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441.&LIPPINCOTT WILLIAMSo WILKINS A Wolterr Kluwcr Company
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441.&LIPPINCOTT WILLIAMSo WILKINS A Wolterr Kluwcr Company
Baltimore New York London Buenos Aires Hong Kong Sydney Tokyo Philadelphia
Acquitirions Editor: Eli~abcthA. Nicginrki Editorid Director oj Detuhplnm~t:Julie hdnrtiner DcrvL~pnmtEditor: Karln h4. Schroedcr . Srr~ior.\tamgirrg Editor: Alny G. Dinkel
a Co&t-ight0 I&W by Lippincott \Villiims & Wilkips. All rights reserved. +is &k is prcltectd by copyright. No part of it may k r r d u c e d . stored in a rerrieval $-stem, o r tnnsrnitrd, in any form or by any means-electronic, mech;lnical, p h o r ~ o p yrecording. , or othenrise--without the prior written permission of the publisher, except for briefquotations einturdied in critical articles, reviews, and testing and e\.nluation materiaL by the publisher r o sch=ls that have adopted its accompanying textbook. Print& in h e United States of America. For information, \\-rite Lippincon Williams & W i l k h , 227 East Washington Square. Philadelphia, PA 191@6. =
~ i t e r i a l appearing s in this b c d prepared by individuals as part of their official duties as U.S. Go\-ernnenc employees are not covered by the ah-e-mentioned copyright.
Fix, Jaiies D. Hish-yield n~~tronnatomy / James D. Fix.-2nd p. ;cm. - (High-yield series) Includes index.
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ISBN @-653-30721-5 1. Neuroanatom).-Ourlines, syllabi. etc. 2. Neuroanatomy-Examinations. questions. e c c I. Title. 11. Series. iDNLh!: I. Nervous System-anatomy Sr histology-Esamination Questions. 2. Xervous Sptem-anatomy & histolo~--Outlines.3. Nen-ous System Diseasec-Esamination Questions. 4. Nervous System Diseasej--Outlines. \WL 18.2 Fj66h ZkW] Qxftjl .F%8 2039 61 1'.Sf07f;~2l 99-051352
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Care has been caken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the authors, edirors, and publisher 2re nor responsible . fcr erron or omissions or for any consequences from application of the information in this book and make no u.arranc)., express or implied. uith respect to the contena of the publication. T h e authors, editors, and publisher have esened ever{ efforr ro ensure that drug selection * and d o s g e set forth in this text.are in accordance with current recommendations and practice at the time of pubiicacion. However, in view of ongoing research, changes in governmen: regulations, and the constant flow of information relating to drug therapy and drug reactions, t h e reader is urged to check the ~ a c k a g einserr for each drug for any change in indications and dosage and for added warnings and precautions. This is particularly important when c h i recommended agen: is a new or infrequently ernploycd drug. Some drugs a n d 5 e d i w l devices presented in this publication have F d and Drug Ad-minixration (FDA) clearance for limited use in restrictcli research settings. It is the r e s e n s i biliry of the health care provider to ascertain the FDA status of each drug or device plahned for use in their clinical practice. '
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The second edition of Hi.&-Yield Ne~troni~aro~~lv is still neuronnatainv at its irreduc;ible minimum. con* raining most, if n o t all, of the national board themes. The sole purpose of the book is to get you through the nert-ous system topics covered on the Uniced States Medical Licensing Exatnination (USMLE) Step 1. Substi~ntialsdditions ha\-e been inade to accointnodate student requests and suggestions.
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TO THIS EDITION
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Mini-atlas of nuclear ~nagneticinlasing scans Carorid and vertebral digital subtraction angiography Nuclear magnetic angiopra~h!. Additional figures of cranial nen-e function conlponents Chapter o n aphasia. aprasia. and dysprosody Index
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TO THE STUDENT To make the most. of chis book, study the illustrations, computed tomography scans, and magnetic resonance images carehlly, and read the legends. Many board-type questions come from this source. In fact, the answers t o a t least 20 common USMLE questions are found wichin this preface. Finally, remember these tips as you scan the chapters:
Chapter I: T h e mini-atlas provides you \vith the essential examination strucrures labeled o n compuced tomography scans and magnetic resonance images.
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Chogter 2: Cerebrospinal fluid pach\vays are \\'ell demonstrated in Figure 2-1. Cerebrospinal fluid is produced by the choroid plesus and absorbed by the arachnoid villi that jut into the venous sinuses. Chapter 3: T h e essential arteries and the functional areas that they irrigate are shown. Study the carotid and verrebral angiograms and the epidural and subdural hematomas in computed tomography .,. scans and magnetic resonance images.
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Chapter 4: T h e neural crest and its derivatives, the dual origin of the pituitary gland, and the difference between spina bifida and the Arnold-Chiari ~nalformationare presented. Study the figures that illustrate the Arnold-Chiari and Dandy-Walker malformations. Chnprer 5 : W h a t is the difference betiyeen Lewy and Hirano bodies'? Nerve cells contain Niss! substance in their perikaq-a and dendrites, but not in their axons. Remember that Nisslsubstance (rough endoplasmic reticulum) plays a role in protein synthesis. Study Figure 5-2 on t h e localization and pre\*alenceof common brain and spinal cord tumors. Remember that, in adults, glioblascoma multifortne is che most common brain tumor, follo\\~edby astrocycoma and meningioma. In children, astrocyroma is the most common brain tumor, followed by rnedulloblastoma and ependymoma. In the spilial cord, ependymoma is the most common tuhor. Chnptcr 6: Tile adult spinal cord tcrrninatcs (conus ter~ninalis)ac the lo\ver border of the first lumbar \vertebra. Thc newborn's spinal cord extends to thc third lumbar vcrtcbra. In adults, the cauda equina csrentls froni \-crtcbral le\*clsL-2 to Co. Cliaf)tC)'7: The tracts of the spinal cord arc rcduccd to four: corticospinnl (pyramidal), dorsal co!::-:nz,
pnii~n l l c l tctnpcraturc, and Horncr's. Know the111cold.
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I . I ......................................................................................................................................................................................................... I Choptrr B,? a11L4 d I I chapter IO: CN C N V-2;C N CN iV, C N VI, I I Chaprer Vestibule-ocular . . 12-3). I Chaptzr I Chapizr 14I -
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Preface
S: Study thc eight classic natic~t~nl \\onr~lle3ic)ns of the spiunl cord, Four l ~ c a \ ]litters .~ arc: Rro\rrn-SCqu;~rJsyi~tlrotne, nCitnminosis (si~baci~te ccli~~l\ii~eJ ilcgct~eration),syringo1lIyelia, ; ~ l l l s ~ ~ r ~l;lteri~l ~ p l ~sclerosis ic (Lou Cellrig's ireasc).
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Chaptc~-9:S t t ~ d yt l ~ trnns\:crse e sections uirhc brain SC~III, nnci locali:e t h e c r m i a l ner\.e ~ ~ u c l eStudy i. t]le ventral surface r)f the brain steln, and id~nrifytllc exiting and e!~reringcranial ner\.i.s. On tlte L{orsal rtlrfa& of the brain srcrtn, identify t h t ur~lyesiting crnninl ner\*e, the trochle;lr nerve. .
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Cri~nialnerve.(CN) 11-1 is the afferent limb of the corneal retles. \!-I, a11d the postg;~i~glionic syinpathetic fibers are all found in the cavernous sinus.
Chapter 11: Figure 11.1 shotvs the auditory pathivay. \What iIre the causes of conJucrio~.ra n d sensorineural denthess? Describe the IVeber and Rinne tuning fork-tests. Remember t11at the auditoV 1.ren.e and the organ of corti and derived fro111 the otic placoclc.
12: This chilpt& describes the rs.o types of \.ertibuli~rn;*stagmus: postrotational and caloric'
(CO\VS acronym). ure
refleses in the'unconscious patient arc also discussed (sek Fig-
13: This chapter on the cranial nerves 'is pivotal. It spawns Inore ncuroanatomy examination questions than any other chapter. Carefully study all of the figures and legends. The seventh cranial nrr\.e deserves special consideration (see Figures 13-3 and 13-4). Understand the diiierence bet\veen a n uFFer motor neuron and a lo~ver.mot@r neuron (Bell's pals!.).
I?: T h e three most i l n ~ o r t a nlesions t of the brain stem zre occlusion of t h e anterior spinal artery (Figure 13-I), occlusion of the posterior inferior cerebellar artery (Figure 1), and medial longitudinal fasciculus syndrome (Figure 14-2). \VeL.er's syndrotne is t h e most c o m m o n tllidbrain lesion (Figure 14-31.
Chapter IS: Figure 15-1 shows the most important cerebellar circuit. T h e inhibitor). y-aminobuq-ric acid (GABA)-ergic Purkinje cells give rise co the cerebellodentatothalamic tract. W h a t are mossy a n d climbing fibers? .
Chaprer 16: Figure 16-1 shows eveqthing you need to know about what goes in a n d what comes our of the thalamus. Know the anatomy of the internal capsule; ic \\rill be o n t h e esamination. W h a t is t h e blood supply of the internal capsule (stroke)?
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Chapwr 17: Know the lesions of the visual s!-stem. Ho\\rsareq u a d r a n t a n ~ ~ i created? as There are two major lesions of the optic chiasma. Know thein! \Vhac is Mej-er's loop?
Chaprcr IS: T h e important anatomy of the autonomic nervous system is clear!). seen in Figures 18-1 a n d IS-2. Chapter 19: Figures 19-1 ilnd 19-2 shour t l ~ att l ~ parat.entricular e and supraoptic nuclei synthesize a n d release antidiuretic l~ormoncand osptocin. The suprachins~nacicnucleus receives direct input from t h e retina andplays a role in the regulation of circadian rhythms.
Chapter 20: Bilateral lesions of the amygdala result in Kliiver-Bucy syndrome. Recall t h e triad hyperphagia, hypcrsexuality, and psychic blindness. Memory loss is associated \\.it11 bilateral lesions of t h e hippocampus. \Vernicke9senccphalopnthy results from a deficiency of tllia~nine(vitainin B,). Lesions ~ ~ , ~nidbraint c g ~ n c n t u ~(Figure n 20-3). Know the Paare found in the rnamillnry Lxxlics, t h a l i ~ m iand Fez circuit, 3 common bo;ird iji~estion.
Chap[cr2 I : Figure 2 1-3 sl~oiirthe circuitr). of the basnJ ganglia ntld thci r associn tcd n e u r o r r a n s t ~t-~ i tcrs. Parkinson's discasc is associatctf \\.it11 a depol?\~larionof netirons in t h e suhstantia nigra. H u n t ington's discnse results in n loss of ncr\.c cells in thc cautinrc n u c l r ~ ~ and s put;lnlcrl. I-fcrniballis~nrcsults from infarction of thr contrnl;ltcr;ll subthalamic nuclcus.
ChnptCr 22: In this chnprc.r, the ~>nth\r*;lys of t l ~ c111;ljorn c u r o t r n ~ ~t tcis , ~ ~ ;Is<: ~ i :;i>c,:t*ni 11 sc.!,;)::r r e t!>;>ps< : i ? , . i r : . ; , ~ ~i s: i1t c1 1 ~: ~ ~ : \ j o r c x c i [ ~ t s t; ~o:i~~s ,~, ~~i t~t ,of:i)t: :r
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- -- L L L ~ - C ~ ~ L I I I I ilrc vnBA-ergic. In Alzheilllrrk disease, there is n loss nccr).lcbolinrrgic n c t ~ r o n rin tllr 1.nsal nucleus of Mcynerr. In Parkinson's disease, there is n loss dopnmincrgic netlmns in the si~l,)mnrinnigr;,.
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~ h n p r k 23: r This c11;r~reidescrihzsthe corricnl locslirilrion of fitnctionnl areis of rl;e hrnin. Holv di . t h e donlinnnt h e o ~ i s ~ ~ ldiffer ~ r r efrolll the nonti.ominnnr hemisphere? Figure 23-4 slrows the effects various lllajor llelnisplreric lesions: \Vllat s!-nlproms result froin n lesiorr of the inferior pariel lobe! \Vhat is G e n r m a n n i sytrdrome? Chnprcr 24: This clli~pterdescri1.e~ n p m s i ~ ' . aphasia fr6m Wemicke's nphasia.'Whrr is cvnuucrlolr aphasiil! 1 his is h ~ n r d - r ~ lmaterial. ~ ~ ~- ~------nt I wish you good luck. *
Jatncs D. Fix
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