Microneurosurgery I (volume. 1)

Microneurosurgery in 4 Volumes

M.G.Yasargil Microsurgical Anatomy of the Basal Cisterns and Vessels of the Brain, Diagnostic Studies, General Operative Techniques and Pathological Considerations of the Intracranial Aneurysms II Clinical Considerations, Surgery of the Intracranial Aneurysms and Results

III Clinical Considerations and Microsurgery of the Arteriovenous Racemose Angiomas

IV Clinical Considerations and Microsurgery of the Tumors Georg Thieme Verlag Stuttgart • New York

Thieme Stratton Inc. New York

V

Acknowledgement

I am deeply indebted to my colleagues Drs. R. D. Smith, P. H. Young and P. J. Teddy for their very capable assistance in writing and reviewing the English manuscript of both volumes. I wish to express my sincere appreciation to Dr. R. D. Smith, New Orleans, who, with the exception of Chapters 6-11, Vol. II, played the initial role of '^Ghostwriter" for the entire manuscript. After detailed discussions with the author concerning the concept and|ayput_of the scheduled monograph and after being presented with the anatomical, pathological, radiological, surgical and clinical aspects, results and statistical material, he composed the primary text for each chapter. Very special thanks go to Dr. P. H. Young, St. Louis, who reviewed and elaborated on the entire manuscript. After detailed discussions and after being presented with statistical material, he also composed the text for Chapters 6-11, Vol. II, and for the figures and illustrations. I am very grateful to Dr. P. J. Teddy, Oxford, who made a final, very careful review of the entire manuscript, made many relevant suggestions and helped to fully restructure the galley-proofs. I appreciate the assistance of Dr. H. J. W. Nauta who wrote the English text concerning the anatomy of perforating arteries, and Dr. Ho and Dr. Slater who elaborated on the English text concerning the anatomy of the middle cerebral artery, Chapter 1, Vol. I. Dr. H.-G. Imhof studied and analyzed Chapter 8, Vol. II. Dr. R. C. Janzer wrote the section of embryology.

Dr. C. Gasser composed Chapter 4, Vol. I, and Dr. M. Curcic, neuroanesthetist since 1977 in my department, reviewed the manuscript and brought it up to date. Mrs. G. Siegenthaler deserves special thanks for her excellent work in controlling the internal medical aspects of treatment. I am very grateful to the assistance of the following colleagues in Zurich, Mrs. M. Fuchs, T. Grauer, M. J. Maraqa, A. Monshi, R. Munch, Mrs. C. Piischel, A. Sarioglu and Mrs. U. Schmid-Sutro for studying the clinical material and presenting some of the statistics. I am convinced that the artistic skills of Mr. P. Roth have enhanced the teaching quality of this publication. The first volume could not have been realized without the generous help of the Institutes of Pathology (Prof. C. Hedinger, Prof. J. R. Riittner, Dr. J. Schneider) and Radiology (Prof. J. Wellauer, Dr. A. Valavanis) and the Department of Surgical Photography (Mr. O. Reinhard) at the University Hospital of Zurich. Very special thanks go to my long-time secretary Mrs. M. Traber who not only typed the whole manuscript, but also performed countless duties related to this project. Finally I would like to thank cordially Dr. h.c. G. Hauff, owner of Georg Thieme Verlag, Stuttgart and his staff especially Mr. R. Zeller and Mr. R. Zepf, for their understanding and cooperation in the preparation and publication of this book.

VI

Preface This book and the succeeding volumes are the product of a rather extraordinary team effort. The team has comprised not only myself and the staff at the University Hospital, Zurich, but also colleagues from all parts of the world too numerous to name who have visited our department for varying lenghts of time over the past sixteen years. Throughout this period all our craniotomies have been performed using microsurgical techniques. The operations have each been displayed on a television monitoring system starting with the drilling of the sphenoid wing and continuing until dural closure. This has allowed close observer participation on every step of the procedure. Discussion during and after surgery and on reviewing the videotapes has stimulated thought, generated research projects and produced many innovative ideas concerning anatomy, clinical problems and techniques which have therefore been constantly evolving throughout the period studied. After carrying out over 4200 microsurgical procedures (1400 for aneurysms, 400 arteriovenous malformations and 2400 cranial and spinal tumors) in the past 16 years I have come to several general conclusions. First, and perhaps the most important, is that in no single case can one totally predict the outcome or peroperative difficulties from either the general or specific condition of the patient or from neuroradiological investigations. Cerebral and extracerebral responses to surgery remain intermittently quite unpredictable and detailed anatomy can only be properly evaluated by microsurgical exploration rather than by X-ray. Secondly, we need to know a great deal more regarding the pathophysiology of events following subarachnoid hemorrhage. In particular we must study the involvement of the cisternal systems, the hemodynamics of the central nervous system, and the reactivity and finer anatomical details of the vessels themselves. It is not only aneurysm location and size which makes for difficult surgery but

the construction of the wall of the sac and the involvement of perforating vessels particularly at the major bifurcations and at the anterior communicating artery. Thirdly, the skill of the individual surgeon still plays a critical role in determining outcome and such skill must embody the concepts of tactic and technique. There is still a common misconception that simply to use a sucker, bipolar coagulation and clips means competence in microsurgery. In fact, these form only the material part of the techniques involved and the real skill has to be learned not just in the operating theatre but by meticulous laboratory training over many months. A further misconception is that the optimally trained microneurosurgeon must have protracted operating experience before he can hope to obtain good results. Previous generations of neurosurgeons have been able to develop their skills by virtue of having large practices but the greatly increased number of trainees today must be provided with modern teaching facilities incorporating slides, tapes and television. A good training in microsurgical technique is no guarantee of success but compared with his macrosurgical colleagues the young neurosurgeon of today should have a much greater opportunity and the distinct advantage of being able to see fine anatomical structures far more clearly. Some colleagues still express doubts as to the real advantage of microsurgery to the patient expecting, for instance, that in some mystical way it may help improve operative results in Grade III-V SAH. The importance and advantages of microtechniques are to be seen best in cases of Grade O-II in whom morbidity rates have, in some hands, reached less than 0.5% even with early operation in many patients. I am convinced that microtechniques are advantageous because they enable one to work in a small gap, minimize trauma to the brain and presumably by reducing retraction and manipulation minimize the "stress"

Preface which may arise in the early days after aneurysmal surgery. I have had the opportunity to develop microsurgical methods and this has led to experience in aneurysm surgery in a considerable number of patients. Over the past three years there has been a gradual decline in the number of cases of ruptured

VII

aneurysm presenting in our clinic. Although this may be due to a variety of factors, I would like to think that the main reason is that colleagues welltrained in microtechniques are now able to successfully take on much of this work themselves. If so, a long-term ambition will have been fulfilled. M. G. Ya$argil

Introduction

Introduction The successful treatment of ity, loss of consciousness, cranial nerve palsies, cerebral aneurysms has become an important contribution by the neu-rosurgeon to patients suffering from cerebrovas-cular disease. The development of an adequate method of treating these lesions demanded first an understanding of the pathogenesis of the lesion itself in order that a diagnosis could be made in life, and subsequently an evolution of the means to perform a delicate surgical procedure that promised both hope for recovery and cure of the lesion. In the 18th century, Morgagni (1761) and Biumi (1778) first described cerebral aneurysms and showed that their rupture might lead to subarachnoid hemorrhage. These observations were not further evaluated until 1859, when Sir William Gull gave recognition to the pathological nature of the lesion with his often quoted statement "Whenever young persons die with ingravescent apoplexy, and after death a large effusion of blood is found, especially if the effusion be over the surface of the brain, in the meshes of the pia mater, the presence of an aneurysm is probable". It is curious that he nevertheless concluded, "Although we may from the circumstances sometimes suspect the presence of aneurysm within the cranium, we have at the least, no symptoms upon which to ground more than a possible diagnosis". The latter half of the 19th century saw considerable investigation into the pathological nature of cerebral aneurysms although clinically, little progress was made. Beadles (1907) addressing the Royal College of Surgeons stated "...the conclusion that I have been forced to draw from a careful study of a large series of cases is, therefore, that it is quite impossible to diagnose an aneurysm of any one of the cerebral arteries except in the most unusual of circumstances. Only two or three have ever been diagnosed in life, and even in these cases it can scarcely be said to have been an absolutely certain diagnosis". Fearnsides (1916) echoed this opinion, although in his analysis of 31 patients who had died of a ruptured cerebral aneurysm, he noted severe headache, nuchal rigid-

hemiparetic syndromes, and papilledema in the clinical histories. It remained for Sir Charles Symonds (1923, 1924) to put together the clinical syndrome of subarachnoid hemorrhage and to stress the importance of ruptured cerebral aneurysm as the most probable etiology. During this era, surgeons occasionally encountered aneurysms during intracranial operations for "tumors" around the sella turcica - a misdiagnosis that can still occur today despite the most advanced radiological methods. Sir Victor Horsley in 1885 is reported to have exposed an aneurysm in the area of the optic chiasm that he treated with bilateral cervical carotid artery ligation (Keen, 1890). Harvey Gushing (1929) in his extensive pituitary tumor experience reported opening an aneurysm and packing it with muscle. More often, though, these lesions were left undisturbed. In such an era of diagnosis by bedside neurological examination combined with investigation only by air contrast encephalography, aneurysms remained lesions that with few exceptions were diagnosed only during incidental operation or at the autopsy table. In 1927, Egas Moniz introduced cerebral angiography to the medical community, and clinicians finally had a method by which cerebral aneurysms could be documented in life. As Dandy (1944) was later forced to admit, "There is no doubt whatever of the excellent demonstrations of aneurysms by this method (cerebral angiography); it is unquestionably the most important, if not the only function that this procedure serves." With the ability to localize the source of subarachnoid hemorrhage, the neurosurgeon could now initiate a coherent plan of operative management. In 1933 Pott brought together the important findings that had been reported in the preceding decade. He presented to the medical and surgical society of Edinburgh a series of eight patients who had undergone angiography with the diagnosis of subarachnoid hemorrhage, describing the location of their aneurysms and reporting his operative

Introduction results. With this work the essential ingredients of cerebral aneurysm surgery were finally defined, i.e. cerebral aneurysms as a common cause of spontaneous subarachnoid hemorrhage, the demonstration of an aneurysm by cerebral angiography, and the possibility of operative treatment for these lesions. Although operations for cerebral aneurysms remained hazardous, reports of intracranial procedures for aneurysm began to appear (Tonnis 1936; McConnell 1937). Krayenbiihl's (1941) monograph described his experience with 31 patients of whom several were treated by carotid ligation and three underwent intracranial procedures. Dandy (1944) subsequently published a series of 108 patients, 30 of whom had undergone intracranial operation. Between 1950 and 1965, neurosurgeons became increasingly committed to the prospect of operative management for cerebral aneurysms. Improvements in operative technique, in anesthesia, and in radiology resulted in many favorable reports of intracranial operative management (Norlen and Olivecrona 1953; Uihlein and Huges 1955; Poppen 1960). However, these reports did not go unchallenged. Other investigators pointed out that the natural history of a ruptured cerebral aneurysm had not been adequately defined and that operations were usually performed only on the more favorable cases; so reports ascribing some benefit to operative treatment might indeed represent only favorable case selection (Magladery 1955; Slosberg 1960; Richardson et al 1966). The difficulty of adequately delineating the natural history of a disease that is both episodic in nature and variable in severity of presentation and that keeps the patient at risk over his lifetime was soon apparent. Nevertheless, considerable progress was made in defining the natural history of intracranial aneurysms and this work will be discussed in the following chapter. With an improved understanding of the nature of cerebral aneurysms, attention could then be directed toward the pathophysiological complications of ruptured aneurysms and the importance of clinical presentation in determining the need and timing of operative therapy. By the middle 1960's it was recognized that the operative management of cerebral aneurysm patients was not producing the significant reduction in morbidity and mortality that had been hoped for. While many neurosurgeons with considerable experience were able to achieve a marked reduction in mortality in favorable cases, larger studies continued to show disappointing mortality and morbidity attending the operative treatment

of these lesions (McKissock et al 1965; Skultety and Nishioka 1966). As a result, other methods of treatment including hypothermia (Botterell et al 1956), proximal occlusion (Logue 1956) coating and wrapping (Dutton 1956; Selverstone 1963) intraluminal thrombosis (Mullan and Dawley 1968) and stereotactic thrombosis (Alksne et al 1965, 1971, 1977, 1980) were tried with varying degrees of success. Along the same lines Serbi-nenko (1974), Debrun et al (1975, 1977, 1981), Taki et al (1979), Mullan et al (1980) and Romo-danov and Shcheglov (1982) used detachable ballon catheters to successfully treat a variety of intracranial aneurysms. It became evident that the morbidity associated with the surgical treatment of aneurysms was to some degree related to a variety of technical difficulties encountered during these procedures, including the close proximity of the lesion to vital structures at the base of the brain, the frequent formation of adhesions between the aneurysm and jhe jT^ejv^jvesse^pgrforating arteries or other adjacent structures, and the propensity of the lesions to rupture during manipulation. To overcome these difficulties it seemed reasonable that the operating microscope and microsurgical methods might prove helpful by allowing more accurate dissection and control of these lesions. The operating microscope would also, perhaps, give the neurosurgeon a. chance to avoid significant brain retraction that all too often produced premature rupture of the aneurysm or created spasm in neighboring small vessels. Additionally the microscope would provide the neurosurgeon with a well-illuminated binocular view of the aneurysm in the depths of a narrow operating field, and when combined with microsurgical techniques, further damage to an already compromised brain would be minimized. Early reports of the application of microsurgical techniques to intracranial aneurysms were not disappointing (Kurze 1964; Adams and Witt 1964; Pool and Colton 1966; Rand and Jannetta 1967). Subsequent series of patients (Guidetti 1973; Adams et al 1976; Pia 1976) operated upon using the microscope confirmed the better results achieved with this method. At a conference in Giessen, Germany in 1977, several distinguished neurosurgeons in the field of aneurysm surgery presented their operative techniques and results (Pia et al 1979). It was apparent then that the benefits of the microsurgical approach to the aneurysm surgery were finally becoming appreciated. Still, the use of the microscope remained individually variable with many aneurysm surgeons employing it only briefly

Introduction during an otherwise classical operation. Therefore .jntelligible_ comparisons of microscopic and classical approaches remained impossible. In 1979 Suzuki reported excellent surgical results in over 1000 aneurysm patients undergoing operation without microsurgical techniques. While there is no question that a few accomplished neu-rosurgeons with a wealth of clinical material can achieve a high standard of operative results with classical or other ^sophisticated approaches to aneurysm surgery, for most neurosurgeons, there nevertheless remains the need of a comprehensive plan of operation fully utilizing the benefits of the microsurgical technique; a plan that incorporates microsurgical principles into the entire procedure from craniotomy to closure. The main principle of microneurosurgery is the ability of the surgeon to perform all the necessary manipulations through a small "key-hole" approach. For the mastery of tactics and techniques of this "key-hole" surgery it is absolutely necessary to be familiar with a new perspective of the anatomy of the cisternal and neurovascular systems. The former techniques of neurosurgery allowed one to perform explorations mainly in subduraltranscerebral approaches whereas the microtechnique enables the neurosurgeon to dissect and expose cerebral aneurysms, arteriovenous malformations and tumors in a natural pathway within the subarachnoidal cisterns, presenting all important surrounding structures, especially the cerebrovascular system in stereoscopic deep sharp focus. The subarachnoidal cisterns are the road-

maps for microneurosurgeons. Taking this very important fact into consideration a chapter of 50 pages in Volume I is devoted to cisternal anatomy. Furthermore, our knowledge concerning the anatomy of the neurovascular system is still not fully completed. Despite the many contributions of the anatomist, pathologist, neurosurgeon and stereotactic surgeon towards an understanding of the cerebral vasculature, the operative microscope provided the microsurgeon with a new approach / for detailed study of the living brain vasculature. ' During microsurgical operations for intracranial' aneurysms, arteriovenous malformations and tumors considerable effort has been made in the present series of patients to delineate the anatomy of the cerebral vasculature in order to familiarize the surgeon with the various anomalous configurations often encountered with other anatomical works. Volume I will present anatomical, neuroradiologi-cal, operative, neuroanesthetic and pathological considerations. The second volume will deal with clinical considerations, early and late results of operated intracranial aneurysms at different locations in 1312 patients, the problems and results in cases with giant and multiple aneurysms, the results of nonoperated cases and finally the complications of aneurysm surgery. Volume III and IV will present microsurgery of arteriovenous malformations and tumors.

Contents Acknowledgement Introduction

1 Operative Anatomy Subarachnoid Cisterns . . . . . . . . . . . . . .

5

Introduction . . . . . . . . . . . . . . . . . . . . . Early Anatomists . . . . . . . . . . . . . . . . . Neuroradiology and Modern Anatomists . . Embryology of Meningeal Development . . . Microneurosurgical Observations . . . . . . . Compartmentalization . . . . . . . . . . . . Intracisternal Arachnoidal Trabeculation . Cisternal Junctions . . . . . . . . . . . . . . . Apposition of Arachnoid and Ependyma . Pathological Thickening and Reduplication of Arachnoid . . . . . . . . . Relationship to Pathological Processes . . Normal Cisternal Anatomy. . . . . . . . Supratentorial Cisterns . . . . . . . . . . . . . . Anterior (Parasellar) . . . . . . . . . . . . . Lateral (Parapeduncular) . . . . . . . . . . . Posterior (Tentorial Notch) . . . . . . . . . Superior (Callosal) . . . . . . . . . . . . . . . Infratentorial Cisterns . . . . . . . . . . . . . . Anterior . . . . . . . . . . . . . . . . . . . . . Lateral . . . . . . . . . . . . . . . . . . . . . . Posterior . . . . . . . . . . . . . . . . . . . . .

5 5 12 13 14 14 20 20 20 23 23 25 26 26 39 46 46 47 47 49 52

Intracranial Arteries. . . . . . . . . . . . . 54 Introduction . . . . . . . . . . . . . . . . . . . . . Internal Carotid Artery . . . . . . . . . . . . . Ophthalmic Artery . . . . . . . . . . . . . . . Superior Hypophyseal Arteries . . . . . . . Posterior Communicating Artery . . . . . . Anterior Choroidal Artery . . . . . . . . . . Dural Artery of Internal Carotid Artery . Middle Cerebral Artery . . . . . . . . . . . . . Superior Lateral Group or Temporal Vessels . . . . . . . . . . . . . . . . Inferior Medial Group or " Lenticulostriate or Striate Vessels" . . . Middle Cerebral Bifurcation . . . . . . . . . Anterior Cerebral Artery Complex ...92 Proximal Anterior Cerebral Artery . . . . Anterior Communicating Artery . . . . . . Distal Anterior Cerebral Artery .... . . . . . Vertebrobasilar System . . . . . . . . . . . . . Vertebral Artery . . . . . . . . . . . . . . . . Basilar Artery . . . . . . . . . . . . . . . . . .

54 56 60 60 60 66 70 72 73 77 84 92 99 116 128 128 131

Perforating Arteries to the Basal Ganglia and Brain Stem

I. Basal Perforation Zones . . . . . . . . . . . 145 la. Anterior Perforated Substance and Extensions: Anterior Perforation Zone . 145 Ib. Posterior Perforated Substance and Extensions: Posterior Perforation Zone . 151 Ic. Pontine Perforation Zone . . . . . . . . 155 Id. Basal Medullary Perforation Zone .. 155 II. Dorsal Perforation Zones . . . . . . . . . . 158

3 General Operative Techniques. . . . .

Ila. Dorsal Midbrain Perforation Zone . lib. Dorsal Thalamic Perforation Zone . Cerebral Veins . . . . . . . . . . . . . . . . . . Parasellar Area . . . . . . . . . . . . . . . . . . . Dorsal Mesencephalic Area . . . . . . . . . . . Ventrolateral Posterior Fossa . . . . . . . . . . The Inferior Surface of the Frontal Lobe . . .

158 162 165 165 165 165 168

2 Diagnostic Studies. . . . . . . . . . . . . Lumbar Puncture . . . . . . . . . . . . . . . . . Xanthochromia . . . . . . . . . . . . . . . . . Uniformity of Blood Concentration . . . . 169 Cellular Changes . . . . . . . . . . . . . . . . 169 Increased Pressure . . . . . . . . . . . . . . . Electroencephalography (EEG) . . . . . . . . Radiological Investigation . . . . . . . . . . . . Background . . . . . . . . . . . . . . . . . . . Plain Skull Radiography . . . . . . . . . . . Pneumoencephalography . . . . . . . . . . . Radioisotopic Brain Scan . . . . . . . . . . . Radioisotopic Cisternography . . . . . . . . Digital Subtraction Angiography . . . . . . Positron Emission Tomography . . . . . . . Nuclear Magnetic Resonance . . . . . . . . Cerebral Angiography . . . . . . . . . . . . . . Method of Angiography . . . . . . . . . . . General Information Derived from Angiography . . . . . . . . . . . . . . . . . . .

169 169

169 170 170 170 170 170 171 171 171 171 171 171 171

172 Specific Technical Details for Given Aneurysms Internal Carotid Artery Aneurysms . . . . 182 Middle Cerebral Artery Aneurysms . . . . 184 Anterior Cerebral-Anterior Communicating Artery Aneurysms . . . . 184 Upper Basilar Artery Aneurysms . . . . . . 187 Vertebrobasilar Aneurysms . . . . . . . . . 187 Diagnostic Difficulties in Cerebral Angiography Anatomical Problems . . . . . . . . . . . . . 188 Inadequate Clinical Information . . . . . . 188 False Positive Angiography (Negative Exploration) . . . . . . . . . . . . 189 Unexpected Location of Aneurysm . . . . 190 Equivocal Angiograms (Positive Exploration) . . . . . . . . . . . . . 192 Discussion . . . . . . . . . . . . . . . . . . . . 193 Multiple Aneurysms with one or more Unrecognized Angiographically . . . . . . 195 Postoperative Angiography . . . . . . . . . 195 Complications of Angiography . . . . . . . 196 Rupture of Aneurysm During Angiography . . . . . . . . . . . . . . . . . . . 198 Computerized Tomography Method of Computerized Tomography . . 199 Information Derived from Computerized Tomography: Identification of Aneurysm . 199 Pitfalls of Computerized Tomography . . . 205 Timing of Radiological Procedures . . . . . . 206 Apparatus and Instruments . . . . . . . . . . . 208 Operating Microscope . . . . . . . . . . . . . . 208 Optical Principles . . . . . . . . . . . . . . . . 208

Lighting System . . . . . . . . . . . . . . . . . Microscope Stand . . . . . . . . . . . . . . . . Accessories to the Microscope . . . . . . . . Microsurgical Instrumentation . . . . . . . . . Stability . . . . . . . . . . . . . . . . . . . . . . Mobility . . . . . . . . . . . . . . . . . . . . . . Post-Operative Care of Instruments . . . . Aneurysm Clips . . . . . . . . . . . . . . . . . Temporary Vascular Clips . . . . . . . . . .

208 210 210 210 211 211 212 212 213

Operating Room Organization. . . . . . . . . 213

Personnel . . . . . . . . . . . . . . . . . . . . . . 213 Operating Room Lay-Out . . . . . . . . . . . . 214 Operative Approach. . . . . . . . . . . . . . . 215 Interfascial Pterional (Frontotemporosphenoidal) Craniotomy . . 215 Position of the Patient . . . . . . . . . . . . . 215 Draping . . . . . . . . . . . . . . . . . . . . . . 217 Incision . . . . . . . . . . . . . . . . . . . . . . 217 Interfacial Temporalis Flap . . . . . . . . . 217 Craniotomy . . . . . . . . . . . . . . . . . . . 220 Other Craniotomies. . . . . . . . . . . . . . . 234 Anterior Paramedian Frontal Craniotomy . . . . . . . . . . . . . . . . . . . 234 Combined Frontal Paramedian and Pterional Craniotomy . . . . . . . . . . . . . 236

Subtemporal Craniotomy . . . . . . . . . . . 237 Lateral Suboccipital Craniotomy . . . . . . 238 Variations . . . . . . . . . . . . . . . . . . . . 239 Occipital Craniotomy . . . . . . . . . . . . . 244 Aneurysm Clipping . . . . . . . . . . . . . . . . 245 Preparation . . . . . . . . . . . . . . . . . . . 245 Microtechniques of Aneurysm Obliteration 260 Stepwise (Staging) Elimination of Aneurysm Sac . . . . . . . . . . . . . . . . . . 260 Efficacy of Clipping . . . . . . . . . . . . . . 263 Summary . . . . . . . . . . . . . . . . . . . . . 264 Alternative Methods of Aneurysm Treatment Cervical Carotid Artery Ligation . . . . . . 265 Intracranical Parent Artery Ligation and Trapping Procedures Aneurysm Ligation . . . . . . . . . . . . . . . 265 Wrapping and Coating Techniques . . . . . 265 Microsurgical Vascular Repair and Anastomosis Induced Thrombosis and Internal Occlusion . . . . . . . . . . . . . . . . . . . . . 266 Special Operative Problems . . . . . . . . . . . 267 Multiple and Bilateral Aneurysms . . . . . 267 Giant Aneurysms . . . . . . . . . . . . . . . . 268 Intraoperative Rupture . . . . . . . . . . . . 269 Intraoperative Vasospasm . . . . . . . . . . 271 Summary of Methods Applied in the Current Series271

5 Pathological Considerations. . . . . .

4 Anesthesia for Microsurgical Procedures in Neurosurgery Introduction . . . . . . . . . . . . . . . . . . . . . 272 Anesthetic Principles and Pharmacological Considerations Preoperative Care . . . . . . . . . . . . . . . 273 Premedication . . . . . . . . . . . . . . . . . . 273 Induction of Anesthesia . . . . . . . . . . . . 273 Maintenance of Anesthesia . . . . . . . . . 274 Brain Relaxation . . . . . . . . . . . . . . . . 274 Postoperative Care . . . . . . . . . . . . . . . . 275 Induced Hypotension . . . . . . . . . . . . . . . 275 Deliberate Hypotension Induced by Halothane . Deliberate Hypotension Induced with Trimetaphan Induced Hypotension with Sodium Nitroprusside Hypothermia . . . . . . . . . . . . . . . . . . . . 277 Vertebro-Basilar Aneurysms . . . . . . . . . . 277 Anesthetic Management of Posterior Fossa Microsurgery in the Sitting Position . . . . . . 277 Premedication . . . . . . . . . . . . . . . . . . 277 Cardiovascular and Respiratory Complications Monitoring and Air Embolism . . . . . . . 278 Cranial Nerve Examination . . . . . . . . . 278 Postoperative Care . . . . . . . . . . . . . . . 278

Epidemiology of Cerebral Aneurysms . . . . 279

Incidence . . . . . . . . . . . . . . . . . . . . . . Classification . . . . . . . . . . . . . . . . . . . . I. Saccular Aneurysms . . . . . . . . . . . . II. Other Types of Cerebral Aneurysms . Infectious (Mycotic) Aneurysms . . . . Traumatic Aneurysms . . . . . . . . . . Dissecting Intracranial Aneurysms . . Arteriosclerotic Ectatic Aneurysms . . Aneurysmal Enlargement . . . . . . . . . . Distribution . . . . . . . . . . . . . . . . . . . . . Location of Cerebral Aneurysms . . . . . .

279 280 280 281 281 282 285 285 295 299 299

Latoatity . . . . . . . . . . . . . . . . . . . . .

299

Age . . . . . . . . . . . . . . . . . . . . . . . . 299 Sex . . . . . . . . . . . . . . . . . . . . . . . . . 300 Multiplicity . . . . . . . . . . . . . . . . . . . . 301 Familial Occurrence of Cerebral Aneurysms 304 Occurrence with a Described Hereditary Syndrome Coarctation of the Aorta . . . . . . . . . . . 304 Ehlers-Danlos Syndrome . . . . . . . . . . . 304 Pseudoxanthoma Elasticum . . . . . . . . . 304 Friedreich's Ataxia . . . . . . . . . . . . . . . 304 Hypertension . . . . . . . . . . . . . . . . . . 304 Fibromuscular Dysplasia . . . . . . . . . . . 305 Occurence without a Described Hereditary Syndrome Associated Vascular Anomalies . . . . . . . . 306 Development Abnormalities . . . . . . . . . 306 Persistent Carotid-Basilar Anastomosis . . 306

Persistent Hypoglossal Artery . . . . . . . . 306 Proatlantal Intersegmental Artery . . . . . 307 Agenesis and Aplasia of the Internal Carotid Artery . . . . . . . . . . . . . . . . . 307 Accessory Middle Cerebral Artery . . . . . 308 Fenestration and Duplication . . . . . . . . 308 Arteriovenous Malformation . . . . . . . . 309 Coincidental Association of Aneurysm and Occlusive Vessel Diseases . . . . . . . . 313 Moya-Moya Disease Associated with Aneurysms Association of Brain Tumor and Cerebral Aneurysm Pathology of Saccular Aneurysm Formation and Rupture . . . . . . . . . . . . . . . . . . . . . 321 Natural History of Ruptured Cerebral Aneurysms Mortality and Morbidity . . . . . . . . . . . 324 Necropsy of Fatal Aneurysm Rupture . . . 325 Spontaneous Thrombosis of Cerebral Aneurysms Pathophysiological Complications of Ruptured Cerebral Aneurysm . . . . . . 334 Hematoma Formation . . . . . . . . . . . . . 334 Subdural Hematoma . . . . . . . . . . . . . . 334 intracisternal Hematoma . . . . . . . . . . . 336 Intracerebral Hematoma . . . . . . . . . . . 336 Intraventricular Hematoma . . . . . . . . . 342 Cerebral Ischemia and Infarction . . . . . . . 342 Vasospasm . . . . . . . . . . . . . . . . . . . . . 343 Prolonged Chronic Spasm or Narrowing of Arteries . . . . . . . . . . . . . . . . . . . . . . 343 Our Observations . . . . . . . . . . . . . . . . 344 Hypothalamic Injury . . . . . . . . . . . . . . 345 Cerebral Edema . . . . . . . . . . . . . . . . . . 345 Ventricular Dilatation and Communicating Hydrocephalus Unexplained Subarachnoid Hemorrhage . . 347

References

Operative Anatomy

1 Subarachnoid Cisterns

Early Anatomists

Introduction Although many of the clinical pathophysiological processes occurring in the subarachnoid space have been well described (i.e. subarachnoid hemorrhage, meningitis, circulatory disturbances of CSF, tumors, AVM's etc.), it is surprising that an accurate topography of the basal cisterns has jnot been adequately worked out.] Knowledge of 1 the neural and vascular contents of each of the basal cisterns is of particular value to the neurosurgeon in the planning and execution of intracranial procedures. The neurosurgeon may chart his intracranial approach like a road map in terms of • the basal cisterns. Many of the subarachnoid cisterns can be considered to be anatomically distinct compartments, but others are not, these being separated from each other by a porous trabeculated wall with various sized openings. Under normal circumstances this permits a continuous exchange of CSF from one compartment to another. These apertures can become plugged and partially or totally obliterated after subarachnoid hemorrhage, infectious meningitis, chemical meningitis, (e.g. craniopharyngioma) spread of malignant cells in the subarachnoid space (e.g. carcinomatous meningitis) and spread of proteinaceous exudate (e.g. meningioma, acoustic neuroma), thus hindering the normal CSF circulation. At surgery the release of CSF from the basal cisterns provides a quick effective reduction of cerebral volume and facilitates the intracranial approach. A good example of this is the opening of the lateral cerebello-medullary cistern prior to exploration of tumors, aneurysms, and angiomas in the cerebello-pontine angle. Similarly, the Sylvian, carotid, chiasmatic and interpeduncular cisterns are opened for approaches to aneurysms and parasellar tumors.

While Galen and Vesalius had made general reference to membranes over the brain in 1555 Blaes (Blasius) is credited with naming of the arachnoid in 1666. Vieussens (1690) noted that the pia and arachnoid existed as two separate membranes, and Ruysch (1697) showed that the arachnoid extended over the convexities of the brain. Pac-chioni (1729) recognized fluid around the brain, but this was considered by others to be a pathological condensation until Cotugno (1770) verified the normal presence of cerebrospinal fluid. In 1802, Bichat proposed that the arachnoid formed a serous cavity similar to the peritoneal cavity. He felt the arachnoid cavity communicated with the ventricular system by extensions of the arachnoid • into the ventricles. Magendie (1822) gave the first modern description of the subarachnoid space as containing cerebrospinal fluid that circulated under pressure and was intercommunicating in all areas. He described the basal cisterns and the extensions of the arachnoid along cranial nerves II, V and VIIVIII. His ideas were accepted by anatomists of the nineteenth century (Kolliker 1850; Virchow 1854; Luschka 1855; Quain 1844), and are generally considered valid today. In 1875, Key and Retzius published a monumental work in which they presented drawings of the subarachnoid space that had been injected with blue dye (Berliner-Blau) to demonstrate the extensions and divisions of the subarachnoid system (Fig 1A). They were able to demonstrate that the subarachnoid space, although intercommunicating, is also compartmentalized. They showed the relationship of the cerebral vessels to the arachnoid and the numerous trabeculae which suspend these vessels from the walls of the cisterns. This outstanding study remains valid today, although an appreciation of the importance of these findings for neurosurgery had to await the introduction of the operating microscope (Figs 1BK)

6

1 Operative Anatomy

Fig 1 A This original figure from the monograph (1875) by Key and Retzius shows the ventricular, arachnoid, and cislernal spaces outlined by Berliner Blue.

Early Anatomists g 1 B This precisely drawn picture depicts a dissection of Tie basal cisternal compart"lents. including the olfactory, gitasmatic. SyMan, carotid, in'.erpedLincular, crural, prepontine. cerebellopontine, and an_terior spinal cisterns.

Fig 1 C Dissection of the interpeduncular cistern with its trabeculae invaginating the pia mater of the ventral pons.

8

1 Operative Anatomy Fig 1 D Dissection of the cerebellopontine, lateral cerebellomeduilary and anterior medullary cisterns.

--.a'

Fig 1 E A perfect depiction of the perimesencephalic cisterns (the interpeduncular, ambient, and quadriqeminal).

\'in !•

Early Anatomists Fig 1 F Incresed density of fibers around the Galenic vein.

FigIG A unique representation of the completely dissected lamina terminalis cistern. Chiasmatic cistern closely surrounding the optic nerves.

9

10

1 Operative Anatomy Fig 1H An illustration of the perioptic cistern, extending along the optic nerve within its sheath.

Fig 1 i Arachnoidal compartments in a sulcus and dense organization of the fibers around the artery.

Early Anatomists - g 1J Arachnoid fibers within the sulcus.

Fig 1 K A microscopic representation of arachnoid trabeculae from the work of Key and Retzius. Arachnoid trabeculae from different areas are composed of differing fiber organizations.

The figures (1 A-K) have been taken from the excellent monograph by Key and Retzius (Stockholm 1875). This two volume masterpiece contains several hundred extremely accurate pictures and it should be consulted for further details.

11

12

1 Operative Anatomy

Neuroradiology and Modern Anatomists j l n 1919 Dandy described the injection of air into ' the lumbar subarachnoid space in order to outline the cerebral ventricles. While it was seen that the basal subarachnoid cisterns were also demonstrated in this manner, attention was primarily fixed on the size and shape of the ventricles. Locke and Naffziger (1924) undertook a corrosion cast study of the subarachnoid cisterns in dogs and humans, and demonstrated the shapes and intercommunications of the subarachnoid space. They gave general names to the subarachnoid cisterns, and admitted that the finer points of the system had probably not been demonstrated by this method. Vital dye studies and a somewhat different classification were reported by Spatz and Stroescu (1934). In 1937, Davidoff and Dyke published a textbook on the normal pneumoencephalogram in which they discussed the shape and extension of the subarachnoid cisterns in some detail. Corrosion casts had displayed the subarachnoid system as freely intercommunicating while fractional pneumoencephalography suggested more j:om-partmentalization of the subarachnoid space. Liliequist (1959) employed both techniques to provide a working normal anatomy of the subarachnoid space. For the most part he used the terminology of Key and Retzius to name the cisterns. Since this monograph, several radiological and anatomical papers have discussed the subarachnoid space (Epstein 1965; Wilson 1972; Lang 1973), but little attention was directed toward the subarachnoid cisterns. The relationship of the fine structure of the subarachnoid cisterns to subarachnoid hemorrhage was discussed by Arutiunov and associates^ 1974), and electron microscopic studies oftne intricate pattern of membranes and fibers which form this system were reported by Andres (1967), Alien and Low (1975), Suzuki et al (1977, 1979), Barrio-nuevo et al (1978), and Julow et al (1979). The anatomical relationship of the dura and arachnoid was disputed for many years (Clara 1953; Pease and Schultz 1958; Ham 1974), until the advent of microsurgical procedures, where the careful elevation of the dura under magnification revealed multiple, fine reticular attachments between the jfeiia and arachnoid.. This observation provided" the impetus_for Schachenmayr and Friede (1978) to develop a technique for the in situ fixation of human meninges in order to finally document the ultrastructure of the dura-arachnoid interface.

Their results refuted the existence of a subdural jjpace (real or potential). They concluded that all disease processes originally thought to exist in this space, occur in a cleavage plane within the innermost layer of cells of the dura (what are termed "dural border cells") (Fig 2)._____________ Many other questions remain to be answered about the structure and function of the leptome-ningeal arachnoid membrane. Unresolved problems, such as the role of epithelial cells and the importance and tensile strength of elastic bands (Fig IK) in the arachnoid need to be studied further, and would be of interest to the neurosur-geon. Some of these questions may eventually find answers in electron microscopic studies of the arachnoid similar to the one described above. Interface layer

DURA MATER Subarachnoid space Dense collagenous Trabecula

Fig 2 Typical relationship existing at the dura-arachnoid interface (For more detail consult the publication by Friede and Schachenmayr, Amer. J. Path. 1978). __

Embryology of Meningeal Development 1 3

Embryology of Meningeal Development The brain and spinal cord are enclosed within membranous structures collectively known as meninges. They are commonly subdivided into Pachymeninx (Dura mater) and Leptomeninx (Arachnoidea and Pia mater). Anatomical organization and development of these different parts of the meninges show considerable species-dependent differences. Findings in other species cannot be extrapolated to humans without reservation. Sensenig (1951) has described 75 human embryos and fetuses at the Carnegie Institute of Embryology most thoroughly, but ultrastructural investigations of the human meningeal development are still lacking. At Carnegie stage XI (gestational age (days) 23-26; 2.5-4.5 mm CR) a single layer of cells is first seen along the lateral aspect of the primitive neural tube. These cells are continuous with and probably derived from the neural crest. This layer participate in the later formation of the intima pia. In stage XII (gestational age (days) 26-30; 3-5 mm CR) vascularization begins in tissues around the neural tube and in stage XV (35-38 days, 7-9 mm CR) the neural tube is completely surrounded by developing vessels. At the same time a loose, sparsely cellular area lying between the neural tube, somites and notochord is descernible. This mesoderm derived tissue is called meninx pri-mitiva. At stage XVI (37-42 days, 8-11 mm CR) the meninx primitiva has surrounded the neural tube. It has contributed to the single cell layer adjacent to the neural tube, which is now continuous and represents the primitive intima pia. Laterally the meninx primitiva is adjacent to the vertebral primordia. At stages XVII-XVIII (42-48 days; 11-17 mm CR) vascular channels penetrate the neural tube, carrying cells of the intima pia and meninx primitiva as their adventitia. At certain sites the second component of the pia mater, the epipial tissue, forms as a stratified cell layer upon the single cell layer of the intima pia. At stage XIX-XX (48-53 days; 16-22 mm CR) the meninx primitiva begins to cavitate. The outermost part of the cavitated meninx primitiva forms a compact layer, which correspond to the dura mater. At this stage, it is in continuity with the perichondrium of the vertebrae, which are already chondrified. At cranial levels, there will never be a separation of these two layers, but in the spinal cord an epidural space begins to form at stage

XXIII (56-60 days; 27-31 mm CR). This corresponds to the end of the embryonic period of development. With the cavitation of the meninx primitiva a primitive subarachnoid space is formed before any arachnoid is identifiable with certainity. The sequence of arachnoid development is much less certain than the above mentioned development of the dura mater and pia mater. From the sparse data available on humans it can be said that it probably develops from the inner aspect of the dura, that it is of mesodermal origin, and that it is the last of the three meninges to differentiate. A recent ultrastructural study (Schachenmayr and Friede 1978) of adult human meninges has shown that there is no subdural space, but a complex tight layer of cells, the interface layer, composed of the innermost portion of the dura mater (the dural border layer) and the outermost portion of the arachnoid (the arachnoid barrier layer) (see Fig 2). The exact embryological development of these ultrastructurally defined subdivisions of dura mater and arachnoidea is not yet elucidated. The formation of the basal cisternae is correlated with a total regression of the arachnoid trabecu-lae. The cisterns are formed by the end of the embryonic stages, at the same time as the foramen of Magendie.

14

1 Operative Anatomy

Microneurosurgical Observations The operating microscope has provided a unique opportunity for the observation of the subarach_noid spacf in vivo under close to physiological conditions with the chance to note fine anatomical details. An important contribution of the operating microscope and microsurgical technique to neurosurgery has been a better understanding of the important role of the subarachnoid cisterns in I the dissection and exposiirePof" cerebTaT d£eu-| rysms, arteriovenous malformations, and tumors. • It has been recognized that the subarachnoid space and, in particular, the cisterns, can provide a natural pathway for dissection that preserves all important brain structures and have an important relationship to the cerebrovascular system. The observations presented here are based on i over 4200 intracranial and spinal procedures and i 200 cadaver dissections performed under the , microscope by the senior author (MGY). During the early stages, there was developed this operative concept of utilizing the subarachnoid cisterns as natural pathways for the surgeon, thus providing easier access to deep brain structures and allowing operation on a variety of pathological lesions. Particular attention was directed toward the topography of the cisterns and associated arachnoidal adhesions and trabeculae in operative approaches to intracranial aneurysms, vascular malformations, and a variety of basal tumors, such as gliomas, meningiomas, neurinomas, craniopharyngiomas, epidermoids, and chordomas. The pathophysiological effects of these processes on the cisterns were carefully observed and recorded on 35 mm slides, movies, video tapes and sketches.

Compartmentalization The traditional view of the subarachnoid space as a freely communicating channel for the flow of cerebrospinal fluid around the cerebral-spinal axis and between the arachnoid and pia is inadequate to explain the findings at operation. The arachnoid partitions the subarachnoid space into relatively discrete chambers. Sheets of arachnoid form the walls of the cisterns whicri_ retard, and perhaps direct the flow of cerebrospinal fluid. Thus the opening of one subarachnoid cistern does not allow the immediate egress of fluid from the adjoining cisterns and collapse the entire sub-arachnoid space. The arachnoid and pia can be considered connective tissue rather than mesothelial elements. This

connective tissue forms fibers and trabeculae that bridge the subarachnoid space and are continuous with the adventitia of vessels within the subarachnoid space. The arachnoid fibers and membranes are in fact, noted to be regularly thicker and tougher where the arteries pass through the trabeculated wall from one cisternal compartment to another. ____________________. These barriers to cerebrospinal fluid flow are seen in numerous locations, providing a rationale for naming them as individual subarachnoid cisterns. For example, at pneumoencephalography air is often prevented from ascending into the subarachnoid space around the optic chiasm by a well developed bridge of arachnoid (Liliequist 1959) thus forming a wall between cisterns differentiated as interpeduncular and chiasmatic (Key and Ret-zius 1875; Epstein 1965). Undoubtedly the more fragile cisternal boundaries are partially destroyed by corrosion techniques, and autopsy studies are limited by the difficulty in avoiding disruption of the subarachnoid system on removing the brain and by autolysis after death. Microsurgical operations have thus provided a new, previously unobtainable look at the Compartmentalization of the , basal subarachnoid cisterns as they remain distended with cerebrospinal fluid and to some extent' remain in their natural physiological state. It is to • be expected that the degree of competence of the walls between cisterns varies with the individual patient and with the effects of the disease process. In addition some cisterns are easily accessible for observation while others can be only partially explored at operation. Some correlation with radiological information is therefore required to develop an overall concept of Compartmentalization within the subarachnoid space (Figs 3A-C, 4A-B).

Microneurosurgical Observations

15

iry cistern————-^ Premedullary cistern-Fig 3 A Schematic representation of the cisterns in lateral view, which can also be demonstrated on contrast CTscan.

16

1 Operative Anatomy

Fig 3B-C Schematic representation of the basal cisterns as observed during microsurgical procedures and inforrnalin-fixed brains. B The relationship between the basal cisterns (Arabic numbers) and the cranial nerves {Roman numerals).

1 Olfactory cistern 2a Callosal cistern 2b Lamina terminalis cistern 3 Chiasmatic cistern 4 Carotid cistern 5 Sylvian cistern 6 Crural cistern

7 Interpeduncular cistern

8 9 10 11

Ambient cistern Prepontine cistern Superior cerebellar-pontine cistern Inferior cerebeliar-pontine cistern (lateral cerebellomedullary) 12 Anterior spinal cistern 13 Posterior spinal cistern

Microneurosurgical Observations

ant.cho. a. p.c.{P,)

V.a. PICA

A.sp.

3C The relationship between the basal cisterns (Arabic numbers) and the ventral cerebral arterial system.

A

= A! + A2 + Anterior communicating artery

ex MCA ICA p.co.a. ant.cho.a. p.c. (PT)

B = = = = =

Middle cerebral artery Internal carotid artery posterior communicating artery anterior choroidal artery posterior cerebral artery

sea compl AICA V.a. PICA A.sp.

= = = = =

superior cerebellar artery Basilar artery anterior inferior cerebellar artery Vertebral artery posterior inferior cerebellar artery anterior spinal artery

17

18

c

1 Operative Anatomy

D Fig 4 A-D Perioptic and basal cistern visualized by computed tomography with dye injection.

Microneurosurgical Observations 1 9

ICA

sup.tr. MCA MCABi.

Fig 4 E

Schematic representation of the basal cistern seen on Fig 4 A-D.

A3 ICA sup.tr. MCA MCABi. inf.tr. MCA ant.ch. p.co.A.

= = = = = = =

A2 segment Internal carotid artery superior trunk of MCA MCA Bifurcation inferior trunk of MCA anterior choroidal artery posterior communicating artery

P!

P2

= P, segment = P2 segment

Hip.

= Hippocampus

Ba.Bi.

= Basilar Bifurcation

Pa

= P3 segment

P«

= PA segment

20

1 Operative Anatomy

Intracisternal Arachnoidal Trabeculation Numerous connective tissue strands bridge the subarachnoid space adhering to, and supporting, the vessels and nerves within the cisterns (Fig 5AE). The cisterns vary in the strength and density of these trabeculae. Key and Retzius (1875) presented the relationship of the arachnoid trabeculae to cerebral vessels in elaborate detail. Mayet (1965) found neural elements including complicated nerve endings within the arachnoid and arachnoid trabeculae of the cisterna magna of man. The shape of these nerve endings in the arachnoid was variable but complex end formations such as knobs, loops, varicosities, and fine baskets up to 1 mm in length were found in the trabeculae. It was concluded that these nerve endings might convey information about the cere-brospinal fluid pressure. Arutiunov et al (1974) described similar nerves within the trabeculae and felt that they might relate to cerebral vasospasm. Hirano and associates (1976) found capillaries in the arachnoid trabeculae of the rat, and tiny vessels over the posterior wall of the cisterna magna have been seen in man during microneurosurgical operations (see Figs 5B and 35).

Cisternal Junctions There are some areas where several cisterns come together. At these points there are though reinforcements of the arachnoid fibers that hold the neural and vascular structures firmly_in position. These areas are important surgical landmarks and provide a key to understanding the subarachnoid space. The cisterns will be discussed in detail in the following pages, but the junction points will be mentioned briefly here: Parasellar Area Above the internal carotid artery bifurcation is a confluence of the carotid, chiasmatic, olfactory, lamina terminalis, Sylvian, crural and interpeduncular cisterns. Thickened bands of arachnoid run across the origins of the anterior and middle cerebral arteries from the area of the olfactory trigone to the lateral optic nerve and mesial temporal lobe. Additional thickened fibers are closely applied between the posterior communicating artery and oculomotor nerve as both pierce the interpeduncular cistern, and between the anterior choroidal artery and the mesial temporal lobe as the carotid and crural cisterns meet. This forms a triangle of firm arachnoid fibers joining the posterior communicating artery, anterior choroidal artery, and oculomotor nerve.

Foramen of Luschka At the foramen of Luschka is a confluence of the lateral cerebellomedullary, cerebellopontine, premedullary and prepontine cisterns and the lateral recess of the fourth ventricle. The flocculus of the cerebellum is just above this junction and the choroid plexus of the fourth ventricle is frequently visible. The pontomedullary sulcus is medial and from this point cranial nerves VII and VIII run superolaterally, while cranial nerves IX and X run inferolaterally. Pineal Area Above the pineal gland is a confluence of the superior cerebellar, quadrigeminal, ambient, pericallosal and velum interpositi cisterns. This is near the area of the tentorial notch posterior to the quadrigeminal plate. The posterior cerebral and superior cerebellar arteries approach the midline in this area, and the internal cerebral veins, basal veins of Rosenthal, pericallosal veins, and occipital veins converge to form the great vein of Galen.

Apposition of Arachnoid and Ependyma In certain areas of the brain, the subarachnoid space and ventricular system are in close approximation. Knowledge of these areas helps in understanding the general plan of the subarachnoid space, and may be of some therapeutic importance. \ Lamina Terminalis The lamina terminalis cistern and the third ventricle are separated by this thin membrane which contains also neural elements. A small venous plexus is usually found in this area (Duvernoy et al 1969). Choroid Fissure The crural cistern and the temporal horn of the laterale ventricle are separated only by the arachnoid and a single pial layer as the anterior and lateral posterior choroidal arteries enter the temporal horn to supply the choroid plexus. Velum Interpositum The cistern of the velum interpositum is separated from the third ventricle by arachnoid and ependyma and contains the medial posterior choroidal arteries and the internal cerebral veins.

Microneurosurgical Observations Fig 5 A Operative photograph (right pterional approach) demonstrating the numerous trabeculae that extend from the arachnoid over the frontoorbital gyrus to gain attachment to the orbital dura. These are normally present in many areas but can be appreciated only after the most delicate dural opening.

Fig 5B Membranous arachnoidal layer between the frontoorbital gyrus and orbital dura (arrows). Note: this membrane has its own micro-vasculature.

Fig 5C Operative photograph (supracerebellar approach) showing innumerable trabeculae that suspend the cerebellar vermis.

21

221 Operative Anatomy Fig 5D Operative photograph illustrating the more delicate trabeculae extending from the anterior quadrangular lobule to the tentorium.

Fig 5 E Operative photograph (right Sylvian cistern) demonstrating numerous trabeculae that suspend the middle cerebral artery (M) within the cistern. Microscissors (sc) are seen over the artery. Arachnoidal membrane over Sylvian fissure (arrows).

Microneurosurgical Observations

Foramen of Luschka The lateral recess of the fourth ventricle opens into the lateral cerebellomedullary cistern as described above. Again a fine incomplete membrane is present separating the ventricle from the cistern. Foramen of Magendie The fourth ventricle opens in the midline into the cisterna magna. A thin membrane separating the ventricle from the cistern has been observed.

Pathological Thickening and Reduplication of Arachnoid There are two important changes in the arachnoid which the surgeon may encounter during operations for cerebral aneurysm. First, hemorrhage leads to staining and thickening of the arachnoid making visualization of structures and dissection more difficult. Second, with aneurysm growth, reduplications of the arachnoid are encountered as the aneurysm carries the arachnoid of its original cistern against the arachnoid of adjacent cisterns. Thus the aneurysm becomes invested with the arachnoid of neighboring cisterns. This allows tension to be transmitted to the fundus of the aneurysm even when dissection is being carried out some distance away, but it also provides an invaluable plane of dissection to allow easier separation of the aneurysm from adjacent structures.

23

Relationship to Pathological Processes If the arachnoid cisterns are to be utilized as a plane of dissection to separate pathological lesions from the brain, cranial nerves, and vascular system, the precise relationship of these lesions to the arachnoid must be appreciated. Such a relationship for various lesions is outlined diagrammatically in Fig. 6A-C for the sellar area, although the general concepts are valid throughout the intracranial cavity and spinal canal. Processes that originate outside the dura will with growth indent the dura and be separated from normal neural and vascular structures by the dura and the arachnoid (Fig 6A). Such lesions include pituitary adenomas, osteomas, chordomas, chon-dromas, glomus jugulare tumors, and epidural metastases. Processes arising between the dura and arachnoid will be invested with various reduplications of the subarachnoid cisterns depending on the particular location (Fig 6B). These lesions are primarily meningiomas and schwannomas such as acoustic neuroma. Most important to the present discussion are those lesions that arise within the subarachnoid cisterns (Fig 6C). With growth, these lesions encroach upon adjacent cisterns and become invested with various reduplications of arachnoid. These arachnoid layers are the planes by which the lesion can be separated from adjacent structures and removed. Such lesions include subarachnoid cysts, craniopharyngiomas, exophytic gliomas, dermoids, epidermoids, and of course, cerebral aneurysms and arteriovenous malformations.

24

1 Operative Anatomy

Fig6A-C Schematic representation of the relationship between the parachiasmal cisterns and expanding masses in the area. Cisterns (blue), dura mater (green), skull (black). A Pituitary adenomas, osteomas, chordomas and glomus tumors arise in the epidural space and are covered by both dural and arachnoid membranes (A-,). B Meningiomas and schwannomas originate in the subdu-ral space and extend subdurally, but epiarachnoidally. They are covered by two or more cisternal layers depending on the number of cisterns traversed (B,). C Craniopharyngiomas, optic and hypothalamic gliomas, AVMs, and aneurysms arise wilhin the cisternal spaces, If confined to a single cistern, they are covered by a single cisternal layer only (d).

Normal Cisternal Anatomy

25

Normal Cisternal Anatomy In describing and naming the subarachnoid cisterns, certain limitations present themselves: 1) While most of the cisterns can be almost completely explored at microneurosurgical operations, only portions of some cisterns are available for inspection. 2) During exploration the jlimsy walls of some cisterns may be torn with only minimal retraction, thereby altering the normal topography. 3) In other cases cisternal walls may be deficient as part of a pathological process or as the usual anatomical variation. 4) Embryological studies are still incomplete concerning development of the subarachnoid cisterns, so the basis for any current categorization is only empirical.

With these limitations in mind, a concept of the subarachnoid space is presented that attempts as accurately as possible to describe what has actually been observed at operation. The structures are placed into surgically relevant groups, and an easily understood nomenclature is employed. The cisterns are divided into two major groups supratentorial and infratentorial (Table 1), both for convenience and to parallel neurosurgical approaches.

Table 1 Subarachnoid Cisterns I. Supratentorial Cisterns A) Anterior (parasellar) 1) Carotid cistern 2) Chiasmatic cistern 3) Lamina terminalis cistern 4) Olfactory cistern 5) Sylvian cistern B) Lateral (parapeduncular) 1) Crural cistern 2) Ambient cistern (anterior part) C) Posterior (tentorial notch) 1) Quadrigeminal cistern 2) Velum interpositum cistern D) Superior (callosal) 1) Corpus callosum cistern - anterior portion 2) Corpus callosum cistern - posterior portion 3) Hemispheric cistern II. Infratentorial Cisterns A) Anterior 1) Interpeduncular cistern 2) Prepontine cistern 3) Premedullary cistern B) Lateral 1) Ambient cistern (posterior part) 2) (Superior) cerebellopontine cistern 3) Inferior cerebellopontine or lateral cerebellomedullary cistern C) Posterior 1) Cisterna magna 2) Superior cerebellar cistern D) Superior 1) Vermian cistern 2) Hemispheric cistern

26

1 Operative Anatomy

Supratentorial Cisterns Anterior (Parasellar) Carotid Cistern

This cistern, described radiologically by Lewtas and Jefferson (1966) and by Wackenheim and associates (1973) is bordered superiorly by the dura over the anterior clinoid process and the orbitofrontal lobe, and inferiorly by the cavernous sinus (Figs 7, 8A-B). The arachnoid does not follow the internal carotid artery into the cavernous sinus nor is it attached to the anterior cfmoid process. There are one or two millimeters of jiaked internal carotid artery which are between the investment of the carotid cistern and the dura of the cavernous sinus. Medially the cistern shares

a wall with the chiasmatic cistern and laterally is bounded by the mesial temporal lobe and the free margin of the tentorium. Opening the carotid cistern does not always release cerebrospinal fluid from the chiasmatic and interpeduncutar cisterns, justifying its designation as a separate cistern. The cistern is relatively free of trabeculated fibers except around the origins of the posterior communicating and anterior choroidal arteries which have their own sleeves of arachnoid within the carotid cistern (Figs 9A-D, 10). The inferior part of the carotid cistern and superior part of the mterpeduncufar cistern are in apposition sometimes creating a single (Lilie-quist's) membrane, which may be thick or thin -but normally forming two separate layers. The carotid cistern may sometimes extend 1-2 cm deep inferiorly.

cistern cistern

Pco.A.

Carotid cistern Ant. ch. A.

Ambient

cistern Crural cistern Sylvian cistern

Interpeduncular Chiasmatic Olfactory cistern Callosal cistern Lamina terminalis cistern Fig 7 Schematic representation of the parachiasmal and neighboring cisterns as encountered during the pterional approach. Chiasmatic cistern contains Chiasm (Ch) and stalk (st) Carotid cistern contains Carotid artery (C) and branches

Lamina terminalis cistern contains Anterior communicating and A, segment

Sylvian cistern contains Middle cerebral artery (M) Olfactory cistern contains Olfactory tract Interpeduncular cistern contains Basilar artery (B) and branches Crural cistern contains Anterior choroidal artery (Ant. ch. A.) Ambient cistern contains P2 segment of posterior cerebral Oculomotor nerve (III) has its own sleeve of arachnoid.

Supratentorial Cisterns

Fig 8A-B The parachiasmatic cisterns as recognized under the operating microscope from the pterional approach. 1 Sylvian cistern with middle cerebral artery 2 Olfactory cistern (base) with olfactory tract 3 Carotid cistern with internal carotid artery 4 Interpedunojlar cistern (lateral recessj with posterior communicating artery 5 Crural cistern with anterior choroidal artery 6 Chiasmatic cistern with chiasm 7 Lamina terminalis cistern with anterior cerebral and

27

anterior communicating artery 8 Callosal cistern (ant, part) with distal anterior cerebral artery A2

28

1 Operative Anatomy

Fig 9 A Operative photograph (right pterional approach) pointing out the proximal Sylvian and carotid cisterns (Ca-C) already partially exposed (arrows).

Fig 9 B The opened arachnoidal membrane over the right internal carotid artery. Strong membranous fibers at the proximal part of the Sylvfan fissure between the fronto-orbital and temporal gyrus (arrows).

Fig 9C The proximal limit of the carotid cistern with ophthalmic artery (arrows). Vasa vasorum over the sclerotic right internal carotid artery.

Fig9D Vasa vasorum over the sclerotic right internal carotid artery. Large sclerotic ophthalmic artery (arrow) also with vasa vasorum. Compression of the right optic nerve without clinical signs and symptoms.

Supratentorial Cisterns

29

Fig 10 Schematic drawing of the superiorly opened carotid cistern showing the posterior communicating artery entering the lateral recess of the interpeduncular cistern, while the anterior choroidal artery (arrow) is entering the crural cistern.

Especially important relationships of the carotid cistern are to the posterior communicating artery, dorsum sellae, oculomotor nerve, and interpeduncular cistern, since aneurysms commonly arise fromjhe lateral wall of the internal carotid artery and involve these structures. The arachnoid of the cistern is easily separated from the anterior cli-noid process and anterior cavernous sinus, is not attached to the free edge of the tentorium, and is contiguous with the_ mterpeduncular cistern^ Nevertheless a sleeve of arachnoid around the origin of the posterior communicating artery is in some cases densely adherent to the dura over the posterior clinoid process, and the artery may lie in a sulcus within the dorsum sellae. This accounts for much of the difficulty encountered in isolating some inferiorry directed posterior communicating artery aneurysms and is responsible for their often sudden rupture when attempts are made to place a clip before adequate division of the adherent bandsjFigs 11-131__________________ A second point of aracrmoidal reinforcement is where the posterior communicating artery penetrates the interpeduncular cistern and the oculo-

motor nerve with its own arachnoidal sheath, Jeaves the cistern to enter the dura of the cavernous sinus. Dense arachnoid trabeculations often bind the artery and nerve at this point. A final area of dense arachnoid fibers is between the carotid and crural c^ierns and the uncus of the temporal lobe, where the anterior choroidal artery leaves the carotid cistern to enter the crural cistern. These regularly observed areas of thickened arachnoid bind the posterior communicating and anterior choroidal arteries and oculomotor nerve firmly and must be divided sharply to gain mobility during dissection. Additional areas of thickening are similarly present at the bifurcation of the internal carotid artery, but these are discussed with the lamina terminalis and Sylvian cisterns as they relate primarily to these cisterns. ______ ! The carotid cistern contains the supraciinoid~por-tion of the internal carotid artery, the origins of ophthalmic, posterior communicating and anterior choroidal arteries, small arteries to thg_gp_tic_ jierves and pituitary stalk, a small but regularly seen artery to the dura over the anterior clinoid process (see Figs 11A and 47A-C), and variably

30

1 Operative Anatomy

Fig 11A Operative photograph of the opened carotid cistern: d = dural artery, posterior communicating artery (arrow 1) , anterior choroidal artery (arrow2).

Fig 11 B Operative photograph of the lateral portion of the right carotid cistern demonstrating the posterior communicating artery (arrow 1 ) , the oculomotor nerve (III), the anterior choroidal (arrow 2) and uncal arteries.

Fig 12 The arachnoidal sleeve (arrow) encasing the right oculomotor nerve (III) has been opened in this operative photograph.

Fig 13 The left oculomotor nerve (III) and its arachnoidal sleeve within the interpeduncular cistern as seen (arrow) from a dorso-lateral approach in the sitting position after the removal of a meningioma from the upper cerebellopon-tine angle. The basilar artery is well seen (Ba).

Supratentorial Cisterns

31

Fig 1 4 A The chiasmatic cistern has been partially opened on the right side in this operative photograph. The roof of the cistern is closely applied to the dorsal surface of the optic nerves and chiasm, as demonstrated by the dissecting forceps (arrow). Fig14B Subchiasmal part of the chiasmatic cistern, seen between the right internal carotid artery and the optic nerve (arrow). Fig 1 4 C Pituitary stalk after opening of the chiasmatic cistern (arrow).

/present frqntqorbital veins which lie just overjhe J internal carotid artery and drain into the sphenoj parietal sinus. "~™ ~' Chiasmatic Cistern (Cisterna Chiasmatica) This cistern encloses the subarachnoid space, around the optic nerves and chiasm. Superiorly it is tightly adherent to the superior surface of the optic nerves and chiasm and caudal to this contiguous with the inferior part of the lamina termina-lis cistern (Fig 14A-C)._______________ Interiorly it shares a common wall with the interpeduncular cistern, this thick arachnoid joining the chiasmatic and interpeduncular cisterns being called "Liliequist's membrane" (Fig 15A-D). Anteroinferiorly it extends to the infundibulum and pituitary stalk and is bounded by the diaphragma sellae. When the diaphragma is incom-

petent, the chiasmatic cistern may send extensions inside the sella. Often a remarkable density of arachnoid fibers bind the inferior surface of the optic nerves to the pituitary stalk, sometimes completely enclosing the stalk in the form of a collar. Anteriorly the cistern is limited by the limbus sphenoidale except at the optic foramina where short extensions of the subarachnoid space follow _the optic nerves into the orbit./ Laterally the cistern shares a common wall with the carotid The chiasmatic cistern contains the optic nerves, pituitary stalk, and numerous small internal carotid branches to both structures. The ophthalmic artery enters the chiasmatic cistern within the optic canal.

32

1 Operative Anatomy

Fig 1 5 A The inferior border of carotid and superior border of the interpeduncular cistern is composed of tough trabecular fibers (also known as Lillequist's membrane) as seen through the opened carotid cistern, beneath the right carotid artery (ICA) in this operative photograph.

Fig 15 B Sugero-medial wall of Liliequist's membrane is opened (arrow) between the right optic nerve and right internal carotid artery.

Fig 1 5 C Inferior wall of carotid cistern and superomedial wall of Liliequist's membrane are separately seen (arrow).

Fig 1 5 D Lateral perspective to the stalk (arrow 1 ) . Pathway of the right P-, segment (arrow 2).

Supratentorial Cisterns

Fig 16 Schematic drawing of the lamina terminalis cistern containing both anterior communicating artery and branches.

Lamina Terminalis Cistern (Cisterna Laminae Cinerae Terminalis) This cistern is defined primarily by the anterior / cerebral arteries (Fig 16). Its anteroinfcriorjirmt is the superior surface of the optic chiasm where it is contiguous with the chiasmatic cistern. Anterosuperiorly the rostrum of the corpus callosum covers the cistern. The posterior boundary is jhe lamina_ terminalis^; Extensions laterally enclose !each anterior cerebral artery with the anterior 'perforated substance above and the optic chiasm below, before the cistern joins several cisterns above the internal carotid artery bifurcation, it Thickened bands of arachnoid running from the olfactory area to the optic nerve demarcate the most lateral limit of the cistern. These form a jtunnel through which the anterior cerebral artery |must pass on leaving the carotid and entering the lamina terminalis cistern (Figs 17-19)

33

and proximal part of A2 segment and

In the center of the cistern dense, but very fragile trabcculatcd fibers _arc present running between the anterior communicating artery and the lamina terminalis (Fig 20). Near the origins of the frontopolar arteries, similar thickened arachnoidal bands bind the A2 segments of the anterior cere bral arteries to each other. Finally, throughout the anterior extension of the cistern in the interhemisphcric fissure, short tough fibers connect both re_ctus^gyri. __________ _________ The lamina terminalis cistern contains the anterior cerebral arteries, medial striate branches (the recurrent artery of Heubner), the anterior com municating artery complex, arteries to the hypothalamus, the most proximal A2 segments of the anterior cerebral arteries, frontoorbital arteries, and occasionally the origin of the frontopolar arter ies. Anterior communicating and anterior cerebral veins also lie within the cistern (Figjl^______

34

1 Operative Anatomy

Fig 1 7 A Opening of the lateral part of the right lamina terminalis cistern.

Fig 1 8 A The proximal portion of this right A, segment is nearly strangulated by similar trabeculations as seen at operation (arrow), su = sucker.

Fig 17B In this operative photograph, the right carotid and Sylvian cisterns have been opened. The entrance of the right A, segment into the lateral part of the lamina terminalis cistern is marked by the presence ofjough trabeculae (arrow) extending betwen the optic and~olfactory nerves. ~

Fig 1 8 B After opening of the arachnoidal fibers over the right A, segment.

Supratentorial Cisterns

35

Fig 20 Numerous trabeculae and a few small perforating vessels suspending the anterior cerebral artery complex within the lamina terminalis cistern in a formalin-fixed specimen. These fibers are easily disrupted during dissection and thus are seldom recognized at operation. A = Anterior cerebral artery, ArSegment.

Fig 1 9 A In this operative photograph, the right portion of the chiasmatic cistern has been opened. At the tip of the sucker (su) is the edge of the left gyrus rectus (gr). Fig 1 9 B Left wing of the lamina terminalis cistern seen from the right sided pterional approach. I. A1 = left A, segment, H = left Heubner's artery, CH = chiasm, r. A1 = right A, segment. Fig 1 9 C Left internal carotid artery (ICA) seen from the right sided pterional approach. Op = optic nerves, left A, and M, segment.

36

1 Operative Anatomy

OL.

Fig 21 Bilateral medial orbitofrontal arteries (arrows) arising from the A2 segments and disappearing into the olfactory sulci beneath the olfactory tracts (OL.) in this formalin-fixed specimen and coming to the surface of (small arrows) lateral to the right olfactory tract. Ch = Chiasm.

Olfactory Cistern This cistern is formed by the arachnoid over the olfactory tract between the orbital gyri laterally and the gyrus rectus medially. The olfactory sulcus between the gyri may be several (usually 5-10) millimeters deep with the cistern expanding slitlike into the sulcus (Fig 22). Inferiorly it is bounded rostrally by the floor of the anterior fossa including the cribriform plate of the ethmoid bone and caudally by the chiasmatic cistern. Posteriorly it joins several other cisterns above the internal carotid artery bifurcation. The olfactory cistern contains the olfactory bulb and tract, parts of frontoorbital and olfactory arte^_ jies^ their branches, and several frontobasal veins. The frontoorbital artery characteristically dips into the olfactory cistern as it passes laterally across the orbital surface of the frontal lobe.

Fig 22 Basal view of the right olfactory cistern following retraction of the tract (arrow 1) in a formalin-fixed specimen. The olfactory cistern extends to a depth of 1-2 cm and within it the medial orbito-frontal artery (arrow 2) divides. Its branches leave the cistern on its lateral border (arrows 3).

Sylvian Cistern (Cisterna Fossae Sylvii, Cisterna Fissurae Lateralis) This cistern is transitional between the basal cisterns and the subarachnoid space over the convexities. The most medial and inferior extent of the Sylvian cistern is at the origin of the middle cerebral artery from the internal carotid (Fig 23). Thickened bands of arachnoid completely enclose the origin of the middle cerebral as it arches from the area of the olfactory trigone on the lateral orbitobasal frontal lobe to the mesiobasal temporal lobe (see Fig 9B). These form a tunnel through which the middle cerebral artery passes before entering the Sylvian fissure. Slightly more distal there are very often numerous frontotemporal

Supratentorial Cisterns

Fig 23

37

Schematic drawing of the proximal part of the Syivian cistern containing the M-, segment and branches.

fibers within the Syivian cistern, crossing over the artery and almost forming a second membrane on top of the artery. The cistern narrows superiorly as the frontal and temporal lobes approach each other over a length of 15-20 mm. The width of the cistern is usually about 0.5-1.0 cm on the surface. In some cases however, the ftwnftrf sad temporal lobes are closely approximated on the surface thereby covering the substance of the cistern (Fig 24A-B). For this reason the Syivian cistern and its investing arachnoid can be categorized as follows:

Category \ 2 3 4

dsiernal Size Large Small Large Small

Arachnoidal Characteristics Transparent + Fragile Transparent + Fragile Thickened + Tough Thickened +JTqugh_

Microsurgical dissections of the Syivian cistern during the pterional operative approach are increasingly more difficult as the category of cistern increases according to the above classification. Thus the exposure of a category 3 cistern is quite tedious, but certainly easier than that of a category 4, post-meningitic cistern, which is almost impossible.

38

1 Operative Anatomy

Tern.

Fig 24A-B The variations of the width of the proximal Sylvian cistern and the position of the middle cerebral artery (M). Tem. = Temporal lobe, Fr. = Frontal lobe.

B Fig 25 A-B The proximal part of the lateral fronto-orbital gyrus (Fr.) herniating into the temporal lobe (Tem.). M = Middle cerebral artery (A). The proximal part of the superior temporal gyrus herniating into the lateral fronto-orbital gyrus (B).

Supratentorial Cisterns Rarely is the cistern clearly visible on the surface. Usually the lateral orbital gyrus firmly indents the temporal lobe inside the proximal Sylvian fissure thereby compressing the cistern, pushing it laterally, and concealing its deeper portion (Fig 25A-B). At the limen insulae the cistern enlarges to encompass the middle cerebral artery bifurcation. Thickened arachnoid fibers are present over the origins of both major trunks. These trunks diverge in a gentle curve and then reapproximate after 10 to 15 mm, still within the cistern. Numerous arachnoid trabeculae stretch between the two trunks as they diverge, and as the trunks recon-verge they are again covered with these thickened arachnoid fibers. Over the insula, the cistern is large, even though it appears small on the surface. Scattered arachnoid fibers course across the cistern and they are reinforced around the middle cerebral branches as the arteries exit from the Sylvian fissure. The Sylvian cistern contains the middle cerebral artery and the origins of the lenticulostriate, tem-poropolar and anterior temporal arteries, the middle cerebral artery bifurcation and the origins of the major branches. The superficial and deep Sylvian veins (with insular branches) are also within the cistern.

bral peduncle and the interpeduncular cistern, and its lateral boundaries are supratentonally the mesial temporal lobe and infratentorially the lobu-lus quadrangularis of the cerebellum. Inferiorly it shares an arachnoid wall with the cerebellopontine cistern. Anteriorly the cistern is related to the crural cistern. It has yet to be determined whether the lateral posterior choroidal artery must cross a cisternal wall to gain access to the crural cistern. The anterior choroidal and posterior lateral choroidal arteries enter the choroidal fissure within a few millimeters of each other. There is a superior extension of each ambient cistern which was named the wing of the ambient cistern by Liliequist (1959). This includes that portion of the cistern which extends from the I uncus of the temporal lobe, over the pulvinar of the thalamus, and anteromedially to the area of the velum interpositum near the foramen of Monro. The ambient cistern contains segments of the posterior cerebral artery, numerous arteries to the midbrain from both PCA's, and the basal vein of Rosenthal. The superior cerebellar artery and the trochlear nerve have their own arachnoid sleeves around the peduncle.

Lateral (Parapeduncular) Crural Cistern The crural cistern (see Fig 11A-B) lies between the parahippocampal gyrus _and the cerejjral peduncle. The cistern extends to the carotid • cistern anteriorly and lies on top of the interpeduncular cistern with the ambient cistern lateroposterior.|The crural cistern is clearly demarcated from the carotid and interpeduncular cisterns between the anterior choroidal and posterior communicating arteries./t has been recently possible at operation (selective hippocampectomy) to clearly separate the cistern posteriorly and infe-riorly from the ambient and interpeduncular _cisterns.jThe importance of this cistern lies in the valuable surgical plane it establishes between the anterior choroidal and posterior communicating arteries. The crural cistern contains the anterior choroidal and medial posterior choroidal arteries and the basal vein of Rosenthal. Ambient Cistern (Gisterna Ambiens) This cistern covers the lateral aspect of the mesencephalon and is both supra- and infratentorial justifying its inclusion in both categories (Figs 26A-D, 27A-J). Its medial boundary is the cere-

39

40

1 Operative Anatomy Fig 26A Schematic drawing of the right parapeduncular cistern (right subtemporal approach}.' ~~ " '"

Fig 26 B The right parapeduncular cistern; posterior cerebral artery within the ambient cistern, superior cerebellar artery has its own sleeve as has the trochlear nerve (IV). The anterior choroidal (cho) artery is seen in the opened crural cistern. Ill - oculomotor nerve, sea = superior cerebellar artery, P2 = P2 segment.

Supratentorial Cisterns

Fig 27A

The right lateral portion of the

Fig 26C Operative photograph of the right parapeduncu-lar cistern. Fig 26D The right lateral wing of the interpeduncular cistern seen on the operative photograph after elevation of the tentorial edge by forceps (Fore.) sea = right superior cerebe/lar artery. right carotid cistern (ICA) has been opened (arrows) following retraction of the temporal pole to reveal the posterior communicating artery (pco), tuberomammillary artery (tu) and anterioT choroidal artery (cho). Ill = oculomotor nerve.

41

42

1 Operative Anatomy Fig 27 B Lateral portion of the right carotid cistern, superolateral part of the interpeduncular cistern and the beginning of thejimlbient cistern (arrows) are 6pe~riedTfh~= thalamoperforating vessels.

Fig 27 C The P! segment and the perforating vessels from the P, and P2 segments of the posterior cerebral artery can be better seen (th), before the P2 segment enters the ambient cistern.

Supratentorial Cisterns Fig27D The right posterior communicating artery, tuberomammillary artery (tu) and the arachnoidal membrane (arrows) at the beginning of the ambient cistern.

Fig 27 E Following a right selective amygdalo-hippocampectomy, the crural and ambient cisterns have been opened, revealing: - the P2 segment of the posterior cerebral artery, as well as the anterior cho-, roidal artery (cho). op = optic tract.

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44

1 Operative Anatomy Fig 27 F The parapeduncular section of the ambient cistern is opened. The P2 segment and branches are better seen. The superior cerebellar artery (sea) is seen within its own arachnoidal sleeve.

Fig 27 G The end of the posterior cerebral artery P2 segment as it branches into temporal and parieto-occipital arteries (P3) and the posterior lateral choroidal artery (arrows) as it enters the choroid plexus.

Supratentorial Cisterns Fig 27 H The parieto-occipital branches (Pr, Oc) of the P3 segment and temporal branch (Te) after removal of a temporobasal astrocytoma.

Fig 27 i The trochlear nerve leaving the quadrigeminal cistern and entering its own sleeve along the tentorial edge.

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46

1 Operative Anatomy

Posterior (Tentorial Notch) Quadrigeminal Cistern (Cisterna Venae Magnae Galeni) This cistern (Fig 28A-C) is jpmewhat arbitrarily divided from the ambient cistern. The vein of Galen has well-developed, sometimes dense arachnoid attachments which form a clear boundary dorsally. Laterally, however, it has been difficult to demarcate this area because any retraction quickly ruptures the arachnoid membranes and there are no specific anatomical structures defining the limits of the cistern. The anterior limits of the cistern are the dorsal mesencephalon, the quadrigeminal plate, and the pineal gland. Posteriorly arachnoid is attached to the tentorium and extends from the splenium of the corpus callosum inferiorly to the lingula of the cerebellar vermis, above the anterior medullary velum of the fourth ventricle. The cistern is contiguous superiorly with the velum interpositum cistern and laterally with the ambient cisterns. The quadrigeminal cistern contains the medial posterior choroidal arteries, the great vein of Galen, the terminal portions of its tributaries, and the internal cerebral, basal, pericallosal, and occipital veins. The origins of the posterior pericallosal arteries and the continuation of the posterior cerebral arteries are also contained within this cistern. Velum Interpositum Cistern This small cistern extends from the habenular commissure to the foramen of Monro (see Fig 3C). It is located beneath the splenium of the corpus callosum above the velum interpositum, with the roof of the third ventricle below. Anteriorly it is beneath the fornix, converging to a point at the foramen of Monro. It lies between the pulvinar thalami, the arachnoid margins blending with the tela chorioidea. Posteriorly there is no clear distinction from the quadrigeminal cistern. The cistern contains the medial posterior choroidal artery, the splenothalamic branches of the pericallosal arteries, and the internal cerebral veins.

Superior (Callosal) Corpus Callosum Cistern - Anterior Portion (Cisterna Corpus Callosi, Cisterna Fissurae Interhemisphaerica) This cistern extends from .he falx cerebri medially to the pia over the cingulate gyri laterally (see Fig 3C). Anteriorly the cistern follows the falx to the

Fig 28A-B Quadrigeminal and Galenic cisterns; original drawing from the work of Key and Retzius (1875). Fig 28C Operative view of the quadrigeminal cistern (supracerebellar approach).

Infratentorial Cisterns

47

crista galli and joins the lamina terminalis cistern near the rostrum of the corpus callosum. Although there are reinforced arachnoidal fibers at the branching of the pericallosal and callosomarginal arteries, no distinct division of the corpus callosum cistern has been noted, and the arbitary division of this cistern into anterior and posterior portions is merely for convenience in discussing regional anatomy. The cistern contains the pericallosal arteries, and the origins of the frontopolar and callosomarginal arteries. Small anterior cerebral veins may be present sometimes making connections with the inferior sagittal sinus. Corpus Callosum Cistern - Posterior Portion Beyond the branching of the callosomarginal and pericallosal arteries, the corpus callosum cistern is narrower as the falx conies closer to the corpus callosum. Arachnoid forming the roof of the cistern is suspended from the inferior margin of the falx. Inferiorly the cistern joins the quadrigeminal and velum interpositum cisterns at the end of the splenium. The posterior portion of the corpus callosum cistern contains the pericallosal arteries which may end anywhere between the gyrus precuneus and the foramen of Monro. When the pericallosal arteries are not long, posterior pericallosal arteries arise from the parietooccipital branch of the posterior cerebral artery and run forward in the corpus callosum cistern. This cistern also contains the posterior pericallosal veins.

Fig 29 Dissection of a formalin-fixed brain demonstrating the interpeduncular (arrow 1) and prepontine (arrow 2) cisterns.

Infratentorial Cisterns Anterior Interpeduncular Cistern As the cerebral peduncles emerge from between the two optic tracts, they converge to enter the pons so that the subarachnoid space between them forms a cone-shaped cul-de-sac occupying the interpeduncular fossa. This is the most posterior recess of the interpeduncular cistern. The roof of the cistern is formed by the inferior surface of the mesencephalon and the lower diencephalon, the posterior perforated substance, and the mammillary bodies. The anteroinferior boundary is the clivus, and laterally tEe~cisfern joins the ambient cistern inferiorly and superiorly is limited by the carotid and crural cisterns and the mesial temporal lobes (Figs 29,

The anteroposterior wall of the interpeduncular cistern is especially well-developed. It stretches like a curtain from one mesial temporal surface to another and is fused with the chiasmatic cistern around the infundibulum and pituitary stalk. This membrane was described by Key and Retzius (1875) but j§ commonly referred to as, Liliequist's membrane (Liliequist 1959). Following subarachnoid hemorrhage, this arachnoid membrane may become thickened and create ajoculation of cerebrospinal fluid in the interpeduncular and prepontine area. Opening of this membrane at operation almost always results in \he escape of some cerebrospinal fluid, even in the presence of profuse lumbar drainage.

48

1 Operative Anatomy

Fig 30A-B Diagonal arachnoidal membranes along the inferior border of the interpeduncular cistern as seen in a formalinfixed specimen, on both, right (A) and left (B) sides. The arachnoid trabeculae crossing the cistern (B).

The inferior aspect of the cistern extends in a tine to the cerebellopontine cistern. Just above the triangular shape down to the middle portion of the level of this artery a plane separates this cistern basilar artery. The origins of the superior cerebel- superiorly from the interpeduncular cistern. The lar arteries lie within the interpeduncular cistern lateral extent of the prepontine cistern is limited as there is no significant arachnoid membrane by bilateral arachnoid membranes that form the between these arteries and the posterior cerebral medial walls of the cerebellopontine cisterns. The arteries, but at the level of the third nerve the inferior arachnoidal wall of the cistern is thickened superior cerebellar arteries acquire their own as the vertebral arteries join to form the basilar arachnoid sleeves and the Pj segments enter the artery beneath the pontomedullary sulcus. The ambient cistern (see Figs 26 and 27). The cistern contains the basilar artery, the origin of the interpeduncular cistern contains the upper 1A of the anterior inferior cerebellar artery, and the entire basilar artery and the origins of the posterior free course of the abducens nerve from the pons to cerebral and superior cerebellar arteries, medial Dorello's canal. posterior choroidal and thalamogeniculate arteries, and their branches, the basal veins of Rosenthal, and the oculomotor nerves. The oculomotor nerves Premedullary Cistern (Anterior Medullary can be seen to have their own distinct sleeve of Cistern) arachnoid when leaving the cistern. This cistern extends superiorly from the pontomedullary sulcus over the ventral aspect of the Prepontine Cistern medulla to the upper cervical area inferiorly. It is This cistern lies between the anterior surface of limited anteriorly by the clivus. The lateral extenthe pons and the clivus surrounding the basilar sion of the cistern is not as great as the vertebral artery (see Figs 29, 30A). Arachnoidal fibers arteries and hypoglossal nerves are in the adjacent encircling the anterior inferior cerebellar artery lateral cerebellomedullary cistern. The cistern denote the passage of this artery from the preponcontains the anterior spinal artery and the anterior medullary vein.

50

1 Operative Anatomy

Fig 32 A-C Operative photographs of the right cerebellopontine angle revealing: A The lateral cerebello-medullary or inferior cerebellopontine cistern containing cranial nerves IX, X, and XI (arrows). B The inferior cerebello-pontine cistern has been opened revealing cranial nerves IX, X, and XI, while nerves VIII and VII remain hidden within the upper cerebello-pontine cistern (arrow). C Both upper und lower cerebello-pontine cisterns have now been opened revealing cranial nerves VII, VIM, IX, X and XI, along with dense interposing trabeculae and a loop of anterior inferior cerebellar artery (arrow).

Laterally the cistern extends along the posterior petrous portion of the temporal bone entering the internal auditory meatus and extending outwards into Meckel's cave. Posteriorly the cistern is covered by the posterior quadrangular and superior semilunar lobulus of the anterior cerebellar hemisphere. Medially the flocculus is immediately posterior to the cerebellopontine cistern (Fig 32AC). Operative and cadaver observations show that the trigeminal nerve has its own cisternal sleeve which is separate from, but which forms a recess into the cerebellopontine cistern (Fig 33). This situation is analogous to the oculomotor nerve in the interpeduncular cistern, which carries

its own arachnoid sheath and is separate from the cistern. Anatomically, however, leaving the trigeminal nerve within the cerebellopontine cistern simplifies the topographical concept and leads to no particular change in operative planning or dissection (Fig 34A-B). The cerebellopontine cistern contains the anterior inferior cerebellar artery and the auditory artery if this has an independent origin, cranial nerves V, VII and VIII, and the lateral pontomesencephalic vein. The superior petrosal vein (Dandy vein) lies just outside the cistern except medially where it is located between the superior wall of the cerebellopontine cistern and the recess of the trigeminal nerve.

1 Operative Anatomy

52

Lateral Cerebellomedullary Cistern (or Inferior Cerebellopontine Cistern) This lateral cerebellomedullary cistern lies anterior and lateral to the medulla (see Figs 31-33). Its anterosuperior border is the sulcus between the medulla and the pons. Arachnoid over cranial nerves IX, X, and the cranial portion of XI separate this cistern from the cisterna magna dorsally and from the cerebellopontine cistern superiorly. Ventrally a less clear arachnoid sheet separates the cistern from the premedullary cistern. The cistern extends from the pontomedullary sulcus superiorly to the foramen magnum inferiorly, and reaches laterally along the occipital bone with short sleeves into the jugular and hypoglossal foramina accompanying the respective nerves. The cistern contains the vertebral artery, the origin of the posterior inferior cerebellar artery, the retroolivary and lateral medullary veins, and cranial nerves IX, X, XI and XII.

Posterior Cisterna Magna (Cisterna Cerebellomedullaris Dorsal is) As the dorsal spinal subarachnoid space opens into the intracranial cavity through the foramen magnum, it widens into a large cistern, the cisterna magna. This cistern is limited anteriorly by the dorsal surface of the upper spinal cord and lower medulla, and extends to the posterior medullary velum. Superiorly in the midline it runs beneath the vermis between the tonsils to communicate with the fourth ventricle at the foramen of Magendie, forming a cephalad extension of the cistern called the vallecula (Fig 34 C). Dorsally over the vermis the cistern has a variable i_^ VJl. \JX*1JL»

VJ

>"*il

*»»*.""»

fr^M. n.TU.13

„».»,.

_ ——— -_ _ _ ———

———_ . _

„

-_-_

_

-

expansion depending to some degree on the development of the falx cerebelli. It usually ends near the lobulus pyramis of the vermis but may extend all the way up the tentorium. Posteriorly, the cistern conforms to the inner table of the occipital bone except in the midline where the falx cerebelli partially divides the cistern. Laterally over the cerebellum, the cistern is limited by the fusion of the arachnoid to the pia and laterally over the brainstem by the arachnoid over the bulbar nerves forming the lateral cerebellomedullary cistern. Numerous tough trabeculae are seen in the cisterna magna stretching between the dorsal medulla and the posterior arachnoidal wall of the cistern. Similar fibers arch between the medulla, the cerebellar tonsil and the ipsilateral posterior

Fig 34 C Median suboccipital craniotomy. Arachnoidal membrane of the cisterna magna with vascularization of the membrane.

inferior cerebellar artery. Often a median sheet of arachnoid divides the cistern into sagittal halves, and at the level of Q-C2 two additional paramedian septi are formed and extend to the level of Tu_i2, thereby dividing the dorsal spinal subarachnoid space into several distinct compartments (Key and Retzius 1875). This cistern contains the inferior vermian branches of the posterior inferior cerebellar arteries and the median tonsillar veins. Several small vessels including draining veins between the medulla and overlying dura are adherent to the dorsal wall of the sinus.

Superior Cerebellar Cistern This cistern covers the superior vermis and blends laterally with the subarachnoid space over the cerebellar hemispheres. Anteriorly it meets the tentorium and the quadrigeminal and ambient cisterns. The cistern contains the terminal branches of the superior cerebellar arteries and the superior cerebellar and vermian veins (Table 2).

JSupra- and Infratentorial Cisterns | Table 2 Summary of anatomical relationships within various cisterns Cistern

Artery

Vein

Nerve

Internal carotid artery Origin ophthalmic artery Origin posterior communicating artery Artery to the dura of anterior clinoid Origin of anterior choroidal artery,

Occasionally fronto-orbital vein draining to sinus sphenoparietale or to basilar vein

None

Optic venous plexus

Optic nerves Pituitary stalk Olfactory nerve

Parasellar area Carotid

branches to the stalk and optic nerve Chiasmatic Olfactory

Hypophyseal arteries Chiasmal arteries Olfactory artery

Medial fronto-orbital artery Lamina terminalis

Anterior cerebral artery (A,-A2) Anterior communicating artery Proximal medial striate artery Recurrent artery of Heubner Perforating branches (to chiasma)

Olfactory vein Orbital veins Anterior cerebral vein Lamina terminalis venous plexus Orbital veins

None

Medial fronto-orbital artery (origin) Olfactory artery (origin) Distal anterior cerebral artery (A2) Frontopolar artery (origin) Callosomarginal artery (origin) Middle cerebral artery (M,)

Anterior cerebral vein

None

None

Anterior choroidal artery

Superficial middle cerebral veins Deep middle cerebral veins Basal vein of Rosenthal

Basilar artery (upper)

Pontomesencephalic veins

Oculomotor nerve

Lateral pontomesencephalic vein Basal vein of Rosenthal

Trochlear

Vein of Galen

Trochlear origin

Medial posterior choroidal artery Splenothalamic artery Dorsal (posterior) callosal artery Superior cerebellar artery (distal)

Internal cerebral veins

None

Precentral cerebellar vein Superior vermian veins

None

Corpus callosum (posterior) Posterior fossa

Posterior pericallosal arteries

Pericallosal veins

None

Cisterna magna Premedullary Prepontine

PICA (distal)

Inferior vermian vein

C,-C2

Anterior spinal artery Basilar artery AICA (origin) Perforating arteries

Median medullary vein Pontine veins

Abducens

Lateral cerebello-

Vertebral artery

Inferior petrosal vein

Glossopharyngeal

medullary

PICA (origin)

Anterior portion corpus callosum Sylvian _ __ Crural Interpeduncular

and its branches

None

Posterior cerebral artery (origin) P, Thalamoperforating arteries Med. posterior choroidal artery (origin) Quadrigeminal artery

Dorsal mesencephalon Ambient j

Posterior cerebral artery (P2-P3)

Quadrigeminal

Posterior cerebral artery (P4)

Superior cerebellar artery Lateral posterior choroidal artery (origin) Quadrigeminal artery Quadrigeminal artery

Velum interpositum

Superior cerebellar

Cerebellopontine (inferior) Cerebellopontine (superior) Superior vermian and hemispheric cistern

Occipital veins

Vagus

AICA and its branches

Superior petrosal vein Lateral recessus vein

Medial and lateral terminal branches of superior

Branches to the tentorial dura and straight sinus, branches to the precentral cerebellar veins

cerebellar artery

Accessory Hypoglossal Facial Vestibular Trochlear Trigeminal

53

54

1 Operative Anatomy

Intracranial Arteries Introduction The initial descriptions of the cerebral vasculature were produced by anatomists such as Thomas Willis, who in 1664 laid the framework for cerebral vascular anatomy (Fig 35 A). During the next two centuries, the fascination of the anatomists in the field of cerebral vasculature was reflected in the work of the pathologists. Textbooks such as those by Quain (1844), Luschka (1867), Henle (1868), and Duret (1874) and the description of the mesencephalic arteries by Alezais and d'Astros (1892) laid the foundation for the present-day understanding of the cerebral Fig 35A Ventral aspect of the brain and basal circle of arterial circulation. In 1872, Heubner recognized the need circulation as envisaged by Willis and published in 1664, for a more detailed description of the cerebral drawing by Sir Christopher Wren. arteries and with infusion techniques detailed many of the smaller cerebral arteries including the one that bears his name. Windle (1884, 1888) reported anomalies and variations in the cerebral vasculature in 200 cadaver examinations and Lazorthes et al 1956, Lazorthes 1959, 1961; pointed out the scant literature available on that Krayenbuhl and Ya§argil 1959; Baptista 1963; subject. Westberg 1963; Ostrowski et al 1964; Kaplan and Over the next several decades, increased attention Ford 1966; Ahmed and Ahmed 1967; Gillilan was paid to the anatomy of the cerebral vessels 1968; Stephens and Stilwell 1969; Wollschlaeger and their distinct distribution areas, and neurolo- and Wollschlaeger 1970; Krips and Kleihues 1971; gists in particular, began to define clinical syn- Waddington 1974; Newton and Potts 1974; Ya§ardromes associated with particular vascular territories gil et al 1975; Dunker and Harris 1976; Marino (DeVriese 1905; Testut 1904; Fawcett and 1976; Perlmutter and Rhoton 1976; Lazorthes et Blachford 1906; Looten 1906; Beevor 1907; Ayer al 1976; Schlesinger 1976; Salamon and Huang 1907; Aitken 1909; Kramer 1912; Stopford 1916; 1976; Duvernoy 1978; Brunner 1978; Lang and Shellshear 1920, 1921, 1927; Foix and Hillemand Brunner 1978; Lang 1979; Rhoton et al 1979) 1925; Bonne 1926; Adachi and Hasebe 1929; (Fig35B-C). Critchley 1930; DeAlmeida 1933; Kleiss 1941/42). It will become obvious to the careful reader that Anomalies in the circle of Willis were also noted (Lautard 1893; Longo 1905; Blackburn 1907; wide discrepancies exist among many of the anaBusse 1921; Hansenjager 1927; Slany 1938) and tomical descriptions (Fig 35B-C). developmental (Padget 1944, 1948) and phyloge- However, it must be realized that many of the netic (Abbie 1933/34; Watts 1934) aspects dis- topographical observations from both past and cussed. present work are based on fundamental differenWith the advent of arteriography and the active ces. As previously stated, these studies have been treatment of cerebral aneurysms, important con- performed by anatomists, pathologists, neuroratributions were made by the neuroradiologists and diologists, and surgeons, each with a different neurosurgeons. The relationship of aneurysms to perspective and each utilizing a different method anomalies of the circle of Willis was described. of examination. Among other things, the effects (Wilson et al, 1954; Stehbens 1963; Riggs and of formal fixation, latex perfusion, high pressure Rupp, 1963). In addition the introduction of ste- contrast injection, coexistant intracranial pathology reotactic surgery renewed interest in the fine ana- including vasospasm, (whether non-operative or tomy of the cerebral vasculature. (Kaplan 1950; surgically induced) CO2 levels, the examiners degree of precision etc., must be taken into considKaplan et al 1954; von Mitterwallner 1955; eration.

Introduction

Fig 35B

Circle of Willis at skull base (Clara).

( 1 ) Anterior communicating a. (2) Posterior communicating a. (3) Anterior choroidal a. (4) Pontine ramus. . (5) Basilara. (6) Anterior spinal a.

(7) Vertebral a.

(8) Posterior spinal a. (9) Cristagalli. (10) Anterior cerebral a. (10a) Pericallosal a. (11) Ophthalmic a. ( 1 2 ) Middle cerebral a. (13) Posterior cerebral a. (14) Superior cerebellar a. (15) Labyrinthine a. ( 1 6 ) Anterior inferior cerebellar a. (1 7 ) Middle inferior cerebellar a. ( 1 8 ) Posterior inferior cerebellar a. (19) Great foramen (From Krayenbuhl, H., M. G. Yasargil: Cerebral Angiography, 2nd Ed. Thieme, Stuttgart 1982)

Fig 35C (1) (2) (3) (4) (5) (6)

(7)

55

A contemporary drawing of the Circle of Willis.

Internal carotid artery Anterior choroidal artery Plexus A, segment Anterior communicating artery Heubner's artery MT segment

(8) Vertebral artery (9) Basilar artery

(10) P2 segment

(11) Posterior inferior cerebellar artery (12) Anterior inferior cerebellar artery (13 /1 4) Pontine branches (15) Superior cerebellar artery (16) Posterior communicating artery (From Kahle, W., H. Leonhardt, W. Platzer: Color Atlas and Textbook of Human Anatomy, Vol. III. Thieme, Stuttgart 1978)

56

1 Operative Anatomy

It is vital that the microsurgeon should have a sound knowledge of cerebrovascular anatomy in order that all brain vessels be preserved at surgery. At first, the idea that the _trainee should acquire such a detailed anatomical knowledge, especially of the arterial perforators, is formidable^ However, as this study shows, a pattern emerges that can easily be mastered and applied in the operating room. The fundamental concept is that any given area of the brain requires a blood supply that is fairly constant from one patient to another, and hence the arterial supply is constant. The difference between patients is in the size of the vessels, which can vary greatly and often with one or more dominating (socalled "hyperplastic"). This size difference may be so great that it appears that the primary feeding artery for a given region varies from brain to brain. However, when the underlying pattern is understood, a basic picture emerges. In aneurysm surgery, the need for detailed knowledge of cerebrovascular anatomy reaches its height. Preoperatively, the surgeon plans an approach based on his basic knowledge of the arrangement of the vascular tree. Using angio-grams, he can work out the relationship of the neck of the aneurysm to the vessels, in particular the perforators, in the vicinity. Should the aneurysm rupture, he has a plan based on his anatomical knowledge, of how to deal with the situation in a controlled fashion. Similar principles apply to tumor surgery. The surgeon works out the distortion of the normal vascular pattern pre-operatively. At surgery, he recognizes the normal vasculature and then works towards the tumor, dealing with all tumor surface vessels as though they were distorted brain vessels, until he can prove otherwise. Armed with a full vascular knowledge, the operator approaches surgery with complete command of the situation; a confidence that is frequently repaid by excellent post-operative results.

Internal Carotid Artery The intracranial internal carotid artery begins as the vessel exits from the carotid canal at the apex of the petrous pyramid. At this point the artery is just medial to the Gasserian ganglion and may be separated from it by only a dural sleeve. As it passes upward, forward and medially over the foramen lacerum, the vessel reaches the lower lateral portion of the posterior sella turcica and enters the cavernous sinus.

The intracavernous portion of the artery follows a somewhat tortuous course with the vessel first ascending for a short distance along the posterolateral aspect of the sella turcia. It then curves anteriorly continuing along the lateral aspect of the sella and enters the carotid sulcus. As it approaches the anterior portion of the sella, it then curves upward and medially and continues in this direction to emerge from the cavernous sinus infero-medial to the anterior clinoid process.____ This segment of the carotid artery has traditionally been considered to lie within the cavernous sinus, encased in venous blood, and studies by Bedford (1966) and Harris and Rhoton (1976) support this ' concept. However Parkinson (Parkinson and Shields 1974) maintains that the cavernous sinus is not a simple, single venous channel but actually a trabeculated plexus of veins. He believes that in this intricate maze of venous channels, the carotid artery and the other components of the sinus are each compartmentalized and separated from con-tact with venous blood by sinus endothelium.____ Branches of the intracavernous carotid artery have been studied by Bernasconi and Cassinari (1956), de la Torre and Netsky (1960), Schnurer and Stattin (1963), Parkinson (1964), Pribram et al (1966), Wallace et al (1967), Hacker and Alonso (1968), Lehrer (1970), Manelfe et al (1974), Wollschlaeger and Wollschlaeger (1974), Harris and Rhoton (1976) and Lang (1979). The meningohypophyseal trunk (dorsal main stem) is a constant vessel arising from the dorsal aspect of the artery near the beginning of its anteriorly directed segment. Branches include tentorial (supplying the mass of the tentorium and its petrous attachment), dorsal meningeal (supplying the dura of the dorsum sellae and clivus), and inferior hypophyseal (supplying the posterior "pituitary). A second vessel regularly arises further distally along the cavernous carotid artery called the artery of the inferior cavernous sinus (lateral main stem). It supplies branches to the nervous components of the cavernous sinus, its wall, the Gasserian ganglion and the surrounding dura in the floor of the middle fossa, and the free edges of the tentorium. Final branches of the cavernous carotid termed capsular arteries by McConnel (1953) ramify both anterior and posterior to the pituitary in the dural floor of the sella. However, these vessels were found by Harris and Rhoton in only 28 per cent of specimens.

Internal Carotid Artery

57

The persistent primitive trigeminal artery occurs with a frequency of 0.1-0.2 per cent (Rupprecht and Scherzer 1959; Madonick and Ruskin 1962; Krayenbiihl and Yas,argil 1965; Lie 1968). This artery arises from the intracavernous carotid artery proximal to the meningohypophyseal trunk (Parkinson and Shields 1974). The vessel passes posteriorly through the cavernous sinus and emerges at the dorsum sellae where it curves medially and enters the basilar artery between the superior and anterior inferior cerebellar arteries (see Figs 238239). As the carotid artery emerges from the cavernous sinus infero-medial to the anterior clinoid, it enters the dura and carotid cistern. The anterior clinoid process can cover the proximal, supra-clinoid internal carotid artery and the origin of its proximal vessels to a variable degree and may even indent the internal carotid at this point (Newton and Potts 1974). The artery then passes upward, posteriorly, and slightly laterally towards its bifurcation and is within the carotid cistern for its entire course. The length, caliber, direction, and tortuosity of this vessel varies and its termination at the bifurcation, although usually occurring inferior to the anterior perforated substance, may occur as high as the Sylvian fissure. The artery is immediately lateral to the optic nerve and may course parallel to it, or it may describe a convex or concave curve in relation to the nerve. At times this tortuosity of the artery will severely indent the nerve as it enters the optic canal (see Fig 9C-D), but no clinical syndrome has been recognized from this. This relationship of the supraclinoid carotid artery and optic nerve is particularly important in frontotemporal exposures to the basilar artery bifurcation (see chapter 3). Vasa vasorum normally are present along the internal carotid artery only to the point of origin of the ophthalmic artery, but can also extend to the level of the bifurcation when atherosclerotic changes are present in the vessel wall (see Fig 9C). An autonomic plexus covers the artery (Fig 36). The diameter of the proximal intracavernous carotid artery varies between 3.3-5.4 mm while the proximal supraclinoid portion measures 2.4—4.1 mm (Wollschlaeger et al 1967).__________ Unilateral and bilateral instances of hypoplasia of the internal carotid artery have been reported (Hyrtl 1848; Orr 1906; Schmeidel 1930; Tondury 1934; Priman and Christie 1959; Van den Zvan and "Fossen 1962; Brihaye and Dhaene 1962;

Fig 36 The autonomic plexus covering the right carotid artery as seen at operation.

Fields et al 1966; Lie 1968; Smith et al 1969; Lhermitte et al 1968; Steimle et al 1969; Teal et al 1973d). In the present series, the right and left carotid arteries were of equal size in all cases except in two; in one of these an anomalous short right common carotid artery and an aneurysm at the left internal carotid artery bifurcation were seen (Fig 37A-B) and in the other case an aplasia of the internal carotid artery was seen (see p. 308) (Fig 38A-F). Several examples of bilateral aplasia have been reported (Fisher 1913: da Silva 1936; Wolff 1944; Keen 1946: Fields et al 1965: Hills and Sament 1968; Lie 1972; Dilenge 1975; Rosen et al 1975; Teal et al 1980). No examples of fenestra-tion or duplicated carotid arteries have been reported. Aplasia of the left internal carotid artery associated with an aneurysm of the anterior communicating artery, a transverse carotid anastomosis at the base of the skull and 8 other cases have been published by Huber (1980). A transsellar intracavernous intercarotid collateral artery was associated with agenesis of the internal carotid artery in a case of Staples (1979).

58

1 Operative Anatomy

Fig 37A-B Arteriograms revealing (A) an anomalous short right common carotid artery (black arrows), (B) aneurysm at the left internal carotid bifurcation and A, segment (white arrows).

Fig 38A-F Two unusual cases: Fig 38A A ruptured saccular aneurysm (large arrow) at the junction of the P, and P2 segments of the right posterior cerebral artery (left vertebral injection) and spontaneous visualization of the right middle cerebral artery (small arrow).

Internal Carotid Artery

59

I Fig 38B Filling of the right middle cerebral artery through the right P, segment by left vertebral injection (arrow). The right internal carotid artery is aplastic.

Fig 38 C The operative findings are expressed diagrammatically. Dotted lines indicate the aplasia of the right ICA and the right A, segment. The right MCA originating from the right P-|-P2 corner.

Fig 38D Another patient with an aneurysm of the anterior communicating artery showed aplasia of the right internal carotid artery. Fig 38 E The right middle cerebral artery (arrow) is spontaneously visualized by vertebral angiography.

Fig38F The operative findings in diagrammatic form. The right ICA is aplastic. The right MCA originating from the right P1-P2 corner. Black arrow indicates the blood flow from right P, segment to the right distal internal carotid artery and its branches.

60

1 Operative Anatomy

The branches of the supracavernous internal caro tid artery include the ophthalmic artery, several small superior hypophyseal arteries arising from the infero-medial carotid and supplying the pitu'itary stalk, anterior pituitary lobe, and chiasm, the posterior communicating artery arising from the infero-lateral carotid, the anterior choroidal artery and occasionally 2-3 smaller branches to the area of the uncus arising from the distal infero-lateral carotid, a commonly present, small artery to the dura of the anterior clinoid arising from the supero-medial carotid, and finally the terminal branches - the anterior and middle cerebral arter ies. ______

Ophthalmic Artery The ophthalmic artery is the first major branch of the internal carotid artery and is the only large branch directed medially. The ophthalmic artery usually arises from the antero-medial (53.6%) or supero-medial (31.5%) surfaces of the carotid artery (Hayreh 1974). The exact site of origin is somewhat variable as attested by Hayreh and Dass (1962) who studied 168 specimens. In 83 per cent the origin of the artery was in the subdural space just at the point where the carotid artery enters the dura after leaving the cavernous sinus. In 2 per cent it arose just proximal to this point so the artery was partially subdural and partially extradural. In 7.5 per cent it originated even further proximally, so that it was intracavernous and completely extradural. In the remaining 6.5 per cent, it arose within the most anterior portion of the carotid cistern within 1 mm of its most anterior portion. The initial course of the ophthalmic artery is intimately related to the body of the sphenoid and to the proximal part of the suprachiasmatic internal carotid artery to which it is frequently adherent for some distance (Hayreh 1974). The artery most frequently lies within the subdural space for its entire intracranial course attached to the undersurface of the optic nerve by a loose meshwork of connective tissue. The artery is infero-medial to the nerve in 43 per cent of cases, directly inferior in 37 per cent, infero-lateral in 16 per cent, or rarely directly medial or lateral in 2 per cent each (Hayreh and Dass 1962). As it enters the optic canal beneath the optic nerve (infero-lateral 25.9 per cent, directly inferior 32.7 per cent, inferomedial 41.4 per cent - Hayreh and Dass 1962), it pierces the optic nerve dural sheath to lie between this sheath and the periosteum of the optic canal. As it courses through the optic canal, the ophthalmic artery lies infero-lateral (84.5%) or infero-

medial (15.5%) to the optic nerve (Hayreh and Dass 1962). Shortly after penetrating the orbit, the artery crosses over (82.6%) or under (17.4%) the nerve to continue a more medial course. The entire orbital course, branches, anastomoses, and anomalies of the ophthalmic artery are beyond the scope of this book. Interested readers should consult Hayreh in Newton and Potts 1974, Chapter 61, for a detailed description of these topics. The diameter of the ophthalmic artery varies between 1.0 and 2.0 mm. No cases of duplication or aplasia were seen in the present series, but in one case an artery was noted to originate from the ophthalmic, course with the optic nerve, and penetrate the anterior perforated substance. The topographical anatomy of the ophthalmic artery has been discussed by Bock and SchwarzKarsten (1955), Hayreh and Dass (1962), Hayreh (1974) and Vignaud et al (1972). A complete list of references is given by Hayreh (1974) and Lang (1979). Radiological anatomy has been studied by Bregeat et al (1952), Decker and Schlegel (1957), Di Chiro (1961), Dilenge et al (1965), Salamon et al (1965), Vignaud et al (1975), Lasjaunias et al (1975), Huber (1975).

Superior Hypophyseal Arteries Several small but constant arteries leave the infero-medial internal carotid artery and course beneath the optic nerves through the carotidjmd chiasmatic cisterns to supply the pituitary stalk, tuber cinereum, anterior lobe of the pituitary, and inferior surface of the optic nerves and chiasm (Stephens and Stilwell 1969). These arteries anastomose with similar vessels from the opposite side and with the inferior hypophyseal branches to form a longitudinally oriented vascular plexus around and along the stalk - the hypophyseal portal system. The visualization of this plexus of vessels is helpful at surgery in identifying the pituitary stalk.

Posterior Communicating Artery The posterior communicating artery takes origin from the infero-lateral wall of the supraclinoid internal carotid artery within a few millimeters (2-8 mm) of the anterior portion of the carotid cistern. From its origin at the internal carotid artery to the point where it leaves the carotid cistern by piercing the interpeduncular cistern, the posterior communicating artery does not lie freely within the cistern, but is encased in a sleeve of arachnoid that is adherent to a similar sleeve encasing the oculomotor nerve. As with most

Internal Carotid Artery

PcoA = P-]

c

PcoA > PI

B

D

PcoA

2nd PCA

Fig 39A-D Variations between the posterior communicating artery and P, segment. A Posterior communicating artery and P, are equal. B P, is larger. C Posterior communicating artery is larger. D A second posterior cerebral artery (arrow).

intracranial arteries, it is further stabilized by bands of arachnoid suspending it from the walls of the cisterns. As the artery courses posteriorly to join the posterior cerebral artery, impasses close to the dura overlying the posterior clinoid process. In some cases it may be adherent to the dura in this region over a few millimeters or it may even lie in a sulcus within the process. These attachments of the artery may at times hinder attempts to mobilize the vessel during aneurysm operation. The calibre of the posterior communicating artery is highly variable. Dilenge (1962) found the artery to be larger than 2 mm in 38.7 per cent of cases, between 1-2 mm in 41.5 per cent, and less than 1 mm in 18.9 per cent. In children a greater proportion of large calibre postcommunicating arteries are seen (38.5-75%) as compared to adults (829%), suggesting that this vessel diminishes in size with increasing age (De Vriese 1905; Padget 1944). In 67.5 per cent of cases the posterior communicating artery is Ys to '/2 the size of the corresponding posterior cerebral artery. However

61

in 8.0 per cent of cases the posterior communicating artery is of similar calibre to the posterior cerebral artery and in 24.5 per cent it is actually larger (Fig 39A-D). In these situations (PcoA > PCA), the proximal portion of the posterior cerebral artery (P^ is often hypoplastic, thereby demonstrating a persistence of the fetal type of circulation (Table 3). Hypoplasia of the posterior communicating artery is not at all infrequent and multiple cases of apla-sia have been described. The incidence of aplasia varies from 3-11 per cent for unilateral cases and 0.3-1.5 per cent for bilaterally absent vessels (Windle 1888; Stopford 1916; Fettermann-Moran 1941; Padget 1944). Other variations of the posterior communicating including duplication and fenestration of the vessel have been presented by Hasebe (1928), Kleiss (1941), Dandy (1944), von Mitterwallner (1955), Alpers et al (1959), Wells (1960), Riggs and Rupp (1963), Kaplan and Ford (1966), Krayenbiihl and Ya§argil (1968), Wollschlaeger et al (1969), Ozaki et al (1977), Saeki and Rhoton (1977), and Lang and Brunner (1978). In the present series three cases of duplication of the posterior communicating artery were seen at operation (Figs 40-42). In these cases the artery that originated distally did not join the posterior cerebral artery but coursed independently along the medial-basal temporal lobe and functioned as a temporal artery. One such a case was also encountered during 200 cadaver brain dissections (see Fig 42C). Similar cases were described by Windle (1888) who found one (1 case) or two (1 case) vessels arising from the internal carotid artery in the position of the posterior communicating artery; "In one case two arteries sprang from the internal carotid artery in the position normally occupied by the posterior communicating artery. Instead however, of joining the posterior cerebral artery, they passed to the under surface of the temporo-sphenoidal lobe which they supplied. A few filaments from each of these anastomosed with slender twigs from the posterior cerebral artery." Dandy (1944) also describes this variation. Wollschlaeger and Wollschlaeger (1974) in: Newton and Potts, p. 1178, describe two main branches of the posterior cerebral artery which may arise separately. In this variation the temporo-occipital branch arises from the internal carotid artery and the parieto-occipital branch from the basilar artery. Also in this series one case of fenestration of the posterior communicating artery and two cases of another unusual variation were seen (Fig 43A-C).

62

1 Operative Anatomy Fig 40 A Left lateral angiograms demonstrating a second posterior cerebral artery (arrows) arising just proximal to the anterior choroidal artery and ending in the medialbasal occipital pole.

Fig 40 B AP view of the second posterior cerebral artery. It does not give rise to parieto-occipital branches.

Fig40C Operative picture of the left second posterior cerebral artery (arrows 12). Anterior choroidal artery (arrow 3).

Internal Carotid Artery

63

Fig 41 A-C A second posterior cerebral artery that ends in the parieto-occipital lobe and does not give any temporal branches. A AP angiogram showing the distal supply of the second posterior cerebral artery (arrows). B Vertebral angiogram portraying the terminations of the real right posterior cerebral artery that gives only temporal branches (arrow). C Operative photograph of two posterior cerebral arteries (arrows 1 and 2), anterior choroidal artery (arrow 3).

64

1 Operative Anatomy

Fig 42 A A rare variation of the Circle of Willis observed in a formalin-fixed brain. The right P,-P2 junction is duplicated as in the anterior communicating artery. The left fronto-polar and Heubner's arteries have a common trunk, as do the left lateral fronto-orbital and lateral striate arteries. Fig 42B Another unusual anomaly showing two right posterior cerebral arteries joined by a bridge and 3 Aa segments. Again the left lateral fronto-orbital and striate arteries have a common trunk. Fig 42 C An example of two completely separate right posterior cerebral arteries.

Table 3 Variations of the posterior communicating artery in 200 cadaver brains (400 hemispheres) Left

Right

Total

(%)

Aplasia

unilateral bilateral

6 -

.

2

8

2.0 67.5%

Hypoplasia

unilateral bilateral

112 .

62

174

43.5 22.0

88

Equal to P,

unilateral bilateral Hyperplasia (larger than P,)

7 12

unilateral bilateral

29

13

20

5.0 3.0 32.5%

53

16

82

20.5 4.0

Fenestration

unilateral bilateral

2 -

2

0.5 -

1 -

1

0.25 -

Duplication

unilateral bilateral

Internal Carotid Artery

65

Fig 43A-C An unusual case of a posterior communicating artery aneurysm. A Schematic representation of the posterior communicating artery aneurysm arising on a fenestrated posterior communicating artery, B Lateral angiogram showing the aneurysm but failing to show the complexity of the situation. C Operative photograph showing the fenestrated posterior communicating artery (arrow 1) and the coagulated aneurysm neck (arrows 2).

The posterior communicating artery has along its course 2-10 branches that generally begin about 2-3 mm from the origin of the artery and run posteroinferiorly and medially into the interpe-duncular cistern. Perlmutter and Rhoton (1976) found that more of these branches are located on the anterior half of the artery in 54 per cent of cases, on the posterior half in 25 per cent and are equally distributed in the other 21 per cent. These branches were called the "anterior thalamoperfo-rating arteries" by Westberg (1966) and supply the

inferior optic chiasm, optic tract, tuber cinereum, mammillary bodies, subthalamus, posterior jiypothalamus, and the anterior and vertebral portion of the thalamus. Most of these branches are quite variable in size and may branch early or run a long course, except one larger vessel that regularly passes in front of the mammillary bodies and then penetrates the brain (see Fig 44, p. 66). This artery was designated the "premammillary" by Stephens and Stilwell (1969) and Perlmutter and Rhoton (1976) and the "thalamotuberal

66

1 Operative Anatomy

Fig 44 Tubero-mammillary (premammillary) (2), other perforating branches of the posterior communicating artery (1), and the anterior choroidal artery (3) are well seen.

artery" by Haymaker (1969) and Foix and Hillemand (1925a). In the present series, this vessel was identified in all cases (Fig 44). In only one instance was this vessel seen to arise directly from the internal carotid artery. The mammillary bodies themselves are supplied by either these branches from the posterior communicating artery or from branches of the proximal posterior cerebral artery (P^. In 65 per cent of cases each mammillary body is supplied by ipsilateral vessels, in 23 per cent by bilateral arteries, and in 12 per cent of cases both are supplied by one side (Putz and Poisel 1974). Dunker and Harris (1976) described some nutriment of these structures by proximal anterior cerebral branches (A,). Even when the posterior communicating artery is hypoplastic, rather stout penetrating branches may be seen to exit from the artery. In the present experience, no branches to the temporal lobe were seen to originate from the posterior communicating artery. In one case an artery originated from the posterior communicating artery and coursed toward the crural cistern, but this probably represented an anomalous origin of the anterior choroidal from the posterior communicating artery. Further details about the topography of the posterior communicating artery can be found in the work of Zeal and Rhoton (1978).

Anterior Choroidal Artery The anterior choroidal artery arises 2-5 mm (1.19.0 mm, Rhoton et al 1979) distal to the posterior communicating artery and 2-5 mm

(2.0-8.0 mm, Rhoton et al 1979) proximal to the carotid bifurcation from the infero-lateral aspect of the internal carotid artery. In every case except one in the present series, the anterior choroidal artery arose as the first infero-lateral branch of the internal carotid artery after the posterior communicating artery. In one case, the posterior communicating and anterior choroidal arteries were seen to arise from exactly the same level with the former from the medial-inferior wall and the latter from the lateralinferior wall. It is surprising that Carpenter et al (1954) and Rhoton et al (1979) found branches between the posterior communicating and anterior choroidal arteries in 10 and 32 per cent of cases respectively. Rhoton describes these branches as most frequently terminating in the optic tract, medial temporal lobe, and posterior perforate substance. In our cases, we found branches emerging from the intero-medial wall of the internal carotid artery between the posterior communicating and the anterior choroidal arteries and supplying the optic tract and posterior perforate substance that could represent the vessels described by Rhoton. However, branches tojhe medial-basal temporal lobe in our experience always originate from the infero-lateral internal ' carotlcTTfista/ to^the anterior choroidal artery. Without exception the second infero-lateral branch of the internal carotid artery after the posterior communicating artery is the anterior choroidal artery or arteries. When duplicated one or more trunks of the anterior choroidal artery occur. The uncal artery is always distal to the anterior choroidal artery or may originate from the lateral wall of the proximal middle cerebral artery (Waddington 1979). As mentioned under the posterior communicating artery, in one case from the present series, an anterior choroidal artery may have originated from the posterior communicating artery but this was not verified (Figs 45A-E, 46A-G). The calibre of the anterior choroidal artery varies from 0.5-1.5 mm (0.7-2.0 mm, Rhoton 1979). In 70 per cent of cases in the present series, the anterior choroidal artery aros^^s_a_singlejrunk that usually then divided either immediately or within 2-5 mm into two trunks. In 30 per cent of cases in the present series, the anterior_chprpidal_ artery arose as 2-4 independent vessels/ Saeki and Rhoton (1977) found a single trunk in 96 per cent of 100 brains and Rhoton et al (1979) found only single trunks in 50 brains. Several authors have found the anterior choroidal artery to occasionally arise from the bifurcation of the internal carotid artery, from the middle cerebral artery, or from

Internal Carotid Artery

Fig 45A-E Variations of the anterior choroidal and uncal "arteries (u). " "————————————— A Three separate arteries originating from internal carotid artery. B Uncal artery originates from middle cerebral artery. C Uncal artery originates from anterior choroidal artery. D Uncal artery originates from internal carotid artery. E Anterior choroidal artery originates from posterior communicating artery (extremely rare). Fig 46A-G Variations of the anterior choroidal and uncal arteries as seen at operation. A Right anterior choroidal (arrow) and uncal (u) arteries arising from the common trunk. B Right anterior choroidal (2) and uncal (u) arteries arising independently at the same level. Posterior communicating artery (1). C Separated origin of anterior choroidal artery ( 1 ) and uncal artery (u). PcoA = posterior communicating artery.

67

68

1 Operative Anatomy

46 D Three separate branches (black arrow) of the anterior choroidal and uncal arteries. White arrow indicates the posterior communicating artery.

E Tubero-mammillary artery (arrow 1) , anterior choroidal artery (arrow 2), uncal artery (arrow 3). PcoA = posterior communicating artery.

F Left pterional approach: Posterior communicating artery (1), anterior choroidal artery (2), uncal artery (3), large proximal lateral striate artery (4). M = middle cerebral artery.

G Anterior choroidal artery (1), uncal artery (2), temporal pole artery (3) in a case with an AVM of the temporal pole, tu = tuberomammillary artery.

Internal Carotid Artery

69

Table 4 Arteries with origin at the anterior choroidal artery Anatomic studies in cadavers

No. of arteries examined

ICA

ICB

MCA

PcoA

AchA absent

Bevoor 1907

174

100%

-

-

-

-

Carpenter et al 1 954

60

76.6%

3.3%

1 1 .7%

6.7%

1 .7%

Von Mitterwallner 1955

360

97.0%

L. 0.3% R. 0.0%

L. 2.0% R. 0.5%

L. 2.0% R. 1 L. 1 .2% R. 1 .6% .6%

Otomo 1 965

778

99.2%

0.4%

-

0.4%

-

Herman et al 1 966

74

85%

7%

8%

-

-

Saeki and Rhoton 1977

100

100%

-

-

-

-

Rhoton et al 1979

50

98.0%

-

-

2.0%

-

Own 1982

200

99.5%

_

_

0.5%

_

. Angiographic studies Sjogren 1956

88%

2.0

3.0

Cooper 1954

92%

%

%

the anterior communicating artery (Table 4). In the present series of over 2000 operative exposures in this area and 200 cadaver brain examinations by the senior author (MGY), the anterior choroidal artery was seen to arise only from the internal carotid artery in every case but one.____ From its origin, the anterior choroidal artery passes postero-medially in the carotid cistern to reach the optic tract postero-lateral to the posterior communicating artery. At this point it diverges from the posterior communicating artery and follows in the general direction of the optic tract between the mesial temporal lobe and the cerebral peduncle to enter the crural cistern. If the artery arises as two separate vessels or as a single trunk that divides into two vessels, one of them, the uncal artery ramifies immediately to supply the uncus piriform cortex, the postero-medial amygdala, the anterior hippocampal and dentate gyri and the tail of the caudate nucleus. The other generally larger vessel continues in the crural cistern as the main anterior choroidal artery with proximal branches that supply the inferior aspect of the optic chiasm, the posterior % of the optic tract, the medial 2 segments of the globus pallidus, the genu of the internal capsule, the middle '/i of the cerebral peduncle, the substantia nigra, upper parts of the red nucleus, a portion of the subthalamus, and a lateral portion of the ventral anterior and ventral lateral thalamic nuclei (Abbie 1932). The main anterior choroidal artery then courses through the wing of the ambient cistern to enter the choroidal fissure and join the choroid plexus of the temporal horn. Branches of this portion of the anterior choroidal artery supply the antero-

lateral half and hilum of the lateral geniculate body, the inferior half of the posterior limb of the internal capsule, the retro-lenticular portion of the internal capsule and the optic radiations. The anterior choroidal artery supplies the choroid plexus of the lateral ventricle in association with the posterior lateral choroidal artery. The anatomy and distribution of the anterior choroidal artery have been discussed by Abbie (1933), Carpenter et al (1954), Morello and Cooper (1955), Mounier-Kuhn et al (1955), von Mitterwallner (1955), Sjogren (1956), Otomo (1965), Herman et al (1966), Wollschlaeger et al (1969), Goldberg (1974), Theron (1976), Saeki and Rhoton (1977), Rhoton et al (1979), and Lang (1979). A marked reciprocal relationship between the arterial distribution areas of the anterior choroidal artery and surrounding branches of the internal carotid, posterior cerebral, posterior communicating, and middle cerebral arteries has been noted (Rhoton et al 1979). Rich anastomoses between branches of these major vessels permit inter-changeability in their distribution of blood such that if one is smaller than usual, others are larger than normal to compensate. This phenomenon has been noted in the present series of patients but not studied. Other than duplicated or triplicated anterior choroidal arteries, there usually are no additional branches of the infero-lateral internal carotid artery between the anterior choroidal artery and the bifurcation. However in one case from the present series, an anterior temporal artery took origin proximal to the bifurcation, and in another case an accessory middle cerebral artery arose

70

1 Operative Anatomy

from the infero-lateral wall of the internal carotid artery just distal to the anterior choroidal artery origin.

Dural Artery of Internal Carotid Artery A consistent small branch arises from the superomedial aspect of the internal carotid_artery 3 to 5 mm proximal of the bifurcation and courses to the dura in the area of the anterior clinoid process (Fig 47A-F). Rarely this artery may arise from

the anterior cerebral artery (Aj), and in one case bilateral symmetrical branches of the anterior cerebral arteries (Aj) ran to the limbus sphenoidale. Retraction may blanch this artery so it appears only to be a strand of arachnoid, and when accidentally avulsed from the parent artery it may be a source of unrecognized bleeding, especially after a local sympathectomy and the application of papaverine to the internal carotid artery.

Fig 47A-C Operative photographs (right pterional approach) illustrating a small but regular branch (arrow) of the internal carotid artery, leaving its distal, superomedial wall and supplying the dura over the anterior clinoid (A).

B Dural branch of internal carotid artery (arrow).

C Rarely this branch arises from the A, segment (arrow).

продолжение

Internal Carotid Artery продолжение Fig47D Dural artery (arrow) to the tuberculum sellae arising from the right A, segment. Fig47E Dural artery (arrow) to the area of the tuberculum sellae arising from the left A, segment. Fig 47F An unusual branch (arrows) of the right A, segment to a vascular network within the prechiasmatic arach-noidal membrane.

71

74

1 Operative Anatomy

polar temporal artery is enlarged one might expect to see that the anterior temporal artery is hypoplastic or absent. It is then the enlarged polar temporal artery supplying both the polar temporal and anterior temporal regions. Occasionally, during surgical dissection one may observe that both the polar temporal and anterior temporal arteries may be hypoplastic or absent and their cortical areas are supplied by a single large middle temporal branch that arises from the inferior trunk of the M2 bifurcation (Fig 51). Infrequently a single large cortical branch arises at the site of the hypoplastic or absent polar temporal or anterior temporal arteries (Figs 52A-H). It is very important to be aware of these different patterns along the superior lateral wall of the Mj segment, both at angiography and at the time of surgery. These different anatomical patterns can lead to_confusion of the position of the true middle cerebral artery bifurcation. The examples cited in Fig 52A-E, are referred to as examples of the false early bifurcation occurring along the superior lateral MI segments. If the position of the true bifurcation is mistaken, it is understandable to find that the length of the Mt segment has been incorrectly identified as being 0 to 30 mm in length.

Fig 51 Variation of the M, segment with no branches arising from its lateral wall. The polar-temporal and anterior temporal branches originate instead from the inferior trunk ofM2.

Fig 52A False bifurcation (giving the impression of an early true bifurcation) due to the presence of a larger than normal polartemporal branch from the lateral wall of the proximal M-, segment. This temporal artery may give rise to multiple temporal lobe branches as depicted in this diagram. ___.

Fig 52 B Similar situation with the temporal artery arising more distally on the M-, segment.

Middle Cerebral Artery

2 \A) 3 Fig 52C Variations of the origin of the temporal trunk: (1) from ICA, (2) from proximal M,, (3) from distal M,.

Fig 52 D AP angiograms showing a false early bifurcation due to the origin of a large right temporal artery from the most proximal MI segment (arrow 1). The left temporal artery is small (arrow 2).

Fig 52 E Operative photograph showing the false (arrow 1) and true (arrow 2) bifurcations.

75

76

1 Operative Anatomy

Fig 52F A large temporal artery trunk arising from the internal carotid artery (arrow). The lenticulostriate arteries arising from M-,.

Fig 52G Left sided carotid angiogram of the same case showing normal anatomy of middle cerebral artery, the lenticulostriate artery arising from distal M,.

Fig 52 H Operative diagram of an unique example of another large temporal artery trunk arising from the internal carotid artery (arrow) in a case with ruptured aneurysm of the anterior choroidal artery.

Middle Cerebral Artery

Inferior Medial Group or "Lenticulostriate or Striate Vessels" The inferior medial group of vessels along the Mj segment are the striate arteries which number 215. At their origin they form "vascular loops" on their way to supply the sub-cortical areas of the brain after entering the lateral two-thirds of the anterior perforated substance (Newton and Potts 1974; Ring 1974; Leeds 1974; Lang and Brunner 1978). Since they originate on the inferior surface of the Mj segment it is necessary to gently retract this segment of the artery in order to observe the sites of origin of these arteries.] The striate vessels supply the substantia innominata, the lateral portion of the anterior commissure, most of the putamen, the lateral segment of the globus pallidus, the superior half of the int. capsule and adjacent corona radiata, and the body and head (except the antero-inferior portion^ of the caudate nucleus (Stephens and Stilwell 1969). In our experience three patterns of origin of the striate arteries from the Mt segment have been observed. Most frequently, occurring 40 per cent of the time, we observed that all the striate arteries arose from one single large artery, a stem, artery that then divided after 2-10 mm into many branches (Fig 53A). Two other patterns of striate origin were seen each in 30 per cent of the cases. These patterns consisted either of two large parallel arteries that immediately divided to give off the numerous branches of the striate group (Fig 53B), or numerous small twigs (10-15) of striate arteries that arose directly from the whole inferior medial Mj segment (Fig 53C).

Fig 53A-C Variation in the origin and number of proximal and distal lateral lenticulostriate arteries. A A large and small proximal trunk side by side. B Two large proximal trunks. C Multiple small arteries arising along the whole infero-medial wall of the M, segment.

77

The striate arteries have never been seen to arise from the superior or lateral aspect of M1. In most cases, these vessels arise from the infero-medial aspect of the Mj segment, along either its proximal, mid-portion, or distal segments or along the proximal middle cerebral trunks distal to the bifurcation (M2 segment). Generally they can be separated into proximal, middle and distal groups. Lang et al (1979) found that the striate branches often arose from several areas. Proximal Mj branches were seen in 71 per cent, mid-portion branches in 86 per cent, distal Mj branches in 44 per cent, proximal M2 branches in conjunction with M] branches in 41 per cent and proximal M2 branches only in 14 per cent.

78

1 Operative Anatomy

Thus the striates originate from one or a combination of the following 5 zones: 1) Proximal segment of Mj 2) Mid-portion of M1 3) Distal segment of Mj, bifurcation 4) Superior trunk of M2 5) Inferior trunk of M2 (Fig 54). In the present experience, the major stem(s) of the striates arose from the superior or inferior trunk of M2 in 10 per cent of cases (Figs 55-60). Fig 54 The 5 origins of the Jatera^ proximal and distal lenticulostriate arteries arisingIrorrTthe proximal ( 1 ) or distal (2) M, segment, from the Mt bifurcation (3), or from the superior (4) or inferior (5) trunks of the M2 segment. Combinations of the above are also seen especially distal M, and proximal M2 origins for these branches.

Fig 55 Angiographic demonstration of the lateral distal striate arteries arising from the superior trunk of the left M2 segment (arrow).

Fig 56A-D Aneurysm of the left middle cerebral artery bifurcation with the lateral distal striates (arrow) arising from the superior trunk of the M2 segment (A) angiogram, (B) operative diagram.

Middle Cerebral Artery

Fig 56 C-D Other examples of the lateral distal striate arteries arising from the M2 segment.

Fig 57A-D Examp1eofalargelateralstriate(arrow)arising from the right proximal M, segment (A) operative photograph, (B) schematic diagram.

79

80

1 Operative Anatomy

Fig 57 C Operative photograph of a right carotid bifurcation aneurysm (arrow 1) and a large proximal lateral striate artery (arrow 2).

Fig 57D Operative photograph of a left carotid bifurcation aneurysm. H = Heubner's artery. Arrows = proximal lateral striate arteries.

Fig 58 Operative photograph of multiple distal lateral striate arteries arising from the most distal portion of the right M, segment at the bifurcation (arrow 1) and from the superior trunk of M2 (arrow 2).

Middle Cerebral Artery

A

81

B

Fig 59A-B The right middle cerebral artery bifurcation as seen at operation from behind showing several large distal lateral striates (arrows) arising just below the bifurcation (A) and (B) after elevation of the superior trunk (arrow).

Fig 60 Operative photograph of the left middle cerebral (M) artery showing the origin of several distal lateral striate arteries from the most distal portion of M, (arrow).

82

1 Operative Anatomy

An important variation of the origin of the lenticulostriates occur in the other 3 per cent of cases. In this instance the striate vessels arise either from a large single lateral fronto-orbital branch or from a common stem with the lateral fronto-orbital artery. The usual origin of the lateral fronto-orbital artery is either from the superior trunk of M21-10 mm after the bifurcation or as a common stem with the prefrontal artery from the superior trunk (Figs 61A-C, 62A-C). However, when associated with the striate vessels the lateral orbito-frontal artery originates from the infero-medial aspect of M1. When this anatomical arrangement occurs and especially if the lateral fronto-orbital artery is large, one can be misled into believing that this is the area of the bifurcation. Some aneurysms may arise in this area and the surgeon must be aware of the possible striate topography as these vessels are often hidden by the aneurysm neck (Fig 63AD).

In the current series, no regular branches originating from M! and coursing to the frontal-orbital cortex and anastomosing with the medial frontal-orbital branches of A2 were ever seen. This arrangement was described by Lang (1979) as occurring in 6 per cent of cases, but represents the association of the orbitofrontal artery and striates described above. It is important to keep in mind all of the possible variations of striate origin to avoid injury to this most important group of vessels during surgical exploration in this area. The vascular territory of the striate arteries will be discussed later in this chapter. There is a reciprocal relation between each of the proximal and distal striate branches of the Mj segment, proximal and distal striate branches of the A, segment and between the Al and Mj striate arteries.

B ii.

Fig 61 A-C Schematic (A) and angiographic (B) demonstrations of the right distal lateral striates and the lateral fronto-orbital arteries arising as a common trunk (arrow), (C) operative photograph.

1

2

Fig 62A Relation of lateral fronto-orbital, lateral striate and prefrontal arteries: 1 Separate origin of the lateral fronto-orbital artery from M2 2 Common trunk of lateral fronto-orbital ( 1 ) and prefrontal arteries from M2(2).

3 Common origin of lateral fronto-orbital ( 1 ) artery together with lateral striate artery from M,. 4 Common origin of lateral striate, lateral fronto-orbital ( 1 ) and prefrontal arteries (2) from M,.

Middle Cerebral Artery

Fig 62B The variation may give the impression of an early bifurcation. ,

Fig 62C Common trunk as seen in the angiogram. Arrow indicates the lateral striate artery.

83

84

1 Operative Anatomy Fig 63A-D Operative photographs of the left middle cerebral artery demonstrating an aneurysm at the origin of the lateral fronto-orbital artery (arrow) from M, (A) and its relationship to the distal lateral striate branches (small arrows) of the lateral fronto-orbital artery (large arrow) (C). Schematic representations of A (B) and C (D).

Middle Cerebral Bifurcation The true bifurcation of the proximal middle cerebral artery (Mj) always occurs at the high point of the limen insulae (see Fig 48). The portion of the middle cerebral artery distal to the bifurcation -the M2 segment - is composed of two trunks, the superior and inferior trunks. Distal to the bifurcation, the trunks turn postero-superior to reach the surface of the insula, thereby describing a more or less pronounced curve called the genu. The area of the bifurcation may also be described as forming an "Omega" pattern because of the trunk's initial divergent but then convergent courses.

Arachnoid fibers stretch between both trunks like ajiarp. The major trunks diverge at the bifurcation, but reapproximate in the Sylvian fissure after 10 to 22 mm. The inferior trunk is frequently under the temporal operculum and may not be identified, especially if early branching of the superior trunk is accepted as the principal bifurcation. The majority of arterial branches near the bifurcation are large and occasionally the same diameter as the superior and inferior trunks. When large branches arise from either the superior or inferior trunks in close proximity to the bifurcation, an

Middle Cerebral Artery

Fig 64A-D The superior or inferior M2 trunks may divide just after the bifurcation giving the false impression of a trifurcation (arrow) as seen diagrammatically (A-B), angio-graphically (C), and intraoperatively (D).

85

86

1 Operative Anatomy

Fig 65A An early division of both superior and inferior M2 trunks may also occur giving the false impression of a quadrification.

impression of a "pseudo-trifucation" or "pseudoquadrification" may be given (Figs 64A-D, 65AB). When precisely dissected these usually represent superior or inferior trunk bifurcations immediately adjacent to the true bifurcation. However_LangJ_1979) has reported that in 20 per cent of cases a trifurcation, tetrafurcatlcmTbr even pentafurcation is present. Similarly Gibo et al (1981) found a true bifurcation in 78 per cent, a trifurcation in 12 per cent, and a division into 5 or more trunks in 10 per cent of cases. There was also a misinterpretation in the monograph of Krayenbuhl and Ya§argil (1965) analysing the carotid angiograms of 1000 cases, that a right-sided trifurcation was found in 43 per cent, a left-sided one in 65 per cent, a tetrafurcation in 16 per cent, and a pentafurcation in 3 per cent. An awarness of these possible patterns is important during aneurysm surgery dissection since the majority of middle cerebral artery aneurysms arise at the true branching point of the middle cerebral artery. Distal to the bifurcation, the trunks of the middle cerebral artery pass over the insula and distribute cortical branches to the lateral frontal, parietal, occipital, and temporal lobes. According to Gibo et al (1981) the superior trunk is dominant in 28 per cent of cases, the inferior is larger in 32 per cent, both trunks are of equal calibre in 18 per cent, and multiple trunks of various sizes are found in 22 per cent.

Fig 65B Operative photograph of the right middle cerebral artery with pseudo-quadrification (arrows).

The arterial branches from the superior trunk usually supply the regions of the inferior frontal cortex, the frontal opercular cortex, the parietal and central sulcus territories. The branches from the inferior trunk generally supply the middle temporal cortex, the posterior temporal cortex, the temporal occipital regions as well as the angular and posterior parietal regions. _________ 'Named peripheral branches of the middle cerebral group include lateral orbitof rental, pref rental, frontoopercular, precentral, central sulcus, angular, and posterior temporal arteries. Discussion of these arteries is beyond the scope of this book, but the reader is referred to excellent descriptions by Gabrielle et al (1949), Duroux et al (1952), Vlahovitch et al (1968), Waddington and Ring (1968), Salamon (1973), Salamon and Huang (1976), Michotey (1972), Waddington (1974), Szikla et al (1977), Huber (1979), Lang (1979), and Gibo et al _ At times anomalies were observed in this study. They were not encountered frequently, but must be considered. A fenestration of the middle cerebral artery was seen in two of one hundred cadaver dissections and in three angiographical examinations and surgical dissections for aneurysms (Figs 66A-C, 67AB). When present it occurred near the origin of the middle cerebral artery. Three cases were also radiographically identified by Iro et al (1977).

Middle Cerebral Artery

87

Fig 66 A—C Examples of fenestrated right distal M, segments. A Angiogram. B Intraoperative photograph (arrows). C Diagram.

продолжение

88

1 Operative Anatomy

Fig 67A Fenestration of the left M, segment (arrow). Fig 67B Schematic illustration of the operative finding of fenestration of M, and A, segments with aneurysm of anterior communicating artery, before clipping (1) and after clipping (2).

Two cases of accessory middle cerebral artery were seen (Fig 68A-D). Both occurred at the Aj-A2 junction opposite the anterior communicating artery. This duplication also gave the origin to the Heubner branch. In another four cases the accessory MCA arose from the proximal Al (Fig 69A-B), and in two cases bilaterally (Fig 70A-B). In another case it arose from the internal carotid artery distal to the anterior choroidal artery (Ya§argil and Smith 1977). Crompton (1962) described ten cases (2.9%) of accessory middle cerebral arteries originating from the internal carotid artery distal to the anterior choroidal artery and one case of this vessel originating from the junction of the A, and A2 segments of the anterior cerebral artery. Jain (1964) found accessory middle cerebral arteries in nine of three hundred brains (30%), with one bilateral and noted it arising from the internal carotid in two cases and the anterior cerebral artery in eight cases.

B There were two cases in which there was no right internal carotid artery. In this situation the middle cerebral artery arose from the posterior cerebral artery (see Fig 38A-F). In only one patient a unique variation was observed with a coiled inferior trunk (Fig 71A-B). Finally, we would like to mention that on no occasion have we ever identified the anterior choroidal artery arising from the proximal Ml segment as stated to occur in 11.4 per cent by Carpenter et al (1954). We have only identified the uncal artery arising in 70 per cent of the cases from the internal carotid artery and 30 per cent of the cases from the proximal M1 segment. It is our belief that it was probably the uncal artery which was mistaken for the anterior choroidal artery in Carpenter's study. Finally we have seen two cases in which the uncal artery was large giving off a branch supplying the temporal polar area.

Middle Cerebral Artery

89

Fig 68A Accessory middle cerebral arteries arising from the A!-A2 junction (large distal medial striate artery gives rise to the accessory MCA). B Accessory middle cerebral artery arising from the A!-A2 junction associated with an aneurysm of the anterior communicating artery and circular stenosis of the proximal M, segment. C Right carotid angiogram with partial stenosis of middle cerebral artery (arrow). D Left carotid angiogram showing an aneurysm of the anterior communicating artery (arrow 1) and accessory middle cerebral artery (arrow 2).

90

1 Operative Anatomy

Fig 69A-B Accessory middle cerebral artery arising from the right proximal part of A, at a spot where a large proximal A, perforator is usually present. A AP angiogram showing the origin of the lateral striate (arrow 2) and lateral fronto-orbital (arrow 3) arteries from this vessel 1. B Diagrammatic representation of A. Fig 69C Symmetrical anomaly on the left with larger branch from left A, (arrow).

Fig 70A-D Another example of bilateral accessory middle cerebral arteries arising from the right (A) and left (B) A, segments (arrow), intraoperative photograph (C); Pr = large proximal medial striate artery gives rise of the accessory middle cerebral artery. Arrow 1 = right A, segment, arrow 2 = right accessory middle cerebral artery.

Middle Cerebral Artery

91

Fig 70D Schematic representation of the origin ot the ace. MCA. Origin from lateral A, (1) , origin from A,-A2 junction (2). The ace. MCA is striped.

Fig 71A-B Unique variation of the right M2 segment in a case with bilobular aneurysm of the middle cerebral artery bifurcation (arrow): the enlarged inferior trunk is_coiled (Mg). A Angiogram (arrow indicates the aneurysm and coiling of inferior trunk). B Operative photograph (arrow indicates clipped aneurysm).

92

1 Operative Anatomy

Anterior Cerebral Artery Complex Proximal Anterior Cerebral Artery (Synonyms: precommunicating segment, "Aj segment") The anterior cerebral artery is generally the smaller of the two arteries leaving the internal carotid artery bifurcation (71%), although it may be equal in size to the middle cerebral artery (24%) or it may be larger in caliber than the middle cerebral (5%) especially if the opposite A1 is aplastic or very hypoplastic.) The size of the anterior cerebral artery is usually 1.0-3.0 mm but hypoplastic (< 1.0 mm) and very hypoplastic (< 0.5 mm) arteries are frequently seen. Angiographically demonstrat-_ed aplasia is almost never confirmed at surgery. The artery courses medially and often somewhat anteriorly, to the interhemispheric fissure, passing over the optic nerves and chiasm with a slightly posterior convex curve to join the contralateral anterior cerebral artery through the anterior communicating artery .1 As the artery leaves the internal carotid artery bifurcation it is crossed by thick-ened bands of arachnoid coursing from the olfactory trigone to the lateral part of the optic nerve and forming a tunnel through which the artery enters the lamina terminalis cistern. (The exact course of the artery is somewhat variable as it may loop underneath the orbitofrontal lobe so its junction with the anterior communicating artery may be quite anterior. Fig 72A-F Variations between the perforating branches of the M, and A, segments are constant. One may distinguish proximal lateral ( 1 ) and proximal distal (2) branches of MCA which are called 'lateral lenticulo-striate arteries" in the literature. The proximal A, perforators (3) are j neglected in the literature or called "medial lenticulostriate arteries", whereas the distal A, perforator (4) is well known as Heubner's artery. These vessels have a reciprocal relationship between the size and distribution not only concerning 1 and 2, or 3 and 4, but also between the groups 1-2 and 3-4. If one or two of these arteries are hypo- or dysplastic, then the others are larger and vice versa. Note also that 3 and 4 may give rise to frontopolar and assessory middle cerebral arteries.

Several small perforating arteries arise along the infero-posterior aspect of the proximal anterior cerebral artery (Aj segment). These arteries do not usually arise directly from the internal carotid artery bifurcation, but rather 2-5 mm distal. They are more frequent and larger in the lateral anterior cerebral area beneath the anterior perforated substance, jit "has been shown that these perforating arteries supply the septum pellucidum, the medial portion of the anterior commissure, the pillars of the fornix, the optic chiasm, the paraolfactory area, the anterior limb of the internal capsule, the anterior-inferior part of the striatum and the anterior hypothalamus (Critchley 1930; Abbie 1933/34; Lazorthes et al 1956; Ostrowski et al 1964; Dunker and Harris 1976; Perlmutter and Rhotonl976). As with most small perforating arteries, there is commonly (46%) a stem vessel that originates from the proximal anterior cerebral artery in this location and runs a recurrent course for several millimeters before dividing into several fine arteries that penetrate the brain substance. In most cases this vessel is of smaller caliber than the recurrent artery of Heubner, but courses with Heubner's artery to the medial anterior perforated substance. On occasion, especially if the lateral striate arteries are small, this vessel may be quite large, even larger than Heubner's artery, and supply branches to the lateral parts of the anterior perforated substance (Figs 72A-F, 73A-G).

1 Lateral proximal striate arteries of MCA 2 Lateral distal striate arteries of MCA

3 Medial proxima\ striate arteries 4 Medial distal striate (Heubner's) artery.

Anterior Cerebral Artery Complex

Fig72B-F

B If the lateral striate arteries (1 and 2) are aplastic or hypoplastic, the medial proximal striate (3) and Heubner's (4) arteries are well developed. C The large medial proximal striate artery (3) also gives rise to Heubner's artery (4). D The large medial proximal striate artery (3) gives rise to Heubner's (4) and fronto-polar arteries (Fp). E The large medial proximal striate artery (3) gives rise to the accessory middle cerebral artery and lateral striate arteries (2). F Unique case with large fronto-polar arising from the proximal lateral striate artery (1) (see Fig 74A).

93

94

1 Operative Anatomy

Fig73A-G Operative photographs of: A A large right proximal medial striate artery originating from a large A, segment (arrow). A, larger than M,. B A large right proximal medial striate artery (arrow). C A hypoplastic right A, segment giving rise to several small perforators (arrow 1 ) , two large medial striates (arrows 2-3), and Heubner's artery (H) D A large right proximal medial striate (arrow) originating from a hypoplastic A, segment.

In four cases from the present series, both this vessel and the recurrent artery of Heubner had a common origin from the proximal anterior cerebral artery, while in 2 cases this vessel, Heubner's artery, and a frontopolar artery all arose from a common stem in this location. In one case a large vessel arose in place of an aplastic A, segment and penetrated the brain alongside a normal Heubner's artery. In one case this artery gave origin to the large frontopolar artery (Fig 74A-B).

Anterior Cerebral Artery Complex

95

Fig73E-G E The right Heubner's and fronto-polar arteries (arrow 2), and proximal medial striate branches (arrow 1) all arising from a common trunk of A,. F The right Heubner's artery (H) arising from the proximal A, segment and running a recurrent course with very small proximal medial striate branches from the more proximal A, (arrow). G A hypoplastic right A, segment ending as a proximal medial striate (arrows). No connection to the anterior communicating artery. Fig 74 A The large left frontopolar artery (arrow) arises at the same level as the proximal medial striate artery of A,. The left carotid angiogram gives the impression of a duplication of the left anterior cerebral artery.

96

1 Operative Anatomy

Fig 74 B Schematic representation of the origin of medial fronto-orbital (1) and fronto-polar (2) arteries. 1 Separate origin from A2. 2 Common origin of medial fronto-orbital together with fronto-polar artery. 3 Common origin of 1 x 2 and Heubner's artery (H) from A,-A2 junction. 4 Common origin from proximal A!

Fig 75 Unusual origin of the proximal A, perforator (medial proximal striate artery) from the antero-inferior wall of A, (usually arising from the superior wall). Notice also the common origin of the lateral striates of the M, segment and the lateral fronto-orbital artery in this operative diagram.

This important vessel and these variations have not been previously recognized by dissection of the area (Dunker and Harris 1976, Perlmutter and Rhoton 1976). It may represent the accessory artery of Charcot described by previous investigators (Wollschlaeger and Wollschlaeger 1969). In one case this artery originated from antero-inferior wall of A! segment (Fig 75).

Anterior Cerebral Artery Complex

Inequality of the proximal anterior cerebral arteries (AI segments) has been reported to occur in 7 per cent (Riggs and Rupp 1963), 8 per cent (Kleiss 1941/42), 25 per cent (von Mitterwallner 1955), and 46 per cent (Adachi and Hasebe 1929) of unselected cases. In the senior author's (MGY) angiographic studies, cadaver dissection, and operative experience (Table 5), the incidence of proximal anterior cerebral artery inequality is quite variable depending on the mode of examination and the definition as to what degree of size difference is significant. These variations may be due to the effects of pressure injection at angiography, the consequences of formal fixation in cadaver specimens, or the effects of operative or subarachnoid hemorrhage induced vasospasm. Similarly the incidence of A1 size differences visualized at surgery would diminish if only marked differences (> 1.0 mm) were counted instead of more minor variations. Kwak and Suzuki (1979) reported hypoplasia of AI in 68.1 per cent of cases with an aneurysm of the anterior communicating artery. Patients with an aneurysm of the anterior communicating artery in the present series showed some inequality of the Aj segments in 80 per cent of cases, with the left larger in 51.2 per cent and the right larger in 26.6 per cent (Fig 76A-B). Other less frequent anomalies of the proximal anterior cerebral artery in the present series included aplasia on the right side in 5 cases (severe hypoplasia < 0.1 mm in 3 cases and true aplasia in 2 cases), aplasia on the left side in 4 (severe hypoplasia in 2 cases and true aplasia in 2 cases), fenestration in 9 cases (right Al 5 cases, left At - 4 cases), duplication in 1 case (left AI) and an extremely short Al segment (R.)

in one case (Fig 77). In another case (craniopharyngioma), the left anterior cerebral artery coursed beneath the ipsilateral optic nerve as has been reported by Nutik and Dilenge (1976) and Bosma (1977). Isherwood and Dutton (1969) presented two cases of the anterior cerebral artery arising just above the ophthalmic artery in one case bilaterally. Eight similar cases were collected by Nutik and Dilenge (1976). Other authors have reported the incidence of aplasia of the proximal anterior cerebral artery to be between 1-2 per cent (Windle 1888; Padget 1944; von Mitterwallner 1963). Duplications of the A, segment have been described by Perlmutter and Rhoton (1976) (2 cases) and Windle (1888) (1 case). No cases of bilateral aplasia have been reported.

Table 5 Anomalies and variations of A, segments. Neuroradiological observations 1965/1968 7305 Cadaver brains

Both A, equal

58 %

Left A, larger

22 %

Right A, larger Severe 14 % 4 hypoplasia Aplasia

% 1.3%

200 Angiographies

41.5% 36.0%

21 .0% 41.3% 1.0% (right/left) 0.5% (right)

97

Operative observations 375 cases 20.0% 51 .2% 26.6% 1 .3% 1.1%

98

1 Operative Anatomy Fig 76A-B Variations of the anterior communicating artery complex with equal and unequal A, segments. A A hidden aneurysm of the anterior communicating artery (white arrow) with equal sized A, segments (black arrows). B An aneurysm of the anterior communicating artery (white arrow) with hypoplasia of the right A! segment (black arrow).

Fig 77 AP arteriogram revealing a very short right A^ segment (arrow) with distortion of the entire anterior communicating artery complex and an anterior communicating artery aneurysm situated over the olfactory tract.

Anterior Cerebral Artery Complex

99

or midportion. Section of the vessel showed that the lumen was traversed by a trabeculated^parEmbryologically, the anterior communicating titition that bound the arterial walls and narrowed artery develops from a multichanneled vascular the lumen perhaps functioning as a valve. Similar network which coalesces to a variable degree by anatomical studies have been reported by Busse the time of birth (Padget 1944). As classically (1921), Adachi and Hasebe (1929). De Almeida conceived, this short artery unites the paired ante- (1931), Kleiss (1941/42), von Mitterwallner (1955), rior cerebral arteries in the lamina terminalis and Perlmutter and Rhoton (1976) (Figs 82A-D, cistern to provide an important anastomotic channel 83A-C, see also Fig 97). Aplasia of the anterior for collateral circulation through the circle of communicating artery was not observed either in Willis. Direction of blood flow through the artery the cadaver dissections or operative cases, but would depend on slight variance in pressure extreme hypoplasia (< 0.1 mm) was seen in 3 between the anterior cerebral arteries of each cadaver brains (1.5%) and 5 operative cases side. (1.3%). In one cadaver brain there was no anterior The anterior communicating artery is commonly communicating artery as the two anterior cerebral between 0.1-3 mm long. Its normal caliber is arteries were fused in the prechiasmatic region (Fig between 1.0-3.0 mm, but hypoplastic (0.5-1.0 84). Duplications were seen frequently (Table 6, mm), very hypoplastic (0.1-0.5 mm), or even see Fig 81A-B), and in the aneurysm cases, the hyperplastic (> 3 mm) vessels are not infrequently lesion could originate from either the primary or seen. By definition, the normal anterior communi- secondary vessel. cating artery is one that connects two Aj segments of equal size. As previously discussed, this occurred in only 20 per cent of anterior communicating aneurysm cases, as in most cases a large A, segment divided into the two distal anterior cerebral arteries (A2) and the anterior communicating artery in such cases could only be defined by the entry point of the hypoplastic contralateral At segment.]Wilson et al (1954) found that 85 per cent of anterior communicating aneurysms were associated with hypoplasia of one At segment and attributed the formation of an aneurysm in these instances to resultant hemodynamic abnormalities. This concept has been supported by Stehbens (1963) and Suzuki and Ohara (1978).________ Overall, the anterior communicating artery probably exists as a single channel in about 75 per cent of cases (von Mitterwallner 1955). In other cases a spectrum of anomalies exists between the multichanneled network of the embryo and the single anterior communicating artery. Busse (1921) examined 400 cadaver brains using a binocular microscope and recorded 227 variations in the anterior communicating artery. These included duplications and triplications, fenestrations, reticular patterns, and loops and bridges (Fig 78A-C) which indent the artery and may function as valves. These were also seen under the operating microscope in examinations of cadaver brains by the senior author (Figs 79A-D, 80A-E, 81A-D). In 14 of 200 brains (7%), the anterior communicating artery was strictured and deviated in its lateral

Anterior Communicating Artery

100

1 Operative Anatomy

Table 6 Variations of the anterior communicating artery recorded in our own and in other series Windle 1888

Perlmutter/ Rhoton 1976

Own ( Cadaver brains :ases Operations

200 cases*

50 cases

200 cases

375 cases

One AcoA

159 (79.5%)

60%

1 1 4 (57%)

224 (59.7%)

Aplasia Fusion short unpaired long (1 A2) Hypoplasia 0.1-0.2 mm 0.3-1.0 mm 1.1-1.5 mm Normal 1 .5-3.0 mm Hyperplasia > 3 mm

2 (one A,)

7

-

-

8 1

? 7

5 3

4 8

? ? ? ? ?

? 7 ? 7 ?

2 4 8 90 2

4 5 11 186 6

Duplication one very small 0.1-0.2 mm one small 0.3-1.0 mm both equal

14 (7%)

30%

41 (20.5%)

84 (22.4%)

7 ? ?

7 ? ?

8 15 18

22 27 35

Triplication

7 (3.5%)

10%

37 (18.5%)

57 (15.2%)

one very small two very small three equal triangular bridges

? ? ? ?

7 ? ?

12 6 1 18

27 18 3 9

Network

-

-

8 (4%)

10 (2.7%)

200

375

* ( 1 9 1 in original work)

9

Fig 78 Variations of the anterior communicating artery as described by Busse ( 1 9 2 1 ) . (From Busse, O.: Virchows Arch, path. Anat. 229: 178-206, 1 9 2 1 ) .

Anterior Cerebral Artery Complex

59 years 9

47 years 9

55 years

82 years d

13 years 9

59 years

44 years 9

43 years 9

63 years d

28 years 9

6 months 6

42 years

37 years 9

36 years 9

59 years 9

86 years <S

45 years

9 years 9

49 years <5

17 years <5

33 years 9

31 years 9

60 years <5

27 years 9

101

102

1 Operative Anatomy

Fig 79A Fenestration of the anterior communicating artery (1-7).

Anterior Cerebral Artery Complex 10 3

Fig 79C Fenestration of both A, segments with aneu-rysm of MCA-bifurcation.

Fig 79B

Fenestration of both A, segments (1-2).

Fig 79 D Three A2 segments with fenestration.

Fig 80 A Angiographic demonstration of a fenestrated anterior communicating artery (arrow).

104

Fig 80B-C

D

1 Operative Anatomy продолжение

Schematic illustration of two operative observations with fenestration.

E

Fig 80D-E Operative observations of fenestration (arrow) of left (D) and right (E) A, segments.

Anterior Cerebral Artery Complex 10 5

Fig 81A Operative observation of a triplex anterior communicating artery (arrows).

Fig 81 B

Schematic illustration of (A),

2 //

e

-^^

D

Fig 81C-D Schematic illustrations of other operative observations before (1) and after (2) clipping.

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1 Operative Anatomy

Fig 82A-D Trabecular indentations of the anterior communicating artery: A Diagram from Busse showing the trabecular nature of the indentation. (From Busse, O.: Virchows Arch. path. Anat. 229:178-206, 1 9 2 1 ) . B A probe through such an indentation (arrow). C Forceps demonstrating the indentation (arrow) in an opened artery. D Operative observation of a trabecular indentation (arrow).

Anterior Cerebral Artery Complex 10 7

Fig 83 A-C Other variations of the anterior communicating artery including A Aplasia - never observed in own material, B An azygous A2 arising from two A, segments, C Three A2 arising from two A, segments.

Fig 84 Angiographic demonstration of a very short (fused) anterior communicating artery (arrow).

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1 Operative Anatomy

Fig 85 A-B Illustration of the A, segment and anterior communicating artery perforators as described by Lazorthes (1959) in coronal section (A). Distribution areas of these perforators in the anterior hypothalamus (B) with paraventricular (1), anterior commissural (2), supraoptic (3), and infundibular (4) regions.

Anterior Communicating Artery Branches For some time a number of authors failed to mention that the anterior communicating artery had branches (Sobotta and McMurrick 1909; Tilney and Riley 1921; Robinson 1927; Critchley 1930; Ranson 1941) or they emphatically stated that the artery had no branches (Critchley 1930; Grinker 1934). Despite this several of these authors even presented illustrations that showed some of these branches (Grinker 1934; Spalteholz 1929). The presence of small perforating arteries! that arise from the postero-inferior aspect of the anterior communicating artery and course to the infundibulum, optic chiasm, subcallosal area, and preoptic areas of the hypothalamus has been demonstrated by Senior (1923), Lewis (1936), and Rubinstein (1944). In a study of 100 cadaver brains, Rubinstein saw branching of the anterior communicating artery in 47. Of these 25 had two or more branches and 22 had one thin twig. These branches were closely traced to the region of the infundibulum and optic chiasrrr where they penetrated the brain substance to continue into the preoptic area of the hypothalamus. The branch to the optic chiasm passed either ventral or dorsal to this structure. Lazorthes et al (1956) examined these arteries and noted their possible importance in anterior communicating aneurysms, but there was little further mention of these vessels in the neurosurgical literature despite the increasingly frequent operations for aneurysms and tumors in this area (Figs 85A-B, 86).

Fig 86 Unique angiographic visualization of the hypo-thalamic perforators (small arrows) in a patient with an aneurysm (large arrow) and segmental vasospasm of the A! segment.

Anterior Cerebral Artery Complex

Since 1969 the senior author has repeatedly demonstrated these anterior communicating artery perforating branches and noted their importance, and in the last few years increasing attention has been given to these vessels (Krayenbiihl and Ya§argil 1972; Ya§argil et al 1975; Dunker

Fig 87 A—B An injected specimen demonstrating the hypothalamic branches (arrow) from the anterior communicating artery, their penetration immediately below the level of the anterior commissure (B), and their branches supplying the anterior hypothalamus. CH = chiasm, h = left Heubner's artery.

Fig 87 C Branches to the anterior hypothalamus (arrow 2) and to the subcallosal gyrus (arrow 3) originating from the anterior communicating artery (arrow 1).

109

and Harris 1976; Perlmutter and Rhoton 1976; Crowell and Morawetz 1977; Lang 1979). The tracing of these branches into the preoptic region has been reported by Clark et al (1938) and Foley et al (1942) (Figs 87A-C, 88A-B).

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1 Operative Anatomy

Fig 88A-B Another injected specimen (given by Dr. Andre Combalbert and Georges Salamon, Marseille, France) showing the origin of hypothalamic branches (white arrows) from the subcallosal artery (black arrow) (A). A radio-opaque injection of the same subcallosal and hypothalamic vessels (B).

Anterior Cerebral Artery Complex

111

A B

c

Fig 89 A-C Variations of A, segments and the origin of the hypothalamic arteries.

If the proximal anterior cerebral arteries (A,) are of equal size, these vessels will arise from the midportion of the anterior communicating artery, b~uTif tEfTAj segments are unequal then the vessels will arise from the anterior communicating artery on the side ipsilateral to the larger Aj. Thus they bear the same relationship to the anterior communicating artery as do aneurysms arising at this location. As a result the vessels will generally be found on the antero-inferior side of the aneurysm neck (Fig 89A-C). The surgeon approaching the anterior communicating artery will be faced with several variations (Figs 90A-H) in the region of the hypothalamic branches. 1) If they originate from the anterior communicating artery then in 65 per cent of cases there will be a single stem artery which will emerge from the anterior communicating artery and divide after 2-5 mm into many fine branches. In the remaining 35 per cent, 3-10 fine branches will emerge

directly from the anterior communicating artery (Fig90A-B). 2) In case of a small or moderate or fully developed third A2 the hypothalamic branches will arise from the inferior wall of the third A2 just at the origin or 5-15 mm distal to it (Fig 90E-F). 3) In case of a unpaired A2 segment, these branches will arise at the origin of the unpaired A2 or 5-10 mm distal to it (Fig 90G). 4) In one cadaver dissection these vessels arose from a stem which originated on a normal AT segment 12 mm distal to the anterior communicating artery (Fig 90H). 5) It should be added that these hypothalamic vessels frequently arise from the anterior communicating artery even in cases in which the artery is quite hypoplastic (Fig 91C). 6) They may also arise only from the first or second or third anterior communicating artery or a combination of them (Figs 90D, 91A-E, 92A-C).

fr

F

G

Fig 90A-H Variations in the origin and number of hypothalamic perforators as related to normal (A-B), hypoplastic (C), and duplicated (D) anterior communicating arteries, and to triplicated (E, F), and single A2 segments (G) and from A2 segment (H).

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1 Operative Anatomy

Fig 91A-E Dissections of formalin-fixed brains to show the hypothalamic arteries (A-E). Note the origin of a hypothalamic perforator from the hypoplastic and duplicated anterior communicating artery seen in C and D.

Anterior Cerebral Artery Complex 11 3

Fig 92A-D Operative photographs showing A A hypothalamic artery arising from a very hypoplastic anterior communicating artery with two equal sized A, segments. B The hypothalamic artery (arrow) arising from a second anterior communicating artery. C A hypothalamic artery (arrow) arising from the superoposterior wall of the anterior communicating artery and dividing immediately.

It is probable that occlusion of these arteries has been partially responsible for the mental changes (Webster et al 1960; Taren 1965) andTelectrolyte disturbances (the author's cases investigated by Landolt 1972) associated with trapping procedures for anterior communicating artery aneurysms between 1967-1969. Recurrent Artery of Heubner In 1872 Heubner described a recurrent artery originating from the anterior cerebral artery and then reversing its course to run back along the proximal anterior cerebral artery to the anterior perforated substance. Critchley (1930) noted that the vessel can originate from Aj near the anterior

perforated substance, from the internal carotid

D Equal sized A, segments, but the clipped aneurysm is exceptionally sited on the left corner of the anterior communicating artery (arrow 1). The hypothalamic arteries (arrow 2) arising from the left A2. Op = optic nerve.

artery bifurcation, from the middle cerebral artery, or from the anterior communicating artery. Ostrowski et al (1960) found it just proximal to the anterior communicating artery in 26 of 28 brains, and just distal in the other two. Ahmed and Ahmed (1967) and Dunker and Harris (1976) described it as originating from the anterior cerebral artery at the level of the anterior communicating artery. In a study of 177 brains by Kribs and Kleihues (1971), the artery was present bilaterally in 95 per cent of cases and in over 50 per cent of these, the origins of both recurrent arteries were at or distal to the anterior communicating artery. In only one case did both recurrent arteries arise proximal to the anterior communicating artery. Perlmutter and Rhoton (1976) found it emerging

114

Fig 93 A-D

1 Operative Anatomy

Variations in the origin of Heubner's artery (see Table 7 for explanation).

from the A2 segment in 78 per cent of cases, from the A! in 14 per cent, and at the level of the anterior communicating artery in the remaining 8 per cent. The variability of the origin of the recurrent artery of Heubner in the present series is noted in Table 7 (Fig 93A-D). The size of the recurrent artery of Heubner varies from 0.2-2.9 mm (Perlmutter and Rhoton 1976). From its origin the artery is contained within the lamina terminalis cistern. It usually runs anterior to the A] segment (60%), but also frequently courses postero-superior to it (40%) (Fig 94A-B). Table 7 The variation of Heubner's Artery Cadaver brains Operations 375 200 cases cases A) Bilateral AcoA-corner

76 (38.0%)

174

(46.4%)

B) Bilateral A,

3 ( 1.5%)

2

( 0.5%)

C) Bilateral B2

51 (25.5%)

102

(27.2%)

19 ( 9.5%) 15 ( 7.5%) 30 (15.0%)

26 30 31

( 6.9%) ( 8.0%) ( 8.3%)

D) Asymmetrical A,/A2 1) 2) 3) E) Rare variations (see Fig 95A) 1) from frontopolarisorcallosomarginalis 2) from proximal A, branch

Fig 94 A The course of the right Heubner's artery as related to the right A, segment. B An example of double right Heubner's from A2.

2 ( 1.0%)

4 ( 1 .1 % ) 3 ( 0.8%)

3) from proximal A,

2 ( 1.0%) 2 ( 1.0%)

4) from access. MCA

0

1 (

2 ( 0.5%)

Anterior Cerebral Artery Complex 11 5

It follows the anterior cerebral artery proximally to the internal carotid artery bifurcation and the proximal portion of the middle cerebral artery before turning into the anterior perforated substance. The field of distribution of the recurrent artery of Heubner was studied by Ostrowski et al (I960) and Dunker and Harris (1976) with subtle injection techniques. JThe artery supplies the anterior part of the caudate nucleus, the anterior Yi of the putamen, a small portion of the outer segment of the globus pallidus, and the anterior limb of the internal capsule. Kribs and Kleihues (1971) found that occlusions of the recurrent artery generally

I I ©

©

resulted in an area of infarction in the rostral i corpus callosum but could relate no clinical syn-i drome to it. Critchley (1930) presented a patient with aphasia, severe weakness in the upper extremity, and slight paralysis of the face, palate and tongue due to recurrent artery occlusion. There is no doubt that occlusion of this vessel can result in a clinical syndrome of aphasia (dominant), hemiparesis, and paralysis of the face and tongue (Fig 95A-C).________________________ When the anterior cerebral artery is hypoplastic, the recurrent artery may be hypoplastic also. In this case there is frequently a large artery arising Fig 95 A Variations of the Heubner's artery and proximal medial striate of A, segment. 1 The right Heubner's artery and right fronto-polar artery from the same trunk. 2 The right Heubner's and proximal medial striate arteries from the same trunk. 3 The right proximal medial striate artery originating from the A, gives rise to the fronto-polar and Heubner's arteries. 4 The accessory middle cerebral artery originates from the corner of A,-A2 and gives rise to Heubner's artery. B The rare

angiographic visualization of both Heubner's arteries in a patient with a large anterior communicating artery aneurysm (arrows). C In another case

both Heubner's are visualized. True aplasia of the right A, segment.

116

1 Operative Anatomy

from the lateral or midportion of the proximal anterior cerebral artery that functions as an accessory artery of Heubner. In one case a large vessel arose from the carotid bifurcation in the place of an aplastic Al segment and penetrated the brain alongside a normal Heubner's artery. The recurrent artery may also rarely arise from the frontopolar or callosomarginal branches of the distal (A2) anterior cerebral artery (see Table 7). Lang (1979) described duplication of the recurrent artery in 29.4 per cent of cases (left 13.7%, right 15.7%). In the present series duplicated (21) or triplicated (1) recurrent arteries were seen in 22 operative cases (11.8%) and in 32 cadaver dissections (16% right - 14, left - 12, bilateral - 4). Aplasia of this vessel was seen in eight operative cases (1 bilateral) and in 6 cadaver dissections. Other reports specifically addressing the recurrent artery of Heubner include Abbie (1934), Lazorthes et al (1960), Westberg (1963), and Lang (1979).

Distal Anterior Cerebral Artery ... (Synonyms: posterior-communicating portion of the anterior cerebral artery, pericallosal artery, "A2 segment" of the anterior cerebral artery) The distal (A2) anterior cerebral artery is that portion of the anterior cerebral artery distal to the anterior communicating artery. After its origin at the anterior communicating artery, the pericallosal segment ascends in the lamina terminalis cistern in front of the lamina terminalis, passes between the hemispheres in the longitudinal fissure, enters the callosal cistern, makes a wide arc around the genu of the corpus callosum, and passes backward, superior to the corpus callosum distributing branches to the medial frontal, parietal, and occipital lobes and the corpus callosum. In most cases (90%), the distal anterior cerebral arteries are equal in size, and each vessel supplies only the ipsilateral hemisphere. In addition to this classical type of A2 distribution, however, there are a

D

variety of commonly encountered anomalies (Fig96A-H). Fig 96A-H Variations of A2 segments with (A) an azygous A2, (B) equal A2 segments with ipsilateral hemispheric branches most common. (C) unequal A2 with the larger left giving bihemispheric branches, (D) unequal A2 with the larger right giving bihemispheric branches, (E) three A2 segments with the third (small) ending at the genu of the corpus callosum, (F) three A2 segments with the third (large) giving bihemispheric branches.

Anterior Cerebral Artery Complex

117

Fig 96(G) Three A2 segments with the left giving rise to the medial fronto-orbital and fronto-polar arteries and the other two supplying ipsilateral hemispheric branches, (H) three A2 segments with both the right and the left giving rise to medial fronto-orbital and frontopolar arteries and the third supplying bihemispheric branches.

Unpaired A2 (Arteria Pericallosa Azygous) In 1885 Wilder _coined_the term "arteria termatica" to describe the fusion of both A2 segments to form a single artery. This unpaired artery perfusing the surface of both hemispheres is also known as the azygous pericallosal artery. In 1888 Windle described a case in which "the two anterior cerebral arteries united to form a single trunk that ran as such to its termination in the longitudinal fissure, giving branches of either side to the surface of the hemispheres". The incidence of the anomaly varies in the literature from 0.0-5.0 per cent (Table 8). In the present series it was seen in 2 per cent of cadaver dissections and in 2.1 per cent of operative cases. Recently Huber et al (1980) reported the incidence of aneurysm formation in a series of angiographically demonstrated azygous pericallosal arteries to be 41.1 per cent, and concluded that "the highest incidence of aneurysm .... occurs at the bifurcation of a large unpaired pericallosal artery." The study of carotid angiograms of 7782 patients in Bern (1959-1979) showed in 17 cases (0.2%) unpaired A2; 7 of these 17 cases had a pericallosal aneurysm (41.2%). Two own cases and 37 cases of the literature of azygous pericallosal aneurysms have been reported as reviewed by Niizuma et al (1980). Kondo et al (1979) found that aneurysms of unpaired anterior communicating artery either ruptured or unruptured are extremely rare. In our own cases there were only 2 cases with aneurysm of the unpaired A2 of 23 pericallosal artery aneurysms (Figs 97, 98A-E). Median Callosal Artery (Synonyms: A. cerebri anterior mediana, A. mediana corporis callosi, A. corporis callosi superior, "third A2")

Fig 97 Anatomical dissection in a formalin-fixed brain showing an azygous A2 opened at the level of a short frontopolar artery with trabecular indentations into the lumen (arrow).

118

1 Operative Anatomy

Fig 98A-E The association of as seen (A) on the AP an azygous A2 (large arrow) angiogram (arrow), (C) in the operative photographs as the aneurysm (arrows) is being with an aneurysm (small arrow) angiogram, (B) on the lateral angiogram (arrow), (C) in the operative ohotoaraohs as the ane dissected and (D) clipped.

Anterior Cerebral Artery Complex

Fig 98 E

Diagram of the operative findings.

Another variation of the A2 segments occurs when an additional artery arises from the postero-inferior surface of the anterior communicating artery and courses around the genu of the corpus callosum with the two pericallosal arteries. This artery has been termed the medial anterior cerebral artery, the median callosal artery, the superior callosal artery and the third A2 artery. This artery was described by Windle (1884, 1888): "In nine instances a third vessel was present. It arose in each case from the anterior communicating artery, and passed forward in the longitudinal fissure between the two companion branches, for about % of the length of the corpus callosum. It then divided into branches for both opposed surfaces of the hemispheres." The incidence of anomaly varies between 0.5 per cent and 64 per cent in reported cases (see Table 8). The third A2 segment may be quite short and terminate at the genu of the corpus callosum supplying the structure, the adjacent cortex, the septal nuclei, septum pellucidum, and the upper portion of the columns of the fornix, or it may be as long as the other A2 segments (Fig 99). In the present series of patients, a third A2 was found in 9 per cent of cadaver dissections and in 9.6 per cent of operative cases. In the surgical cases it was not possible to follow the artery along its course for a longer distance than 10-20 mm, but the size of this vessel was seen to be about 1.0 mm in 6 cases, between 1.0-2.0 mm in 9, and 2.0-3.0 mm in the other 21 cases (in 3 cases with a fenestration at the origin , see Fig 103). In the cadaver dissections, the terminations of the A2 arteries were dissected. In 2 brains the small vessel ended at the Fig 99 Three main types of A2 segments after Lazorthes etal (1956). 1 = short, 2 = medium, 3 = long.

продолжение

119

120

1 Operative Anatomy продолжение

genu, in 3 a moderate sized vessel ended as a pericallosal artery and in 13 brains a large third A2 supplied uni- (3) or bihemispheric (10) branches (Figs 100-104). De Vriese (1904) found a higher incidence of third A2 arteries in newborns and fetuses than in adults and hypothesized that third A2 vessels are commonly present at birth and then atrophy with age. This was disputed by Padget 1948 and Baptista 1963. No children were examined in the present cadaver series. Additional description of the distal anterior cerebral artery and its anomalies can be obtained from the work of Duret (1874), Heubner

(1874), Beevor (1907), Foix and Hillemand (1925), Shellshear (1927), Godinov (1929), De Almeida (1933), Gabrielle et al (1949), Curry and Culbreth (1951), Ruggiero (1952), Marino (1976) and Lang (1979). Baptista (1963) studied the distal segment (A2) of the anterior communicating artery in 381 human brains. Arterial anomalies were found in 25 per cent of these brains and could be classified into 5 groups. In combination with our own findings, the following modified classification is proposed.

Table 8 Frequency of anterior communicating artery variations in the literature Author

Year

No. of cases

Unpaired 1 A2

Bihemispheric AcoA

Triplex

Windle

1888

200

1 (0.5%)

No mention

9 ( 4.5%)

De Vriese

1904

50

-

-

11 (22.0%)

De Vriese

1905

100

5 (5.0%)

1?

64 (64.0%)

Fawcett et al Blackburn

1905/6

700

-

1907

400

7 (1.7%)

No mention 1?

23 ( 3.2%) 42 (10.5%)

Hasebe Adachi and Hasebe

1928

83

1 (1.2%)

1929

1420

9

No mention No mention

15 (18.0%) 136 ( 9.0%)

Kleiss

1942

325

2 (0.6%)

No mention

12 ( 3.6%)

Von Mitterwallner Lazorthes et al

1955

360

1956

35

? -

No mention No mention

25 ( 7.0%) 7 (20.0%)

Alpers et al

1959

350

6 (1.7%)

No mention

28 ( 8.0%)

Van der Ecken Baptista

1961

90

1 (1.1%)

1963

381

1 (0.2%)

12 (13.3%) 45 (11.8%) R.AcoA to L. 20 and reverse 25

4 ( 4.4%) Unihemisph. 27 Bihemisph. 23

Le May and Culebras

1972

107

4 (3.7%)

cases No mention

• 8 ( 7.4%)

Perlmutter and Photon

1976

50

-

No mention

1 ( 2.0%)

Marino

1976

24

No mention

4 (16.0%) 1 unihemisph. 3 bihemisph.

Dunker and Harris

1976

20

1 (0.5%)

200 brains

4 (2.0%)

Our dissections

adults Ow operated cases

375

8 (2.1%)

A2 in about 90 per cent is of equal size in about 10 per cent one A2 is larger - (may be bihemispheric A2)

2 (10.0%) 22 (11.0% ) R. to L. 10 cases L. to R. 12 cases Only to genu-rostrum Ending as pericallosal Unihemispheric 3 } Bihemispheric 10 j

18 ( 9.0%) Small

2

Middle 3 Large 1 0 2 short 3 long 36 (9.6%) Small 6 Middle 9 Large 21

Anterior Cerebral Artery Complex

121

Fig 100A-C Anatomical dissection showing three A2 segments with the middle one supplying bihemispheric branches (A). Anatomical dissection of two other examples showing three A2 segments (arrows) with the right one supplying only fronto-orbital and frontopolar arteries (B), and in (C) left fronto-orbital and frontopolar arteries (arrows).

1) 1 A2 = fused, unpaired artery, irrigating the mesial surface of both cerebral hemispheres (bihemispheric 1A2). 2) 2 A2 present (classical type) a) Left and right, each one supplying its homolateral(ipsi-) hemispheres (unihemispheric A2). b) Both A2 are present. One of them sends forth one or more branches which cross the midline to be distributed to the mesial surface of the contralateral hemisphere (one unihemispheric A2, one bihemispheric A2). 3) Third A2 (accessory A2 - Triplex) Besides the right and left A2 a third middle or median artery is present, a) The third A2 may distribute only to one hemisphere (unihemispheric third A2).

b) The third A2 may distribute to both hemispheres (bihemispheric third A2). (The third A2 did not always bifurcate to irrigate both cerebral hemispheres).

122

1 Operative Anatomy

Fig 101 A-C Example of a case with three A2 segments (arrow 1) and an anterior communicating artery aneurysm (arrow 2) as seen on angiography (A) and at operation after coagulation of its neck (B). Anterior rotation of the aneurysm demonstrates better the three A2 segments (C).

Fig 102A-B Another case with three A2 segments and a double anterior communicating artery with an aneurysm seen at operation. In (A) the aneurysm (arrow) and two A2 segments are initially visible; however, upon further dissection and elevation (B) the third A2 comes into view (arrow).

Anterior Cerebral Artery Complex 12 3

Fig 103A-B Another case with three A2 segments with fenestration (arrow). The operative findings are shown diagrammatically in (B) before (1) and after (2) clipping.

Fig 104A-E Schematic illustrations of other cases with three A2 segments and with aneurysms before ( 1 ) and after (2) clipping.

124

1 Operative Anatomy

in*

2

2

B

C

D

E

Fig 104B-E Hidden third A2 segment in four other cases before (1) and after (2) clipping

Anterior Cerebral Artery Complex

In surgical approaches to aneurysms in this area, the operators must consider the possible variation of the distal anterior cerebral artery. When present a third A2 usually lies beneath the principle pericallosal arteries and is hidden from immediate view, especially when the fundus of a superiorly or posteriorly directed aneurysm overlies it. Attention should be directed to the possibility of a third A2 being present on the A-P view angiogram and to the origin of the callosomarginal branches on the lateral views. At surgery the right AJ and A2 segments should be gently elevated to expose a third A2 if present (Figs 105A-E, 106A-D).

Fig 105A-E The A2 variations (1) recognizable on lateral view of the angiogram (2): A Normal lateral view. B A third A2 extending to the genu of the corpus callosum.

125

126

1 Operative Anatomy

Fig 105C Three equal A2 segments. In the lateral view of the angiogramtwo large arteries are visualized.

1 D Early origin of a fronto-polar or calloso-marginal artery from the A,-A2 junction.

E An azygous A2 segment.

Anterior Cerebral Artery Complex Fig 106 A Angiogram demonstrating three A2 segments with an aneurysm in the left A!-A2 corner and vasospasm of the right A2.

Fig 106B Lateral view (arrow). .

127

128

1 Operative Anatomy

As the distal anterior cerebral or pericallosal artery follows the corpus callosum several regular branches are distributed to the surrounding cerebrum. The recurrent artery of Heubner is often the first branch of the anterior cerebral artery beyond the anterior communicating artery, and has been described above. A small artery often arises just distal to the anterior communicating artery and courses to the olfactory nerve where it lies alongside it in the olfactory cistern. A larger artery usually arises 2 to 5 mm beyond~lhe~ anterior communicating artery and courses perpendicularly or diagonally across the olfactory tract, often arching deeply into the olfactory cistern, but finally reemerging on the orbital surface of the cortex. This artery is commonly termed the medial fronto-orbital artery. Thejnedial fronto-orbital arteries generally arise several millimeters beyond the anterior communicating artery and define a plane of separation between the lamina terminalis and corpus callosum cisterns. These arteries course forward on the medial aspect of the fronto-orbital lobes.___ The calfosomarginal artery is the primary division of the anterior cerebral artery and may give many of the major cortical branches. Some authors (Krayenbiihl and Ya§argil 1968; Huber 1979) call the continuation of the anterior cerebral artery beyond the callosomarginal artery the pericallosal artery, while others (Stephens and Stilwell 1969; Lin and Kricheff 1974) use the term pericallosal artery to describe the anterior cerebral artery beyond the anterior communicating artery.jAneurysms arising from the anterior cerebral artery distal to the anterior communicating artery usually arise at the origin of the frontopolar or the callosomarginal artery, other locations being very rare. The medial fronto-orbital and frontopolar arteries may have a common origin or both may arise from a low branching callosomarginal artery. In four cases in the present series the recurrent artery of Heubner, medial fronto-orbital and frontopolar arteries all arose from a common trunk. In another case an accessory middle cerebral artery arose opposite to the A1/A2 corner, gave off the artery of Heubner, and continued into the Sylvian fissure (see Fig 68AB). When the callosomarginal artery is especially large and gives most of the cortical branches, the pericallosal artery continues as a diminutive vessel. As the pericallosal artery courses posteriorly over the corpus callosum it gives off small branches laterally which supply the cingulate gyrus. Branches directed inferiorly into the corpus callosum are rarely seen. The pericallosal artery

tapers^ after the precuneal branch, but may continue around the splenium of the corpus callosum giving parietal and occipital branches (Huang and Wolf 1964). It may even extend to the foramen of Monro as a spleniothalamic artery (Schlesinger 1976). More commonly posterior pericallosal branches of the posterior cerebral artery supply this area.

Vertebrobasilar System Between 1953 and 1964, the senior author was involved in a study of the vertebrobasilar system. The results of 400 cadaver brain dissections were presented in 1957 and 1965, and since then, he has concentrated his anatomical efforts on the anterior cerebral circulation. Recent work of Saeki and Rhoton (1977), Zeal and Rhoton (1978), and Fujii et al (1980) supplements the work of Radner (1947), Olsson (1953), Sjogren (1953), Hauge (1954), Decker (1955), Krayenbiihl und Yas,argil (1957), Wackenheim and Metzger (1962), Wolf et al (1962), Economos and Prosalentis (1963), Greitz and Sjogren (1963), Khilnani and Silver-stein (1963), Goree et al (1964), Tiwisina (1964), Bret (1965), Hermann and Seeger (1965), Krayenbiihl and Ya§argil (1965/1968), Ruggiero (1965), Scatliff et al (1965), Dilenge and David (1967), Leman et al (1967), Takahashi et al (1967), Symon and Kendall (1973), Newton and Potts (1974), Takahashi (1974), Duvernoy (1978), and Huber (1979). Lasjaunias (1981) has made a significant contribution to the understanding of vertebral artery anatomy. A superb description of the vertebrobasilar venous system can be found in Huang et al (1965, 1967, 1968) and additional references in Wolf et al (1963, 1966), Takahashi et al (1967), Ben Amor et al (1971), Bull and Kozlowski (1970), Tournade et al (1971) and Duvernoy (1975).

Vertebral Artery The vertebral artery (0.92-4.09 mm in diameter) leaves the foramen transversarium of the atlas and passes through the atlanto-occipital membrane to enter the posterior fossa through the foramen magnum. Intracranially, the artery lies within the lateral cerebellomedullary cistern and courses antero-medially along the medulla just below the hypoglossal rootlets to reach the pontomedullary sulcus where it joins with the opposite vertebral artery to form the basilar artery. Reinforcing fibers of arachnoid at the pontomedullary sulcus demarcate the beginning of the prepontine cistern and basilar artery.

Vertebrobasilar System

129

Fig 107 Variations and anomalies of the vertebral arteries. (From Krayenbuhl, H., M. G. Yasargil: Die vaskularen Erkrankungen im Gebiet der Arteria vertebralis und Arteria basialis. Thieme, Stuttgart 1957).

The site of junction of the vertebral arteries is usually at the lower border of the clivus but this union is variable and tortuosity of the arteries with age may change its position. The two vertebral arteries are usually different in caliber, with the left being more often larger (Fisher 1965; von Mitterwallner 1955) (Fig 107). A not uncommon anomaly (0.2%) is for one vertebral artery to end as the posterior inferior cere-bellar artery and the other to continue as the basilar artery (Morris and Moffat 1956; Krayen-biihl and Ya§argil 1965). Fenestrations and duplications of the vertebral arteries have been reported (Lasjaunias 1980; Rieger 1983) and these

anomalies are frequently associated with intracranial vascular abnormalities including AVM's and aneurysms (Kowada et al 1973; Mizukami et al 1972; Nakajima et 31 1976; Miyazaki et al 1981). We observed only one case with fenestration of the right vertebral artery, a microaneurysm within the fenestration and a ruptured aneurysm of the right VA just after the entrance through the dura (Fig 108A-B). Complete atresia can also occur (Mitterwallner 1955; Krayenbuhl and Ya§argil 1957). Tsukamoto (1981) described a case with proatlantal intersegmental artery with absence of bilateral vertebral arteries.

Fig 108A-B Schematic representation of vertebral artery fenestrations (A) with a ruptured aneurysm of the vertebral artery and an unruptured microaneurysm. (B) Operative photograph.

130

1 Operative Anatomy

Fig 109 Variation of anterior spinal artery (after Stop-ford).

Branches of the vertebral artery include several small branches to the anterolateral, lateral, and posterolateral medulla, the anterior spinal artery which joins with its opposite mate at the pyramidal decussation to run a recurrent course in the premedullary cistern to the cervical spinal cord (Fig 109), and the posterior inferior cerebellar artery. Small posterior spinal arteries usually originate from the posterior inferior cerebellar arteries (73%) but can arise from the vertebral arteries. They descend along the postero-lateral aspect of the medulla and spinal cord as a plexus of fine vessels. Posterior Inferior Cerebellar Artery The posterior inferior cerebellar artery is the largest (0.65-1.78 mm) and most distal branch of the vertebral artery. This vessel has a variable site of origin from the vertebral artery, at times as low as the extracranial portion of the vertebral artery and at times as high as the vertebral artery junction or basilar artery (Fig 110). The site of origin to some extent determines its course. Most commonly, the artery arises 14-16 mm below the vertebral artery junction, in the anterior medullary cistern and winds around the lower end of the olive within the lateral cerebellomedullary cistern superior to or between the hypoglossal nerve rootlets. The artery then turns caudally and passes between the rootlets of cranial nerve XII anteriorly and cranial nerves IX, X, and XI posteriorly. In this position it is between the lateral medulla and the biventer

lobule of the cerebellum and supplies fine branches to the lateral and postero-lateral medulla. It continues interiorly and forms a caudal loop around the cerebellar tonsil to enter the cisterna magna. In 35 per cent of cases the artery will extend a few millimeters lower than the tonsil or the foramen magnum, the position of the caudal loop as seen on angiography is not an entirely reliable sign to assess tonsillar herniation. The artery then ascends on the tonsil behind the roots of the cranial nerves IX and X again supplying posterolateral medullary branches, until it reaches the posterior medullary velum where it supplies branches to the anterior tonsil and choroid plexus of the fourth ventricle. It then reverses direction and forms a loop over the superior pole of the tonsil and branches into tonsillo-hemispher-ic and vermian branches that supply the under-surface of the cerebellar hemisphere (including the tonsil) and the inferior vermis, respectively. As will be discussed under the anterior inferior cerebellar artery, an inverse relationship often exists between the size of the posterior inferior and anterior inferior cerebellar arteries. The posterior inferior cerebellar artery is present as a single vessel in 90 per cent of cases, duplicated in 6 per cent, and absent in 4 per cent (Fujii and Rhoton 1980).

Vertebrobasilar System

131

Fig 110 Variations of anterior and posterior inferior cerebellar arteries.

Basilar Artery The basilar artery begins in the area of the pontomedullary sulcus by the junction of the two vertebral arteries, and courses upward in the prepon-tine cistern in a shallow groove on the surface of the pons. The distal segment reaches the interpeduncular cistern at about the level of the dorsum sellae where it divides into two posterior cerebral arteries. With increasing age the basilar artery becomes more tortuous and elongated and the bifurcation may lie more superiorly, even encroaching on the posterior third ventricle. A perfectly straight course of the basilar artery is found in only 25 per cent of cases, as the artery is frequently deviated from the midline, especially in older age groups. The proximal basilar artery is usually concave toward the larger vertebral artery (Newton andTotts 1974). Embryologically, the vertebral arteries run as paired channels to the posterior cerebral arteries, thus allowing for several anomalies of union to occur. Busch (1966) described in 3 cases out of 1000 cadaver brains full indentation of the wall of

basilar artery (2 mm large) transversely or longitudinally 3-8 mm distal to the vertebral junction, similar to the valvular findings of anterior communicating artery. The basilar artery may be formed by one vertebral artery with the other ending as the posterior inferior cerebellar artery. Busch (1966) reported 13 such cases in 1000 cadaver brains (1.3%), in 12 cases proximally and in one case distally localized. Fenestrations of the basilar artery are not uncommon (1%). Kawamoto et al (1972) studied 216 vertebral angiograms and reported on 4 cases with fenestration in the verte-bro-basilar system. Takahashi et al (1973) saw only 3 cases in 500 vertebral angiograms. Complete duplication, or persistence of the paired basilar arteries of the embryo has been described only twice (Fig 111). Fenestrations are associated with basilar artery aneurysms (Hoffmann and Wilson 1979, Hemmati and Kim 1979, Matricali and Van Dulken 1981). Persistent carotid-basilar anastomoses such as primitive trigeminal, optic, hypoglossal, or proatlantic arteries may fill the basilar artery or vertebral arteries from the carotid

132

1 Operative Anatomy

the abducens nerve and in one case the nerve passed through a fenestration in the artery. Within the cerebellopontine cistern the artery traverses somewhat inferiorly in close relationship to the pons and supplies small branches to the lateral pons from its medullary junction to the upper onethird. Near the origin of the cranial nerves VII and VIII the anterior inferior cerebellar artery usually bifurcates and either one or both main trunks then turn laterally to course with these nerves, generally on their ventral-medial surface. At this turn of the artery, one or more fine branches (lateral medullary arteries, Foix and Hillemand 1925), may course to the area of the olive and lateral medullary fossa. In most instances one of the anterior inferior cerebellar artery trunks traverses infero-medially 1 case 1 case 1 case 1 case near the brain stem to reach the inferior cerebellar from Piersol from Berr and surface while the other follows cranial nerves VII Anderson and VIII toward the internal auditory meatus for a Fig 111 Variations of the basilar artery. variable distance before looping medially beneath the cerebellum. Sunderland (1945) and Mazzoni (1969) described this segment of the artery as circulation (see p. 306). The diameter of the basilar reaching or actually protruding into the internal artery ranges from 2.7-4.3 mm (Wollschlaeger et al auditory canal in 64 per cent and 67 per cent of 1967), ..making it roughly,, the same size as each cases respectively. Martin et al (1980) confirmed of the internal carotid arteries. The basilar artery this in 54 per cent of 50 brains. In a majority of gives off paramedial and circumferential cases this segment of the artery is located anteroperforating arteries that supply most of the pons inferior or between the nerves, and supplies recurrent and mesencephalon as well as its larger branches, perforating branches to these nerves and to the the anterior inferior cerebellar artery, the internal portion of the pons surrounding their entry auditory artery (15 per cent), the superior cerebellar zones. After looping out of internal acoustic meatus artery, and the posterior cerebellar arteries and arriving back at the base of the middle (Kaplan and Ford 1966). Two twig arteries arising cerebral peduncle, this so-called "nerve-related" from the most proximal portion of the basilar anterior inferior cerebellar artery trunk gives artery and penetrating the antero-medial medulla branches to the middle cerebral peduncle and to from the pyramid to the pyramidal decussation the inferior cerebellar surface adjoining the horiwere seen frequently in the present series. These zontal fissure. The other "nerve-un-related" AICA perforators have never been previously mentioned trunk supplies the flocculus, choroid plexus, and and still need to be precisely described (see Fig infero-medial cerebellar surface (Martin etal!980). Rich anastomoses exist between peripheral bran137). ches of the anterior inferior cerebellar artery, the posterior inferior cerebellar artery and to a limited Anterior Inferior Cerebellar Artery degree the superior cerebellar artery. There is The origin of the anterior inferior cerebellar usually an inverse relationship between the size of artery from the basilar artery is usually solitary the anterior and posterior inferior cerebellar ar(58%) but may be duplicated (20%), triplicated teries. When one cerebellar artery is small, the (20%) or rarely absent (2%) (Fujii and Rhoton adjacent ipsilateral or contralateral arteries are 1980). The artery arises from the lower third of larger. According to Fujii and Rhoton (1980), the the basilar in 75 per cent of cases, from the middle anterior inferior cerebellar artery is hypoplastic in third in 16%, and within a few millimeters of the 20 per cent of cases with corresponding enlargevertebral junction in 9 per cent (Stopford 1916). ment of the ipsilateral PICA or rarely the ipsilateral The artery courses backward around the pons and superior cerebellar. In 32 per cent of cases, PICA may cross cranial nerve IV dorsally or ventrally as it is hypoplastic with the ipsilateral AICA or the passes from the prepontine cistern to the cere- contralateral PICA being larger (see Fig 110). bellopontine cistern (Watt and McKillop 1935). In six cases in the present series the artery perforated

Vertebrobasilar System

133

Fig 1 1 2 Variations of the superior cerebellar artery.

Sunderland (1945) reported that the internal auditory artery arises from the anterior inferior cerebellar artery in about 85 per cent of cases and from the basilar trunk in the other 15 per cent. However, reports by Adachi (1928), Fisch (1968), and Martin et al (1980) describe-this vessel as arising from the anterior inferior cerebellar artery in all cases (100%). The internal auditory artery enters the internal auditory canal and branches to supply the nearby bone and dura, the nerves within the canal, the vestibular apparatus, and the cochlea. Superior Cerebellar Artery The superior cerebellar artery is the most consistent in terms of origin and location of all the posterior fossa arteries (Hardy and Rhoton 1978). Most frequently the superior cerebellar artery arises from the basilar apex below, but directly adjacent to the origin of the posterior cerebral arteries. When the bifurcation is a deep cleft, the superior cerebellar arteries may appear to originate from the base of the posterior cerebellar arteries. In a few cases (Fig 112) the artery may arise several millimeters from the bifurcation or from the posterior cerebral artery. Its origin is considered to lie within the interpeduncular cistern, but as the artery courses laterally, separated from the posterior cerebral artery by the oculomotor nerve, it acquires its own arachnoid sleeve. Small branches are given within the inter-peduncular cistern (see p. 151 and Fig 131)./U] encircles the brain stem in a groove between the! pons and mesencephalon. Within the ambient | cistern of the lateral side of the brain stem, the artery makes a shallow caudal loop and then divides into a lateral and medial branch. At this point

either the trunk itself or one of the branches often comes into direct contact or distorts the emerging trigeminal nerve (Hardy and Rhoton 1978; Haines and Janetta 1980). The superior cerebellar artery trunks then course posteriorly in the infratentorial portion of the ambient cistern in close relation to the brainstem but near the free edge of the tentorium, the trochlear nerve, the basal vein of Rosenthal and the posterior cerebral arteries. The lateral branch (marginal branch, Critchley and Schuster 1933) courses antero-laterally to follow the quadrangular lobule of the cerebellum above the trigeminal nerve and then extends postero-laterally in the region of the horizontal fissure to supply the jupero-lateral cerebellar hemispheres and deep nuclei.] The medial branch encircles the ponto-mesencephalic junction as the trunk of the superior cerebellar artery gives origin to several hemispheric branches and then reaches the caudal tectum in the area of the inferior colliculus where it enters the quadrigeminal cistern. This branch supplies fine perforating vessels to the area of the brachium conjunctivum and inferior colliculus. It then approximates the contralateral vessel and turns interiorly over the superior vermis as the superior vermian artery. The hemispheric branches reach the superior cerebellar surface and fan out in a radial pattern toward the horizontal fis-sure supplying the supero-medial cerebellar hemisphere and dentate nucleus (Stephens and Stilwell 1969). All of the superior vermian and hemispheric branches may form anastomoses with the anterior inferior or posterior inferior cerebellar arteries. Also numerous fine anastomoses occur between the superior cerebellar artery medial

134

1 Operative Anatomy

branch and branches of the posterior cerebral artery in the quadrigeminal cistern. Critchley and Schuster (1933) called these anastomoses a plexus pedunculi, but Duvernoy (1978) pointed out that most of these anastomoses are ipsilateral. The size of the superior cerebellar artery varies from 0.721.50 mm (Wollschlaeger et al 1967). The superior cerebellar arteries are of equal size in 33 per cent of cases, the right is larger in 31 per cent, and the left in 38 per cent of cases (Stopford 1916). Duplication of this vessel is seen on the right in 8 per cent and on the left in 13.3 per cent (von Mitterwallner 1955). Mani et al (1968) found duplication in 28 per cent of cases, while Blackburn (1907) found it on the right in 2 per cent, on the left in 1 per cent, and bilateral in 1 per cent of 270 cases (see Fig 131). It is generally considered that a double origin is equivalent to the lateral branch of the artery having its own origin from the basilar artery (see Fig 112).

Posterior Cerebral Artery The terminal bifurcation of the basilar artery within the interpeduncular cistern bifurcates 1-3 mm distal to the origin of the superior cerebellar artery inferior to the much larger paired posterior cerebral arteries (0.65-1.78 mm, Wollschlaeger et al 1967). From its origin the posterior cerebral artery curves superior to the oculomotor nerve in relation to the antero-medial portion of the peduncle and joins the posterior communicating artery. This segment of the posterior cerebral artery from its origin to the posterior communicating artery is termed the Pj segment (Krayenbiihl and Ya§argil 1968). Synonyms include the mesen-cephalic, precommunicating, circular, peduncular, and basilar segment (Figs 113A-E, 114). Most commonly the posterior cerebral artery (Pr segment) is larger than the posterior communicating artery (see Fig 113B-C), but the Pl segment may be smaller than the posterior communicating artery in up to 20-40 per cent of cases (Alpers et al 1959; Riggs and Rupp 1963; Kaplan and Ford 1966; Krayenbiihl and Ya§argil 1968). Embryo-logically the posterior cerebral artery arises from the internal carotid artery (carotid segment). With development the Px segment of the posterior cerebral artery (basilar segment) usually enlarges to form a major connection between the basilar and posterior cerebral arteries with subsequent diminution in the size of the posterior communicating artery. In 22 per cent of cases Saeki and Rhoton (1977) found a small P! segment and a larger posterior communicating artery (unilateral 20%, bilateral 2%) with persistence of the fetal type of

Fig113A-E Relationship between the posterior communicating artery (striped) and the P, segment of the posterior cerebral artery: A Equal size, B Hypoplasia of the posterior communicating artery, C Aplasia of the posterior communicating artery, D Hypoplasia of the P-, segment, E Aplasia of the P, segment.

продолжение

Vertebrobasilar System продолжение Normal

Large

Hypoplasia

Aplasia

135

Duplication

transitional primitive

Fig 1 1 4 Variations of the posterior portion of the Circle of Willis. From Krayenbuhl, H., Yas.argil, M. G.: Die vaskula-ren Erkrankungen im Gebiet der Arteria vertebralis und Arteria basialis. Thieme, Stuttgart 1957.

posterior cerebral circulation arising from the internal carotid artery. In the present series, the posterior cerebral artery was perfused primarily from the basilar artery in 67.5 per cent of cases, from the internal carotid in 24.5 per cent, and equally from both in 8 per cent. Kameyama and Okinaka (1963) reported similar results. Angiographic demonstration of the posterior cerebral arteries occurs in 14-41 per cent as reported in the literature (Krayenbuhl and Ya§argil 1968). It should be noted that in both angiographic and cadaver studies, the fetal type of circulation with a large posterior communicating artery seems to occur with much greater frequency on the right (Tables 9 and 10).

Course of P2-P3-P4 After connecting with the posterior communicating artery, at the anterior margin of the peduncle, the posterior cerebral artery arches postero-later-ally around the cerebral peduncle and enters the ambient cistern. The artery then parallels the course of the basal vein of Rosenthal which lies superior, and the trochlear nerve, tentorial edge, and superior cerebellar artery, which all lie inferior. As the vessel approaches the mesencephalic tectum inferior temporal branches arise. This portion of the posterior cerebral artery from the posterior communicating artery to the origin of the inferior temporal arteries is called the P2 segment (Krayenbuhl and Ya§argil 1968). Synonyms

136

1 Operative Anatomy

Table 9 Posterior cerebral artery arising directly from internal carotid artery

(Cadaver studies)

Total

Bilateral

Right

Left Q

o/

Windle 1888

24 %

4

de Vriese 1905 Fawcett and Blachford 1906

28 % 10 %

20 %

8 %

D

4 %

Blackburn 1907

22 %

-

10 %

7

Stopford 1 9 1 6

10 %

2 %

5 %

3 0 /

Sunderland 1948 von Mitterwallner 1955

32 %

O

13

13 %

19

3.6%

9.7%

4.7%

Ours

24.5%

4.5%

13.3%

7.3%

°/

°/

/o

11

%

/o %

5 %

/o

/o

Table 10 Further anomalies of the posterior communicating and posterior cerebral arteries

3) a) Duplication from a basilar origin (0.5%, Gordon-Shaw 1 9 1 0 ) b) Duplication from a basilar origin with fusion into a single trunk (Windle 1888) c) Origin of the anterior choroidal artery (von Mitterwallner 1955; Krayenbuhl and Yasargil 1965) d) Separate origin of the posterior temporal branch from the internal carotid artery (Critchley and Schuster 1933)

include the ambient, postcommunicating, and perimesencephalic segments. Zeal and Rhoton (1978) divided this segment into equal halves, the P2A (anterior) and P2P (posterior).fThe branches of this segment include peduncular perforating arteries (1-6) that penetrate the cerebral peduncle and supply the corticospinal and corticobulbar pathways, the substantia nigra, red nucleus, and other mesencephalic segmental structures, the medial and lateral posterior choroidal arteries, and the thalamogeniculate arteries (Figs 114-118). After the origin of the inferior temporal branches, the posterior cerebral artery continues to curve around the mesencephalic tectum until it pierces the quadrigeminal cistern and reaches the lateral geniculate body under the pulvinar thalami. Here the vessel divides into its terminal divisions, the parietal occipital and calcarine arteries. The segment of the posterior cerebral artery from the origin of the inferior temporal branches to the origin of the parieto-occipital and calcarine arteries is termed the P3 or quadrigeminal segment. The segment after the origin of the parieto-occipital and calcarine arteries is called the P4 segment. Branches of the P3 segment (in addition to the inferior temporal branches) include the posterior pericallosal arteries. Additional information concerning the anatomy of the posterior cerebral artery can be obtained from the work of Margolis et al in Newton and Potts (1974) and Zeal and Rhoton (1978).

Branches From the inferior and posterior surface of the PI segment multiple (1-13) perforating branches arise and supply the interpeduncular fossa, the mammillary bodies, the cerebral peduncle, and the posterior mesencephalon. From this same area of P1; short circumflex branches arise and pass a short distance around the brain stem medial to the posterior cerebral artery supplying branches to the cerebral peduncle, tegmentum and medial geniculate. Other branches from this segment include the thalamoperforate and quadrigeminal arteries. The branches of the posterior cerebral artery are listed in Table 11 and shown in Fig 115. Table 11 Branches of the posterior cerebral artery I. Central or brain stem branches A) Direct perforation branches 1) From P, segment a) Thalamoperforating arteries 2) From P2 segment a) Thalamogeniculate arteries b) Peduncular perforating arteries B) Circumflex branches 1) Short 2) Long II. Ventricular, choroid plexus branches, dorsal thalamic branches A) Medial posterior choroidal artery B) Lateral posterior choroidal artery III. Cerebral cortical branches

Vertebrobasilar System

Fig 1 1 5 A—B Posterior cerebral artery and branches. A Posterior cerebral artery (p. C.A.) (A) Circular segment (B) Cortical segment ( 1 ) Paramedian arteries (intrapeduncular, intercrural, perforating) (2) Quadrigeminal arteries (3) Thalamic arteries (medial and lateral) (4) Medial posterior choroidal arteries (5) Pre-mammillary arteries (of the posterior communicating artery) (6) Peduncular artery (7) Lateral posterior choroidal arteries (anterior and posterior) (8) Lateral occipital artery (a) Anterior temporal arteries (b) Middle temporal arteries (c) Posterior temporal arteries (9) Medial occipital artery (a) Dorsal callosal artery (b) Posterior parietal artery (c) Occipito-parietal artery (d) Calcarine arteries (e) Occipito-temporal artery

B Basilar artery (B) (p.co.A.) Posterior communicating artery ( 1 ) Thalamic arteries (2a) Medial posterior choroidal artery (2b) Lateral posterior choroidal artery (3) Dorsal callosal artery (4) Medial occipital artery (a) Posterior parietal arteries (b) Occipito-parietal arteries (c) Calcarine arteries (5a) Anterior and middle temporal arteries (5b) Posterior temporal artery Regions of vascular supply of posterior cerebral artery: Substantia nigra, red nucleus, mammillary body, oculomotor nerve, trochlear nerve Quadrigeminal bodies Central nucleus, medial nucleus, ventro-lateral nucleus of the thalamus, pulvinar, lateral geniculate body, internal capsule (posterior portion) Epithalamus, pineal gland, tela chorioidea of the porencephalon Tuber cinereum, cerebral peduncle, ventral nuclei of the thalamus, nuclei of the hypothalamus, chiasm Hippocampal gyrus, lateral geniculate body, pulvinar, dentate fascia, hippocampus, anterior basal cortex of the temporal lobe Choroid plexus of the temporal horn, trigone, dorsolateral nuclei of the thalamus Latero-basal aspects of the temporal and occipital lobe Splenium Cuneus, pre-cuneus Calcarine gyrus, occipital pole Latero-basal occipital lobe

(From Krayenbuhl, H., M. G. Ya§argil: Cerebral Angiography. Butterworth, London, Tnieme, Stuttgart 1968).

137

138

1 Operative Anatomy

sea

Fig 1 1 6 Schematic drawing of the parapeduncular course of the posterior cerebral (Pa—PS) and superior cere-bellar arteries.

Ill = Oculomotor nerve sea = superior cerebellar artery

P? = P2 segment P3 = P3 segment

Vertebrobasilar System

139

MCA

med.post. ch.a.

Gal.

Fig 1 1 7 Schematic drawing of the Circle of Willis and parapeduncular and peripheral course of the posterior cerebral artery (P2, P3, P4) and its branches.

A MCA

= Anterior communicating artery complex

= Middle cerebral artery ant.cho. = anterior choroidal artery PE = Ps segment med. post. ch. a. = medial posterior choroidal artery lat. post. ch. a. = lateral posterior choroidal artery P3 = P3 segment P4 = P4 segment Cal. = Calcarine artery

140

1 Operative Anatomy Fig 118 A-B Operative photog raphs of two examples of a hitherto unknown anatomical variation of the oculomotor nerve observed in 2 patients during selective amygdalohippocampectomies: the left P2 segment is in a tunnel of a separated branch of 111 nerve (arrows), which takes its origin not in the lateral part of the interpeduncular fossa, but from the antero-lateral part of the peduncle.

Thalamoperforating Arteries (Posterior Thalamoperforating or Interpeduncular Thalamoperforating Arteries) The thalamoperforating arteries consist of one or more arteries usually originating on the central segment of P1; but occasionally originating from the medial 1 mm P1 (8%) or the lateral 1 mm (5%) (Saeki and Rhoton 1977) or rarely even arising from the posterior portion of the posterior communicating artery (Peele 1961). Saeki and Rhoton (1977) found that the P; branch nearest the bifurcation was the largest branch of P, in 56 per cent of cases and almost always was a thalamoperforating artery. Lang and Brunner (1978) described four patterns of thalamoperforating arteries in an examination of 50 cadaver brains. In type I (20%) bilateral, multiple thalamoperforating branches

were seen from P^ In type II (26%) only one side had multiple thalamoperforating branches, as the other Pj had 1-2 larger "stem" thalamoperforating arteries arising that then divided into 3-8 branches. In type III (42%), both P! segments had larger stem thalamoperforating branches, and finally type IV (8%), one Pl had no thalamoperforating branches, while the other had a large stem thalamoperforator that supplied branches bilaterally. Similar cases of unilaterally aplastic thalamo-perforators with contralateral crossover have been described by Westberg (1966), Percheron (1973) and Saeki and Rhoton (1977). Grand and Hopkins (1977) pointed out that hypoplastic Pj segments often have large thalamoperforators (Figs 119-122).

Vertebrobasilar System

141

Fig 119A-B Schematic representation of thalamoperforating artery variations with equal (A) and unequal (B) P, segments.

The thalamoperforating arteries enter the posterior perforated substance and supply the anterior and part of the posterior thalamus, posterior limb of the internal capsule, hypothalamus, subthal-amus, substantia nigra, red nucleus, and portions of deep rostral mesencephalon (see Figs 130-137). Thalamogeniculate Artery The thalamogeniculate artery regularly arises from the mid-portion of the P2 segment of the posterior cerebral artery, but has been described to originate from P3 (Stephens and Stilwell 1969, Lazorthes et al 1976). Between 3-6 thalamogeniculate arteries arise and course superiorly to penetrate the base of the thalamus and geniculate bodies|^They supply the posterolateral thalamus, the posterior limb of the internal capsule, and the geniculate bodies.

Quadrigeminal Artery (Long Circumflex or Collicular Artery) The quadrigeminal arteries usually arise from the P! segment (80%), but may arise from the proximal P2 segment (20%; Zeal and Rhoton 1978). Lang and Kapplinger (1979) described their origin from PI in 53.9 per cent, from P2 in 6.5 per cent, and from both in 40 per cent. From their origin they encircle the midbrain medial to the posterior cerebral artery, sending fine branches to the peduncle, geniculate bodies, and tegmentum. They end by forming a rich arterial network over the superior and inferior colliculi (see Fig 145). Duvernoy (1978) consistently saw an accessory quadrigeminal artery paralleling the course of the quadrigeminal artery and supplying the lateral aspect of the superior colliculus.

142

1 Operative Anatomy

Fig 120A-B Operative observations of the basilar bifurcation as seen through the transcallosal, transventricular approach, following the removal of a craniopharyngioma that had opened the infundibular recess. A Bilateral equal sized thalamoperforating arteries arise from the proximal 3-4 mm of the P, segment (arrows).

B A large thalamoperforating trunk arises from the right P, segment and gives branches to both sides (arrow).

Medial Posterior Choroidal Artery The medial posterior choroidal artery has a somewhat variable origin. Lang and Kapplinger (1979) described this vessel as arising from the Pj segment in 9.4 per cent of cases, from P2 in 83.3 per cent, from both Pl and P2 in 1.2 per cent, and from distal posterior cerebral artery segments in 7.1 per cent. Zeal and Rhoton (1978) confirmed these findings with the medial posterior choroidal arising from P, in 12 per cent of 50 cadavers, from P2 in 71 per cent, from P3 in 4 per cent, and from P4 in 13 per cent. Single medial posterior choroidal arteries are seen in 54 per cent of cases, duplications in 32 per cent, and triplications in 14 per cent (Zeal and Rhoton 1978). After arising from the posteromedial aspect of the posterior cerebral artery, "the medial posterior choroidal encircles the midbrain medial to the posterior cerebral artery distributing branches to the peduncle, tegmentum, geniculate bodies and colliculi.llt passes the pulvinar and turns forward lateral to the pineal gland to enter the roof of the third ventricle between the thalami and end at the Fig 1 2 1 Operative photograph (right pterional approach) of a large thalamoperforator arising from the left P, segment foramen of Monro in the choroid plexus. This (arrow).

Vertebrobasilar System

143

Fig 122 A Anatomical dissection demonstrating a large thalamoperforate trunk (large arrow) arising from the right PI and supplying bilateral perforating branches (small arrows). B Schematic representation of single thalamoperforators.

medial choroidal fissure to supply the pulvinar, posterior commissure, body of the fornix. and dorsal-medial thalamus (Yamamoto and Kageyama 1980). Cortical Branches The inferior temporal arteries include the hippocampal and the anterior, middle, posterior, and common temporal arteries. They supply the inferosegment supplies the pulvinar, pineal, roof of the medial portions of the temporal lobe including the hippocampal gyrus, hippocampal 3rd ventricle, habenula, dorsal-medial thalamus, uncus, formation, and dentate gyrus. The posterior and choroid plexus (Schlesinger 1976; Yamamoto pericallosal (splenial) artery arises from the and Kageyama 1980). parietal-occipital artery in 62 per cent, the calcarine in 12 per cent, the medial posterior choroidal in 8 per cent, the posterior temporal in 6 Lateral Posterior Choroidal Artery per cent, P2 in 4 per cent, P3 in 4 per cent, and the The lateral posterior choroidal artery has quite a lateral posterior choroidal artery rn 4 per cent variable origin. Zeal and Rhoton (1978) found the (Zeal and Rhoton 1978). From its origin this origin of the vessels to be P2 (51%), P3 (30%), P4 vessel ascends the splenium of the corpus callosum (15%), and the medial posterior choroidal artery and courses anteriorly for a variable distance to (4%). Of the 30% arising from P3, 8% originated finally anastomose with the anterior pericallosal from the hippocampal artery, 10% from the anterior artery. temporal, 9% from the posterior temporal, 2% The parieto-ocdpital artery consistently arises as a from the middle temporal and only 1% from the single branch and runs in the parieto-occipital main stem P3. The number of lateral posterior fissure to supply the posterior parasagittal region, choroidal arteries in each hemisphere ranges from cuneus, precuneus, lateral occipital gyrus and 1-9 with the average being 3-4 (Galloway and occasionally the superior parietal lobule (Zeal and Greitz 1960). From their origin, the lateral poste- Rhoton 1978). rior choroidal arteries course laterally into the The calcarine artery arises as a single trunk in 90 lateral choroidal fissure to supply the choroid per cent of cases and courses in the calcarine plexus of temporal horn and the glomus of the fissure to reach the occipital pole. It supplies the choroid plexus in the atrium of the lateral ven- lingual gyrus and inferior cuneus (Zeal and Rhoton tricle and then pass upward over the pulvinar and 1978). beneath the columna of the fornix to enter the

продолжение

144

1 Operative Anatomy продолжение

Perforating Arteries to the Basal Ganglia and Brain Stem Because cerebral aneurysms arise most commonly in the basal areas of the brain, around the circle of Willis and along the basilar end of the vertebral artery trunks, the vascular organization of the base of the brain and the brain stem is an important consideration in the pathogenesis of these lesions and in their operative elimination from the arterial tree. Over the past 15 years, the senior author (MGY) has examined over 200 cadaver brains, many with latex injection of the arteries, to follow the perforating arteries within the sub-arachnoid space and to identify their precise site of penetration into the brain stem. Distinct and regular patterns of blood supply to the corpus striatum and brain stem have emerged from these studies, and a complete description of these will constitute reports to be published in the future. Within the contex of this book, however, a preliminary summary of these findings is appropriate. The primary arterial supply to the central nervous system is found on the anterior surface of the brain and spinal cord. There is a basic pattern of arterial distribution with the major trunk or trunks anteriorly, giving origin to two groups of branching arteries. One arises near the midline and converges medially (paramedian arteries) and the other courses laterally around the brain or spinal cord and then penetrates at various levels (circumferential arteries). At the level of the medulla oblongata the primary anterior trunks are the vertebral arteries and the anterior spinal artery. The organization at pontine and mesencephalic levels is similar because the paired basilar arteries of the embryo have coalesced to form a single anterior trunk, the basilar artery. At diencephalic levels, the system again diverges to allow the hypothalamus and optic structures to pass forward into the base of the skull. The primary anterior trunks at this level are the P! segments of the posterior cerebral arteries, the posterior communicating arteries, the internal carotid arteries between the posterior communicating and anterior cerebral arteries, the A! segments of the anterior cerebral arteries, and the anterior communicating artery. This loop, of course, constitutes the circle of Willis. Paramedian arteries issue from each of these major trunks, but tend to be small since they are close to their area of tissue distribution. Circum-

ferential arteries on the other hand, can be quite large if their area of distribution is great. From the vertebrobasilar trunk these arteries include the posterior inferior cerebellar, anterior inferior cerebellar and superior cerebellar arteries, and the P2 and P3 segments of the posterior cerebral arteries, which embryologically were branches of the internal carotid artery. Smaller circumferential branches include the medial and lateral posterior choroidal arteries and the collicular arteries. Circumferential branches of the internal carotid artery include the anterior choroidal artery, the middle cerebral artery, and the distal anterior cerebral artery. In this section the entire paramedian arterial blood supply will be discussed, but only the circumferential blood supply to the basal ganglia and brain stem will be described as that to the cerebral or cerebellar hemispheres was discussed earlier. Entry sites of the perforating arteries into the brain substance are not randomly scattered, but have well-defined patterns. These entry patterns are far more regular than the origins of the arteries themselves. A new catalogue of the perforated substance areas runs the risk of introducing terms which either conflict with those already in general use or are arbitrary and inexact by themselves. The new terms used in the following section were chosen with these pitfalls in mind and aim to be as descriptive and self-explanatory as possible. Terms already in general use are kept within their traditional meanings. Because a major goal of the present work was to provide intra-operative landmarks for the neurosurgeon, the terms were chosen to emphasize identifiable constellations of perforation sites. The temptation simply to name sites by their afferent vessel has been avoided since in many cases the identifiable clusters of perforation sites have a compound vascular origin. Thus the perforation sites of a particular source vessel may not by themselves form a recognizable grouping although contributing to a larger constellation which is recognizable and therefore useful as an intraoperative landmark.

An outline of the terms used is provided in Table 12.

I. Basal Perforation Zones

145

Table 12 Basal and dorsal perforating zones

I. Basal perforation zones a) Anterior perforation zone 1) antero-medial extension 2) antero-lateral extension 3) inferior-lateral extension b) Posterior perforation zone 1) interpeduncular group ^ 2) periinfundibular group 3) peri-mammillary group 4) retro-optic group c) Pontine perforation zone 1) medial pontine group 2) lateral pontine group d) Medullary perforation zone 1) medial medullary group 2) para-olivary group 3) lateral medullary group 4) basal cerebellar group II. Dorsal perforation zones a) Dorsal thalamic perforation zone 1) medial posterior choroidal group 2) lateral posterior choroidal group 3) cingulothalamic group b) Dorsal midbrain perforation zone 1) peri-collicular group 2) circumgeniculate group 3) lemniscal trigone group

I. Basal Perforation Zones la. Anterior Perforated Substance and Extensions: Anterior Perforation Zone The anterior perforation zone (Fig 123) encompasses the basal surface of the brainstem anterior to the optic chiasm and tract and therefore includes the anterior perforated substance as traditionally defined (Ranson 1959) plus three distinct extensions on each side. As can be seen in Fig 124B, the zone resembles a five-pointed star in overall shape (Fig 124A-C). Located centrally in this zone, the classically-described anterior perforated substance is bounded by the olfactory trigone, the optic tract and the uncus. This triangular field of grey matter is studded with entry sites of vessels which pass first through the subjacent olfactory tubercle and sub-stantia innominata before reaching the head of the caudate nucleus, putamen, pallidal complex and

internal capsule. Some branches reach as far as the thalamus before dissipating. Many of the vessels perforating this region are known to arise directly from the first segment of the middle cerebral artery (Mj) with a variable number contributed from the first segment of the anterior cerebral artery (At). Expanding on these observations, it was possible in the surface denuded specimens to appreciate three distinct extensions of the classical anterior perforated substance. One such extension of punctate entry sites continues as an arc running antero-medially and remains between the lamina terminalis and the posterior margins of the paraterminal gyrus deep in the interhemispheric fissure before being stopped by the corpus callosum rostrum. It is necessary to retract the hemispheres laterally to see all the perforation sites of this group (as shown in Fig 124). When this is done the antero-medial extensions of each side line up to form two parallel rows, the entry sites becoming

146

1 Operative Anatomy

FP

Fig 123 An illustration of the classical anterior portion of the Circle of Willis and perforating arteries. The arteries are abbreviated as follows: ophthalmic (Oph), dural (d), chiasmatic (ch), posterior communicating (PcoA), tuberomammillary (tu), anterior choroidal (AchoA), uncal (u), middle cerebral artery (M-, segment) superior, and inferior trunk (M2), polar and anterior temporal (Po, a. temp.), lateral proximal and distal striate (I. pr. str., I. d. str.), A, segment (A,), medial proximal striate (m. pr. str.), medial distal striate (m. d. str.) or Heubner's, anterior communicating (AcoA), hypothalamic (Hy), A2 segment (A2), medial fronto-orbital (m. fr. orb.), lateral fronto-orbital (I. fr. orb.), and fronto-polar (Fp) arteries.

smaller towards the rostrum of the corpus callosum (Fig 126). A second extension of the classical anterior perforated substance can be followed antero-laterally towards the limen of the insula. A third extension follows along the anterior edge of the optic tract caudolaterally to the lateral geniculate body. These three extensions, termed respectively the antero-medial, antero-lateral, and inferolateral extensions are shown diagramatically in Fig 124 with further details shown in Figs 124 through 140. Dissection of the source vessels in the latex injected specimens revealed that the antero-medial extension receives an initial contribution by the A! segment but that the majority of its rostral extent is supplied by small branches of the anterior communicating artery or its hypothalamic branch (see Figs 87, 88). More rostral entry sites may be filled by small branches of the A2 segment. Dissection along the small perforating vessels themselves sug-

gested that the rostromedial extension supplies at least part of the septal area, the anterior columns of the fornix and medial part of the anterior commissure (Figs 125,126). The antero-lateral extension represents the entry sites of vessels arising from the M! segment and typically appears to supply the lateral putamen and internal capsule. A distinct lenticulostriate artery typically reaches the lateral sites in the extension while branches of Heubner's artery can often be seen to enter the brainstem just at the base of the rostrolateral extension in a region still within the classical anterior substance (Figs 127129). The infero-lateral extension represents the entry sites of branches from the anterior choroidal artery. An uncal branch is often encountered as a distinct early branch of the anterior choroidal artery and typically perforates the uncus at its medial apex near the base of the infero-lateral extension.

I. Basal Perforation Zones 14 7

Fig 124A Topography of ventral brain stem perforating vessels. Ventral view with (A) the subarachnoid vessels still attached.

148

1 Operative Anatomy

Id3

Fig 1 2 4 B All vessels and surrounding arachnoid removed to show the pits marking the sites of entrance of ventral perforating vessels into the brain. Basal perforation zones a) Anterior perforation zone 1) antero-medial extension 2) antero-lateral extension 3) inferior-lateral extension b) Posterior perforation zone 1) interpeduncular group

2) peri-infundibular group 3) peri-mammillary group 4) retro-optic group ' c) Pontine perforation zone 1) medial pontine group 2) lateral pontine group

d) Medullary perforation zone 1) medial medullary group 2) para-olivary group 3) lateral medullary group 4) basal cerebellar group

I. Basal Perforation Zones

LenticulostriateA. (M,)

149

Subcallosal knee

AcoA

Heubner's A.

Basilar A.

AICA

Ant. spinal A.

Fig 124C The organization of these perforator pits into specific well defined zones each receiving penetrating vessels from a specific penetrating artery.

150

1 Operative Anatomy

125

126

Fig 125 Dissected specimen showing the perforating zone for the hypothalamic arteries just above the opened lamina terminalis (through which the anterior commissure is visible). Fig 126 The perforating zone of the hypothalamic arteries is seen extending along the subcallosal gyrus just under the genu of the corpus callosum. The perforating pits become smaller and less distinct as the distal edge of the zone is approached. Fig 127 Dissected specimen demonstrating the lateral portion of the so-called 'anterior perforate substance' with Heubner's (H) artery penetrating the brain just below the trigone of the olfactory nerve (OL). Ch = chiasm, tu = tubero-mammillary artery. 127

I. Basal Perforation Zones

Fig 128 Formalin-fixed specimen showing the medial and lateral portions of the so-called 'anterior perforate substance' with both the striate (Lstr) and Heubner's (H) arteries penetrating the brain, tu = tubero-mammillary artery.

Ib. Posterior Perforated Substance and Extensions: Posterior Perforation Zone The posterior perforation zone encompasses the basal surface of the brain stem between the optic tracts and the converging cerebral peduncles and therefore includes the traditionally recognized posterior perforated substance plus several additional clusters of perforation sites. Its overall rhomboid shape can be appreciated in Fig 124 A-B. Within this zone, the classically described posterior perforated substance is centered between the converging cerebral peduncles, the mammillary bodies and the rostal edge of the pons. The vessels perforating this region are well known to arise from the posterior cerebral and superior cerebellar arteries with additional branches coming from the basilar artery near its termination. It is well known that these perforating branches supply a major part of the mid-brain, caudal thalamus, and upper pons (see Stephens and Stilwell 1969 for a review) and thus requires little further emphasis (Figs 130-132).

151

Fig 129 The lateral portion of the "anterior perforate substance' after removal of the vessels.

Expanding on these classical observations, it seems important to note that entry sites in the interpeduncular fossa usually form two parallel rows interpeduncular group (Figs 124B, 136), one on each side of the mid-line and the entry sites become progressively smaller caudally towards the pons (Fig 124B). Also noteworthy is the occasional finding of a branch from the P! segment of one side filling entry sites on both sides of the midline (see Figs 119-122). In almost all cases, the larger rostral sites are filled by the Pl branches, those further posterior by the superior cerebellar branches, and the most caudal small sites are filled by the basilar itself. In the surface denuded specimens several additional clusters of perforation sites can be appreciated within the boundaries defined for the posterior perforation zone. One such site encircles the base of the infundibulum and is here termed the periinfundibular group (Fig 124B), while a second locus forms a crescent around the lateral margins of the mammillary bodies and can be termed the perimammillary group. A third cluster extends laterally behind the optic tract and is therefore termed the retro-optic group (Figs 133, 134, 137).

152

1 Operative Anatomy Fig 130 An injected specimen il lustrating a dense maze of thalamoperforate arteries above the basilar bifurcation.

Fig 1 3 1 Formalin-fixed specimen showing the origin of penetrating arteries that enter the interpeduncular fossa from the superior cerebellar and P, segment arteries (arrows).

Fig 132 Injected specimen revealing symmetrical thalamoperforators arising from both P, segments and penetrating either directly or in a circular fashion around the mammillary bodies (Mb).

Basal Perforation Zones

Fig 133 Injected specimen demonstrating the right lateral portion of the so-called 'posterior perforate substance' with the tubero-mammillary branch (tu) of the posterior communicating artery entering the brain in the peri-mammillary area through large and small branches. Mb = right mam-millary body. Op. Tr. = optic tract.

In the latex injected specimens, the source vessels of the perforation sites were identified. Those entering the peri-infundibular group arise from the internal carotid artery directly. The anterior sites in the perimammillary group usually arise from the posterior communicating artery while the posterior sites of this group originate from the first segment of the posterior cerebral artery (P t ) (Figs 133, 134). Branch vessels entering the retro-optic group arise from the posterior communicating artery and typically, a prominent perforating branch enters just at the angle between the optic tract and the peduncle (see Fig 137). The inter peduncular group sites are filled by branches from the Pj segment and superior cerebellar artery (Figs 130,131,132, 135, 136).

153

Fig 134 Injected specimen showing the left posterior communicating artery and the tubero-mammillary branch (tu) with small branches to the left peri-mammillary area (Mb).

I. Basal Perforation Zones

Fig 133 Injected specimen demonstrating the right lateral portion of the so-called 'posterior perforate substance' with the tubero-mammillary branch (tu^ of the posterior communicating artery entering the brain in the peri-mammillary area through large and small branches. Mb = right mam-millary body. Op. Tr. = optic tract.

In the latex injected specimens, the source vessels of the perforation sites were identified. Those entering the peri-infundibular group arise from the internal carotid artery directly. The anterior sites in the perimammillary group usually arise from the posterior communicating artery while the posterior sites of this group originate from the first segment of the posterior cerebral artery (P,) (Figs 133, 134). Branch vessels entering the retro-optic group arise ' from the posterior communicating artery and typically, a prominent perforating branch enters just at the angle between the optic tract and the peduncle (see Fig 137). The interpeduncular group sites are filled by branches from the P: segment and superior cerebellar artery (Figs 130,131,132, 135, 136).

153

Fig 134 Injected specimen showing the left posterior communicating artery and the tubero-mammillary branch (tu) with small branches to the left/peri-mammillary area (Mb).

154

1 Operative Anatomy

Fig 135 The peri-mammillary and interpeduncular areas as seen after the removal of the vessels. Fig 136 View of the interpeduncular fossa beneath the mammillary bodies (Mb) showing the perforation pits which diminish in size towards the pons. Ill = remnants of the oculomotor nerves. Fig 137 The lateral portion of the 'posterior perforate substance' illustrating the presence of perforation pits (arrows) along the optic tract (Op. Tr.) Ch = chiasm. 137

I. Basal Perforation Zones

155

AICA

PICA

Ant. spin. A

Ic. Pontine Perforation Zone The pontine perforation zone encompasses the basal surface of the pons. Here, in the surface denuded specimens, a linear array of perforation sites may be appreciated near the midline of the pons on its basal surface. Although generally small, the sites of this medial pontine group are consistently present and are not significantly influenced in their distribution by the often deviated course of the basilar artery. Additional perforation sites are seen scattered more laterally over the pons and brachium pontis to form a lateral pontine group (see Fig 124B-C). In latex injected specimens small branches from the undersurface of the basilar artery were seen to enter the medial pontine group while branches of the superior cerebellar and anterior inferior cere-bellar arteries were seen to enter the scattered sites noted more laterally.

Id. Basal Medullary Perforation Zone Denuded specimens revealed rich arrays of perforation sites on the basal surface of the medulla. One such array, the medial medullary group is evident in the midline extending from the foramen caecum caudally (see Fig 124B-C). The caudal limit of this group is not apparent and it clearly continues to spinal levels in the anterior median fissure. As shown in Figs 138A-C and 139A-C the two Fig 138A-C Regular penetrating arteries arising from the most distal vertebral arteries (beyond the anterior spinal arteries) or pyramids must be retracted laterally to expose two parallel paramedian rows of perforation sites, the most proximal basilar artery and entering the brain in the neighborhood of the foramen caecum. A Injected specimen. B largest of which are located rostrally at the foramen Schematic drawing. caecum. The sites become progressively smaller C Formalin-fixed brain after the reflexion of the vertebrocaudally. basilar arteries. Perforators from basilar artery (arrows).

156

1 Operative Anatomy

Fig139A-C The ventro-median ponto-bulbar perforate zone

in a dissected specimen (A). Notice the symmetrical organization of the perforation pits in rows (B). This zone gradually blends in with the anterior spinal artery perforate zone as one descends (C).

I. Basal Perforation Zones

157

Fig 140A-C The peri-olivary perforate zone for penetrating branches of the vertebral, basilar, posterior inferior cerebellar and anterior inferior cerebellar arteries as seen on the right (A) and left (B) sides following removal of the vessels. (C) Injected specimen showing the right peri-olivary penetrating arteries from vertebral, basilar arteries and AICA and PICA (arrows).

A particularly rich array of perforation sites, the para or circumolivary group forms such a conspicuous ring around the olivary eminence that it warrants separate mention although it may be considered part of a lateral medullary group which extends caudally to spinal levels (Fig 140A-C). A group of perforation sites, the basal cerebellar group is evident only on retracting the basal cerebellar folia to expose the white matter deep in the horizontal cerebellar fissure. On this white matter surface are two linear arrays of small vascular entry sites converging laterally and separated medially to accommodate the flocculus and para-flocculus (see Fig 141A-B). In the latex injected specimens the source vessels corresponding to these medullary perforation areas were determined. The smaller inferior sites of the medial medullary group derive from the anterior spinal artery while the larger anterior sites derive from the basilar artery.

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Fig141A-B Lateral to the olive, the origins of cranial nerves V, VII, VIII, IX, X, the choroid plexus, and the flocculus (FL) are seen (A) and lateral to this, another perforate zone on the most lateral extension of the horizontal sulcus (arrow) (B). Branches of posterior inferior cere-bellar, anterior inferior cerebellar, and the superior cerebel-lar arteries penetrate in this area.

The circumolivary group appears to have a more complex composite derivation as shown diagramatically in Fig 124C. The anterior sites in the ring correspond to branches from the anterior inferior cerebellar artery (AICA) and basilar artery, while the posterior sites correspond to branches from the posterior inferior cerebellar artery (PICA). Medial sites in the ring may come from the vertebral artery. The more caudal sites in the lateral medullary group correspond to branches from the PICA and vertebral artery. In the basal cerebellar group, both the anterior and posterior rows described above derive from the AICA and superior cerebellar arteries.

Ma. Dorsal Midbrain Perforation Zone

In denuded specimens three clusters of perforation sites could be identified on the dorsal surface of the midbrain (Fig 142A-C). Small sites could be seen to encircle each of the quadrigeminal bodies individually and are therefore termed the pericollicular group. An especially conspicious ring of punctate vascular entry sites, the circumgeniculate group was seen to encircle the medial geniculate body (Figs 143, 144A-B). A third group of perforations overlies the lemnis-caltrigone. The respective source vessels were again determined in latex injected specimens. Rostral perforation sites in the pericollicular group derive from branches of the P2 segment of the posterior cerebral artery and especially from its medial posterior choroidal branch. Where a separate "collicular artery" exists (Duvernoy 1978), this vessel makes a II. Dorsal Perforation Zones prominent contribution (Fig 145). The caudal The basal surface of the brain stem has consider- perforation sites usually derive from the medial ably more area and opportunity for vascular per- superior cerebellar artery. The perforation sites in foration than does the dorsal surface. This circum- the circumgeniculate group derive largely from stance arises largely as a matter of definition the medial posterior choroidal artery with addibecause the great cerebral and cerebellar hemi- tional branches coming from the P2 segment of the spheres are elaborated from the dorsal aspect of posterior cerebral artery directly. The lemniscal the embryologic neural tube but excluded by the trigone group of perforations represent the entry term "brain stem". jience the following discussion points of branches from the superior cerebellar can-be limited almost erftTFely-tc; the dorsal aspects artery and the collicular artery when present. of the midbrain and thalamus.

I. Dorsal Perforation Zones

Fig 142A-C Topography of dorsal brain stem perforating vessels. Dorsal view with the subarachnoid vessels still attached (A).

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1 Operative Anatomy

Fig142B All vessels and surrounding arachnoid removed to show the pits marking the sites of entrance of dorsal perforating vessels into the brain.

Dorsal perforation zones a) Dorsal thalamic perforation zone 1) medial posterior choroidal group 2) lateral posterior choroidal group 3) cingulothalamic group b) Dorsal midbrain perforation zone 1) peri-collicular groups 2) circumgeniculate group 3) lemniscal trigone group

II, Dorsal Perforation Zones

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Lat. post. chor. A. Cingulo-thalarnic branch

Fig 1 4 2 C The organization of these perforator pits into specific well defined zones: each receiving penetrating vessels from a specific penetrating artery. SCA - superior cerebellar artery.

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Mb. Dorsal Thalamic Perforation Zone In denuded specimens, three distinct linear arrays of perforation sites are evident on the dorsal surface of the thalamus. A medial row, the medial posterior choroidal group, extends along the stria medullaris and line of attachment of the choroid plexus roofing the third ventricle. A few perforation sites of this group extend caudally to puncture the posterior commissure in its recess behind the pineal gland (Figs 146, 147A-B). The afferent vessel for this medial posterior choroidal group is the medial posterior choroidal artery, which in turn is derived from the posterior cerebral artery. A lateral row of perforation sites, the lateral posterior choroidal group, follows the junction of the lamina affixa with the choroid plexus of the lateral ventricle. These sites receive afferents from the lateral posterior choroidal artery, a vessel which also derives from the posterior cerebral artery. Between these two rows, an intermediate row, the cingulothalamic group is evident and is best described by its corresponding source vessel the cingulothalamic artery. Fig 148 illustrates the Circle of Willis and its penetrating branches. Fig 143 The dorsal mesencephalon after removal of the vessels.

A

\

B

Fig 144 A-B The dense circular distribution of perforating pits around the left (A) and right (B) medial geniculate bodies.

II. Dorsal Perforation Zones

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Fig 146 Injected demonstration of the dorsal mesencephalon with the collicular and medial posterior choroidal arteries (arrows). Pi = pineal body. Fig 145 The right collicular artery (arrow) supplying branches to both the superior (s. Col) and inferior colliculi (i. Col).

B Fig 147 A-B The perforate zone of the posterior medial choroidal artery (arrows) in the dorsal mesencephalon (A) and near the posterior commissure and habenula (B), after superior rotation of the pineal body with forceps.

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1 Operative Anatomy 6 Inferior-lateral zone with anterior choroidal artery; A Anastomosis between anterior choroidal and postero-lateral choroidal arteries. B Anastomosis between posterolateral choroidal and cingulothalamic arteries. C Anastomosis between posterolateral choroidal and postero-medial choroidal arteries at the level of Foramen Monroi. D Anastomosis between splenothalamic and posteromedial choroidal arteries. 7 Dorsal perforation zone with branches from posterior cerebral artery.

Fig 148 Schematic representation of the Circle of Willis and its penetrating branches: 1 Medial medullafy-perfoTatoTs-ftom vertebral, basilar, and anterior spinal arteries. ~~~~ 2 Lateral medullary perforators (para-olivary group) from PICA, AICA and basilar arteries. 3 Posterior perforation zone with branches from superior cerebellar (a), P-, (b), internal carotid and posterior communicating arteries (c). 4 Medial anterior zone with hypothalamic branches. 5 Antero-lateral zone with perforation: a Proximal and distal lateral striates b Proximal medial striate c Heubner's artery.

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Ventrolateral Posterior Fossa продолжение

Cerebral Veins The cerebral venous system was less well studied in the present series than the arterial system. While it is generally considered that the venous system in the brain has a well developed collateral system, attempts were made to preserve all veins during dissection. At times one or two or more veins had to be sacrificed, and no untoward symp-toms postoperatively could be definitely attribut^ ed_to loss of these veins. Nevertheless, there is a need to study the importance of the venous system as related to microsurgical operations in the brain, the contribution of venous occlusions to cerebral swelling and infarction, and the functional capabilities of venous anastomoses (Fig 149A-B)._____ In this book, the venous system will be discussed only in the areas where microsurgical operations of aneurysms were commonly performed - in the parasellar area, the posterior mesencephalic area, and the ventrolateral posterior fossa. For further excellent descriptions of the cerebral venous system, the reader is referred to the work of Wolf and~Huang (1963), Stephens and Stilwell (1969), Stein and Rosenbaum (1974), Huang and Wolf (1974), Duvernoy (1975), and Salamon and Huang (1976).

Parasellar Area The veins of the anterior fossa and parasellar area jnpre or less parallel the arteries in their initial segments. Anterior cerebral veins that course with the anterior cerebral arteries give branches to the inferior sagittal sinus as they continue anteriorly and may have a communication which is analogous to the anterior communicating artery (Duvernoy 1975). Each anterior cerebral vein then turns laterally beneath the olfactory tract where it is joined by the olfactory vein jind by striate veins exiting from the anterior perforated substance. The veins lie inferior to the anterior -cerebral artery in the lamina terminalis cistern. At the junctiofKpf the lamina terminalis and crural cisterns beneatfiht|ie internal carotid artery bifur-cation, the anterioKcerebral vein joins the_deep middle cerebral vein (formed by the convergence of insular veins) to give rise to the basal vein of Rosenthal. From this point, the directions of the veins and arteries separate, as the basal vein runs posteriorly and slightly superiorly in the crural cistern between the uncus and cerebral peduncle, enters the ambie_nt_ cistern to course with the gosteriorcejebraj^and superior cerebellar arteries,

and finally in the quadrigeminal cistern empties into the great vein of Galen. In two cases in the present series, the anterior cerebral vein did not join with the basal vein, but crossed the internal carotid artery superiorly to empty into the sphenoparietal sinus, hampering dissection in the carotid cistern. Superficial middle cerebral veins (Sylvian veins). lie on the temporal side of the Sylvian cistern. There may be one or more large veins. These veins usually follow the Sylvian cistern anteriorly and empty into the sphenoparietal or cavernous sinuses. In some cases the veins continue around the temporal pole and drain into the superior petrosal sinus. There are often several veins from the lateral frontoorbital lobe that join the superficial middle cerebral veins across the Sylvian cistern anteriorly or enter to the basal vein of Rosenthal. It should be noted that attempts to preserve these delicate vascular structures during dissection will occasionally prove futile, but the Sylvian vein will only exceptionally be sacrificed (Figs 150A-C, 151A-C).

Dorsal Mesencephalic Area The paired internal cerebral veins are formed by the union of the thalamostriate and septal veins at the foramen of Monro. The internal cerebral veins continue posteriorly beneath the fornix in the velum interpositum cistern and merge to form the great vein of Galen which lies in the quadrigeminal cistern (cisterna vena Galeni) and receives the basal veins from the ambient cistern, the perical-losal and occipital veins from the corpus callosum cistern, and the precentral cerebellar vein from the superior cerebellar cistern, as well as the internal cerebral veins from the velum interpositum cistern. Thus in this area the cisternal system seems more defined by the veins than by the arteries (see Fig 149B).

Ventrolateral Posterior Fossa The superior petrosal vein (Dandy 1929) is the principal collecting vein of the anterolateral posterior fossa structures. According to Huang et al (1968), this vein receives the lateral anterior pontomesencephalic vein, transverse pontine veins, brachial (cerebellar) veins, the vein of the hori-

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1 Operative Anatomy Fig 149A-B Schematic representation of the basal and dorsal brain stem veins (after Duvernoy). A = anterior cerebral veins, M = Sylvian group, R = vein of Rosenthal, P = pontine veins, D = Dandy's vein, ICV = internal cerebral veins.

vein of orbital lobe deep middle cerebral vein ant, cerebral vein

basitar vein draining to the great cerebral vein

Ventrolateral Posterior Fossa

zontal cerebellar fissure, and the vein of the lateral recess of the fourth ventricle. Each of these major tributaries may enter the superior petrosal sinus independently. The superior petrosal vein courses anterolaterally, more or less parallel with the trigeminal nerve, to enter the superior petrosal sinus between the internal auditory meatus and Meckel's cave. The vein is posterior and usually slightly superior to the trigeminal nerve, although Duvernoy (1975) found the vein anterior to the nerve in one case.

Fig 150A-C Schematic drawing of the variations of the Sylvian vein. A The fronto-orbital, fronto-parietal and anterior temporal veins draining into one Sylvian vein (1). B Two superficial Sylvian veins with separated basal vein draining into ( 1 ) the sphenoparietal and (2) Rosenthal's vein. C Two superficial Sylvian veins (1 ) draining into the spheno-parietal and (3) into the superior petrosal veins.

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Veins of the more inferior portion of the cerebellopontine and lateral cerebellomedullary cisterns are less constant. Salamon and Huang (1976) described a vein coursing with the vagus nerve that drains preolivary and retroolivary veins and called it the inferior petrosal vein. A vein is often seen within the lateral cerebellomedullary cistern which empties into the sigmoid sinus. This vein is easily injured when opening the cistern in an approach to the cerebellopontine angle. The vein seems to correspond to the lateral medullary vein described by Duvernoy (1975) which he found in about 35 per cent of cases.

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1 Operative Anatomy

A

D Fig 151-A-E Superficial and deep middle cerebral (Sylvian) veinsx A The vein is draining into the spheno-parietal sinus (1), or partially into the vejn of Rosenthal (2) or into the superior petrosalsinus(3). B Pronto-parietal and^ temporal branches of the Sylvian vein are joined.

C Temporal branches draining to the vein of Labbe (4). D There is only a deep Sylvian vein. E There are superficial and deep Sylvian veins. In both cases (D-E) the fronto-orbital veins are draining into the deep Sylvian vein.

The Inferior Surface of the Frontal Lobe Most of the commonly used approaches for aneurysm surgery and for removing lesions in the region of the optic chiasm require some degree of retraction and manipulation of the frontal lobe. Although surgeons are frequently working around the lateral basal portion of this lobe and it appears to have important neurophysiological functions, the regional anatomy is only poorly described in most anatomical and operative surgical texts. The reader is recommended to study the description of the anatomy of the inferior surface of the cerebral hemisphere as described in Chap. 7 of Gray's Anatomy (35th Ed. 1975), see p. 233, Fig 199L.

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Diagnostic Studies

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Lumbar Puncture Because of the wide spectrum of clinical symptomatology in patients who suffer rupture of an intracranial aneurysm, it is important that the physician not be reticent in performing the diagnostic manoeuvers which will separate this condition from more benign or less treatable conditions. Lumbar puncture is especially important in cases where the symptoms and signs are enough to suggest subarachnoid hemorrhage, but are not of such severity that hospitalization or further diagnostic workup will be undertaken in the absence of subarachnoid hemorrhage. In these cases, lumbar puncture can usually be safely performed and may allow treatment to be instituted before a more devastating hemorrhage occurs. It will also serve to exclude bacterial meningitis. Opinion is more divided over cases in which the history is characteristic, and the patient presents with papilledema or lateralized mass effect. Many feel that a few drops of cerebrospinal fluid taken with a small bore needle to confirm the diagnosis is a safe manoeuver. It must be remembered, however, that spinal fluid will continue to leak from the arachnoid puncture site into the subdural and epidural spaces, thereby lowering intracranial pressure and increasing transmural pressure across the aneurysm wall. As computerized tomography becomes more readily available, it is reasonable to perform a computerized scan first in all patients and then to base the need for lumbar puncture on the results of the scan. The use of repeated lumbar punctures to lower intracranial pressure before operation can be dangerous and is generally not advised. Difficulty sometimes arises in determining whether bloody spinal fluid is due to subarachnoid hemorrhage or a traumatic tap. Indications that subarachnoid hemorrhage has in fact occurred include:

Xanthochromia Xanthochromia of the supernatant following centrifugation of the cerebrospinal fluid is generally a reliable indication that subarachnoid hemorrhage has occurred.

Uniformity of Blood Concentration Following a traumatic puncture the spinal fluid tends to clear as successive samples are removed. Subarachnoid hemorrhage should show about the same concentration of blood in all specimens.

Cellular Changes Hemolysis and crenation of red blood cells may be observed under the microscope in cases of subarachnoid hemorrhage. Phagocytosis of red blood cells by mononuclear cells indicates red blood cells have been in the cerebrospinal fluid for some time.

Increased Pressure Cerebrospinal fluid pressure is usually increased following subarachnoid hemorrhage, especially within the first week. Walton (1956) found that 146 of 154 cases having lumbar puncture within the first week after subarachnoid hemorrhage had elevated pressure. Nevertheless, the finding of normal spinal fluid pressure certainly does not rule out a subarachnoid hemorrhage as this condition exists in many cases of mild bleeding. Furthermore, there seems to be no clear correlation between the pressure observed at lumbar puncture and the clinical condition of the patient. Thus an elevated pressure found at lumbar puncture in the presence of bloody spinal fluid can do no more than support the probability that subarachnoid hemorrhage has occurred. It should be noted that the lumbar cerebrospinal fluid can be entirely clear in the presence of a ruptured aneurysm. In eight cases from the present series (1 AcoA, 7 PcoA aneurysms), lumbar punc-

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ture was negative but an aneurysm was demonstrated at angiography. At operation, there was blood clot or staining of the arachnoid limited to the area immediately around the aneurysm and the blood hat not percolated into the general cerebrospinal fluid circulation. As indicated this situation was seen most often with aneurysms of the internal carotid-posterior communicating artery.

tials have been used to evaluate the structural integrity of the brain stem (Symon et al 1979). Techniques such as this might find application in the prognosis of comatose patients and in determining case selection for operation.

Radiological Investigation Background

Electroencephalography (EEC) While EEG has little use in the diagnosis and localization of ruptured cerebral aneurysm, it nevertheless finds some application in the evaluation of brain function in patients who are obtunded or comatose following subarachnoid hemorrhage. Hanhart (1959) reviewed the existing literature concerning the application of EEG to ruptured cerebral aneurysms and discussed the findings in 52 cases of anterior communicating artery aneurysm which had been seen at the University of Zurich. Ten cases (19%) had normal EEG tracings. The most common abnormality, found in 17 patients (33%), was bilateral frontal delta activity, and this could be generally correlated with decreased levels of consciousness. A variety of focal disturbances were found in other patients and these seemed to have no specific correlation with level of consciousness. The few patients who were moribund showed polymorphic delta activity and periods of marked slowing on the EEG tracing. Van der Drift (1961) summarized the findings on EEG in patients with ruptured cerebral aneurysm and noted that EEG findings basically paralleled disturbances in cerebral blood flow, but noted that the EEG tracing tended to normalize within 6 weeks of hemorrhage while blood flow alterations could persist. In an interesting recent case in the author's series a 45 year old woman presented with subarachnoid hemorrhage and angiography revealed bilateral middle cerebral artery aneurysms. Computerized tomography was not helpful in determining which of the lesions had bled. An EEG, however, showed dysfunction on the left cerebral hemisphere. Because the right sided aneurysm was significantly larger than the left, operation was carried out on the right side and an unruptured aneurysm found. Subsequent left sided exploration revealed the aneurysm which had bled. In this case EEG proved more helpful than angiography for localization of hemorrhage. Newer diagnostic tools such as recording the auditory evoked brain stem poten-

Cerebral angiography was introduced in 1927 (Moniz), and has been the mainstay of diagnosis in cerebral aneurysms ever since. In the past, the purpose of angiography has been twofold: 1) to define the aneurysm and the anatomical and physiological state of the blood vessels associated with it, and 2) to detect hematoma, hydrocephalus and brain shifts associated with rupture of the aneurysm. Most of the cases in the present series were evaluated in this way by angiography. With the coming of computerized tomography, there has necessarily been a change in the application of angiography to patients with ruptured cerebral aneurysm. While angiography remains the most accurate method of delineating an aneurysm, of determining the presence of multiple aneurysms, and of assessing the cerebral circulation, computerized tomography has proved more useful in defining the real size of an aneurysm in determining the degree of thrombosis, and in evaluating associated hydrocephalus, infarction, and intracerebral hematomas. These two methods of radiological investigation are thus complimentary in attempting to accurately depict the intracranial pathological state of the aneurysm patient.

Plain Skull Radiography Although most smaller intracranial aneurysms cause no abnormalities on roentgenograms of the skull, larger aneurysms may show erosion of the base of the skull, particularly in the sphenoid bone and sella turcica, or the lesion itself may be partially calcified (see Vol. II, Fig 79B).

Pneumoencephalography In the past, pneumoencephalography has found application in two situations concerning cerebral aneurysm. First when a patient presented with an enlarged sella turcica or visual and endocrine abnormalities as primary complaints, he might have undergone this study to diagnose a suspected pituitary or parasellar tumor. The need for angiog-

Cerebral Angiography 17 1

raphy in such cases is obvious. Second, pneumoencephalography was used for many years to diagnose hydrocephalus, especially in the postoperative period. Computerized tomography has replaced pneumoencephalography as a basic diagnostic investigation for mass lesions and hydrocephalus in most neurosurgical centers.

to ensure proper aneurysm obliteration postoperatively, and to sequentially evaluate the status of vasospasm. Future applications of digital subtraction angiography to the diagnosis of patients with cerebral aneurysms will certainly improve the neurosurgeon's ability to initiate successful treatment.

Radioisotopic Brain Scan

Positron Emission Tomography

Brain scan may show an arteriovenous malformation or cerebral tumor to be the cause of a subarachnoid hemorrhage. In the subacute period, 1 to 6 weeks following hemorrhage, areas of infar-cion may be recognized on the brain scan. These diagnostic contributions have been largely supplanted by computerized tomography. Dynamic brain scanning provides an innocuous method to evaluate the cerebral circulation.

Positron Emission Tomography or PET scanning is an in vivo autoradiographic technique for measuring cerebral blood flow and metabolism. A variety of radioactive short half-life materials are injected intraarterialh. necessitating the immediate availability of a cyclotron. This drastically limits the widespread use of PET scanning, at present confining it to use as a research tool. With its ability to quantitate cerebral blood flow and metabolism. PET scanning is being applied to aneurysm patients with associated vasospasm. Efforts are underway to demonstrate that symptomatic patients with vasospasm have an uncoupling of cerebral blood flow and metabolism. Future work with this new investigative device will certainly shed light on the pathophysiology of subarachnoid hemorrhageinduced vasospasm.

Radioisotopic Cisternography In the present series of patients, radioisotope cisternography has been used several weeks after hemorrhage in addition to pneumoencephalography and computerized tomography to confirm the diagnosis of communicating hydrocephalus prior to permanent shunt insertion.

Nuclear Magnetic Resonance Digital Subtraction Angiography This new diagnostic approach to cerebrovascular diseases allows the visualization of vascular channels that contain only very small quantities of contrast material. This permits arteriographic examinations of both extracranial as well as intracranial vessels to be performed after the intravenous administration of contrast. This drastically reduces the procedural risk, especially the risk of cerebral infarction (Seeger et al 1982). The applications of digital subtraction angiography to the diagnosis of cerebral aneurysms are currently being defined. It seems likely that a majority of extracranial aneurysms can be adequately defined by this procedure alone, without the need for standard arteriography. Intracranial aneurysms on the other hand, are not well delineated by this test. Standard arteriography supplemented perhaps with arterial-injected digital subtraction films will remain the hallmark for precise aneurysm definition. Digital subtraction angiography can be helpful in screening for aneurysms, for example in patients with enhancing suprasellar masses on CT scan. It can be used repeatedly with little risk to follow the status of untreated or partially treated aneurysms,

Nuclear Magnetic Resonance or NMR scanning allows a tomographic picture of tissue based on its electron density. At the present time, the application of imaging and metabolic NMR to cerebral aneurysms awaits further development.

Cerebral Angiography Method of Angiography It is important that the entire cerebral circulation be visualized to determine the presence of multiple aneurysms, evaluate collateral circulation, and detect vascular anomalies. Angiography is best performed by the catheter technique which allows the entire cerebral circulation to be investigated through one arterial puncture, and provides selectivity of injections, and flexibility to the procedure. The method of angiography used at the University of Zurich since 1975 consists of the introduction of a flexible polyethylene catheter into the right femoral artery over a guide wire and advancement of the catheter into the carotid and vertebral arteries in the neck. Angiography in this institution is performed under general anesthesia based on the fact that this provides a higher quality study with less anxiety to the patient.

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lodinated contrast medium is injected by hand, with 8 ml used for carotid studies and 6 ml for vertebral studies. A maximum of 40 ml is given. Films are routinely taken in the lateral projection and in an anteroposterior projection which superimposes the orbital roofs on the petrous pyramids. Stereoscopic lateral and anteroposterior views have been especially useful in separating aneurysms on adjacent vessels (Krayenbiihl and Ya§argil 1968) and in disclosing hidden aneurysms. Increased or decreased angulation in the anteroposterior projection, oblique views, magnification and subtraction techniques, and angiotomography are essential in given cases to further delineate an aneurysm (Newton and Potts 1974; Huber 1979). It should be remembered however that angiography at best gives only a luminal representation of the lesion and cannot portray the precise relationship of an aneurysm to surrounding structures. It is therefore not advisable to persist with examination trying to obtain a perfect study when this might increase unnecessarily the risk to a patient.

General Information Derived from Angiography Confirmation of Diagnosis Angiography will demonstrate the presence and location of an aneurysm, or may show an arteriovenous malformation, vascular tumor, or intracerebral hemorrhage to be the source of subarachnoid hemorrhage. It may also show coincidental occlusive disease, and subdural hematomas. Delineation of the Aneurysm Of importance are the size, shape, number of lobules, direction of fundus projection, presence of irregularities or loculations in the aneurysm wall, and relationship of the aneurysm neck to the parent arteries. The presence of thrombus within the aneurysm is often suggested by angiography, but in other cases angiography may be quite misleading as to the true size and shape of the fundus. Computerized tomography supplements angiography in this regard in that substantial intraluminal thrombus may be demonstrated giving a more complete picture of the lesion. Multiplicity Multiple aneurysms of significant size are present m about 20-30 per cent of cases, emphasizing the need for complete angiography. Clues that suggest which of two or more aneurysms has bled include the burger aneurysm, secondary loculations on the

aneurysm, the presence of localized vascular spasm, and the presence of localized mass effect (Taveras and Wood 1964). In only one case in the present series, both a middle cerebral and an anterior communicating artery aneurysm had simultaneously ruptured, but this is an extremely rare phenomenon. At operation additional tiny (micro) aneurysms are seen in about one-third of cases, but these small lesions can rarely be visualized at angiography. Collateral Circulation Variabilities and anomalies in the circle of Willis in association with cerebral aneurysms are discussed in Chapter 1. With angiographic demonstration of hypoplasia in various segments of the circle of Willis, the surgeon has some flexibility in attack on aneurysms at given locations. Compression of one carotid artery during angiography gives an appreciation for the crossfilling from one side to the other and from the vertebrobasilar circulation. Variations in the distribution of the more peripheral arteries should also be noted. Degenerative Vascular Changes Elongation, tortuosity, and atherosclerotic narrowing of cerebral vessels are noted at angiography. These degenerative changes increase the risk of manipulation of the vessels and may demand additional measures at the time of aneurysm clipping. Vascular occlusions by thrombosis or emboli may also be demonstrated. Vasospasm Cerebral vasospasm is defined angiographically as a narrowing of one intraluminal diameter. This is thought to be due to the contraction of the muscular arterial wall (Fig 152A-B). Vasospasm is generally (although not exclusively) seen in conjunction with ruptured cerebral aneurysm. It usually involves the basal arteries around the circle of Willis, particularly in the vicinity of the ruptured aneurysm, but may involve any or all of the cerebral arteries. Vasospasm is usually confined to vessels within the subarachnoid space and does not extend back into the subclinoid internal carotid or the extracranial vertebral arteries. Peripheral arterial dilatation may be associated with vasospasm of the circle of Willis. Although there may be a brief period of vasospasm at the time of rupture (but never observed during surgery), sustained vasospasm generally appears about the third day after subarachnoid hemorrhage and usually persists for 2 to 3 weeks (ref.). Chronic arterial changes may occur.

Cerebral Angiography

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Fig 152A-B Schematic respresentation of the portions of the Circle of Willis that are most susceptible to induced vasospasm (A) and an operative view of induced vaso-spasm (arrow) on the proximal right A, segment (B).

The clinical effects of vasospasm are related to its degree and extent, and it is important to note and consider this when judging its relevance to a given case. Radiologists generally grade vasospasm as mild, moderate or severe (Zingesser and Schech-ter 1968; Taveras and Wood 1976), relating it as a 25, 50, or 75 per cent reduction in diameter. Vasospasm may be confined to a localized segment or be diffuse and may be unilateral, bilateral, or general. A precise relationship to clinical condition can be drawn only in cases with severe diffuse and generalized spasm, whereas the localized, mild, or moderate spasm around the aneurysm is usually benign (Figs 153-158).____________ Vasospasm must be distinguished from other causes of arterial narrowing seen at angiography: Atherosclerosis. Atherosclerosis, especially in the Fig 153 Mild local vasospasm of both distal A, segments following rupture of an anterior communicating aneurysm (arrows).

internal carotid and proximal middle cerebral arteries may occasionally be confused with vasospasm. In general luminal narrowing from atherosclerosis tends to be more irregular and patchy than vasospasm, although this is not always the case. Technical difficulties. Proper demonstration of the cerebral vasculature by angiography is de pendent on adequate filling of the vessels with contrast medium. When the arteries are not com pletely filled, they may give the appearance of being in spasm. The following factors contribute * c £x to poor filling of the cerebral vasculature: -a " a) Poor cerebral perfusion increased intracranial 'r pressure or systemic circulatory failure will not permit the contrast medium to fill the cerebral arteries. General poor filling may be interpreted as diffuse spasm.

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b) Inadequate contrast medium may lead to layering of the contrast medium which is interpreted as spasm. c) Streaming and dilution as a stream of blood meets with the stream of contrast medium, layering may occur giving the impression of spasm. This is most common in the basilar and anterior cerebral arteries. Hypoplastic segments. Hypoplastic segments of the circle of Willis may be interpreted as being in spasm. At times both processes are occurring. Difficulty is most often encountered with the proximal anterior cerebral artery (A1 segment) and the posterior communicating artery.

Fig 154 A-B Moderate perifocal vasospasm (white arrows) of the right internal carotid, A, segment, and middle cerebral arteries following rupture of a right middle cerebral artery aneurysm (black arrow) (A). The left sided arteries are normal in size, whereas the right sided are spastic (white arrows) (B).

Fig 155A-B Moderate perifocal vasospasm involving the right (A) and left (B) internal carotid, A,, A2, M-,, and left M2 arteries following rupture of an anterior communicating aneurysm.

Cerebral Angiography 17 5 Fig 156A-C Angiographic demonstration of severe perifocal vasospasm with involvement of both AT (A) and A2 (B) segments with evidence of early filling veins (C) indicating luxury perfusion in ischemic areas. The 52 year-old female patient died before surgery. Autopsy revealed a large callosal hematoma.

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2 Diagnostic Studies Fig 157 Extreme generalized vasospasm of both proximal and distal arteries with poor distal perfusion, indicating severe cerebral edema, following rupture of a posterior communicating aneurysm. The 34 year old patient developed non reacting pupils immediately after SAH and died within a few hours.

Fig 158A-B A ruptured anterior communicating aneurysm causing extreme generalized vasospasm with no filling of the anterior circulation (A).

An aneurysm may escape detection at angiography because of vasospasm, or it may be better demonstrated in the presence of vasospasm. Eight cases in the present series showed only vasospasm on the original study, but later an aneurysm could be demonstrated. Therefore, in cases of subarachnoid hemorrhage where only vasospasm is present, it is advisable to repeat the study in two or three weeks or later as it is quite probable that an aneurysm may be present. Hydrocephalus Hydrocephalus may be suspected angiographically by elevation and stretching of the pericallosal arteries, lateral displacement and straightening of the striate and thalamoperforating arteries, and widening and stretching of the subependymal

Perfusion of the vertebrobasilar system is visible (B). The 33 year old patient died within 24 hours.

veins, particularly the thalamostriate vein in the anteroposterior projection. Intracranial Hematoma Subdural and intracerebral hematomas, particularly in the temporal lobe are demonstrated indirectly by appropriate shifts of the vascular system. Hematomas in the frontal lobes and within the ventricle are often not recognized by angiography. Cerebral Ischemia and Infarction In addition to the arterial phase of the angiogram, one should not forget to pay strict attention to the capillary and venous phases. Luxury perfusion with early filling veins may be the only evidence of cerebral infarction, or prolonged transit time may indicate poor cerebral perfusion. Often a good

Cerebral Angiography 17 7

correlation exists between changes evident in these phases of the angiogram and the patient's clinical condition. The combination of vasospasm and the localized absence of superficial cerebral veins on the venous phase in a patient with subarachnoid hemorrhage implies superficial venous thrombophlebitis and impending cerebral infarction. Direction of Fundus a) It should be especially noted that neuroradiological descriptions are usually presented in the standard anatomical position with the head upright. For the neurosurgeon planning an intracranial procedure in the usual supine position (with the head inclined 90° from the vertical this can be quite misleading. One must be aware that structures described as projecting anteriorly are found to be superior at surgery, those situated superior now become posterior, something originally described as posterior is found inferior, and an inferior structure is revealed anterior. Thus an operative procedure to correct a relatively simple posteriorly directed anterior communicating artery aneurysm on angiograms (film) will in reality show it to be an inferiorly directed aneurysm with adherent perforators behind it. The descriptions presented throughout this work are those appreciated by the neurosurgeon at surgery, but these discrepancies must be recognized (Figs 159-168). b) The diagnosis of intracranial aneurysms is readily made from the standard AP view angiogram. In planning surgical aneurysmal obliteration, though, it is absolutely essential to delineate the exact direction of fundus projection. In some instances (i.e. posterior communicating and basilar aneurysms) this information is available from the routine lateral view angiogram. In other cases (i.e. anterior communicating and middle cerebral aneurysms) this precise information is not always available from the standard lateral view due to the supra-imposition of vessels that obscure fine detail in these areas. Even the addition of lateral subtraction films may not be helpful in many of these cases. The recent application of angiotomography to these situations has provided this important missing link. The addition of lateral angiotomographic films to routine and subtraction lateral angiograms allows a precise definition of fundus projection, especially in anterior communicating and middle cerebral artery aneurysms, and should now be considered essential in the radiographic investigation of these lesions.

Fig 159A-B Schematic representation of the difference between the description of the aneurysmal projection given by the radiologist (A) and that actually found by the surgeon at operation (B) because of a 90 degree rotation of the head from the upright position normally seen by the radiologist to the supine position during surgery. A = anteriorly, I = inferiorly, P = posteriorly, S = superiorly directed fundus of aneurysms.

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2 Diagnostic Studies

Fig 160 A

Anterior

Superior

Superior

Posterior

Posterior

Inferior

Postero-inferior

Fig 160A-F Schematic representations of possible fun-dus projections as appreciated by the surgeon at operation. A Carotid-ophthalmic aneurysms B Posterior communicating aneurysms C Carotid bifurcation aneurysms D Middle cerebral bifurcation aneurysms E Anterior communicating aneurysms F Basilar bifurcation aneurysms Fig 160C

Anterior

Inferior

Superior

Posterior

Inferior

Inferior

Cerebral Angiography

Anterior

Superior

Posterior

Inferior

Fig160D

Fig 1 6 0 E

Fig 1 60 F

Anterior

Superior

Post. Inferior

Posterior

Inferior

Complex

Inferior

179

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2 Diagnostic Studies

Fig 161 This anteriorly directed anterior communicating (arrow) aneurysm as described by the radiologist will appear superior when approached by the surgeon with the head in the standard supine operating position (rotated 90 degrees from the orientation of the radiologist).

Fig 162 This radiographically described antero-superior (arrows) aneurysm will appear supero-posterior at operation.

Fig 163 This aneurysm seemingly extending superiorly (arrow) on x-ray will be posterior at surgery.

Fig 164 The radiologist's concept of this aneurysm as having anterior, superior, and posterior parts (arrows) conflicted with the surgeon who found superior, posterior, and inferior bulges.

Cerebral Angiography

Fig 165 The generally easier posteriorly directed anterior communicating aneurysm (as appreciated by the radiologist) becomes the more difficult supero-posteroinferiorly (arrows) directed one when approached at surgery. Fig 167 An inferiorly directed aneurysm of the posterior

communicating artery (on x-ray) is seen anterior at exploration.

Fig 168A-B A complex anterior communicating aneu-rysm will be described by both the radiologist and the surgeon as having anterior, superior, posterior, and inferior bulges, but with a 90 degree rotation.

181

Fig 166 This posterior communicating aneurysm that appears to have lobes projecting posteriorly and inferiorly on angiogram will be found at operation to be inferior and anterior (arrows).

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2 Diagnostic Studies

Specific Technical Details for Given Aneurysms While in many hospitals neurosurgeons either perform cerebral angiography or are actively involved in the procedure, there has been a trend in the larger neurosurgical centers for neuroradiologists to take full responsibility for the study. This is not without merit as with greater experience a study can be more safely and expeditiously performed, and more advanced techniques employed. Nevertheless, it is important that contact be maintained between the neurosurgeon and neuro-radiologist in order that the radiologist knows what information the surgeon requires. The following points have been noted in relation to the angiography of specific aneurysm locations:

Internal Carotid Artery Aneurysms Intracavernous It is important to check collateral circulation both from the contralateral carotid and from the vertebrobasilar systems as these aneurysms are generally treated by carotid artery ligation.

Ophthalmic a) With aneurysms at this location it may be difficult to decide the true origin of the aneurysm. Aneurysms of the anterior communicating artery, the anterior choroidal artery and the internal carotid bifurcation and especially the inferior wall of internal carotid artery may be confused with ophthalmic aneurysms, in the anteroposterior projection. The neck should be visible just above the carotid siphon in the lateral view, but special oblique views may be required (Fig 169A-B). b) With giant aneurysms it is important to carefully evaluate the collateral circulation as it may be necessary to compress or to ligate the internal carotid artery. These large aneurysms may be extremely difficult to distinguish from inferior wall and bifurcation aneurysms. c) Aneurysms at this location show a high incidence of bilaterality and thorough investigation of the opposite side should be carried out. In addition, ophthalmic aneurysms are frequently associated with aneurysms at other locations, requiring investigation of the entire cerebral circulation. d) It is recommended whenever possible to have computerized tomography performed as these lesions often contain significant thrombus and may present at operation considerably larger than was noted by angiography. When totally throm-bosed. the aneurysm may present as a sellar tumor (Rhonheimer 1959; Krayenbiihl and Ya§argil 1968).

Fig 169A-B The origin of this right sided aneurysm (arrow) is unclear in the right oblique projection (A), while the opposite oblique view shows a clear internal carotid-ophthalmic lesion (B).

Cerebral

Fig 170A-C Internal carotid artery aneurysms that appears to be arising at the bifurcation on the AP view (A), at the posterior communicating on the lateral view (B), and from the carotid itself on the oblique view (C) are actually arising from the inferior wall of the carotid.

Inferior Wall of Internal Carotid Artery a) Aneurysms at this location present a typical appearance: in the lateral projection, the fundus is directed posteriorly suggesting a posterior communicating artery aneurysm; in the antero-posterior view the aneurysm is directed medially suggesting an ophthalmic artery or carotid-bifurcation aneurysm. The posterior communicating artery aneurysms are not directed medially and can therefore be distinguished from aneurysms of the inferior carotid artery wall in the anteroposterior projection (Fig 170A-C).

b) Because these aneurysms are more difficult to control at operation and one may need to apply the technique of trapping, it is necessary to carefully evaluate the collateral circulation. Posterior Communicating and Anterior Choroidal Arteries a) The problem of infundibular widening versus a small aneurysm may be difficult to resolve. If the artery is coming directly out of the widened area there is probably not a surgically treatable aneurysm. This is often better appreciated in the

184

2 Diagnostic Studies

anteroposterior and anteroposterior oblique pro- tion should also be evaluated as extracranialjections. Clinical factors such as an oculomotor intracranial bypass operation may be considered, e) palsy or temporal lobe hematoma may help to The direction of the aneurysm fundus should be resolve the question. clearly identified by routine lateral and angiob) With larger aneurysms, one should try to tomographic views. demonstrate the anterior choroidal artery, which is seen best in lateral and in anteroposterior oblique Peripheral view. One must consider mycotic aneurysm at peripheral The identification of the anterior choroidal artery locations. With their tendency to spontaneous is important because its relationship to the an- thrombosis, angiography should be repeated just eurysm should be precisely defined. However, prior to operation. often it is difficult or even impossible to predict the relationship of the aneurysm to the posterior communicating and anterior choroidal arteries and the Anterior Cerebral-Anterior real topography is often uncovered only at surgery. c) Rarely, a second posterior cerebral artery will Communicating Artery Aneurysms take direct origin from the internal carotid artery. a) Hypoplasia or aplasia of an anterior cerebral artery should be noted. The location of the aneurysm on the anterior communicating artery will Bifurcation a) This location must be carefully examined when bear a given relationship to the relative caliber of subarachnoid hemorrhage occurs in children and the anterior cerebral arteries - on the ipsilateral side of the larger vessel or in the middle when the young adults. b) These aneurysms are occasionally bilateral and segments are equal. the opposite internal carotid artery must be care- b) A third A2 segment (median callosal artery) is present in about 8% of cases. This may be difficult fully checked. c) Effort should be made to identify the striate to see in the anteroposterior projection because it can be covered by the pericallosal and callosomararteries, and the anterior choroidal artery. d) With large aneurysms, any collateral circulation ginal arteries. In the lateral view however, it is must be carefully evaluated, including the extracra- useful to note whether a low origin of the frontoponial circulation with a view to carrying out extracra- lar arteries exists and whether the callosomarginal arteries are present. nial-intracranial vascular anastomosis. c) In 8 cases of the present series, a single A2 e) Computerized tomography is valuable in segment arose from the two A! segments. This evaluating the amount of thrombus which may be artery will be larger in caliber than either of the two considerable. proximal arteries and will be seen to supply both hemispheres (see Figs 105,106). d) Redundancy of vessels and complexity around Middle Cerebral Artery Aneurysms the anterior communicating artery may make a small aneurysm difficult to verify. Stereoscopic Proximal (M1 Segment) The relationship of the aneurysm to anterior tem- views, angiotomography, oblique and submenporal and striate branches should be noted as some tovertex projections help to clarify the situation (Figsl71A-B,172A-B). aneurysms may have their origin at this level. e) The direction of fundus projection of small and moderate sized aneurysms is not usually clearly Bifurcation defined on routine lateral views. The lateral a) The size and location of the major trunks angiotomogram may be necessary for more precise should be evaluated. definition (see Figs 164,165). b) The origin of the striate arteries is noted. f) Angiographic demonstration of the origin of the c) Although bilaterality is frequently mentioned recurrent artery of Heubner on either side is only with aneurysms at this location, only 9 of 184 cases rarely possible, and demonstration of the hypoin the present series had bilateral aneurysms. thalamic arteries is not possible. Nevertheless, careful evaluation of the opposite g) While it is helpful to know the direction of the side is necessary. fundus and its shape, angiography is frequently d) With giant aneurysms, collateral circulation inadequate to accurately predict the findings at may be well developed from the anterior and operation, especially the relationship of the fundus posterior cerebral arteries. The external circulato adjacent arteries (Fig 173A-D).

Cerebral Angiography

185

Fig 1 7 1 A-B Suspected aneurysm of the anterior communicating artery (arrow) on AP view (A) is better appreciated by turning the head to obtain an oblique view (B) it confirms the aneurysm (arrow) and also shows a small ophthalmic artery aneurysm.

Fig 172A-B Another example of an anterior communicating artery aneurysm (arrow) that is inconspicuous on the AP view (A) but well defined (arrow) on the oblique view (B).

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2 Diagnostic Studies

Fig 173A-D The finer details about aneurysm size, shape, origin, projection, and relation to surrounding vessels are not usually found in the angiogram as the AP (A), oblique (B), and lateral (C) views of this anterior communicating aneurysm demonstrate, in schematic illustration (D) after surgical observation.

Diagnostic Difficulties in Cerebral Angiography

187

B

Fig 174A-B A right carotid angiogram visualized both A2 segments and segmental spasm of the left A2 segment (arrow) but no aneurysm (A), while the left carotid angiogram (B) performed at the same time identifies the lesion (arrow).

Distal Anterior Cerebral Artery Aneurysms An aneurysm on the pericallosal artery may fill from only one side (ipsilateral or contralateral) despite the filling of both pericallosal arteries from an internal carotid artery. It is, therefore, necessary to examine the anterior cerebral arteries from both sides. Aneurysms at this location can also be bilateral (Fig 174A-B).

Upper Basilar Artery Aneurysms a) It must be determined whether the aneurysm is actually on the basilar bifurcation, just below it, or on a posterior cerebral artery. Of 63 aneurysms in the vicinity of the basilar bifurcation in the present series, 50 were actually on the bifurcation, 9 were on the proximal segments of the posterior cerebral arteries, and 2 on the superior cerebellar artery. b) The size and direction of the posterior communicating artery on each side must be evaluated, and the contribution of the posterior communicating artery to the posterior cerebral artery on each side noted. c) The relative size of the posterior communicating artery to the P, segment of the posterior cerebral artery on each side is evaluated, and perforating arteries from each vessel noted. d) The direction of fundus projection and its relationship to the thalamoperforate vessels will be best seen on lateral angiotomographic films.

e) As these aneurysms may contain thrombus, computerized tomography is especially important to determine the real size and shape of the aneurysm.

Vertebrobasilar Aneurysms a) Most aneurysms occur at the origin of the posterior inferior cerebellar artery, and this area should be carefully investigated. b) An aneurysm may involve the vertebral artery of one side above the posterior inferior cerebellar artery, and be large and mostly thrombosed. Angiography then shows the vertebral artery on that side to end at the PICA and perhaps a small amount of aneurysm to fill from the opposite side giving the impression that the aneurysm is originating from the opposite vertebral artery.

Diagnostic Difficulties in Cerebral Angiography The introduction of cerebral angiography by Moniz in 1927 was, of course, a significant breakthrough in the diagnosis of intracranial pathology, and especially cerebrovascular disease. Since that time considerable effort has been expended to improve and further refine angiographic studies. The complex topographical anatomy of cerebral vessels has required that new techniques be developed to

188

2 Diagnostic Studies

adequately portray intracranial lesions, so stereoscopic angiography, subtraction and magnification techniques, and angiotomography have been introduced over the years. Many textbooks of angiography are now available (Krayenbuhl and Ya§argil 1968; Newton and Potts 1974; Taveras and Wood 1976; Huber 1979). In recent years, emphasis has been placed on fine anatomy of the cerebral vasculature, and texts treating difficult areas in great detail have been of immense value to neurosurgeons (Stephens and Stilwell 1969; Duvernoy 1975/ 78; Salamon 1976; Schlesinger 1976; Salamon and Huang 1976; Nadjmi 1977; Szikla et al 1977). Improvement in contrast media and selective catheter techniques have allowed a variety of projections to be performed during one examination, limited only by the amount of contrast medium that can be safely injected. These advances in neuroradiology have let physicians come to expect that pathological entities will be clearly defined, and this is usually the case. Nevertheless, from the experience at the University of Zurich including angiograms received from departments around the world, it is apparent that the excellent angiographic demonstration of cerebral aneurysms usually encountered in publications is not always to be found in daily work. Many referring centers simply do not have the experience or expertise to perform more than a basic examination. It is a pity that frequently the x-rays are not clearly marked with "left" or "right". In even the largest centers, however, inconclusive results may be obtained despite the best efforts of experienced neuroradiologists. Two factors especially contribute to suboptimal studies:

Anatomical Problems The resolution of angiography is at times inadequate to portray fine anatomical detail, especially the precise position of larger vessels and perforators surrounding an aneurysm. Small aneurysms are not easily distinguished from infundibular widenings, especially of the posterior communicating, lenticulostriate, anterior temporal, fronto-polar, and posterior inferior cerebellar arteries. Vessels seen end on may appear to be small aneurysms. It is not only small aneurysms that create difficulty in angiographic interpretation, however, as aneurysms of considerable size may be hidden by superimposition of normal vessels and go unrecognized (see Fig 173A-D). Finally anatomical variations and anomalies may be mistaken for aneurysms. Examples of these various anatomical problems will be presented in the following pages.

Inadequate Clinical Information Providing the neuroradiologist with specific clinical information will help direct his attention to a suspicious area. An oculomotor palsy will suggest an aneurysm of the lateral wall of the internal carotid artery or the basilar bifurcation, while a visual deficit will suggest an aneurysm of the medial wall of the internal carotid artery or the anterior communicating artery. The value of an increased index of suspicion in radiographic interpretation is illustrated by the following case (Fig 175A-B). When diagnosis remains uncertain, it is generally advisable to attempt different projections and techniques to clarify the situation and avoid an unnecessary or suboptimal operative procedure. Repetition of the study or additional investigation may or may not provide useful information, however, and causes additional stress to the patient. Angiographic studies require interpretation and are therefore subject to human error. The previous experience, confidence, and disposition of the radiologists and neurosurgeons evaluating the studies will influence this interpretation. Thus in some cases unnecessary operative procedures will be performed, while in others lesions will be missed and patients will rebleed and die. In still other cases an aneurysm will be successfully treated despite equivocal findings on angiography. It should be noted that angiography may not always be diagnostic in terms of defining an aneurysm in those patients who undergo aneurysm clipping but then suffer another episode of subarachnoid hemorrhage. When the bleeding has resulted from the formation of another bulge at the base of a previously clipped aneurysm (proximal to the clip), the clip itself often conceals the lesion. If the hemorrhage can be confirmed by LP or CT scan, then these patients should undergo exploration of the previously clipped aneurysm despite the lack of angiographic confirmation (eight own cases see p. 263, Vol. I, and p. 194, Vol. II).

продолжение

Diagnostic Difficulties in Cerebral Angiography продолжение___189

Fig 175 A-B In this patient with a right homonymous hemianopsia, a small aneurysm at the beginning of the P3 segment of the left posterior cerebral artery was suspected on AP (A) and lateral (B) vertebral angiograms (arrows). This was confirmed at operation.

False Positive Angiography (Negative Exploration) As discussed in Chapter 5, it is not infrequent that no angiographic cause for subarachnoid hemorrhage can be found. Some of these cases will be found months and years later to have had an aneurysm, either by repeat angiography or at autopsy. However the problem of a "false positive" angiogram, where an aneurysm is thought to be present on angiography, but is not found at operation is less often discussed. In the present series, 15 patients underwent operative exploration for intracranial aneurysm with no lesion found (Fig 176A-D).

Fig 176A-D The radiographic diagnosis seemed certain of (A) anterior communicating aneurysm (arrow), (B) anterior communicating aneurysm (arrow).

190

2 Diagnostic Studies Fig 176C—D Anterior communicating aneurysm (C) (arrow), and (D) right middle cerebral (M,) aneurysm (arrow), but in each case no aneurysm was found at exploration.

Unexpected Location of Aneurysm In two cases, the aneurysm did not turn out to be at the location suggested by angiography (Fig 177AB). These two cases differ from those with negative exploration only in that the unexpected aneurysm was present at operation to explain the subarachnoid hemorrhage. The ruptured lesion had not been accurately documented angiographi-cally. The presence of a suspicious lesion, of course, has the tendency to make further examination of the study less critical. Nevertheless, either of these aneurysms could be easily missed, even with the rest of the study unremarkable. Of particular relevance here is the adequate opening of the basal cisterns at operation (as described on pp. 226-233). Not only does this provide for free egress of loculated collections of CSF thereby reducing the need for brain retraction and manipulation but it also facilitates the demonstration of hitherto unsuspected incidental aneurysms.

Diagnostic Difficulties in Cerebral Angiography

191

Fig 177A—B The presence of a large ruptured left carotid-ophthalmic aneurysm (arrows) was hidden on the AP and lateral left carotid angiogram (A) and recognized by exploration of the basilar artery aneurysm seen in the lateral vertebral angiogram (B).

Fig 1 7 8 A In this case an aneurysm of the right M, segment was suspected on the angiogram (small arrow). Exploration showed, however, a small remnant of a ruptured and thrombosed aneurysm at the origin of the right posterior communicating artery (larger arrow).

Fig 178B Right carotid angiogram with cross-compression produced good filling on both sides and demonstrated a welldefined aneurysm on the right M-, segment. At operation this aneurysm was found to be unruptured but an inferiorly directed aneurysm of the right carotid bifurcation (arrow) had ruptured. Even retrospective study of the lateral angiograms failed to reveal the hidden aneurysm.

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2 Diagnostic Studies

Equivocal Angiograms (Positive Exploration) An equivocal angiogram to one examiner may be quite conclusive to another with more experience or a higher degree of suspicion. However, 37 patients have undergone angiography in this series where no agreement could be reached among members of the departments of radiology and neurosurgery as to the presence of an aneurysm, but were nevertheless explored and found indeed to have a ruptured aneurysm. Unoperated, some of these patients would surely have rebled and died. A few such angiograms are presented to allow a comparison with those from patients described above under negative exploration (Figs 178, 179AC,180A-C). Attention should be paid to the problem of rerupture of an incompletely clipped aneurysm. Repeat angiography can often fail to demonstrate recurrent aneurysm formation or enlargement at the site of an incorrectly applied clip. In 8 such cases postoperative angiograms failed to demonstrate small newly-developed aneurysms between the parent vessel and the clip which were discovered at reexploration (see Fig 221, p. 263).

Fig 179A-C Right AP (A) and left oblique (B) carotid angiograms suggested the presence of an anterior communicating aneurysm (arrow) arising from the left corner. This was confirmed at surgery (C).

Diagnostic Difficulties in Cerebral Angiography

193

Fig 180A-C The finding of hematoma and infarction in the left medial-basal temporal lobe on CT scan (A) suggested the presence of a left carotid aneurysm, but left AP (B) and lateral (C) carotid angiograms showed only seg-mental spasm of the internal carotid, A,, and M^ arteries. A well developed left internal carotid-anterior choroidal aneurysm was found at operation.

Discussion Pertinent findings in the 15 cases of negative exploration are summarized in Table 13. Nine of these patients had one or more lumbar punctures showing bloody spinal fluid in a referring hospital. These patients were first seen from 1 to 9 weeks after hemorrhage, and it was not considered useful to repeat the lumbar puncture. Five of the 6 patients initially evaluated in Zurich had bloody spinal fluid, and in 2 of these the supernatant was recorded as xanthochromic. One patient did not have a lumbar puncture performed. All 15 patients had rather typical histories for subarachnoid hemorrhage, and all demonstrated meningism when first examined. Aneurysms were suspected on the anterior communicating or anterior cerebral arteries in 6 cases, the proximal middle cerebral artery in 3 cases, the middle cerebral artery bifurcation in 3 cases, the

internal carotid posterior communicating artery in 2 cases and the basilar artery bifurcation in one case. In only one case were the subarachnoid cisterns filled with hematoma. and in 3 additional cases, yellow stained arachnoid was seen. The other eleven cases showed normal subarachnoid cisterns upon surgical exploration. There was one death in these 15 patients. The cause of the intimal dissection in the internal carotid artery in this case, and its temporal relationship to angiography and operation are not clear. It appears certain that this man sustained a true subarachnoid hemorrhage, but the etiology could not be determined. One case required a ventriculoatrial shunt in the postoperative period, and she was the only patient that had extensive hematoma in the basal cisterns. None of the cases has been subsequently found to have had an aneurysm.

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2 Diagnostic Studies

Table 13 Negative explorations Patient

Age

Sex

LP

Men.

Grade

Angiogr.

Op. find.

Postop.

W. W.

33

M

Bl*

+

la

R MCA bif.

Neg.

Good

A. K.

32

M

Bl*

+

la

Good

61

F

Bl*

+

lla

ACoA L MCA bif. occ. branch

Xan. cisterns

A. K.

Neg.

Good

C. S.

45

F

Bl*

+

lla

M-1 (L)

Neg.

Good

A. N.

55

M

Bl*

+

la

AA-1 (R)

Neg.

Hypertension

L. F.

35

F

0

+

la

M-1 (R)

Neg.

Seizures

C. R.

62

F

Bl*

0

Illb

MCA bif. (R)

Neg.

Good

K. M.

37

F

Bl*

+

la

M-1 (L)

Neg.

Good

S. O.

29

F

Xan

la

ACoA (L)

Neg.

Good

C. C.

64

M

Bl*

+

Ilia

ACoA (R)

Neg.

Good

E. H.

56

F

Bl

+

lla

Bas. Bif.

Cisternal hem.

Hydrocephalus - shunt

W. Z.

47

M

Bl

+

lla

ACoA (L)

Neg.

Good

A. B.

48

M

Xan.

+

la

ACoA (M)

Xan., on R. opt. nerve.

Died, autopsy did not reveal an aneurysm. Intimal dissection of the right ICA on the neck due to the angiography Good Good

The above 15 cases of negative exploration thus must be classified as cases of unexplained subarachnoid hemorrhage. Four of the cases had clear evidence for subarachnoid hemorrhage seen at operation. In the other 11, there was no real evidence that blood had been present in the subarachnoid space. On two previous occasions when four vessel angiography had been negative, myelography had revealed a spinal arteriovenous malformation. One of these fifteen cases underwent myelography and it was negative. At other times, tumors have proven to be the source of subarachnoid hemorrhage, but in none of the above cases was there evidence for tumor either during hospitalization or in the follow-up period. For the 11 patients with clear subarachnoid cisterns, it must be assumed that at least some had a false positive lumbar puncture, and that symptoms were in fact related to some other cause. Whether lumbar puncture is bloody or clear, however, there is no way to be certain that subarachnoid hemorrhage has not occurred. While computerized tomography can further corroborate the presence of subarachnoid blood, it cannot prove that blood is not present. Cases have been seen at operation where bleeding is confined to the area immediately around the aneurysm despite normal

CT-scan. If one accepts only the obvious cases of subarachnoid hemorrhage, and operates on only the aneurysms which are distinct on angiography, a number of patients harboring an aneurysm will be left at risk. These are patients who are often in good condition and who can benefit most from an operation. Aneurysms which are questionable on angiography are not always small, as noted above. Furthermore the fact that a patient has presented with subarachnoid hemorrhage, shows that his aneurysm is capable of rupture whatever the size. Frequently, small aneurysms seen at operation are transparently thin and certainly capable of rupture. One must of course strive to limit false positive and false negative studies, but in any large series a small group of these will unfortunately occur. Social and psychological pressures on the neurosurgeons must also be considered. Not infrequently patients will build certain expectations from discussions with referring physicians which may be inappropriate to the circumstances. Physicians should refrain from advising a certain mode of therapy until all those involved in the care of the patient have had an opportunity to review the findings. Secondly the surgeon cannot help but be influenced by his recent experience. A successful

Diagnostic Difficulties in Cerebral Angiography 19 5

case may lead to a subsequent negative exploration. An operative disaster may dampen enthusiasm for the next several cases. Factors such as these influence radiographic interpretation and the willingness to operate in the face of equivocal findings. While it is certainly more emotionally trying for a neurosurgeon to perform a negative exploration than to defer operation, he must remain cognizant of his responsibility to patients who are denied operation and subsequently succumb to aneurysm rupture.

Multiple Aneurysms with one or more Unrecognized Angiographically In about 20 to 30 per cent of the cases, multiple aneurysms will be seen on angiography. In some cases however, multiple aneurysms will be found at operation, but one or more will not be recognized on angiography. In the latter group it may occasionally be the ruptured lesion which is not appreciated on the radiographic study (see Vol. II, Chapter?). It has been a relatively common experience that additional aneurysms are encountered at operation which were not appreciated on angiography. These aneurysms are not necessarily small. The surgeon must keep in mind the limitation of angiography to completely exclude the presence of an aneurysm, and at operation pay attention to the common sites of aneurysm formation.

Postoperative Angiography Several neurosurgeons have stated the need for postoperative angiography to ascertain the accuracy of clip placement and the patency of surrounding vessels (Allcock and Drake 1963; Quest and Countee 1977; Servo and Puranen 1977). Incomplete clipping of the lesion demonstrated by angiography has ranged from 4 to 26% of cases depending to some extent on criteria used (Drake and Vanderlinden 1967). It would seem logical that the use of the operating microscope would negate the necessity of routine postoperative angiography when the lesion has been completely visualized, and clipped. Postoperative angiography was of course also used before (1976) for evaluation of patients with an unsatisfactory postoperative course to look for intracranial hematoma, vessel occlusion, hydrocephalus or cerebral vasospasm. Postoperative angiography has not been performed routinely in the present series of patients. In most cases the fundus of the aneurysm, after thorough coagulation, has been resected close to the base and clip placement and staged clipping

checked under the operating microscope. The high closing pressure of the Aesculap clip minimizes the possibility of clip slippage in the postoperative period, although particular care must be taken with clip placement in arteriosclerotic aneurysms. Reasons for postoperative angiography in this series have included some cases with postoperative deterioration, rerupture of clipped aneurysms before the technique of staged clipping was initiated and at the request of patients, relatives or referring physicians. In cases with reruptured aneurysms however the visualization of the newly developed aneurysm between the clip and parent artery may be very difficult, even impossible, if the lesion is small and the clip itself covers the lesion. In such cases the only way of dealing with this acute problem is that of reexploration (see Fig 221C-G). Since it became available in 1976, a pre- and postoperative CT scan has been performed routinely in all our cases. In patients with a normal postoperative course the CT scan always presented a normal picture, whereas in patients with delayed recovery it frequently showed a developing hydrocephalus. In patients with a permanent paresis the CT scan showed, on about the tenth day, an area of infarction correlating with the clinical symptoms.

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Complications of Angiography

Table 14 Potential complications in cerebral angiography

With improved techniques, cerebral angiography I. Anesthetic complications performed in patients with ruptured cerebral aneut rysm has become a relatively safe procedure. Increase of intracranial pressure during intubation Evaluating 7165 angiographic procedures from the Hypo- or hypertension Cooperative Study, Ferret and Nishioka (1966) Reaction to anesthetic drugs found the overall incidence of complications was 6.43%, although figures from various centers II. Angiography technique ranged from 1.4% to 15.7%. A slightly higher A) Local incidence of complications was found in patients Hematoma intramural who had suffered subarachnoid hemorrhage than periarterial Spasm those who had not. Complications increased with (local) Thrombosis age and with the amount of contrast medium used, Arteriovenous fistula and there was a slightly higher rate of complications Infection with general anesthesia than with local anesthesia. B) Systemic Dilenge and Ramee (1966) reported 520 (1.2%) Allergic reaction Embolic transient and 44 (0.1%) permanent complications in phenomenon Ischemic 43,450 studies for various disease processes. The symptomatology death rate was 0.15%. Niizuma et al (1979) (in the Vasospasm intracranial Rupture of aneurysm monograph of Suzuki 1979) encountered 1080 cases of intracranial saccular aneurysms over a period of about 14 years (1961-1975). All but 80 cases were Some of the major causes of deleterious sequelae subjected to direct operation. Cerebral angiography include: was performed on those cases and occasionally In the early days after angiography was introcaused complications. Complications were found in duced the contrast medium itself was frequently 34 (3.6%) of the 939 cases studied and in 36 (1.2%) thought to be the cause of complications. Injury of of the 3093 angiograms. Coddon and Krieger the carotid artery due to intramural injection, (1958) observed complications in 17.8 per cent of Rupture of aneurysm during angiography, Emboli 483 cases of SAH subjected to angiography, and in from an intimal plaque, Vasospasm (Pribram 24.2 per cent of 33 cases with intracranial [1965] mentioned that cerebral vasospasm might aneurysms among his cases. Fields et al (1962) readily be induced by angiography), Hypotension found complications in 2.5 per cent of their total during anesthesia (Fig 181A-D). cases and in 3.3 per cent of the cases of SAH: death from rerupture occurred in 2 cases. Reisner et al (1980) reported on the complications of 1628 patients undergoing direct carotid or brachial angiography and 1000 patients undergoing transfemoral angiography for CNS disorders. A total of 80 complications occurred in both groups combined (3.04%). Local technical complications occurred most frequently in older patients with vascular diseases. Transient or permanent neurological deficits occurred in only 1.78 per cent of brachial and carotid studies as compared to 5.10 per cent of transfemoral studies. Although the total complication rate of transfemoral angiography was much higher, most of the complications were mild (only 0.33% permanent neurological deficits) as compared to the complication rate of direct brachial and carotid angiography in which most of the complications were permanent. Also the only 2 deaths in the series occurred in this latter group (Table 14).

Diagnostic Difficulties in Cerebral Angiography___19 7

Fig 1 8 1 A-D Embolic occlusion (arrow) of the right distal A, segment of the anterior cerebral artery by a small aneurysm of the proximal A, segment was suspected on the right (A) and left (B) carotid angiography and confirmed at surgery (C). The embolus was pushed back along the right A, segment and removed through the resected aneurysm (D).

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2 Diagnostic Studies

Rupture of Aneurysm During Angiography Since the report of Jenkinson et al in 1954 concerning a case of rupture of aneurysm during angiogra-phy there have been several studies published. Koenig et al (1979) reported 10 cases of intracranial aneurysm that ruptured during cerebral angiogra-phy, and reviewed 28 cases in the literature. Onuma et al (1979) reported 2 cases and collected 21 cases from the literature. Dublin and Freud (1980) reported one case and reviewed 30 cases of the literature in detail: The average age was 41 years. There is a preponderance of females over males. 71% to 29%, the clinical grade, using Botterell's classic grading scale was III. The distribution of the site of the aneurysm was in 6 cases ICA, in 8 cases PcoA, in 7 cases MCA, in 6 cases ACA, one case in each of PICA vertebral junction, basilar tip and one unknown. 21 cases demonstrated cisternal, 13 cases intracerebral and 10 cases intraventricular extravasation of the contrast material. Of 14 cases whose pre-angiographic blood pressure was known 11 were definitely elevated and hypertensive. Most angiograms were performed under local anesthesia and in only one case under general anesthesia. Most studies employed direct carotid puncture (18 cases). One direct vertebral puncture, one retrograde brachial study and four transfemoral studies were performed. The average time interval from SAH to angiographic evaluation was 4.7 days (14 cases within 1 day after SAH). Twenty of 27 (75%) of patients with known follow-up died. Of the seven survivors only 2 were completely normal. Table 15 Preoperative mortality cases after angiography

The use of general anesthesia, stabilization of hypertensive patients before and during angiography seems to be the answer to this problem. I In our series cerebral angiography was always performed under general anesthesia, but the injec tion technique altered. Direct puncture of the carotid and axial or brachial puncture for the vertebral angiography was used from 1967-1975, thereafter only the technique of femoral-catheterization (and this under general anesthesia) was used. In the present series of 1114 cases (1012 cases operated, 24 patients refused operation, 78 pa tients died before surgery) there were no cases of infection, arteriovenous fistula, or thrombosis of ICA. Similarly no cases of aneurysm rupture dur ing angiography occurred, but there were severe complications encountered in 28 patients (2.5%) with impairment of consciousness and 14 of the 28 patients died. Mild or moderate but transient hemisyndrome with or without speech impairment and visual field loss was observed in 22 cases (1.97%): 12 cases in grade Ha, 8 cases in Ilia, 2 cases in IV. Severe and persistent hemisyndrome was seen in 4 cases (0.35%): 2 in grade Ilia, 2 in IV. The analysis of the 14 preoperative mortality cases (1.2%) showed the following relations concerning the site of aneurysm, year of angiography, sex, age, pre-angiographic condition and time of angiography after SAH (Table 15).

Site

Year

Age

Sex

Condition

Time of angiography

Time of death

AcoA

1967

61

F

lla

2d

1d

1969 1972 1971

37 52 40

M F M

Ha IV IV

7d 6d 14 d

3 hours 6d 12d

1972

42

F

IV

4w

hours

1967 1974

60 56

M F

Nib IV

10d 1d

2d 9d

IC-Bi

1969

64

M

IV

7d

10d

MCA

1972

67

F

Ilia

7d

7d

1970 1974 1971

55 54 63

M F F

1Mb Ilia IV

12d 4d 3d

3d 2d 4d

1969

49

M

IV

9d

hours

1974

47

M

IV

9d

11 d

PcoA

B-Bi

Computerized Tomography

The impression has been gained from our series that the rate of complications goes up first with the worsening clinical condition of the patient and then with the age. Patients in grades I and II have rarely had complications, while patients in grades III to V often show mild, moderate, or severe deterioration. Since the use of the femoral technique in combination with routine general anesthesia there have been no deaths. Since the CT scan has been available, those patients with ischemia demonstrated on CT are not scheduled for angiography.

Information Derived from Computerized Tomography: Identification of Aneurysm

199

v

At the present time the diagnosis of intracranial aneurysms on the CT scan is only approximate, as only angiography gives in most of the cases a clear picture. However, the CT diagnosis of aneurysms down to 6 mm in size has been possible (Schubiger etal!980). By good discrimination between relatively similar densities within the cranial vault, computerized tomography is able to portray many of the pathogenetic sequelae of ruptured cerebral aneurysm much better than angiography and with remarkable clarity: Fresh blood within the Computerized Tomography Intracranial Hematoma cranial cavity is quite easily distinguished from Method of Computerized Tomography brain tissue and cerebrospinal fluid. It is Following a routine scan, 1 to 1,5 cc 50% Hypaque important that the initial scan be done without or Conray-60 per kilogram is given intravenously contrast medium in order that fresh blood not be over about 15 minutes, beginning 5 minutes before confused with enhancing tissue. Subdural, the scan. This technique must be adjusted to the intracisternal, intracerebral and intraventricular time frame of the scanner, as the newer models hematoma can be recognized. When correlated with require less time per study. This will allow visualishifts of the ventricular system, the mass effect of a zation of the larger intracranial vessels and give hematoma can be appreciated. The recumbent enough time for contrast medium to pass into areas position of the patient will allow blood in the where the blood brain barrier is no longer effective. ventricular system to gravitate to the occipital While newer, faster scanners have minimized horns, and may result in layering out of blood cells motion artefact, it is preferable to have the patient in a subdural hematoma. As blood lyses, its attenuquiet and immobile. As patients with subarachnoid ation factors will change and it may become hemorrhage are frequently restless, sedation is isodense with brain for a period of time. This must often indicated. Children may require general be remembered when CT is done a few hours or anesthesia. several days after ictus (Fig 182A-B).

Fig 182 A In a 34 year old male, in grade Ilia, the CT scan showed intracerebral and intraventricular hematomas. Full recovery of the patient ensued after clipping of the aneurysm of the anterior communicating artery and removal of the hematomas 8 hours after hemorrhage. B A 40 year old female in grade V showed a large frontal hematoma on CT scan. The ruptured aneurysm of the middle cerebral artery was clipped and the hematoma removed 6 hours after hemorrhage, but the patient did not recover and died within 24 hours.

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2 Diagnostic Studies

Cerebral Infarction As ischemic tissue becomes edematous, its density decreases and these areas can be distinguished . from normal brain. After a few days, the blood brain barrier is no longer competent and contrast medium will pass into the infarcted areas. After several weeks, the area becomes cystic, and is of low density, again impermeable to contrast medium. The time course of these events must be considered when evaluating the scan. Initial compression of the ventricular system by edematous brain and subsequent expansion of the ventricle into the area of cystic degeneration complement the picture of cerebral infarction (Figs 183-186). Hydrocephalus Ventricular size is clearly demonstrated by computerized tomography and may be followed serially to see whether an early ventricular dilatation or late hydrocephalus occurred (Fig 187A-C). Demonstration of Lesion If a scan is made during infusion of contrast medium, the major vessels are displayed with increased density. At times, an aneurysm can be recognized (see Fig 189A-E). Arteriovenous malformations, tumors, and other lesions in the differential diagnosis of subarachnoid hemorrhage are usually visible on the scan. Multiple Aneurysms Two aneurysms have been diagnosed by CT scan in 3 cases and three aneurysms in one case (see Vol. II). Site of Ruptured Aneurysm In cases of multiple aneurysms the presence of localized hematoma or infarction may suggest which of the lesions had bled (see Vol. II). Following Angiography Repeat computerized tomography should generally be performed following angiography on some patients with large or giant aneurysms prior to surgery, because the tendency of these aneurysms to thrombose following angiography is well documented. Thrombus Within an Aneurysm

Thrombus within an aneurysm is usually well shown by computerized tomography. It is very important to compare the CT scan with the angiogram to assess the amount of thrombus within the lesion and gain a better appreciation of its size.

Fig 183A-B The finding of a left temporal infarction in a neurologically normal patient (42 years old) following subarachnoid hemorrhage (A) suggested the presence of a left middle cerebral aneurysm, that was confirmed at angiography (B) arising from the origin of the anterior temporal artery. This patient suffered postoperative epileptic seizures.

Computerized Tomography

201

Fig 184A-B In this 33 year old patient with a subarach-noid hemorrhage and severe neurological deficits (right hemisyndrome, aphasia, and right homonymous hemianopsia), the presence of a large left occipital infarction (A) was related to a basilar bifurcation aneurysm (B) also found on the CT scan.

Fig 1 8 4 C-D In this 38 year old patient with subarachnoid hemorrhage and left hemiparesis the angiography (C) showed a partially thrombosed aneurysm of the right P, segment and the CT scan a thalamic infarction (D).

202

2 Diagnostic Studies Fig 185A-B A large right temporal lobe infarction (arrows) from a ruptured right middle cerebral aneurysm in a neurologically normal patient (A). Three weeks after a subarachnoid hemorrhage, a large right mesial frontal lobe infarction (arrow) from a pericallosal artery aneurysm (arrow) was discovered on CT scan in a neurologically normal patient (B). Fig 186A-B This 61 year old female patient with a left-sided hemiplegia had a normal CT scan 24 hours after a subarachnoid hemorrhage (A). A repeat scan two weeks later, however, showed an area of infarction (B).

Computerized Tomography

203

Fig 187 A-C Segmental spasm of the A,, M, and internal carotid arteries but no clearly defined aneurysm (anterior communicating = arrow) was seen in this patient (26 years old) on angiography in 1968 (A) following a subarach-noid hemorrhage. Ten years later the patient developed headaches following an auto accident and CT scan (B) showed a large right frontal porencephalic cyst, probably related to the previously ruptured but not enlarged anterior communicating aneurysm (C) that was confirmed at operation (1978).

Giant aneurysms have at times gone unsuspected pre-operatively because of the small lumen seen at angiography (Fig 188A-G). Kazner and Lanksch (1979) correlated the CT findings on admission with clinical grades and found that a normal scan or hydrocephalus were the only pathological findings occurring in Grade I+11 patients while the poorest grade patients (IV-V) consistently showed evidence of subarach-noid hemorrhage, intracranial hematoma, cerebral edema and/or hydrocephalus. One half of the patients with signs of infarction as a sequel of vasospasm died, although this was the only abnor-

mal finding on the CT scan. However, if this was combined with other complications like tam-ponade of basal cisterns, circumscribed hematomas or intraventricular hemorrhages, the outcome was always fatal. The CT scan experience in our cases within the last six years is similar, but not identical; as we have also observed patients in Grade I and II, who have cisternal and intracerebral hematomas on the CT scan, without neurological symptoms.

204

2 Diagnostic Studies

Fig 188A-B The true size of a partially thrombosed basi-lar bifurcation aneurysm (arrow) is better appreciated on the CT scan (B) than on the angiogram (A) (26 year-old male).

Fig 188C-I The true size of an asymptomatic, partially thrombosed giant aneurysm of the anterior communicating artery ( 1 ) and a ruptured basilar aneurysm (2) on the CT scan (C-D-E) and on the angiogram (F-G-H) (35 year old female), and postoperative CT (I).

Computerized Tomography

205

Fig 188F-H The carotid (F-G) and vertebral (H) angio-grams confirming the presence of two aneurysms.

Pitfalls of Computerized Tomography The computerized tomographic evaluation of aneurysm patients is not without its difficulties. Not infrequently definite areas of increased density are seen without contrast in the cisterns or ventricles and initially interpreted as signifying a subarachnoid or intraventricular hemorrhage. In a few of these patients, subsequent evaluation by angiography and spinal tap will reveal no evidence of aneurysm or prior hemorrhage. In other circumstances, patients with proven ruptured aneurysms may have persistently normal computerized tomographies, and patients with significant subdural, intracerebral or intraventricular (isodense) hematomas or areas of infarction found at operations may have no evidence of these abnormalities on prior computerized tomography. These misleading interpretations of computerized tomography though infrequent, emphasize the complementary roles of CT and angiography in the evaluation of the aneurysm patient and should be recognized. Fig 1881

Postoperative CT scan.

206

2 Diagnostic Studies

Timing of Radiological Procedures Until the last few years, it has generally been recommended that angiography be performed early following subarachnoid hemorrhage (at least in younger patients below 50 years) to document the lesion responsible for subarachnoid hemorrhage aneurysm, arteriovenous malformation, tumor, thrombophlebitis, - and to look for possible complications - intracerebral hematoma, hydrocephalus, vasospasm, or vascular occlusions. The introduction of computerized tomography into the neuroradiological armamentarium, however, has necessitated a reappraisal of the proper timing for angiography. Although angiography is reasonably safe in patients who remain in good condition following subarachnoid hemorrhage, patients in poorer condition have seemed to suffer a higher complication rate when angiography is done early. Facilities without computerized tomography will have to depend on angiography as has been done in the past to evaluate brain shifts and ventricular size in patients in clinically poor condition. In units that have computerized tomography, however, this modality will be used first in all cases of subarachnoid hemorrhage. It is easily tolerated by the patient, will show hematomas, infarction and ventricular size, and in some situations with contrast enhancement will show an aneurysm, arteriovenous malformation, or other cause for subarachnoid hemorrhage. The presence of blood within the subarachnoid cisterns and ventricles confirms that subarachnoid hemorrhage has actually occurred. With patients in poor condition in whom no lesion requiring an emergency procedure is found, angiography may be deferred until the patient has improved. If operation is planned, angiography is usually performed first to define the aneurysm, unless the patient's condition demands immediate intervention. Patients in good condition will continue to have angiography performed early, and proceed to operation. The patient's general condition including hypertension, diabetes, cardiac, pulmonary, and renal disease, and blood dyscrasias, must also be considered when planning proper timing for angiography. It is becoming increasingly more common for patients with ruptured cerebral aneurysms to be referred to neurological centers for care. This being the case, it is recommended that patients with subarachnoid hemorrhage not be taken acutely to angiography in smaller referring hospitals merely for the sake of diagnosis where no therapy is contemplated. Often the study will be

suboptimal or a change in the patient's condition will require the study to be repeated. Angiography in cerebral aneurysm patients should be considered as the first step of the operative procedure, and should therefore be performed at a center where a neurosurgeon can participate in the decision. The following outlines the practice in this department. 1) Angiography is deferred in patients in poor condition in whom CT scanning has shown no significant hematoma or has shown infarction. 2) Unilateral angiography is done immediately in the patient with hematoma showing significant mass effect on CT scan. 3) Bilateral carotid angiography is performed early in patients in grades I and II in whom an aneurysm is identified at CT in the carotid territory. The left side is demonstrated first if CT shows an aneurysm in the ACA location, since in 50% of cases this will be the side of a larger A! segment. 4) Vertebral angiography is performed first if signs of vertebrobasilar aneurysm rupture are seen on CT. 5) In the absence of CT signs suggesting the site of aneurysm bilateral carotid angiography is first performed. 6) If bilateral carotid angiography is negative then vertebral angiography is performed, first one side then the other if a crossfilling not occurred. 7) In case of a re-rupture of an aneurysm before the scheduled angiography, immediate exploration without angiography can be occasionally recommended providing the CT scan is helpful in delineating the site of the lesion (4 own cases) (Figl89A-E).

Timing of Radiological Procedures Fig 189 A The CT scan showed in a 39 year old patient a temporal hematoma with a bifurcation aneurysm of the middle cerebral artery (arrow). The immediate exploration with removal of hematoma and clipping of aneurysm was successful. Fig 189 B The CT scan showed a left insular hematoma in a 35 year old patient, who then began to develop neurological impairment. Immediate exploration with removal of the hematoma, clipping of the bifurcation aneurysm of the middle cerebral artery (arrow) and papaverine application to the spastic vessels was lifesaving.

Fig 189C A 45 year old patient in grade lla showed right frontal and bilateral intraventricular hematomas and a suspected aneurysm of the anterior communicating artery (arrow). An immediate exploration was performed without angiography, the hematomas removed and the aneurysm clipped with a successful result. Fig 189D-E A 60 year old patient in grade lla was scheduled for angiography the following day. Two hours prior to angiography the patient showed signs of another rupture. On the repeat CT scan an aneurysm of the right posterior communicating artery was convincingly demonstrated (arrow). Immediate exploration without angiography confirmed fresh basal cisternal hematomas, which were removed and the aneurysm successfully clipped. Lateral view of CT scan (E): aneurysm (arrow).

продолжение

207

208 продолжение

3

General Operative Techniques

Apparatus and Instruments Operating Microscope The technical details and specifications of each type of microscope are available from the various manufacturers and are beyond the scope of this book. The present discussion will be limited to four topics: optical principles, the lighting system, the microscope stand, and the various accessaries to the microscope.

Optical Principles Two optical principles are of importance to the neurosurgeon concerning the operating microscope, namely magnification and stereoscopic perspective.

operations take place in a small space at the base of the brain through a narrow gap and in these cases it is more important to the neurosurgeon that he maintains well-lit binocular vision in the recesses of the field. This stereoscopic perspective is thus the more useful function of the surgical microscope in these situations (Fig 190A).The operating microscope allows stereoscopic vision in small spaces by reducing the necessary interpupillary distance required for binocular vision. The distance between the anterior lenses of the binocular tube of the microscope is only 16 mm, whereas the average interpupillary distance is around 60 mm. This means that light reflected from deep basal structures towards the operating microscope during surgical procedures employing fissure, sulci or transcortical approaches, will result in a stereoscopic image when only a 16 mm image enters the microscope aided eye. Even when assisted with magnification loupes, the eyes are unable to maintain stereoscopic vision in such a narrow space. Thus the real importance of the surgical microscope as it relates to most neurological procedures is not the magnification it supplies, but in the clear visual perspective it provides. With this the surgeon can avoid excessive brain retraction and yet still reach every point in the central nervous system, adequately visualizing deep structures either along the basal cisterns or through a transcerebral tunnel.

Magnification The enlargement of objects in the operating field is the most widely recognized but actually least important function of the surgical microscope. Optical principles relate the final magnification obtained through any microscope, to the magnification lens and the magnification of the ocular pieces. This relationship varies among different "microscopes, thus changing the quantification of the final magnification. In the neurosurgical operating room at Zurich, an operating microscope is used with a 300 mm objective and 12.5 oculars for all cranio-vertebral surgery except superficial anastomoses when a 200 mm objective and 12.5 ocular lens are more conve- Lighting system nient. The light intensity is a fundamental aspect of gaining visual resolutions under the operating miStereoscopic Perspective croscope. Unfortunately, adequate lighting has A few neurosurgical procedures such as microvas- been one of the most difficult design problems of cular anastomoses and nerve repairs are performed the operating microscope and even today remains on the surface of the operating field, and in these imperfect. Light intensity is determined by the the magnification and depth of field are primary objective lens and the diameter of the lighted field considerations. However, most neurosurgical

Operating Fig 190 A Diagram of the difference I pillary distance (PD) and interocular erating microscope (a).

16-22 mm

Fig 190B The prototype counterbalanced Contraves stand for the operating microscope in use at the University Hospital of Zurich since 1972.

Fig 190C H = hand-switch, M = mouth-switch, F = photo- or movie camera, T = Hitachi colour TV camera now available with three tubes.

210

3 General Operative Techniques

that is projected through it, i.e. illumination units lumens or foot candles/units of area. As the magnification is increased, less of the illuminated field is used, resulting in a proportionally diminished intensity of illuminated object as viewed through the microscope. Beam splitters to allow for observer tubes and televisions or camera equipment further decrease the amount of light actually reaching the eyes of the surgeon. A system of lighting has been developed in this department of attempting to maximize light intensity. The primary light source is focused through the objective lens onto the field of vision, as in all Zeiss microscopes. This primary light is a 50 watt tungsten bulb, powered at 10 volts. This bulb is manufactured to accept only 6 volts and overloading the bulb significantly reduces its life, so it is changed after each operation. The system must be ventilated by a suction apparatus placed within the microscope drape to prevent its overheating. This primary light system is supplemented by a fiberoptic light source with a 150 watt, 15 halogen lamp. The actual light delivered through this system is about 90,000 lux. With this system it is important to keep the microscope properly centered on the illuminated field so as to maximize the available light.

Microscope Stand One of the primary impediments to the widespread use of the operating microscope by neurosurgeons has been the need to manually change the position of the microscope. This often forced the surgeon to accept uncomfortable positions of his head or body during delicate procedures because he could not release instruments to repeatedly move the microscope. It was estimated that about 40% of the surgeon's time while using the microscope was spent merely adjusting and moving it around (Fig 190B-C). For over 5 years (1967-1972), the department of neurosurgery in Zurich worked on a solution to this problem. A variety of methods providing a freely mobile yet stable microscope were evaluated. Finally the counterbalance idea of Malis proved most practical, and in 1972 working with the Contraves Company a microscope stand was developed in which the microscope and its accessaries were completely balanced by adjustable counterweights mounted on the microscope stand. Then by incorporating a system of electromagnetic brakes into the various joints of the stand, absolute stability of the instrument could be maintained when the microscope was in any desired position. The final addition of a mouth switch allowed all movements

(including focusing) in the primary axes to be controlled by the surgeon's head. Only rotatory movements of the microscope require hand adjustment by a pistol-grip switch. This stand permitted effortless microscopic mobility and adapted the operating microscope to suit all microsurgical procedures. Subsequent commercially available stands, though unfortunately not possessing quite this degree of effortless mobility nonetheless contribute further to making the operating microscope indispensable for most neurosurgical operations.

Accessories to the Microscope The freely mobile operating microscope has diminished the effectiveness of additional surgeons attempting to assist during the microsurgical part of an operation. Similarly the scrub nurses and anesthetists have not been able to adequately follow the operation process through an observer tube that is constantly moving. Fortunately the optical characteristics of the operating microscope permit its easy adaptation to include the use of closed circuit television monitoring, thereby allowing these members of the surgical team (and others) to more actively participate in the operation itself. Also this allows an operation to be simultaneously taped and still camera photographs taken for later documentation of the pathology and for educational purposes. In fact these photographic facilities have proved to be an exceptionally helpful way for the surgeon to disseminate operative information to his collegues at meetings and to educate medical students, residents, and visitors. Recently (1980) a vidicon tube (RGB-Hitachi mod. SSOO) color TV camera was installed in Zurich, which has markedly increased the resolution and true color rendition of microsurgical procedures.

Microsurgical Instrumentation The application of microsurgical techniques to neurosurgery has necessitated the development of instrumentation which properly exploits the advantages offered by the operating microscope. As instrumentation is basically an extension of human physical abilities, principles of instrument design must account for the surgeon's physical requirements as well as the job to be undertaken. Just as the body requires stabilization of the larger parts in order that small parts may carry out fine movements, instrumentation was developed to provide stability as well as to enhance mobility (Ya§argil etal!977).

Microsurgical Instrumentation

211

Stability

Mobility

Instruments are required to provide stability to the patient, to the surgeon, and to the operating field.

With stability of the operating field achieved, the surgeon requires instrumentation which will maximize mobility in precise dissection and hemostasis. Sharp accurate dissection must be accomplished in deep narrow openings with instruments that are delicate yet strong and that do not interfere with vision. In Zurich, the microinstruments are separated into two sets - a basic set that includes those microinstruments that are most frequently used and a special set that is composed of instruments used in special situations only. Both sets of instruments are gas sterilized (ethylene oxide gas at 53°C) and available for all procedures.

Head immobilization (Mayfield-Kees) For microneurosurgical operations the head is best immobilized in a three-point skeletal fixation device. This allows the head to be fixed in a variety of positions and prevents pressure on bony prominences and eyes. Soft Tissue Retraction Spring retractors, composed of sharp hooks and a bulldog clamp joined by a coil spring have been developed to provide steady retraction of soft tissues with easy repositioning. Brain Retraction Hand-held retraction by an assistant is inadequate for microsurgical operations. A linked-socket type retractor was developed to provide gentle but steady retraction of the brain in almost any direction. This retractor is now held by a metal post attached to the side bar of the operating table. A coupling head with multiple clasps for the attachment of several retractors allows one or more retractors to be used from either one or both sides of the operating table. Further refinements of this retractor in the future hopefully will provide more precise retraction, presently lacking for example in sitting position procedures. Operating Stool The sitting position is generally more comfortable and more stable for the surgeon. An operating stool has been developed which rests on a cylinder of compressed synthetic liquid-gas. The material has an expanding force of 30 kilograms allowing the stool to slowly follow the surgeon up when released by a foot pedal, yet permitting the full weight of the surgeon to depress the stool. This stool is placed on casters to allow free mobility around the operating field. Arm Rest A spring loaded arm rest mounted on a ball and socket joint stabilizes the surgeon's forearms or hands during microsurgical dissection. It is released vertically by a foot pedal and is freely movable around the circumference of the ball and socket attachment.

Bipolar Coagulation The concept of bipolar coagulation originally conceived by Greenwood (1940-1950) but later perfected by Malis (1950-1960) was applied by the senior author in 1966 to use under the operating microscope. The precise control and even repair of small blood vessels and the preparation of an aneurysm with bipolar coagulation have added new dimensions to dissection in and around the brain. The principle of bipolar coagulation has been welldescribed by Malis (1967/1969) and several commercial current generators are available. The neurosurgeon will be most concerned with the size, shape, weight, and spring of the bipolar coagulation forceps. A variety of tip sizes and shaft lengths are required for different situations and should be clearly marked to avoid confusion at the operating table. The longest available blade length is 13.0 cm while the longest point from the surface of the brain \ to the base of the skull measures about 12.0 cm. ' The bayonet shape is required to avoid the surgeon's hand blocking the field of vision. A moderate degree of spring will aid in dissection with the forceps. It is desirable to have the blades isolated as current may pass between the blades proximal to the tips of both blades resting on a low resistance structure. As with the other microinstruments, the bipolar forceps are gas sterilized (ethylene oxide at 53°C). It is particularly important with the bipolar forceps to avoid cleaning them with hydrogen peroxide or steam autoclaving them at 135° C as these modes seem to increase their tendency toward sticking during coagulation. The tips of the bipolar forceps need to be checked regularly. The most important factor in preventing forceps adherence to tissue during coagulation is avoiding the use of forceps whose tips are discolored or rough. Forceps displaying these characteristics need to be returned to

212

3 General Operative Techniques

the instrument maker for polishing and realignment. Duplicate bipolar forceps should be available at all times during procedures to allow one pair to be frequently cleaned while the other is in use. Intraoperative cleaning should consist of thoroughly wiping the tips with a moistened gauze 'sponge. The tips should never be scraped with a knife as this may scratch or dull the finish and promote further sticking during use. Scissors Squeeze grip and jilligator type scissors are available in a variety of sizes and shapes. They should have a smooth closing action and cut cleanly. Scalpels A perfectly satisfactory blade for microsurgical work is not available. Small microscalpels in various shapes are available as are holders for broken razor blades. Nevertheless the precise incision of the vessel wall is rarely possible with these instruments. Suction Apparatus The suction tip is an integral part of the dissection instrumentation serving as a retractor and manipulator as well as a sucker, so its proper design is important. Suction tips used in this department have a smoothly rounded edge to prevent damage to brain structures during dissection, and have external diameters down to 1,5 millimeters. The shafts are generally about 30 cm long and bent at an angle to give a working length of about 20 cm. Also important for delicate microscopic work is the amount of suction. Smooth low suction is preferred as high suction may rupture small blood vessels as well as aneurysms and damage neural structures. To achieve this, sucker shafts without pressure ' regulating holes and an electrical suction pump whose pressure is closely regulated have been introduced. High-Speed Drill An important concept in the microsurgery of aneurysms has been the removal of bone from the base of the skull to create the necessary gap for operating without significant brain retraction. To remove this bone, and electrical high-speed drill with tungsten steel cutting and diamond burrs has been found most satisfactory. The speed is more accurately controlled than with air driven instruments and the direction of rotation of the drill can be reversed.

Post-Operative Care of Instruments At the conclusion of surgery, all microinstruments are washed and dried by hand. Each instrument is then carefully inspected and checked to ensure proper working order. Particular attention is paid to the microscissors (to ensure that the blade tips are not barbed and that the closing action is smooth) and to the bipolar forceps (to be sure that the blade tips are also not barbed and that the alignment of the blades upon closing is precise). Magnification including a magnifying glass, loupes, or sometimes even the operating microscope is often necessary during this inspection depending on the size and precision of the particular instrument.

Aneurysm Clips During the early stages of our experience, a variety of clips then available was used. Plain silver Week clips were applied in several cases and found unsatisfactory due to their immobility. Once initially Jastene_d_ on the aneurysm, they could not be removed and repositioned without great difficulty and hazard to the aneurysm and surrounding vessels. Thus it was impossible to use a stepwise technique of obliterating the aneurysm and any perforators inadvertantly included in the initial clip were almost certainly irretrievably damaged. Commercially available aneurysm clips such as the Scovilie were also utilized and found lacking. These clips could be easily removed and repositioned, but frequently were seen to slip off. the aneurysm shortly after application.! Coagulation was developed to narrow the neck of broadbased aneurysms to permit clip placement and to prevent subsequent clip slippage, but it was still felt that a better clip was needed.____________ To meet these needs, a clip was designed and developed with narrow blades for easy application and with a high enough closing pressure to prevent clip slippage (A.esculap)( Initial clip shapes were simple and of a limited range, but the demands of neurosurgeons around the world resulted in clips of many shapes and sizes. Later larger clips were also developed for the giant sized lesions previously not amenable to clipping. At the present time, this series of clips is satisfactory for closing the majority of aneurysms encountered in Zurich. Not a single clip failure has been seen in over 1500 aneurysms so treated. It is important that the aneurysm clip maintain a high closing force as specified by the particular manufacturer, so that when applied, they hold and do not slip. Although many manufacturers state that aneurysm clips can be steam autoclaved, in

Personnel Zurich they are gas sterilized (ethylene oxide at 53° C) only. As a consequence of their utilization characteristics, some aneurysm clips are sterilized several times before their actual use, and we feel the less traumatic gas sterilization technique is a useful precaution against clip closing force weakening. To minimize the number of times an individual clip is re-sterilized, two sets of aneurysm clips are used. One set includes only the more commonly used clips and is opened at every case; the other contains a wide selection of clips and is opened as needed. Unnecessary, repetitive opening of the blades of aneurysm clips is to be absolutely avoided. This will result in a reduction of the clip closing force and in some cases a malalignment of the blades. The first time an aneurysm clip should be widely opened is immediately before it is applied to an aneurysm. A wide range of aneurysm clips are currently available (Aesculap). Frequent changes and modifications in those commercially available place a complete list of them beyond the scope of this book. Interested readers are referred to the various manufacturers for catalogues and specifications.

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Temporary Vascular Clips Temporary vascular clips differ from aneurvsmf clips in that they have_a lower closing pressure { which is sufficient to just occlude an artery without' damaging its wall. Unlike aneurysm clips which are designed for permanent implantation, temporary clips are for intra-operative use only and should j n £Y5.L^?.e leftJErJg06 permanently. For this reason many temporary vascular clips are gold-plated for easy identification. In situations that require permanent vessel occlusion, temporary clips already applied should be exchanged for aneurysm clips or other permanent vascular occlusive techniques (such as coagulation or ligation) employed. Many of the situations requiring the use of temporary vascular clips occur suddenly without warning and demand swift and steady action. To anticipate these situations, one or two temporary clips should be immediately available in their applying forceps.

Operating Room Organization Personnel To fully utilize the operating microscope and microsurgical instruments, a well-trained team of surgeons, anesthesiologists, and nurses is required. The proper education and training of the operating room personnel are critical if valuable time during the procedure is not to be wasted. Confidence and timing are especially important ingredients of a successfully performed aneurysm operation and will only be gained with practice and experience. Each phase of a neurosurgical procedure, beginning the moment the patient enters the operation room suite, follows a specialized but orderly routine. The microsurgical technique, when applied to almost any speciality, requires undivided attention to many small details. Each operation team member must be knowledgable concerning: a) The positioning of the patient on the operation table b) The layout of the operation suite c) The operation of the surgical microscope and its draping d) The use of drills, retractors, suction apparatus, etc.

e) The position and control of both unipolar and bipolar coagulation f) The organization and applications of basic and microinstrumentation g) The use of video equipment including the TV and 16 mm cameras. In our department, there are seven members of the operating team - the surgeon and his assistant, the anesthesiologist and his assistant, the scrub nurse and two circulating nurses ./The scrub nurse is responsible for passing instruments during the operation. With the surgeon's attention directed through the operation microscope, it is especially important that the scrub nurses know enough about the operation that they can follow the procedure on the television monitor and be prepared with the necessary instrumentation and equipment at the appropriate time. Scrupulous attention must be given to the cleanliness of the instruments as many of them are not usable when contamined with only minor amounts of blood or tissue. One circulating nurse takes responsibility for maintenance of equipment in the room, moving the operating microscope into place, adjusting the coagulation units, running the drilling equipment,

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3 General Operative Techniques

and caring for the television monitoring. The other nurse_p£ocures_necessary instruments, solutions, adjusts the suction apparatus and works closely with the scrub nurse to ensure the smooth coordination of the procedure.

Operating Room Lay-Out

Fig. 191 The operating room set-up in use in the neurosurgical department in Zurich. A Anesthetic apparatus B1B2 Table of instruments C,-C2 Bipolar and unipolar coagulators D Suction apparatus E Monitors for anesthesiology F Electric drill TV 3 TV monitors for the use of anesthesiology, nurses and other observers.

The basic organization of the operating room during cerebral aneurysm operations is shown in Fig 191. The patient is positioned for a given aneurysm operation. The surgeon sits or stands directly behind the patient with his assistant to the right. At the time the operating microscope is brought into the operating field, the assistant will move to sit or stand behind the surgeon where he can observe the television monitor. The anesthesiologist and his equipment are to the patients left. The front instrument table covers the patient and the back table is behind the scrub nurse. The video monitor should be in a position that the scrub nurse and assistant can both see the progress of the operation. Retractor posts and operating microscope are draped into the operating field at the beginning of the procedure. Power equipment for craniotomy is on a trolley and can be moved into position behind the surgeon's right side as needed. Left-handed surgeons may prefer to have these various positions reversed.

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Interfascial Pterional (Frontotemporosphenoidal) Craniotomy продолжение

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Operative Approach Interfascial Pterional (Frontotemporosphenoidal) Craniotomy In principle it would be ideal if the brain could be left completely undisturbed while the dissection and clipping of an intracranial aneurysm was carried out. To approach this ideal, a craniotomy must take advantage of those natural planes and spaces which nature has provided to expose the base of the brain without significant brain retraction.!One such plane is provided by the sphenoid ridge as it separates the frontal and temporal lobes. Another is provided by the roof of the orbit as it projects superiorly and mdents the basal surface of the frontal lobe. These planes project from the surface of the brain directly to the parasellar area and form the base of a small pyramidal space whose apex is formed by the junction of the frontal and temporal lobes. This natural space can be expanded along its base by the removal of bone from the sphenoid ridge and the flattening of the orbital roof. Further enlargement of this space along its apex is accomplished by o_gening the basal Sylvian fissure, thereby forming a pyramidal shaped working space whose apex is directed towards the limen insulae. The width of this pyramid is the shortest possible distance from the calvarium to the sella. Through this small pyramid, the arachnoid attachments between the frontal and temporal lobes, and between the basal frontal lobes and the optic chiasm and internal carotid arteries can be opened, thereby allowing the entire forebrain to fall away from the base of the skull with minimal or no retraction. Then utilizing the magnification, lighting, and especially the stereoscopic binocular vision provided by the operating microscope, the entire undersurface of the brain is exposed bilaterally from the parasellar and suprachiasmatic areas down beyond the interpeduncular and prepontine cisterns to the cerebellopontine cistern and porous acusticus. The craniotomy to be described is useful for an-eurysms of the anterior circulation and upper basi-lar artery, as well as for tumors of the orbital, retroorbital, sellar, parasellar, chiasmatic, sub-frontal, retroclival, and prepontine areas. Only minimal retraction of the laterobasal frontal lobe and little if any retraction of the temporal lobe are required, j Positioning of the head, adequate removal of bone from the base of the skull, release of spinal fluid from the basal cisterns, and a sys-

Itematic dissection within the subarachnoid space are the key points of this technique. Other factors of importance include the ability of the surgeon to carry out fine manipulations through a tiny gap and the availability _of fine precision manufactured instruments of adequate length.

Position of the Patient The patient is positioned supine with the head at the foot end on a standard operating table. A three-point skeletal fixation device such as Mayfield-Kees, is placed at the foot of the table (Fig 192A-D). A right-sided craniotomy is preferred for mid-line as well as right-sided lesions for the right handed surgeon (with some exceptions). The head is directed about 20° vertex down, elevated slightly, and rotated about 30° to the left to bring the malar eminence to the superior point of the operating field./This position will cause the operat-ing field to incline slightly toward the surgeon. allowing the frontal lobes to fall away from the orbital roof. The sphenoid ridge will be directed vertically in the operating field. Exact positioning of the head establishes an unobstructed visual axis through the surgical microscope along the sphenoid ridge to the anterior clinoid and parasellar area. In positioning the head, care must be exercised to avoid extreme positions that strangu- \ late or compress the trachea, jugular vein, carotid ; or vertebral arteries. The skeletal fixation device should be placed with one prong behind the ear, just above the ipsilateral mastoid and with the two pronged side on the left side of the head. The prongs should be high enough on the skull (above the linea terminalis) that they do not enter the temporalis muscle which will lead to instability as well as unnecessary bleeding.

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Fig 192 A-D The position of the head with fixation device (after Mayfield-Kees) (A-B) and the surgeon's plane of vision (arrow) centered at the junction of the frontalzygomatic process and the zygomatico-frontal process (C-D).

Interfascial Pterional (Frontotemporosphenoidal) Crankrtomy

Draping Following antiseptic preparation of the scalp, a semicircular incision (see under Incision) is outlined in ink. An adherent sterile plastic drape is placed over the operating field, and a windowed waterproof sheet laid on top of this, secured by a second plastic drape. Double sterile sheets are used throughout. The self-retaining retractor holders are affixed to the operating table and covered with specially made drapes that fit like stockings. The microscope proper and mounting arm are draped and a single drape is placed around the microscope stand.

Incision The precise location of the incision varies somewhat from patient to patient depending upon the intracranial site of interest, the cranial bone and sinus topography, and the position of the hairline. As a general rule, the scalp incision begins 1 cm superior to the anterior aspect of the auricle and extends to the temporal crest in a direction perpendicular to the zygoma. Care is exercised during this part of the incision to avoid injury to the more anteriorly placed superficial temporal artery and temporal branch of the facial nerve. From the temporal crest, the incision curves sharply anterior, ending at the hairline, 1-2 cm shy of the midline(Figl92A-D).

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superficial of these (superior layer) contains only fat, the temporalis branch of the facial nerve, and a large temporal vein. The deeper layer (inferior layer) covers the temporalis muscle and contains a deep temporal artery and vein. The superior and inferior layers of the superficial temporalis fascia attach in an arched fashion along the anterior portion of the linea temporalis and- on the lateral and medial surfaces respectively, of the frontalzygomatic process and zygoma. Beneath the superficial temporalis fascia there is a fine investment of fascia covering the entire temporalis muscle, which maintains the shape of the muscle despite incisions into the fascia. Finally the deep temporalis fascia is present beneath the muscle and though thin, it nonetheless allows the separation of the muscle intact from the underlying skull. On the basis of the above anatomical findings, retraction of the temporalis muscle and fascia is currently performed through an interfascial approach between the layers of the superficial temporalis fascia.

Interfacial Temporalis Flap Throughout the years different methods of incising and retracting the temporalis muscle have been tried. A free bone flap has been preferred and a variety of ways to retract the temporal muscle investigated accordingly. Ideally one wishes to maximally retract the muscle away from the craniotomy site but at the same time avoid damage to the tetngoralis branch of the facial nerve which innervates the frontalis muscle. Subgaleal dissection of the skin flap with separate reflection of the temporalis muscle and fascia carries a 30% incidence of frontalis paralysis, while turning a combined skin and muscle flap may limit exposure (Fig 193 A-B) The anatomy of the soft tissues over the area of the pterion is, of course, more complex than that of the rest of the cranium due to the interposition of the temporalis muscle and fascia. The galea aponeurotica covers the entire area with the superficial temporal artery and vein lying on its outer aspect in the subcutaneous tissue. The anterior onefourth of the superficial temporalis fascia splits to form two overlying fascial planes. The more

Fig 1 9 3 A Upon retraction of the skin flap, pericrania! lines of incision are carried out through the fascia and periosteum underneath the fronto-zygomatic process (1), '/2 cm superiorly to the temporal line (2), and diagonally along the frontal bone (3). The pericranium of the frontal area is carefully separated and retracted.

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3 General Operative Techniques

Fig 193B Over the anterior 1/5 of the temporal muscle, just behind the fronto-zygomatic process there is a sickle shaped fat layer between two fascia layers (open arrow), which should be separately dissected to avoid injury to the frontal branch of the facial nerve. A regular large vein within the fat layer (arrow V) and a regular small artery penetrating bone (arrow A) are seen.

Interfascial Pterional (Frontotemporosphenoidal) Craniotomy The galea is separated from the pericranium and temporalis fascia to within 4 cm of the orbital rim, until its remaining fascial attachment constitutes a plane overlying the anterior one-fourth of the temporalis muscle. In this process a scalp flap is reflected toward the orbit. Along this plane the separation of the superficial temporalis fascia into

Rg 194A-B The deepest pericranium of the temporalis muscle is separated from the inferior surface of the fronto-zygomatic process (A) and from the temporal fossa (B) and retracted.

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superior and inferior layers can be identified by a small quantity of fat concealed between the layers. The superior layer is incised all along this arched plane from its attachment on the inferior temporal line to near its attachment on the zygoma, separated from the inferior layer, and reflected along with the skin flap. This protects the frontal branch

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of the facial nerve contained in the superior layer. The separation ends upon insertion of the superior temporalis fascia on the lateral surfaces of the zygoma and frontal zygomatic process. When completed this dissection reveals a sickle-shaped anterior quarter of the temporalis muscle still covered by the inferior layer of fascia and variable amounts of fatty tissue (Fig 194A-B). The inferior layer of the temporalis fascia is incised at its attachment anteriorly on the medial surfaces of the zygoma and frontal zygomatic process. The contiguous pericranium and deep temporalis fascia is also incised starting near the medial part of the frontal zygomatic process, continuing around the semi-circular superior temporal line, and ending near the scalp edge several cm. past the coronal suture. A short anteriorly directed slit of the frontal pericranium allows its deflection as a triangular flap towards the orbit. The incised pericranium above the superior temporal line is reflected away from the temporal fossa. The temporalis muscle and its adherent fascia are stripped first from the linea temporalis, then downward from most of the temporal fossa, ending on a line parallel to the zygoma near the floor of the middle cranial fossa. The temporalis muscle (and its supporting fascias) is then reflected postero-inferiorly along the line of its tendonous attachment. This unroofs most of the temporal fossa revealing the pterion and a large portion of the squamous temporal, sphenoid, and zygomatic bones, plus portions of the frontal and parietal bones extending into the fossa.

periosteal elevator utilizing a gentle semicircular motion in the epidural space, rather than a linear plunging or pushing movement. Small grooves are rongeured from the first and second holes, anterosuperiorly along the frontal zygomatic process and anterolaterally into the frontal bone respectively. With a Gigli saw the anterior margin of the bone flap is then arched rostrally, while the medial and posterior margins are completed in the usual linear fashion. Using a high speed electric drill, the lateral margin is grooved obliquely downward from the first and fourth holes, along the zygomatic sphenoid suture, across the squamous temporal bone, then spanning the greater wing of the sphenoid near the line of the zygoma. This groove allows a gentle, atraumatic, and precisely limited fracture across the sphenoid when raising the bone flap(Following elevation of the bone flap, the tension of the intracranial compartment can be readily assessed and 10 or 20 cc. of CSF may be released if necessary through a previously placed spinal needle to provide a measure of decompression/ The squamous temporal and greater wing sphenoid bones are rongeured further inferiorly toward the floor of the middle fossa (thereby allowing more mobility of the anterior temporal lobe necessary in some cases) to reach the tentorial edge and providing in all cases a degree of decompression.

Craniotomy The bone flap is initiated with a frontal burr hole just superior to the frontal zygomatic suturejmder the linea temporalis. A second hole is placed in the frontal bone 3-4 cm superior to the first and 1-2 cm above the orbital rim, avoiding if possible the frontal sinus. A third hole is positioned in the parietal bone along the linea temporalis variably behind the coronal suture, depending on the intracranial site of interest. The final corner of the bone flap is marked by a burr hole in the squamous temporal bone behind the spheno-temporal suture, about 4 cm inferior to the third hole and 3 cm posterior to the first (Fig 195A-D). For many years these burr holes were drilled by hand, but since 1976 an electric powered perforator which stops automatically as the dura is encountered has been employed. The bone dust is saved to be replaced in the holes. The dura underlying the anterior, medial, and posterior margins of the bone flap is most effectively and safely separated with a small curved

Fig 195 A

indicated.

Four burr holes are placed in the order and site

Interfascial Pterional (Frontotemporosphenoidal) Craniotomy

221

Fig 195B-C Small anteriorly directed troughs are placed in holes 1 and 2 (B) to allow the subsequent Gigli bone incision (C) to extend in an anterior direction.

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Fig 195 D The inferior portion of the bone flap is completed with a high-speed drill in a curvilinear fashion.

Enlarging the Base of the Pyramid With the aid of the surgical microscope, a high speed electric drill, and gentle frontal lobe retraction, the rough bony convolutions of the posterolateral orbital roof are smoothed (adjacent to the frontal sphenoidal suture). Generally one or two small dural vents are cut along the frontal and/or temporal portions of the planned dural incision prior to smoothing this rough surface. These provide a measure of CSF release (or in some cases subdural hematoma), thereby reducing the need for retraction during this procedure (Fig 196A-C). Although the thickness of the orbital roof is individually quite variable (1-10 mm), with experience only the inner table and diploe of bone are removed, preventing injury to the outer table with inadvertant penetration into the orbit or sinus. In a similar fashion the posterior ridge of the greater wing of the sphenoid is progressively flattened until a small ridge representing the most lateral aspect of the lesser wing is reached (Fig 197A-B). A small bridging vessel, the orbital-meningeal artery (anastomotic branch of the ophthalmic artery to the

middle meningeal artery) can almost always be seen marking this spot. Throughout this process, variable amounts of hemorrhagic oozing should be expected from the middle of the sphenoid ridge in the distribution of the orbitomeningeal artery and from each side to the ridge along the sphenosquamosal and sphenofrontal sutures in the distribution regions of two orbitomeningeal artery branches. The bleeding can be easily controlled by coagulation and wax application to the bone or compression of a piece of muscle between the bone and the dura. During this process the frontal sinus may be inadvertantly entered if it extends far laterally. When this occurs, the mucoperiosteal lining of the sinus should be stripped from the walls in the area of the penetration and tucked back into the sinus toward its narrowing aperture. In most instances the trabeculated nature of the sinus will confine this process to a small localized section of the whole sinus, but in rare instances a larger cavity is entered demanding additional bone removal in the area of penetration and formal mucosa stripping. In either

Interfascial Pterional (Frontotemporosphenoidal) Craniotomy

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case, once the mucosa has been displaced towards the sinus opening, a small stamp of muscle is placed over the mucosa to cover the aperture. The muscle is then surrounded by gelfoam and sealed with layers of an acrylic adhesive (Aron- Alpha A). This is permitted to harden during the operation, but upon closing a small amount of bone wax is gently applied to completely seal the defect. Similarly the orbit may occasionally be entered but the defect can be simply covered with a small piece of bone. Fig 196A-C Following small dural incisions (A) to release cerebrospinal fluid or subdural hematoma, the dura around the sphenoid wing is separated (B) and the spine of the wing rongeured (C).

A

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Fig 197A-B Using a high-speed drill, the sphenoid ridge and bony indentations of the orbital roof are removed (A) producing a smooth, flat sphenoid surface (B) along which the plane of vision is directed. Notice the orbito-meningeal artery (arrow) and branches (temporal and frontal) that provide rich vascularization to this area.

Interfascial Pterional (Frontotemporosphenoidal) Craniotomy Dural Opening The dura is opened in a semi-circular fashion around the Sylvian fissure, arched toward the sphenoid ridge and orbit (Fig 198A-B). Bipolar coagulation (rather than metallic clips) is applied to the meningeal vessels. The temporal end of the dural opening is protected with a through-andthrough suture to prevent the dural incision from tearing beneath the bony margin toward the floor of the middle fossa. The dural flap is snugly tented over the sphenoid ridge, again securing an unobstructed line of vision along the ridge to the base of the brain. With a relaxed brain the dural edges can now be secured to the bony margins through small drill holes thus preventing oozing into the operating field or into the temporal-parietal sub- or epidural spaces during the procedure. iThe frontal I lobe is gently retracted allowing easy access and; entrance into the carotid, chiasmatic, and lamina terminalis cisterns, thereby releasing CSF and providing the necessary room for easy dural tacking. In a few cases this manoeuvre does not provide sufficient fluid release, necessitating opening the con-tralateral cistern and/or the interpeduncular cistern to gain adequate decompression. The lamina terminalis can also be incised allowing CSF release from the 3rd ventricle, but this should be reserved only for those instances when the other previously mentioned measures fail especially if the basal cisterns are blocked by adherent hematomas. __

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Fig 198 A-B The middle meningeal and orbital-frontal arteries are coagulated and the dura incised in a semicircle facing the sphenoid wing (A). The dura is draped on the sphenoid wing and fixed (B).

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Arachnoid Opening Arachnoid dissection is the real key to successful aneurysm operations. The direction and sequence of cisternal openings depends to some degree on the location of the lesion and these details are discussed with each specific aneurysm. It is important that the neurosurgeon be familiar with the anatomy of the subarachnoid cisterns as described in Chapter 1. For most lesions approached through a pterional craniotomy, both the Sylvian cistern between the basal frontal and temporal lobes and the whole lamina terminalis cistern adhering the frontal lobes to the optic nerves and chiasm are opened. Enlarging the Apex of the Pyramid With sharp dissection utilizing a round arachnoid knife, the Sylvian cistern is entered at the level of the opercular frontal gyrus. The arachnoid of the Sylvian cistern may be thin and transparent allowing good visualization of structures within the cistern, but often it is milky, yellow, or even opaque following a subarachnoid hemorrhage. In a few cases there is gelatinous hematoma and degenerate arachnoid that can be easily removed by gentle suction. There may be a 2-3 mm space on the surface between the frontal and temporal lobes allowing easy entry into the cistern and rapid identification of the major vessels. At times the arachnoid and pia of the frontal and temporal lobes may be superficially adherent7 but after a few millimeters the cistern is entered and separation ^from there^bfljis not difficult. In some cases the direction of the cistern may be obscured from the surface, but the orientation of the cistern can be discovered by following a superficial artery into the fissure toward the middle cerebral track. Meticulous dissection avoiding any injury to the middle cerebral artery candlelabra and the superficial middle cerebral venous system is essential. The superficial middle cerebral veins are one or more large venous channels that course on the temporal side of the Sylvian fissure, ffhey generally empty into the sphenoparietal or cavernous sinuses, but will occasionally continue around the temporal pole to the superior petrosal sinus. The arachnoid of the Sylvian cistern should be opened on the frontal side of these veins so that they will not cross the Sylvian fissure when the frontal lobe is retracted. Occasionally 2-3 fronto-orbital venous tributaries that cross the Sylvian fissure to enter the middle cerebral vein must be sacrificed to complete the dissection. There has been no way to assess possible neurological changes induced by damage to these veins. With experience, the arachnoidal

(sleeve surrounding the frontal-basal veins can be incised, thereby allowing retraction of the frontal lobe without torsion or tearing of them (Fig 199A-B)7 ———— Both as a congenital variant and following subarachnoid hemorrhage, arachnoidal and pial attachments within the Sylvian fissure may occur. Occasionally the frontal and temporal lobes may be tightly adherent down to the middle cerebral artery. In these cases opening the fissure is quite difficult and usually results in some damage to the frontal and/or temporal surfaces. It is important in these instances to follow the arteries proximally for accurate orientation (Fig 199C-D). The final stages of this dissection around the most anteromesial temporal lobe are often the most tenous due to its tight adherence to the frontal lobe. Most often the orbital frontal gyrus sharply indents the corresponding temporal lobe, thereby distorting this portion of the Sylvian cistern. To avoid damaging the gyrus, the cistern must be followed laterally around it./The frontal lobe can be retracted away from the M[ segment of the Middle Cerebral artery with relative ease because the M! never supplies branches to it. However in 3% of cases it must be remembered that frontalorbital branches arise together with the striates. When completed this division of the Sylvian cistern allows the frontal and temporal lobes to fall apart away from the sphenoid ridge and orbital roof thereby enlarging the apex of the pyramidal space. When combined with the previously mentioned opening of the carotid, lamina terminalis cisterns bilaterally and interpeduncular cistern (medial or lateral to the ICA), a large empty pyramidal space is thus created, bordered at its base by the flattened sphenoid ridge and orbital roof and on its upper and lower margins by the separated frontal and temporal operculi (with its apex directed into the limen insulae). This pyramidal space highlights the value of the pterional approach for through it with minimal or no brain retraction, a line of vision is constructed from the eye of the surgeon through the surgical microscope to the base of the brain (Fig 199E-K). More specific details of the approaches to individual aneurysms will be given in the following section.

Interfascial Pterional (Frontotemporosphenoidal) Craniotomy

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Fig 1 9 9 A After opening of carotid and interpeduncular cisterns medial {arrow 1) and lateral (arrow 2) to the internal carotid artery to release liquid and to gain optimal relaxed brain condition, the basal Sylvian cistern is then opened medial to the Sylvian vein (3).

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3 General Operative Techniques Fig 199 B The Sylvian cistern is opened and the middle cerebral artery (M, segment) dissected free.

Fig 199C The carotid cistern is opened first medially and then laterally, revealing the carotid artery and branches.

interfascial Pterional (Frontotemporosphenoidal) Craniotomy

Fig 199D-E The supero-medial border of the interpeduncular cistern ^Liliequist's membrane) is opened (D) revealing the terminal basilar artery and its branches (E).

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Fig199F-G The chiasmatic (F) and lamina terminalis (G)

Lamina terminalis cistern

G cisterns are now opened revealing the optic nerves, chiasm, A, segments, and anterior communicating artery complex.

Interfascial Pterional (Frontotemporosphenoida!) Craniotomy

Fig 199H-I For posteriorly directed anterior communicating aneurysms, a small cortica incision is made between the olfactory and fronto:orbitaf arteries in the gyrus rectus (ff), allowing better visualization of the anterior communicating artery complex (if it is hidden) (I).

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Fig 199 J Dissection is carried through the lamina termin-alis and chiasmatic cisterns to the opposite carotid cistern to visualize the opposite carotid artery and bifurcation.

Closure The dura is reapproximated with a continuous 4—0 water-tight silk suture and the bone flap secured with 0 silk sutures. Prior to replacing the bone flap, two drill holes are made on the anterior temporal line for securing the temporalis muscle to the bone. The fascia and galea are closed in layers with interrupted sutures, and the skin is closed with a running, locked atraumatic nylon suture. Sub-

galeal drainage at a low suction pressure is routinely employed for 24 hours. The wound is sprayed with a skin adhesive and dressed with gauze and tape.

Interfascial Pterional (Frontotemporosphenoidal) Craniotomy

Fig 199 K For more superiorly sited anterior communicating arteries and associated aneurysms it may be necessary to dissect the olfactory nerve from the olfactory sulcus.

Gyrus rectus Olfactory sufcus MediaLorbital gyrus Anterior orbital gyrus

Orbital sulci .Lateral orbital gyus

Posterior orbital gyrus

Fig 199L The orbital surface of the right frontal lobe. (Adapted from Gray's Anatomy, Eds. Warwick R. and P. L. Williams, 35th Ed., 1975).

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Other Craniotomies

While most aneurysms can be treated through the ptcrional or lateral suboccipital craniotomy (or one of its modifications), a few lesions will require

other approaches.

Anterior Paramedian Frontal Craniotomy (For callosal aneurysms) A bifrontal incision behind the hairline and 1-2 cm anterior to the coronal suture is used. The skin flap is turned to the orbital rim and 3 burr holes are placed: 1) 2-3 cm superior to the orbital rim and 1 cm to the left of the midline 2) 3 cm posterior to 1 3) In the right frontal area 3-4 cm from both 1 and 2(Fig200A-D). Following elevation of the bone flap, a triangular dural flap is draped across the sinus. The topography of the draining veins in this region is quite variable but usually a 3 cm gap can be developed between two veins. The medial surface of the frontal lobe is then retracted away from the falx and a small tunnel thus established. Frontal branches of the pericallosal artery are then followed towards the corpus callosum. A false impression of having reached the corpus callosum may be gained as the falx ends and adherent cingulate gyri are encountered. However gentle separation of the cingulate gyri will reveal the strikingly white corpus callosum hidden beneath. The pericallosal arteries are seen atop the corpus callosum. In the majority of proximal pericallosal aneurysms, the lesion will be located proximal to the section of artery first encountered. Papaverine is applied to this section and the artery is followed anteriorly for 1-2 cm to reach the aneurysm.

Fig200A-B Parasagittal craniotomy for pericallosal aneurysms. Uni- or bi-frontal skin flaps (A), burr holes and bone flap (B).

Other Cramotornies

Fig 200C-D Parasagittal dissection along the falx with retraction of the mesial frontal lobe to visualize the aneurysm (C) and clip it (D).

235

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3 General Operative Techniques

Combined Frontal Paramedian and Pterional Craniotomy •(For callosal aneurysms associated with internal carotid, middle cerebral, or basilar bifurcation aneurysms) A bifrontal incision behind the hairline and extending down on the side to the antero-superior margin of the auricle is used. Standard frontal paramedian and standard pterional craniotomies are previously described. Triangular, dural flaps are positioned superiorly and laterally along the superior sagittal sinus and sphenoid wing respectively (as previously described under frontal paramedian and pterional craniotomies) (Fig201A-B).

Fig 201A-B Separate pterional and parasagittal craniotomies (A) for pericallosal and other aneurysm combinations (B).

Other Craniotomies

Subtemporal Craniotomy This standard approach is seldom necessary in aneurysm surgery because most basilar bifurcation, proximal posterior cerebral (P,), and an-eurysms located between Pt and superior cerebel-lar artery can be better handled through the pte-rional approach without temporal lobe retraction sequelae. However, this approach does provide better access to ambient segment (P2) posterior cerebral artery aneurysms and may be helpful in some cases of large or giant aneurysms at the distal end of the basilar artery (Fig 202A-B).

Fig 202A-B Posteriorly extended pterional approach (A) for (he exploration of the parapeduncular segments of the posterior cerebral and superior cerebellar arteries (B). Ill = oculomotor nerve Ba. Bi. = basilar bifurcation sp. c. a. = superior cerebellar artery P2 — P2 segment

P3

= P3 segment

Ba. Bi.

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3 General Operative Techniques

Lateral Suboccipital Craniotomy (See p. 102-108, Advances and technical standards in neurosurgery, Vol. 4,1977) Aneurysms of the vertebral circulation below the origin of the superior cerebellar arteries are operated upon through a lateral suboccipital craniotomy, in the sitting position. As with the pterional craniotomy, the principle of this craniotomy is to remove bone laterally, in this case from the mastoid area, so that a pyramidal shaped working area is fashioned along the medial aspect of the petrous bone with minimal retraction of the cerebellum. This exposure will display most aneurysms originating near the vertebral or basilar trunks. Position

The anesthetized patient is placed in the sitting position on several layers of cushions, with the legs wrapped in elastic bandages and elevated. The head is flexed slightly and cocked, rotated about 30° toward the side of intended craniotomy so that an unobstructed visual plane is established between the petrous bone and the lateral surface of the cerebellum. The degree of neck flexion should allow two fingers to pass comfortably between the chin and manubrium sternum to avoid compressing the trachea and jugular veins. The head is immobilized with three point skeletal fixation (Mayfield-Kees) (Fig203A). Fig 203A-B Left lateral suboccipital craniotomy (A) for the dissection and clipping of distal vertebral and proximal PICA aneurysms (B). AICA = anterior inferior cerebellar artery PICA = posterior inferior cerebellar artery

AICA

PICA

Other Craniotomies

Incision A paramedian vertical incision beginning 2-3 cm above the superior nuchal line and extending inferiorly about 7 cm is carried through the skin and galea. This tissue is undermined about 1 cm on each side of the incision to allow the placement of hemostatic clamps. The periosteum and more superficial muscles below the superior nuchal line (splenius capitis, trapezius, and sternocleidomastoid) are incised with electrocautery in line with the skin incision. The deeper muscles (obliques and rectus capitis) do not usually need to be incised unless the aneurysm is close to the foramen magnum. Similarly the extracranial vertebral artery lies in a fatty triangle behind the arch of the atlas and is usually not exposed. At this point it is worthwhile to take a small piece of muscle for hemostasis should a dural sinus be torn during the craniotomy. This can be placed flat over the defect and held for 10-30 seconds thereby tamponading the bleeding. Craniotomy Three burr holes are placed: 1) At the apex of the incision about 1-2 cm over the superior nuchal line. 2) On the superior nuchal line just behind the mastoid process. 3) 3 cm medial to (2). The superior parts of the burr holes may be connected with a wire saw, but the inferior part will be opened with the high speed electric drill as mastoid emissary veins can be identified and coagulated before they are torn. The bone flap is removed from the operative field and wrapped in a moist sponge. With the electric drill further bone is removed from the mastoid until the sigmoid sinus is exposed. The sigmoid sinus will limit opening of the dura laterally, so further removal of bone will be of no benefit. The mastoid air cells must be carefully waxed and coated with acrylic to prevent subsequent cerebrospinal fluid rhinorrhea. Dural Opening It is preferable to first decompress the posterior fossa by releasing cerebrospinal fluid from the subarachnoid cisterns before fully opening the dura. This prevents sudden outward herniation of the cerebellum. A small triangular flap of dura, one centimeter on each side is incised at the inferolateral corner of the craniotomy. The cerebellar hemisphere is retracted upward a few millimeters to expose the lateral cerebellomedullary cistern, or if it is blocked then the lateral part of the cisterna magna, which is opened releasing cerebrospinal fluid and generally relaxing the

239

cerebellum. When opening this cistern care must be taken to avoid injuring a small vein that runs across the cistern toward the jugular foramen and collects branches from the medulla, the cerebellar tonsils, and the biventer lobule of the cerebellum. The dural incision is now completed with the lateral portion of the dural flap being divided into three triangles based on the transverse sinus, the sigmoid sinus, and the base of the craniotomy respectively. The medial portion of the dura is left overlying the cerebellum and will help protect it during retraction. The dural flaps are retracted with 4-0 silk sutures to the adjacent muscle and galea. Opening of Arachnoid The inferior cerebellopontine cistern is opened by following the spinal accessory nerve to the jugular foramen to identify the glossopharyngeal and vagus nerves. These are then followed superome-dially to the brain stem where an important confluence of cisterns - the inferior and superior cerebellopontine. and the prepontine - is identified near the pontomedullary sulcus. Here also the flocculus of the cerebellum is noted, and choroid plexus within the tela protrudes from the foramen of Luschka. Cranial nerves IX, X, and XI run inferolaterally and cranial nerves VII and VIII superolaterally from this point. The vertebral arteries join to form the basilar ventrally, and the origin of the anterior inferior cerebellar artery is always just superior to this junction. Further details of the anatomy of this region are given in Fig 31. Dissection will, for the most part, be dictated by the location and size of the given aneurysm, and will thus be discussed under vertebrobasilar an-eurysms.

Variations This standard rhomboid-shaped, lateral suboccipital craniotomy is useful for most aneurysms arising from the vertebrobasilar trunks at the origin of the AICA and PICA. In many instances though, a modification of this approach is more helpful in obtaining the best possible access to the aneurysm. The following variations will be briefly described: Paramedian Infracerebellar Approach (For small proximal PICA aneurysms) In this modification a smaller paramedian incision is employed beginning at the superior nuchal line and extending 5 cm inferiorly. A single burr hole is placed along the line of the incision 1-2 cm beneath the superior nuchal line. Using a high speed electric

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3 General Operative Techniques

drill, obliquely angled cuts are made inferomedially and inferolaterally from this hole extending to the floor of the posterior fossa. A small triangular bone flap is thus removed (Fig 203B). This approach allows satisfactory mobilization of the interior cerebellar surface for access to many small, proximal posterior inferior cerebeflar artery aneurysms (Fig 203C-D).

Fig 203 C-E Paramedian infracerebel-lar approach (C) for a small left PICA aneurysrn (C-E).

V- a. = Vertebral artery PICA = posterior inferior cerebellar artery

Fig 203E Clipped aneurysm of left PICA.

Other Craniotomies

241

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3 General Operative Techniques

Paramedian Supracerebeltar Approach (For peripheral aneurysms of the superior cerebel-lar artery)

The previously described paramedian incision is performed, but the 4 burr holes are placed differently as illustrated in Fig 204A-B. This modification allows greater mobilization of the superior cerebellar surface especially helpful in many peripheral superior cerebellar artery aneurysms. Fig 204A-B Superior-paramedian-suboccipital osteoplastic craniotomy for supracerebeliar dissection of aneu rysms of the left distal superior cerebellar artery.

left sea = left superior cerebellar artery

A

Other Craniotomies

Median Suboccipital Approach (For peripheral PICA aneurysms, Fig 205A-B)

A midline incision is used beginning just above the external occipital notch and extending 5-6 cm inferiorly. Four burr holes are placed as illustrated inFig205A-B. The superior and lateral margins of the bone flap are completed with a wire saw, while the inferior margin is connected with the foramen magnum using the electric drill. This approach permits mobilization of both cerebellar tonsils allowing easy access to most distal posterior inferior cerebellar aneurysms including those arising at the choroidal point.

Fig 205A-B Midline suboccipital craniotomy in the sitting position (A) for distal PICA aneurysms (arrows) (B).

\

PICA artery

posterior inferior cerebellar

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3 General Operative Techniques

Occipital Craniotomy

(For distal posterior cerebral artery (P^) aneurysms) A horse-shoe shaped occipital skin flap is fashioned across the sagittal and transverse sinuses as outlined in Fig 206A. Three or six burr holes are placed as illustrated in Fig 206A. The dura is hinged medially toward the sagittal sinus permitting mobilization of the medial occipital lobe and access to distal (P^) posterior cerebral artery aneurysms in the quadrigeminal cistern (Fig 206A-C). Fig 206A-C Parasagittal parietaloccipital craniotomy in the sitting position (A) for the dissection (B) and clipping (C) of distal posterior cerebral (P3-P4) aneu-rysms. Aneurysm

Aneurysm Clipping

245

Parietoocc. A. = Parietooccipital artery P4 = P,, segment CalcarineA. = Calcarine artery

Parietoocc. A.

Calcarine A

Aneurysm Clipping Preparation Application of a spring clip across the neck of an aneurysm is at present the most practical and satisfactory method of eliminating the lesion from the circulation. Clips must possess adequate clos ing pressure to prevent delayed slip from the neck of the aneurysm, yet at the same time must be delicate enough so that their application to the neck of the lesion can be easily accomplished. The physical requirements of aneurysm clips were dis_cussed on p. 212. Of importance at operation is that a variety of shapes and sizes of aneurysm clips be available to deal with the wide spectrum of aneurysms encountered. _ _ _ _ ..._ Prior to the application of a clip, the aneurysm neck must be free of adhesions to surrounding jirteries and neural structures and must be of such a size and compressibility that the clip blades are able to close and completely exclude the aneurysm fundusjrom circulation. In cases of ''simple aneurysms", with a narrow and well defined neck a clip can be placed across the base and slowly closed with the surgeon making sure that the clip includes the whole an eurysm neck, does not compromise the parent

vessels and does not include a perforating artery between the blades. The solid clips allow the holding of the head of the clip with forceps which may be elevated!_an_d^rotated to check the surround^ njj^reaj Following placement of the clip, the fundus of the aneurysm is resected and the cut) edges are sealed completely by bipolar coagulation. The clip can then be removed and the rest of the aneurysm held with smooth-edged ring forceps and slightly rotated to ensure that the whole sac is occluded and all the perforators arc secured. The bulging parts of aneurysms are then perfectly coagulated down to the level of the parent vessel. After such stepwise or staging elimination, a final perfectly sized clip can be applied (Figs 207A-G and208A-B). __________________ In cases of a "complex aneurysm". with a broad irregular base and an atherosclerotic or thrombotic sac, the aneurysm is often not amenable to initial clipping, even if the neck is adequately dissected, In order to perform a perfect clip placement with- out strangulation of the parent vessels and per-forators. the following techniques have proven useful to prepare the aneurysm for clip application.

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3 General Operative Techniques

Fig 207 A 1 Staging (stepwise) coagulation and clipping. Small aneurysm at the origin of the right posterior communicating artery (arrow). The posterior communicating artery itself is not visible, but the perforating branches are. 2 The aneurysm sac is shrunk with the aid of bipolar coagulation. The posterior communicating artery is now well seen (arrow).

3 Another case with an aneurysm of the left posterior communicating artery (large arrow). Anterior choroidal artery (small arrow). 4 After application of an initial clip the proximal part of posterior communicating artery is visualized (white arrow).

5 Coagulation and stepwise shrinkage of the aneurysm (arrow). 6 Final small clip applied (arrow).

Aneurysm Clipping

247

Fig 207 B 1 A superior-anteriorly directed, small aneurysm with a large base from the anterior communicating artery (arrow). 2 Shrinkage of the aneurysm sac (arrow). 3 Aneurysm sac fully shrunk with the aid of bipolar coagulation will then be clipped (black arrow). The sclerotic right internal carotid artery with numerous vasa vasorum (white arrow).

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3 General Operative Techniques

C1

Fig 207 C 1 Medium sized aneurysm (An) of the left internal carotid artery bifurcation. The fundus is displaced laterally to demonstrate the dissected Heubner's artery (H) underneath the aneurysm sac (arrows). 2 The aneurysm sac is coagulated and temporarily clipped (CL). The fundus of the aneurysm is resected. 3 The initial clip is removed for_proper coagulation of the inferiorly bulging part of the aneurysm beneath the bifurcation of the internal carotid artery. 4 Fully coagulated aneurysm sac (arrow). 5 The final clip is applied (CL). Heubner's and striate arteries are readily visible (arrows). Ill = left oculomotor nerve lateral to the posterior communicating artery.

Aneurysm Clipping___249

Postero-inferiorly directed aneurysm (An) of the anterior communicating artery. A, = both A, segments. Initial clip applied and fundus coagulated. Removal of the clip. Rotation of the aneurysm and coagulation of the inferiorly bulging parts (arrow). Final clip applied.

продолжение

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3 General Operative Techniques

drill, obliquely angled cuts are made inferomedially and inferolaterally from this hole extending to the floor of the posterior fossa. A small triangular bone flap is thus removed (Fig 203B). This approach allows satisfactory mobilization of the interior cerebellar surface for access to many small, proximal posterior inferior cerebeflar artery aneurysms (Fig 203C-D).

Fig 203 C-E Paramedian infracerebel-lar approach (C) for a small left PICA aneurysrn (C-E).

V- a. = Vertebral artery PICA = posterior inferior cerebellar artery

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3 General Operative Techniques

Fig 207 E 1 A large based aneurysm (arrow) hiding the right posterior communicating artery. 2 Initial clip (CL), aneurysm rotated. The posterior communicating artery and the proximal part of the aneurysm are visible (arrow). 3 Coagulated fundus (small arrow) after removal of the clip. Large arrow indicates the posterior communicating artery. 4 Full coagulation of the aneurysm. 5 Final clip (CL) applied. Posterior communicating artery (Pco), anterior choroidal artery (arrow) are now better seen. An = aneurysm.

Aneurysm Clipping

251

F4

Fig 207 F 1 Aneurysm of the right anterior choroidal artery (arrow).

2 After dissection of the neck and bipolar coagulation (arrow 1), posterior communicating artery (arrow 2). 3 Initial clip applied and fundus of the aneurysm shrunk by coagulation (arrow). 4 Initial clip removed, the aneurysm is fully coagulated (arrow 1) , anterior choroidal artery (arrow 2), posterior communicating artery (arrow 3). 5 Final clip applied.

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3 General Operative Techniques

Fig 207 G 1 Broad-based aneurysm of the right middle cerebral artery bifurcation (arrow). 2 After initial clipping (arrow). 3 Coagulation of the fundus, removal of the clip, further coagulation of the aneurysm sac. 4 Final clip applied

Aneurysm Clipping

253

Fig 208A Stepwise "staging" elimination of an aneurysm of the anterior communicating artery with inferiorly bulging parts: 1 Initial clip application to the dissected neck of the aneurysm (1). 2 Puncture of the sac. 3 Cutting of the fundus. 4 Coagulation along the cut edges of the aneurysm with the aid of bipolar forceps. 5 A second clip (2) is applied in cases of sclerotic aneurysm. 6 Removal of the first clip. 7 Anterior rotation of the aneurysm. removal of the second clip, dissection of the hypothalamic arteries from the inferiorly bulging parts of the aneurysm and shrinkage of the remaining parts of the aneurysm. 8-9 Application of a smaller final clip (3).

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3 General Operative Techniques

Fig 208 B 1 -7 Same procedure performed with the aid of ring-ended grasping forceps.

Aneurysm Clipping Bipolar Coagulation Bipolar coagulation has been found useful in | shrinking and shaping an aneurysm, not only in the area of the neck but in all parts of the aneurysm. It is now almost a routine part of the microscopic obliteration of an aneurysm, not only as a prelude to the initial application of the clip, but also as a help during the further application of the clip, and during the further manipulation of the aneurysm . before final clip placement. Surgery on an aneu_, rysm does not always start at the neck. Small, thin . lesions or an entire lobule can be coagulated and shrunk by the intermittent application of low amperage current, permitting a more precise obliteration of the aneurysm while preserving surrounding vessels. [Bipolar coagulation is especially help-i ful in shaping and shrinking amorphous, bulging areas of some aneurysms and the neck of broad based aneurysms and in preventing the rupture o thinwalled areas during manipulation.fine wall of the sac will be thickened, the volume of the aneurysm reduced, and the fundus will be separated spontaneously from the surrounding tissue or it will become easier to dissect it with the forceps or dissectors. The bipolar coagulation technique is also helpful in eliminating the thickened arachnoid fibers adherent between the sac and the surrounding arteries. Not infrequently there are newly , developed or dilated veins over and around the ! aneurysm in relation to cisternal or intracerebral hematomas; these veins can be distinguished from normal veins, separated, and coagulated before they rupture, simulating an aneurysm rupture and concealing the dissection area, especially underneath the AcoA and MCA-bifurcation. The moistened tips of the coagulation forceps are passed across the neck of the aneurysm and the tips : I gently squeezed and released as short bursts of ,' current are applied. Usually a setting of 25 on the Malis bipolar coagulation unit is satisfactory. The tips must be released frequently from the aneurysm surface and repeatedly cleaned to prevent adhers ence and to evaluate the degree of shrinkage. Several sets of forceps should be available for the surgeon and a single forceps should not be used for an extended period of time. They should be changed frequently._________________ prhe use of bipolar coagulation is also very effective in complicated situations such as the premature, rupture of aneurysms or unexpected rupture of an aneurysm immediately after clip application (see p. 269-271 staging technique). The bleeding corner can be controlled by coagulation. f However, the bipolar coagulation of an aneurysm is not without hazard. Excessive heating of the aneurysm will cause it to rupture. If the forceps-tips

255

stick to the aneurysm, its wall may be ruptured or its neck may be avulsed from the parent artery. Before bringing bipolar coagulation to the operating room, the surgeon should thoroughly acquaint himself with this technique on blood vessels in the laboratory. Then he will have proper experiences to judge which parts of aneurysm should be first coagulated and how much the forceps-tips should ' be squeezed when coagulating to achieve the , required shrinkage (Fig 209). Bipolar coagulation cannot be applied to every aneurysm. Aneurysms that are directed interiorly or postero-mferiorly are usually adherent to and surrounded by perforating vessels that will be injured by primary coagulation of the base. Only after adequate dissection and separation of the jvessels should coagulation be attempted/ Those aneurysms with very broad, sclerotic, even calcified bases or those which are thrombosed cannot be shaped with this technique., Pertuiset (1979) recommended tangential application of monopolar coagulation. We used other manoeuvers such as ligature or temporary clipping and removal of the sclerotic or thrombotic material. Suction Tip The suction tip can be a useful instrument for dissection and preparation of the aneurysm neck. With the suction turned to a low vacuum, so that small vessels and strands of arachnoid will not be trapped in the suction tip, the tip can be used to depress the aneurysm to see behind the fundus, and to help empty the aneurysm of blood to soften it for clip application. This may be done over a small s^pon^ejfthe^neurysrnjeems especially thin. If any leakage from the aneurysm occurs, it should be controlled if possible with continued low suction and application of a small piece of Jiammered muscle or a sponge over the leakage point. Excessive suction can further damage the aneurysm and associated small arteries, and may turn a small leak into a major site of rupture. Forceps Normal forceps held in the nondominant hand can be used to narrow the aneurysm and shape the neck for clipping, or they can be used to hold the aneurysm closed if there is a rent in the fundus while the clip is being applied. Round headed forceps (smooth surfaced or with teeth) are especially useful to provide traction on an aneurysm so that a clip can be seated.

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3 General Operative Techniques

Fundus

Middle

Neck

Fig 209 This schematic illustration represents the technique of selective bipolar coagulation in relation to the different parts of the aneurysm sac.

Temporary Clips Several years ago the routine application of temporary clips to the parent vessels was advised for [ aneurysms ^n some locations in order to decompress the aneurysm and facilitate dissection and . permanent clip application. With the operating microscope and microsurgical technique to aid the surgeon in dissection, the routine use of temporary ^lips has generally been abandoned. Nevertheless, there are situations especially with premature rupture of the aneurysm and in the treatment of giant aneurysms where the judicious application of temporary clips is useful. Temporary clips possess a much lower closing force than regular aneurysm clips thus preventing mural vascular injury in their application. They are generally gold plated for easy identification and should never be permanently implanted. Ljunggren et al (1983) have recently reported their observations on temporary clipping during early operation in 16 cases of ruptured aneurysms. Especially important for the surgeon is a firm grasp of the anatomical relationship for a given case, both from angiography and from evaluation during dissection, to have in mind where he will place temporary clips if needed. Whenever possible, perforating arteries should not be isolated from the circulation although with middle cerebral and anterior communicating artery aneurysms this sometimes cannot be avoided. The usual sequence of temporary clip application hasjbeen as follows: I Internal carotid artery; Temporary clips are less useful with aneurysms proximal on the internal carotid artery. There is seldom space to place a clip below an ophthalmic aneurysm or inferior wall aneurysm of the ICA and the anesthesiologist must

be advised that compression of the cervical carotid may be necessary (Figs 210A-B, 211A-B). With aneurysms at the posterior communicating artery origin there may or may not be room to place a clip proximal to the aneurysm .^A_clip distal to the aneurysm should be proximal to the anterior choroidal artery so that this artery receives blood from the contralateral circulation through the anterior communicating artery (Fig 212A-D). Because these aneurysms are close to the tentorial edge, it is usually found that if clips are placed above and below the aneurysm and on the posterior communicating artery, there is little room left for dissection. Generally, one can only hope that a proximal clip will slow bleeding enough so that the neck of the aneurysm can be defined or that bleeding can be stopped with compression. With aneurysms at the origin of the anterior choroidal artery clips can be placed above and below the lesion, and with aneurysms at the internal carotid artery bifurcation, a temporary clip should be placed on the internal carotid artery distal to the anterior choroidal artery (Fig 213). The rupture of an aneurysm at the bifurcation of ICA may be treated as shown in Fig 214A-C.

Aneurysm Clipping

257

Fig 210A-B Ruptured carotid-ophthalmic aneurysm controlled by (A) cervical carotid compression and distal clip, (B) proximal clip (1) only, or distal clip (2) combined with a clip (3) to the posterior communicating artery.

Fig 2 1 1 A-B Inferior wall carotid aneurysm with rupture controlled by (A) cervical carotid compression and distal clip, (B) only proximal clip (1) or combined distal clip (2) and a clip to the posterior communicating artery (3).

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3 General Operative Techniques

Fig 212A-D Posterior communicating ruptured aneurysm controlled by (A) neck compression (see Figs 210-211), (B) proximal clip, (C) proximal ( 1 ) and distal clips (2), and (D) proximal (1), distal (2), and posterior communicating clips (3).

Fig 213 Anterior choroidal aneurysm rupture can be controlled stepwise by a single proximal clip (1) or combined proximal (1) and distal clips (2).

Fig 214A-C Ruptured carotid bifurcation aneurysm controlled stepwise by (A) neck compression, (B) only proximal clip if the A! segment is hypoplastic, and (C) distal carotid (1), proximal A, (2), and proximal M, clips (3).

Aneurysm Clipping Middle cerebral artery: A clip (1) on the middle :erebral trunk should be_distal to the lenticulostri-aie arteries if possible although in many cases of 'aneurysm, these perforating arteries arise at the bifurcation or from the primary branches (Fig 215). If vigorous bleeding persists after temporary clipping of the middle cerebral trunk, it is desirable to place temporary clips on one or more of the major branches (2-3). Back bleeding suggests that collateral circulation is well-developed and isolating the rent with distal clips avoids a sump effect of lowering perfusion pressure in the distal middle cerebral artery distribution. Anterior cerebral-anterior communicating arteries: A temporary clip should be applied first to the larger Aj segment and attempts made to control the bleeding. If unsuccessful a clip is placed on the smaller A1 segment. Occasionally a temporary clip must also be applied to one or both A2 segments (Fig 216A-D). Clips are ideally placed medial to the perforating arteries, although if both A, segments are clipped, blood supply to the hypothalamic arteries and recurrent arteries of Heubner will be compromised. Basilar artery: If possible a temporary clip should be placed distal to the superior cerebellar arteries although the distance between the superior cerebellar and posterior cerebral arteries is often too short to accomplish this. If the bleeding is not controlled by clipping the basilar trunk (1), clips may be required on one (2) or both (3) posterior

259

Fig 215 Middle cerebral ruptured aneurysm controlled stepwise by distal M, clip (1), or distal M, and proximal M2 clips (2, 3).

cerebral arteries or posterior communicating arteries. Location of perforating arteries and size of the various components of the posterior circle of Willis will determine the proper placement of temporary clips (Figs 217, 218). Temporary clips should be applied for the minimal time possible and the blood pressure normalized to support the collateral blood flow. The surgeon should therefore have some idea of what he intends

Fig 216A-D Ruptured anterior communicating aneurysm controlled stepwise by (A-C) dominant A, clip, (D) bilateral A, clips, and (E) bilateral A, and single or bilateral A2 clips.

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3 General Operative Techniques

Fig 21 7 Ruptured basilar aneurysm controlled by distal basilar clip (1), distal basilar and uni- or bilateral Pn clips (23).

to do prior to applying temporary clips, so that the necessary manoeuvers can be performed as quickly as safety allows. In large thrombosed aneurysms, much of the hematoma can be removed before it is necessary to apply a temporary clip. In bulky but non-thrombosed aneurysms, attention should be directed to the neck of the lesion and the fundus cut away to allow placement of a standard aneurysm clip before final dissection is performed.

Fig 218 Ruptured vertebral PICA and junction aneurysms controlled by a proximal (1) or additional distal clip (2).

Aneurysms with accessible and definable necks, isolated away from the parent vessel and dissected free of adherent perforators, may be precisely clipped at the proximal neck without further manipulation. Following application, the clip should be carefully inspected to ensure the inclusion of the entire neck and the continued patency of the parent vessel without tension or torsion. In most cases this can be followed by gentle bipolar coagulation and Microtechniques of Aneurysm excision of the fundus to prove adequate clip Obliteration placement, occasionally to remove any fundusThe precise microscopic obliteration of an intracra- associated mass effect, and possibly to prevent nial aneurysm involves the selective application of subsequent tension of neighboring neurovascular the most suitable techniques from the surgeon's structures by the fibrosing fundus. Any necessary armamentarium. Certainly no single technique of repositioning of the clip can be easily accomplished aneurysmal correction will achieve satisfactory following further bipolar coagulation of the anresults in every case and quite often a single eurysmstoma, creating a hemostaticplug. aneurysm demands the utilization of several techniques. Occasionally, the direct microscopic Stepwise (Staging) Elimination of method must be supplemented or even superceded Aneurysm Sac by an indirect approach, such as proximal carotid Aneurysms with adherent or inaccessible bases ligation for intracavernous aneurysms or a trapping should be first clipped at the most proximal accesprocedure for fusiform carotid aneurysms. The sible portion to prevent rupture during manipula-tion ideal procedure should provide complete isolation with the philosophy "first place the lasso ' around of the aneurysm (including the entire neck) from the neck of the aneurysm and then it is / possible to the intravascular compartment (without damaging tame it in a desirable fashion." Following further nearby neurovascular structures), and yet should dissection along the base, the clip can then be ensure the continued patency of the parent cere- repeatedly advanced or a second clip will be applied bral vessel. With experience it becomes obvious proximal to the first clip, which will then be removed, that even though these goals cannot be realized in and the freed corners coagulated again. With one or every case, a microscopic procedure consisting of two clips a stepwise fashion is used, until the neck is individual techniques applied somewhat differ- completely obliterated. Sequential bipolar ently in each case, produces the best results. coagulation of the fundus beyond the clips can be used to prevent hemorrhage

Aneurysm Clipping

261

Fig 219 Inordertosecureall the aneurysm base into the clip, a stepwise "staging" clip application is necessary as in Fig 208 A-B.

from friable areas during the clip advancement, or two or more clips can be advanced over one another. Coagulation and excision of the fundus prior to final clip positioning can sometimes provide additional working space. Broad-based aneurysms with necks too wide for simple clip placement are better handled with gentle bipolar coagulation. This softens and coalesces the base, thus producing a clippable

neck. With experience bipolar coagulation of low amperage can be safely applied to aneurysms in short bursts without adherence. Other techniques to flatten the base for permanent clipping include suture ligation, temporary clip application above the base, and temporary forceps occlusion. In all these neck-forming techniques, care should be taken to avoid damaging any small perforating vessels (often adherent along the base) and to

262

3 General Operative Techniques prevent placing any tension or torsion on the parent vessel. A. stepwise (staging) method of advancing the clip with sequential replacement proximally following further dissection along the base can be quite helpful. Following needle puncture, excision of the fundus (with or without prior bipolar coagulation) can be instituted at any point along this clip advancement to promote an easier dissection. Then by grasping the coagulated aneu-rysmal stoma with the other hand, the clip can be slid into final position at the base, and the perforators can be saved in a more secure way (Fig 219, see also Fig 208A-B). Aneurysms with broad but very firm proximal portions can generally be handled with bipolar coagulation along the base to soften the neck. However, sometimes (especially with larger an-eurysms), thrombotic and/or atheromatous material is sequestered in the base thereby prohibiting secure clip closure for complete obliteration. In these cases excision of the obstructing material can be accomplished with temporary clipping proximally along the base at the parent vessel or along the parent vessel itself. Removal of this material will permit tighter closure of the clip across a softer base thereby better obliterating the aneurysm. The proximal portion of many aneurysms is quite irregular and despite proper clip placement, some degree of bulging along the base proximal to the clip remains. This can be handled by gentle bipolar coagulation of the protruding area, coalescing the adventitia and shrinking the bulge. The resulting coagulum also provides a nidus for subsequent fibrosis. Other fibrosis-producing substances such as beaten muscle or sponge fibers can also be applied, or for larger bulges a protective wrapping such as acrylate can be added (Fig 220 A-D).

Fig 220 A-D Complex anterior communicating aneurysm clipping techniques (A) over the right A2 segment, (B) under the A2 segment, (C) anterior to the anterior communicating artery, and (D) with two separate clips. Small bulges still remaining are covered with muscle and sponge fiber. This technique was used in two cases as the hypo-thalamic arteries were closely attached to the wall of the aneurysm which therefore could not be entirely dissected and clipped.

Aneurysm Clipping

263

every case within 2 to 4 weeks, leading to rerupture

Efficacy of Clipping The clipping of an aneurysm is generally consicferecf curative despite occasional1 reports of clip slippage or breakage. In the present series the entire aneurysm was not included in the clip in 10 cases of the internal carotid and basilar arteries, to avoid any strangulation of the parent vessel. These patients suffered subsequent subarachnoid hemorrhage. In all cases from this group (8 anterior communicating, 1 posterior communicating and 1 basilar artery bifurcation aneurysm), the aneurysm projected inferiorly and appeared to be satisfactorily clipped, though slight bulging around the base could not be included in the clip without compromising hypothalamic branches. Despite the

placement of a small piece of muscle around the area, recurrent aneafysaK developed ia / (Fig 221A-B). To combat this during the last four years, the weakened areas have been handled by a staging technique of successive coagulation and reclipping with the final application of muscle and/ or sponge fibers attached to the clip by an acrylic bonding agent. The number of reruptured aneurysms decreased, but this problem does not seem to have been fully resolved, as in 1982 two further cases of rerupture occurred, in spite of meticulous use of the above mentioned staging technique (see Fig 221C-G).

Fig 221 A-B In cases of incompletely clipped aneurysms without elimination of the inferiorly bulging parts another aneurysm may develop j/\/itlTiriJ::£wjeeks_between the clip and the parent artery.

Fig 221 C An aneurysm of the anterior communicating artery (see Fig 221D) with a posterior-inferiorly directed fundus was coagulated and clipped smoothly, the postoperative course was without any problems and the 49 year old patient left for home on the 14th postoperative day. However, three days later she suddenly developed severe headache; lumbar puncture confirmed a subarachnoid hemorrhage and the CT scan showed an intraventricular hematoma (arrows).

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3 General Operative Techniques

Fig 221 D An interiorly directed aneurysm of the anterior communicating artery (arrow) was clipped with staging technique. Fig 221E-G The patient had initially a smooth postoperative course but after two weeks had a second sub-arachnoid hemorrhage. This was confirmed by LP and CT scan (see Fig 221C), but 4-vessel-angiography (E-G) failed to demonstrate an aneurysm. On reexploration a small newly developed aneurysm was found between the clip and anterior communicating artery. This new aneurysm was extremely thin-walled, difficult to handle, but was finally successfully reclipped.

Summary Despite the experienced application of these various techniques, the successful microscopic obliteration of some aneurysms remains most difficult. Regardless of location, aneurysms directed anteriorly or superiorly can usually be handled quite well, but in our experience those aneurysms directed inferiorly or postero-inferiorly remain quite difficult. Due to their position, these aneurysms are frequently directed away from the operator into a maze of adherent perforating ves-

sels. This dissection, though simplified somewhat in the smaller sized aneurysms, is quite tedious in most cases, and almost impossible in the larger aneurysms. As a result the current morbidity and mortality associated with the micro-obliteration of aneurysms lies primarily in the inferiorly and post eriorly directed cases. Improvements in the micro scopic approach to these patients await newer j techniques. «

250

3 General Operative Techniques продолжение

Fig 207 E 1 A large based aneurysm (arrow) hiding the right posterior communicating artery. 2 Initial clip (CL), aneurysm rotated. The posterior communicating artery and the proximal part of the aneurysm are visible (arrow). 3 Coagulated fundus (small arrow) after removal of the clip. Large arrow indicates the posterior communicating artery. 4 Full coagulation of the aneurysm. 5 Final clip (CL) applied. Posterior communicating artery (Pco), anterior choroidal artery (arrow) are now better seen. An = aneurysm.

Aneurysm Clipping

251

F4

Fig 207 F 1 Aneurysm of the right anterior choroidal artery (arrow).

2 After dissection of the neck and bipolar coagulation (arrow 1), posterior communicating artery (arrow 2). 3 Initial clip applied and fundus of the aneurysm shrunk by coagulation (arrow). 4 Initial clip removed, the aneurysm is fully coagulated (arrow 1) , anterior choroidal artery (arrow 2), posterior communicating artery (arrow 3). 5 Final clip applied.

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3 General Operative Techniques

Fig 207 G 1 Broad-based aneurysm of the right middle cerebral artery bifurcation (arrow). 2 After initial clipping (arrow). 3 Coagulation of the fundus, removal of the clip, further coagulation of the aneurysm sac. 4 Final clip applied

Aneurysm Clipping

253

Fig 208A Stepwise "staging" elimination of an aneurysm of the anterior communicating artery with inferiorly bulging parts: 1 Initial clip application to the dissected neck of the aneurysm (1). 2 Puncture of the sac. 3 Cutting of the fundus. 4 Coagulation along the cut edges of the aneurysm with the aid of bipolar forceps. 5 A second clip (2) is applied in cases of sclerotic aneurysm. 6 Removal of the first clip. 7 Anterior rotation of the aneurysm. removal of the second clip, dissection of the hypothalamic arteries from the inferiorly bulging parts of the aneurysm and shrinkage of the remaining parts of the aneurysm. 8-9 Application of a smaller final clip (3).

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3 General Operative Techniques

Fig 208 B 1 -7 Same procedure performed with the aid of ring-ended grasping forceps.

Aneurysm Clipping Bipolar Coagulation Bipolar coagulation has been found useful in | shrinking and shaping an aneurysm, not only in the area of the neck but in all parts of the aneurysm. It is now almost a routine part of the microscopic obliteration of an aneurysm, not only as a prelude to the initial application of the clip, but also as a help during the further application of the clip, and during the further manipulation of the aneurysm . before final clip placement. Surgery on an aneu_, rysm does not always start at the neck. Small, thin . lesions or an entire lobule can be coagulated and shrunk by the intermittent application of low amperage current, permitting a more precise obliteration of the aneurysm while preserving surrounding vessels. [Bipolar coagulation is especially help-i ful in shaping and shrinking amorphous, bulging areas of some aneurysms and the neck of broad based aneurysms and in preventing the rupture o thinwalled areas during manipulation.fine wall of the sac will be thickened, the volume of the aneurysm reduced, and the fundus will be separated spontaneously from the surrounding tissue or it will become easier to dissect it with the forceps or dissectors. The bipolar coagulation technique is also helpful in eliminating the thickened arachnoid fibers adherent between the sac and the surrounding arteries. Not infrequently there are newly , developed or dilated veins over and around the ! aneurysm in relation to cisternal or intracerebral hematomas; these veins can be distinguished from normal veins, separated, and coagulated before they rupture, simulating an aneurysm rupture and concealing the dissection area, especially underneath the AcoA and MCA-bifurcation. The moistened tips of the coagulation forceps are passed across the neck of the aneurysm and the tips : I gently squeezed and released as short bursts of ,' current are applied. Usually a setting of 25 on the Malis bipolar coagulation unit is satisfactory. The tips must be released frequently from the aneurysm surface and repeatedly cleaned to prevent adhers ence and to evaluate the degree of shrinkage. Several sets of forceps should be available for the surgeon and a single forceps should not be used for an extended period of time. They should be changed frequently._________________ prhe use of bipolar coagulation is also very effective in complicated situations such as the premature, rupture of aneurysms or unexpected rupture of an aneurysm immediately after clip application (see p. 269-271 staging technique). The bleeding corner can be controlled by coagulation. f However, the bipolar coagulation of an aneurysm is not without hazard. Excessive heating of the aneurysm will cause it to rupture. If the forceps-tips

255

stick to the aneurysm, its wall may be ruptured or its neck may be avulsed from the parent artery. Before bringing bipolar coagulation to the operating room, the surgeon should thoroughly acquaint himself with this technique on blood vessels in the laboratory. Then he will have proper experiences to judge which parts of aneurysm should be first coagulated and how much the forceps-tips should ' be squeezed when coagulating to achieve the , required shrinkage (Fig 209). Bipolar coagulation cannot be applied to every aneurysm. Aneurysms that are directed interiorly or postero-mferiorly are usually adherent to and surrounded by perforating vessels that will be injured by primary coagulation of the base. Only after adequate dissection and separation of the jvessels should coagulation be attempted/ Those aneurysms with very broad, sclerotic, even calcified bases or those which are thrombosed cannot be shaped with this technique., Pertuiset (1979) recommended tangential application of monopolar coagulation. We used other manoeuvers such as ligature or temporary clipping and removal of the sclerotic or thrombotic material. Suction Tip The suction tip can be a useful instrument for dissection and preparation of the aneurysm neck. With the suction turned to a low vacuum, so that small vessels and strands of arachnoid will not be trapped in the suction tip, the tip can be used to depress the aneurysm to see behind the fundus, and to help empty the aneurysm of blood to soften it for clip application. This may be done over a small s^pon^ejfthe^neurysrnjeems especially thin. If any leakage from the aneurysm occurs, it should be controlled if possible with continued low suction and application of a small piece of Jiammered muscle or a sponge over the leakage point. Excessive suction can further damage the aneurysm and associated small arteries, and may turn a small leak into a major site of rupture. Forceps Normal forceps held in the nondominant hand can be used to narrow the aneurysm and shape the neck for clipping, or they can be used to hold the aneurysm closed if there is a rent in the fundus while the clip is being applied. Round headed forceps (smooth surfaced or with teeth) are especially useful to provide traction on an aneurysm so that a clip can be seated.

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Fundus

Middle

Neck

Fig 209 This schematic illustration represents the technique of selective bipolar coagulation in relation to the different parts of the aneurysm sac.

Temporary Clips Several years ago the routine application of temporary clips to the parent vessels was advised for [ aneurysms ^n some locations in order to decompress the aneurysm and facilitate dissection and . permanent clip application. With the operating microscope and microsurgical technique to aid the surgeon in dissection, the routine use of temporary ^lips has generally been abandoned. Nevertheless, there are situations especially with premature rupture of the aneurysm and in the treatment of giant aneurysms where the judicious application of temporary clips is useful. Temporary clips possess a much lower closing force than regular aneurysm clips thus preventing mural vascular injury in their application. They are generally gold plated for easy identification and should never be permanently implanted. Ljunggren et al (1983) have recently reported their observations on temporary clipping during early operation in 16 cases of ruptured aneurysms. Especially important for the surgeon is a firm grasp of the anatomical relationship for a given case, both from angiography and from evaluation during dissection, to have in mind where he will place temporary clips if needed. Whenever possible, perforating arteries should not be isolated from the circulation although with middle cerebral and anterior communicating artery aneurysms this sometimes cannot be avoided. The usual sequence of temporary clip application hasjbeen as follows: I Internal carotid artery; Temporary clips are less useful with aneurysms proximal on the internal carotid artery. There is seldom space to place a clip below an ophthalmic aneurysm or inferior wall aneurysm of the ICA and the anesthesiologist must

be advised that compression of the cervical carotid may be necessary (Figs 210A-B, 211A-B). With aneurysms at the posterior communicating artery origin there may or may not be room to place a clip proximal to the aneurysm .^A_clip distal to the aneurysm should be proximal to the anterior choroidal artery so that this artery receives blood from the contralateral circulation through the anterior communicating artery (Fig 212A-D). Because these aneurysms are close to the tentorial edge, it is usually found that if clips are placed above and below the aneurysm and on the posterior communicating artery, there is little room left for dissection. Generally, one can only hope that a proximal clip will slow bleeding enough so that the neck of the aneurysm can be defined or that bleeding can be stopped with compression. With aneurysms at the origin of the anterior choroidal artery clips can be placed above and below the lesion, and with aneurysms at the internal carotid artery bifurcation, a temporary clip should be placed on the internal carotid artery distal to the anterior choroidal artery (Fig 213). The rupture of an aneurysm at the bifurcation of ICA may be treated as shown in Fig 214A-C.

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257

Fig 210A-B Ruptured carotid-ophthalmic aneurysm controlled by (A) cervical carotid compression and distal clip, (B) proximal clip (1) only, or distal clip (2) combined with a clip (3) to the posterior communicating artery.

Fig 2 1 1 A-B Inferior wall carotid aneurysm with rupture controlled by (A) cervical carotid compression and distal clip, (B) only proximal clip (1) or combined distal clip (2) and a clip to the posterior communicating artery (3).

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3 General Operative Techniques

Fig 212A-D Posterior communicating ruptured aneurysm controlled by (A) neck compression (see Figs 210-211), (B) proximal clip, (C) proximal ( 1 ) and distal clips (2), and (D) proximal (1), distal (2), and posterior communicating clips (3).

Fig 213 Anterior choroidal aneurysm rupture can be controlled stepwise by a single proximal clip (1) or combined proximal (1) and distal clips (2).

Fig 214A-C Ruptured carotid bifurcation aneurysm controlled stepwise by (A) neck compression, (B) only proximal clip if the A! segment is hypoplastic, and (C) distal carotid (1), proximal A, (2), and proximal M, clips (3).

Aneurysm Clipping Middle cerebral artery: A clip (1) on the middle :erebral trunk should be_distal to the lenticulostri-aie arteries if possible although in many cases of 'aneurysm, these perforating arteries arise at the bifurcation or from the primary branches (Fig 215). If vigorous bleeding persists after temporary clipping of the middle cerebral trunk, it is desirable to place temporary clips on one or more of the major branches (2-3). Back bleeding suggests that collateral circulation is well-developed and isolating the rent with distal clips avoids a sump effect of lowering perfusion pressure in the distal middle cerebral artery distribution. Anterior cerebral-anterior communicating arteries: A temporary clip should be applied first to the larger Aj segment and attempts made to control the bleeding. If unsuccessful a clip is placed on the smaller A1 segment. Occasionally a temporary clip must also be applied to one or both A2 segments (Fig 216A-D). Clips are ideally placed medial to the perforating arteries, although if both A, segments are clipped, blood supply to the hypothalamic arteries and recurrent arteries of Heubner will be compromised. Basilar artery: If possible a temporary clip should be placed distal to the superior cerebellar arteries although the distance between the superior cerebellar and posterior cerebral arteries is often too short to accomplish this. If the bleeding is not controlled by clipping the basilar trunk (1), clips may be required on one (2) or both (3) posterior

259

Fig 215 Middle cerebral ruptured aneurysm controlled stepwise by distal M, clip (1), or distal M, and proximal M2 clips (2, 3).

cerebral arteries or posterior communicating arteries. Location of perforating arteries and size of the various components of the posterior circle of Willis will determine the proper placement of temporary clips (Figs 217, 218). Temporary clips should be applied for the minimal time possible and the blood pressure normalized to support the collateral blood flow. The surgeon should therefore have some idea of what he intends

Fig 216A-D Ruptured anterior communicating aneurysm controlled stepwise by (A-C) dominant A, clip, (D) bilateral A, clips, and (E) bilateral A, and single or bilateral A2 clips.

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3 General Operative Techniques

Fig 21 7 Ruptured basilar aneurysm controlled by distal basilar clip (1), distal basilar and uni- or bilateral Pn clips (23).

to do prior to applying temporary clips, so that the necessary manoeuvers can be performed as quickly as safety allows. In large thrombosed aneurysms, much of the hematoma can be removed before it is necessary to apply a temporary clip. In bulky but non-thrombosed aneurysms, attention should be directed to the neck of the lesion and the fundus cut away to allow placement of a standard aneurysm clip before final dissection is performed.

Fig 218 Ruptured vertebral PICA and junction aneurysms controlled by a proximal (1) or additional distal clip (2).

Aneurysms with accessible and definable necks, isolated away from the parent vessel and dissected free of adherent perforators, may be precisely clipped at the proximal neck without further manipulation. Following application, the clip should be carefully inspected to ensure the inclusion of the entire neck and the continued patency of the parent vessel without tension or torsion. In most cases this can be followed by gentle bipolar coagulation and Microtechniques of Aneurysm excision of the fundus to prove adequate clip Obliteration placement, occasionally to remove any fundusThe precise microscopic obliteration of an intracra- associated mass effect, and possibly to prevent nial aneurysm involves the selective application of subsequent tension of neighboring neurovascular the most suitable techniques from the surgeon's structures by the fibrosing fundus. Any necessary armamentarium. Certainly no single technique of repositioning of the clip can be easily accomplished aneurysmal correction will achieve satisfactory following further bipolar coagulation of the anresults in every case and quite often a single eurysmstoma, creating a hemostaticplug. aneurysm demands the utilization of several techniques. Occasionally, the direct microscopic Stepwise (Staging) Elimination of method must be supplemented or even superceded Aneurysm Sac by an indirect approach, such as proximal carotid Aneurysms with adherent or inaccessible bases ligation for intracavernous aneurysms or a trapping should be first clipped at the most proximal accesprocedure for fusiform carotid aneurysms. The sible portion to prevent rupture during manipula-tion ideal procedure should provide complete isolation with the philosophy "first place the lasso ' around of the aneurysm (including the entire neck) from the neck of the aneurysm and then it is / possible to the intravascular compartment (without damaging tame it in a desirable fashion." Following further nearby neurovascular structures), and yet should dissection along the base, the clip can then be ensure the continued patency of the parent cere- repeatedly advanced or a second clip will be applied bral vessel. With experience it becomes obvious proximal to the first clip, which will then be removed, that even though these goals cannot be realized in and the freed corners coagulated again. With one or every case, a microscopic procedure consisting of two clips a stepwise fashion is used, until the neck is individual techniques applied somewhat differ- completely obliterated. Sequential bipolar ently in each case, produces the best results. coagulation of the fundus beyond the clips can be used to prevent hemorrhage

Aneurysm Clipping

261

Fig 219 Inordertosecureall the aneurysm base into the clip, a stepwise "staging" clip application is necessary as in Fig 208 A-B.

from friable areas during the clip advancement, or two or more clips can be advanced over one another. Coagulation and excision of the fundus prior to final clip positioning can sometimes provide additional working space. Broad-based aneurysms with necks too wide for simple clip placement are better handled with gentle bipolar coagulation. This softens and coalesces the base, thus producing a clippable

neck. With experience bipolar coagulation of low amperage can be safely applied to aneurysms in short bursts without adherence. Other techniques to flatten the base for permanent clipping include suture ligation, temporary clip application above the base, and temporary forceps occlusion. In all these neck-forming techniques, care should be taken to avoid damaging any small perforating vessels (often adherent along the base) and to

262

3 General Operative Techniques prevent placing any tension or torsion on the parent vessel. A. stepwise (staging) method of advancing the clip with sequential replacement proximally following further dissection along the base can be quite helpful. Following needle puncture, excision of the fundus (with or without prior bipolar coagulation) can be instituted at any point along this clip advancement to promote an easier dissection. Then by grasping the coagulated aneu-rysmal stoma with the other hand, the clip can be slid into final position at the base, and the perforators can be saved in a more secure way (Fig 219, see also Fig 208A-B). Aneurysms with broad but very firm proximal portions can generally be handled with bipolar coagulation along the base to soften the neck. However, sometimes (especially with larger an-eurysms), thrombotic and/or atheromatous material is sequestered in the base thereby prohibiting secure clip closure for complete obliteration. In these cases excision of the obstructing material can be accomplished with temporary clipping proximally along the base at the parent vessel or along the parent vessel itself. Removal of this material will permit tighter closure of the clip across a softer base thereby better obliterating the aneurysm. The proximal portion of many aneurysms is quite irregular and despite proper clip placement, some degree of bulging along the base proximal to the clip remains. This can be handled by gentle bipolar coagulation of the protruding area, coalescing the adventitia and shrinking the bulge. The resulting coagulum also provides a nidus for subsequent fibrosis. Other fibrosis-producing substances such as beaten muscle or sponge fibers can also be applied, or for larger bulges a protective wrapping such as acrylate can be added (Fig 220 A-D).

Fig 220 A-D Complex anterior communicating aneurysm clipping techniques (A) over the right A2 segment, (B) under the A2 segment, (C) anterior to the anterior communicating artery, and (D) with two separate clips. Small bulges still remaining are covered with muscle and sponge fiber. This technique was used in two cases as the hypo-thalamic arteries were closely attached to the wall of the aneurysm which therefore could not be entirely dissected and clipped.

Aneurysm Clipping

263

every case within 2 to 4 weeks, leading to rerupture

Efficacy of Clipping The clipping of an aneurysm is generally consicferecf curative despite occasional1 reports of clip slippage or breakage. In the present series the entire aneurysm was not included in the clip in 10 cases of the internal carotid and basilar arteries, to avoid any strangulation of the parent vessel. These patients suffered subsequent subarachnoid hemorrhage. In all cases from this group (8 anterior communicating, 1 posterior communicating and 1 basilar artery bifurcation aneurysm), the aneurysm projected inferiorly and appeared to be satisfactorily clipped, though slight bulging around the base could not be included in the clip without compromising hypothalamic branches. Despite the

placement of a small piece of muscle around the area, recurrent aneafysaK developed ia / (Fig 221A-B). To combat this during the last four years, the weakened areas have been handled by a staging technique of successive coagulation and reclipping with the final application of muscle and/ or sponge fibers attached to the clip by an acrylic bonding agent. The number of reruptured aneurysms decreased, but this problem does not seem to have been fully resolved, as in 1982 two further cases of rerupture occurred, in spite of meticulous use of the above mentioned staging technique (see Fig 221C-G).

Fig 221 A-B In cases of incompletely clipped aneurysms without elimination of the inferiorly bulging parts another aneurysm may develop j/\/itlTiriJ::£wjeeks_between the clip and the parent artery.

Fig 221 C An aneurysm of the anterior communicating artery (see Fig 221D) with a posterior-inferiorly directed fundus was coagulated and clipped smoothly, the postoperative course was without any problems and the 49 year old patient left for home on the 14th postoperative day. However, three days later she suddenly developed severe headache; lumbar puncture confirmed a subarachnoid hemorrhage and the CT scan showed an intraventricular hematoma (arrows).

264

3 General Operative Techniques

Fig 221 D An interiorly directed aneurysm of the anterior communicating artery (arrow) was clipped with staging technique. Fig 221E-G The patient had initially a smooth postoperative course but after two weeks had a second sub-arachnoid hemorrhage. This was confirmed by LP and CT scan (see Fig 221C), but 4-vessel-angiography (E-G) failed to demonstrate an aneurysm. On reexploration a small newly developed aneurysm was found between the clip and anterior communicating artery. This new aneurysm was extremely thin-walled, difficult to handle, but was finally successfully reclipped.

Summary Despite the experienced application of these various techniques, the successful microscopic obliteration of some aneurysms remains most difficult. Regardless of location, aneurysms directed anteriorly or superiorly can usually be handled quite well, but in our experience those aneurysms directed inferiorly or postero-inferiorly remain quite difficult. Due to their position, these aneurysms are frequently directed away from the operator into a maze of adherent perforating ves-

sels. This dissection, though simplified somewhat in the smaller sized aneurysms, is quite tedious in most cases, and almost impossible in the larger aneurysms. As a result the current morbidity and mortality associated with the micro-obliteration of aneurysms lies primarily in the inferiorly and post eriorly directed cases. Improvements in the micro scopic approach to these patients await newer j techniques. « продолжение

Alternative Methods of Aneurysm Treatment продолжение

Alternative Methods of Aneurysm Treatment Cervical Carotid Artery Ligation Ligation of the common or internal carotid arteries in the neck was the first method of treatment for intracranial aneurysms. Nishioka (1966) analysed a large series and found only 56 per cent were considered successful. Death occurred in 19 per cent. Tindall and Odom (1969) have reviewed this subject, and feel that common carotid artery ligation may be effective in internal carotid aneurysms and in those anterior communicating artery aneurysms associated with a hypoplastic Al segment. Cervical carotid artery ligation was used in the present series of patients in 15 cases of intracavernous carotid artery aneurysms and in two cases of inferior wall carotid artery aneurysm. However, improved results with intracranial operations have relegated carotid ligation to a less important role in management of these lesions.

Intracranial Parent Artery Ligation and Trapping Procedures Logue (1956) recommended clipping of the larger anterior cerebral artery (At segment) as an alternative to dissection and clipping of the lesion itself in cases of anterior communicating aneurysm. Some subsequent workers (Pool and Potts 1965; McKissock et al 1965) did not find this operation to be of benefit, but more recently reported series have stated good results with this method (Scott 1973; Hockley 1975). No patient in the present series was treated by proximal anterior cerebral artery occlusion. Trapping procedures should normally be avoided, although in some instances there will be no alterna tive. If a trapping procedure to treat, for example, a large or complex aneurysm of the internal carotid artery is contemplated, it is necessary preoperatively to evaluate the collateral circulation. A variety of diagnostic tests can be employed, such as angiography or electroencephalography with com pression. If unsufficient collateral circulation is suspected then a bypass procedure such as a super ficial temporal to middle cerebral artery anas tomosis might be considered as a preliminary treat ment for fusiform middle cerebral artery aneurysm to provide additional collateral blood flow/Trap ping of the anterior communicating artery should be avoided as it deprives hypothalamic branches of blood flow and is associated with a high postopera tive incidence of mental changes and electrolyte disturbances. _________

265

Aneurysm Ligation A silk ligature, usually 2-0 or 3-0. may be used to occlude the neck of the aneurysm (see previous publications). Ligature occlusion has been preferred by some neurosurgeons for aneurysms of the internal carotid and middle cerebral artery bifurca- | tions. Care must be taken that only the neck of the aneurysm is included in the ligature. The ligature is first passed beneath the parent vessel, and the ends of the ligature then brought individually between the neck of the aneurysm and the branches at the bifurcation. The ligature is drawn up behind the neck of the aneurysm so that the knot can be tied on the top of the neck under direct vision. In some cases it will be useful to tie a second ligature to the first in order to pull the ligature through the space between the aneurysm neck and parent " artery. ___ _________ Ligation of an aneurysm is generally less satisfac- , tory than clipping because j 1) It distorts the parent vessels by drawing them together 2) Small perforating arteries are easily injured when attempting to tighten the ligature. 3) If the aneurysm wall is sclerotic, the ligature may cut through it. The advantage of a ligature is the small space which it occupies and the degree of flexibility in applica tion. _________________

Wrapping and Coating Techniques The operating microscope has provided a better appreciation of the relationship of an aneurysm to its parent arteries. Two important concepts have developed over the time span of the present series: First, fusiform aneurysm formation of the parent artery such as the anterior communicating artery (2/380) and middle cerebral artery bifurcation (21 180) are much less common than once thought. Secondly, with the exception of basilar bifurcation aneurysms it is very uncommon for a saccular aneurysm to give rise to an arterial branch and therefore be unamenable to clipping. In both these situations arachnoid adhesions may create a false impression as to the origin, shape, and relationship of the aneurysm. Thus with increased experience there has been less need for an alternative method to clipping. Nevertheless, there do remain a few cases where clipping is not possible. In the present series two carotid-ophthalmic aneurysms were partially extradural, one vertebral, one middle cerebral the entire segment Ml and two anterior communicating artery aneurysms were fusiform and

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seven basilar bifurcation aneurysms could not be adequately dissected from the adherent thalamoperf orators. Muscle was first used to cover an aneurysm to stimulate fibrosis around the lesion and thus prevent further bleeding (Dott 1933). Experimentally, * Sachs (1972) did not find that adequate fibrosis occurred with muscle to protect a patient in the first month - the time of greatest likelihood of rupture. j Fabrics such as cotton (Northfield 1952) and muslin «(Gillingham 1958; Mount and Antunes 1975) have been used in a similar manner. Button (1956, 1969) introduced a method of aneurysm encasement with methylmethacrylate, and Selverstone and Ronis (1958) suggested a two-layered investment with polyvinyl applied directly to the aneurysm covered with a layer of stronger epoxy resin. Cyanoacrylates subsequently became popular because they are both adherent to tissue and provide adequate strength. Use of these compounds was reviewed by Handa and associates (1969). In these aneurysms not amenable to complete clipping, pieces of muscle and sponge fiber have usually been applied to the aneurysm and then cyanoacrylate (Aron Alpha A) has been used to stabilize the muscle to a clip. It is not applied directly to a vessel as there is some concern over tissue reactivity to this compound. As discussed previously small basal bulgings beyond the clip are shrunk with bipolar coagulation and similarly f covered. The ultimate fate of the cases in which this i treatment is used is not yet clear.

performed. The middle cerebral artery remained patent, but the superior trunk of MCA remained occluded as before. The need to repair an injured artery is dependent on the collateral circulation and determined by review of the angiography, evaluation of the size of collateral vessels at operation, and the degree of backbleeding from the distal side of the damaged vessel. A further application of microvascular techniques is the creation of an extracranial-intracranial arterial bypass anastomosis to allow a more proximal artery to be sacrificed (Ya§argil 1967, 1969). Usually an end to side anastomosis between the superficial temporal artery or occipital artery and a cortical branch of the middle cerebral artery has been employed. Nine cases in the present series required arterial bypass procedures. Two were giant intracavernous aneurysms and another four were aneurysms of the internal carotid artery bifurcation, one ophthalmic artery, two middle cerebral artery bifurcation and one posterior communicating artery aneurysm respectively. The other two were fusiform aneurysms of the inferior wall of the internal carotid artery. In the first seven cases, the anastomosis was performed during the same operation for treatment of the aneurysm, while in the last two cases, a prophylactic bypass was created in anticipation of possible sacrifice of the internal carotid artery. As this type of vascular anastomosis has evolved into a relatively safe procedure with a high rate of longterm patency, it should probably be considered more often in applicable cases.

Microsurgical Vascular Repair and Anastomosis

Induced Thrombosis and Internal Occlusion

The introduction of microvascular suturing techniques has created the possibility of directly repairing injured arteries. In 7 cases in the present series, the aneurysm had a very broad base or was torn at its base or it was too sclerotic to be clipped. Repair with 8-0 suture was therefore performed; two cases were posterior communicating artery aneurysms, one case a middle cerebral artery bifurcation aneurysm, one case an anterior communicating artery aneurysm, one case a proximal A2 aneurysm (Fig 222A-C) and one case each of aneurysms of the medial wall of the internal carotid artery and the pericallosal artery. In two cases of giant aneurysms (one middle cerebral bifurcation and one P2 segment of the posterior cerebral), the lesion was trapped with temporary clips, an aneurysmectomy performed, and the parent artery repaired with 8-0 sutures. Because of thick walls an endarterectomy of the occluded superior segment of MCA was

The authors have had no experience with these techniques, and can only provide a list of references for the interested reader. Induced thrombosis 1) Animal hair (Gallagher 1962) 2) Electrical thrombosis (Mullan et al 1969; Hosobuchi 1975) 3) Wire thrombosis (Mullan 1974) 4) Iron fillings (Alksne and Fingerhut 1965). Internal occlusion 1) Catheter ballon occlusion (Serbinenko 1974, 1979; Romodanov and Shcheglov 1979, 1982; Debrun et al 1978, 1981) 2) Plastic injection (Alksne and Smith 1977,1980).

Special Operative Problems

Fig 222 A-C

girl.

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Excision of a fusiform aneurysm of the proximal right A2 segment by micro suture technique in a 9 year old

Special Operative Problems Multiple and Bilateral Aneurysms (See also Vol. II, Chapter 7) A pterional craniotomy provides access to much of the Circle of Willis and often permits the clipping of more than one aneurysm at the same operation. This is particularly true of multiple aneurysms on the same side. On occasion, multiple bilateral aneurysms can be approached from one side. The key to exposing the multiple sites of aneurysm formation is an adequate dissection of the subarachnoid cisterns, especially the Sylvian cistern in the basal Sylvian fissure and the carotid, chiasmatic and lamina terminalis cisterns in the subfrontal area.

When more than one aneurysm is seen at angiography. the operative approach can be planned to include clipping the additional aneurysms if they are at accessible sites. Aneurysms usually accessible from one side include: a) Ipsilateral internal carotid, middle cerebral, or anterior cerebral artery aneurysms b) Any of the above plus a basilar apex aneurysm, or c) Any of the above plus a contralateral ophthalmic, contralateral internal carotid bifurcation, contralateral proximal anterior cerebral (Aj), contralateral proximal middle cerebral (Mj), or rarely contralateral posterior communicating or contralateral anterior choroidal artery aneurysms .

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3 General Operative Techniques

Bilateral staged operations are usually necessary for: a) Ipsilateral internal carotid, middle cerebral existing with a contralateral posterior communicating, anterior choroidal, or distal middle cerebral artery aneurysm. b) On the vertebrobasilar circulation, basilar artery bifurcation aneurysms, aneurysms on the Pj segment of the posterior cerebral artery, and aneurysms of the upper basilar trunk can be reached through a pterional craniotomy, but other vertebral aneurysms require another approach: e.g. if there is a rare combination of a vertebral and basilar bifurcation aneurysm as was found in one case. If multiple aneurysms include an aneurysm on the distal anterior cerebral artery, the craniotomy can be fashioned to include the interhemispheric area for example a combined pterional and frontal flap placed forward for an anterior communicating artery aneurysm and a distal anterior cerebral artery aneurysm, or a combined flap placed more laterally for a pericallosal artery and a middle cerebral artery or basilar bifurcation aneurysm (see Fig 201A-B, p. 236). Frequently, aneurysms which were poorly visualized or not recognized on angiography are found at operation. Under normal circumstances, the carotid, lamina terminalis, Sylvian and interpeduncular cisterns are opened. Thus the ipsilateral internal carotid, anterior, and middle cerebral arteries, the contralateral internal carotid, anterior cerebral and most proximal middle cerebral arteries, and the anterior communicating and upper basilar artery will be visualized. If the brain is swollen, the arachnoid cisterns unyielding, the patient elderly or in poor medical condition, the exploration should be limited to the ruptured lesion or to easily accessible aneurysms seen on angiography. Usually the ruptured aneurysm is treated first, since if difficulties are encountered, the operation may have to be terminated, and one does not wish to leave the ruptured aneurysm undipped. However, sometimes it is more convenient to isolate and coagulate or cover the unruptured aneurysm with muscle until the ruptured aneurysms have been clipped because the clip on an unruptured aneurysm might hinder dissection of the main lesion. For example a clip placed on an unruptured posterior communicating artery aneurysm could make exploration of a ruptured basilar artery bifurcation aneurysm quite difficult. Small "baby" aneurysms are usually coagulated and covered with muscle or sponge fibers. At times coagulation will cause them to retract into the

lumen of the artery only to reappear later. The precise fate of these lesions is not clear but followup angiography would seem warranted. In one case in this series, a patient with a posterior communicating artery aneurysm was noted at operation to have a baby aneurysm on the basilar artery bifurcation. Ten years later this presented as a medium sized ruptured lesion.

Giant Aneurysms (See also Vol. II, Chapter 6) As aneurysms enlarge beyond 3 crn_in diameter, two processes compound difficulty with their treatment. First, the neck may become broad and sclerotic and encroach further on the wall of the parent arteries or the origins of the perforating arteries. Second, there is a tendency for such ^ajieurysms to undergo thrombosis, and the thrombus prevents clip application and excision of the aneurysm. These aneurysms can be discussed in three groups relative to the degree of thrombosisnonthrombosed, subtotally thrombosed, and totally thrombosed. Nonthrombosed giant aneurysms at times may have a surprisingly narrow neck despite a large fundus, and clipping is not particularly difficult. Following clipping the fundus can be resected and the neck further shrunk with bipolar coagulation to obtain ideal clip placement. More often, however, the neck is broad and a combination of long clips, bipolar coagulation, and compression to empty the aneurysm may be required. As with smaller aneurysms, the parent arteries and perforating arteries must be dissected from the neck, and attempts made to form a neck that will accept the clip. Usually, giant aneurysms contain considerable thrombus. With these aneurysms, shrinkage with bipolar coagulation and piecemeal resection is unlikely to succeed until a substantial amount of thrombus has been removed. Temporary clips to the parent arteries may or may not be necessary. If possible it is better to go directly to the neck and try coagulation, removal of some thrombus and reclipping until the aneurysm is separated from the parent arteries. The fundus can then be removed and further adjustments of the clip made without the unwieldly bulk of aneurysm present. In some cases, however, especially when thrombus is almost complete, it is possible to open the aneurysm fundus without application of temporary clips, and begin removal of thrombus. This is continued until brisk bleeding is encountered, when temporary clips to the parent arteries or a large clip across the base of the aneurysm can be placed.

Special Operative Problems

269

In some cases, the aneurysm will involve the parent arteries to such an extent or be in such a position that it is not feasible to attempt clipping of the neck. This situation arises with almost all intracavernous aneurysms, and with giant an-eurysms of the internal carotid artery and middle cerebral arteries, occasionally with anterior communicating artery aneurysms, and not uncommonly with vertebrobasilar aneurysms. Treatment mal ligation (see Figs 228, 229, 231, 232). When there are preexisting deficits, or collateral circulation at angiography and at operation seems adequate, trapping or ligation may proceed directly. This technique often includes gradual occlusion of the parent artery such as by the application of Selverstone or Crutchfield clamps to the cervical internal carotid artery, or by the tourniquet occlusion of the vertebral or basilar arteries as described by Drake (1975). Increasingly reports have shown the value of performing a preliminary superficial temporal artery-middle cerebral artery anastomosis to support the middle cerebral artery circulation before attempting occlusion of the internal carotid or middle cerebral arteries (Gelber and Sundt 1980; Spetzler et al 1980). This technique was carried out in 8 patients with giant aneurysms in the present series (see Figs 230,252). Finally, there is a group of patients with giant totally thrombosed aneurysms (see Fig 243). There is generally little reason to attempt resection of these lesions unless they are in an especially favorable location and mass effect is clearly symptomatic. Some of these patients will benefit from ventricular shunting when an aneurysm has obstructed the ventricular system, or from extra-cranialintracranial bypass when there are symptoms of ischemia in the distribution of the parent artery. Enlargement of the aneurysm seen by CT scan might prompt more active intervention (see p. 328).

Intraoperative Rupture If rupture of the aneurysm occurs early in the operation during craniotomy or opening of the dura, the case should not be abandoned. The dura is quickly opened and the frontal lobe retracted medially to expose the area of the aneurysm. Placing a sucker into the area of bleeding, the field is cleared of blood, working the suction tip toward the point of bleeding until the aneurysm is brought into the suction. A temporary clip may then be placed across the aneurysm or the parent arteries while a definitive dissection is performed. More commonly, however, rupture occurs while dissection is being performed in the vicinity of the

Fig 223 A Types of aneurysm rupture ( 1 ) at the base, (2) beneath an attached clot, (3) at the dome, and (4) complete rupture (after Pertuiset). ______________

aneurysm. In our experience in most cases rupture occurred in the very final stage of dissection rather than prematurely. Pertuiset (1979) gave a very practical illustration concerning the site of the rupture (Table 1, p. 399, Pia et al 1979) (Fig223A). Often bleeding is from a small opening in the aneurysm, and although brisk for a few moments

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3 General Operative Techniques

will diminish with application of a cottonoid sponge or jstarnp of muscle over the lesion and gentle pressure with the suction (Fig 223B)._Brisk movements and large bore suctions will often increase the damage to the aneurysm. Sometimes the rent in the aneurysm wall can be closed with bipolar coagulation, reducing the diameter of the hole, thus reducing the size of the aneurysm. At other times temporary clips must be applied to the aneurysm or parent vessels. 1 Rupture may occur with attempts to shrink the aneurysm with bipolar coagulation, either from a sudden increase in pressure within the aneurysm from heating and squeezing or from penetration of the lesion by a tip of the forceps. If the dome has

Fig 223 B The premature rupture (1) of an aneurysm can be controlled by suction only (2), or with gentle counter pressure on a cotton sponge (3), or muscle (4), coagulation (5), clip application (6), resection of the fundus of the aneurysm (7), coagulation of the interiorly bulging parts of the aneurysm (8), removal of the clip and full coagulation of the aneurysm (9), and application of the final small clip (10).

ruptured or a thin spot in the wall of the aneurysm above the forceps tips is the source of bleeding, further coagulation may control the bleeding. Therefore, this should be tried for a few seconds. Drawing the aneurysm into the suction tip or closing it with forceps held in the other hand may allow coagulation to proceed. If further coagulation results in increased bleeding, however, the tip has probably penetrated the aneurysm and the clip should be withdrawn and reapplied between the bleeding point and the neck of the aneurysm. By coagulation of the fundus down to the ruptured

Summary of Methods Applied in the Current Series

corner and with reapplication of the clip the situation can be controlled. Temporary clips are applied to the parent vessels when these manoeuvers are unsuccessful (see Figs 210-218). Finally, rupture of the aneurysm may occur during application of the clip or after clip application when the aneurysm is opened. This is generally due to one of the following situations: 1) The clip is not completely across the base of the aneurysm 2) One blade of the clip has penetrated the aneurysm 3) The clip will not completely close because of atherosclerotic plaque or thrombus 4) At a bifurcation, one artery is not dissected free of the neck and its lumen remains open to the aneurysm 5) The clip has torn the base of the aneurysm from the parent artery. In the first situation, the clip may be advanced onto the aneurysm or a longer or different shaped clip tried while the aneurysm is held in the suction or with forceps. In the next three situations, either reapplication of the clip or use of temporary clips will be required to allow further dissection and clarification of the situation. In the last situation, bursting of the sac at the base, temporary clipping of the parent vessels and microvascular suture repair will probably be required; unless the surgeon feels that collateral circulation will permit sacrifice of the parent artery. The technique of "suture repair" can be applied easily if the base of the aneurysm is superior; in cases with posteriorly, anteriorly and laterally localized bases the clip may be of help to rotate the artery superiorly for repair. If the base of the aneurysm is inferiorly located, the suturing technique can be extremely difficult or even impossible. In such cases sacrifice of the parent vessel is the only way to overcome this dangerous situation. One must hope for a well developed collateral system or perform an extra-intracranial anastomosis.

Intraoperative Vasospasm As discussed in previous chapters, vasospasm frequently accompanies rupture of a cerebral aneurysm, and may be aggravated by manipulation of the vessels during operation. Adequate dissection of the arachnoid cisterns is helpful in relieving I this spasm. The compartmentalization of the basal subarachnoid cisterns allows blood to collect in some cisterns, often tightly distending them, while adjacent cisterns may be quite free of blood. It is important to clear all blood from the subarachnoid space to improve the circulation of cerebrospinal

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fluid and to minimize any deleterious effect of blood on the arterial walls. The cisterns should be opened and well irrigated. It has been noted in patients receiving antifibrinolytic agents, that clot within the subarachnoid cisterns may be quite tenacious and adherent to vascular structures, making clearing of the cisterns more difficult. Direct application of 4% papaverine to the arteries at operation will result in their dilatation within a few minutes. Usually papaverine is applied after the aneurysm has been clipped, but with middle cerebral artery bifurcation aneurysms and aneurysms of the distal anterior cerebral arteries, it is advisable to apply papaverine to the distal branches early in dissection, as these smaller vessels are especially prone to spasm. In approaching a basilar bifurcation aneurysm through Liliequist's membrane, the internal carotid artery should receive papaverine as it will be unavoidably manipulated during dissection with resultant spasm. Following application of papaverine, the adventitial sympathetic nerve plexus will become well delineated, presenting as white strands against the pink background of the vessel wall. These nerves can be gently elevated from the vessel wall and divided, perhaps giving further protection against vasospasm.

Summary of Methods Applied in the Current Series 1) Aneurysms with definable necks a) Clip directly coagulation and resection b) Temporary clip to parent vessel in case of large aneurysm, puncture of aneurysm, then final clip and removal of temporary clip. 2) Broad-based aneurysms a) Coagulation and clip b) Ligature and clip c) Temporary clip on the aneurysm, puncture to collapse the sac, better dissection of the surrounding area, better visualization of the perforators, coagulation, a second clip proximal to the first, removal of the first, coagulation stepwise, then final clip, removal of the second clip (staging technique) d) Temporary clip, resection, coagulation and/ or suture, then final clip. 3) Unclippable aneurysms a) Trapping b) Trapping with extra-intracranial anastomosis when collaterals not well developed, 4) "Baby" aneurysms a) Coagulation and cover with muscle or sponge fiber cemented by acrylic.

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4

Anesthesia for Microsurgical Procedures in Neurosurgery

Introduction Anesthesia for neurosurgery has been the subject of many monographs and reviews. The anesthetic techniques for microsurgical procedures as well as for neuroradiology are well documented in the literature, including those of Michenfelder et al. (1969/72), Gordon (1975), Smith and Wollmann (1972), Lassen (1976), Hunter (1975), and Shapiro (1975). Particularly helpful is Michenfelder's monograph (1975) "Anesthesia for intracranial surgery" in which one will find a summary of all the problems in neurosurgical anesthesia and how they might be handled, including intracranial pressure, ventilation, jdiuresis, cerebral metabolic rate, the anesthetics themselves etc. It must be noted that there are almost as many methods of anesthetizing patients for neurosurgical procedures as there anesthesiologists and that an experienced anesthesiologist will usually give better anesthesia with a method he knows than with a new one unfamiliar to him. Thus, looking back on our experiences over the years there were many different neuroanesthesiologists using a variety of methods with each benefitting those patients placed in that particular person's hands. In the sixties we used mainly methoxyflurane or ether, supplemented later with halothane and positive-negative pressure ventilation. The diuretic used at this time was urea. In the late sixties and early seventies we replaced urea with mannitol and introduced neuroleptanesthesia with fentanyl, haloperidol and nitrous oxide. Later haloperidol was replaced by droperidol, used in the ratio fentanyl: droperidol = 1:1. Then there was the time when we omitted completely the neuroleptic drugs, giving just fentanyl in a very high dosage. Up to 1974 we had performed hundreds of controlled hypotensive episodes using a 0.1% solution of trimetaphan (Arfonad) and since 1975 we have induced over 600 controlled hypotensive periods with sodium nitroprusside (Nipride).

This chapter will include descriptions of our method for anesthetizing patients for neurosurgical operations with neuroleptanesthesia, hyperventilating them, restricting infusions with balanced electrolyte-glucose solutions, supplementing neuroleptanesthesia with enthurane, and inducing hypotension artificially.

Anesthetic Principles and Pharmacological Considerations The principles for anesthesia in neurosurgery are the same as for general anesthesia. In all procedures N2O/O2(-endotracheal anesthesia) is used as a basic anesthesic. In addition we use initially the combination of fentanyl and droperidol although at times other i.v. narcotics as well as inhalation anesthetics are used. One has to be aware that some anesthetics are either potent cerebrovascular dilators or constrictors. As a rule of thumb it may be said that all volatile anesthetics are vasodilators while all intravenous anesthetics are vasoconstrictors, with one notable exception: ketamine, an i.v. narcotic is a potent cerebral vasodilator (Michenfelder 1975).

Anesthetic Principles and Pharmacological Considerations

On this basis one might believe that volatile anesthetics are contraindicated for neurosurgical anesthesia. However, hyperventilation alone when induced before the use of inhalation anesthesia can suppress the vasodilator effects of volatile anesthetics . For example, if a Pco, of 25 mm Hg (3.5 kPa) is achieved before halothane is used, then halothane will not induce vasodilatation. Michenfelder (1975) calls this phenomenon a physiologic competition between the vasodilating effect of halothane and the vasoconstricting effect of hypocarbia. For this reason we start anesthesia with a fair amount of barbiturate (3-5 mg pentothal per kg bodyweight), perform endotracheal intubation after relaxation with succinylcholine (1 mg/kg), initiate hyperventilation and then after 5 to 10 minutes begin halothane. In most cases though, our method of choice is neuroleptanesthesia combined with N2O/O2 hyperventilation and muscle relaxants. The term neuroleptanesthesia is derived from the use of the combination of a neuroleptic drug like Droperidol and a potent analgesic like Fentanyl or l^O. Fentanyl is a very potent but short acting analgesic. Since it causes marked respiratory depression, controlled mechanical ventilation is mandatory. Droperidol, a butyrophenone, is a neuroleptic drug that mildly sedates the patient and puts him in a state of dissociation from his surroundings. It is also a mild alpha-adrenergic blocker as well as an excellent antiemetic. Furthermore it helps the patient tolerate the endotracheal tube better and prevents him from coughing. A disadvantage of droperidol is that it may cause some undesirable extrapyramidal effects. Both fentanyl and droperidol drastically reduce CBF (Fitch et al 1969). As a muscle relaxant we use the nondepolarizing, steroidal muscle relaxant pancuronium, which produces no change in peripheral resistance but slightly increases the cardiac output (Kelman and Kennedy 1971). The depolarizing muscle relaxant suxamethonium is used only for emergency cases where the patients are assumed to have full stomachs and therefore rapid intubation is a question of survival. Suxamethonium acts very quickly and is the most useful agent to facilitate rapid intubation; however, due to fasciculations it produces a rise in blood pressure and thus an increase in intracranial pressure (Halldin and Wahlin 1959).

Preoperative Care The day before the operation the patient is seen by the anesthesiologist accompanied by the internist who examines the patient and takes his history.

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ECG, chest x-ray, differential blood picture, prothrombin time and electrolytes are checked carefully and if necessary corrective therapy is initiated. Antiepileptic drugs, antibiotics, and dexamethasone are prescribed prophylactically. The usual orders for an adult the day before the operation include: 1) A strict fluid restriction of 1000 cc/24 h. 2) Moderate activity restriction (allowed to use lavatory rather than bed-pan). 3) 100 mg of diphenylhydantoin every 8 hours orally. 4) 4 mg of dexamethasone every 6 hours i.m. 5) 1 gm of chloramphenicol every 6 hours orally.

Premedication A fully awake patient receives an appropriate dose of an oral sedative (0.5-1.5 mg flunitrazepam) the evening before the operation that provides a night free of anxiety. Pre-operative medication is given '/: hour prior to being brought to the OR. It consists of Innovar which is a combination of fentanyl and droperidol and atropine. While Innovar keeps the patient relaxed, atropine suppresses the vagal reflexes caused by the induction of anesthesia. The doses for an adult of about 70 kg bodyweight are: 1.5 ml Innovar (i.e. 0.02 ml pro kg bodyweight) and 0.75 mg atropine (i.e. 0.01 mg pro kg bodyweight) .

Induction of Anesthesia Since all our patients are at risk of developing increased intracranial pressure, induction is one of the most critical parts of anesthesia. Increases of intracranial pressure were found to be related to apprehension caused by the face mask, inadequate depth of anesthesia for laryngoscopy, incomplete muscle paralysis for intubation, and hypoxia and hypercapnia during laryngoscopy. Being aware of these factors, our present technique is to start anesthesia with 0.1 mg per kg bodyweight droperidol followed by a paralyzing dose of pancuronium (0.1 mg per kg bodyweight). Then we inject about 0.008 mg per kg bodyweight fentanyl followed by a sleeping dose of methohexital (about 0.5 to 1.0 mg per kg bodyweight). We introduce a face mask and assist ventilation with 100% of oxygen until the corneal reflexes disappear. At this moment controlled hyperventilation is initiated. When the patient is fully curarized, the intubation is performed with an armoured endotracheal tube and controlled hyperventilation is taken over by a

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4 Anesthesia for Microsurgical Procedures in Neurosurgery

respirator. Endexpiratory CO2 is monitored continuously throughout the procedure. Then the insertion into a peripheral vein of a 16 g needle is performed. A radial or a dorsalis pedis artery is canulated to monitor continuously arterial blood pressure using a pressure transducer. Through a cubital subclavian or jugular vein a 16 g catheter is inserted to allow the monitoring of central venous pressure. The correct position of the catheter is checked by a chest x-ray or by an intravascular ECG. Body temperature is monitored by a rectal thermistor if the length of operation is expected to exceed 2-3 hours, and diuresis is controlled by measuring urinary output. The ECG is monitored continuously.

Maintenance of Anesthesia Before the skin incision additional doses of fentanyl (about 0.006 mg per kg) and droperidol (about 0.07 mg per kg) are given to counteract painful stimuli which increase blood pressure. The patients are hyperventilated with N2O/O2 in a ratio of 3:1 or 2:1, which is reduced to 1:1 during controlled hypotension. The degree of hyperventilation is checked by blood gas samplings, corrected to the actual body temperature, which should indicate a high P0i (above 80 mm Hg) and a low PCOi (between 25 to 30 mm Hg). Therapy with dexamethasone, chloramphenicol and diphenylhydantoin is continued. Blood losses are replaced with plasma, packed expanders, such as dextran or gelatine, except in posterior fossa surgery, where a fall in blood pressure due to orthostatic reaction in the sitting position may be treated by volume substitution. When the use of controlled hypotension is contemplated the patients are normoventilated with an N2O/O2 ratio of 1:1 to avoid hypoxia since during prolonged hypotension the respiratory physiological dead space may increase to as much as 80% of the tidal volume (Eckenhoff et al 1963). In all craniotomies, the positioning of the patient is of utmost importance. The head must be elevated, in the supine position about 10°. This assists venous drainage and prevents TCP increase due to venous congestion. To prevent corneal abrasions we apply eye ointment and close the eyelids with tape. The whole body and the arms are wrapped in sheets to maintain core temperature and to prevent any injuries to peripheral nerves. To maintain anesthesia about 0.002 mg per kg of fentanyl is given in 30 minute intervals until the surgeon starts the closure of the dura. After the closure of the dura anesthesia is deepened with enflurane (0.4-0.6%) to avoid blood pressure increases due to painful stimuli caused by skin closure. The remaining

interval until the completion of the operation allows the patient to metabolize the narcotics. Thus, on the one hand we achieve a deeper depth of anesthesia for the skin sutures, while on the other hand we end up with a quickly reusable patient with minimal narcotic hang-over. This also provides a painless early postoperative period with sufficient spontaneous respiration. We try to avoid the use of antagonists such as nalor-phine or naloxone since they not only reverse respiratory depression but also analgesia resulting occasionally in an uncontrollable blood pressure elevation. We would rather continue artificial ventilation than use antagonists. However, when anti-narcotics have to be given, one should carefully titrate them (i.e. 1 mg nalorphine every 5 minutes) until the patient's respiration is adequate. For the final minutes of the operation the patient is ventilated with pure oxygen to prevent diffusion hypoxia. While the patient is still paralyzed, the trachea and pharynx are sucked out. Only after spontaneous respirations have occurred is the remaining effect of the nondepolarizing relaxants completely reversed with a mixture of atropine and prostigmine. The extubation is performed when the patient's respiration is adequate and his pharyngeal reflexes have returned to normal. In some cases of AVM we continue sedation, relaxation, and even deliberate hypotension for another one or two days, avoiding any blood pressure increase until the dangers of rebleeding and brain edema have become minimal.

Brain Relaxation A relaxed brain is essential for a non-traumatic procedure. Apart from a well chosen anesthetic technique brain relaxation is achieved through fluid removal from the three intracranial compart-ments. Cerebrospinal fluid drainage by lumbar puncture may prevent damage to the brain when drilling burr holes and facilitate retraction of the dura during drilling of the orbital roof and sphenoid wing. Cerebrospinal fluid drainage also helps to keep the operating field dry during dissection of the aneurysm. Occasionally, inspite of lumbar drainage relaxation of the brain occurs only after opening the basal cisterns. | The intraventricular compartment can be positively influenced with respect to relaxing the brain by: correct positioning of the head to promote venous outflow and hvperventilation, inducing cerebral vasoconstriction. The degree of hypocar-bia is monitored by serial blood gas analyses. About three years ago we abandoned routine diuretic therapy and we now limit fluid administration to 1000 cc glucose-electrolyte solution

Induced Hypotension (Aeguifusion, Hausmann) within the first 24 hours after the start of surgery. Fluid administration is gradually increased on the second or third postoperative day, depending on the blood levels of the urea and creatinine. The stabilizing effect of dexamethasone on the blood-brain barrier may be of benefit to the patient's postoperative recovery. Although no unequivocal difference in the patients treated with dexamethasone and those not receiving the drug has been established, patients undergoing aneurysm surgery are given 4 mg dexamethasone every six hours beginning one day prior to operation. The drug is slowly withdrawn after the second postoperative day, depending upon the condition of the patient.

Postoperative Care After surgery the patients are monitored in the neurosurgical intensive care unit. To avoid hypoxia we administer ajiurnidified 40% oxygen-air mixture by mask to all patients postoperatively. Po2, PCo2, pH, BE and O2-saturation of the arterial blood are checked regularly. Arterial blood pressure, temperature, central venous pressure and ECG are monitored continuously. Hypertension (greater than 140 systolic) is treated with hydrallazine, reserpine, clonidine, diazoxide or beta-adrenergic receptorblocking agents. The dexamethasone therapy is tapered off over 5-10 days, and chloramphenicol and diphenylhydantoin are continued for one day more. Fluid is restricted to approximatively 0.6 liter_5% glucose solution with 40 mg potassium chloride per m2 of body surface per 24 hours. Oral fluids are begun the morning after surgery, but the fluid restriction (1 liter per day) is continued postoperatively for 3—4 days. Should the patient become hypernatremic (Na > 145), larger amounts of oral fluids are prescribed accompanied by furosemide for salt diuresis. For analgesia we use pentazocine (30 mg i.m. every 4 hours) for adults. Pentazocine is a strong analgesic from the group of morphine antagonists but causes less respiratory depression than morphine. Ambulation and physiotherapy is started the first postoperative day, and as a result atelectasis and venous thrombosis are rarely seen. However, mobilization is delayed in those patients who have undergone early (days 1-7) surgery, particularly if there is any subjective complaint of dizziness or faintness on assuming the upright posture (see Vol. II). The patient's status is monitored continuously by the neurosurgeon, the internist and the anesthesiologist.

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Induced Hypotension Operative bleeding during microsurgical procedures is generally minimal, but occurs to varying degrees. The aim of lowering blood pressure during surgery is not only to reduce bleeding, but to avoid the rupture of coagulated aneurysms. A dry surgical field certainly improves the working condition for the surgeon and offers the patient a better chance for a good result, even though the techniques of induced hypotension are not without their inherent danger. During the last three decades different methods have been used to induce controlled hypotension. In 1946 Gardner produced hypotension , by blood letting / through an arteriotomy. In 1950 Enderby introduced the technique of ganglionic blockade to produce hypotension. Later, deep halothane anesthesia alone was used to induce hypotension. A list of the most commonly used drugs and their action to induce hypotension is as follows: Halothane, by vasodilatation combined with a variable degree of myocardial depression Trimetaphan, by ganglion blockade Sodium nitroprusside, by direct vasodilation of the vessels. There is a paucity of published data regarding the optimal degree of hypotension for neurosurgical patients. From our experience over the last 4 years (600 cases) of providing deliberate hypotension with sodium jiitroprusside we recommend that the mean arterial blood pressure not be lowered below 40 mm Hg in normotensive and not below twothirds of the preoperative value in hypertensive patients. Below a mean arterial blood pressure of 30 mm Hg Finnerty et al (1954) found signs of cerebral ischemia in normotensive individuals. Although we do not hesitate to lower arterial blood pressure drastically for a few minutes to support an essential step in the operation, we see no need for the routine use of profound hypotension. For this reason good communication between the anesthetist and surgeon is of particular importance.

Deliberate Hypotension Induced by Halothane Halothane may be a useful agent to lower blood pressure in neurosurgical procedures. However, one must be aware that halothane is a potent vasodilator and if a patient is not hyperventilated it may increase brain bulk and thus raise the intracranial pressure. Theoretically, one could lower blood pressure with halothane beyond the levels at which autoregulation is able to maintain cerebral blood flow thus decreasing brain bulk and improving

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4 Anesthesia for Microsurgical Procedures in Neurosurgery

operating conditions. However, one of the dose dependent effects of halothane besides a reduction in stroke volume and cardiac output is an increase in right atrial pressure (Prys Roberts et al 1974) thereby expanding the cerebral venous system and the brain bulk. Thus this procedure cannot be recommended without reservations.

Deliberate Hypotension Induced with Trimetaphan Ganglion blocking agents, such as trimetaphan, block sympathetic vasoconstriction, opening the peripheral vascular bed and thereby reducing blood pressure (Enderby 1950). Trimetaphan also relaxes capacitance vessels and blocks other sympathetic reflexes. Thus, cardiac output is slightly reduced. Trimetaphan inactivates the pupillary reflexes and may interfere with the postoperative neurological evaluation of the patient. At the University of Zurich up to 1974 we performed hundreds of controlled hypotensive episodes with trimetaphan (0.1% solution). The initial dose for an adult is about 3 mg per minute (i.e. 60 drops per minute), but to maintain hypotension the drip is reset to 1 mg per minute (i.e. 20 drops per minute). The combination of halothane and trimetaphan is particularly effective in achieving a desirable level of hypotension due to the suppression of vasomotor responses.

Induced Hypotension with Sodium Nitroprusside Sodium nitroprusside (SNP; Na2FeCN5 -NO • 2H2O) was first isolated in 1849 and its pharmacological effect was described in 1886 by Hermann. In 1929 Johnson differentiated its hypotensive action from its toxic action, which was regarded to be similar to sodium cyanide. Johnson's suggestions for the therapeutic application of the hypotensive effects of SNP remained unnoticed until 1950 when Page (1951) confirmed these findings and described the clinical use of SNP. In some centers SNP has been used to produce deliberate hypotension since 1962 (Tinker and Michenfelder 1976). SNP acts by direct vasodilation: it dilates the peripheral resistance vessels as well as the peripheral capacitance vessels, thereby pooling the blood and reducing not only the afterload but also the preload of the heart (Moraca et al 1962). Heart rate increases initially but returns slowly back to normal. Renal blood flow is maintained or increased, but coronary blood flow is reduced (Wang et al 1977). The potential toxicity of SNP is

now recognized and is the result of cyanide released from the nitroprusside molecule (Wang et al 1977). Cyanide is then converted to thiocyanate via the rhodanase system (Wiedemann 1976). For detecting the development of cyanide toxicity the best indicators are the pH and lactate levels as well as the levels of plasma cyanide and thiocyanate (Wiedemann 1976). SNP is supplied as a 50 mg lyophilized dry powder and it has to be dissolved with 5% glucose. Since it is sensitive to light it must be shielded with aluminium foil. To initiate hypotension with SNP Tinker and Michenfelder (1976) recommend titrating the dose between 0.5 to 1.5 meg per kg per minute. The total intraopera-tive dose should not exceed 3-3.5 mg per kg (Wiedemann 1976). Lawson et al (1976) showed that there is a relation between age, weight and required dose of SNP, and formulated a nomogram to easily estimate the quantity of SNP needed. From 1975-1978 we performed over 300 controlled hypotensions with SNP. In analyzing 138 cases we found the necessary amount of SNP averaged 2.44 + 1.1 SD meg per kg per minute. These findings agree with the data of Stoelting et al (1977) who found in his series a need for 2.4 + 1.1 meg per kg per minute SNP for profound hypotension. However, in another analysis of 153 cases we found 15 cases in which the demand for SNP was of 6.54 + 1.24 meg per kg per minute. To explain this we postulated that the phenomenon of tachyphylaxis probably occurred and from this data the incidence of tachyphylaxis might be as high as 10%. SNP is a very potent and fast acting antihyperten-sive drug. Since it produces hypotension by direct arteriolar vasodilation independent of the auton-omic nervous system (Schlant et al 1963) there is no available antidote. However, its duration of action is so short that it has to be administered by continous infusion, so its hypotensive effect is reversed merely by discontinuing the drip. It can be convenient to give a 0.01% solution at about 4 drops per minute, but in our department we use a 0.1% solution with a perfusor pump starting with 1 meg per kg per minute. At 30 minute intervals we check the blood gases to detect the occurrence of acidosis and to prevent hypoxia. In some cases of AVM we have induced profound hypotension with SNP for over 48 hours without any sign of cyanide intoxication or renal failure. However, in such cases it is advisable to check cyanide and thiocyanate levels routinely (the plasma cyanide should not exceed 300 n mol%) and, if necessary, to initiate therapy with hydroxy-cobalamine. Routinely, a second hypotensive agent (clonidine hydrochloride or dihydrallazin) is administered as

Anesthetic Management of Posterior Fossa Microsurgery in the Sitting Position

the SNP is being tapered to prevent a sudden reflex rise in blood pressure.

Hypothermia

277

Anesthetic Management of Posterior Fossa Microsurgery in the Sitting Position

(Aneurysms of the vertebral artery. PICA, vertebral junction, AICA) In our department the sitting position is used for all posterior fossa surgery, since it provides the best surgical access to the operation field and improves venous drainage (Albin et al 1976). Conversely, the sitting position can present the following dangerous complications: Postural hypotension (Michenfelder et al 1969; Michenfelder 1975; Hunter 1975; Albin et al 1976). Air embolism (Michenfelder et al 1969; Michenfelder 1975; Hunter 1975; Albin et al 1976; Michenfelder et al 1972). Cardiac arrhythmias (Michenfelder et al 1969; Michenfelder 1975; Hunter 1975; Albin et al 1976) Deterioration of the O? saturation by changes in the ventilation/perfusion ratio (Eckenhoff et al 1963). Faced with these problems anesthesiologists may fear the sitting position. However, according to the Vertebro-Basilar Aneurysms literature (Albin et al 1976, 180 cases) as well as to In surgery of vertebro-basilar aneurysms the ques- our own experience (over 500 cases, most of them tion arises as to the advantage of spontaneous tumors and AVM's) there is no increased mortality ventilation as a reliable monitor of brain stem associated with this position. The anesthesia for the function. Authors who have used this method sitting position is given according to the guidelines report alterations in cardiac rhythm, blood for microsurgical anesthesia already described in pressure and respiration as valuable warning sig- this chapter. One can minimize the complications nals of excessive manipulation in the region of the of the sitting position by taking additional measures: brain stem. Spontaneous breathing as an alternative to controlled ventilation is not used in our clinic because we give priority to optimal conditions for both Premedication patient and surgeon which we believe are offered by neurolept-anesthesia with moderate hyperven- To avoid pooling of the venous blood in the lower tilation. Problems which can arise in spontaneously extremities, the legs are wrapped with elastic breathing patients (coughing, respiratory efforts, bandages. Atropine sulfate (0.01 mg i.m.) is given hypoventilation etc.) do not occur. Therefore thirty minutes before the induction of anesthesia to anesthetic management in surgery of vertebro- prevent unwanted vago-mimetic responses as well basilar aneurysms is no different from that for as to increase heart rate in patients with intracranial pressure related bradycardia. In such patients other vascular lesions. the use of morphine or drugs with a morphine-like action must be totally avoided since they may cause a profound and persistent respiratory depression (Hunter 1975). The electrolyte status in these patients who may have repeated emesis with a related hypochloremic alkalosis should be closely monitored. Under hypothermic conditions the brain can safely tolerate the cessation of perfusion for a predictable time corresponding to the degree of cooling. Since the fifties this method has been applied with enthusiastic and disappointing results. Although its property of protecting the brain is beyond dispute its value in neurosurgery remains controversial. Indeed, there is little evidence that the outcome of surgery, which also depends on many other factors, has been improved by this method. We have had only limited experience with hypothermia (one basilar aneurysm and a few cases of arterio-venous malformation) and have never used the technique routinely. The technique is currently rarely employed. Moreover, constant advances in microsurgical techniques have developed to a degree that the use of hypothermia with its potential risks is not imperative.

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4 Anesthesia for Microsurgical Procedures in Neurosurgery

Cardiovascular and Respiratory Complications The upright position can seriously affect the cardiovascular status of the patient (Millar 1972; Martin 1970). The effect of gravity and the alphareceptor blocking effect of anesthetics (e.g. halothane, ethrane, droperidol etc.) produce a decrease in systemic blood pressure due to venous pooling. For this reason we wrap the legs with bandages. The pressure transducer for continuous intraarterial blood pressure measuring is mounted at the level of the head to accurately monitor the intracranial arterial pressure. Otherwise the pressure measured at the heart level must be reduced by 2 mm Hg for every inch of vertical height above the heart. To avoid hypoxia due to the reduced ventilation/perfusion ratio of the lungs in the upright position (Eckenhoff et al 1963), the patients are ventilated with 50% oxygen and nitrous oxide.

performed as an intraoperative functional test. The following cranial nerves can be examined in this manner: A) Vagus - Bradycardia, hypotension B) Trigeminal - Bradycardia, hypertension (sensory); Jaw jerk (motor) C) Facial - Twitch of face or platysma, salivation D) Accessory - Shoulder shrug.

Postoperative Care The postoperative treatment of patients who have had posterior fossa surgery does not differ from those who have had supratentorial surgery; however, the competency of the larynx must be carefully proved since its innervation may have been disturbed.

Monitoring and Air Embolism Routine monitoring consists of continous direct arterial and venous blood pressure recording, display of a standard ECG lead on an oscilloscope, intermittent arterial blood gas analysis, and continuous auscultation of the heart sounds ("jTullwheel" murmers in case of air embolism) with an ultrasonic device (Doppler) (Michenfelder et al 1972). The microphone of this device is placed over the right atrium. The tip of central venous catheter has to be precisely in the right atrium to allow the aspiration of air in case of embolism. The correct position of the catheter is controlled prior to the operation by a chest radiograph or by an intravascular ECG (Martin 1970; Hufnagel 1976). The frequency of air embolism can be as high as 25% (Albin et al 1976), but serious consequences can be minimized by early diagnosis and prompt treatment (Michenfelder et al 1972). Therefore adequate monitoring in the sitting position cannot be accomplished without a Doppler air bubble detector and a previously inserted right atrial catheter (Albin et al 1976).

Cranial Nerve Examination The use of the sitting position for posterior fossa surgery also enables the anesthesiologist to monitor the slightest surgical manipulation of certain cranial nerves such as the vagus, so as to prevent associated cardiac arrhythmias and inadvertent nerve injury (Giessen 1976). Similarly the stimulation of other nerves such as the facial can be

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Pathological Considerations

Epidemiology of Cerebral Aneurysms Incidence The incidence of cerebral aneurysms has been the subject of several large autopsy reports (McDonald and Korb 1939; Richardson and Hyland 1941; Housepian and Pool 1958; Jellinger 1977). In the general population the incidence of intracranial aneurysms is about 1 per cent which corresponds to their average frequency in large autopsy statistics (Heidrich 1972), although their incidence in various postmortem series ranges from 0.2-9 per cent (Jellinger 1979). More recent studies have tended to show an increasing incidence of cerebral aneurysms with the suggestion that a more careful examination of the cerebral arteries at autopsy has led to a greater number of aneurysms found. Stehbens (1963a) found an incidence of 5.6 per cent in his autopsy series. Evaluating 7,650 autopsies in patients over 10 years old, McCormick and Nofziger (1965) found 153 patients with aneurysms (2.0%), 127 ruptured and 26 unruptured. However in an addendum to their report, they noted that of 197 recent autopsies, 17 (8.6%) had cerebral aneurysms with only five of these ruptured. By inclusion of aneurysms less than 2 mm in diameter, Hassler (1961) found an incidence of 16 per cent ruptured and unruptured lesions. The clinical incidence of cerebral aneurysms is equally difficult to assess. Some large studies group all subarachnoid hemorrhage patients together when speaking of cerebral aneurysm, while others fail to consider unruptured aneurysms which may have presented through mass effect, intracerebral hemorrhage, or carotid artery - cavernous sinus fistula. The most accurate study of incidence of ruptured cerebral aneurysm is probably that of Pakarinen (1967) who related the confirmed cases of subarachnoid hemorrhage to the population of Helskini. He found an incidence of 15.7 per 100,000 per year. The incidence of subarachnoid

hemorrhage caused by verified aneurysm was 10.3 per 100,000 per year. In about 20 per cent of cases, a source of subarachnoid hemorrhage could not be found, and undoubtedly some of these cases had undisclosed ruptured aneurysms. Van der Werf (1972) reported the incidence of subarachnoid hemorrhage in the Netherlands to be 10 per 100,000 per year, and Rasmussen and associates (1980) found an incidence jrf_3_.4 patients per 100,000 per year admitted to neurosurgical departments in Denmark with verified ruptured cerebral aneurysm. An analysis of statistics from Switzerland for the past 13 years shows: From January, 1967, to July, 1979 the incidence of subarachnoid hemorrhage caused by operatively or postmortem verified aneurysms was 624/1.1 million population in the Canton of Zurich; 397 patients were admitted to the Neurosurgical Department of the University Hospital of Zurich, whereas 227 patients died before admission, either at home or at the district hospitals of the Canton of Zurich. The autopsy rate for all deaths in Zurich for this time period was about 40 per cent. Autopsies are not performed randomly, however, and it is not justifiable to extrapolate these figures toward 100 per cent population mortality statistic to calculate the total incidence of cerebral aneurysm in the population. For example, younger patients who died suddenly are likely to be routinely autopsied, while older patients who are found dead at home often do not come to autopsy. Government statistics show about 25 to 30 deaths per year in this older population group from subarachnoid hemorrhage, but another 140 deaths per year from intracerebral hemorrhage, less than half of which are associated with hypertension. Undoubtedly, some of this latter group represent ruptured cerebral aneurysms.

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5 Pathological Considerations

Classification Several types of aneurysm in the central nervous system (CNS) have been described. The traditional classification separates mycotic, luetic, arteriosclerotic and congenital forms. Krauland (1957) distinguished two major types on the basis of morphological description. As the etiology is still not clear, especially the relationship of congenital factors and acquired degenerative changes, it seems to us reasonable to follow this morphological classification with a slight modification. Type I. Saccular or berry aneurysms (99%) 1) Congenital form 2) Acquired degenerative changes a) unknown factors b) mycotic aneurysms, resulting from inflammatory and embolic lesions c) syphilitic aneurysms d) traumatic aneurysms e) dissecting aneurysms

95-98%

0.4-2.5% very rare < 1.0% very rare

II. Fusiform aneurysms (1%) (synonyms: arteriosclerotic aneurysms, sclerotic aneurysms, megadolicho-arteria, serpentine arteries) a) congenital factors b) arteriosclerosis c) a + b combined

Saccular Aneurysms This type accounts for 66-90 per cent of all aneurysms (Dandy 1944; Housepian and Pool 1958; Sugai and Shoji 1968), but 98 per cent in 1116 cases of Suzuki (1979) and 98 per cent in 1012 of our own cases. Size Saccular aneurysms may be divided into three, i.e. small, medium and large (Sugai and Shoji 1968), four (Freytag 1966; Gabor and Potondi 1967), five (Locksley 1966) and even six groups (Housepian and Pool 1958; McCormick and Acosta-Rua 1970). We distinguished in our material:

1) Baby aneurysms (discovered during operative dissections) 2) Small size 3) Medium size 4) Large size 5) Giant aneurysms

(<2mm) ( 2- 6mm) ( 6-15 mm) (15-25 mm) (25-60 mm)

The saccular aneurysm arises: (1001 cases) a) At the end-bifurcation of the main arteries; 632 cases (63.1%) carotid, basilar, MCA, ACA. b) Distal to the origin of larger branches from the main arteries; 240 cases (24.0%) ophthalmic, PcoA, AchoA, temporal arteries, pericallosal arteries, PICA, AICA, SCA. c) At the origin of small arterioles or perforators from the main arteries: 84 cases (8.4%) cavernous portion of the 1C A, inferior and medial wall of ICA, at the origin of premammillary artery from PcoA, at the origin of uncal artery from AchoA, at the origin of medial and lateral striate arteries (A^Mj), thalamoperforators (P1-P2), hyp-othalamic arteries (AcoA). d) At the origin of distal branches of ACA, MCA, PCA, PICA, AICA, SCA 45 cases (4.5%).

Appearance The neck of the saccular aneurysm may be small (1-3 mm) or large (4-10 mm) and well defined or not defined at all. The shape is variable. Uni-, bi- or multilobular configurations with and without single or multiple thin or thick walled bulging parts and even with well defined secondary aneurysms are seen. A false sac may be localized only in the fundus or dome of the aneurysm; or it can even start at the neck and present itself as a whole sac. Nevertheless this can and should be identified at the time of surgery. Although small aneurysms are generally thought to have thin walls and the larger aneurysms increasingly thicker walls, we have not infrequently found unusual varieties. Usually the neck of an aneurysm has a thicker wall than the fundus and dome, but here again there are also variations: 1) With a thin walled neck and a thick walled fundus, 2) With a thin walled neck and a thin walled fundus, 3) With a thick walled neck and a thick walled fundus,

Classification 4) With a thick walled neck and a thin walled fundus. These findings are sometimes even more complicated as the relative thickness of the wall can be variable over the entire aneurysm surface. Each aneurysm appears to have its own "structural dynamics" or "natural history of development" (Nystrom 1979).

II. Other Types of Cerebral Aneurysms Infectious (Mycotic) Aneurysms The term "mycotic aneurysm" was first used by Osier in 1885. Subsequently Stengel and Wolferth (1923) reported 217 cases, including their own, of aneurysms developing during bacterial infections. Among these 42 cases had intracranial aneurysms, and since that time at least 30 cases of mycotic aneurysms have been reported (Iwabuchi et al 1979, in Suzuki, p. 694). Prior to the antibiotic era, cerebral aneurysms secondary to infected emboli from the vegetations of endocarditis were not uncommon. At the beginning of the century, mycotic aneurysms were thought to account for about one-fourth of intracranial aneurysms. A clearer picture of the nature of saccular aneurysms developed in the next thirty years. A review of 1126 cases of intracranial aneurysm in 1939 (McDonald and Korb 1939) showed an incidence of 6% mycotic aneurysms. Following the introduction of treatment of subacute bacterial endocarditis, bacterial cerebral aneurysms have become quite rare. A more likely error in present-day diagnosis is the failure to consider an aneurysm to be of bacterial embolic origin. Infectious cerebral aneurysms differ from saccular aneurysms in being more frequently peripherally located. The presence of multiple peripheral aneurysms is highly suggestive of an embolic origin. < Bohmfalk et al (1978) reviewed existing reports of infectious cerebral aneurysms from 1954 to 1977 and added four cases of their own. In this time period, 82 documented and 13 suspected cases of bacterially caused cerebral aneurysm. 4 cases of fungal aneurysms, and 1 case of a phytotic aneurysm were reported. Of these 6 were related to meningitis, 6 to thrombophlebitis, 1 to cardiac myxoma, and the rest to valvular heart disease with endocarditis. Overall mortality was 46% with an 80% mortality for those whose aneurysms ruptured during the course of treatment. These authors recommended operative therapy for single peripheral aneurysms and those associated with mass lesions, and conservative antibiotic therapy

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for proximal and most multiple aneurysm cases. They emphasized the importance of sequential radiological investigation with angiography and computerized tomography. Bingham (1977) has also established guidelines for the treatment of infectious cerebral aneurysms. Two patients in the present series underwent operation for mycotic cerebral aneurysms. and a third patient died while under antibiotic treatment: K. B., a 43 year old man, was seen in 1972 with a history of rheumatic endocarditis at age 10. He developed symptoms of bacterial endocarditis in 1960 and suffered a subarachnoid hemorrhage. Angiography was not performed at that time. In Jan 72, he developed fever, chills, and a bleeding tendency, and a week later experienced sudden onset of a left hemiparesis and nuchal rigidity. He was receiving penicillin and streptomycin at the time. Mitral insufficiency was noted on examination. The patient became progressively more obtunded, and lumbar puncture revealed bloody spinal fluid. He was then transferred to our hospital. At the time of admission he was comatose, febrile, and demonstrated marked nuchal rigidity. Angiography showed an aneurysm of the right pericallosal artery, and suggested an associated intracerebral hematoma. He was taken to the operating room on 25 Jan 72, where the hematoma was removed and the aneurysm clipped. A smaller aneurysm on the left pericallosal artery was coagulated. The bone flap was not replaced. Postoperatively the patient remained semicomatose. He bled from the wound and the following day was returned to the operating room for evacuation of an epidural hematoma. His endocarditis was treated with cephalothin and streptomycin. Staphylococcus aureus was grown from the blood. For a week he remained unresponsive, and then gradually began to improve. He first spoke on 19 Feb 72. Despite a rather severe urinary tract infection, he continued to make good progress and was transferred to the medicine clinic on 14 Mar 72. In Jul 72 he returned for bone-flap replacement. At that time he complained only of an occasional seizure for which he was taking medication. The left hemiparesis had completely resolved. He was seen in the clinic in Jun 79 during which time he had returned to part-time work. In 1980 his general condition was good and he was working part time. He has had no further hemorrhage. C. R., an 18 year old girl with known congenital heart disease developed fever and polyarthralgia in Sep 76. She experienced a sudden severe headache which abated. In Oct 76. she was stepping from the bath and noted diminished vision on the right side, right-sided weakness and difficulty with speech. These symptoms disappeared over the following week. Angiography showed an aneurysm on a frontoopercular branch of the left middle cerebral artery, and computerized tomography demonstrated a frontal intracerebral hematoma. At the time of her referral to Zurich in Nov 77, she was alert with no speech difficulty, but still showed a mild right hemiparesis. Angiography was repeated and showed partial thrombosis of the aneurysm. At operation on 24

282

5 Pathological Considerations

A B Fig 224 A-B AP (A) and lateral (B) right carotid angiograms show a large anterior communicating aneurysm with spasm of the internal carotid artery and occlusion of the inferior trunk of the middle cerebral artery (arrow) in a patient with subarachnoid hemorrhage and endocarditis. Histology confirmed a mycotic aneurysm. Nov 76, the vessel was clipped and the aneurysm resected. The postoperative course was uneventful, and she was discharged to continue antibiotics for 2 to 3 months. Histological examination including electron microscopy showed a thinning of the elastica, but no sign of active inflammation. It was presumed from the history and location and gross appearance of the aneurysm that this represented a mycotic lesion. In 1980 she suffered a recurrent hemorrhage with severe right sided hemiparesis. The repeated angiography in another hospital showed another small aneurysm in a peripheral branch of the left MCA. M. F., a 25 year old student suffered rheumatic fever in 1954 and 1960. Seven years later aortic and mitral insufficiency and a septal defect where diagnosed. On 29 May 68 he developed an acute febrile state and 2 days later he showed general deterioration. In a septic coma he was admitted to hospital. The bacteriology revealed streptococcus and staphylococcus sepsis. After antibiotic therapy he first started to improve, but on 9 Jun 68 he had a sudden onset of left sided hemiplegia. The lumbar puncture showed bloody spinal fluid. Right sided angiography showed an occlusion of the right MCA and an aneurysm of the AcoA. Because of his poor general condition surgery dould not be performed. The patient died 3 weeks later. An autopsy showed embolic occlusion of the right MCA, a large intracerebral hematoma in the right frontal lobe and clot in the ventricular system. The ruptured aneurysm was on the right corner of the AcoA. Histological examination confirmed the diagnosis of a mycotic aneurysm (Fig 224A-B).

All of these patients had known valvular heart disease and presented with clinical symptomatology of bacterial endocarditis. However, the symptoms of subacute bacterial endocarditis may consist

only of lethargy and a low-grade lever, as often the disease may not be recognized as the etiology of an aneurysm. The peripheral location of these aneurysms makes the patients more prone to neurological deficit. All three patients presented with a hemiparesis. The third case is unusual with the coincident occurrence of occlusion of the right MCA and a ruptured aneurysm of the AcoA. Frazee et al (1980) reported on 13 mycotic aneurysms associated with bacterial endocarditis. They found an alarming incidence of aneurysm formation in patients with endocarditis (3%) and recommended frequent repeated angiography for endocarditis patients. Bacterial endocarditis associated with mycotic aneurysms has been rarely seen in Zurich, probably because patients with bacterial endocarditis receive earlier, effective medical treatment thereby preventing intracranial dissemination. Traumatic Aneurysms Aneurysms of the cerebral arteries may arise as the result of damage to the arterial wall from skull fractures, penetrating foreign bodies, or during angiography or surgical manipulation. For the most part these lesions represent "false" aneurysms, i.e., aneurysms formed by the recanaliza-tion of periarterial hematomas which have been created around lacerations in the arterial wall. In a few cases the arterial wall has remained intact although damaged, giving rise to a true aneurysm more like a typical saccular aneurysm. Johnson et al (1980) described an unusual case of a 12 year old

Classification

boy with a traumatic dissecting aneurysm of the MCA. Wortzman et al (1980) reported a rare case of a traumatic aneurysm in the posterior fossa and reviewed the literature. Traumatic aneurysms are found most often on the large basal arteries or on the middle meningeal arteries, although cases have been described involving the peripheral branches of the anterior and middle cerebral arteries. Delayed posttraumatic carotid-cavernous fistulae may have their origin from such a lesion. Asari and associates (1977) have reviewed 58 cases of traumatic peripheral aneurysms reported in the literature and have added two of their own cases. Peripheral traumatic aneurysms are seen mainly in the MCA distribution (58%) or in the anterior cerebral artery distribution (39%). Other aneurysms of the anterior choroidal, posterior cerebral, and superior cerebellar arteries have been reported. Traumatic aneurysms are diagnosed in patients with a history of severe head injury who angiographically demonstrate aneurysms arising at sites other than arterial bifurcations. The usual interval from injury to aneurysm rupture is 3 weeks. The overall mortality is 32 per cent in ruptured cases. Laun (1979) reported three of his own cases with traumatic aneurysm among his series of 450 aneurysms and collected 70 other cases from the literature. The aneurysms were located on the AcoA in 13 cases (18%), on the MCA in 29 cases (40%) and in a single case each on the AchoA, PCA and VA. Twenty patients had aneurysms of the middle meningeal arteries. Fourty-two patients had false while only three had true aneurysms. In only 15 cases (21%), and if iatrogenic aneurysms are excluded, in only 10 (13%) was a preoperative diagnosis established. The prognosis is unfavorable because of a difficult pre-operative diagnosis. The clinical course is characterized by unexpected rapid deterioration from rupture usually 2 or 3 weeks after the trauma. It seems that in such cases of acutely developing raised intracranial pressure, one should keep in mind the possibility of traumatic aneurysm and complement the preliminary diagnosis by computer tomography and angiographic investigation. Parkinson and West (1980) reported 11 of his own cases and found that there are a few more than 100 cases recorded in the world literature (73 references). Their conclusion is "because of the superficial location of these lesions, the operative mortality should be close to zero, and the overall mortality is that of the associated brain damage. Unfortunately, they are rarely recognized until their presence is heralded by delayed deterioration, at

283

which time the salvage rate is markedly decreased. Earlier recognition can only be accomplished by more frequent use of angiography following head injuries and/or more sophisticated scanning". In the years between 1967-1979. we observed two cases, in whom head trauma had occurred 6 days and 3 weeks before subarachnoid hemorrhage. The angiograms showed aneurysms of MCA and AcoA. After completion of the present series the following interesting case presented: B. M., a 28 year old female suffered on 4 May, 1980. a severe car accident as a rear seat passanger. She was comatose for 4 hours and presented at admission with no neurological deficit, but with complex fractures of mandibular and maxillary bones and a Le Fort III. The CT scan showed no suggestion of an aneurysm. Fixation of the fractures was performed. The patient regained consciousness and presented a normal neurostatus. Twelve days later she suffered acute deterioration with dilatation of the left pupil and right sided hemiparesis. The CT scan showed in addition to a large left frontal and an intraventricular hematoma. a hint of an aneurysm at the level of the left 1C A. Left sided carotid angiography confirmed the diagnosis of an inferior wall aneurysm of the left 1C A. Five hours later surgical exploration was performed and the hematomas in the left frontal lobe and in the intraven-tricular areas were totally removed and the aneurysm clipped; papaverine was applied to the basal arteries. The patient made a satisfactory recovery. She still has a mild hemiparesis and dysphasia (Fig 225A-F).

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5 Pathological Considerations

Fig 225 A-F A 28 year old woman with severe facial fractures following an auto accident had a normal CT scan (A). Ten days later, she suddenly lost consciousness and repeat CT scan showed a left frontal intracerebral hema-toma (B) and a large left carotid aneurysm (C). AP (D) and lateral (E) left carotid angiograms confirmed the presence of a carotid aneurysm and showed segmental spasm of the A 1 : M,, and internal carotid arteries, in addition to diffusion of contrast into the insular subarachnoid space from the leaking aneurysm (F). Following removal of the frontal hematoma at operation, the aneurysm ruptured; no clip-pable neck could be created, so the aneurysm was trapped as depicted. The patient survived and made a fairly good recovery (mild right sided hemiparesis remained).

I

Classification

285

aneurysm arises having no relation to the arterial forks with considerable sclerosis of the parental artery. In Suzuki's series (1979) eleven of 1116 aneurysm cases (1%) had sclerotic aneurysms: nine patients had a single saccular aneurysm, one patient had a single fusiform aneurysm, and one multiple aneurysm case had one fusiform and two saccular aneurysms. The age at the time of onset ranged from 32 to 60 years with an average of 53. There were seven male and four female cases. Two fusiform aneurysm of the basilar artery were seen and of the five saccular aneurysms one each was located on the ICA, on the VA, and on the PICA, with two on the MCA. Moseley and Holland (1979) reported five of their own cases of ectasia of the basilar artery, and reviewed 40 cases of the literature, which had reasonably full clinical details including confirmation of the diagnosis by vertebral angiography or autopsy. Thirty-one cases were male and nine female. The mean age of diagnosis was 59 years, only five patients being aged less than 50 years. They found "that CT scan examination yields in most cases a picture sufficiently characteristic as to render pneumography and vertebral angiography, which is not without risk in those patients, unnecessary for the diagnosis of a condition for which specific treatment is not available". The vertebrobasilar system is most commonly affected by the degenerative process (Bladin and Donnan 1963; Arteriosclerotic Ectatic Aneurysms Boeri and Passerini 1964; Jellinger 1977). However in approximately 80 per cent of cases, the internal The term "arteriosclerotic aneurysm" is used to carotid artery is found at angiography to be involved describe fusiform dilatation of a cerebral vessel in as well (Greitz and Hind-marsh 1974; Jellinger which the wall has undergone atheromatous degeneration. The first comprehensive discussion of 1979; Goldstein and Tibbs 1981). Fewer than 75 cases of cerebral arterial ectasia have been reported this entity was by Dandy in 1944, who encountered 11 cases of elongated and tortuous vascular arteries in the medical literature (Goldstein and Tibbs 1981). The majority of patients are more than 40 years old in the course of posterior fossa procedures. Such and are mildly or moderately hypertensive. Males serpentine dilatation of the vertebral-basilar or are affected somewhat more frequently than internal carotid arteries is a frequent occurrence in patients with severe atherosclerosis (Jellinger 1979). females in a ratio 3:2 (Boeri and Passerini 1964; Co\HN\\\e 1961-, GteVxz. and Uiisxedx \954y These lesions are usually classified as Intracavernous aneurysms occurring in hypertensive aX\\e,xos,ck.TOX\c avve.\K^K\s, a\X\vo\x%\v Vtve.^ ate TYOX women over the age of 40, may be either fusiform necessarily associated with senile ectasia or atherosclerosis of the vessel, e.g. Marfan syndrome, or, more often, saccular in shape associated with atherosclerosis (Jellinger 1979). megalodolichobasilaris or idiopathic medianecrosis. Atherosclerotic aneurysms accounted for about 50 per cent of the lesions in older statistics (McCormick and Acosta-Rua 1970) and are found in 8 to 16 per cent of Housepian and Pool (1958) and Jelliger's (1979) series. Ohara et al (1979) distinguished two types of arteriosclerotic aneurysms. One is the type where the trunk arteries, such as the basilar artery, themselves, swell to a fusiform shape (fusiform aneurysm). The other is the type where a saccular Dissecting Intracranial Aneurysm The cause of dissection has been ascribed to trauma, arteritis, congenital defects, or developmental abnormalities of the vessel wall (Stehbens 1972), e.g. focal absence and duplication of the internal elastica (Adelman et al 1974). Yonas and associates (1977, 1980) have reviewed the reported cases of dissecting intracranial aneu-rysm and have determined that patients so afflicted can be divided into two groups. In the first group, dissection takes place between the internal elastic layer and the media. These cases usually present with ischemic symptomatology. The etiology of these dissecting aneurysms may be congenital, traumatic, or inflammatory. In the second group, dissection is within the media or between the media and adventitia. In these cases, subarachnoid hemorrhage is more common. These cases appear to have hematoma formation in the wall independent of the lumen, and rupture of the vasa vasorum was postulated as the most probable etiology. The occurrence of dissecting aneurysms of the intracranial arteries in association with the Moya-Moya type of multiple progressive intracranial arterial occlusion (Adelman et al 1974) or with fibromuscu-lar dysplasia has also been noted (Pilz and Hartjes 1976).

286

5 Pathological Considerations

Table 16 Our cases of ectatic aneurysms

= 26

Related to our own observations this problem is more complex and it needs a more definite approach (Table 16). We have noted that: a) At surgery an aneurysm may occur in the presence of any degree of atherosclerosis from the slightest to the most severe. Thus the question arises as to what degree of sclerosis and ectasia is significant. b) Approximately 10 per cent of aneurysms present with mild to severe sclerosis of portions of the fundus or the entire sac. This is with or without sclerosis of the parent vessel and with or without the appearance of vaso vasorum on the sclerotic parts. Fifty cases from the present series had significant enough sclerosis throughout the sac to be classified in this group. c) The sclerotic aneurysms with serpentine ectasia are not only seen in older patients (over 40 years), but also in younger patients, and even in children. d) The sclerotic ectatic aneurysms occur not only in the trunk of the vertebral (2 cases), basilar (6 cases) and internal carotid arteries (4 cases), but also in their branches, i.e. PCA in P, segment (1 case), P2 segment (2 cases), MCA (3 cases), ACA (A,) (3 cases), AcoA (2 cases), A2 (2 cases). e) The clinical features of sclerotic ectatic aneurysms include: Cranial nerve dysfunction Pituitary dysfunction Ischemic symptoms (every degree and pattern) Aqueduct stenosis - hydrocephalus Pseudotumor symptoms. It should be noted that rupture, i.e. SAH, is rarely observed (Bladin and Donnan 1963; Goldstein and Tibbs 1981) (Figs 226-232).

Classification

287

Fig 226A-B AP (A) and lateral (B) right carotid angiograms demonstrating an unusual fusiform aneurysm (arrows) of the entire right A2 segment in a 62 year old hypertensive patient on anticoagulants who presented with coma and left hemiplegia. Partial occlusion of the right middle cerebral artery (B).

Fig 227A-B Fusiform aneurysm (arrow) of the anterior and middle cerebral arteries in a 25 year old patient (A). Eleven years later the patient suffered a stroke and repeat angiography revealed complete occlusion of the superior trunk of M2 with no change in the size of the aneurysm (arrow) (B).

288

5 Pathological Considerations

-J

Fig 228A-C Giant fusiform aneurysm of the anterior communicating artery (A) with no visualization from the right carotid angiogram (B) in a patient with chiasmal and psychoorganic syndromes. The right superior branch of the middle cerebral artery is also segmentally fusiform (arrow). At operation (C) this sclerotic and partially throm-bosed fusiform dilatation of the anterior communicating artery could be trapped and removed. The 43 year-old patient made an uneventful recovery.

Classification

Fig 229A-G CT scan in a 15 year old patient with progressive headaches and postural amaurotic seizures revealed a possible aneurysm at the base of the left frontal lobe (A). Bilateral carotid angiography (B and C) demonstrated a large fusiform aneurysm involving the distal A, anterior communicating, and A2 (D) segments of both anterior cerebral arteries.

289

D

290

5 Pathological Considerations

Fi g229E-G At surgery a calcified sclerotic fusiform lesion was trapped and resected (E). Repeat computerized tomography following an uneventful recovery showed no evidence of infarction (F and G), although right A,-A2 have been clipped and the hypothalamic arteries could not be identified.

Classification

Fig 230A-H A hyperdense, calcified lesion was found on CT scan (A) in the left Sylvian fissure of a 13 year old patient with recurrent headaches. Angiography (B and C) revealed a giant fusiform aneurysm along the middle of the M, segment. At operation the entire aneurysm (D) was trapped

291

292

5 Pathological Considerations L. ICA

Fig230E-H

and resected (E) and an EC-IC bypass (arrow) performed (F). The child made a good recovery without signs of infarction on repeat CT scan (G and H).

Classification

Fig 231A-E After visiting the dentist, a 20 year old patient developed a left hemisyndrome and on CT scan had a dense lesion in the right medial temporal area (A). AP (B) and lateral (C) vertebral angiograms showed a giant fusiform aneurysm of the P2 and P3 segments of the right posterior cerebral artery. Fig 231 D and E

293

294

5 Pathological Considerations Fig 231 D-E Carotid angiograms showed good collateral from the right distal middle cerebral artery to the distal posterior cerebral distribution, so no infarction was evident clinically or on post-operative CT scan (D and E) even though at surgery the P2 segment was clipped proximal to the aneurysm.

Fig 231 D

Fig 232A-D Vertebral angiography (A, B and C) revealed a large fusiform aneurysm of the left P2 segment in a 43 year old patient with progressive hemiparesis and dysphasia. At surgery a 5 cm sclerotic aneurysm (D) was resected and the patient's condition slowly improved.

Classification

Aneurysmal Enlargement McCormick (1971) has shown that while intracranial aneurysms are relatively common in adult life, they are rare in childhood. This of course suggests that aneurysms enlarge with time. Similarly, he has shown a definite relationship between the size of an aneurysm and its likelihood of rupture, implying in general that aneurysms grow with time. Kassell and Torner (1983) suggest that patients with incidental unruptured aneurysms greater than 5 mm in diameter should be considered for surgery. However, relatively little is known about the actual growth propensity of individually diagnosed aneurysms. Allcock and Conham (1976) reported on the growth of 82 aneurysms over a time period of a few days to 10 years. They found 17 per cent decreased in size, 15 per cent remained the same, while 69 per cent enlarged significantly (Winn et al 1977). No standard rate of growth could be ascribed to aneurysms from the available data as this varies tremendously between individual sacs. A few smaller aneurysms have been shown to greatly enlarge over a short period of time, while several intermediate lesions changed very little over many years. One can conclude at the present time that the growth potential of an individual aneurysm is unpredictable and as a result, no aneurysm regardless of size

295

can be considered safe from enlargement and rupture over any period of time. The relationship of infundibular widening to aneurysm formation remains obscure. Stuntz et al (1970), Yoshimoto and Suzuki (1974), Young et al (1971), Waga and Morikawa (1979), and others have demonstrated the enlargement of a posterior communicating artery infundibulum into a saccular aneurysm. Others believe that this condition is never pre-aneurysmal (Epstein et al 1970). Winn et al (1977) followed 364 patients for up to 21 years, who suffered a subarachnoid hemorrhage from an aneurysm either of the posterior communicating or anterior communicating artery and who were not surgically treated. In this series an increase in aneurysm size as judged by routine arteriography six months after initial hemorrhage did not correlate with rebleeding. However, an increase in the size of the aneurysms had occurred in all patients who were studied angiographically at the time of their late rebleeding. In the present series of patients, there are several documented instances of the temporal enlargement of both previously recognized and unrecognized aneurysms. A few cases are illustrated in Figs 233237.

Fig 233 A-D Progressive enlargement of an anterior communicating aneurysm (arrows) in a 31 year old female as seen in AP (A) and lateral (B) angiograms over a three year period (C and D).

296

5 Pathological Considerations

Fig 234 A-B Enlargement of an anterior communicating aneurysm (arrows) (A) over a four month period (B) heralded by the development of a chiasmal syndrome in a 40 year old man.

D Fig 235 A-D Progressive enlargement of a posterior communicating aneurysm (arrows) as seen on AP (A) and lateral (B) angiograms over a ten year period (C and D) in a 60 year old female.

Classification

297

Fig 236A-D This inferiorly directed basilar bifurcation aneurysm as seen on AP (A) and lateral (B) angiograms was explored following a subarachnoid hemorrhage but could only be wrapped with muscle. Two years later, after another hemorrhage, repeat angiography (C and D) showed enlargement of the aneurysm; it was again explored but again could not be clipped. The 19 year old patient died after a third hemorrhage 3 years later.

298

5 Pathological Considerations

Fig 237A—E The posterior communicating aneurysm (arrow) pictured in (A) ruptured and was uneventfully clipped in 1968. Ten years later the patient suffered another subarachnoid hemorrhage; vertebral angiography (B) demonstrated a basilar bifurcation aneurysm (arrow) that was not visible on the prior examination (arrow) (C). Another aneurysm had also developed on the left middle cerebral artery M, segment (arrow) (D). A plain skull film (E) following a second operation shows three aneurysm clips each in the position of a previous aneurysm, all placed from a right pterional approach.

продолжение

Distribution продолжение

Distribution

Table 17 Incidence of aneurysms

at given locations No. of cases

Location of Cerebral aneurysms

%

The frequency of symptomatic aneurysms at various locations on the cerebral arteries in the present series is shown in Table 17. The most common location for aneurysms was the anterior communicating artery followed by the internal carotid artery at the origin of the posterior communicating artery and the bifurcation of the middle cerebral artery. These numbers generally agree with those of the Cooperative Study of Locksley (1966) and Suzuki (1979), while population studies including autopsy material such as that of Pakarinen (1967), tend to show a higher frequency of middle cerebral aneurysms. This may suggest a higher mortality or perhaps less accurate diagnoses with regard to aneurysms located on the middle cerebral artery. Despite the suggestion by autopsy and radiological investigations that 15 to 20 per cent of aneurysms are found on the posterior circulation, none of the large clinical series except Drake s (1979) have shown an incidence of ruptured posterior circula-

Internal carotid artery

| 319 .

Intracavernous Medial wall:

13

1.3

Ophthalmic Distal Superior wall Inferior wall Lateral wall: Post. comm. artery Ant. chor. artery Bifurcation Middle cerebral artery

33 2 1 21

3.3 0.2 0.1 2.1

173 21 55 184

17.1 2.1

Proximal (M,) Bifurcation Distal

Anterior cerebral artery

22 152 10 | 412|

2.2 15.0 0.98 40.7

Proximal (A,) Ant comm artery Pericallosal artery

14 375 23

1.4

tion aneurysm greater than 10 per cent.

Basilary artery Bifurcation SCA and PCA Mid-basilar trunk Mid-basilar fusiform Post, cerebral Interpeduncular (P,) Ambient (P,/2) P2 P3 (distal) Superior cerebellar art. (distal)

| 79 | 50 5 3 5

7.8

0.5 0.3 0.3 0.3 0.2 1.8

Laterality Laterlization of aneurysms in the present series is presented in Table 18. Aneurysms on the internal carotid and middle cerebral arteries are slightly more common on the right side, while aneurysms of the anterior communicating artery arise more frequently from the left side.

31.5

5.4 18.2

37.1 2.3 4.9 0.5 03 0.5

Age

Vertebral artery

5 3 3 3 2 | 18

In the present series, the peak age for presentation

PICA origin PICA distal

10 5

0.98 0.5

of a ruptured intracranial aneurysm is 46 years with 68 per cent of the patients under age 50 (Table 19). This represents a slightly younger group than that reported by the Cooperative Study where the peak age was closer to 52. Aneurysms at different locations varied considerably with respect to the most common age of presentation (Table 20). Aneurysms of the anterior communicating, middle cerebral, and internal carotid-posterior communicating arteries were most common between the ages 40 to 60, while 40 per cent of aneurysms of the posterior cerebral artery and 59 per cent of aneurysms of the internal carotid artery bifurcation, were found in patients under 30 vears old. Aneurysms occurring in childhood are discussed in Vol. II, Chapter 1.

Vertebral trunk Fusiform

2 1

0.2 0.1

1012

.

299

300

5 Pathological Considerations

Table 18 Lateralization of 1 0 1 2 symptomatic aneurysms Total No. Cavernous

6

Ophthalmic Medial wall Superior wall Inferior wall P.co. Ant. chor. Bifurcation

14

M.c.

A, 13

7 (42.4%)

1

19 148

14

171

(46.4%)

73 11 29

(53.6%)

477

Sex

(47.1%)

33 2 1

7

21

100

(57.8%)

173

(52.7%)

10 26

(47.3%)

21 55

92

(50%)

10

(71.4%)

197

Ba.Bi. Ba.Br. 8 PICA origin PICA distal

(57.6%)

2 -

(42.2%)

92

(52.5%)

9 (42.8%) Ba-Trunk 4 ' Vertebr. Trunk 1 3

(28.6%) (43.5%) (27.7%)

12 622

50 (57.2%) (55.6%)

74 50

(50%)

104

.. Pericallosal 4 10 (19.7%)

(56.5%)

A.co.

13

184

14 23 376 21 8 10 35

(44.4%)

132

Women accounted for 53.5 per cent of cases in the present series. This is compared to 59 per cent in the Cooperative Study (Locksley 1966), 60.0% in the Danish series (Rasmussen et al 1980) and 60.3% in Pakarinen's series (1967). There is a general trend for the incidence to increase in women with increasing age (Table 21). Distribution between the sexes also varied significantly in relation to the location of the aneurysm (Table 22). Especially noteworthy is the clear predominance in male patients presenting with anterior communicating artery aneurysms, and in female patients presenting with aneurysms located on the proximal portion of the intracranial internal carotid artery. Children most commonly present with aneurysms on the carotid bifurcation and vertebro-basilar arteries (Table 23).

(13.1%)

403

(39.8%)

1012

Table 19 Age of occurrence of 1012 aneurysms

Age

Cases

0-1 0 years 4 11 - 0.4% 3.7% 11.1% 21 .0% 32.0% 20 years 37 2 1-30 690/1012 = 68.2% years 112 31 -40 years 213 41-50 years 324 51-60 years 61-70 years > years

234 23.1% 8.2% 0.5% 83 70 31.8% 5

322/1012 =

Distribution

301

Multiplicity McKissock and associates (1964) showed that one in every five to six patients with a cerebral aneu-rysm will have one or more additional aneurysms. In the Cooperative Study (Locksley 1966) multiplicity ranged from 18.5 per cent in cases diagnosed by angiography to 22 per cent of cases seen at autopsy. Of these patients, 3.5 per cent had three aneurysms and 1.4 per cent had four or more aneurysms. The distribution of 449 double aneurysms showed 21 per cent to be ipsilateral, 47 per cent contralateral, 29 per cent midline plus one side, and 3 per cent both midline. Suzuki and Yoshimoto (1979) reported that the incidence of multiple aneurysms in a clinical study was 166 of 1080 saccular aneurysm cases (15.4%) and 17 of 34 necropsy cases (50%). Only multiple aneurysms of more than 1 mm in diameter were considered for the necropsy study. In the present series, multiple aneurysms were present in 243 patients (24.0 per cent) of cases with 451 aneurysms 3 mm or larger and 169 aneurysms 2 mm or smaller. The total number of aneurysms was 1389 in 1012 patients (Table 24a-b). Multiplicity was found most commonly with internal carotid ophthalmic, anterior choroidal, and pericallosal artery aneurysms and concurrently these were often symmetrical. Anterior communicating artery aneurysms were associated with other aneurysms in only 12 per cent of cases. Multiplicity was not seen with basilar artery trunk aneurysms or aneurysms arising from the inferior wall of the internal carotid artery (see Vol. II, Chapter?).

302

5 Pathological Considerations

Table 21 Sex difference in aneurysm occurrence

Age

Male

Female

Cases

0-10 years

25 %

75 %

4

11 -20 years 21-30 years 31-40 years 41-50 years 51-60 years 61-70 years 70 > years

62.2% 50.9% 48.8% 49.7% 42.7% 30.1% 0 %

37.8% 49.1% 51.2% 50.3% 57.3% 69.9% 100 %

% 0.4

37

3.7

112 213 324 234 83 5

11.1 21.0 32.0 23.1 8.2 0.5

Table 22 Sex difference with respect to aneurysm location (more than 10 cases)

Location Post cerebral A. co. Pericallosal I.C.A. Bi I.C.A. inf.

Male -

Female

Total

i 19 (65.5%) 231 (61.6%)

10 (34.5%) 1 4 4 (38.4%)

29 (2.9%) 375 (37.1%)

14 (60.9%)

9 (39.1%)

23

(2.3%)

31 (56.4%)

24 (43.6%)

55

(5.4%)

11 (52.3%)

10 (47.6%)

21

(2.1%)

A. chor.

10 (47.6%)

11 (52.4%)

21

(2.1%)

Ba.Bi.

22 (44.0%)

28 (56.0%)

50

(4.9%)

M.c.

71 (38.6%)

1 1 3 (61.4%)

184 (18.2%)

Cavernous Vertebral P.co. A, Ophthal.

5 (38.5%)

8 (61.5%)

13

(1.3%)

6 (33.3%)

12 (66.7%)

18

(1.8%)

46 (26.6%)

127 (73.4%)

173 ( 1 7 . 1 % )

2 (14.3%)

12 (85.7%)

14

(1.4%)

33

(3.3%)

3

(9.1%)

i

30 (90.9%)

r

1009 + 3 single cases (medial and superior wall of ICA) Table 23 Age ranges for various aneurysm locations Med. Age Sex Ca Oph Wall

Inf

P.c.

A.cho

Ca. Bi

M.c

Youngest

Fern.

33

29

27

50

9

26

9

Youngest

Male

18

38

-

41

25

25

Eldest

Fem.

50

71

64

70

72

Eldest

Male

57

42

-

64

64

A.co

Ba

V

17

5

15

10

20

13

14

61

53

73

69

61

64

64

63

56

50

Distribution Table 24a Multiplicity Site of aneurysms Total No.

Single

Multiple

1

2

Additi nal

urysm

o3

ane 4 s 5

6

8

Intracavernous

13

11

2

2

-

-

-

-

-

-

Ophthalmic

33

17

16

11

4

1

-

-

-

-

Medial wall Superior wall

2

2

-

-

-

-

-

-

-

-

-

-

1

-

-

1

-

-

Inferior wall

21

20

1

1

-

-

-

-

-

PcoA

173

122

51

28

14

2

4

-

2

1

AchA

21

10

11

9

1

1

-

-

-

-

ICA-Bi

55

37

18

11

5

2

-

-

-

-

MCA

184

125

59

41

6

6

5

-

14

11

3

1

2

-

-

1 -

-

A,

-

-

AcoA

375

330

45

35

6

2

2

-

-

PcA

23

11

12

10

2

-

-

-

-

-

Ba-Bi

50

32

18

11

5

1

1

-

-

-

Ba-Br

29

26

3

2

1

-

-

-

3

3

-

-

-

-

-

-

-

VA

-

-

PICA origin

10

8

2

2

-

-

-

-

-

-

PICA distal

5

3

2

1

1

-

-

-

-

-

1012

769 (76%)

243 (24%)

165

47

15

12

1 0.1 2 0.2 1 0.1

16.3 67.9

4.6 19.3

1.5 6.2

1.2 4.9

0.4

Symptomatic aneurysms ...... . f Macro aneurysms Additional 4 ... [ Micro aneurysms

0.8

0.4

303

% of 1 0 1 2 cases

% of 243 cases

1 0 1 2 208 16 9

1389

Table 24b Multiplicity of aneurysms at given locations in

Bilateral

order of descending frequency AchoA

11/21

52.4%

1/21

4.8%

Pe Oph PICA distal Ba-Bi ICA Bi MCA PcoA

12/23 16/33 2/5 18/50 18/55 59/184 51/173 3/ 14 2/10 2/13 1/21 45/375 3/21

52.2%

10/23

43.5%

48.5%

6/33

18.2%

40.0% 36.0%

2/5 -

40.0% -

32.7%

3/55

5.4%

32.1%

8/184

4.3%

29.5%

3/173

1 .7%

21 .4%

0/14

20.0%

0/10

15.4% 4.8%

2/13 0/21

15.4%

12.0%

8/375

2.1%

14.3%

0/29

243/ 1012

= 24.0%

A,

PICA orig. Intracavernous ICA inferior AcoA Ba trunk and branches

304

5 Pathological Considerations

Familial Occurrence of Cerebral Aneurysms Occurrence with a Described Hereditary Syndrome Poly cystic kidney disease. The association of cerebral aneurysms with polycystic disease was recognized by Dunger (1904) following the report of a case by Borelius (1901). Forster and Alpers (1943) described a case of cerebral aneurysms and polycystic kidneys in a young child, lending support to a congenital basis for both lesions. Dalgaard (1957) in a comprehensive analysis of 284 patients with polycystic kidney disease, was able to draw a statistically significant correlation between this disease and the presence of cerebral aneurysms. He warned, however, that increased interest in such a correlation might have resulted in a more careful pathological search for cerebral aneurysms. He also noted that a history of hypertension was common at the time that cerebral aneurysms were diagnosed. Ditlefsen and Tonjum (1960) reported on a family of 99 members of whom 15 had recognized polycystic disease. Six of these had died from cerebral hemorrhage, 3 probably from ruptured cerebral aneurysms. Sahs (1950) found the incidence of polycystic kidneys in aneurysm patients to be 2.7 per cent and Stehbens (1972) 0.9 per cent. Wakabayashi et al (1983) found 7 cases of unruptured aneurysm in 17 patients with polycystic kidney disease including 5 with no evidence of hypertension. They recommend early investigation (and treatment) to exclude aneurysms in patients with polycystic disease although Levey et al (1983) suggested that prophylactic investigation was rarely indicated. Three patients in the present series, all women (0.3 per cent) had associated polycystic kidney disease which had been discovered by intentional investigation. No routine pyelography was performed, so the correct number of cases cannot be given.

contemporary cases of combined coarctation and cerebral aneurysm including one of his own. He noted that these patients usually had hypertrophy of the left ventricle consistent with chronic hyper tension. Four male patients in the present series had coarctation of the aorta all were between 20 and 30. , *

Ehlers-Danlos Syndrome This syndrome is an autosomal dominant disease characterized by hyperextensibility of the joints and easy bruising of the skin. Rubinstein and Cohen (1964) reported the case of a left internal carotid aneurysm in a female patient with Ehlers-Danlos syndrome, and suggested that the disorganized collagen matrix within the vessel wall may have contributed to aneurysm formation. Imahori and colleagues (1969) presented a case of a woman with Ehlers-Danlos syndrome in which arterial findings predominated. In addition to multiple lesions of the peripheral arteries, two anterior •communicating artery aneurysms and a vertebral artery aneurysm were present. These were his-tologically similar to the usual saccular cerebral aneurysm. Tridon and associates (1969) described a case of Ehlers-Danlos syndrome with a right middle cerebral artery aneurysm and a cerebral arteriovenous malformation, and Bannerman and colleagues (1970) presented cerebral aneurysms in two sisters with Ehlers-Danlos syndrome.

Pseudoxanthoma Elasticum Scheie and Hogan (1957) described 10 patients with this autosomal dominant or recessive disorder who exhibited generalized arterial abnormalities, especially in the lower extremities. One of these patients had an intracranial aneurysm. Considering the widespread disturbance of elastic tissue formation in this disorder, it is perhaps surprising that intracranial aneurysms have not been found more often.

Coarctation of the Aorta

Friedreich's Ataxia

Reifenstein and associates (1947) analysed 104 cases of death in patients with coarctation of the aorta. Five of these patients had suffered a fatal cerebral aneurysm rupture. In two others, subarachnoid hemorrhage was present, but a ruptured aneurysm could not be found. An unruptured aneurysm was present in one of these cases. Two patients who did not have an autopsy performed were thought to have died from cerebral hemorrhage. Wright (1949) reviewed the above 104 cases, 200 cases described by Abbott (1928) and several

Brisman and Abbassioun (1971) presented three pairs of family members with cerebral aneurysms. One pair suffered from Friedreich's ataxia. The known abnormalities of the aorta and heart were noted by the authors.

Hypertension Hypertension occurs in about 18 per cent of the population, and its genetic basis gains evidence from a high concordance rate in twins and its

Occurrence Without a Described Hereditary Syndrome familial and ethnic incidence (Fox and Robins 1978). Stehbens (1954) examined 156 cases at autopsy who were noted to have cerebral aneurysms, ruptured and unruptured. Eighty-nine of these (57%) were considered to have had preexisting hypertension. Left ventricular hypertrophy was present in 77 cases, and in the other 12 at least two of the following factors were present: cardiomeg-aly, chronic renal disease, or a known premortem blood "pressure greater than 150/90. In a similar study, Wilson and associates (1954) found that 27 of 40 patients under 40 years old (68%) with cerebral aneurysms at autopsy had cardiomegaly, usually left ventricular hypertrophy. The association of cerebral aneurysm and systemic hypertension has recently been questioned by McCormick and Schmalstieg (1977) who found no increase in hypertension in 250 cerebral aneurysm patients over age and sex matched controls. This opinion was also supported by Franks (1978). In the present series, 195 patients were considered to be hypertensive showing sustained blood pressure greater than 160/95.158 were known hypertensives under treatment, and the other 37 diagnosed following admission. A recent Swiss screening program had shown an incidence of hypertension of 18 per cent in the general population. The conclusion from this series of patients is that the incidence of hypertension is not increased in patients presenting with a ruptured cerebral aneurysm.

Fibromuscular Dysplasia First described in the renal arteries, fibromuscular dysplasia has been reported in most of the larger arteries of the body (Wylie et al 1966). An increased incidence of cerebral aneurysms was recognized in association with renal artery fibromuscular dysplasia, but it remained uncertain as to whether this was secondary to a primary arterial defect or to the hypertension associated with renal disease (Belber and Hoffman 1968). In a comprehensive report analysing 70 cases of cervical and cranial fibromuscular dysplasia, Manelfe and associates (1974) found intracranial aneurysms in 39% of cases. Twenty-two patients (31%) of the total series had hypertension, but the relationship of hypertension to cerebral aneurysm was not given. Even for severe hypertension, however, this would represent an extremely high incidence of cerebral aneurysm. It is not known whether fibromuscular dysplasia represents a familial disease. Bolander et al (1978) reported an infant (11 months old) with fibromuscular hyperplasia of the renal arteries and an aneurysm of the anterior communicating artery.

305

Occurrence Without a Described Hereditary Syndrome Evidence of a familial basis for cerebral aneurysms without an associated known hereditary disorder comes from scattered reports of the occurrence of aneurysms in more than one member of a family. Two sets of twins were reported to have probably each died from subarachnoid hemorrhage, but autopsy proof of aneurysms was lacking in both reports (O'Brien 1942; Jokl and Wolffe 1954). Chambers and colleagues (1954) reported the occurrence of aneurysms in a father and son, and Ulrich and Sugar (1960) presented findings in four families where more than one family member had ruptured intracranial aneurysm. Graf (1966) reported on two sets of siblings who had ruptured aneurysms at identical locations. Kak and associates (1970) reported two sets of brothers who had sustained ruptured intracranial aneurysms. We operated on a patient with a ruptured aneurysm of the anterior communicating artery and his brother died some months later from a ruptured aneurysm of the anterior communicating artery. In another case a patient had a ruptured aneurysm of the anterior communicating artery and an incidental anterior choroidal artery aneurysm. His sister, a medical doctor, performed"4 vessel angiography on his twinbrother but could demonstrate no anomalies. Thierry and colleagues (1971) described two sisters with ruptured aneurysms and reviewed those cases where a genetic factor might be implicated. AcostaRua (1978) presented 6 families where two members had suffered ruptured aneurysms, in 3 of whom the aneurysms were at the same location. Hashimoto (1977) reported a consanguineous family in which four members suffered subarachnoid hemorrhage from ruptured aneurysm, and in which asymptomatic aneurysms were found in two additional family members. He subjected the family of patients to chromosome analysis and no abnormalities were found. The family described by Patrick and Appleby (1983) with aneurysms, cerebral hemorrhages and cortical blindness, is quite remarkable. In the present series. 85 patients (8.4%) could give a history of some family member suffering a "stroke". Of these. 39 (3.8%) knew of a family member with subarachnoid hemorrhage, and 15 (1.4%) of these had confirmation of ruptured cerebral aneurysm either at operation or autopsy. Therefore the incidence of relatives with ruptured cerebral aneurysm is about 1.5 per cent in our

306

5 Pathological Considerations

cases, a figure compatible with the usual incidence of cerebral aneurysm in the population, but somewhat higher than that expected for ruptured cerebral aneurysm. These figures suggest some family tendency to cerebral aneurysm rupture, but do not demonstrate a definite genetic basis for aneurysm formation.

Associated Vascular Anomalies Developmental Abnormalities Inequalities and Anomalies of the Circle of Willis The frequent anomalous configurations of the circle of Willis have been related to cerebral aneurysms in several studies (Riggs and Rupp 1943; Padget 1944; Riggs and Rupp 1963; Kirgis et al 1966; Krayenbuhl and Ya§argil 1968). Inequalities within the circle of Willis are so common even without the presence of an aneurysm, however, that the relevance of these configurations to cerebral aneurysm formation has been questioned (Stehbens 1963). In the present series of patients, considerable attention has been paid to anomalous arterial constructions, and these are presented in detail in Chapter 1. In general, aneurysms are found at areas of increased flow, for example on the side of the anterior communicating artery which receives the larger anterior cerebral artery, in association with a "fetal type" posterior communicating artery, or toward the side of the larger trunk at the middle cerebral or basilar artery bifurcation. However, aneurysms are not invariably seen in these instances, so simple flow dynamics do not seem to explain all cerebral aneurysm formation. In the early stages of the human embryo, some anastomoses between the carotid and basilar circulatory system occur. These channels are the primitive trigeminal, otic, hypoglossal, proatlantal intersegmental and cervical intersegmental arteries which when persistent may be also combined with the occurrence of intracranial aneurysms and AVMs. Persistent Carotid-Basilar Anastomoses Persistent trigeminal artery. Persistent trigeminal artery has been noted in about 3 cases per 1000 at angiography and autopsy and 134 cases of persistent trigeminal artery reported previously in 1964 (Woflschlaeger and Wollschlaeger 1964). An aneurysm of a persistent trigeminal artery was first mentioned by Davis in 1956. Eggers et al

(1982) reported two cases of asymptomatic aneurysms of a primitive trigeminal artery and found nine cases in the literature. Wolpert (1966) presented 3 cases of persistent trigeminal artery associated with cerebral aneurysm, one of which was on the trigeminal artery itself. George and associates (1971) reviewed their 19 cases and the angiographic studies previously reported, and concluded that in the presence of a persistent trigeminal artery, the incidence of cerebral aneurysm was about 14%. Including their own case, four aneurysms arising from the trigeminal artery or its junction with the internal carotid or basilar arteries had been noted. Sugar (1951) suggested that intracavernous aneurysms and spontaneous carotid-cavernous fistulae might arise from aneurysms located at the embryonic origin of the trigeminal artery. Enomoto and colleagues (1977) have observed a case of a large aneurysm of the trigeminal artery which ruptured to form a carotid-cavernous fistula. It has been pointed out by Krayenbuhl and Ya§argil (1968), however, that the origin of the trigeminal artery is generally below the cavernous sinus, and subarachnoid hemorrhage is the more common presentation of trigeminal aneurysm rupture (see Figs 238, 239A-B). Morrison and colleagues (1974) presented a case of aneurysm on the trigeminal artery which they could treat by operation and Eggers et al (1982) reported 2 cases of unruptured aneurysms of a persistent trigeminal artery. Persistent Hypoglossal Artery Drake (1968) encountered one aneurysm at the junction of the basilar artery and a persistent hypoglossal artery. Huber and Rivoir (1974) reported an aneurysm on a persistent left hypoglossal artery. Springer and associates (1974) reported a superior cerebellar artery aneurysm in a patient with a persistent hypoglossal artery, and Kodama et al (1976) presented two cases of persistent hypoglossal artery in which there was an anterior communicating artery aneurysm in one and an aneurysm arising from the embryonic artery in the other. Kodama et al (1979) reported 8 cases from the literature. In five of these cases the aneurysm arose from the persistent hypoglossal artery itself, in three cases from the ICA, in one case from the SCA. Only three of the five originating from the persistent hypoglossal artery itself were treated surgically (Udvarhelyi et al 1963; Drake 1969; Kodama etal 1979). Persistent otic artery. No case of aneurysm has been reported with this rare anomaly.

Associated Vascular Anomalies

307

Proatlantal Intersegmental Artery Tsukamoto et al (1981) reported a unique case of proatlantal segmental artery with absence of bilateral vertebral arteries and a ruptured aneurysm of the anterior communicating artery. The aneurysm was successfully clipped. Tsukamoto et al (1981) reviewed the literature and found only 9 reports with persistent proatlantal intersegmental artery, but there were no other cases coincident with aneurysms.

Fig 238 A posterior communicating aneurysm (black arrow) is seen in a patient with a persistent trigeminal artery (white arrow).

Agenesis and Aplasia of the Internal Carotid Artery (See Chapter 1, Anatomy, p. 57) Lie (1968) defined "agenesis" of the ICA as a total absence of the entire length of the artery and used the term "aplasia", when a vestige or a portion of the ICA remained, such as the carotid siphon. These anomalies concerning one or both carotid arteries have been described with or without the coincidence of symptomatic or incidental cerebral aneurysms. Lagarde et al (1957) reported a case of aplasia of the ICA above the PcoA in a patient with an AcoA aneurysm. Burmester and Slender (1961) reported two cases and Moyes (1969) one case of aneurysm and aplasia of ICA, and Lie (1968) showed an example in his book on carotid artery anomalies. Huber (1980) reported a case of an intracranial transverse carotid anastomosis, with

Fig 239A-B An anterior communicating aneurysm (arrow) is demonstrated in a patient whose entire anterior circulation is filled after injection of the right common carotid artery without contralateral compression (A). The left carotid angiogram (B) reveals a large persistent trigeminal artery (arrow) with filling of the vertebro-basilar system almost exclusively.

308

5 Pathological Considerations

aplasia of the left ICA and an aneurysm of the AcoA. He also found 8 cases in the literature. In a case of Staples (1979) there was a trans-sellar intracavernous intercarotid collateral artery with agenesis of the ICA, but no cerebral aneurysm. Servo (1977) reported a case of left ICA aplasia, associated with an aneurysm of the right ICA and he reviewed the literature on this subject. Handa et al (1980) reported a 52 year old female patient who suffered a subarachnoid hemorrhage. Angiography did not reveal any cerebral aneurysm but did show an anomaly of the left ICA. The intracranial portion of the left ICA as well as the left ophthalmic artery were not visualized below the level of PcoA. Tomographic studies of the petrous bone demonstrated no bony carotid channel on the left side. Rosen et al (1975) reported an interesting case of aplasia of both carotid arteries associated with an aneurysm of the basilar artery bifurcation. Beresini et al (1981) reported a unique case of a 54 year old patient with a primary cerebral neoplasm on the right temporal lobe and bilateral aplasia of ICA. Bilateral carotid angiography failed to show of the internal carotid arteries, but did show collaterals from the left external carotid via a transsellar intracavernous anastomosis to both the anterior and middle cerebral arteries. Vertebral angiography showed filling of the right carotid artery in its cavernous portion via the trigeminal artery. Beresini et al reviewed the literature and found bilateral absence of the ICA reported only four times in vivo (Fisher 1914; Dilenge 1975; Rosen et al 1975; Teal et al 1980), and five times at post-mortem examination (Da Silva 1936; Wolff 1944; Keen 1946; Fields and Sahs 1965; Hills and Sament 1968). Interestingly, there is not a single case reported in the literature with agenesis or aplasia of the vertebral artery combined with an aneurysm, butTsukamoto et al (1981) presented a case of an intersegmental artery with bilateral absence of the vertebral arteries and a ruptured aneurysm of the anterior communicating artery. In the present series we observed only one case with agenesis of the right ICA in a patient who had a ruptured aneurysm at the junction of the right PcoA and PCA. The right MCA was filled during vertebral angiography via the enlarged right PcoA. Surgical exploration confirmed the angiographic findings (see Fig 38A-C, p. 58-59). After completing the present series an interesting case was observed as already described in Fig 38D-F, p. 59.

Accessory Middle Cerebral Artery (See also Chapter 1, Anatomy). Crompton (1962) described an artery coursing with the MCA, arising from both the distal ICA and from the area of the AcoA, in association with an aneurysm of the MCA and he termed it an "accessory middle cerebral artery". Fig 69A-C shows two cases with an accessory MCA. Fig 70A-C shows bilateral MCA with an associated aneurysm of the basilar bifurcation. In these cases the accessory-MCA is arising from the proximal A1. Handa et al (1968); Stabler (1970); Teal et al (1973); and Ito et al (1975) reported further cases. Waga et al (1977) have also described a case of an aneurysm arising from the accessory MCA. Ya§ar-gil and Smith (1976) published 2 cases in which the anomaly was associated with an aneurysm of the anterior communicating artery and fibrous seg-mental stenosis of the right middle cerebral artery in one case (see Fig 68A-D), and fibrous stenosis of the left internal carotid artery bifurcation in the other. This resulted in a "Moya Moya" type of vascular anomaly in the left frontobasal area. It seems from this experience that the accessory MCA is like a secondary enlargement of either the proximal perforators or of Heubner's arteries. Fenestration and Duplication Fenestration of the anterior cerebral artery was reported in only one case (0.1%) by Fawcett and Blachford (1906). Its reported occurrence varies: Fawcett and Blachford (1906) Hasebe (1928) Kleiss (1942) von Mitterwallner (1955) Alpers et al (1959) Baptista (1964) ' McCormick (1969) Perlmutter and Rhoton (1976)

1/700 6/83 2/325 3/360 3/350 12/417 12/1000 2/50

0.1% 7.2% 0.6% 0.8% 0.8% 2.8% 1.2% 4.0%

Crompton (1962) reported an aneurysm at the proximal end of a fenestration of the anterior cerebral artery in an autopsy case. Ito et al (1981) reported two cases of tumors (meningioma and pituitary adenoma) and one case of an aneurysm of the pericallosal artery in which angiographically demonstrated fenestration of the anterior cerebral artery was seen. An aneurysm at the fenestration of vertebral and basilar arteries was reported by Mizukami et al (1972), Hoffmann and Wilson (1979), Hemmati and Kirn (1979), and Matricali and Van Dulken (1980). Miyazaki et al (1981) reported a case of multiple aneurysms of the ver-

Associated Vascular Anomalies

tebrobasilar system associated with fenestration of an intracranial artery. A search of the world literature revealed 56 other cases of vertebral artery fenestration mainly in reports from Japan. Fenestration of the left Aj segment is shown in the monograph of Krayenbiihl and Ya§argil (1965/68) with a duplication of the left A, (Fig 40B). An excellent visualization of an A[ fenestration is shown in Fig 100 of Huber (1979). Krayenbiihl and Ya§argil (1965/68) pointed out that the pronounced waviness of the posterior communicating artery at its point of origin from the internal carotid artery could, on antero-posterior projection, give the impression of fenestration of the anterior communicating artery. In our series there are 14 cases with fenestration of ACA, MCA, PcoA and VA: No. of cases —- AcoA MCA PcoA VA 9 151 3 11 (see Figs 43, 66, 67, 79, 80, 108).

Arteriovenous Malformation The association of cerebral aneurysms and cerebral arteriovenous malformations has been discussed by several authors. Paterson and McKissock (1956) reported that of 110 cases of arteriovenous malformation, 3 had associated cerebral aneurysms. BoydWilson (1959) reviewed the existing literature and added three cases of his own. He felt that on the basis of Paterson and McKissock's study, the frequency of cerebral aneurysm associated with arteriovenous malformation was scarcely above that expected for chance occurrence. He also pointed out that no constant relationship between the location of the cerebral aneurysms and the arteries feeding the arteriovenous malformation could be determined. Anderson and Blackwood (1959) examined 9 cases of arteriovenous malformation at autopsy and found that five of the cases contained single or multiple aneurysms. Of the 12 aneurysms found, nine were on arteries feeding the malformation and three were not. They suggested that there was a greater association between aneurysms and arteriovenous malformations than previously recognized by angiography. Perret and Nishioka (1966) in the Cooperative Study found 37 aneurysms out of 490 cases (7.6%). Cronqvist and Troupp (1966) examined angiograms of 150 patients with arteriovenous malformations and found single aneurysms in 8 patients and multiple aneurysms in 5. In 9 of the 13 cases, aneurysms were on the arteries supplying the malformation. Voigt and associates (1973) have presented a case of a young woman with bilateral arteriovenous

309

malformations and multiple aneurysms of the intracranial and extracranial vessels. Higashi et al (1979) encountered 4 cases of coexisting aneurysms and arteriovenous malformation in a series of 43 consecutive cases with AVM (9.3%). Concerning the etiology of coexisting intracranial aneurysms and AVM, the following theories have been advocated: 1) The increase in flow in a vessel feeding an AVM predisposes toward the development of an aneurysm on this vessel. 2) Multiple congenital disorders of cerebral vessels tend to occur simultaneously. 3) These two vascular lesions are of incidental occurrence. Suzuki and Onuma (1979) observed in 10 out of 1080 symptomatic aneurysms the coexistence of an AVM, whereas 9 out of 140 patients with a symptomatic AVM had associated intracranial aneurysms (6.4%). Shenkin et al (1971), (citing Hispaki) reported a case in which the removal of an AVM of the brain resulted in a distinct reduction in the size of a large aneurysm located on its principal feeding vessel. The Cooperative Study showed a death rate of 60 per cent (9/19) in cases which were managed conservatively, whereas the result was better in the operated cases (29% mortality 4/14). Small aneurysms in the proximity of an AVM are quite common, but larger aneurysms along the increased flow system were observed in only 10 of 350 AVM's in our series (2.8%) (see Table 25). Only in case No. 6 was there also a second large aneurysm of the contralateral ICA, that did not show an increased blood flow on Doppler examination. The aneurysms on the basilar bifurcation and on the enlarged right posterior cerebral artery were in relation to increased blood flow, as was the case in the other 9 patients. In two cases (9, 10) the aneurysm ruptured and was immediately fatal. In 8 cases the AVM's ruptured, and the well developed aneurysms were asymptomatic. In 4 cases the AVM and the aneurysm were successfully operated upon (3 cases in one session, 1 case in two sessions). In four other patients the asymptomatic aneurysms were successfully clipped. Two patients with left sided parietal and right occipital lesions are scheduled for the second operation. The 54 year old female (No. 8) with a large parietal AVM and severe right sided hemiparesis, hemianesthesia, and hemianopia (hemisyndrome) died six months later of a second hemorrhage, although at surgery for the pericallosal aneurysm, two large feeders to the AVM were clipped. Case 5, who before aneurysm surgery had five SAHs from his left sided parietal AVM, has fortunately had no recurrent bleeding for six years.

310

5 Pathological Considerations

Table 25

Clinical details of 10 cases of aneurysm associated with AVM

Name

Age

1) Fa

50

2) Sch

34

M

1978

3) Ma

28

F

1978

4) Pe

64

F

1979

5) Ha

35

M

1976

6) Br

29

F

1979

7) Ri

56

M

1979

8) Wi

54

F

1979

9) Ma

44

M

10) Du

43

M

Sex M

Year

Site of aneurysm

Site of AVM

Course

R. cerebellar

3 SAHs from AVM AVM extirpated, aneurysm clipped

Good

R. MCA

R. occipital

1 SAH from AVM with mass effect

AVM extirpated, aneurysm clipped 3 months later

Good

L. MCA

L. temporal

1 SAH and seizures

AVM extirpated, aneurysm clipped

Good

AcoA

L. frontal

1 SAH, seizures

AVM extirpated, aneurysm clipped

Good

AcoA

L. parietal

5 SAHs

No treatment of AVM, Good aneurysm clipped

R. occipital

1 SAH from AVM

Clipping of Good aneurysms treatment of AVM scheduled

R. occipital

1 SAH, mass effect Clipping of aneurysm Good and enlarged PCA treatment of AVM scheduled

L. pericall.

L. parietal

1 SAH, mass effect Clipping of aneurysm Death hemisyn-drome and feeders. Died after another bleeding 6 months later

1977

L. MCA

L. Sylvian

Seizures 13ys. SAH lead to death

Autopsy revealed the Death aneurysm as source of hemorrhage

1976

AcoA

L. parietal

SAH lead to death

Autopsy revealed the Death aneurysm as source of hemorrhage

1971

R. PICA

L. ICA, BaBi P2

Basil. Bi

Our policy, in general, is to plan the operative elimination of both lesions, AVM and aneurysm, especially in cases with well developed saccular aneurysms, because the rupture of such an aneurysm with increased flow frequently ends fatally (Figs 240-243).

Follow-up

Result

Associated Vascular Anomalies Fig240A-C Case 5, Table 25. A large anterior communicating aneurysm and a parasagittal left parietal AVM (white arrow) with bilaterally enlarged A, segments and an enlarged left A2 segment (A, B and C). The asymptomatic aneurysm arising from the left corner of the anterior communicating artery was clipped at operation; the unruptured AVM remains untouched, as the patient refused a second operation.

311

312

5 Pathological Considerations

Fig 241A-B Case 10. A large anterior communicating aneurysm (arrow) (A) with no relationship to a large left parietal AVM (arrow) (B).

Fig 242 A-C Case 6. A large left carotid superior wall aneurysm (arrow) (A) and a basilar bifurcation aneurysm (B) with only the basilar aneurysm seemingly related to the right occipital AVM. At surgery both aneurysms were clipped from a pterional approach (C); the AVM is scheduled for another procedure.

Associated Vascular Anomalies

313

Fig 242 C

Coincidental Association of Aneurysm and Occlusive Vessel Diseases There are three types of such associations to distinguish. 1) Patients with symptomatic intracranial aneurysms and an incidental finding of stenosis. 2) Patients with transient ischemic attacks and an incidental finding of a cerebral aneurysm. 3) Patients with symptomatic cerebral aneurysm and symptomatic stenosis of the carotid artery. 1) The angiographic examination of a patient with a symptomatic aneurysm may occasionally reveal an incidental asymptomatic extracranial carotid stenosis or occlusion. Pool and Potts (1965) and Fields and Weibel (1970) each described a patient who had bled from a right PcoA aneurysm and who had bilateral carotid stenosis. Contralateral endar-terectomy was performed because carotid ligation was planned. The patient of Fields and Weibel died of SAH shortly after operation. The patient of Pool and Potts underwent muscle wrapping of her intracranial aneurysm and died after this procedure , (see Stern et al 1979). Portnoy and Avellanosa (1970) presented a patient with SAH from a right PcoA aneurysm, who also had transient ischemic attacks referable to the left internal carotid artery. This patient underwent a left carotid endarterec-tomy, then clipping of the contralateral aneurysm and has done well. Stern et al (1979) reported 5

patients, 4 of them with SAH and one with a rapidly progressive third nerve palsy, all of whom showed significant carotid stenosis at angiography. Three of these patients first underwent clipping of the aneurysm and then endarterectomy of the ipsilateral internal carotid artery. One patient also had an aneurysm on the contralateral side, and another had an aneurysm and an AVM on the contralateral side. These patients have had no recurrence of symptoms. One patient, operated upon in 1962, presented with a progressive right third nerve palsy and underwent a left common carotid - left internal carotid artery bypass, with subsequent muscle wrapping of the right posterior communicating artery aneurysm. This patient suffered a fatal subarachnoid hemorrhage one month after craniotomy. The other patient had a left carotid endarterectomy and one week later underwent the successful clipping of a right posterior communicating artery aneurysm. This patient has had no neurological sequelae. 2) Gurdjian et al (1962) noted the presence of an incidental aneurysm in six of 205 patients who were evaluated angiographically for carotid disease. Although one of these patients later died of a SAH, no mention is made of whether this or any of the other five patients, actually underwent endarterectomy. Fields and Weibel (1970) presented four patients, two of whom were admitted for recurrent transient ischemic attacks and underwent uneventful endarterectomy. with an aneurysm on the ipsilateral internal carotid artery. Angiograms 1 year later (postoperatively) did not show an increase in

продолжение

314

5 Pathological Considerations продолжение

the size of the aneurysm. Neither of these patients had a SAH or recurrence of their TIA's. Denton and Gutmann (1973) presented a similar case, but the postoperative angiogram demonstrated delayed emptying of the aneurysm, which arose from the ipsilateral MCA, and it was subsequently encased with plastic. Shoumaker et al (1976) performed bilateral carotid endarterectomies in a patient with bilateral aneurysms. The first operation was carried out on the symptomatic ICA. A follow-up angiogram 7 months later revealed increased stenosis in the contralateral asymptomatic carotid, and an endar-terectomy was performed on this artery. This patient had aneurysms of the right MCA and right ACA, as well as a left PcoA aneurysm. None has bled postoperatively. The case of Adams (1977) presented with TIA's referable to the left ICA. Angiography revealed bilateral carotid stenosis and an aneurysm of the left PcoA. The patient underwent an uneventful left carotid endarterectomy, but died 7 months later from a SAH. Stern et al (1979) reported 15 patients with TIA's. Angiography in 4 cases showed bilateral and in 11 cases unilateral aneurysms: 5 intracavernous, 1 ophthalmic, 5 PcoA, 3 MCA, and 1 ACA. One patient had 2 aneurysms and one patient had 3 aneurysms. None of the patients in this group who presented with TIA's and incidental asmyptomatic aneurysms and who underwent endarterectomy suffered SAH. Fourteen patients refused surgery of the aneurysm, so only one of this group of patients has had the aneurysm clipped. The very complex therapeutic problems encountered with these combined lesions was discussed. Matsuda et al (1983) reported seven cases. Surprisingly, there are only a few publications dealing with this subject. The question arises in cases of symptomatic aneurysms as to whether the extracranial portion of internal and common carotid arteries has been examined carefully. Still, despite the fact that many thousands of patients throughout the world with stenotic carotid artery disease have undergone cerebral angiographic studies, the number of discovered incidental asymptomatic aneurysms is very few. There also are to date no cases in the literature of coexistent aneurysms and stenosis within the vertebrobasilar system. In the present series we observed 9 patients with symptomatic stenotic disease. In three cases the angiogram revealed stenosis of the left extracranial internal carotid artery and in addition an asymptomatic aneurysm of the bifurcation of the left middle cerebral artery. The unruptured aneurysm was clipped first and subsequently an endarter-

ectomy was successfully performed (in a 42 year old female and two males ages 52 and 58). One unusual case a symptomatic severe stenosis of the intracavernous portion of the right internal carotid artery combined with a thrombosed aneurysm of the basilar trunk (Fig 243A-D). No surgical treatment has been performed. In 3 patients presenting with TIA's the angiogram showed a large, sclerotic, unruptured aneurysm with occlusion of branches of the middle cerebral artery. In 2 patients with SAH the angiogram showed a saccular aneurysm of the anterior communicating artery and a tight stenosis of the MCA (see Fig 68B, p. 89). After completing this series a further interesting case presented. A 58 year old woman diagnosed as having poliomyelitis after developing a right hemiparesis at the age of 2 was thought to have had a minor cerebrovascular accident in 1975. In 1983 she presented with a massive intraventricular hemorrhage and obstructive hydrocephalus as demonstrated on CT scan. Initial treatment by insertion of a VP shunt produced a marked improvement. Subsequent angiography revealed a large anterior communicating artery aneurysm and complete occlusion of the supraclinoid portion of the left internal carotid artery - probably the cause of her original hemiparesis. This raised the possibility that the chronically increased flow from right to left through the anterior communicating artery may have contributed toward the formation and rupture of the aneurysm which was successfully clipped on 23. 6. 83. She made an uneventful recovery (see Fig 244A-B, p. 316).

Associated Vascular Anomalies

315

Fig 243A-D A large fusiform basilar aneurysm is visualized on the left vertebral angiogram following subarachnoid hemorrhage in a 19 year old patient (A). Right carotid angiography reveals a three segment stenosis (arrows) in the petro-cavernous segment (B) with collateral filling from the left side. Repeat angiography (C) one month later shows complete thrombosis of the aneurysm with occlusion of the distal basilar artery (arrow) and filling of the posterior cerebral and superior cerebellar arteries from the left carotid (D).

316

5 Pathological Considerations

Fig 244A—B 58 year old female suffered subarachnoid and large intraventricular hemorrhages and angiography revealed an aneurysm of anterior communicating artery visualized from right sided angiograms (A) whereas left carotid angiography showed an old occlusion of internal carotid artery on the neck (B). In the history of the patient it is known that she had at the age of 2 an insult of unknown aetiology, she had a right hemiparesis and hypomelia.

Moya-Moya Disease Associated with Aneurysms Over 1000 cases of Moya-Moya disease had been reported up to 1979. Since a case with Moya-Moya disease associated with intracranial aneurysm was first reported by Pool et al (1967), 56 cases showing this association have been reported (Yabumoto et al (1983). We saw in the same time period (1967-1979) only two cases of Moya-Moya disease, and in no instance was an association with an aneurysm observed. However, in two other cases with symptomatic ruptured aneurysms, angiography revealed severe circular stenosis of a short segment of Mj combined with an accessory MCA and the visualization of a network of small arterioles around the M,-segments: a picture similar to that seen in Moya-Moya disease (see publication Ya§argil and Smith 1976).

In 1981 another unique case came to our attention. A 9 year old girl developed a right sided VI nerve palsy. The panangiograms, uncovered an asymptomatic occlusion of the left internal carotid artery just distal to the origin of the ophthalmic artery, and severe segmental stenosis of the upper % of the basilar artery. There were networks of arterioles on the left carotid and vertebral angiograms (Fig 245A-E) similar to that seen in Moya-Moya disease. The right carotid angiogram showed an unusual enlargement of the right ICA along its entire length, with two saccular aneurysms in the intracavernous portion and excellent collaterals through an enlarged right Al to the left hemisphere. There was also good collateral circulation from the stenotic basilar artery via both PcoA to MCA. The patient has experienced no complaints other than diplopia due to a right VI nerve palsy.

Associated Vascular Anomalies

317

Fig 245A-E A large saccular right internal carotid aneu-rysm (arrows) is demonstrated on right carotid angiogra-phy (A and B) with excellent cross-filling of the left middle cerebral artery despite no cross compression during the injection. Left carotid angiography (C and D) reveals severe supraclinoid carotid occlusive disease (Moya-Moya) with telangiectasia (arrows). Similar changes are seen in the basilar artery (small arrow) (E).

318

5 Pathological Considerations

Association of Brain Tumor and Cerebral Aneurysm Pia and associates (1972) conducted an extensive evaluation of the association of brain tumors with cerebral aneurysms including personal cases, cases taken from the literature, and cases obtained by questionnaire to neurosurgeons throughout the world. They were able to collect 116 cases. Overall the frequency (0.2%) of association did not seem greater than the expected frequency of cerebral aneurysms in the population, but they did notice an increased frequency of meningiomas and pituitary adenomas compared to the expected frequency of brain tumor types. Middle cerebral artery aneurysms were more often associated with convexity tumors, and internal carotid artery and vertebrobasilar aneurysms with basal tumors. The authors advised operative treatment of both lesions in cases of benign tumor. Jakubowski and Kendall (1978) performed routine angiographic studies and found 11 (6.0%) of 150 pituitary adenomas and 33 craniopharyngiomas had an associated silent aneurysm (6 of the aneurysms occurred in the 29 eosinophile adenoma patients and 1 of the aneurysms in the 33 craniopharyngioma cases. Four aneurysms arose from the intracavernous, 4 from the supraclinoid carotid, and 3 from the anterior cerebral artery complex. Wakai et al (1979) found coexisting aneurysms with pituitary adenomas in 7 cases (7.4%). This was a significantly higher incidence than that found with other brain tumors (1.1%) (Figs 246A-C, 247, 248A-B).

Fig 246A-C (Case 16; Vol. II, Table 14). A right internal carotid-ophthalmic aneurysm (arrows) (A and B) and an enlarged sella from a pituitary adenoma (arrow) (C) in a 27 year old patient. The aneurysm was clipped, and the adenoma extirpated.

Associated Vascular Anomalies

319

Fig 247 Case 9. A small left ophthalmic artery aneurysm and an anterior choroidal aneurysm in a patient with a large left frontal sarcoma.

Fig 248A-B Case 5. A bilobular anterior communicating aneurysm (arrow 1) in a patient with a right sphenoid wing meningioma (arrow 2) (A). Following removal of the meningioma at operation, the aneurysm (arrow 1) and a very hypoplastic right A, segment (arrow 2) were seen (B).

320

5 Pathological Considerations

Our cases are listed on Table 26. Six of our cases had meningiomas in association with cerebral aneurysms, and one each had a pituitary adenoma, a sarcoma, an astrocytoma, and a glioblastoma. Nine of the ten cases occurred in women. This series thus helps substantiate the idea that aneurysms occur more often with meningiomas and pituitary adenomas than with other brain tumors. The few cases observed, however, cannot support more than a chance occurrence between tumors and intracranial aneurysms. The aneurysms were ipsilateral to the meningiomas in each of these cases. In only one case (No. 2) was the aneurysm

the symptomatic lesion. Surprisingly in case three, the tumor had bled and the patient presented with the clinical picture of a ruptured aneurysm. In case 7 evidence of mass effect on angiography was incorrectly interpreted as being due to a thrombosed aneurysm. The cause of her visual deficit was pressure from the tumor on the optic nerve and the anterior cerebral artery. The aneurysm did not seem to have injured the optic nerve. In case 10, operation was not indicated because of a widely infiltrating glioblastoma. In all other cases both lesions were treated.

Table 26 Association of brain tumor and cerebral aneurysm Name

Year

Age

Sex

Location of aneurysm

Type of tumor

Course

Result

1) Si

1974

63

F

(R) PcoA

Meningioma (R) convexity

Seizures and focal deficit, improved with removal of tumor, clipping of aneurysm

Good

2) Cu

1975

55

F

(R) MCA

Meningioma (R) sphenoid wing

Headache, vertigo, decreased (R) corneal reflex; both lesions treated at operation

Good

3) Wa

1976

45

F

(L) ICA-Bi + (L) ophthal.

(L) parasagittal meningioma frontal

SAH from tumor; both lesions treated at operation

Good

4) Ro

1975

57

F

(L) ICA-Bi

(L) sphenopetro-clival meningioma

(L) exophthalmus and di-plopia; both lesions treated at operation

Good

5) Na

1979

66

F

(L) AcoA

(R) sphenopetro-clival meningioma

Visual field defect; both lesions treated at operation

Good

6) Ma

1979

47

F

(L) MCA

(L) parietal meningioma SAH from the aneurysm; both lesions treated at operation

Good

7) Tu

1976

47

F

(R) Ophthal.

Pituitary adenoma

Optic atrophy, fatigue; both lesions treated at operation

Good

8) Ha

1978

64

M

AcoA

(R) frontal astrocytoma

Personality change; both lesions treated at operation

Good

9) Al

1976

70

F

(L) AchoA

(L) frontal reticulum cell Personality change; both lesions sarcoma treated at operation

Good

10) Sh

1976

47

F

(R) PcoA

Bifrontal glioblastoma

Three months headache and personality change. Died without operation

Death

Pathology of Saccular Aneurysm Formation and Rupture

Pathology of Saccular Aneurysm Formation and Rupture The pathophysiology of saccular aneurysm formation on cerebral arteries has been debated for over a century, and a complete understanding of this lesion is still not to hand. In the first half of the 19th century there were only occasional reported cases. Lebert in 1866 examined 86 cases of cerebral aneu-rysms and felt that in most instances a paren-chymatous arteritis of undetermined nature had caused the formation of an aneurysm. He rejected the idea of his day that syphilis and atherosclerosis were the most common etiologies of cerebral aneurysm. Church (1870) presented evidence that infected emboli from subacute bacterial endocarditis were the more common etiology of cerebral aneurysm. Over the next 30 years these theories of embolism versus syphilis were debated in many reports. Eppinger made a comprehensive study of aneurysms occurring in all organs in 1887 and r emphasized the destruction of the elastic layers as I important in the formation of aneurysms. He felt that congenital abnormalities of the elastic layer might be responsible for these findings. He did not distinguish aneurysms in the cerebral circulation from other aneurysms. Simple aneurysms for which he could not find an etiology were ascribed to trauma. Interestingly, he shows a figure of an aneurysm at the bifurcation of the middle cerebral artery as such an example.

Fig 249 Histological preparation of the anterior communicating artery of a 58 year old man showing 'weakening of the wall to form an aneurysm' (after Busse 1921).

321

Von Hofmann (1894) pointed out that cerebral aneurysms generally occur at bifurcations or points of division of arterial branches. He felt that syphilis, atherosclerosis, and trauma were not significant factors in cerebral aneurysm formation. but atheroma and hypertension might contribute to aneurysm rupture. Fearnsides (1916). following the work of Turnbull (1915), introduced the concept of medial degeneration as the most common cause of non-inflammatory cerebral aneurysm formation and suggested a congenital weakness of the arterial wall at the junctions of the major arteries. Fearnsides found that hemorrhage was the cause of death in 81 per cent of non-embolic aneurysms. He further noted that multiple episodes of leakage had occurred in 42 per cent of patients, and that rupture seemed often related to "the violent muscular effort of acute emotion". These studies set the modern tone for the pathological nature of cerebral aneurysm. Otto Busse (1921) found the anterior communicating artery especially prone both to aneurysm formation and to anomalous construction. He systematically examined the anterior cerebral-anterior communicating complex in 400 cadavers using a binocular dissecting microscope and found 39 ruptured aneurysms. He described the anomalies present in 55 per cent of cases, and noted intraluminal bands and weakened areas in the arterial wall. He concluded that syphilis played no role in aneurysm formation in this area, and he postulated that anomalous development associated with hypoplasia of a portion of the arterial wall led to the growth of an aneurysm (Fig 249).

322

5 Pathological Considerations

Forbus (1930) noted defects in the tunica media of the cerebral arterial wall occurring at the branching of the major vessels, sites corresponding to the more common locations of intracranial aneurysms. As these defects were also found in children, he considered them a congenital defect. This "congenital" etiology of cerebral aneurysms gained general acceptance. Many pathologists, however, have tended to mitigate the importance of medial defects, noting that they are present in a majority of the population. Glynn (1940) stressed the importance of the internal elastic layer in giving strength to the vessel wall, and Carmichael (1950) and Stehbens (1963, 1972) emphasized the role of atherosclerosis and degenerative change. Kernohan and Woltman (1943) raised the possibility of inflammatory factors. In a careful analysis of autopsy specimens, Hassler (1961) found small aneurysms in up to 17 per cent of specimens. He could relate the presence of h aneurysms to an increase in the number and size of medial defects at arterial branchings, but not to presence of atheroma. He confirmed the presence of intraluminal bridges in the basilar and anterior communicating arteries in 16 per cent of specimens . He noted that intimal cushions across from a medial defect might direct the stream of blood into the area of the defect thereby giving rise to an aneurysm. Even tiny aneurysms showed changes in the internal elastic layer including thickening, round cell infiltration and clumps of eosinophilic fibrinoid material. Hassler ascribed these changes to the force of blood directed against the wall, and felt that atherosclerosis was a secondary phenomenon. The impression should not be gained from this analysis that the aneurysm wall is smoothly tapered from a thicker base to a thin dome. Experience with aneurysms at operation has shown that frequently the transition from parent vessel wall to aneurysm is quite abrupt, with a thin, dark red aneurysm neck protruding from the thicker, whitishpink vessel wall. Small outpouchings may occur from the neck and may easily be ruptured during dissection. Furthermore, pathological changes can extend into the parent artery. In 11 cases in the present series - 8 anterior communicating artery, 2 basilar artery, and 1 internal carotid-posterior communicating artery aneurysm - a clip was placed low across the neck, but over weeks to months a new aneurysm arose beneath the clip and ruptured. Crompton (1966) evaluated factors relating to growth and rupture in 289 autopsy specimens of both ruptured and unruptured aneurysms. He was impressed by the evidence of inflammation.

Stehbens (1972) presented a detailed microscopic study of small and large aneurysms and pointed out that atherosclerosis indicated by the presence of foam cells and/or cholesterol clefts has been found histologically in 96 per cent of 100 cases in which the arterial forks with aneurysms were serially sectioned. In a later electron microscopic study, Stehbens (1975) found a variable thickness of the endothelium, a thickened basement membrane occasionally containing collagen fibers or cell debris, and a severely degenerate media containing atrophic smooth muscle cells and some monocytic infiltration. He felt that the finding of such degenerative changes in even the smallest aneurysms supported his concept of an acquired degenerative lesion. Ebhardt and associates (1976) however, also submitted a few aneurysms to electron microscopy and noted no atherosclerotic plaque in the resected fundi which they felt tended to refute the concept of atherosclerotic destruction of the vessel wall as the basis for aneurysm formation. They found hyperplastic smooth muscle cells which they related to hypertension. Meyermann (Meyermann and Ya§argil 1978) was given 120 aneurysm fundi from the present series of patients for examination by electron microscopy. He found the endothelium intact in only 10 per cent of specimens, and the internal elastic lamina disorganized. Thrombus in various stages of development, sometimes with capillary proliferation and a growth of fibroblasts was present in most specimens. The smooth muscle cells of the media had become hypertrophied and assumed some characteristics of fibroblasts similar to the so-called "sub-endothelial cells" seen in hypertension and atherosclerosis. Sites of rupture showed an infiltration of erythrocytes and fibrin into the aneurysmal wall (Fig 250). Suzuki and Ohara (1978) have recently examined 45 aneurysms at autopsy, 23 unruptured and 22 ruptured specimens. They felt that medial defects formed the basic pathological substrate, but that the impact of the blood stream and elevated blood pressure were contributory factors. They emphasized the importance of minor rupture into and through the wall of the aneurysm in the growth of the lesion. They formulated the following pathogenesis for cerebral aneurysm: The constant tension applied to the medial defect by the blood stream leads to a thin bulging of the arterial wall. At this stage the aneurysm is less than 3 mm and is composed of fibrous tissue similar to the adventitia of the parent vessel. Turbulence and other hemodynamic forces lead to further growth of the lesion, but also elicit reparative processes which lead to increased thickness of the neck or the dome.

Pathology of Saccular Aneurysm Formation and Rupture

323

Fig 250 A—B Electron microscopic section of clinical intracranial aneurysm showing the discontinuity of the endothelial cell layer (after Meyermann 1978).

Endothelial cells, fibroblasts, and elastic fibers are involved in this process. With increased growth the wall becomes primarily collagenous tissue, and thin areas develop as potential sites of rupture. In those aneurysms which rupture, fibrin and arachnoid reinforce the site of rupture. After about three weeks, this tissue is better organized with capillary proliferation and thickening of the arachnoid. However, intraluminal hemorrhages may occur from these immature capillaries, and these again

lead to aneurysm growth and new sites of potential rupture. Ferguson (1972b) has studied the physical factors contributing to aneurysm formation. He emphasized the force of impact of the axial blood stream against a bifurcation leading to the initial disruption of the internal elastic layer and subsequent aneurysm formation. While not finding turbulence a significant factor in initial aneurysm formation, he did feel that turbulence might lead to

324

5 Pathological Considerations

growth and further degeneration of the wall within a l of 43 per cent from the initial hemorrhage, with 74 | formed aneurysm. Increased stress is applied to the per cent of these patients dying within the first 24 wall of an aneurysm with increasing size. He found hours. For patients who arrive alive at a hospital i and that the pressure within an aneurysm was directly thus fall into clinical statistics, the gross mortality rates related to the pressure within the parent artery for ruptured cerebral aneurysm without operation (Ferguson 1972a). When a critical pressure is (averaging several studies) is about 25 per cent for the exceeded, the aneurysm ruptures. Nornes (1973) has first week, 50 per cent at two _ months and 70 per discussed the factors that lead to jgssation of bleeding cent at five years.________ As Ask-Upmark and in the ruptured aneurysm. He noted that during Ingvar (1950) have stated, given five patients who bleeding (ruptured cases) there was a marked have sustained rupture of an aneurysm, at the end of increase in intracranial pressure as measured five years three will have died, one will be disabled, and epidurally that in effect tamponaded the bleeding by the last will be alive and well. temporarily causing a cessation of blood flow. The gross mortality of ruptured cerebral aneurysms During this time, hemostatic mechanisms form a includes many patients who suffer a fatal brain plug of platelets and fibrin in the rent. Vasospasm at injury at the time of hemorrhage. An opera-tion is the time of rupture was suggested as a contributory generally directed towards the prevention ol factor in the control of hemorrhage. In evaluating the rebleeding. From the "Cooperative Study", Lockspresence of blood clot within the cisterns at the time ley (1966) determined a rate of recurrent hemorof microsurgical operation, it could be construed that rhage of 10 per cent for the first week, 12 per cent the acute filling and distension of the arachnoid for the second, 7 per cent for the third, 8 per cent cisterns around the site of aneurysm rupture might for the fourth, and 14 per cent for between 5 and 12 contribute to hemostasis. Rerupture of a cerebral weeks. Mortality from the second hemorrhage was aneurysm implies a reversal of the protective between 41 and 46 per cent depending upon the mechanism which follow rupture. Increased location of the aneurysm. Pakarinen found the fibrinolytic activity of the cere-brospinal fluid mortality from recurrent hemorrhage to be 24 per following subarachnoid hemorrhage has been well cent at one month, 34 per cent at two months and documented (Tovi 1972). dissolution of the clot 38 per cent at one year. Winn and associates (1977) prior to the formation of adequate scar tissue, found a late rebleeding rate of about 3 per cent per decrease in the intracranial pressure, and relaxation year on patients randomly allocated to non-operaof vasospasm may all be considered factors tive treatment and followed for up to 20 years. contributing to the rerupture of an aneurysm. Jane (1981) summarized his studies of the natural history of saccular intracranial aneurysms and concluded that approximately two thirds of patients die as the result of the first bleeding episode and many do not reach medical attention. Jane compared his patients who rebled after 14 days to those who did not and formulated the following:

Natural History of Ruptured Cerebral Aneurysms Mortality and Morbidity

1) The shorter the time duration since the first episode of bleeding, the more likely is rebleedIt has been difficult to ascertain the precise natural ing. The rebleeding incidence curve flattens out mortality associated with ruptured cerebral aneuat about 6 weeks. However, rebleeding from rysm because of the selection factors which are anterior or posterior communicating artery anapplied to patients referred to centers interested in eurysms after 6 months continues over the years cerebrovascular surgery. The "Cooperative Study" at a rate of 3 to 4 per cent per year for at least 20 (Locksley 1966b) found an eventual mortality of 68 years. The mortality rate of such late rebleeding per cent, evaluating 830 cases of first bleeding, is approximately 67 per cent. single aneurysm, non-operated patients. There was aj.0 per cent mortality for the first 24 hours and a 27 12) The worse the clinical grade on admission the more likely rebleeding is. per cent mortality for the first week. Pakarinen (1967) probably gives a more accurate picture of 3) Hypertension increased the likelihood of rebleeding among Jane's patients with a diastolic the mortality of ruptured cerebral aneurysms by blood pressure below 90 mm Hg. 25 per cent including in his statistics patients who died before rebled, whereas of those with a diastolic arriving at a hospital and who were subjected to pressure above 109, 75 per cent rebled. forensic autopsy as well as those who died in the 4) Older patients are more prone to rebleeding. various hospitals in Helsinki. He found a mortality

Natural History of Ruptured Cerebral Aneurysms 5) Aneurysms pointing down are less likely to rebleed than those pointing up in the direction of the jet stream of the blood. 6) Short broad aneurysms rebleed more frequently than long narrow aneurysms 7) Posterior communicating artery aneurysms rebleed at a higher rate than do anterior communicating artery and vertebrobasilar aneurysms. 8) Angiography performed 6 months after the initial hemorrhage can provide prognostic information. Among Jane's patients 6 of 21 (29%) who had a documented increase in size of their aneurysm and 11 of 28 (39%) with no change in size experienced rebleeding. In contrast, only 1 of 11 (9%) with a decrease in aneurysm size rebled. __________.________.— Bucy (1983) has summarized the statistical analysis and management concepts of Kassell and Drake regarding the overall mortality and morbidity from aneurysmal SAH, the figures agree closely with those found in the Canton Zurich (see below).

Necropsy of Fatal Aneurysm Rupture

325

those dying hours to days later had such hematomas. She found an incidence of 22 per cent of subdural hematomas in these fatal cases. She also found an _8 per cent incidence of ischemic infarction, but felt that this was explained by the fact that only 11 per cent of such cases lived longer than one day, liijdra and van Gijn (1982) studied 31 patients dying within 24 hours of a ruptured cerebral aneurysm and found that 25 had significant intracerebral and/or intraventricular hematoma. Imhof (1980) has analysed the autopsy findings in 303 patients who died of ruptured intracranial aneurysm in the Canton of Zurich between Jan. 1967 and Jul. 1979. Seventysix patients died in the University Hospital of Zurich (USZ) and the other 227 died in various community hospitals. Of the 303 patients, 27 (8.9%) were found dead and another 130 (42.9%) died within the first day (Table 27a). Of patients surviving longer than 24 hours, another 92 had a progressive downhill course and died within 2 weeks, while 54 (17.8%) stabilized or made some recovery and then had a secondary deterioration, either from rebleeding or from medical factors. These patients went on to die 2 to 4 weeks after the initial hemorrhage. Except for a few patients sent to USZ in a moribund condition, the acute deaths occurred outside this hospital (Table 27a-b). 62.7 per cent of the patients had an intracerebral hematoma and 49.1 per cent had an intraventricular hematoma. There is a higher percentage in cases of acute death. Autopsy findings in this series thus support Crompton's contention that cerebral infarction and intracerebral hematoma account for the majority of deaths following aneurysm rupture. The incidence of cerebral infarction seems quite low, but is probably explained by the short survival times of many patients not allowing the full expression of an infarct and the lack of microscopic examination on many of the autopsied. Edema was present in 174 patients (57.4%) and this probably resulted from ischemia if not frank infarction in most cases. Subdural hematoma was found in 5 per cent of patients (Table 27c). Aneurysms of the anterior communicating artery formed the single largest group at autopsy account ing for 47.5 per cent of cases. There were 69 cases of middle cerebral aneurysm and 37 cases of inter nal carotid-posterior communicating artery aneu rysm. Multiple aneurysms were seen in 9.2 per cent I of cases (Table 21A).

Crompton (1964) analysed the factors causing death in 159 patients with ruptured cerebral aneurysm, noting that subarachnoid hemorrhage, per se, is not an adequate explanation for brain death. While ^ognizant. of the frequent occurrence of intracranial hettiatoma in fatal aneurysm rupture, he emphasized the importance of ischemic infarc-: Hon which he found in 119 of 159 patients (72%). The incidence of infarction was highest with aneurysms at the internal carotid-posterior communicating artery junction and the middle cerebral artery. Intraarterial thrombus was found in only two cases. Venous thrombosis overlay areas of pale infarction in five cases. He concluded that both cerebral infarction and intracerebral hematomas \were important causes of death following rupture 'of an aneurysm. Robertson (1949) found hematomas in 60 of 80 patients at autopsy. From the findings of the "Cooperative Study", Locksley (1966b) reported that 90 per cent of 1 patients dying within the first 12 hours had intracra' nial hematomas. He felt that this explained the high mortality associated with middle cerebral and distal anterior cerebral artery aneurysms which were more prone to form intracerebral hematomas. Freytag (1966) in a survey of 250 autopsy cases of ruptured intracranial aneurysm, found that only 24 per cent of patients who died within hours had , Patients who died are divided into groups and intracerebral hematomas, while 71 per cent of expressed as percentages relating their time of death and the site of aneurysm rupture in Table 27e.

326

5 Pathological Considerations

Table 27a Analysis of patients dying from subarachnoid hemorrhage in the Canton of Zurich Table 27b Findings at autopsy

Total

27 (8.9%) Immediate death (Forensic) Death within 1 day (Acute) Death within 2d-2w 130 92 54 (Progressive) Death within 2w-1 m (Delayed)

227 (74.9%)

IVH.

Edema

Infarction

174 57.4%

33 10.8%

ICH

IVH

Edema

8

(77.8%)

16(59.3%) 78 19 98

50 27

(68.5%)

(60.0%) 39 17 14 14

Severe SAH

303 =

3 0.9%

Table 27c

The findings at autopsy

200 16 190 150 49.5% 66.0% 5.3% 62 7% related to the time of death following rupture

Forensic

27 (8.9%) 130

17

Acute

(42.9%) 92 (30.4%)

89 3

Progressive 54(17.8%)

3

Prominent SDH

1

ICH.

SDH autops.

21 108 48

4

27 (100%) 15(11.5%) 34 (36.9%) 27 115(88.5%) 58 (63.0%) 27 (50.0%) (50.0%)

76(25.1%)

Not performed

Severe

Other Hospitals of Canton Zurich

303

Total No.

No. SAH

USZ

Infarct.

7 43 12

30

Delayed 303 Table 27d

No.

3

200

16

190

150

174

33

Site of aneurysms and section

Severe

SDH

A.co. M.c. 144(47.5%) 69

ICH section

2

P.co.

(22.8%) 37(12.2%) 19 4 1

I.C.A. Bi.

(6.3%) 26 (8.6%) 8

Ba.Bi.

(2.6%)

-21

IVH

SAH

92

8 39

29

1 13

36

Edema

1 0 1 49 20 8 10

76 33 17 6

72

2

11

7 16

7

13

-

Infarct.

18 48 4 3 19

16

Vertebr.

303

3

200

Table 27e

Site of fatal rupture related to time of death

Site of Aneurysm

Forensic/Acute

16 Table 27f

190

150

Site of fatal rupture related to

174

33

initial grade

(2d-2w) (2w-1 m) Site of Progressive-Intermittent Aneurysm

No. of Cases

ll-lll

IV-V-Forensic

A.co. M.c. 50% 54% 56% 63%

50%

144 69 19 37

25.0% 27.5%

75.0% 72.5%

P.c. Ca.Bi

M.c. 44%

Ca.Bi 37%

8 26

2 1 . 1 % 35.3% 78.9% 64.7%

Vertebr.

P.c. 25%

Vertebr. 62%

Ba.Bi.

Ba.Bi.

75% 38%

A.co. 46%

37.5% 38.5%

62.5% 61 .5%

Natural History of Ruptured Cerebral Aneurysms

327

Table 27g Aneurysm location with respect to age and mortality Site of Aneurysm

No. of Cases

A.co.

144 (47.5%)

1

1

M.c. P.c.

69 (22.8%)

1

4

37(12.2%)

Ca.Bi.

19 (6.3%)

Ba.Bi. Vertebr.

1-10

11-20

21-30

31-40

Age 41-50

51-

61-70

71-80

81-90

90 >

60 14

31

34

34

24

6

16

17

19

6

3

5

6

11

9

3

-

-

1

4

5

2

7

-

-

-

26 (8.6%)

1

3

9

8

4

1

8 (2.6%)

1

1

1

5

-

-

-

-

303

1

33

68

77

73

34

2

3

13

194

(64%)

Upon initial clinical statistical evaluation, patients with anterior communicating, middle cerebral and carotid bifurcation aneurysms present more frequently as grade IV, V and forensic cases, than posterior communicating vertebral or basilar bifurcation aneurysm patients. The patients with aneurysm of the Aco, Pco arteries and basilar bifurcation have a less acute, extended time course before I dying, whereas vertebral and carotid bifurcation I aneurysms cause the rapid demise of their host. Thirty-six per cent of patients who died were over 60 years old, whereas only 8.7 per cent of operated patients were over 60. No location of aneurysm showed a special predilection for the older age group (Table 27g). There was a trend for older patients to die in outside hospitals rather than being transferred to USZ. Of female patients 45.2 per cent were over 60 as compared to 25.9 per cent of male patients. This conforms to the expected increase in incidence of aneurysms in females with advancing age. Clinical or post-mortem evidence of hypertension was present in 91 of the 303 cases (30.0%). While the incidence of hypertension in men was unremarkable (15.6%), 70 of the 168 women (41.7%) had hypertension, far above the expected 19 to 20 per cent in general population. The incidence of diabetes, heart disease, kidney disease, and other general medical problems did not appear increased in this group of patients. The great majority of these patients were unsalvageable from the time of their initial ictus. Only 25 per cent of these patients were seen at USZ and of these more than half remained semicomatose (grades IV or V) until death.

Spontaneous Thrombosis of Cerebral Aneurysms Thrombus formation within an aneurysm is common. Considering the disturbance of laminar blood

1

1

-

-

1

1

109 (36%)

flow within an aneurysm, it is perhaps surprising that thrombosis does not occur more frequently. Various degrees of thrombosis may occur within aneurysms of any size, but thrombosis within larger lesions is more common. Thrombosis within an aneurysm is important with regard to both the increased difficulty of management at operation and the possible treatment of aneurysms without intracranial procedures by the initiation of thrombosis within the lesion. Aneurysms containing thrombus may be divided into three general groups: partially thrombosed, subtotally throm-bosed, and totally thrombosed.

Partially Thrombosed Aneurysms There is no evidence that an aneurysm found at angiography or computerized tomography to contain some thrombus will go on to complete thrombosis or that the patient is any safer from subsequent rupture or rerupture (Fig 251). Consequently aneurysms in this category are treated in the same way as aneurysms containing no thrombus. Care must be taken at the time of operation to avoid embolization of the clot during manipulation of the aneurysm. Thrombus may cause the aneurysm to rupture as a clip is being applied, and in some instances thrombus will have to be removed before a final clip can be placed. Subtotally Thrombosed Aneurysms Eighteen cases were been seen in this series that demonstrated 80 to 90% thrombosis of the aneurysm. Most of these aneurysms were larger than 25 mm in diameter. In general these aneurysms should undergo operation as hemorrhage may occur despite extensive thrombosis. In addition, mass effect on local neural and vascular structures is often present. The presence of a large thrombus, combined with severe atherosclerosis in the wall of aneurysm, may however complicate the operation

328

5 Pathological Considerations Fig 251 Intraventricular hemorrhage and death was caused by the rupture of this almost completely thrombosed right internal carotid bifurcation aneurysm in a 48 year old man.

to the point that the lesion cannot be adequately treated. In the present series, one patient was treated with only decompressive craniectomy because the risk of attempted resection of a large subtotally thrombosed anterior communicating artery aneurysm seemed too high. Totally Thrombosed Aneurysms Occasional reports of complete spontaneous thrombosis of cerebral aneurysms have appeared. While early reports by Hutchinson (1875) and Lyall (1936) demonstrated that aneurysms may undergo spontaneous thrombosis, this relatively infrequent occurrence was documented by Krayenbiihl (1941) who found only one thrombosed and organized aneurysm in over 7000 autopsies. Other autopsy series however have suggested a higher incidence of totally thrombosed aneurysms (Housepian and Pool 1958). Increased use of angiography to diagnose and follow patients with cerebral aneurysm has resulted in more reports of patients in whom aneurysms spontaneously closed. Epstein (1953) described 3 cases of thrombosis of anterior communicating artery aneurysms in which thrombus had also occluded the anterior cerebral artery. One case was documented at autopsy and in the other two the aneurysm was diagnosed by pneumoencephalography. Marguth and Schiefer (1957) reported the first angiographically demonstrated case of a thrombosed aneurysm of the posterior communicating artery. Schunk (1964) described seven cases of aneurysms with thrombosis of which 2 had undergone complete thrombosis. Lodin (1966) reported 2 cases in which previously discovered aneurysms could not be demonstrated

6 months and 2 years after the original study. Bonnal and Stevenaert (1969) reported 4 cases in which clipping or ligation had only partially occluded an aneurysm, but follow-up angiography revealed no filling of the lesion. Devadiga et al (1969) described spontaneous thrombosis of an intracavernous internal carotid artery aneurysm in a child that may have been of infectious origin. Scott and Ballantine (1972) and Kowada et al (1974) have described cases of spontaneous thrombosis of middle cerebral artery aneurysms. Moritake et al (1981) reported a case of a thrombosed aneurysm of the posterior communicating artery and found 15 other cases in the literature (including the cases of Lodin and Devadiga et al). Nine patients have been seen over the last 12 years with fully thrombosed aneurysms; in two patients the aneurysms were localized at the left M4 segments, in two patients at the origin of the ophthalmic artery, and in one each on the basilar artery, on the proximal anterior cerebral artery, at the origin of the right SCA and at the right P3 segment, and at the internal carotid artery bifurcation. None of the predominant locations for cerebral aneurysms (the anterior communicating artery, the origin of the posterior communicating artery, and the middle cerebral artery bifurcation) has been represented by a spontaneously and fully thrombosed aneurysm, making it difficult to generalize on these 9 cases. Of these 9 patients, 4 underwent operation. Two cases had thrombosed lesions acting as spaceoccupying masses and were best handled by operation. In two other cases it was not known until the time of operation that the aneurysm had throm-

продолжение

Natural History of Ruptured Cerebral Aneurysms продолжение

bosed. Angiography performed closer to the time of operation would have spared a procedure, but angiography performed on one case only two days before operation did not accurately demonstrate the true situation. The other 5 cases did not undergo operation as the aneurysm had become no longer symptomatic and there did not appear to be any benefit in exploration. None of these cases has had a recurrent hemorrhage. It is concluded that those patients in whom an aneurysm undergoes spontaneous complete thrombosis and is asymptomatic should be observed, while those who are experiencing symptoms from mass effect should undergo operation for decompression. With the current interest in iatrogenic thrombosis as a treatment for intracranial aneurysm, it would be very important to know the degree of protection against rerupture afforded by thrombosis. This unfortunately cannot at present be stated with certainty (Figs 252-256).

Fig 252A-B A giant partially thrombosed right internal carotid aneurysm in a 19 year old patient (A) who showed a fully thrombosed aneurysm sac at operation (Case 4; Vol. II, Table 45). An EC-IC bypass procedure was performed in 1969. Postoperative angiogram (B). (From Yasargil, M. G.: Microsurgery Applied to Neurosur-gery. Academic Press, New York, Thieme, Stuttgart 1969).

329

330

5 Pathological Considerations

Fig 253A-E Right carotid angiography was normal (A) but left carotid (B) injections showed a small aneurysm of the left carotid bifurcation (arrow) in a 39 year-old patient following a subarachnoid hemorrhage. The finding of posterior callosal collaterals on vertebral angiography (C) was explained at operation when the aneurysm and the left A, segment were both found to be completely occluded (D and E). (Vol. II, Table 69).

Natural History of Ruptured Cerebral Aneurysms

331

Fig 254A-D Pneumoencephalography (A) and CT scan (B) confirmed the presence of a suprasellar mass in a 65 year old female with chiasmal compression. Right carotid angiography (C) failed to demonstrate an aneurysm despite good crossfilling (arrow). At surgery (right pterional approach) (D) a large, partially thrombosed left carotid-ophthalmic aneurysm with a small neck was clipped and resected (Case 26; Vol. II, Table 14).

332

5 Pathological Considerations

Fig 255A A large distal middle cerebral aneurysm was Fig 255B Repeat angiography four weeks later (prior to found on angiography in a 30 year old patient with Jack- surgery) showed complete disappearance of the lesion, sonian epilepsy.

Fig 256A-F Contrast CT scan in a 44 year-old patient with headaches (A) showed a suspicious right thalamic enhancing lesion (arrows) probably representing a thalamic tumor. Right carotid angiography (B) showed collateralization (arrows) from the distal middle cerebral to the posterior cerebral distribution.

Natural History of Ruptured Cerebral Aneurysms

333

R. PCA

Fig256C-F Vertebral angiography (C) showed occlusion of the right posterior cerebral artery distal to the P2 segment. At exploration (D) the patient was found to have a completely thrombosed aneurysm of the P2-P3 segments at the site of occlusion; the aneurysm was resected (E) and the patient made a good recovery. Postoperative CT (F).

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5 Pathological Considerations

Pathophysiological Complications of Ruptured Cerebral Aneurysm

damage and exert mass effect. These hematomas may be subdural, intracisternal, intracerebral. intraventricular, or a combination of these. The frequency of hematomas occurring with aneurysms at given locations in the present series is discussed in Vol. II.

Hematoma Formation The characteristic syndrome of ruptured intracranial aneurysm with headache, nuchal rigidity, and clouding of consciousness is so clearly identified with blood in the subarachnoid space that the Subdural Hematoma pathological entity has long been equated with Although delicate, the arachnoid is surprisingly "subarachnoid hemorrhage". The pathological strong, and generally prevents blood from a rupimportance of the presence of blood in the sub- tured aneurysm from entering the subdural space. arachnoid space, per se, has not been clearly Subdural hematomas with mass effect occurred in defined, although vasospasm and many toxic | only 11 of the 1012 patients (1.1%) in the present effects of blood and its breakdown products on series - in 6 cases of anterior communicating artery nervous tissue have been proposed. Of considerable ' aneurysm. 3 cases of internal carotid-posterior pathological importance, however, are intra-cranial communicating artery aneurysm, and 2 cases of hematomas which when large cause cortical middle cerebral artery aneurysm (Figs 257A-B, 258A-D).

Fig 257A-B A 39 year old patient presented in grade Illb following a subarachnoid hemorrhage. Left carotid angiography (A) showed a large anterior communicating aneurysm with displacement of the anterior cerebral artery to the right. A later phase of the angiogram (B) showed a large subdural hematoma (arrows) that was larger than suspected at surgery.

\

Natural History of Ruptured Cerebral Aneurysms Fig 258A-B A 43 year old patient with a subarachnoid

hemorrhage and grade 1Mb status presented with a posterior communicating aneurysm, marked perifocal vaso-spasm, and a large subdural hematoma (arrows). The patient died (Case 5; Vol. II, Table 35). Fig 258C-D Another patient with aneurysm of posterior communicating artery and large subdural hematoma (ar rows). D

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5 Pathological Considerations

As blood enters the subdural space under arterial pressure, significant brain shifts and herniations may occur, and in these 11 patients, the subdural hematoma was generally associated with an unfavorable outcome. In cases of SAH with progressive impairment, with or without a hemisyndrome, the possibility of a subdural hematoma should be evaluated by an EEG, a CT scan (which can be misleading), or repeated carotid angiography. A thin layer of subdural hematoma (1-3 mm) without mass effect has been seen in 14 additional cases. In a pathological series subdural hematomas were seen in 15-20 per cent of cases (Jellinger 1979). In our series these occurred in only 5.2 per cent. Intracisternal Hematoma The compartmentalization of the subarachnoid system is such that a given cistern may be tightly distended with hematoma while an adjacent cistern is essentially clear. For example, with an aneurysm of the internal carotid, the carotid cistern is often filled with clot while the chiasmatic cistern is clear. On the other hand, an aneurysm of the anterior communicating artery can be associated with hematoma in the interpeduncluar cistern as well as in the lamina terminalis cistern. The consistency of these hematomas varies from soft clot easily removed with suction, to .tenacious, firm hematoma which must be carefully dissected from delicate vascular and neural structures. The consistency of clot is of course related to the timing of operative intervention. It has also been noted that patients who have received antifibrinolytic agents will have firmer clot which is more difficult to aspirate. It is probable that hematoma in the basal cisterns exerts a mechanical effect as proposed by Johnson and associates (1958) and demonstrated by Arutiunov and co-workers (1974). This may be important in the initial cessation of bleeding at the ' i time of aneurysm rupture . arteries and veins traversing the cisterns however, may be comprom-' ised by distortion and pressure. The cisternal walls are competent enough to allow considerable local pressure to be exerted without a significant increase in general intracranial pressure. To what degree these mechanical forces are related to the phenomenon of cerebral vasospasm is not clear. In addition to the effects on local structures by intracisternal hematoma, cerebrospinal fluid circulation may also be impeded. It is not an uncommon finding at operation, that the removal of hematoma from the interpeduncular cistern or opening of the lamina terminalis will result in an immediate release of cerebrospinal fluid. These observations

suggest the importance of completely clearing the subarachnoid cisterns of blood if optimal recovery is to be expected. It is noted that the interpeduncular cistern often has a hematoma collection in association with a variety of aneurysms, and it is, therefore, important that the anterior wall of the cistern (Liliequist's membrane) be opened and the cistern inspected. Intracerebral Hematoma Saccular aneurysms are situated in the subarachnoid space and may to a greater or lesser extent lie embedded within the cerebral tissue. The incidence of intracerebral hematomas ranges from 43-79 per cent (Heyn and Noetzel 1956). In the series of Jellinger (1979) intracerebral clot occurred in 64 per cent of cases and in our pathological series 62.3 per cent had clot. Jt is common for the jet of blood from a cerebral aneurysm to disrupt the adjacent pia and dissect into the cortex. These intracerebral hematomas lead to focal neurological deficits, exert mass effect, and are associated with increased morbidity and mortality. As is noted (see Vol. II), intracerebral hematomas are most freiquent following rupture of a middle cerebral or distal anterior cerebral artery aneurvsm. At these locations, the brain envelops the arteries and the aneurysms, so that the full thrust of the blood jet from the ruptured fundus may be directed against the pia. Ruptured aneurysms at given locations can be expected to result in recognizable patterns of intracerebral hematoma: Internal carotid artery, medial wall: In 3 cases, internal carotid-ophthalmic artery aneurysms caused hematomas in the orbitofrontal area. In 2 cases, the aneurysm was suprachiasmatic, while in the third case, the fundus was subchiasmatic, but it had extended between the optic nerves to rupture into the gyrus rectus (Fig 259A-B). Internal carotid artery, lateral wall: Aneurysms arising at the origin of the posterior communicating and anterior choroidal arteries rupture most com monly into the adjacent parahippocampal gyrus of the temporal lobe (Fig 260A-C). Middle cerebral artery. Aneurysms of the middle cerebral artery bifurcation ruptured into the tem poral lobe (usually the superior temporal gyrus) in 28 cases, into the insula in 7 cases, into the frontal lobe in 14 cases, and into more than one area in 9 cases (Fig 261 A-B). ,,,,.,» Anterior communicating artery. Aneurysms of the anterior communicating artery rupture most com monly into the adjacent orbitofrontal area around the gyrus rectus (Fig 262A-B). They never rupture through the lamina terminalis into the third ventri cle . The lamina terminalis cistern is well-reinforced

Natural History of Ruptured Cerebral Aneurysms

Fig 259A-B A medially directed carotid-ophthalmic artery aneurysm (arrow) (A) that ruptured between the optic nerves creating a gyrus rectus hematoma (B) (Table 14).

at this location, preventing blood from dissecting up into the corpus callosum. In three cases however, blood escaped from the cistern superiorly and dissected along the corpus callosum from the genu to the splenium (Fig 263A-C). One of these cases died and the remaining two were paraplegic. Blood will dissect into the brain around the frontoorbital arteries, and the appearance of blood on CT in the frontoorbital and olfactory sulci on the surface of the frontal lobes is felt to be pathognomonic for ruptured anterior communicating artery aneurysms (Fig 264A-B). At times hematoma can be quite lateral in the frontal lobe. CT scan may not show these hematomas well because of the proximity of the dense bony orbits. Distal anterior cerebral artery. Pericallosal artery aneurysms rupture laterally into the adjacent radiations of the corpus callosum and cingulate gyri, but never directly into the corpus callosum itself (Fig 265 A-C).

337

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5 Pathological Considerations

Fig 260 A-C Diffuse intraventricular hemorrhage (A) caused by a ruptured right anterior choroidal aneurysm (arrow) (B) that was directed towards the uncus (C) (Vol. II, Table 40).

Natural History of Ruptured Cerebral Aneurysms

339

Fig 261A-B Following removal of this large right insular hematoma (A) and clipping of the middle cerebral bifurcation aneurysm, a grade IV patient made a good recovery.

Fig 262 A-B A frontal interbemispheric hematoma (A) from a ruptured anterior communicating artery aneurysm (arrow) (B), with marked segmental vasospasm of the pericallosal arteries along the clot.

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5 Pathological Considerations

Fig 263 A-C The CT appearance (A and B) of an intra-callosal hematoma from a ruptured anterior communicating aneurysm (arrow) (C). This patient survived with permanent paraplegia.

Natural History of Ruptured Cerebral Aneurysms Fig264A-B An antero-superiorly directed anterior communicating aneurysm (arrow) (A) with subarachnoid and left olfactory intrasulcal hematomas (B).

Fig265A-C Following a subarachnoid hemorrhage (A), the right carotid angiogram was thought to be normal. Two weeks later the patient suffered another hemorrhage (B) with both intracerebral and intraventricular components. Review of the previous angiogram showed a small right pericallosal aneurysm at the origin of the frontopolar artery (C) (arrow).

продолжение

341

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5 Pathological Considerations продолжение

Intraventricular Hematoma Blood may reach the ventricular system either by direct rupture through the cortex or by entering through the cerebrospinal fluid pathways. Pathological investigations in fatal cases showed massive intraventricular hematomas in 42.5 per cent. In the past, intraventricular hematoma has been considered almost invariably fatal. Computerized tomography however has shown intraventricular hematoma not to be uncommon following the rupture of an aneurysm, even in patients in satisfactory condition. A patient in the present series was taken from his card game for a follow-up CT scan to check ventricular size and the entire ventricular system was found to be filled with blood. There is not always a clear correlation between the amount of intraventricular hematoma and clinical condition. The CT scan has shown the resorption time for these clots to average 3-10 days, in rare cases considerably longer. As the ventricular system has not been opened routinely during surgery in this series, the exact percentage of intraventricular hematomas was unknown before the CT-scan era. Since 1976 it has been found on CT scan that 10 per cent of the operated cases have had mild intraventricular hematoma (occipital horn), 2 per cent moderate hematomas (partially filled ventricular system) and 0.5 per cent severe hematomas. Intraventricular hematomas appreciated at operation are generally an extension of an intracerebral hematoma into the adjacent ventricle. Sites of predilection for rupture into the ventricular system coincide with the location of the aneurysm and its associated intracerebral hematoma: Internal carotid artery. Aneurysms on the lateral wall rupture through the parahippocampal gyrus into the temporal horn, while bifurcation aneu-rysms rupture through the anterior perforated substance into the frontal horn. Middle cerebral artery. Aneurysms at this location may enter the temporal horn through the superior temporal gyrus or the frontal horn through the frontal lobe. Anterior cerebral-anterior communicating artery. These aneurysms rupture through the orbitofrontal cortex - the gyrus rectus, area olfactoria, and subcallosal gyrus - to enter the frontal horn near the foramen of Monro. Direct perforation of the lamina terminalis has not been seen at operation. Distal anterior cerebral artery. Aneurysms at this location rupture into the cingulate gyrus and penetrate the corpus callosum laterally to gain access to the frontal horn. It has been noted by computerized tomography that hematomas frequently migrate or form in the

occipital horns because of the patient's recumbejit position. Mohr et al (1983) reviewed 91 cases in which intraventricular hemorrhage was associated with ruptured aneurysm. The mortality rate was 64% and mortality appeared to correlate with changes in ventriculocranial ratio as measured on the initial CTscan.

Cerebral Ischemia and Infarction Focal ischemic symptomatology is frequently associated with ruptured intracranial aneurysm. This may present as a reversible ischemic phenomenon or may be seen as a complete cerebral | infarction. While ischemia is more common in the distribution of the vessel harboring an aneurysm, this is by no means always the case. The pattern of infarction may vary from a single infarct appropriate to a given vessel, to a picture of diffusejpatchy areas of infarction covering much of the brain, where the vascular pattern of ischemia is not apparent (Robertson 1949; Smith 1963; Crompton 1964; Janzer and Friede 1979). Cerebral infarction has been reported in 8 per cent (Freytag 1966) to 80 per cent of autopsy cases after rupture of an aneurysm (Crompton 1964; Hanau et al 1969). It is rather rare in sudden death due to massive intracerebral hemorrhage (Freytag 1966), but occurs more often with subarachnoid hemorrhage into the basal cisterns and Sylvian fissure (Hanau et al 1969). Ischemic necrosis may occur within the territory of the artery bearing the aneurysm (see Figs 184-186), but more often other parts of either hemisphere are involved. Hanau et al (1969) reported "paradoxical" lesions in two thirds of their cases. Some infarcts undoubtedly result from vascular occlusion which occurs either at the time of rupture or thereafter when thrombus seals the rent in the aneurysm. Taptas and Katsiotis (1968) and Antunes and Correll (1976) have pointed out the role of emboli from an aneurysm in producing cerebral infarction. Sakaki (1980) reported 4 cases and reviewed 10 papers in the literature dealing with this subject. Four cases in the present series showed occlusion of the angular branch of the middle cerebral artery with hemiplegia following rupture of a middle cerebral artery aneurysm, and in another case the superior main trunk of the middle cerebral artery was thrombosed. Similarly, cerebral infarction i occurring in the postoperative period may follow

Prolonged Chronic Spasm or Narrowing of Arteries

343

dislodgement of thrombus or atheromatous plaque The mechanism by which rupture of an aneurysm at the time of operation. leads to cerebral vasospasm has been widely invesA patient who was reexplored when he became tigated, primarily in animal models. Proposed hemiplegic following clipping of a pericallosal theories include: a neurogenic response to rupture artery aneurysm showed the lumen of the perical- mediated by an adrenergic nervous system (Peerless losal artery to be occluded by a plaque which had 1969; Flamm et al 1972; Peerless and Kendall 1975), a been fractured from the intima by application of primary myotonic response in the arterial wall (Simeone and Peerless 1975), compromise of the the clip. The artery was thrombosed distally. arterial system by_stretching and tenting of the Crompton (1964), found cerebral infarction in 119 arachnoid (Kapp et al 1968; Arutiunov et al 1974), and of 159 cases in an autopsy series and listed those a pharmacological response of the vessel wall to factors which he felt contributed to cerebral infarc- substances liberated from blood (Kapp et al 1968; tion. These included: atherosclerosis of the cere- Robertson 1949; Zervas et al 1974; Alien et al 1977; bral arteries, poor collateral circulation through Suzuki and Ohara 1978,1979). While blood products the circle of Willis, subarachnoid hematoma espe- are presently the most widely accepted cause of cially dissecting along the perivascular sheath of vasospasm, surprisingly little attention is given to the perforating arteries, systemic hypertension, the fact that patients with ruptured arteriovenous surgical manipulation, and the presence of vaso- malformations may present with subarachnoid spasm on premortem angiography. hemorrhage and the same clinical picture as patients The future treatment of patients with ruptured with ruptured cerebral aneurysm, but vasospasm is aneurysms must take into account these findings. not observed on the angiograms of these patients.; The practice of vigorously lowering the patient's It is also a very interesting phenomenon that systemic blood pressure after subarachnoid hemor- patients with nega-: tive 4 vessel angiography after rhage may precipitate such a pattern of infarction. subarachnoid hemorrhage show spasm in a much lower percentage (1% instead of 30-40% in proven aneurysm cases). These patients also have a lesser degree of Vasospasm spasm, even though in most of the cases the CT Vasospasm following mechanical stimulation of a scan confirms the SAH with hematoma in the basal cerebral artery or application of blood to the cisterns, and in some cases even in the ventricular intracranial vessels of animals has been recognized system. If the presence of blood in the basal for many years (Florey 1925; Echlin 1942). Robert- cisterns should always cause vasospasm, there is no son (1949) suggested vasospasm as the etiology of answer to the question as to why those cases with cerebral infarcts in patients with ruptured cerebral SAH but without an aneurysm rarely show vasoaneurysm for whom there was no other apparent spasm and as to why the cases with ruptured AVM cause for ischemia. Two years later, Ecker and do not show spasm at all._______________ Riemenschneider (1951) reported segmental narrowing of the cerebral vessels seen on angiography in patients who had sustained ruptured aneurysms. A Prolonged Chronic Spasm or straightforward cause and effect picture seemed to emerge following rupture of an aneurysm, some Narrowing of Arteries mechanical factor or a deleterious component of blood in the subarachnoid space caused spasm of There is increasing evidence that whatever is the the cerebral arteries, and this spasm led to ischemia factor initiating constriction, prolonged spasm and infarction. Because of the potential for phar- leads to degenerative changes in the vessel wall macological manipulation of vasospasm, considerable (Ya§argil 1969; Alksne and Greenhoot 1974; Fein et investigative effort has been expended in al 1974; Hughes and Schianchi 1978). The mievaluation of cerebrovascular spasm. Unfortu- crosurgical observations of the reaction of brain nately, a clear picture has not emerged, either arteries to mechanical stress in the laboratory and in concerning the relevance of vasospasm to ischemic the human theatre convinced the senior author that symptomatology, or to the pharmacological control vasospasm has clearly recognizable morphological steps. Initially for only a few seconds, the intima of of the phenomenon in aneurysm patients. the artery becomes swollen causing a narrowing of Hashi and Nishimura (1977) charted the time the intraluminal space (best observed in the rabbit course of vasospasm by means of serial angiography and dog basilar and middle cerebral arteries). This and concluded that spontaneous recovery of is later followed by a segmental narrowing of the vasospasm occurred around 3 weeks after SAH. whole diameter of the artery. This

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5 Pathological Considerations

spasm is rapid in onset, transient in duration and easily counteracted by the local application of papaverine. Prolonged narrowing has been seen in patients with incomplete resorption of a hematoma around the basal arteries after a period of 2-4 weeks or longer. Upon microsurgical exploration and inspection, these vessels appear opaque and greyish-white and they are frequently surrounded by an inflammatory exudate. They dilate poorly if at all to papaverine. Indeed, it may well be that much of the significant persistent vascular narrowing is not primarily vascular hypertonicity but edema and inflammation of the vessel wall. This pathological alteration of the wall may be due not only to the inflammatory stimulus of the surrounding blood but also to interference with the nutritive mechanism of the vessel wall (p. 90, Ya§argil 1969). There is mounting evidence that delayed "vaso-spasm" is not muscular spasm at all, but rather a morphological change in the arterial wall (Wilkins 1980). This vascular injury reaction, which may be a nonspecific reaction to an insult, is also referred to as an acute proliferative vasculopathy. It consists of the initial loss of portions of the endothelial lining accompanied by necrosis of the smooth muscle in the tunica media and followed by intimal thickening.

Our Observations A. G., a 36 year old man, sustained a subarachnoid hemorrhage on 27 August, 1966. In September, 1966, he suddenly became hemiparetic on the left. It is not known whether he suffered a second subarachnoid hemorrhage. Angiography performed on 1 Febuary, 1967, five months after the subarachnoid hemorrhage, showed an aneurysm of the right middle cerebral artery with spasm around the right internal carotid artery bifurcation and the middle cerebral artery. Pneumoencephalography showed expansion of the right frontal horn consistent with atrophy in the right frontal lobe. At operation on 22 Febuary, 1967, the aneurysm was partially thrombosed and atrophic changes were present in the right frontal and temporal lobes. The right middle cerebral artery was spastic and showed proliferation of the vasa vasorum, and the primary branches were thickened and narrowed. The middle cerebral artery did not dilate with application of papaverine. His condition was unchanged post-operatively. His post-operative course included a ventriculo atrial shunt which was revised twice. He was seen in 1978, and though self-sufficient, he has a left hemiparesis. He is taking anti-epileptic medications, and does part time work (Fig 266).

Comment: The process within the Sylvian fissure, presumably initiated by hematoma, had induced chronic changes in the arterial walls of the middle cerebral artery and its branches, including the

Fig 266 Six months following a subarachnoid hemorrhage with a left hemiparesis, angiography revealed a right middle cerebral aneurysm with narrowed internal carotid, A,, and M-, segments. At surgery the middle cerebral artery was chronically narrowed with no response to the application of papaverine or a local sympathectomy. The surrounding frontal and temporal lobes were noted to be severely atrophic.

growth of vasa vasorum into the wall of the middle cerebral artery. The artery showed no response to the application of papaverine. S. A., a 32 year old man, suddenly lost consciousness at a religious meeting on 11, October, 1968. He was hospitalized and angiography showed a left middle cerebral artery aneurysm with spasm of the left internal carotid and the middle cerebral arteries, including its branches. He was discharged, but 3 weeks later had a sudden headache and loss of consciousness. He was subsequently dysphasic with anomia and acalculia, and exhibited a hemisensory loss on the right and a mild distal right hemiparesis. He was referred to Zurich 5 months later. At operation on 1 April 69, the left middle cerebral artery was unremarkable. The major branches, however, were white and narrowed with thickened arachnoid and organized hematoma. There was no reaction to local papaverine application. The aneurysm was clipped. Postoperatively there was no significant change in his neurological condition (Fig 267A-B).

Comment: Again chronic constrictive changes had occurred in the branches of the middle cerebral artery and persisted several months after subarachnoid hemorrhage. Prolonged delay in operation resulted in no clinical improvement. Finally, the relationship of vasospasm to cerebral infarction is also unclear. There are investigations which report a correlation between neurological deficit and vasospasm (Allcock and Drake 1965; Graf and Nibbelink 1974; Fisher et al 1977) and those which find no correlation (Schneck 1964; Millikanl975).

Cerebral Edema

345

A * ^ * B Fig 267A-B A 31 year old patient was operated upon 6 months after two subarachnoid hemorrhages from a left middle bifurcation aneurysm. Angiograms at the time of hemorrhage (A and B) show severe segmental spasm (arrows) of the internal carotid, A,, and M-, segments. At surgery these vessels were pale and chronically narrowed with no dilatation to papaverine or sympathectomy.

Cerebral blood flow measurements correlate somewhat better with neurological deficits, and blood flow alterations may or may not be associated with vasospasm (Zingesser et al 1968; James 1968; Heilbrun et al 1972; Mathew et al 1974; Grubb et al 1975; Meyer 1979; Kohlmeyer 1979). It has been concluded from these observations that factors other than vasospasm such as edema, hematoma, and normal pressure hydrocephalus are of primary importance in reducing CBF and causing ischemia and neurological deficit (Meyer 1979). ___________________ Vasospasm is most probably related to ischemia when the luminal diameter of a vessel is reduced by vasospasm to a degree severe enough to compromise flow in an area where blood flow is already partially compromised by other factors. The radiological pattern of vasospasm is presented in Chapter 3 and the clinical implications of cerebral vasospasm are discussed more fully in Chapter 4.

Hypothalamic Injury The frequent ocurrence of lesions of the hypothalamus in cases of ruptured aneurysms was noted by Crompton (1963). Hypothalamic lesions have been commonly associated with aneurysms of the anterior and posterior communicating arteries, but they have also been seen with aneurysms in almost all locations. Infarctions in the hypothalamus have been both ischemic and hemor-rhagic. In separate reports, Wilkins (1975) and Nagai et al (1976) have reviewed the pathophysiology of the

hypothalamus in subarachnoid hemorrhage, especially as it relates to cerebrovascular spasm. The electrolyte changes, hyperpyrexia, hypertension and cardiac abnormalities associated with ruptured cerebral aneurysm suggest that the hypothalamus is frequently functionally altered in this disease. In our experience, however, disturbances of electrolytes and endocrine function following sub-arachnoid hemorrhage have not occurred. Despite angiographic evidence and even direct observation of severe spasm in the A1; A2, M, and Pl segments, the perforating branches (including those to the hypothalamus) were never involved. On the contrary, these vessels appeared dilated and were more readily identifiable than usual. Explanations of the pathophysiology of vasospasm must take into account this paradoxical response of perforating vessels. Similarly, the mechanical distortion of perforating vessels by large and giant aneurysms may compromise their lumen to a degree, but severe strangulation does not occur. Hypothalamic dysfunction following subarachnoid hemorrhage is more likely due to direct injury or compression of this structure and it is not secondary to the perforating vessels being compromized.

Cerebral Edema While there is slight evidence that a direct toxic effect of blood in the subarachnoid space (Nibbelink et al 1975) or a hypothalamic response (Nagai et al 1976) might lead to cerebral edema following subarachnoid hemorrhage, it is generally

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5 Pathological Considerations

considered that cerebral edema is related to cerebral ischemia. Symon (1978) noted that at the levels of ischemia generally found following SAH, the increased permeability of cell membranes and cellular swelling may play a more important role than the loss of capillary integrity and the breakdown of the blood brain barrier. This may be followed by the transudation of fluid across the capillary due to an increased blood pressure in the absence of autoregulation. He has found experimentally that cerebral edema can accumulate quite readily and lead to rapidly increasing intracranial pressure. It has been noted, however, at operation that although the brain may appear distended as the dura is opened, the subsequent release of cerebrospinal fluid from the basal subarachnoid cisterns will allow the brain to fall away from the dura. The cause of "brain swelling" in these cases is not edema, but rather a disturbance of cerebrospinal fluid circulation akin to those factors that result in hydrocephalus.

Ventricular Dilatation and Communicating Hydrocephalus The fact that ventricular dilatation can be a consequence of blood in the subarachnoid space was first suggested by Bagley in 1928. Krayenbiihl and Liithy (1948) described two patients who had suffered subarachnoid hemorrhage from a ruptured cerebral aneurysm and who showed marked ventricular dilatation at autopsy. Foltz and Ward I (1956) were probably the first authors to recognize . two phases of ventricular enlargement following SAH. The incidence has been variously reported as between 634 per cent (Foltz and Ward 1956; Kibler et al 1961; Shulman et al 1963; Galera and Greitz 1970; Kunst and Quenzer 1971; Griffith et al 1972; Raimondi and Torres 1973; Ya§argil et al 1973; Symon and Dorsch 1975; Mizukami et al 1976; Pertuiset et al 1972; Blaylock and Kempe 1978; Symon 1978; Ishii et al 1979; Julow et al 1979). Before the CT scan era, acute hydrocephalus was diagnosed only with the help of cerebral angiography and chronic hydrocephalus was demonstrated with pneumoencephalography or echoencephalography. Since the CT scan, the dynamics of the blockage and subsequent clearing of the pathways within the ventricular system and along the arachnoid cisterns can be followed and demonstrated. The experience derived from the present series of patients indicate

I that transient ventricular dilatation developing 1 within hours and lasting for 1-3 days, occurs com• monly. Moderate ventricular dilatation was seen in 20 per cent of the operated patients. Postoperatively normalization of the ventricular size within days was seen in 10 per cent of patients, while in 2 per cent of the cases the normalization time extended up to 4-8 weeks. I In 8 per cent definitive treatment (ventriculoatrial or ventriculo-peritoneal shunting) was indicated after the RHISA study was found positive. Vassilouthis and Richardson (1979) performed an exhaustive study and evaluation of CT examinations in 210 patients after SAH and reviewed the literature. They concluded that ventricular dilatation persisting or occurring later than the second week after SAH (late phase), was present in 22 of , the 210 patients_(10.5%}. Of these, enlargement was considered clinically significant in 15 (7%). The authors concluded that this was the incidence of communicating hydro_cephalus in their series./Mechanical obstruction of the cerebrospinal fluid by blood clot or its organization at the level of the exit foramina of the fourth ventricle or within the basal cistern is considered the mechanism responsible for the production of the early ventricular enlargement (Foltz and Ward 1956; Kibler et al 1961; Knibestol et al 1976; Kusske et al 1973; Mizukami et al 1976; Shulman et al 1963). Blockage of the arachnoidal villi by red cells, with subsequent impairment of the absorption of CSF along the superior sagittal sinus, has also been suggested (Blaylock and Kempe 1978; Ellington and Margolis 1969; Shulman et al 1963). Ishii et al (1979) examined the subarachnoid space after SAH with the help of the scanning electron microscope and classified obstructive changes into five grades ranging from patency to total obstruction. They reported a correlation between communicating hydrocephalus and obstruction if an obstruction above grade 3 was found in the para-sagittal region or in the lateral cerebral spaces. Julow and Ishii (1979) studied in 60 dogs the changes of arachnoidal tissue after experimental SAH. Their examination by scanning electron microscope showed resting and activated macro-phages, erythrophagocytosis, and giant cells in the subarachnoid space after SAH. They concluded that the macrophages play an important role in the formation of subarachnoid fibrosis, similar to the role of macrophages in fibrosis at other sitesjThese electron microscopic findings support the hypothesis that the pathogenesis of the second or "chronic" phase of hydrocephalus is explained on the basis c:^asaj_arachngidal adhesions, resulting from a leptomeningeal reaction to the presence of_

t) l

Unexplained Subarachnoid Hemorrhage blood products, thus preventing the CSF from reaching the site of its absorption. The question arises as to whether it is only the severity of the SAH or whether an additional factor may play a role in producing residual hydrocephalus as it occurs in only 6-10 per cent of cases._______ The incidence of hydrocephalus seems to vary considerably with the site of the aneurysm. Symon (1978) noted that of his 12 cases (6%) requiring a shunt following SAH, there was only one middle cerebral aneurysm. Kazner and Lanksch (1979) observed hydrocephalus as a complication predominantly caused by SAH from aneurysms of the

347

subarachnoid hemorrhage carried a more benign prognosis. McKissock and Paine (1959) stated that 390 of their 781 patients with subarachnoid hemorrhage (50%) did not have a definite diagnosis although in 75% of autopsies an aneurysm was found. Walton (1956) extracted 173 carefully autopsied cases from his series and was unable to find a source of bleeding in 14 (8%) although an aneurysm was suspected in some. Hofer (1966) analysed the cases of subarachnoid hemorrhage seen at the University of Zurich from 1940 to 1965. Of 1053 cases, 283 (27%) did not have a clear etiology of hemorrhage determined.

arteries. Sakamoto et al (1979) reported that^ The findings at lumbar puncture revealed: CSF bloody and xanthochromic CSF among 52 shunted cases (21.2% of the series), the bloody but clear supernatent CSF localization of the aneurysm was in 22.6 per cent not bloody but xanthochromic CSF either on the AcoA or the ICA, in 23.1 per cent either on the ACA or multiple, in 14.6 per cent on clear - reported bloody by the the MCA, and in 0 per cent (30 operated cases) on referring physician

the vertebro-basilar arteries. A more detailed presentation by Vassilouthis and Richardson (1979) reveals the following sites of aneurysms: I In cases with acute ventricular dilatation, the site of '' aneurysms was on the ACA or AcoA in 50 per cent, on the ICA in 19 per cent, on the MCA in 15 per cent and on the vertebrobasilar system in 8 per cent. In cases with chronic hydrocephalus, the site of aneurysm was on the ACA/AcoA in 23 per cent, on the ICA in 27 per cent, on the MCA in 9 per cent and on the vertebrobasilar system in 18 per cent. In our series 88 patients (8.7%) were observed with a malresorptive hydrocephalus which needed a shunt procedure. The site of aneurysm was on the ACA in 47 patients (11.4%), on the ICA in 19 patients (6.0%), on the MCA in 10 patients (5.4%), on the basilar artery in 11 patients (14%) and on the vertebral artery in 1 patient (6.7%) (see Vol. II, Chapter 9, Table 129b). anterior communicating and internal carotid

Unexplained Subarachnoid Hemorrhage In any large series of patients with subarachnoid hemorrhage, there exist some cases in which no cause for the bleeding can be found. Hook (1958) reported a group of 138 cases of unexplained subarachnoid hemorrhage. All had undergone bilateral carotid angiography and 38% had vertebral angiography. This series had a median age of 43 years and an average follow-up time of 4.5 years. Within this time period, 6% sustained a fatal recurrent hemorrhage, and Hook concluded that in the absence of a demonstrable angiographic lesion,

206 (73%) 2 (1%) 51 (18%) 24 (8%) 283 The method of angiography employed in these cases was: Bilateral carotid, bilateral vertebral 37 (13%) Bilateral carotid, unilateral vertebral 40 (14%) Bilateral carotid only 125 (44%) "Unilateral carotid, unilateral vertebral 8 (3%) *Unilateral carotid only 39 (14%) Unilateral vertebral only 2 (1%) No angiography 31 (11%) 282 * Bilateral filling was achieved.

233 of the 283 patients have been followed to the time of the publication. 48 patients have died, with 12 of these coming to autopsy and the following diagnosis being made: Ruptured cerebral aneurysm 5 Intracerebral hemorrhage 3 Subarachnoid hemorrhage 1 Cerebral edema 1 Multiple Sclerosis 1 Pneumonia 1 In 21 additional cases a cause of death was given without autopsy: Cerebral hemorrhage 8 Lung carcinoma 5 Cardiac failure _ 5 Suicide '* 3 For the remaining 15 patients, no information was available. Subarachnoid hemorrhage recurred in 29 patients (12%) with 17 of these being represented in the

348

5 Pathological Considerations

mortality statistics. Only 2 of the 12 living who had recurrent hemorrhage have had four vessel angiography. Therefore a cerebral aneurysm in the other 10 has not been definitely excluded. There were 118 (50%) patients symptom free at the time of publication, while 54 (23%) had neurological complaints such as dizziness, headache, nausea, or malaise, without specific neurological findings. 13 (6%) had neurological deficits, such as hemiparesis, extraocular muscle palsies or seizures. The finding of 17 deaths from recurrent hemorrhage (7%) is quite comparable to the study of Hook (1958). There remained a total of 37 cases (27%) in the series who underwent bilateral carotid angiography and at least unilateral vertebral angiography, and in whom no cause of subarachnoid hemorrhage has been found. Four of these died without a source of bleeding being determined, while 27 are living including two who sustained recurrent subarachnoid hemorrhage. In 6, information as to their course is lacking. Grauer (1979) has added to the above analysis those cases seen between 1966 and 1979. In 244 no source of bleeding was found. Findings at lumbar puncture: CSF blood stained and xanthochromic CSF xanthochromic CSF clear

210(86.1%) 26 (10.6%) 8 (3.3%)

244

193(79.1%) 4 (1.6%) 42 (17.3%) 1 (0.4%) 4 (1.6%) 244 * Bilateral vertebral filling was achieved. ** Reasons for incomplete studies including age, poor clinical condition and patient refusal.

Of these 244 patients, complete visualization of the intracranial vasculature (either directly or by retrograde filling of the contralateral side) was obtained in 80.7%. 188 patients could be followed up (mean 4.4years). 17 (9.0%) died in 13 of whom recurrent hemorrhage was not suspected (4 autopsied) and in whom the following diagnoses were made: myocardial

Method of angiography: Bilateral carotid, bilateral vertebral

*Bilateral carotid, unilateral vertebral Bilateral carotid only "Unilateral carotid only **No angiography

infarct 2, accidental death 1, uremia 1, carcinoma 2, unknown 3. 14 patients sustained recurrent SAH (7.4%) in 5 of whom it occurred within one month. Four deaths (2.1%) were certainly attributable to recurrent hemorrhage (3 verified by autopsy of whom 1 was found to have a ruptured posterior communicating artery aneurysm and the others no obvious vascular abnormality). Of the 10 survivors of the recurrent hemorrhage, 6 (3.2%) had further negative angiography and 4 (2.1%) had positive findings - 2 on previously omitted vertebral angiograms (1 AVM, 1 aneurysm). There was one cervical spine AVM demonstrated and in one case a previously suspected but unoperated anterior communicating artery aneurysm was confirmed. Of the 171 known survivors, 51 (29.8%) are symptom free, 34 (19.9%) have minimal complaints and 65 (38%) have moderately severe headaches. Eleven (6.5%) have definite neurological findings. Thus of the 188 patients followed up only 1 case of ruptured aneurysm as a cause for a recurrent bleed was diagnosed at autopsy. Of the 147 cases followed up who had panangiography at the time of their first bleed 6.1% had recurrent hemorrhages but in only 1 case was new, unsuspected pathology found on reinvestigation (spinal AVM). Repeat normal panangiography seems to be justified only in cases with suspicious findings such as spasm. In other cases the natural history should be followed. With regard to spinal tumors and AVMs myelogra-phy was carried out in 17 patients (7.0%) and spinal angiography in 5. Some elements in the history or physical findings suggested the possibility of a spinal lesion but only the one case

of spinal AVM was found. All patients were seen in medical consultation to exclude other causes of SAH. Nineteen per cent of the latter group of patients were hypertensive. In the earlier series this was not recorded. Finally, in this present series a further 83 cases of subarachnoid hemorrhage of indeterminate etiology have presented between September 1979 and December 1981. Of these, 64% were male and 36% female. The average age was 44.0 years (range 22-71 years). In 57% the family history was entirely negative, 16% of patients had a family history of stroke and 17% of cardiovascular disease and diabetes mellitus. There were no cases in which other members of the family had suffered a subarachnoid hemorrhage. 58% of the patients themselves had no significant past medical history, while 6% had previous transient ischemic attacks and 13% evidence of previous cardiovascular disease or diabetes.

Unexplained Subarachnoid Hemorrhage

The hemorrhages occurred during normal daytime activities in 58%, sporting activities in 19%. heavy work in 8%, coitus in 6% and whilst using the lavatory in 5 %. __ Symptoms included headache, vomiting and neck stiffness in 53%, headache and meningism (no vomiting) in 27%, headache alone in 6%, drowsiness (10%), and loss of consciousness (6%). Lateralising or focal neurological deficit occurred in 12%, psycho-organic syndrome in 12% and epileptic seizures in 3.6%.______________ 65% of the patients presented in grade la, 2.5% in grade Ib, 30% in grade Ila, and 2.5% grade Ilia. 75 patients (90%) had a lumbar puncture of which 96% were positive for blood staining and xanthochromia. 41 patients (49%) had an EEG of which 49% showed focal changes and 56% showed non specific change. 81 patients (98%) had a CT scan of which 46 (57%) were normal, 30 (37%) showed subarachnoid blood and a further 5 (6%) were suspected as showing subarachnoid blood. Angiography was performed in all 83 cases. Of these, 72(87%) had four vessel angiography and 11 (13%) had 2 or 3 vessel studies. All angiograms were normal. 3 had subsequent myelography and one a spinal angiogram. All were normal. Forster and associates (1978) reported a series of 529 patients of whom 150 (28%) had negative angiography. 56 of these patients were subjected to repeat pan-angiography and in only 1 patient was an aneurysm found. They felt that repeat angiography was probably not justified as a routine follow-up procedure. They suggested the self-repair of small aneurysms as a probable mechanism. Mujica et al (1981) recently reported a case of an ascending pharyngeal aneurysm as the source of a subarachnoid hemorrhage. This lesion was only identified using selective external carotid angiography. One wonders if perhaps in the future selective external carotid angiography should be routinely performed in cases of subarachnoid hemorrhage with negative four-vessel angiography, but such a case seems to be extremely rare. The diagnosis of occult arterio-venous malformation described by Margolis and associates (1951) and by Crawford and Russell (1965) has remained a popular diagnosis for unexplained bleeding. It is probable that with increased use of computerized tomography, the number of unexplained subarachnoid hemorrhages, especially those related to primary intracerebral hemorrhage and to brain tumor, will diminish. In a recent study, however, by Hayward (1977) in which computerized tomography was used, 91 of 592 cases (15%) of subarachnoid hemorrhage remained unexplained. 51 of

349

these cases had undergone complete angiography. Computerized tomography has been in use at the University of Zurich since 1975. Between 1977 and 1979, 59 patients were examined with unexplained subarachnoid hemorrhage. There were 6 with infarcts, 3 with intracerebral and 4 with intraventricular hemorrhages. 4 vessel angiography failed to reveal any aneurysms, AVMs or tumors. It seems then at present, that an active clinic will continue to encounter cases of apparent SAH for which in life and sometimes even in death a definite cause cannot be found. It may well be that a proportion of these cases are not spontaneous SAH but are iatrogenic in nature. Of some interest in these cases is the small incidence of angiographically demonstrated cerebral vasospasm (2%). Even when it does occur it is usually quite localized, is of minor degree and is clinically undetectable except in those patients shown on repeat angiography a few weeks later to have a hidden aneurysm. Why subarachnoid hemorrhage of undetermined cause, hemorrhages from AVMs and bleeds from tumors should be associated with such a low incidence of diffuse spasm is unclear. It may provide a lead in the search for the etiology of spasm, perhaps indicating that further research into vessel structure itself is required. In terms of treatment of patients with subarachnoid hemorrhage who have no aneurysm on angiography our policy is as follows. Those patients whose angiogram shows spasm judged sufficient to mask a possible aneurysm continue resting quietly until angiography is repeated after 4-8 weeks. If the second angiogram fails to reveal a leasion they are discharged. Patients with a proven subarachnoid hemorrhage but no angiographic abnormality at all are carefully checked for bleeding disorders, hypertension, spinal symptoms, or any form of drug ingestion which may have led to a bleed. If none is found they are merely advised to rest quietly for about four weeks then gradually to | resume normal activities and told that the chance of • recurrent hemorrhage is very small.

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