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Physical Agents in Rehabilitation From Researchto Practice
Physlcal Agents ln Rehabllltatlon From Research to Practice Second Edition
Stichelle H. Cameron, PT, OCS l:est Lecturer l:aCuate Program of PhysicalTherapy j,.:ruel Merritt College I i
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SAUNDERS An Imynntof Elsevrcr 11830WesthneIndustrralDnve St Lours,Mrssoun63146 JnnO
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PHYSICAT ACENTS IN REHABILITAIION FROM RESEARCH TO PRACTICE Copyright @ 2003, Elsevier. AII rights resenzed.
0.7216-9378-4
No part of thrs pubhcatron may be reproduced or transmrtted rn any form or by any means, electroruc or mecharucal, mcludng photocopyrng, recordmg, or any nformailon storage and retneval system, wrthout permrsslon m wntmg from the pubhsher Permrssronsmay be sought drrectly from Elsevrer's Health ScrencesRrghts Department rn Phrladelphra, You may USA phone. (+ l)215-238-7869, fax. 1+ l)215-238-2239, emul:
[email protected]. also complete your request on-lme vta the Elsevrer Screncehomepage (http:/iwww.elsevrer com), by selectrng 'Customer Support' and then'Obtarmng Permrssrons'.
NOTICE Rehabrhtatron ls an ever-changrng field Standard safety precautlons must be followed, but as new research and clrrucal expenence broaden our knowledge, changes m treatment and drug therapy may become necessary or appropnate. Readersare advrsed to check the most current product mformahon provrded by the manufacturer of each drug to be admrmstered to verfiy the recommended dose, the method and durauon of admmrstratlon, and contrarndrcauons It rs the responsrbrlrty of the hcensed prescnber, relyrng on expenence and knowledge of the patlent, to determrne dosagesand the best treatment for each rndrvrdual patlent. Nerther the Pubhsher nor the author assumes any habrlrty for any mlury and/or damage to persons or properq/ ansrng from thrs pubhcatron.
Prevrous edrtron copyrtghted 1,999 Acqus fironsEdrtor'Manon Waldman DevelopmentalEdttors Sue Bredenstemer,Maqory Fraser PublrchmgSerwcesManage r' John Rogers ProlectManagar- Kathleen L Teal Deugner"Kathr Gosche CoverArt Kathr Gosche Pnnted m the Umted States of Amenca Lastdrgrtrstheprmtnumber'9
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tothememoryof Thisboobis dedicated myhusbandanddearest friend Cameron John rnetoaim high encouraging for I Vutmymindto. methatI coulddo whatever andteaching
Michelle H. Cameron, PT, OCS, is the owner of Health Potentials, a health education and consulting company. Sheis a physical therapist clinician, a teacher, researcher, and author, and now also a full-time medical student at the Universiry of California, San Francisco. She wrote the first edition and the currenr edition of this book, PhysicalAgents in Rehabilrtatrcn: FromResearch toPractice,published by Saunders.In addrtion, her research on phonophoresis is published in PhysicalTheraVy,the Journal of the Amerrcan Physical Therapy Association, and in ClinicalManagementmag-
vl11
azine, and earned her the California APTA Clinician ResearchAward. Michelle has also written and edited numerous articles on electrical strmulation, ultrasound and phonophoresis, and wound management, and wrote the section on ultrasound in Saunders'Manual for Physical TheraVy Practice.Michelle's discussions of ultrasound, electrical sumulation, thermal agents, biofeedback, and wound management bring together current researchand practice to provide the decisionmaking and hands-on tools that support optimal care within today's health care envirorunenr.
Acknowledg*ents First and foremost, I want to thank the readers and purchasersof the first edition of thrs book. Wrthout l"ou, there wouldn't be a second editron. In particular, I would like to thank those readerswho took the time to contact me with their comments, thoughts, and suggestionsabout what worked for them and what didn't. And, special thanks are due Dr. Marjorie -ltoore for her review and input on Frgures 3-4 duough 3-7 inthe chapter on pain. Thank you also to my friends, famtly, and col,eagues.Your ongoing support, encouragement, and patience has kept me h.ppy and relatrvely sane :,hroughthis endeavor and the rest of my hfe. I would also like to give specialthanks to: Andrew Allen, publishing director at Elsevier Science,for his consistent support throughout this nroject; As well as Marion Waldman, executive editor; Sue 3redensteiner, developmental editor; and Marjory
Fraser,ancillary and website developer and editor, for therr ongomg support. The contrrbuting authors to the first edition, including David Selkowitz, as well as those who have been part of both editions, and Sara Shapiro who is new to the team; Sara,for her persistenceand dedication with a job that turned out to be much more than she bargained for; Juhe Pryde, Diane Allen, and Gail Widener, who updated their respective chapters thoroughly and promptly; and Linda Monroe for keeping this text in line with the APTA Cuide to PhysrcalTheraprstPractice,second edition, and keeping my neck healthy through my hours at the computer. MichelleH. Cameron
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Lontrtbutors Diane D. Allen, MS, PT Adj unct Assistant Professor SamuelMerritt College FhysicalTherapist T:nterimHealth Care SanJose,California ChaVter(: ToneAbnormalrties
Linda G. Monroe, MPT, OCS PhysicalTherapist PnvatePractice and Guide to Physical ChaVter5: MotionRestictions TherapistPractice(secondeditioncontent) Suzana Otafro-Lata, MS SiomedicalEngineer 3ostonScientificCorp/Symbiosis 1"[iami,Florida Radiation(firstedrtion) Chayter'12:Electrornagnetic
Diana Perez,BSc,P! MSc lart-time Faculry& CourseCoordinator Faculryof Medicine Schoolof Physicaland OccupationalTherapy l-l.cGillUniversity l"tontreal,Quebec
julie A. Pryde, MS, PA-C, PT, OCS, SCS, ATC, CSCS AdjunctAssistantProfessor SamuelMerritt College Oakland,California PhysicianAssistant Muir OrthopaedicSpecialists Walnut Creek,California and Tissue ReVair Chayter2: Inflammation
Sara Shapiro, MPH, PT AssistantClinicalProfessor Universiryof CaliforniaSanFrancisco GraduateProgramin PhysicalTherapy SanFrancisco,California Owner Apex Wellness& PhysicalTherapy Chayter8: ElectricalCurrents
Gail L. Widerter, PhD, PT AssociateProfessor SamuelMerritt College Oakland, California Chayter4: ToneAbnormaliues
ihysical Therapist l"Ledi -Club Physiother apyand Me dicalWellness Center Radiation(firstedition) Chayter'12:Electromagnetic
xl
Pref^ceto theSecond Edition -:: rvriting the first editron of this book I tned to meet = need that I beheved exrsted-the need for a book -r the use of physical agents in rehabilitatron that -:...ered the breadth and depth of this material in a ::adly accessible and easy to understand manner. - rut together a text that leads the reader from the iasic scientificand physiological prrnciplesunderlying :::e applicatlon of physical agents,to the researcheval:.rng their clinical use, and thence, to the practrcal :.--arlsof selectrngand applyrng each specrficphysrcal :.-nt to optrmize patlent outcome. The enthusrasm ",,,:iewhich the first edition of this book was received, -:-:^udrng complimentary comments, adoption by :-;rly educational programs, and purchase by many :5cians, shows that the need was there and I met it. Given how well the first edition of this book was :r:eived, I was Ieery to make too many changes for --:-:ssecond edition. I have done my best to keep all :::. positive aspectsof the first editron whrle updatrng ::-. in-formatronin all chapters. In addition, the con-.:rs and language of the second editron of the -1-:erican Physical Therapy Associailon's Curde to :;:."sical Therapst Pracficeand the principles of evr:=::ce-basedmedicme have been incorporated rnto *-:s new edition, and a few areashave been clarified ::::nproved in other ways. Updates include consideri: rr1of the most recent researchin all areas,with par:::,ar attention to meta-analyses and systematlc ::l-iews of the literature. Over 50 new illustrauons :,:'"-e been added to clarrfy and update content. In : iirion, all aspects of the text, includrng the case ::;dies, have been modified to be conslstentwrth the -:":'-{eto Phyncal TherapistPractrce,second edrtion.* 1:-e order of the chapters has been changed and, the -1= Preferred Physrcal Theraprst Pracfice PatternsSM are copy:;:-:2002 Amencan PhysrcalTherapy Assocratronand are taken :-i:- rrhe Gwde to Physrcal TheraprstPractue (Gurde to Physrcal T:-::aprst Practrce,2"d Ed. Pht,s Ther 200I,81,9-744) All rrghts :r:,=:-.'ed. Preferred Physrcal Theraprst Practrce PatternsSM rs a :l j.:nark of the Amencan Physrcal Therapy Assocratron
origrnal chapter on traction and compressionhas been drvrded mto two separatechapters,in order to reflect patterns of clmrcal practice rather than the physical propertres of drfferent physical agents.The electrical currents chapter has also been rewritten to make its sfyle, content and level of detail more similar to that of the other chaptersin section rwo of the book. This chapter has been shghtly simplified and shortened while strll thoroughly covering all aspectsof the applicatron of electncal currents rn rehabilitation. In additron to updating this book, there is now comparuon Evolve Online Learning Resources,which is available onlne at hW :/ / evolve.elsevier.com/Cameron The Student ResourceCenter provides a Study Guide with many boards-type multiple-choice questions to help students learn and assess their knowledge. Instructors' resourcesare available to instructors who adopt thrs book. The Instructors' Resource Center rncludes suggestlonsfor laboratory activities, means to assessand document student competence in the selection and application of physical agents, and an electronic image collection of most of the figures in the text. Images in the collection can be copied into PowerPoint presentatlons. The Preface to the First Edition states that this book was intended primarily for physical therapy students and physical therapists although I believed that rt would also meet the needs of physical therapist asslstants,occupauonal therapists, chiropractors and physrcrans,and students m these fields learning about the use of physrcal agents. Since the first edition was releasedrt has come to my attention that many others, including athletic trainers, occupationai therapy assistants,osteopaths,veterinariansand animal trainers also find this book to be a useful tool in their practice. I hope that this new edition continues to meet a wide range of professionals'needs for a readily accessrble, ciear, and thorough text on the appiication of physrcal agentsin rehabilitauon. Michelle H. Cameron xl11
Pref^ceto theFirstEdition Teachingclassesand courseson physical agents,I was =equently asked by ^y students,"ls there a book you '.".'ouldrecommend that covers all this information?" ,rd I would respond, "One of these days I'll write :re.' So, when the phone rang and the person on the :--her end of the line said, "l'm calling from the pub''sher W.B. Saunders.Will you write a new textbook :n physical agents for us?" I immediately said "Yes, ;ue.'Then came the shock, the work, the excite::rent, and now, here, a few years and a few life events "-z.er, that book. is dthough there are other texts on physical agents,I ielieve none cover the information with the same breadth and depth as this one. After reading this book -:-e readerwill be familiar with all the physical agents ':sed by rehabilitation clinicians, including thermal =:ients, water, mechanical agents, and electrical ;gents. The reader will also understand the rypes of :aient problems that can be treated effectively with and the physical properties and phys::-,rz5l.u1agents ::iogical effects of physical agents. Additionally, the :eader will be able to apply this knowledge to select physical agents and treatment parame":propriate ::rs and to use safe and effective application tech::ques in order to optimize patient outcome. The :zader will also have a thorough understanding of -"4-:]yusing physical agents benefits patients, the rypes :: benefits that can be achieved by such interven:ons, and the mechanisms by which such interven:ons produce their effects. This book provides rehabilitation students and ::acticing clinicians with a thorough understanding =:d firm basis for applying physical agents in rehabili-jon. Aithough intended primarily for physical therand physical therapists,this publication ":y'srudents : so meets the needs of physical therapist assistants, : ;c,upationaltherapists,chiropractorsand physicians, =d students in these fields learning about the use of ::lvsical agents.The book is structured to be used by
students as a course text with outlines and objectives at the beginning of each chapter, lists that summarize content throughout the text, and chapter reviews; however, it can certainly be used by practicing clinicians as a reference. There is an accompanying instructor's manual and a study guide available to further facilitate the teaching and learning of the presented information. This book is divided into three sections.The first includes chapters about the physiological processes most commonly affected by the application of physical agents, the second includes chapters about the specific different rypes of physical agents and their application, and the third includes chapters about integrating the application of physical agents with other treatment proceduresand provides suggestions for future research on the application of physical agents in rehabilitation. In Section'l , the reader learns about tissue inflammation and healing, pain, tone abnormalities, and motlon restrictions. This information is presented first so that the information gained from assessment of a patient's presentingproblems can be used in making decisions regarding the selection and application of physical agents. In Section2, rhe readerleams about the specificphysical agentsand their recolrunended clinical uses.Details of contraindicationsand precautionsand specific guidelines for clinical application are presented in consistendy formatted passages that are immediately recognizable and make the material easy to understand and review. The physical and physiological bases for the application of physical agentsare describedfirst, followed by an examination of the researchon the effects of physicai agents,in order to provide a basisfor the recommended clinical application guidelines. This section includes chapters on thermal agents, hydrotherapy, traction and compression, ultrasound, electromagnetic fields and electrial currents.
xvr
Preface to the First Edition
Chapter 6, onthermal agents,describesthe mechanisms and effects of decreasing or increasing tissue temperature and the clinical application of both cooling and heating agents. Chapter 7, onhydrotherapy, describesthe basisfor the therapeutic application of water and provides guidelines for using water to cleanseopen wounds or as an environment for exercise.Chapter B covers the application of mechanical force in the forms of traction and compression;the section on traction focuses on the application of mechanical traction to the spine, while the section focuses on the use of compression for controlling edema. Chapter 10, on electromagnetic agents, describesthe electromagnetic spectrum and the physical agents, including ultraviolet, lasers, and diatherml, that apply electromagnetic radiation to achieve therapeutic effects. Chapter 1.t, on electrical currents, describesthe rypes of electrical currents used in rehabilitation and their application to produce muscle contractions, modulate pain, promote tissue healing, and facilitate transdermal drug penetration. All chapters in Sectionsl and 2 include clmical case studies that illustrate the presented material within the context of patient care and demonstrate the clini-
cal decision-making processesused in selectionof the optimal physrcal agentsand treatment parameters. Section3 integrates the information from the prior rwo sections. Chapter t2 discusses how physical agents may be used in conjunction with each other and with other rypes of interventions. A discussion of how physical agents may be used within the context of different health care delivery systems is also provided in this chapter. The final chapter explains why further research on the use of physical agents in rehabilitation is needed to validate and enable the progress of clinical practice and includes suggestions to direct such research. This is the book on physical agents that I and my students have been looking for. The logical and consistent format of each chapter makes the presented information readily accessible,and the depth of information, complete referencing, and illustratrve case studies facilitate the reader's understanding of how physical agents may be applied safely and effectively to enhance patient rehabilitation. Michelle H. Cameron
Contents z T0 PHYSICAL AGENTS, 1 INTR0DUCTION Definitronsand Examplesof PhysicalAgents,z of PhysicalAgents,z Categories History of the Useof PhysicalAgentsin Medicineand Rehabilitation,+ The Roleof Rehabilitationin PatientCare.s The Roleof PhysicalAgentsin Rehabilitation.o Effectsof PhysicalAgents,z GeneralContraindrcations andPrecautrons for the useof PhysicalAgents,ro ChapterReview,ro
Z: 4 TONE ABNORMALITIES, Dtane D. Allen and (]ail L. Widener Muscle Tone Deftned, za Terminology for Tone Abnormalities, zo Measuring Muscle Tone, 77 The Anatomical Basesof Muscle Tone and Muscle Activation, So Abnormal Muscle Tone and It's Consequences,qj Clinical Case Studies, to+ Chapter Review, ro7
lor RESTRICTI0NS, 5 MOT|ON hnda C. tUlonroe
ONE PATHOLOGY ANDPATIENT SECTION PROBLEMS ,s ANDTISSUE REPAIR, 2 INFLAMMATI0N JuheA. Pryde InflamationPhase(Days1-Q, rs ProliferationPhase(Days3-20),z+ Maturation Phase(Duy 9 On),zo ChronicInflammation,30 FactorsAffectingthe HealingProcess,sz Healingof SpecificMusculoskeletal Tissues,s+ ClinicalCaseStudy,sz ChapterReview,.tZ
+r 3 PAIN, Types of Patn,+z Mechanisms of Pain Reception and Transmission, +5 Pain Modulation and Control, sz Measuring Pain,5zt Pain Management Approaches, 57 Clinical Case Studies,rs Chapter Review, 6;
Introduction. t t z Types of Motion, rrz Patternsof Motion Restriction, 445 TissuesThat Can Restrict Motion, 4'tj PathologiesThat Can CauseMotion Restrictions,,t,tb Assessmentof Motion Restrictions,I tq Treatment Approaches for Motion Restrictions, 't23 The Role of Physical Agents in the Treatment of Motion Restrictions. I 26 Clinical Case Studies, rz7 Chapter Review, rz8
AGENTS TWO THEPHYSICAL SEGTION ISS ANDHEAT, AGENTS: GOLD 6 THERMAL Physical Principles of Thermal Energy, ts+ SpecificHeat, t s4 Modesof HeatTransfer,t s+ erapy, 437 Cold-Cryoth Effectsof Cold.rsa xvrl
Contents
xvlll
z,a CURRENTS, ELECTRICAL
Uses of Cryotherapy, 441 Contraindications and Precautionsfor Cryotherapy, 144 Contraindications for the Application of Cryotherapy, t44 Precautionsfor the Application of Cryotherapy,'t4b Adverse Effectsof Cryothercpy, 44b Application Techniques, r47 Documentation, t55 Clinical CaseStudies,rlt
Heat-Thermother rsa Effectsof.Heat,
SaraShadro
Introduction and History, zzo Terminol ogy for Electrical Currents, 220 Effectsof ElectrrcalCurrents, 227 Clinical Applications of Eiectrrcal Currents, zso ElectricalCurrent in ClinicalPracttce,zsz C ontraindications fo r Electri cal Stimulation, zs7 Precautionsfor ElectricalStimulati on, 238 Documentation, 250 ClrnrcalCase Studies,zsr Chapter keview, zs+
apy,', sa
Uses of SuperfictalHeat, rbz Contraindications and Precautionsfor Thermotherapy, rbz Contraindications for the Use of Thermotherapy, rbs Precautionsfor the Use of Thermothercpy, rb+ Adverse Effectsof Thermotherapy, r66 Application Techniques, t 68 Other Means of Applying Therm otherupy, 't77 DocumentatLon, 't77 Clinical Case Studies,rzz
zar HYDROTHERAPY, PhysicalPropertresof Water,262 PhysiologicalEffectsof Hydrotherapy, zos Uses of Hydrptherapy, zzo Contraindications and Precautionsfor Hydrothe rapy, 278 Contraindications for Local Immersion Forms of Hydrotherapy, zza Precautionsfor Local lmmersion Forms of Hydrotherapy, 27q Contramdrcauons for Full Body Immersion Hydrothe rapy, 280 Precautionsfor Full Body Immerston Hydrotherapy, 284 Precautionsfor Full Body Immersion in Hot or V"ry Warm Water, zrz Precautionsfor Nonimmersion Hydrotherapy, 283 Adverse Effectsof Hydrotherapy, zrs Application Techn iques, z8+ Documentation, 2q5 Safery IssuesRegardingHydrothe rapy, Including Infection Control and Pool Safery,zot Clinical Case Studies,zqs Chapter Review, "toz
Choosing Between Cryotherapy and Thermotherapy, r8o ChapterReview,rBc
rar ULTRASOUNDn History,rso Terminology, t87 Generation of Ultrasound, rg3 Effectsof Ultrasound, rg3 Thermal Effects, rqs Nontherm al Effects, r qs Clinical Applications of Ultrasound, tsb Contramdications and Precautionsfor Ultrasound,zo+ Contraindications for the Use of Ultrasound, zoq Precautionsfor the Application of Ultrasound,zob Adverse Effectsof Ultrasound. zoz Applrcatron Technrque,207 Documentation, 2to Clinical Case Studtes,zr r Chapter Review, zr4
:O; 1 0 TRACTION, Effectsof SprnalTraction, .lo8 Clinical Indications for the Use of Spinal Traction, s to Contraindications and Precautionsfor Spina1 Traction, srz Contraindlcatlons for the Use of Traction, ;2.;
,l::ll:' :lll:i:t: illill
xix
CONTENTS
for the Useof Traction,s,t4 Precautions AdverseEffectsof SpinalTraction,sr7 srs ApplicationTechniques, Documentation.ss+ ClinicalCaseStudies,-tst ChapterReview,ssl
s+o 1 1 COMPRESSION, Effectsof ExtemalCompression,s42 Clinicallndicationsfor the Useof External Compression,3+3 for External Contraindicationsand Precautrons s+9 Compression, Contraindicationsfor the Useof Intermittent or CompressionPumps,s+o Sequential Precautionsfor the Useof Intermittent or CompressionPumps,.t5r Sequential 35.r AdverseEffetsof ExternalCompression, ApplicationTechniques,3t 3 Documentation,3b2 ClinicalCaseStudies,soz ChapterReview,s66
',2 ELECTROMAGNETIC soo RADIAT\0N, -llrchelleIL Cameron.Dtana Perez.and Suzana Otafio-Lata
Physical Properties of Electromagnetic Radia tiorr, szt Physiological Effects of Electromagnetic Radi atiorr, szs PhysicalProperties of Ultraviolet Radiation,sz.r Effectsof UltravioletRadiatron,374 ClinicalIndicationsfor the Useof Ultraviolet Radiation,szt Contraindicationsfor the Useof Ultraviolet Radiation,szz Precautions for the Useof Ultraviolet Radiation,szz AdverseEffectsof UltravioletRadiation.sza ApplicationTechniqves,s7q Documentation,382 SelectingaWLamp,ssz ClinicalCaseStudy,saz PhysicalProperties of Lasers,38.3 Effectsof Cold Lasers,s8t ClinicalIndicationsforthe Useof Cold Lasers.s8b
Contraindlcatronsand Precautionsfor Lasers,:8z Contramdrcationsfor the Use of Lasers,.188 Precauuonsfor the Use of Lasers,.taz PhysicaiPropertiesof Diathermy-Thermal and Nonthermal, .lB8 Typ.r of Diathermy ApplLcators,38q Effectsof Diathermy, 3q2 Clinical Indrcations for the Use of Diathermy,3q3 Contraindications and Precautionsfor Diathermy,395 Contramdrcauons for All Forms of Diathermy,3go Contrandications for Thermal-Level Diathermy, iqb Contraindications for Nonthermal Pulsed ShorwvaveDiathermy, 3q7 Precautionsfor A11Forms of Diathermy, 3q8 Precauilonsfor Nonthermal PulsedShorwvave Diathermy, jgg Adverse Effectsof Diathermy, 3qq Applicatron Techn Lques,i qq Documentatton, 402 Selectrnga Diathermy Devic e, 403 Clinical Case Studtes,/to+ Chapter kevtew, +ob
THREEINTEGRATING SECTION AND AGENTS INTOPRESENT PHYSIGAL PRACTICE FUTURE AGENTS INTO PHYSICAL 13 INTEGRATING PATIENT CARE,+,s Attributes to be Consrderedin the Selectionof Physical Agents,+rb Usrng Physical Agents in Combinatron with Each Other or with Other Interventions, +zo Using Physical Agents within Different Health Care Delivery Systems,+27 Chmcal CaseStudres,+za Chapter Revtew,+.17
RESEARCH AND FORFUTURE 14 DIREGTIONS APPLICATI0N, ++, Why Further Researchon the Physical Agents in Rehabilitation Is Needed, ++z
Contents
Areasfor FutureResearchon Physical Agents,++z of Future MethodologicalCharacteristics Researchon PhysicalAgents,++6 Conclusion,4i3 ChapterReview,+5s
APPENDICES Terms, Used A Glossary of Commonly +ss Abbreviations and B Commonly Used Acronyms, +oo C Unils,+ot
Introductionto Ph icalA7ents :,'i l
SUMMARY
OF
IIVFO RMATlOA/
Definitions and Examplesof PhysicalAgents Categoriesof PhysicalAgents History of the Use of PhysicalAgentsin Medicine and Rehabilitation The Role of Rehabilitationin Patient Care
COVERED
The Role of PhysicalAgents in Rehabilitation Effectsof PhysicalAgents GeneralContraindicationsand Precautionsfor the Use of PhysicalAgents Chapter Review t, ,
,.,.,
OB]ECTIVES UVoncomVletion of this chayter,thereaderwill beable to:
t . Describe, categorize, and compare the types of
5 . Identify the physiologic effects of physical
physical agents used in rehabilitation. 2 . Summarize the history of the clinical application of physical agents. 3 . Explain the role of rehabilitation in patient care. 4 . Explain the role of physical agents in rehabilitation.
agents. 6 . Outline the general contraindications and precautions for the use of physical agents.
'l o Introduction
This book is intended primarily as a course text for those learning to use physical agentsin rehabilitation. It was written both to meet the needs of studenrs learning about the theory and practice of applying physical agents and to assistpracricing rehabilitation professionalsin reviewing and updating their knowledge about the use of physical agents. This book describes the effects of physrcal agents, gives guidelines on when and how physical agents can be most effectively and safely appiied, and describes the outcomes that can be expected from integrating physical agents wrthm a program of rehabilitation. The theory underlying the application of each agent and the researchconcerning its effects are covered to provide a rationale for the treatment recommendations. Information is also provided on the physiologlc processesnfluenced by physical agents in general,and regardingthe specific effects produced by specific agents.After reading this book, rhe reader will be able to integrate the ideal physical agenr(s)and treatment parameters within a complete program of rehabilitation care to promore optimal patient outc om e. This book uses a framework for describing the clinical use of physical agenrs based on rhe Gwde to PhysrcalTherapstPracilce,2ndedttion (herein nored as the Guide).1However, this book presentsmore specific, research-basedinformation regarding the theaU, rationale, assessment process, and treatment parametersfor the applicarion of physical agentsthan provided by the Guide. It is important ro note that the Guide is based on descriptions of preferred practice patterns for selected patient diagnostic groups. These practice patterns are not prescriptive, nor are they based on a review of available research evidence. Following this introductory chapter, the book rs divided into three secrions.The first section covers the different rypes of musculoskeletaland neuromuscuiar problems that may be addressed by the use of physical agents. The second section describes the physical properties, physiologic effecrs, and application techniques for the different rypes of physical agents available.The third secrion integrates information from the first wvo and summarizes how different rypes of problems may be influenced by different physical agenrs, how rreatments with physical agents may be integrated into a patienr's compiete plan of care, and how physical agenrsmay be applied under different health care delivery
to Physical Agents
systems.The final chapter discussesdirectionsfor future researchon the useof physrcalagentsin rehabilitation.A glossaryof termsand abbreviations used in describingand documentingthe apphcationof physicalagentsrs provrdedin Appendx A on pages 456-459.
DEFINITIONS ANDEXAMPLES OFPHYSICAL AGENTS Physicalagentsare various forms and means of applying of energy and materials to parienrs. Physical agents include heat, cold, water, pressure, sound, electromagnetrcradratron,and electncalcurrents.The term Vhysicalagentcan be used to describethe general rype of energy,such as electromagnetic radiation or sound; a specific range within the generaltype, such as ultraviolet radiation or ultrasound and the actual means of applying the energy, such as an ultravioiet lamp or an ultrasound transducer.The rerms Vhysical modality and modality are also frequently used in place of the term yhysical agent and are used interchangeably in this book, with variation for ease of reading.
CATEGORIES OFPHYSICAL AGENTS Physical agents are most readlly categorized as thermal, mechanical,or electromagnenc (Table 1-1). Thermal agents include deep-heatingagents,superficial heating agents, and superficial cooling agents. Mechanical agents include traction, compresston, water, and sound. Electromagnetic agents include electromagneticfields and electricalcurrents.
Thermal Agents Thermal agents transfer energy to a patient to produce an increase or decreasein tissue temperature. Different thermal agents produce the greatestchange in temperature in different rypes and areas of tissue. For example, a hot pack producesthe greatesttemperature increasein superficial tissueswith hrgh thermal conductiviry in the area directly below rt. In contrast, an ultrasound produces the most heat in tissues with high ultrasound absorption coefficlents, such as tendon and bone. It produces this effect up to a depth of 5 cm but only in a small area, approximately twice that of the effective radiating area of the transducer.
4 o INTRODUCTION TO PHYSICAL ACENTS
Thermal
Deep-heatmg agents Superficral heatrng agents Cooling agents
Drathermy Hot pack Ice pack
Mechanical
Tracuon Compressron Water Sound
Mechamcal tracuon Elastrcbandage Whrrlpool Ultrasound
Electromagnertc
Electromagnetlc fields Electrrc currents
TENS
Thermal agents that increase tissue temperature are most commonly appliedwhen increasing of circulation, metabolic rate, and soft tissue extensibiliry or the decrease of pain ire expected to promote the goals of treatment. Thermal agents that decreasetissue temperature are most commonly applied when decreasing circulation, metabolic rate, or pain is expected to promote the treatment goals. A full discussion of the principles underlying the processesof heat transfer, the methods of heat transfer used in rehabilitation, and the effects, indications, and contraindications for applying superficial heating and cooling agents is provided in Chapter 6. The principles and practice of applying deep heating agents are discussedin ChapterT inthe section on thermal applicarions of ultrasound and in Chapter 1,2inthe section on diathermy. Ultrasound is a form of sound that cannot be heard by humans becauseof its high frequency. It is defined as sound with a frequency of greater than 20,000 qgcles/second. Ultrasound a mechanical form of enerry composed of alternatingwaves of compression a.rrdrarefaction. Ultrasound is used as a physical agent :n rehabilitation to produce both thermal and nonthernal effects. Thermal effects, including increased deep and superficial tissue temperature, are produced by :ontinuous ultrasound waves of a sufficient intensiry while nonthermal mechanical effects, including caviadon, microstreaming, and acoustic streaming, are ?roduced by both continuous and pulsed ultrasound. l-hermal-level ultrasound is used for the same pur:oses as other thermal agents when deep tissue is rvolved. These purposes include increasing circula-
Ultravrolet
tion, metabohc rate, and soft tissue extensibiliry and decreasing pain. Ultrasound is applied in a pulsed manner to optlmlze the nonthermal effects and facilitate tissue healing or promote transdermal drug penetration. Further information on the theory and practice of applying ultrasound can be found in Chapter 7.
Agents Mechanical Mechamcal agents apply mechanical force to increaseor decreasepressurein or on the body. Water provides resistanceto increaselocal pressure,hydrostatic pressure to increase circumferential pressure, and buoyancy to decreasepressureon weight-bearing structures. Traction decreasesthe pressure berween structures, and compression increases the Pressure between structures. Water can be applied by immersion or nonimmersion techmques.The therapeutic application of water is known as hydrotherafy. Immersion in water produces pressure around the immersed area, provides buoyancy, and, if there rs a difference in temperature between the area and the water, transfers heat to or from the area.Movement of the water produces local pressure,which can be used as resistancefor exercise when an areais immersed and for cieansingor debriding openwounds with orwithout immersion. Further information on the theory and practice of hydrotherapy is provided in Chapter 9. Tracilon is most commonly used to alleviate pressure on structures, such as nerves or joints that produce pain or other sensory changes or that become inflamed when compressed.Tractron application can
4 c Introduction
normalize sensationand prevent or reduce damage or inflammation of compressed structures. The pressure-relievingeffects of traction may be temporcry or permanent, depending on the nature of the underlying pathology and the force, duration, and means of traction application used. Further information on the theory and practice of applying traction is provided in Chapter 10. Compression is used to counteract tluid pressure and control or reverse edema. The force, duration, and means of application of compression can be varied to control the magnitude of the effect and to accommodate different patient needs. Further information on the theory and practice of applying compressionis provided in Chapter 1,1,.
neticAgents Electromag Electromagneti c agents apply electro magnetrc energy in the form of electromagneticradiation or an electrical current. Variation of the frequency and intensity of electromagnetic radiation changes its effects and depth of penetration. For example, ultraviolet radiation, which has a frequency of 7.5 x 1914so 1915 cycles/second,produces erythema and tanning of the skin but does not produce heat, whereas infrared radiation, which has a frequency of 1011 to L014 cycles/second,produces heat only in superficial tissues. Continuous shorrwave diathertrtl, which has a frequency of 10 million to 100 million cycles/second, produces heat in both superficial and deep tissues. When shortwave diathermy is pulsed to provide a low average intensity of energy,it does not produce heat; however, the electromagneticenergy is thought to modify cell membrane permeabiliry and cell function by nonthermal mechanisms and thus acts to control pain and edema. Further information on the theory and practice of applying electromagnetic radiation is provided in Chapter 12. The effects and clinical applications of electrical currents vary according to the waveform, intensiry duration, and direction of the current flow and according to the rype of tissue to which the current is applied. Electrical currents of sufficient intensiry and duration can depolarize nerves, causing sensory or motor responsesthat may be used to control pain or increase muscle strength and control. Electrical currents with an appropriate direction of flow can attract or repel chargedparticlesand alter cell membrane permeabiliry to control the formation of edema, promote
to Physical Agents
tissue healing, and facilitate transdermal drug penetration. Further information on the theory and practice of electrical current application is provided in Chapter B.
AGENTS HISTORY OFTHEUSEOFPHYSICAL ANDREHABILITATION INMEDICINE Physical agents have been a component of medical and rehabilitation treatment for many centuries and are used acrossa wide variery of cultures. For example, the remains of origrnal bath houses with steam rooms and pools of hot and cold water that can still be seen in many major cities of the ancient Romans and Greeks provide evidencethat these cultures used heat and water to maintain health and treat various musculoskeletal and respiratory problems.2 The health benefits of soaking and exercising in hot water regained populariry many centuries later with the advent of health spas in Europe in the late 19th century in areas of natural hot springs. Today, the pracr tices of soaking and exercising in water continue to be popular throughout the world becausethey provide resistance, thereby allowing the development of strength, endurance, and buoyancy, and reducing weight bearing on compression-sensitivej oints. Other examples of the historic use of physical agents include the use of torpedo fish, in approxrmately 400 n.c., to apply electric shocks to the head and feet to treat headachesand arthritis, and the use of amber in the 17th century to generate static electriciry for the treatment of skin diseases,inflammation, and hemorrhage.3 There are also reports from rhe LTth century of charged gold leaf being used to prevent scarringfrom smallpox lesions.a Before the widespread availabiliry of antibiotics and effective analgesic and antiinflammatory drugs, physical agents were commonly used to treat infection, pain, and inflammation. Examples of such applications include the use of sunlight for the treatment of tuberculosis, bone and joint diseases,and dermatologic disorders and infections, and the use of warm Epsom salt baths for the treatment of sore or swollen limbs. Although physical agentshave been used for their therapeutic benefits throughout history over time, new uses, applications, and agents have been developed, and certain other agents and applications have fallen out of favor. New uses of physical agents have developed as a result of increased understanding of
I o INTRODUCTION TO PHYSICAL AGENTS
the biologic processesunderlying disease, dysfunction, and recovery, and in response to the availability of advancedtechnology. For example, the use of transcutaneous electrical nerve stimulation (TENS) for the treatment of pain was developed based on the gate control theory of pain modulation, as proposed by Melzack and Wall. In contrast, the various modes of TENS application now available are primarily the result of the recent development of electrical current generators that allow fine control of the frequency, intensiry, and pulse duration of the applied electrical current. The use or specific application of a physical agent falling out of favor, usually occurs because the treatment is ineffective or because other, more effective ffeatments are developed. For example, infrared lamps were commonly used to treat open wounds because the superficialheat they provide can dry out the wound bed; however, these lamps are no longer used for this appiication because of the knowledge that wounds heal more rapidly when kept moist.5,6 During the early years of the 20th century sunlight was used to treat tuberculosis; however, since the advent of antibiotics, which are generally effective in eliminatnng bacterial infections, physical agents are now rarely used to treat tuberculosis or other infectious diseases.A number of physical agentshave waned in populariry becausethey are cumbersome,have excessive associatedrisks, or interfere with other aspectsof ffeatment. For example, the use of diathermy as a Ceep-heatingagent was very popular 20 to 30 years ago, but becausethe machines are large and awkward :o move around, can easily burn patients if not used appropriately, and the electromagnetic fields can nterfere with the functioning of computer-controlled equipmentnearby, diathermy is rarely currently used -l the United States. This book focuses on the physical agents most :ommonly used in the United States today. Physical sgents that are not commonly of current use in the ',-nited Statesbut were popular in the recent past, and iose that are popular abroad or are expectedto come back into favor as new delivery systems and applica:ons are developed, are covered more briefly. Also -:rcludedin this book is some discussionof modalities being used abroad that are awaiting :urently :nproval by the Food and Drug Administration (FDA) :er clinical use in the United States.The populariry of :arricular physical agentsand applications is basedon :eir history of clinical use and, in most cases,
research data supporting their efftcacy; however, in some cases,their clinical application has continued despite the lack or limitations of supporting evidence. In most cases,more researchis necessaryto elucidate the ideal treatment and patient characteristics for optimal resultsand the precisenature of the outcomes to be expectedfrom the application of physical agents in rehabilitation.
THEROLE OFREHABILITATION PATIENT IN CARE Rehabilitation is a goal-oriented treatment process designed to maximize independence in individuals who have compromised function as a result of underlying pathologic processes and secondary impairments. Rehabilitation generally addressesthe sequelae of pathology rather than the pathology itself. A number of classification schemes exist to categorrze the sequelae of pathology. In 1980 the Wodd Health Orgaruzation (\MHO) published the first classification scheme known as the International Classification of Impairments, Disabilities and Handicaps (ICIDH).7-eThir scheme, based primarily on the work of Wood, classifies the sequelae of pathology as impairments, disabilities, and handicaps.10,11 Shordy thereafter, Nagi developed a model that classified the sequelae of pathology as impairments, functional limitations, and disabilities.12In L993, the National Center for Medical Rehabilitation Research(NCMRR) published a classificationscheme der:ed from a combination of the Nagi model and the original ICIDH mode1.13Most recently, in2001, WHO further revised their classification scheme in their International Classification of Functioning, Disabiliry and Health (ICIDH-2) scheme.la The models of disability and the language used have been revised over time to reflect and creare changesin perceptions of people with disabilities and to meet the needs of different groups of individuals. The original models were intended to differentiate disease and pathology from the limitations they produced. These models were developed primarily for use by rehabilitation professionals. The new expandedmodels have a more positive perspectiveon the changes resulting from pathology and diseaseand are intended for use by a wide range of people, including communiry, national, and global institutions that create policy and allocate resourcesfor persons with
5
4 o Introduction
disabilities. Specifically,the NCMRR model added a category of societallimitations to the functional problems associatedwith disabiliry and it abandoned the previous linear modeling approach to reflect the frequently nonsequential nature of the relationships bewveen categories.The ICIDH-2 has tried to change the perspective of disabiliry from the negative focus of "consequencesof disease"used in the 1980 model to a more positive focus on "components of health." Thus, while the first ICIDH used categoriesof impairments, disabilities, and handicaps to describe sequelae of pathology, ICIDH-2 uses categories of health conditions, body functions, activities, and participation to focus on abilities rather than on restrictions and limitations. This book usesa scheme consistentwith the terminology and framework of the Cuide to Physical TherapistPractice,2nd edition, which is based on the work of Nagi (Fig. 1-1), to evaluate clinical findings and determine a plan of care for the casestudies presented.l
Pathology Diseaseor injury
Functional limitation Restrictionsin the ability to performcomponents of daily life
Disability Inabilityto performtypical activitiesof daily living
Figure1-1, Ciassificationof the sequelaeof pathology. (Data from American Physicai Therapy Association: Cuide to PhysicalTheraqstPractice,ed 2, Alexandria,VA, 200I, The Associatron.)
to Physical Agents
According to the Nagi scheme, the sequelae of pathology are classified as impairments, functional limitations, or disabilities.T,r2Pathologyrefers to the alteration of anatomy or physiology due to diseaseor injury. Lumbar disc herniation and joint inflammation are examples of pathology. are defined as alterations in Impairments anatomic, physiologic, or psychologic structures or functions as the result of some underlying patholagy.7'rzAn impairment is a measure at the organ or organ system level and is equivalent to a sign or an objective measure. For exampie, decreased cervic mobiliry diminished deep tendon reflexes, and absent sensation are all impairments. Impairments may lead to functional limitations or disabilities. A functional limitation, as defined by the Nagi model, is a restriction in the abiliry to perform an acdviry in an efficient, typically expected, or competent manner. Examples of this classification include an inabiliry to lift more than 20lbs or a limitation in sitting tolerance. The Nagi model, then, defines a disabiliry as the inabiliry to perform activities requiredfor self-care,home, work, or community roles. Examples of disabiliry according to the Nagi model are the inabiliry to lift one's child or to walk to the bathroom at home. While medical treatment is genenlly'directed at the underlying pathology or disease, rehabilitation focuses primarily on reversing or minimizing the associated impairments, functional limitations, and disabilities. Essentially, rehabilitation professionals must assessand set goals not only at the level of impairment, such as pain, decreasedrange of motion, or hypertonicity, but also at the level of functional limitation. These goals should include the patient's goals, such as being abie to get out of bed, ride a bicycle, work, or compete in a marathon.
AGENTS THEROLE OFPHYSICAL INREHABILITATION Physical agents are tools to be used, when appropriate, as components of rehabiiitation. The American Physical Therapy Association's (APTA) position statement concerning the exclusive use of physical agents, published in 1995, states that "Without documentation which justifies the necessiryof the exclusive use of physical agents/modalities, the use of physical agents/modalities, in the absenceof other skilled therapeutic or educational intervention, should not be
,I o INTRODUCTION TO PHYSICAL AGENTS
considered physical therapy.'1s This is a clear statement that the APTA believes that the use of physical agents alone does not generally constitute physical therapy, and that, in most cases, physical agents should be applied in conjuncrion with orher inrerventions. The skilled application of physical agents that constitutes a component of physic altherapy involves the integration of the appropriate intervention(s), which may include the application of a physical agent or agentsor the education of the patienr in such application, into the complete program of a patient,s care to facilitate progress toward the functional goals of ffeatment. The aim of this text is to give clinicians a berter understanding of the theory and appropriate applica:ion of physical agents.Therefore the examples, documentation, and clinical casestudies described focus rn the physrcal agent being discussed.Inclusion of all eossible goals and interventions for a given impair:rrent or iimitation is beyond the scope of this book. Physical agents have direct effects primarily at the -evel of impairment. These effects can then promote -:nprovements at the levels of functional limitation disability. Physical agents are used primarily to "nd :educe or eliminate soft tissue inflammation or circu-atory dysfunction, increase the healing rate for soft ::ssue in1ury, modulate pain, modify tone, increase :onnective tissue extensibiliry and length, remodel --:artissue,or treat skin conditions. For example, ther=al agents can be used to increase circulation and ,:celerate the metabolic rate to acceieratehealing, :::d electrical currents can be used to stimulate sen:1ry nerves to control pain or to stimulate motor :-irves to produce muscle contractions. Physical agents are frequently used in conjunction ',-:fi, or in preparation for, other interventions such as --:-erapeuticexercise, functional training, or manual :-cbrhzation to increase the efficacy of these inter=rtions. For example, a hot pack may be applied :=:ore stretching to increase the extensibiliry of the :::erficial soft tissuesand thus promote a more effec:'.'e and safe increase in soft tissue length when the ,:etching force is applied. r,Vhen considering rhe application of a physical .:ent, one should begin the examination by checking : -r physician's referral, if one is required, for a diag--:;is of the patient's condition and any precautionsto :. observed.The examination should include but nor := jmited to the patient's medical history; subjective : : rplaints; review of systems, tests and meisures;
functional status; and disabilities. The examination findings are then evaluated and, when possible, quantified. Following this analysis, a plan of care is established including anticipated goals. Given an understanding of the effects of different physical agents, the clinician can assesswhether treatment using a physical agent may help the patient progress toward the anticipated goals. The clinician can then determine the treatment plan, including the ideal physical agent(s) and treatment parameters if indicated. The treatment plan is modified, as appropriate, when the patient's outcome is assessed.The sequence of examination, evaluation, and intervention is followed in the casesrudiesin Section 2 of this book. Goals and interventions in this text prim afiIy refer to treatment of impairment with the physical agent(s)being discussed.
EFFECTS OFPHYSICAL AGENTS Modiff inflammation and healing Relieve pain Alter collagen extensibility Modiff muscle tone The application of physical agents primarily resulrs in modification of tissue inflammation and healing, relief of pain, alteration of collagen extensibiliry or modification of muscle tone. A brief review of these processesfollows; more complete discussions of these processes are provided in Chapters 2 through 5.
Inflammation andHealing When tissue is damagedby trauma or disease,it usually responds in a similar and predictable way. The first phase of recovery after damage has occurred is inflammation. This is followed by the proliferative phase of healing, which is completed during rhe maturation phase. Modification of inflammation and tissue healing can result in acceleratedpatient progress toward more active participation in rehabilitation and can expedite achievement of the therapy goals. Faster tissue repair can also reduce the risk and severiry of the adverse effects of prolonged inflammation, pain, and disuse. Thermal agents generally modify inflammation and healing by changing the rate of circulation and the
4 o Introduction
rate of chemical reactions. Mechanical agents control motion and alter fluid flo*, and electromagnetic agents alter cell function, particularly membrane permeability and transport. When selected and applied appropriately, physical agents can acceleratethe completion and resolution of the phasesof tissue healing, stimulate necessaryprocessesto resume if they have stopped, accelerate recoveryj and improve the final patient outcome. Physical agents can also minimize the risk of adverse effects from delayed or incomplete healing. However, if selected or applied inappropriately, physical agents may prolong inflammarion, increasethe severity ofassociatedsymptoms, prevent or delay healing, and increase the probabiliry of adverse consequencesand a poor outcome. A brief review of the processesof inflammation and healing and the factors that influence rheir progression follows; a more complete discussion of these processes is provided in Chapter2. During the inflammatory phase of healing, which generally lasts for I to 6 days, the ceils necessary for removing debris and limiting bleeding enrer the rraumatized area. This phase is characterized by heat, swelling, pain, redness, and loss of function. The more quickly this phase is completed and resolved, the more quickly healing can proceed and the lower the probabiliry of joint destruction, excessive pain, swelling, weakness, immobilization, and loss of function. Physical agents generally assist during the inflammatory phase by reducing circulation, reducing pain, reducing enzyme activiry rate, controlling motion, and promoting progression to the proliferative phase of healing. During the proliferative phase, which generally starts within the first 3 days after injury and lasts for approximately 20 days, collagen is deposited in the dama ged areato replace tissue that was destroyed by the trauma; in addition, if necessary myofibroblasts contract to accelerate closure, and epithelial cells migrate to resurface the wound. Physical agents generally assist during the proliferative phase of healing by increasing circulation, increasing errzyme acdviry rate, promoting coliagen deposition, and promoting progression to the remodeling phase of healing. During the maturation phase, which usually srarrs approximately 9 days after the initial injury and can last for up to 2 years, both deposition and resorption of collagen occur. The new tissue remodels itself to resemble the original tissue as closely as possible to
to Physical Agents
best serve its original function. During this phase, the healing tissue changes both in shape and structure to allow for optimal functional recovery.The shape conforms more closely to the original tissue, often decreasingin size from the proliferative phase, and the structure becomes more organized; thus, greater strength is achieved with no change in tissue mass. Physical agents generally assist during the remodeling phase of healing by altering the balance of collagen deposition and resorption and improving the alignment of the new collagen fibers.
PainControl Pain is an unpleasant sensory and emotionai experience associatedwith or describedin terms of actual or potential tissue damage.16-18puitr usually protects individuals by preventing them from performing activities that would cause tissue damage; however, it may also interfere with normal activities and thus result in functional limitation and disability. For example, pain frequently interferes with an individual's ability to sleep,work, or exercise.Relieving pain can allow patients to participate more fuliy in normal activities of daily living and may acceleratethe initiation of an active rehabilitation program, thereby limiting the adverseconsequencesof disuseand ailowing more rapid progress toward the patient's functional goals. Pain may be due to an underlying pathology, such as joint inflammation or pressure on a nerve that is in the processof resolution, or by a pathology, such as a malignancy, that is not expected to fully resolve. In either circumstance,relieving pain may facilitate resolution of the functional limitations and disabiliry that result from the underlying pathology and can therefore assist the patient. The use of pain-relieving interventions, including physical agents, may be continued as long as pain persists and should be discontinued when the pain resolves. Physical agents can control pain by modi Aing pain transmission or perception or by changing the underlying process causing the sensation. Physical agents may act by modulating transmission at the spinal cord level, changing the rate of nerve conduction, or altering the central or peripheral release of neurotransmitters. Physical agents can change the processesthat causepain by modifying tissue inflammation and healing, altering coliagen extensibility, or modifying muscle tone. The processesof pain per-
4 o INTRODUCTION TO PHYSICAL AGENTS
;eption and pain control are explained in greater Cetailin Chapter 3.
Extensibility Collagen Collagen is the main supportive protein of skin, tenCon, bone cartlTage,and connective tissue.19Tissues -hat contain collagen can become shortened as a :esult of being immobilized in a shortened position or -ceing moved only through a limited range of motion. :-mmobilization may be the result of disuse as a result rf debilitation or peripheral or central neural injury, or :nay be due to the application of an external device such as a cast, brace, or external fixator. Movement nay be limited by internai derangement, pain, weak:tess,or poor posture or may be due to the application rf an external device. Soft tissue shortening may ;ause impairment of restricted joint range of motion, shortened muscles,tendons, or joint capsules. To return soft tissue to its normal functional -ength, thereby allowing fuli rnotion without damagng other structures, the collagen must be stretched. Coliagen can be stretched most effectively and safely 'vhen it is most extensible. Since the extensibiliw oF ;ollagen is temperature dependent, increasing in :esponse to increased temperature, thermal agents are frequently applied before soft tissue stretching to cptimize the stretching process20-24(Frg. I-2). The processesunderlying the development and treatment cf motion restrictions are discussed in detail in Chapter 5.
f o ?h z UJ F
x
UJ
z
ul (5 J J
o () TEMPERATURE Figure1-2. Changesin collagenextensibiliqyin response ro changesin temperature.
9
Muscle Tone Muscle tone is the underlying tension that servesas a background for contraction in a muscle.2s Muscle tone is affected by both neural and biomechanical [actors and can vary in responseto a pathology, expected demand, pain, and position.26Abnormal muscle tone is usually the direct result of nerve pathology or is a secondary sequela of pain due to injury of other tissues."' Central neryous system injury, as may occur with head trauma or a stroke, can result in increased or decreased skeletal muscle tone in the affected area, whereas peripheral motor nerve injury as may occur with nerve compression,traction, or sectioning, can decrease skeletal muscle tone in the aFFected area. For example, a patient who has had a stroke may have increased tone in the flexor muscles of the upper extremiry and the extensor muscies of the lower extremity on the same side, whereas a patient who has had a compression injury to the radial nerve as it passesthrough the radial groove in the arm may have decreased tone in the wrist and finger extensors. Pain may cause an increase or decreasein muscle tone. Muscle tone may be increased in the muscles surrounding a painful injured area in order to splint the area and limit motion, or tone in a painFul area may be decreasedas a result of inhibition. Although protective splinting may prevent further injury as a result of excessive activiry, if prolonged it can also impair circulation, retarding or preventing healing. Decreasedmuscle tone as a result of pain-as occursr for example, with the reflexive hypotonicity of the knee extensors-that causes buckling of the knee, when knee extension is painful, can limit activity and thus result in functional iimitation. Physical agents can alter muscle tone either directly, by altering nerve conduction or sensitivity or by altering the biomechanical properties of muscle, or indirecdy, by reducing pain or the underlying problem causing pain. Normalizing muscle tone will generally reduce Functionallimitations and disabiliry allowing the individuai to improve the performance of functional and therapeutic activities. Attempting to normalize muscle tone may also promote better outcomes from passive treatment techniques such as passive mobilization or positioning. The processes underlying changesin muscle tone are discussedfully in Chapter 4.
10
4 e Introduction to Physical Agents
tion to such tissue.Somephysicalagentsaccelerate the growth or metastasisoFmalignanttissue.These effectsarethoughtto resultfrom increasedcirculation or alteredcellularfunction. Care must also be taken when consideringtreatingany areaof the body that Pregnanry currendy has or previously had cancercelis, since Malignanry malignanttissuecan metastasizeand may therefore Pacemaker be oresentin areaswhere it hasnot yet beendetected. Impaired sensation ih" ,rr" of physicalagentsis generallycontraindiImpaired mentation catedwhen rfreenergyof the agentcanreacha pacemakerbecausethe energyproducedby someof these agentsmay alter the functioning of the pacemaker and thus dangerousiychangethe patient'sheartrate. Restrictionson the use of particulartreatmentinterImpairedsensationand mentationare contraindior freventions are categorizedas contraindications Contraindicationsare conditionsthat render cationsor precautionsfor the use of many physical cautions. a particularform of treatmentimproper or undesir- agentsbecausethe end limit for the applicationof theseagentsis the patienl'sreport of how the treatable,while precautionsare conditionsunder which ment feels. For example,for most thermal agents, be applied should of treatment form a particular the patient'sreport of the sensationof heat being absolute The terms limitations.6 special care or with comfortableor painful is used as a guide to limit be can relative contraindications and contraindications the intensity oFthe treatment.If the patient cannot and precautions, place of contraindications used in feelheat or pain due to impairedsensation,or cannot respectively. report this sensationaccurateiyand consistentlydue and preAlthough the specificcontraindications cautions for the application of particular physical to impaired mentation or other factors affecting agentsvary,a numberof conditionsare contraindica- the ability to communicate,the applicationof the tions or precautionsfor the use of most physical treatmentwould not be safe and is thereforecontraindicated. agents.Thereforecautionshouldbe usedwhen conand precautions,includSpecificcontraindications sideringapplicationof a physicalagentto a patient and featuresto assess patient ask the to ing questions with any of theseconditions.In patientswith such of eachphysicalagent, the application before before conditions,the nature of the reslriction,the nalure this book in eachoFthe 2 of in Section are provided and distribution of the physiologic eFfectsof the types of physical different the chaptersconcerning physicalagent,and the distributionof the energyproagents. The ducedby the physicalagentmust be considered. conditionsfor which treatmentwith most physical or requirecautionarc prcg agentsarecontraindicated REVIEW CHAPTER nancy, malignancy,the presenceof a pacemaker, Physicalagentsarevariousforms of energyandmateimpairedsensation,and impairedmentation. rials and their means of applicationas applied to Pregnancyis generallya contraindicationor prepatients.Physicalagentsinclude heat, cold, water, caution for the application of a physical agent if radiation,and elecpressure,sound,electromagnetic the energy produced by the agent or the physiologic effectsof the agentmay reachthe fetus.These trical currents.These agentscan be categorizedas restrictionsapply becausethe influencesof these thermal, mechanical,or electromagnetic'Physical types of energyon fetal developmentare usually agentshave been used for many centuriesand by many culturesand continue to be used today as a not known and because Fetai development is adversely affected by many influences,some oF comoonentof rehabilitation. Rehabilitationfocuseson the treatment oF the which aresubtle. sequelaeof pathology,includingimpairments,funcor precautionfor Malignancyis a contraj.ndication tional limitations,and disabilities.Physicalagentsare the applicationof physicalagentsif the energyproincludedin rehabilitationcareprimarily to afFectthe ducedby the agentor the physiologiceffectsoFthe agentmay reachmalignanttissueor alterthe circuia- impairments dftecrly, thereby reducing functional
CONTRAINDICATIONS GENERAL FORTHEUSE ANDPRECAUTIONS AGENTS OFPHYSICAL
4 I INTRODUCTION TO PHYSICAL AGENTS
limitation and disability. The use oFphysical agents is generally integrated into a program of patient treatment that includes other interventions to optimize the benefit and outcome. When appropriately selectedand applied, physical agents can promote the resolution of inflammation, acceleratetissue healing, relievepain, increasesoft tissue extensi.bllity, and/or modify muscle tone. Most physical agents should not be applied when the energy provided by the agent or the physiologic effects produced can reach a fetus, malignant tissue, or a pacemaker. In addition, physical agents that use the patient's report as a guide for dosage or intensity should not be applied to patients with impaired sensation or mentation.
l1
11. WagstaffS: The use of the InternationalClassification of Impairments,Disabilitiesand Handicapsin rehabilitation, Physiotherayy 68:548-553,1.982. 12. Nagi S: Disability conceptsrevisited.In Pope AM, Tarlov AR, eds:Disabilityin America:Towarda National Agendafor Prevention, Washington,DC, 1,991,, National AcademyPress, 13. National Institutes of Health: ResearchPlan for the Irlailonal Center for Medical RehabilitarionResearch, Bethesda, I\AD,1993,The Institutes. 14. World Health Organization International Classification of FunctioningDkability and Heahh (ICIDH-2), Geneva, 200l, The Organization. 15. American Physical Therapy Association: Positionon exclusiue useof Vhysicalagentsmodalities, Alexandria,VA 1995,Houseof Delegates ReferenceCommrttee,25-95. 16. Sweet WH: Pain: In lield J, Magoun HW, and Hall WE: Handbook of Physiology, Section I, References Neurophysiology, vol. 1, WashingtonDC,1959,Amer 1. American Physical Therapy Association: Guide to PhysiolSoc,pp. 459-506. PhysicalTheraVistPractice,ed 2, .Alexandria,YA, 2001,, 17. BonicaJJ:Pain:What is sciencedoing about rt?Pain The Association. 2:12-15,1975. 2. JohnsonEW: Back to water (or hydrotherapy),J Bacb 18. Merskey H, ed: Classification of chronic pain: Musculosbel Med 4(4):ix,1.994. Descriptionof chronicpain syndromesand definition 3. BakerLL, McNeal DR, BentonLA, et al: Neuromuscular of pain terms,Pain 13(SupplS):s1,, L986. ElectricalStimulation:A PracticalCuide, ed 3, Downey, 1,9. Dorland'slllustrared MedicalDictionaryed2g,PhiadeIphia, CA, 1,993, LosAmigosResearch & EducationInsrirute. 2000,WB Saunders. -1.RobersonWS: Digby'sreceipts,Ann Med HistT(3):216, 20. Lentell,G, Hetherington Eagan et al: The useof ther! J 1925. mal agentsto influencethe effectiveness of low load proJ. Hyland DB, Kirkland VJ: Infrared therapy for skin longed stretch,J Orthoy SVortPhys Ther 16(5):200-207, ulcers,AmJ Nurs80(10): 1800-1801,1980. 1.992. 5. CummingsJ:Role of light in wound healing.In Kloth L, 21,.WarrenC, LehmannJ,Koblanskii: Elongationof rat tail McCullochJM,IeedarJA,eds: rWo und H ealing:Alternativ es tendon:Effectof load and temperature, ArchPhysMed -474, 484,1.97 inManagement, Philadelphia,1990,FADavis. Rehabil 52:465 1.. -. Melvin JL, Nagi SZ: Factorsin behavioralresponse 23. Warren C, LehmannJ, KoblanskiJ: Heat and stretch to impairments, Arch Phys Metl Rehabil 51.:532-537, procedures:An evaluation using rat tarl tendon, Arch 1,970. PhysMed Rehabil 57:122-126,1976. :. SchenkmanM, Buder RB: A model for muitisystem 24. CerstenJW: Effect of ultrasoundon tendon extensibilevaluation,interpretatioq and treatment of individuals rty,AmJPhysMed34:362-369,1955. with neurologic dysfunction,Phys Ther 69(7):538-547, 25. LehmannJ, MasockA, WarrenC et al: Effectof thera1989. peutictemperatureson tendon extensibility,ArchPhys ;. World Health Organization International Classification of M ed Rehab il 5 I :481-487,I970. Imyairments, DisabilitiesandHandicaVs (ICIDH), Geneva, 26. KeshnerEA: Reevaluatingthe theoreticalmodel under1980,The Organization. iying the neurodevelopmental theory: A literature - -,. Wood PHN: The languageof disablement:A glossary review,PhysTher6I:L035-I040,1981. relatingto diseaseand its consequences, Int RehabMed 27. Brooks VB: Motor control: How postureand move2:86-92,1.980. mentsaregoverned,PhysTher63:664-673,1983.
:€-*'
Pathologyand Patient Problems
Inflammation and ssueReVair JulieA. Pryde,MS, PA-C,PT,OCS,SCS,ATC,CSCS SUM,T,IARY O1 lNFOR -nflammation Phase(Days 1-Q lroliferation Phase(Days 3-20) -\laturation Phase(Day 9 on) lhronic Inflammation
WATlOIV
COVERED
Iactors Affecting the Healing Process Healing of SpecificMusculoskeletalTissues Clinical CaseStudy Chapter Review
OBJECTIVES Uponcomyletionof this chaVtet,the readerwill beable to: Define inflammation and identify its possible causes. Identify the five cardinalsignsof inflammation and tfeir causes. List the phasesof tissueinflammation and repair and their relative time ftames. Describethe four responsesof the inflammatory phase. Discussedemaand its qualitative variability. Describethe four processesthat occur in the oroliferation phaseof healing.
7 . Differentiate between the different types of collagenand their rolesin tissuerepair. 8. Describethe differencesbetween the cellular fesponsesin acute and chronic inflammation. 9. Identify local and systemicfactorsthat can affect tissuehealing. 10. Discusshow different types of musculoskeletal tissueheal. 11. List the physical agentsthat can affect or modify tissuehealing.
13
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Trauma or injury to vascularizedtissueresultsin a coordinated,complexJand dynarnic seriesof events collectively refered to as inflammatiotland re7air. Although there are variationsbenveenthe responses of different tissue t)?es, overall the processesare remarkably similar The sequelaedepend on the sourceand site of injury, the stateof local homeostasis, and whether the injury is acute or chronic.The ultimate goal of inflammation and repair is to restore function by eliminating the pathologicalor physical insult,replacingthe damagedor destroyedtissue,and promoting regenerationof noImal tissuestructure. Rehabilitation professionalstreat a variety of inflammatory conditionsresultingftom trauma, surgical procedures,or problematic healing.The clinicianwho is calledupon to managesuchinjuriesneeds to understandthe physiology of inflammation and healingand how it canbe modified. The cliniciancan enhancehealing by the appropriate application of various physical agentsJtherapeutic exercises,or manual techniques.The foundation for a successful rehabilitation program requiresan understandingof biomechanics,the phasesof tissuehealing,and the effects of immobilization and therapeuticinterventions on the healingprocess. Common Causesof Inflammation Soft tissue trasma (spfains, stfains, and contusions) Fractures Foreign bodies (sutures) Autoirnmune diseases (rheurnatoid arthritis) Microbial agents (bacteria) Chemical agents (acid, alkafi) Thermal agents fturns or frostbite) Irradiation (fV or radiation)
This chapterwill provide readerswith information about the processes involvedin inflammationand tissue repair so they can understand how physical agentsmay be used to modify these processesand rmprovepatrentoutcome. The processof inflammationand repairconsistsof three phases:inflammation,proliferation,and maturation. The inflammation phasepreparesthe wound for heaiing;the proliferationphaserebuildsthe damaged structuresand strengthensthe wound; and the marurationphasemodifiesthe scar ussueinto it' matureform (Fig.2-1).The durationof eachphase variesto some degree,and the phasesgenerallyover-
Figure2-1. Flow diagram of the normal phasesof inflam-^-r^-
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-^-^:-
One o PATHOLOGY AND PATIENTPROBLE\4S
Iap. Thus the timetables for the various phasesof healing provided in this chapter are only general guidelines,not precisedefinitions(Fig.2-2).
(DAYS 1-6) PHASE INFLAMMATION Inflammation, from *re Latrn inllamel meaning "to seton fire," beginswhen the normal physiologyof tissue is alteredby diseaseot trauma.l This immediate protectiveresponseattemptsto destroy,dilute, or isolate the cellsor agentsthat may be at fault. It is a norprerequisiteto healing.Ifthere is no nal andnecessary inflammation,healingcannotoccur.Inflammationcan aisobe harmful, particularlywhen it is directedat the '.vrong tissue or is overly exuberant.Ior example, :nappropriatelydirectedinflammatory reactionsthat '-rnderlieautoimmune diseasessuch as rheumatoid :nhritis can causeexcessivescarrinq,which can be
ul
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10 15 20 25 30 35 40 45 s0DAYSFROM TIMEOFINJURY
s
: gure2-2. Time line of the phasesof inflammation and .,1air.
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15
disfiguring and limit joint mobility. Although the inflammatory process follows the same sequence regardlessof the causeof injury somecausestesultin or prolongationof certalnevents. exaggeration CorneliusCelsusfirst describedthe inflammatory phasenearly2000yearsagoasbeingcharacterizedby the four cardinal signsof calor,rubor,tumor,anddolor (Latin terms for heat, redness,swelling, and pain). Functiolaesa(lossof function) was later addedto this list by Virchow, bringingthe numberof cardinalsigns of inflammationto five (Table2-1). An increasein blood in a given area, known as hyyeremia, accountsprimarily for the increasedtemand rednessin the area of acute inflammaperature tion. The onset of hyperemiaat the beginningof the inflammatory responseis conffolled by neurogenic and chemicalmediators.2Localswelling resultsfrom increasedpermeabiliryand vasodilatationof the local blood vesselsand infiltration of fluid into the interstitial spacesof the injured area.Pain resultsftom the pressureof the swelling and from irritation of painsensitivestructuresby chemicalsreleasedfrom damagedcells.2Both pain and swellingmay result in loss of function. There is somedisagreementin the literatureabout the duration of the inflammationphase.Someinvestigatorsstatethat it is relativelyshort,lastingfor less than 4 days,3'aand othersbelieveit may last for up to This discrepancymay be the resultof indi6 days.5,6 vidual and injury-specificvariationor the overlapping natureof phasesof inflammationand tissuehealing. The inflammatory phase involves a complex sequence of interactive and overlapping events includingvascular,cellular,hemostatic,and immune processes. Humoral and neuralmediatorsact to control the inflammatorv phase.
Z-t Cu.airralSignsof Inflammation Sign (Bnglish)
Sign (Latin)
Heat
Calar
Increasedvascularity
Redness
Rubar
lncreasedvasculariry
Swelling
Tumor
Blockageof lymphatic drainage
Pain
Dolor
Physrcalpressureand/or chemical iIIitation of pain-sensitivestructures
Lossof function
Functiolaesa
Painand swelling
l6
2 . Inllamnratiou nnd fi,,ue kfnir
Vascular Response Alterations in the anatomy and function of the microvasculature, inciuding the capillaries, post-
capiliary venules and lymphatic vessels,are among the earliest responsesin the inflammatory phase.T Trauma.such as a lacerarion.sprain.or contusion physicallydisruptsthesestructuresand may produce bleeding,fluid loss,cell injury and exposureof tissues to foreign matedal,including bacteria.The damaged vesselsrespondrapidiy with transientconstdctionin an attempt to minimize blood loss. This response, which is mediatedby norepinephrine,generailylasts for 5 to 10 minutesbut can be prolongedin the small vesselsby serotonin releasedfrom mast cells and platelets. Followingthe transientvasoconstrictionof iniured vessels,the noninjured vesselsnear the injured areadilate.Capillarypermeabilityis also increased by injury of the capillary walls and in responseto chemicalsreleasedfrom injured tissues(Fig.2,3). The vasodilation and increase in capillary permeability are initiated by histamine, Hageman f a c t o r . b r a d y k i n i n .p r o s r a g l a n d i n a s .n d c o m p l e ment fractions.Vasodilationand increasedcapil lary permeabilitylast for up to t hour after tissue damage.
Histamine is released by mast cells, platelets, and basophils at the injury site.dHistamine causesvasodilation and increased vascular permeability in venules, which contributes to local edema (swelling) formation. Histamine also attracts leukocytes to the damagedtissuearea.9Histamine is activefor approximately t hour after tissue injury10 (Iig. 2-4). Separation of endothelialcell junctionscreates gapsallowing leukocyte to escape
Erythrocytes
lvlarginationof leukocytes on endothelialsudace Figure2-3. Vascular responseto wound healing.
I VasoactiveMediators . Histamine . Serotonin . Bradykinin . Anaphylatoxins . Leukotrienes/ Prostaglandins . PlateletActivating Faclors{PAF)
Chemolactic Factors . FormylatedPeptides . LymPhokines . Monoklnes
Activation ol Plateletsand CoagulationSystem
tt Thfombus Formatron
FlecruitrnenV of Stimulation Inflammatory Cells
vasoaclrve Mediators tl
v
Pe-rea5rlity
IncreasedVascular Pemeability Acute lnflammation . PMNS . Platelets
Chfonic lnflammalion . Macrophages . Lymphocytes . PlasmaCells
Fiqure 2-4. Mediatorsofthe inflammatoryresponse.
One . PATHOLOCY AND PATIENT PROBLEMS
Hagemanfactor (also known as dotring faaor Xll), an enzyme found in the blood, is activated by contact with the negatively charged surfaces of the endothelial lining of vesselsthat are exposed when vesselsare damaged.The role of Hagemanfactor is wvofold. First,it activatesthe coagulationsystem to stop local bleeding. Second, it causes vasoconstrictionand increasedvascularoermeabiliw by actlvatingother plasmaproreins.lt conuert"plasminogen to plasmin and prekallikrein to kallikrein, and it activates the altemative complement Dathw a y r l ( F i 82. - 5 ) . Plasmin augmentsvascularpermeability in botlL the skin and lungs by inducing breakdown of fibrin and by cleavingcomponentsof the complementsystem. Plasminalso activatesHageman factor, which initiatesthe cascadethat generatesbradykinin. Plasmakallikrein attractsneutrophils and cleaves kininogen to generateseveralkinins suchasbradykinin. The ability of a chemical to attuactcells is known as cheffiotaxis. Kinins, suchas bradykinin,are biolog! cally active peptides that are potent inflammatory substancesderived lrom plasma. Kinins function similarly to histamine,causinga marked increasein permeability of the microcirculation.They are most prevalentin the early phasesof inflammation, after
Figure2-5. Hageman factor activation and inflammatory tr p.li, f^r
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they ge rapidly destroyedby tissueproteases
oI Ktnlnases.'"
Prostaglandins(PCEs)are producedby nearly all cellsin the body and are releasedin responseto any damageto the cell membrane.Two prostaglandins affectthe inflammatory phase:PGEl and PGEr.PGE, increases vascuJar permeabilityby anragonizing vasoconstdction,and PCE2atffactsleukocytesand synergizes the effects of other inflammatory mediators such as bradykinin. Proinflammatoryprostaglandins are alsothought to be responsiblefor sensitizingpain receptors.In the early stagesof the healingresponse, prostaglandinsmay regulatethe repair process;they are also responsiblefor the later stagesof inflammation.13 Steroids and nonsteroidalantiinflammatory drugs inhibit prostaglandinsynthesis.Ior example, acetyisalicylic acid (aspirin) and acetaminophen (Tylenol@)disrupt the production of prostaglandins but act at different points in their synthesis.Since prostaglandinsare responsiblefor febrilestates,these medicationsareeffectivein reducinsfever. The anaphylatoxins C3a.C4a.andC5aareimportant products of the complement system. These complement fractions causeincreasedvascularpermeabilify andinducemastce11 and basophildegranultaion, causinga further releaseof histamineand thus potentiatinga further increasein vascularpermeabiliqt QabIe2-2). Aside from the chemically mediated vascular changes, changes in physical attraction betlveen blood vesselwalls also alter blood flow. Durins the initial vasoconstriction. rhe opposingwalls oF the small vesselsbecomeapproximated,causingthe lining of the blood vesselsto stick together Under normal physiologicconditions,the cellmembranesof the inflammatory cells and the basement membranes have mutually repulsivenegative chargesjhowever, after injury this repulsiondecreases and the polarity may actuallybe reversed.This resultsin a decreasein the repulsionberween the circulatinginflammatory cellsandthe vesselwalls andcontributesto the adherenceof inflammatory cellsto the blood vessellinings. As blood flow slows resultins from vasoconstriction of the postcapillaryvenulesandincreasedpermeabiliry of the microvasculature,an increasein the cellularconcentrationoccursin the vessels,resulting in increasedviscosiry In the normal physiological state, the cellular componentsof blood within the microvasculatureare confined to a central axial column,and the blood in conractwith the vesselwall
18
2 . Inflauuntion
2-2 Mediators of the Inflammatorv Response Response
Mediators
Vasodilation
Histamine Prostaglandins Serotonin
Increasedvascular permeabihty
Bradykinin C3a,C5a PAF Histamine Serotonin Prostaglandins
Chemotaxrs
Histamrne Monokines Kallikrein Lymphokines
Fever
Prostaglandins
Pain
Prostaglandins Hagemanfactor Bradykinin
is relativelycelf free plasma.Very early in the inflammatory response,neutrophilsin the circulatingblood begin migrating to the injured area.The sequenceof eventsin the journey of these cells from inside the blood vesselto the tissueoutsidethe blood vesselis known as extavasation. The neutrophils,which are a type of leukocyte(white blood cell),breakaway from t}te centralcellularcolumn of blood and start to ro11 along the blood vessellining (the endothelium)and adhere.They line the walls of the vesselsin a process known as margination. Within t hour, the endothelial lining of the vesselscan be completelycoveredwith leukocytes.As thesecellsaccumulate,they lay down in Iayersin a processknown as yavemetting,Certain mediatorscontrol the adherenceof leukocytesto the endothelium, either enhancing or inhibiting this process. for example, fibronectin, a glycoprotein presentin plasmaand basementmembranes,has an important role in the modulation of cellular adherence to vessel walls. After injury to the vessels, increasedamountsof fibronectinare depositedat the injury site. The adherenceof the leukocytesto the endotheliumor vascularbasementmembraneis critical for the recruitmentof leukocytesto the site of the injury.
nnd Ti<
After margination occurs, leukocytes begin to squeezethrough the vesselwalls in a processknown The leukocytesinsert their pseudopods asdiayedesis. junctions into the betweenthe endothelialcells,crawl *rrough the widened junctions, and assumea position betlveen the endothelium and the basement membrane.Then, attracted by chemotacticagents, *rey escapeto reachthe interstitium.This processof leukocytemigration from the blood vesselsinto the perivasculartissuesis known asezgrationFlg.2-C1. Edema is an accumulation of fluid within the extravascularspaceand interstitial tissues.Edemais the result of increasedcapillaryhydrostaticpressure, increasedinterstitial osmotic pressure,and an overwhelmed lymphatic systemthat is unableto accommodate this substantialincreasein fluid and plasma proteins.Edemaformation and control are discussed in detail in Chapter 11.The clinicalmanifestationof edemais swelling. The fluid that first forms edemadurins inflammation has very few cells and very litcle piotein. This fluid is known astransudate. Transudateis madeup of predominandydissolvedelectrolytesand water and has a specificgravity of lessthan 1.0.As the permeability of the vesselsincreases,more cellsand lower molecular weight plasma proteins cross the vessel wall, making the extravascular fluid more viscousand cloudy. This cloudy fluid, known as exudate,has a specificgravity of greaterthan 1.0.lt is alsocharactertzed 6y a high content of lipids and cellular debris. Exudateis often observedearly in the acute inflammatory processand forms in responseto suchminor injuriesasblistersand sunburns. The loss of protein-rich fluid from the plasma reducesthe osmotic pressurewithin the vesselsand increasesthe osmotic pressureof the interstitial fluids.which. in turn. increasesthe outflow of fluid from the vessels,resultingin an accumulationof more fluid in the interstitial tissue.When the exudate'sconcentration of leukocytesincreases,it is known as prs or supFurative exudate.Pus consistsof polymorphonuclear neutrophils, liquefied digestion products of underlyingtissue,fluid exudate,and very often bacteria if an infection is present.When localizedsuppurative exudateoccurswithin a solid tissue,it resultsin an abscess, a localizedcollectionof pusburiedin a tissue,organ,or confined space.Pyogenicbacteriaproduceabscesses. Fourmechanismsare responsiblefor the increased vascularpermeabilityseenin inflammation.The first
One . PATHOLOCY AND PATIENT PROBLEX'IS
19
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Chemoanractant
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:erris. nor ma tnd fluom .uid to!
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Sour"" o, ,nru,, Figure2-6. Illustration of leukocytic events in inflammation: margination, adhesion, diapedesis,and emigration in responseto a chemoattractantemanatingfrom the sourceof the iniury
and predominantmechanismis endothelialcell conraction, which leadsto a widening ofthe intercellular iunctions or gaps. This mechanism affects venules ',vhilesparingcapillariesand arterioles.It is controlled by chemicalmediators and is relatively shortJived, lastingfor only 15to 30 minutes.laThe secondmech anismis a resultof direct endothelialinjury and is an immediate, sustainedresponsepotentially affecting all levelsof the microcirculation.This effect is often seenin severeburnsor lytic bacterialinfections,andis often associatedwith plateletadhesionand thromboendothesis or clot formation. Leukocyte-dependent iralinjury is the third mechanism.Leukocytesbind to lhe area of injury and releasevarious chemicalsand enzvmes that damase the endothelium and thus
increasepermeability.The final mechanismis leakage by regeneratingcapillariesthat lack a differentiated endothelium and therefore do not have tight gaps. This may accountfor the edemacharacteristicof later healinginflammatror.(Frg.2-7).
Response Hemostatic The hemostaticresponseto injury controlsthe blood losswhen vesselsare damagedor ruptured.Platelets, the first cellsat the siteofthe injury enterthe areaand bind to the exposedcollagen,releasingfibrin to stimulate clotting. Plateletsalso releasea regulatoryprotein known as Vlareletderivedgrowthfaaor (PDCF), which is chemotacticand mitogenic to fibroblasts
20
2 . Inflammation and TissueRepair
MECHANISM OF LEAKAGE ANDDISTRIBUTION
Endothelial contraction . venules
Directinjury . all microvessels
Leukocyte-dependant . mostlyvenules .lungcapillaries
Regeneraling endothelium . capillaries . olhervessels
Arteriolar dilatation
Openingof capillary beds
Venular dilatation I
Increased bloodtlow B Figure2-7. A, Illustration of four mechanismsof increasedvascularpermeability in inflammation. B, Vascularchanges associatedwith acute inflammation
and may alsobe chemotacticto macrophages, monocytes,andneutrophils.lsThus plateletsplay a role not only in hemostasisbut also contdbute to the control of fibrin deposition, fibroblast proliferation, and angiogenesis.
When fibrir and fibronectin enter the injured area they form cross-linkswith the collagento createa fibrin lattice.This tenuousstructur€providesa temoorary plug in the blood and lymph vessels,limiting local bleedingand fluid drainage.The lattice sealsoff
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Ore . PATHOLOCY AND PATIENTPROBLEMS
damagedvesselsand confinesthe inflammatory reaction to the areaimmediately surroundingthe injury The damaged,pluggedvesselsdo not reopenuntil later in the heaiingprocess.The fibrin latticeservesas the wound's only sourceof tensilestrengthduringthe inflammatoryphaseof healing.l6
Response Cellular Circulatingblood is composedof specializedcells suspendedin a fluid known as ylasma.These cells include erythrocytes (red blood cells), leukocytes (white blood cells),and piatelets.Redblood cellsplay a minor role in the inflammatory process,although they may migrateinto the tissuespacesif the inflammatory reactionis intense.The primary role of the red blood cells,oxygentransport,is carriedout within the confinesof the vessels.Art inflammatory exudatethat containsblood usually indicatessevereinjury to the microvasculature. The accumulationof blood in a tis sueor organis refeffed to asa hematama; bloody fluid that is present in a joint is called a hemarthrosis. Hematomas in muscle can cause pain and limit m o r i o no r f u n c t i o nr:h e yc a na l s oi n c r e a ssec a r i s s u e formation. A critical function of inflammation is to deliver leukocytesto the area of iniury via *re circulatory system.Leukocytesare classifiedaccordingto their structure into polymorphonucleocytes(PMNs) and mononuclearcells. PMNs have nuciei with several lobes and contain cytoplasmic granules.They are Furthercategorized,by their preferencefor specific histological stains, as neutrophils, basophils, and eosinophiis.Monocytes are larger than PMNs and have a singlenucleus.ln the inflammatory process, leukocytes play the important role of clearing the injured site of debris and microorganismsto set the stagefor tissuerepair(Fig.2-8). Migration of leukocytes into the area of injury occurswithin hours of the in1ury.Eachleukocyte is specialized and has a specificpurpose.Someleukocytes aIe more prominent in early inflammation, whereas others become more impoftant during the later stages.Initially the number of leukocytes at rhe injurysiteis proporrional to theirconcenrration in the circulatingblood (Table2-3). Sinceneutrophils have the highest concentration in the blood, they predominatein the early phasesof inflammation. Chemotacticagentsreleasedby other cells,suchas mast cellsand platelets,attractleuko-
CONNECTIVE TISSUE I\,IATRIX
27
VESSELS
CONNECTIVE TISSUE CELLS
A
Basement
@
membranel Collagentype lV Laminin Fibronectin Proteoglycans Entaclin
Mastcell
n
rioroorast Itl
Elasticfibers
V
td'.\
rg
Collagen fibers
l\,4acrophage
d\+d Proteoglycans
-----,--J
Basophil Figure2-8. Intravascular cells, colnective tissue matdx, and cellsinvolved in the inflammatory response.
$ g
2-3 Cot ."ntration of Leukocytes in Adult Human Blood Typ"
Concentration
Poly morphonuclear Cells Neutrophils Eosinophils Basophils
62.0./. 23% 0.4./.
Mononucleat Cells Monocytes Lymphocytes
5.3./. 30.0%
cytes at the time of injury. Neutrophils rid the injury site of bacteria and debris by phagocytosis. When lysed, the lysosomes of the neutrophils release proteolytic enzymes (proteases)and colwhich begin the lagenolyticenzymes(collagenases),
22
2 c lttllatttttntion
debridementprocess.Neutrophils remain at the site of the injury for only 24 houri, after which time they disintegrate.However, they help to perpetuatethe inflammatory response by releasing chemotactic agentsto attractother leukocytesinto the area. Basophils release histamine after injury and contribute to early increasedvascularpermeability. Eosinophilsmay be involvedin phagocytosisto some degree. Ior 24 to 48 hoursafteran acurernjury.monocytes predominate. Monocytes make up bewveen 4o/o and 8% of the total white blood cell count. The predominanceof thesecellsat this staseof inflammation is thoughr to resuk in parr from rheir longer lite span.Ly'rnphocytessupply antibodiesto mediatethe body's immune response.They are prevalent in chronicinflammatory conditions. Macrophage Products Proteases Elastase Collagenase Plasminogen activator Chemotactic factors fot other leukogztes Complement components of the alternative and classical pathways Coagulation factors Growth-promoting factors for fibroblasts and blood vessels Cl'"tokines Arachidonic acid metabolites Monocytes are converted into macrophages when they migrate from the capillaries into the tissue spaces. The macrophage is considered the most important celi in the inflarnmatory phase and is essen-
nnd Tisstc Reyair
tial for wound healing.Macrophagesare important becausethey produce a wide range of chemicals. They play a major role in phagocytosisby producing enzymes such as collagenase(Fig. 2-9). These enzymesfacilitatethe removal of necrotictissueand bacteria.Macrophagesalso produce factors that are chemotacticfor other leukocytes. Macrophagesalsoprobablyplay a role in localizing the inflammatory processand attractingfibroblaststo the injuredareaby releasingchemotacticfactorssuch as fibronectin. Macrophages chemically influence the number of fibroblastic repak cells activated; therefore,in the absenceof macrophages,fewer, less mature fibroblastsmigrateto the injuredsite. Platelet derived growth factor (PDGI) releasedby platelets during clotting is also releasedby macrophagesand canactivatefibroblasts.In the later stagesof fibroplasia,macrophagesmay also enhancecollagendeposition by causingfibroblaststo adhereto fibrin. As macrophages ingest microorganisms, they excreteproductsof digestionsuchashydrogenperoxide, ascorbic acid, and lactic acid.17Hydrogen peroxideassistsin the control of anaerobicmicrobial growth. The other two products signal the extent of the damagein the area, and their concentration is interyreted by the body as a need for more macrophagesin the area.l8This, in turn, causes increasedproduction of by-products, which then resuitsin an increasedmacrophagepopulation and a more intenseand prolongedinflammatoryresponse. Macrophagesare most effectivewhen oxygen is presentin the injured tissues.However,they can toleratelow oxygen conditions,as is apparentby their presencein chronic inflammatory states.Adequate oxygentensionin the injuredareais alsonecessaryto minimizethe riskof infecrion.I issueoxygentension
Macrophage
Figure2-9. Diagrammatic repres€ntationof the processof phagocl,tosis.
Oqe . PATHOLOCY AND PATIENT PROBLEMS
nt t-
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dependson the concentrationof atmosphericoxygen available for breathing, the amount of oxygen absorbedby the respiratoryand circulatorysystems, and the volume of blood availablefor tlansDortation. as well as rhe stare of the tissues.Local topical application of oxygen to an injured area does not influencetissueoxygen tension as much as the level of oxygenbrought to the injured areaby the circuiating blo6d.le-2t
lmmune Response The immune responseis mediated by cellular and humoral factors. The roles of lyrnphocytes and phagocyticleukocytesin the immune responsewere discussedpreviously.The other mechanisminvolved in the immune responseis the complementsystem which is an important sourceof vasoactivemediators. The complementsystemis one of the most important plasmaprotein systemsof inflammation as its components participate in virtually every inflammatory
ClassicalPathway Activated by immune complexes of antibodies withantigens
23
response.The complementsystem can be activated by antigen-antibodycomplexesand by bacteria,foreignmaterial,and other cellularproducts. The complementsystem is a seriesof enzymatic plasma proteins that is activated by two different pathways, the classical and the alternative.22 Activation of the first componentof either pathway of the cascaderesults in the sequentialenzymatic activationof the downstreamcomponentsof the cascade(Fig.2-10).The end product of the cascade,by either pathway, is a complex of C6, C7, C8, and C9, which form the membraneattack complex (MAC). The MAC creates pores in plasma membranes, *rereby allowing water and ions into the cell. This causesloss of membraneintegrity and cell lysis. The subcomponents generated earlier in the cascade also have important functions. Activation of components C1-C5 produces subunits that enhance inflammationby making bacteriamore susceptibleto phagocytosis(known asopsonization), attractingleukocytes by chemotaxisand acting as anaphylatoxins.
AlternativePathway Activated by cell surfaces
ActivatesClr+C1s
Ite
to on
ActivatesC6, C7, C8, C9 to form membraneattack complex (MAC)
Figure2-10. Overview of the complement system- classicaland alternativeactivation pathways.
24
2 . ltrflarnrnatiortntt/1 li.,ttc Rcfatr
Anaphylatoxinsinducemastcellandbasophildegranu- the classical pathway, C1, C2, and C4 are not lation, causing the release of histamine, platelet involved in the alternativepathway. activatingfactot and leukotrienes.Thesefurther proln summary therearethreemajor consequences of mote increasedvascuiarpermeability. the inflammatory phase.Iirst, fibrin, fibronectin,and The classicalpathway of the complement cas- collagencross-linkto form a fibdn lattice that limits cade is activated by an antigen antibody complex blood loss and providesthe wound widr some initial interactingwith *re first componentof the complestrengdr.Then macrophagesbegin to remove damment cascade, C1.C1 consistsof threeproteins:C1q, aged tissue.finally, endothelialcells and fibroblasts C l r . a n d C l s . C i q b i n d s t o t h e a n t i g e n - a n t i b o d y are recruitedand stimulatedto divide. This sets the complex, resultingin a conformationalchange.Clr stagefor the proliferationphaseof healing(Table2-4). enzymaticallyactivatesC1s so that it can act on C4 and C2. C4 and C2 are cieavedro form C4bC2a,a (DAYS PR0LtFERATt0N PHASE 3-20) complex that acts as a C3 convertase.C3 is cleaved into C3b and C3a by the C3 convertase.C3b then The secondphaseof tissuehealingis known as the cleavesC5, producingC5aand C5b. C5b activatesthe yhase.Thisphasegenerallylastsfor up to Vroliferation production of the terminal products of the cascade, 20 daysand involvesboth epithelialcellsand connecc6-c9. tive tissues.lo Its purposeis to coverthe wound and The alternativepathway of the complementcas- impart strengthto the injury site. cadeis activatedby a variety of cellularand microbial Epithelial ceils form the covedng of mucous and productsand by foreign material.The binding of C3 serousmembranes,and the epidermis of the skin. with tlvo plasmaproteins,factorsB and D, catalyzes Comective tissueconsistsof fibroblasts,ground subthe conversionof C3 to C3bBbwhich functionsas a stance,and fibrous strandsand providesthe structure C3 convertasegeneratingadditional C3a and C3b in for other tissues.The structure,strength,and elastican amplificationstep.C3b then cleavesC5, resulting ity of conn€ctivetissuevariesdependingon the type in the formation of the MAC, C6-C9. In contrastto of tissueit comorises. Fourorocesses occursimultane-
p
,-O ,"--ary
of Eventsof the InflammatoryPhase
Response
Changes in the injured area
Vascular
Vasodilationfollowed by vasoconstnctionat the capillaries,postcaprllaryvenules,and lymphatics Vasodilationmediatedby chemicalmediators histamine,Hagemanfactor,bradykimn, prostaglandins, complementf ractions Slowingofblood flow Margination,pavementing,and ultimatelyemigrationof leukocytes Accumulationof fluid in the interstitialtissuesresultingin edema
Hemostatic
Retractronand sealingoff of blood vessels Plateletsform clotsandassistin burldingoffibrin lattice,which servesasthe wound's sourceoftensile strengthin the inflammatoryphase
Cellular
Delivery ofleukocytesto the areaof injury to rid the areaof bacteriaand debrisby phagocl,tosrs Monocytes,the precursorsof macrophages, areconsideredthe most important cellin the inflammatoryphase Macrophagesproducea numberofproducts essentralto the healingprocess
lmmune
Mediatedby both cellularand humoralfactors Activationof the complementsystemvia the alternativeand classicalpathwaysresultingin componentsthat increasevascuiarpermeability,stimulatephagocytosrs, and act aschemotactic stimuli for leukocytes
One . PATHOLOCY AND PATIENT PROBLEMS
they begin to align themselvesperpendicuincreases, lar to the capillaries. The fibroblastssynthesizeprocollagen,composed of three polypeptide chainscoiled and held together by weak electrostaticbondsinto a triple helix. These chains undergo cleavageby coilagenaseto form Epithelialization tropocollagen.Multiple tropocollagen chains then :oithelialization, *re reestablishmentof the epider- coil together to form collagen fibrils, which then make up collagenfilaments and ultimately combine ::ris,is initiated earlyin prolilerationwhen a wound is ..rperficial.often within a few hours of injury73 to form collagen fibers (Fig. 2-13). CrossJinking .\tLena wound is deep,epithelializationoccurslater, between collagenmoleculesprovides further tensile =:ter collagen production and neovascularization. strengthto the injuredarea. Tissue containing the newly formed capillaries, :oithelialization providesa protectivebarrierto pre-.ent fluid and electroly'telossand to decreasethe risk fibroblasts,andmyofibroblastsis refercedto asgranulation tissue.As the amount of granulation tissue :i infection.Healingof the wound surfaceby epithethereis a concurrentreductionin the sizeof -:alizationalone doesnot provide adequatestrength increases, the fibrin clot, allowing for the formation of a more 3 meet the mechanicaldemandsplacedon most tispennanentsupportstructure.Theseeventsare medi:ues. Suchstrengthis provided by the collagenproated by chemotacticfactorsthat stimulate increased :uced duringfibroplasia. During epithelialization,uninjured epithelial cells fibroblasticactivity and by fibronectinthat enhances misration and adhesionof the fibroblasts.The fibrob:om the margins of the injured area reproduceand tasasinitially produce a thin, weak-structuredcolla:rigrate over the injured area,coveringthe surfaceof --rewound and closingthe defect.It is hypothesized genwith no consistentorganizationknown asty7eIII Thrs period is the most tenuoustime during rat the stimulusfor this activity is the lossof contact collagen. the healingprocessdue to the limited tensilestrength :rhibition that occurswhen epithelial cells are norof the tissue. During the proliferation phase an =ally in contact with one another. The migrating :rithelial cells stay connectedto their parent cells, injured areahas the greatestamount of collagen,yet -:rerebypulling the intact epidermisover the wound its tensile strensth can be as low as 15% of that of normaltissue.2i :Cge. When epithelial cells from one edge meet Iibroblasts also produce hyaluronic acid, a glyrigrating cellsfrom the other edge,they stop moving :ue to contactinhibition (Iig. 2-11).Aithough clean, cosaminoglycan(CAC), which draws water into *re :.oproximatedwounds can be clinically resurfaced area,increasesthe amount of intracellularmatrix, and '.,.'ithin48 hours, larger open wounds take longer to facilitatescellularmigration. It is postulatedthat the compositionof this substanceis relatedto the num]t *ren takes severalweeks for this thin :esurface,24 thereby implyber and location of the cross-bridges, ,ayerto becomemultilayeredand to differentiateinto ing rhat the relationship benveenCAC and collagen =e variousstrataof normalepidermis(Frg.2-12). 17'28 dictatesthe scararchitecture. The formation of cross-1inksallows the newly Production Collagen formed tissueto tolerateearly,controlledmovement without disruption. However, infection, edema, or ibroblasts make collagen. Fibroblast growth, excessive stressonthe healingareamay resultin further takes place in connective tissue. :nown asfibroplasra. and additional depositionof collagen. hflammation :ibroblastsdevelopfrom undifferentiatedmesenchycollagen depositionwill result in excessive Excessive ral cells located around blood vesselsand in fat. that may lirnit the functional outcome. 1ey migrate to the injured areaalongfibrin strands, scarring By the seventhday afterinjury thereis a significant :r responseto chemotacticinfluences,and arepresent increasein the amount of collagen,causingthe tensile i.rroughoutthe injured area.25Adequatesuppliesof strength of the injured area to increasesteadily.By :>,ygen,ascorbicacid, and other cofactorssuch as day 12, the initial immature ty?e IIl collagenstartsto inc, iron, manganese,and copper are necessaryfor :broplasia to occur.26As the number of fibroblasts be replacedby type I collagen,a more mature and :us1y in the proliferation phase to achieve coales:ence and closureof the injured area:epithelializa:on, collagenproduction, wound contraction, and ::eovascularization.
e o t-
d rd o. )le c)e e-
25
26
2 o Itflannation
anl7'issra
Refair
With Injurybasal cells detach irom the basementmembrane.
ce s
The cells migratewhile holdingon to their 'parent'cellsand pulllhem into the center to close the wound. Contact Inhibition
when thetwosrdesmeet,movement ceases,
Basalcells differenliateand proliferate...
...1obecomemultilayered and restorethe epidermis.
Figure 2-11. Schematicdiagramof epithelialization.
strongerform.16,29,30 The ratio of type I to type III collagenincreases sreadilyfrom chispojnron.
Wound Contraction Wound contractionis the finai mechanismfor repairing an injured area.In contrast to epithelialization, which coversthe wound surface,contractionpullsthe edgesof the injured site toged-rer, in effect shrinking the defect.Successfulcontractionresultsin a smaller areato be repairedby scarformation. Contractionof the wound beghs approximately5 days after injury
and peaksafter about 2 weeks.31Myofibroblastsare the primary cel1sresponsiblefor wound contraction. Myofibroblasts,identified by Gabbianiet aI rn 1971, are derived from the same mesenchymaicells as fibroblasts.32 Myofibroblastsare similarto fibroblasts exceptthat they alsopossess the contractileproperties of smooth muscle.Myofibroblastsattachto the margins of the intact skin and pull the entire epithelial layerinward.The rateof contractionis proportionalto the number of myofibroblastsat and under the cell marginsandis inverselyproportionalto the latticecol lagenstructure.
Otc . PATHOLOCY AND PATIENTPROBLEMS
HEALINGBY PRIIVARYINTENTION
27
HEALINGBY SECONDARYINTENTION
24 hours
3 to 7 days
lvlitosis Granulationtissue lvlacrophage Fibroblast New capillary
Fibrous union Wound contraction
; ale rion.
)7r, iasts rties :rar_ :e1ial ral to :cell : col-
Figure2-l2 Diagrammatic comparison of healing by primary intention (left) and secondaryintention (right).
Accordins
rn
rhc
.'.t,''o
tr:mc
th"^^,
.h"
'.vound margin beneath the epidermis is the location :f myofibroblast action.33 A ring of myofibroblasts noves inward from the wound margin. Although :ontractile forces are initially equal, the shape of the
picture frame predictsdre resultantspeedof closure (Frg.2-14).Linear wounds with one narrow dimension contractrapidly;squareor rectangular wounds, wi*r no closeedges,progress at a moderatepace;and circularwounds contractmost slowly.34
28
2 . lrrflotnrnationnnd li..tc Rcynir
Collagen filament Collagen fibril
Primitive coUagen fiber Collagen fibers
Figure 2-13.Dragran-matic representalion of one uopocollagenunit joinirg wirh orhersro lorm collagentilamenrs and, ultimately, collagenfibers.
Figure2-14. Illustration of the picture frame theory of wouno contlactron.
If wound contraction is uncontrolled it can result in the formation of contractures. Contracrures are con ditions of fixed high resistance to passive stretch that may ^result from fibrosis of tissues surrounding a joint.35 Contractures may also result from adhesio'ns, muscle shortening, or tissue damage. Contractures are discussedin greaterdepth in Chapter 5.
Wounds that are rapidly closedwith sutureswith minimallossoltissueandminimalbacterialcontamination can heal without wound contraction.This is known a, healingbv yrimaryunionytimaryinrenrionor When thereis significantlossof tissueor frst ixtention. bacterialcontamhation,wound contractionis necessaryto closethe wound. Wound contractionis the feature that most clearly differentiatesprimary ftom secondaryhealing,alsoknown as healingby secondary intentioxor iadirectuniou.36 Later approximationof a wound's edgeswith suturesor the applicationof skin graftscan reducewound contractionand is krrown as healiugbydelayedyrimatyintention .37'38fo minimize contraction,graftsmust be appliedearlyil the inflammatory phase,beforethe processofcontractionbegins.39 As scartissuematures,it developspressureand tension-sensitivenerveendingsto protect the immature vascularsystem,which is weak and can bleed easilywith any insult. During the proliferationphase, the scaris red and swollen due to the increasein vascularity and fluid, the innervationof the healingsite, and the relativeimmatudty of the tissue.The tissue can easily be damagedand is tender to tension or pressure.
Neovascularization Neovascularization,the developmentof a new blood supply to the injured area, occurs as a result of angiogenesis, the growth of new blood vessels. Healing cannot occur without angiogenesis. These new vessels are needed to suppiy oxygen and nutrients to the injured and healing tissue. It is thought that macrophages signal the initiation of neovascularizatron. Angiogenesis can occur by three different mechanisms: generation of a new vascular network, anastomosts to preexisting vessels,or coupling of the vesselsin the injured area.4o Vesselsin the wound periphery develop small buds that grow into the wound area. These outgrowths eventually come in contact with and join other arterial or venular buds to form a capillary loop. These vesselsfill the injured area,giving it a pinkish to bright red hue. As the wound heals, many of these capillary loops ceaseto function and retract, giving the mature scar a more whitish appearance than the adjacent tissues. Initially the walls of these capillaries are thin, making them prone to injury Therefore immobilization at this stage may help to protect these vesseis and permit further regrowth, whereas excessiveearly
One . PATHOLOGY AND PATIENT PROBLEITIS
/ith
motion can causemicrohemorrhagingand increase 'he likelihood of infection.
29
p ,-s aou"*enTypes
JLS
,or 30r
:om :lary rfa skin nas ma39 and leed
SItC,
ssue nor
looo rgionew ts to that ^-L
f the buds wths artehese rioht
illary ature rt trstnm, tltza^ :ssels early
(DAY PHASE MATURATToN I0N) -\s dre transitionfrom the proliferationto the maturaion stageof healingis made,changesoccurinthe size, :orm, and strengthof the scartissue.The maturation rhaseis the longestphasein the healingprocess.It can rersist for over a year alter *re initial insult. During -Jristime the number of fibroblasts,macrophages, nyofibroblasts,and capillariesdecrease and the water :ontent of the tissue deciines.The scar becomes '.vhiterin appearanceas the collagenmaturesand the '.'ascularitydecreases. The ultimate goal of this phase :srestorationofthe prior functionof the injuredtissue. Severalfactors determine tl-terate of maturation :rrd the final physicalcharacteristics ofthe scar.These :rclude fiber odentation and the balanceof collasen .vnrhesis andlysis. Throughout the maturation phase, synthesis and lysrs of collagen occur in a balancedfashion. llormonal stimulation secondary to inflammation :ausesincreasedcollagendestructionby the enzyme ;ollagenase.Collagenaseis derived from polymor:nogranular leukocytes, the migrating epithelium, ai-rdthe granuiationbed. Collagenaseis ableto break -re strong crossJinkingbonds of the tropocollagen =olecule,causingit to becomesoluble.It is then .xcretedasa wasteby-product.Although collagenase :smost activein the actualareaofthe injury its effects :an alsobe noticed,to a lesserextent,in areasadja-enr to the injury site. Thus remodelrngoccurs --:rrough a processof collagenturnover. Collagen,a glycoprotein,providesthe extracellular :amework for all multicellularorganisms.Although :ore than 27 types of collagenhave been identified, re following discussionis limited to types I, Il, and -llr' f|able 2-5).AII collagenmoleculesaremadeup of -rree separatepolypeptide chains wrapped tighdy :ogetherin a triple left-handedhelix.Type I collagenis re primary collagenfound in bone,skin, and tendon, andis the predominantcollagenin maturescars.Type -l collagenis the major coliagenin cartilage.Type III :ollagenis found in the gastrointestinaltract, uterus, and blood vesselsin adults.It is also the first woe of :olJagen ro be deposited duringrhehealingproceis. During the maturationphase,the collagensynthe;ized and depositedis predominantlyrype I. The bal:nce between synthesisand lysis generallyslightly
Tw"
Distribution
Most abundantform ofcollagen:skn, bone,tendons,and most organs
II
Major cartilagecollagen,vitreoushumor
III
Abundantin blood vessels,rrterus,skin
IV
Ali basementmembranes Mrnor componentof most interstitial ussues
VI
Abundantin most interstitialtissues
VII
Dermal-epidermaljunctron
UII
Endothelium
x
Cartilage
X
Cartilage
favors synthesis.As type I collagenis strongerthan the rype III collagendepositedin the proliferation phase,tensile strengthincreasesfaster than mass.If the rate of collagenproduction is much greaterthan the rate of lysis, a keloid or hypeftrophic scar can result. Both keloids and hypertrophic scarsare the result of excessivecollagendepositiondue to inhibition of lysis. lt is believedthat this inhibition of lysis is due to a genetic defect. Keloids extend beyond the original boundaries of an injury and invade the suffounding tissue,whereas hypertrophic scars, although raised, remain within the margins of the original wound. The treatment of keloid scars through surgery medications,pressure,and iradia44 tion hasonly limited success.42 Collagen synthesis is oxygen dependent,while collagenlysis is not.asThus, when oxygenlevelsare low, the processof maturation is weighted toward lysis,resultingin a softer,lessbulky scar.Hypertrophic scarscan be managedclinicallywith prolongedpressure,which causesa decreasein oxygen,resultingin decreasedoverall collagensynthesiswhile maintaining the level of collagenlysis.37This is one of the basesfor the use of pressuregarmentsin the treatment of patientssufferingftom bums, and for the use of elastomerin the managementof scarsin hand therapy. Eventually,balanceis achievedwhen the scar bulk is flattenedto approximatenormal tissue.
30
2 . Inflannatiou
Collagensynthesisand lysis may last for up to 12 to 24 monthsafreran injury.The high rateof collagen turnover during this period can be viewed as both detrimentaland beneficial.As lonq as the scartissue appearsredderrhanthe surroundingtissue,rernodeling is sLilloccurring.AJthougha joint or rissuesrructure canIosemobiliry quickly duringthis stage,sucha Ioss can still be reversedthrough appropriateinterventron. The physical structure of the collagen fibers is largelyresponsible tor the finalfunctionof rheinlured area.Collagenin scartissueis always lessorganized than collagen in the surrounding tissue. SCarsare inelastic,so redundantfolds are necessaryto Demit mobiliryof the srruturesto which they areattached. To understandthis conceptbetter,onemay considera spring,which, aithoughmadeof an inelasticmaterial, has a spiraledform that, like the redundantfolds of a scar,allows it to expandand contract.If short, dense adhesions are formed, these will restrict motion becausethey cannotelongate. Two theorieshave been proposedto explain the orientation of the collagenfibers in scar tissue:tlre inductiontheory and the tensiontheory.Accordingto the induction theory the scarattemptsto mimic the charactedsticsof the tissue it is healins.46Thus a densetissueinducesa dense.highlycro"s-linledscar, whereasa more pliable tissueresultsin a loose,less cross-linkedscar.Densetissuetypes havea preferential status when multiple tissue types are in close proximity. Basedon this theory, surgeonsattempt to designrepair fields that separatedenseand soft tissues.If this is not possible,as in the caseof repaired tendonleft immobileover bone Fracrures, adhlsions and poorly gliding tendonscan result.In such cases, earlyconrrolledmovementmay be beneficial. According to the tension theory, the intemal and extemalstresses placedon the injuredareaduring the maturationphasedeterminethe final tissuestructure.aoMuscle tension, joint movementJsoft tissue loadingand unJoading. fascialgliding. temperarure changes,and mobilizatjon are alJ forces that are thought to affect collagensfiucture.Thus the length and mobility of cheinjuredareamay be modified-by the applicationof stressduringthe appropriatephases of healing.This theory has been supported by the work of Arem and Madden, which has shown *rat the two most important variablesresponsiblefor successful remodeirngare the phasei of the repair processin which mechanjcal forceswere introduced
and fi>:uc Rerair
and the natureof the appliedforces.aT Scarsneedlowload, long-duration stretch during the appropriate phasefor permanentchangesto occur Studieshaveshown *rat the applicationof tension duringhealingcausesan increasein censilestrength. and immobilization and stress deprivation reduce tensilestrengthand collagenstructure.The recovery curves for tissue experimentallyimmobilized For bet:ween2 and 4 weeks reveal that these processes cantakemonths to reverse,andreversalis oftennever complete. Eachphaseof the healingresponseis necessary and essentialto the subsequentphase.In the optimal scenario,inflammation is a necessarvaspectof the healingresponse and the [irst srept;ward recovery, seting rhe stagefor the ocherphasesof healing.It repeatedinsults or injury occur,however, a chronic inflammatory response may develop that can adverselyafFectthe outcomeof the healingprocess. Acute inflammatory processescan have one of four outcomes.Iirst, and most beneficial,is the complete resolutionand replacementof the injured tissue with like tissue.Second,and most common,is healing by scarformation.The third is the formation of an abscess.Fourth is the possibility of progressionto chronicinflammation.1o
CHRONIC INFLAMMATION Chronic inflammation is the simultaneousproqression of activeinflammation.tissuedestruccion,-and healing.Chronicinflammationcanarisein oneof two ways. The first follows acute inflammation and can be due to the persistenceof the injurious agent(such asa cumulativetrauma)or to someother interference with the normal healing process.The second is a resultof an immune responseto eitheran alteredhost tissueor a foreign material,such as an implant or a suture,or is t}le resultof an autoimmunediseasesuch asrheumatoidarthritis. The normal acute inflammatory processlasts for no morethan2 weeks.II ir continuesfor morechan4 weeks,it is known as subacute inflammation.3 Chronrc inflammationis inflammationthat lastsformonths or years. The primary cells presentduring chronic inflammation aremononuclearcellsincludinglymphocytes, macrophages, andmonocytes(Iig. 2-15).Occasionally eosinophilsare alsopresent.aB The progressionof the inflammatory responseto a chronicstateis a resultof
O e . PATHOLOGY AND PATIENT PROBLEMS
31
Characteristics / Functions
Leukocyte e
Associatedwith . chronic inflammation . phagocytosts
Lysosome
n IJ
e
ibrolyticpathways Regulatescoagulation/f
v
Regulateslymphocyteresponse
)t :S
Ivlonocytesare convertedto macrophageswhen they emigrate from capillanesinto the tissue spaces
:r
v ^l
a
IC
v' If ic
Associatedwith . chronicintlammation
=
immuneresponse Key cell in humoraland cell-mediated
tn
rf :l-
te
Lymphocyte
Ll'
Sparse endoplasmic reticulum
tn
ro
Associatedwilh . allergicreactions . parasiticinfectionsand associatedinflammatoryreactrcns
Granules
Modulatesmasi cell-mediatedreactions rS-
rd 1Q
Eosinophil
ch ce
Assocrated with . acuteinflammation . baclerialandforeignbodyphagocytosis
a )st :a
ch :OI
r4 ric OI
m1ly he oI
@
. Not phagocytic . Contarnshistamine,which causes increasedvascular permeabilfy
Basophil
Figute2-15, Cellular components of acute and chronic inflammation.
32
2 . Itflafltfiatiot
both immunologicand nonimmunologicfactors.The macrophageis an important sourceof inflammatory a n di m m u n o l o g im c e d i a c oa r sn di s a n i m p o r t a ncro m ponent in the regulationof their actions.The role of eosinophilsis much lessclear,althoughthey are often presentin chronic inflammatory conditions that are causedby allergicreactionsor parasiticinfection.4s Chronic inflammation also results in increased fibroblastproliferation,which in turn increasescollagen production and ultimately increasesscar tissue and adhesionformation. This may lead to a loss of function asthe delicatebalancebetweenootimal tensile strengthand mobility of tbe involvei tissuesis lost.
FACTORS AFFECTING THEHEALING PROCESS A number of factors, either local or systemic, can impact or modify the processesof inflammation and repav (Table 2-A1.Localfactors that can affect wound healing include the type, size, and location of the injury infection, blood supply, and external physical forces.
LocalFactors
awl Tissre Repair
Smallerwounds heal faster than larger wounds, and sursicalincisionsheal faster*ran wounds caused by blunl trauma.l6Softtissueinjuriesover bonestend to adhereto the bony surfaces,preventingcontraction and adequateoppositionof the edgesand delaying healing.l6 lnfection Infection in an injured area is the most problematic local factor that can affect healing.Among the complications of wound healing, S0'/" are due to local infection.ll Infections affect collagen metabolism, reducingcollagenproduction and increasinglysis.49 lnfectionoften preventsor delayshealingand encourgranulauon agesexcessive tissueformation.l6 Vascularsupply The healing of injuries largely dependson the availability of a sufficient vascular supply. Nutrition, oxygen tension, and the inflammatory responseall depend on the microcirculatory system to deliver rheir components.50Decreasedoxygen tension resultingfrom a compromisedblood supplycanresult in the inhibition of fibroblastmigration and collagen slmthesis,leadingto decreasedtensilestrengthof the injured area and increasedsusceptibility to infection.2o
Type, size,andlocation oftheiniury Injurieslocatedin well-vascularized tissue,suchas the scalp,heal fasterthan thosein poorlyvascular- Extefnalforces ized areas.16Injuries in areas of ischemia, such as those that may be caused by arterial obstruction or excessivepressure,heal more slowly.16
h p
2-6 FactorsInfluencing Healing Local
Systemic
Type, size,andlocationofinjury Ag" Infection
Infectionor disease
Vascularsupply
Metabolicstatus
Movement/excessive pressure
Nutrition
Temperaturedeviation
Hormones
Topicalmedications
Medication
Electromagnetic energy
Fever
Retainedforeignbody
Oxygen
The application of physical agents including thermal agents,electromagneticenergy,and mechanical forcesmay also influenceinflammation and healing. Cryotherapy (cold therapy), thermotherapy (heat), therapeutic ultrasound electromagnetic radiation, electricalcurrents,and mechanicaipressurehave all been used by rehabilitation professionalsin an attempt to modify the healingprocess.The impact of thesephysicalagentson tissuehealingis discussedin Section2 of this text, which describeseach type of physicalagent,its effects,and its clinicalapplications. Movement Early movement of a newly injured area may delay healing.Thereforeimmobilization may be usedto aid early healing and repair.However, sinceimmobiliry can result in adhesions and stiffness by altering collagencrossJinkingand elasticiry continuouspassive motion (CPM) with stricdy controlled parameters is often usedto remobilize and restorefunction safelv.)rThe use of CPM in coniunctionwi*r short-
One o PATHOLOGY AND PATIENT PROBLEMS
ied nd ac-
rtrc mcal i0, -19
ur-
-:] ofl,
all ver ion' iult 9€n Lhe
:erm immobilization, compared to immobilization alone, has been shown to achieve a better func:onal outcome in some studies; however, odrer srudieshave found differencesonly in early rangeof Ir has also been reponedrhar padents =ocion.5753 :iilizing CPM during the inflammatory phaseof soft :ssue healingafter anterior cruciateligament reconjrruction usesignificandylesspain-relievingnarcotics -,:ranpatientsnot usingcPMs4(Fig.2-10.
Factors Systemic Age -\ge is a factor to be consideredbecauseof variations :r healingbetween the pediatric,adult, and geriatric :opulations.In childhood,wound closure occurs :rore rapidly than in adulthood becausethe physio-rgical changesand cumulative sun exposure that -;cur wtth aging can reducethe healingrace.ss A :ecreasein the density and cross-linkingof collagen, '...'hichresultsin reducedtensile strength,decreased :-umbersof mast cells and fibroblasts,and a lower s- 1n" : rre oI epiLne]ializaLion. occursin the elderly.56 :oor organizationof cutaneous vesselsin olderpeo:le alsoadverselyaffectswound healing.
33
leading to a decrease in local blood flow. Neuropathies, which are alsocommon,canincrease the potential for trauma and decreasethe ability of softtissuelesionsto heal. Patientswho are immunocompromised,such as those with acquired immune deficiency syndrome (AIDS) or those taking immunosuppressivedrugs after organtransplantation,are more prone to wound infections becausethey have an inadequateinflammatory response.AIDS alsoaffectsmany other facets of the healing processthrough its impairment of phagocytosis,fibroblast function, and collagensynthesis.59 Problemsinvolving the circulatorysystem,including atherosclerosis, sicklecell disease,and hypertension, can also have an adverse effect on wound healing since inflammation and healing depend on the cardiovascularsystemfor the delivery of components to the local area of injury Decreasedoxygen tension resulting from a reducedblood supply can result in an inhibition of fibroblast migration and a decreasedcollagensynthesis,resulting in decreased tensilestrengthandmakingthe injuredareamore susceptibleto reinjury Wounds with a decreasedblood supplyarealsomore susceptibleto infection.20'60
tc-
IEI-
ical
LOn,
Disease --.' number of diseasescan affect wound healing ::ther direcdy or indirectly.Ior example,poorly con:ol1eddiabetesmellitus impairs collagensynthesis, r:r.creases the risk of infection due to a dampened and decreases -:rununeresponseJ phagocytosisdue to 58Peripheralvasirerations in leukocytetunction.S0 :.rlar compromiseis alsoprevalentin this population,
I AII an tof dLn rof )ns.
Figure2-16.CIM machine. (Courtesy Thera-l(netics Jompany, Cherry Hill, New Jersey.)
Medications Patientswith injuries or wounds often take medications with systemiceffectsthat alter tissuehealing. Forexample,antibioticscanpreventor fight off infection, which can help to speedhealing but may also havetoxic effectsthat inhibit healing. Corticosteroids,such as prednisoneand dexamethasone,block the inflammatory cascadeearly on by blocking the release of arachidonic acid.61 Corticosteroidshavebeenshown to impair all phases of healingby stabilizingcell membranesand inhibiting the production of prostaglandins.They also decreasethe margination,migration, and accumulation of monocytesat the siteof inflammation.62 They severelyinhibit wound contracture,decreasethe rate of epithelialization,and decreaseahetensilestrength of closed, healed wounds.6366 Corticosteroids that are administeredat the time of injury have a greaterimpact becausedecreasingthe inflammatory responseat this early stagedelayssubsequentphases of healingand increasesthe incidenceof infection. In comparisonwith corticosteroids,nonsteroidal antiinflammatory drugs (NSAIDs)such as ibuprofen are lesslikely to impair healing.They act later in the
34
2 . l la
tnaliol, oud Tis
inflammatory cascade,interruptingthe production of prostaqlandinsfrom arachidonic actd6r Fil 2-77). ih"y Jr. ttot thorrghtto adverselyaffectthe function NSAIDs can of fibroblastsor tissue macrophages.6T causevasoconstrictionand suppressthe intlammatory response,l2however, and some NSAIDs have been found to inhibit celi proliferationduring tendon healing.6B
Studieshave shown that a deficiency of specific nutrients may also affect healing. Vitamin A deficiencvcanretardepithelialization,the rateof collagen synthesis,and croisJinking.TlThiamine (vitamin B) collagenformation, and vitamin ieficiency decreases the tensilestrengthof healed B. deficiencydecreases Vitamin ti"ssue andreducesthe fibroblastnumber.72'73 C deficiency impairs collagensynthesisby fibroblasts, increasesthe capillary rupture potential, arld /a increasesthe susceptibilityof wounds to infection Many mineralsalsoplay an important role in healins. Insufficientzinc can decreasethe rate of epithelialization, reduce-ocollagensynthesis,and decrease tensilesuength.-5 Magnesiumdeficjencymay also causedecreasedcollagensynthesis,and copperinsutto a reduction ficiencymay altercrossJinking,leading in tensilestrength./a
Nutrition Nutrition can have a profound effect on healing tissues.Deficiencyof any o[ a number of important amino acids,vitamins, minerals,or water, as well as insufficient caloric intake, can result in delayed or impairedhealing.This is becausephysiologicalstress from the injury inducesa hypermetabolicstate.Thus if insufficient "fuel" is availablefor the processof inflammationand repair,healingis slowed. ln most cases,healing abnormalities are asso- HEALING OFSPECIFIC ciated with general protein-calorie malnutrition TISSUES MUSCULOSKELETAL rather than depletion of a single nutrient.69Such is The primary determinantsof the outcomeo[ any the casewith patientswith extensivebums who are injury are the type and extent of the injury the rege-nin a prolongedhypermetabolicstate A protein de[ieritive caoaciw of the tissuesinvolved, the vascular ciency can result in decreasedfibroblasticproliferaof damagelo tion, reduced proteoglycanand collagensynthesis, supplvof the iniuredsrte,andthe extent of princrples basic framework.lhe decreasedangiogenesis,and disrupted collagen the extracellulai howall tissues; remodeling./0Protein deficiency can also adversely inflammation and healing apply to which may lead to an increased ever, there is some tissue specificity to the healing affect phagocyto_sis, response.For example,the liver can regenerateeven riskoI infection.ou
Figure2-17, Comparison of the site in the inflammatory cascadeacted on by NSAIDs and steroids
Ore . PATHOLOCY AND PATIENT PROBLEMS
when over half of it is removed, while even a thin hactureline in cartilageis unlikely to heal.
Cartilage
r ) f
:I
Cartilagehas a limited ability to heal becauseit lacks lymphatics, blood vessels,and nerves.77However, ;artilage reactsdifferently when injured alone than -.vheninjured in conjunction with dre subchondral 'cone to which it is attached.Injuriesconfinedto the ;artilage do not form a clot or recruit neutrophilsor nacrophages,and the cells adjacent to the injury ,how a limited capacityto induce healing.This lim:red responsegenerallyfails to heal the defect, and -Jrese lesionsseldomresolve.Ts In injuries that involve both articular cartilage and subchondralbone, the vascularizationof the :ubchondralbone allows for the formation of fibrinibronectin gel, giving accessto the inflammatory -ells and permitting the formation of granulation :ssue. Differentiationofgranulationtissueinto chonCrocytescan begin within 2 weeks. Normafappearng cartilagecan be seenwithin 2 months after the njury However,this cartilagehasa low proteoglycan :ontent and is thereforepredisposedto degeneration :nd erosivechanges./Y
Tendons andLigaments Iendons and ligamentspassthrough similar stagesof realing.Inflammationoccursin the first 72 hours,and :o1lagensynthesis occurs within the first week. - ibroplasiaoccursfrom intrinsic sourcessuchasadja:ent cells,and from extrinsic sourcessuch as those :rought in via the circulatorysystem. The repair potential of tendon is somewhat con=oversial.Both intrinsic cells such as epitendonous :nd endotendonouscellsand extrinsicperitendonous rells pafticipate in tendon repair.The exact role of -Jresecellsand the final outcome dependon several :actors,including the type of tendon, the extent of iamage to the tendonsheath,the vascularsupply,and -he duration of immobilization. The first two stages rftendon healing,inflammationandproliferation,are similar to the healing phasesof other tissues.The -hird phase,scarmaturation,is unique to tendonsin -iat this tissuecan achievea state of repair closeto :egeneration. During the first 4 days following an injury, the with an infiltration of nllammatory phaseprogresses
35
both extrinsicand intrinsic cells.Many of thesecells developphagocyticcapabilities,while othersbecome fibroblastic.Collagensynthesisbecomesevident by days7 to 8, with fibroblastspredominatingat around day 14.Earlyin this stage,both cellsand collagenare oriented perpendicularto the tendon's long axis.80 This orientation changesat day 10, when new collagen fibersbeginto alignthemselvesparallelto the old longitudinalaxis of the tendon stumps.BlFor the following 2 months,thereis a gradualtransitionofalignment, through remodelingand reorientation,parallel to the lone axis. Ultimate maturation of the tissue dependson sufficientphysiologicalloading. If the synovial sheathis absentor uninjured, the relative contributions of the intrinsic and extrinsic cellsare balancedand adhesionsare minimal. If the synovial sheath is injured, the contributions of the extrirsic cellsoverwhelm the capacitiesof the intrinsic cellsand adhesionsarecommon. Factorsaffectingthe repairof tendonsare different from those associatedwith the repair of ligaments.s2 Studieshave shown that mobilization of tendonsby controlled forcesacceleratesand enhancesstrengthening of tendon repair, but mobilization by active contractionof the attachedmusclelessthan 3 weeks after repair generallyresultsin a poor outcome.]he poor resultsmay be a result of the fact that high tension can leadto ischemiaand tendon rupture.Recent studieshavefound no significantdifferencein tendon strengthwhen tendonsare exposedto controlledlow lt or high levelsof passiveforce after repair.8384 appearsthat mechanicalstressis neededto promote appropriate oientation of the collagen fibrils and remodelingof collageninto its mature form and to optimize strength,but the amount of tensionnecessary to promote the optimal clinical responseis not certaln."",""
Many variablesinfluencethe healing of ligamentous tissue,the most important of which are the rype of ligament,the sizeof the defect,and the amount of loadingappiied.For example,injudesto capsularand extracapsularligaments generallystimulate an adequate repair response,while injuries to intracapsular ligamentsoften do not. In the knee,the medial collateral ligament often heals without surgicalintervention, whereasthe anteriorcruciateligamentdoesnot. These differencesin healing may be due to the s)movial environment, the limited neovascularization, or the fibroblastmigrationfrom surroundingtissues.Treatments that stabilize the iniurv site and
36
2 c Inflannatiot
maintainthe appositionof the torn ligamentcanhelp *re ligamentheal in its optimal length and minimize scarring.However, mature ligamentousrepair tissue is still30% to 50oloweakerthan uninjuredligament.sT This does not usually clinically significantly impair joint function becausethe repairedtissue is usually larger than the uninjured ligament. Early, controlled loading of healingligamentscan also promote healing, althoughexcessiveloading may delay or disrupt the healingprocess.88,89
atdTissue Repait
Stages of Fractsre Healing 1. Impaction 2. Induction 3. Inflammation 4. Soft callus 5. Hard callgs 6. Remodeling
Young children have a more elastic bone structure that allows their bones to bend, accountingfor the greenstick-typefracturesseenin this population. Muscle Skeletal Induction is the stage when cells that possess Musclesmaybe injuredby blunttraumacausing a conosteogeniccapabilitiesare activated.lnduction is the tusion,byviolent contractionor excessive stretchcaus- least well-understood stage of bone healing. lt is ing a strain,or by muscle-wastingdiseases. Although thought that the cells may be activatedby oxygen skeletalmusclecellscannotproliferate,stemor reserve gradients,forces,bonemorphogenicproteins,or noncells,known as satellite rclls,can,under some circumcollagenousproteins. Although the timing of this stances, proliferateanddifferentiateto form new skele- processis not known exactly,it is thought to be initital musclecellsafterthe deathof adultmusclefibers.79 ated after the moment of impact.The durationof this Skeletalmuscleresenerationhas beendocumentedin stageis alsonot known, althoughthe influenceof the musclebiopsy tp.ii-".rr kom patientswith diseases induction forcesseemsto lessenwith time. Therefore such as musculardystrophy and poll'rnyositis;howoptimizing the early conditions for healing to miniever, skeletal muscle regenerationin humans after mize the potentialfor delayedunion or nonunionis traumahas not beendocumented.Followins a severe imperative. contusion.a calciFied hematoma.known is nyasiis Inflammationbeginsshordy after impact and lasts ossifcans, may develop.Myositis ossificansis rarefof until somefibrousunion at the fracturesiteoccurs.At lowing surgeryif hemostasisis controlled. the time ofthe fracture,thereis disruptionofthe blood supplyand formationof a fracturehematoma,aswell asa decrease in oxygentensionand pH. This environBone ment favors the growth of the early fibrous or cartilagiBone is a specializedtissuethat is able to heal itself nous callus.This callusforms more easilythan bone with like tissue.Bone can heal by two mechanisms: and helpsto stabilizethe fracturesite, decreasepain, primary or secondaryhealing.Primaryhealingoccurs andlessenthe likelihoodof a fat embolism.lt alsorapwith rigid internalfixation of the bone,while second- idly andefficiendyprovidesa scaffoldfor furthercircuary healingoccursin the absenceof suchfixation. latiorqandfor canilageandendostealboneproduction. Bone goes through a seriesof four histologically The amount of movement at the fracturesite infludistinct stagesin the healing process:inflammation, encesthe amount and quality of the callus. Small soft callus,hard callus,and bone remodeling.Some amounts of movement stimulate callus formation, investigatorsalsoincludethe stagesof impactionand while excessivemovement can disrupt callusformainductionbeforeinflammationin tltis scheme. tion andinhibit bony union. Impactionis the dissipationof the energytrom an The soft callus stage begins when the pain and insult. The impact of an insult is proportionalto the swelling subsideand lasts until the bony fragments energy applied to the bone and is inverselyproporare united by fibrous or cartilaginoustissue. This tional to the voiume of the bone. Thus a fracture is period is marked by a greatincreasein vasculariry more likely to occurif the forceis greatot the bone is ingrowth of capillariesinto the fractufe callus, and small. Energydissipatedby a bone is inverselyproincreasedcellproliferation.The tissueoxygentension portional to its modulus of elasticity.Therefore the remains low. but the oH returns to normal. The bone of a personsufferingfrom osteoporosis,which hematoma becomes organized with fibrous tissue has low elasticiry will sustaina fracturemore easily. cartilageand bone formation; however, no callus is
Orc t PATHOLOGY AND PATIENT PROBLEMS
37
) Clinical CaseStude a The following casestudy summarizesthe conceptsof inflammationand repairdiscussedin this chapter.Based on the scenariopresented,an evaluationof the clinical findingsand goalsoftreatment areproposed.
Case 4
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JPis a 16-year-oldhigh schoolstudent.Sheinjured her right anlle 1 week ago playing soccerand was treated conservativelywith crurches;rest, ice. compression. and elevation (NCE); and NSAIDs. She rcports some improvement,althoughsheis unableto play soccerdue to continued complaints of right lateral ankle pain. Her x-rayfilms showedno kacture,andherfamily physician diagnosed the injury as a grade II lateral ankle sprain. Shecomesto your clinic with an order to (evaluateand treat.' JPsustainedthis injury during a cutting motion while dribblinga soccerball. Shenoted an audiblepop, immediate pain and swelling,and an inabiliry to bearweight. Shereportsttrat herpainhas decreased in intensityftom 8/10 to 6/10 but that it incleaseswith weight bearing and with certain demonstrated movements. The objectiveexam revealsmoderatewarmth of dre skin of the anterolateralaspect of the right ankle. Moderateecchymosisand swellingare alsonoted,with a girth measurement of 34 cm on the right ankle compared with 30 cm on the left. Her range of motion is restrictedto 0 degreesdorsiflexion,30 degreesplantarflexion,10 degreesinversio4 and5 degreeseversion,
with pain noted especiallywi*r plantarflexion and inversion. She exhibits a decreasedstance phase on the right lower extremity. Pain and weakrressoccur on strengti tests of the peroneals,gastrocnemius,and soleusmuscles.JP also exhibits a marked decreasein proprioception,as evidencedby the single-legbalance test.Her anteriordrawertestis positive,and hertalar tilt rsne8at1ve. EVALUATION OF CLINICALFINDINGS The patient presentswith impairmentsof pairl loss of subtalarand talocmalmotioq decreased strengthof the evertomand plantarflexors,increasedgirth of the right ankle, and decreasedproprioceptionresultingin functional iimitation of ambulationand sportsactivitv. She performs home activities independently,without che useof adaptiveequipment. PREFERREDPRACTICEPATTERN Impaired joint Mobiliry, Motor Function, Muscle Performance,and Range of Motion AssociatedWith CoonectiveTissueDysfunction,(4D). PLAN OF CARE The goals of treatment at this time are to control the pain and edema,acceleratethe resolutionof the acute inflammatory phaseof h€aling,and speedthe recovery olJP'snormalrangeof motion, strength,proprioception, and function.
PhysicalTheraPistPracticePattemssMl4DjisCopyright2002AmericanPhysicalTherapy Associatron.All rights reserved. :'reFerred le n.
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visible radiographically.The callusis electronegative :elative to the rest of the bone during *ris period. Osteoclasts remove*re deadbonefrasments. The hard callusstagebeginswhei a sticky.hard ;allus coversthe endsof the fracture,and endswhen 1ew bone uniteswith the fragments.This period cor:espondsto d:)eperiodofclinical and radiologicalfracrure healing.The duration of this period dependson ;he fracture location and the patient's age, and can rangeftom 3 weeksto 4 mon*ts. The remodelingstagebeginswhen the fractureis 'coth clinicallyand radiologicallyhealed.It endswhen -,hebone has returned to its normal state and the catency of the medullary canal is restored. The ibrous bone is convened to lamellar bone, and the nedullary canalis revised.This processcan take severalmonths to severalyearsto complete.90
CHAPTER REVIEW The processesof inflammation and tissue repair involve a complex and dynamic seriesof events,the ultimate goal of which is the restorationof normal function. In these events the involved tissue progressesthrough three stages:inflammation,proliferation, and maturation. The inflammation phase involves interaction of hemostatic.vascular cellular. andimmuneresponses mediatedby a numberof neural and chemical factors.The proliferation phaseis characterizedby epithelialization,fibroplasia,wound contractior\ and neovascularization. The maturation phaseinvolvesbalancedcollagensynthesisand lysis to ultimately remodelthe injuredarea. This seriesof eventsfollows a similar timely and predictablecourse.If the normal healing processis interferedwith however, healingmay be delayedor
38
2 e ln[Iammaion
and Ti>sue Reyair
15. PierceCF,MustoeTA, SeniaRM et al: In vivo incisional wound healingaugmentedby PDCF and recombinant c-sis gene homodimeric proteins, / E^xyMed 167: 975,987,1988. 16. Maninez-HemandezA, Amenta PS:Basicconceptsin wound healing. In Leadbener \48, Buckwalter JA, lxflammatlo4ParkRidge, GordonSL,eds:Spons-lxduced IL, 1990,AmericanAcademyof OnhopaedicSurgeons. 17. Hardy M: The biology of scar formation, Phys Ther 69:1074-1024,1989. 18. RutherfordR" RossR: Plateletfactorsstimulatefibroblasts and smooth muscle celis quiescent in plasma serumto proliferate,J CellBlol69:196-203,1976. 19. Mathes S: Roundtablediscussion:probiem wounds, References PersyectPIasrrc Surg 2 :89-120, 1988 L. Stedmar'sMedrcalDrcnoxaryed 25, Baltimore, 1990, 20. Whimey JD, Heiner S, Mygrant BI et al: Tissue and Williams & Wilkins. wound healingeffectsof sholt duration postoperative 2. Price SA, Wilson LM: Pathophysiology: Cliwcal o*lgen therapy,Biol ResNursJan;2(3):206-215 ed 2, New York, 1982, Coxceptsol DiseaseProtesses, ,2001. 21. Davidson JD, Mustoe TA: Oxygen in wound healing: McCraw Hili. more than a nutrient, \1(/oundReValr Regen May3. KellettJ: Acute soft trssuenjunes a review of the hterature,Med St SVorts Ererc18:489-504,1986. Jun;9 Q):175- 177,2001,. 4. Galrett WE Jr,LohnesJ: Cellularand matrix responses 22. Bell.anttJA,ed: ImnunologyIII, ed 3, Piitadelphia,1985, WB Saunders. to mechanicalinjury at the myotendmousjunction. In 23. Werb A, Cordon S: Elastasesecretionby stimulated Ieadbetter\48, BuckwalterJA, Cordon SL,eds:Spons' macrophages, ItducedInflammauot,Park fudge, IL, 1990,American J ExyMed 142:361-377 , 1975 . 24. Madden JW: Wound healingrbiologic and clinical feaAcademyof OrthopaedicSurgeons. of tures.ln SabistonDC, ed: Davk-ChrktoyherTextbook 5. AndriacchiI SabrstonP, DeHavenK et a1:Ligament: Swgety,ed 1L, Philadelphia,1997,WB Saunders. Injury andrepair InWoo SL-l BuckwalterJA,eds:It4ury 25. Clark RA-F:Overview and general considerationsof and ReVaitof theMusculosleeletal Saftllsaes, Parkfudge, wound repair. In Clark MF, Henson PM, eds: Tle IL, 1988,AmericanAcademyof OrthopaedicSurgeons. Molecular atd Cellular Biology of \Y/oundRepak, New 6. CarrettWE Jr:Musclestraininjuries:Clinicaland basic York, 1988,PlenumPress. aspects, Med Se SponsExerc22:436443,1990. 26. Stotts NA, Wipke-Tevis D: Co"factors in impaired 7. FantoneJC,Ward PA:Inflammation.ln RubrnE, Farber 1996. wound healing,Ostony42(2):44-56, Pl'riladelphra, 1988,JBLippincott. lL, eds:Pathology, L Wrlkerson CB: lnflammauon ln corurectlvelisoue: 27. LevensonS:Practicalapplicationsof experimentalstudies rn the care of primary closedwounds, An J Surg andmanage ment.Athl Ttututkg20:298-301 etrolog'y , 1985. 104:273-282 9. ChristieAI: The tissueinjury cycleand new advances , 1962. toward its managementin openwounds, Athl Trafuing 28. Nemeth-CsokaM. KovacsayA: The effect o[ glycosaminoglycans(CAC) on the intramolecularbind26:274-277 , 1,991. ngs of collagen,ActaBiol30(4):303-308, 1,979. Pathologic 10. RobbrnsSL,KumarV CotranRSet al: Robbins 29. Lachman SM Soft TissueInjuries ut Spotts, St. Louis, BasisofDisease, ed5, Philadelphia,1994,WB Saunders. 1988,Mosby. 11. Fantone JC: Basic concepts in inflammation. In LeadbetterWB, BuckwalterJA, Gordon SL, eds:S7otls- 30. Hunt TK, Van Winkle W Jr: Wound healing. In HeppenstallR3, ed: FractureTreatment and Healing, lwlucedhflamnalox, Park tudge, IL, 1990, American Philadeiphia,1980,WB Saunders. Academyof OrthopaedicSurgeons. 31. Daly T: The repair phase of wound healing: 1.2.PeacockEE\!/oundRepaLr, ed3,Phlladelphia,1984,WB re-eprthehalization and contraction. In Kloth L, Saunders. in McCullochJ,Feederl, eds \X/ound Healing:Abernatives 13. SalterRB,SimmonsDF,Malcom BW et al: The biologiManagement, Phl.adelphia,1990,FA Davis. cal effectsof continuouspassivemotion on the healing oI modified of fu1lthrcknessdefectsin arhcularcartilage,J BaneJoint 32. Cabbiani C, Ryan G, Majeno Gr Presence fibroblastsin granulationtissueand their possiblerole Swg 62-A:1,2321251, 1980. in wound contractioo,Experiertia27:549-550,1971. 14. Majno G, PaladeCE: Studieson inflammauon.L The 33. Watts CT, Grillo HC, GrossJ: Studiesin wound heal effect of histamine and serotoninon vascularpermeing: II. fhe role ofgranulationtissuein contraction,Ar?l ability: an electronmrcroscoprcstudy,/ BnphysBiochem Surg l4B1,53- 1,60, 1,958. Cytolll57l,1961,.
chronic inflammation may result. Various local and systemic factors can influence the progression of inflammation and tissue repair, including physical agents utilized by clinicians to facilitate the healing process. The rehabilitation specialist must assessthe state of inflammation and repair to determine the appropriate agent to incorporate into the treatment plan for an optimal outcome. The reader is referred to the Evolve Website at http://evolve.elsevier.com/ Cameron for study questions pertinent to *Lis chapter.
One . PAIHOLOGY AND PATIENT PROBLEMS
-VcGrath MH, Simon RHr Wound geometry and the kinetics of *re wound contraction,PlastReconstr Surg 72:66-73,1983. Taber's Cyclopedic MedicalDicuonary, ed 75,Philadelphia, 1985,FADavis. Billngham RE, RussellPS:Studieson wound healing, with specialreferenceto the phenomenaofconftacture rn expe mental wounds in rabbit skin, Am Surg 144:961, . , 1,956 SawhneyCP,Monga HL: Wound contracturein rabbits and the effectiveness of skin graftsin preventingitJBlr PlastSurg23:318-321,1970. Stone PA, Madden JW: Biological factors affecting wound contraction,SurgFotuu 26:547-548,1975. RudolphR: Contractionand the control of contraction, VorldI Surg4:279-287,1980. Alvarez OM: Wound healing. In Fitzpatrick T, ed: in CeneralMedicite,ed 3, New York, 1986, Dermatology McCraw-Hill. EyreDR: The collagensof musculoskeletal 5oft tissues. In LeadbetterWB, Buckwalter JA, Cordon SL, eds: SVonsInduced lxflammatiott,Park Ridge, IL, 1990, AmericanAssociarion of Orthopaedic Surgeons. McPhersonJM, Piez KA: Collagenin dermal wound repair.In Clark RAI, HensonPM, eds:Ile Molecularaftd Cellular Biologyof \Yound Repai, New York, 1988, PlenumPress. Kosaka M, Kamrishi H: New concept of ballooncompression wear for the treaffnent of keloids and hypertrophic scars,PlastRecottstr SargOct;108(5): 1454-1,455 , 2001. Uppal RS,Khan U, KakarS et al: The effectsof a single doseof 5-fluorouracilon keloid scars:a clinicaltrial of timed wound irrigation after extralesionalexcision, PlastRecottstt Sutg Oct;108(5):12f8-1224, 2001.. Hunt TK, Van WinlleW: WoundHealing:NormalRepair - Fundamentals of \Yourd Managemettin Swgery,South Plaintield. NJ,1976,Chirurgecom, Inc. MaddenJ:Wound healing:the biologicalbasisof hand surgery,Clh PlastSutg3:3-11,1976. Arem AJ, Madden IW: Iffects of stress on healing wounds: I. Intermittent nonryclica\ tensi.on,J SurgRes 2 0 : 9 31 0 2 , 1 9 7 6 . Fantone JC: Basic concepts of inflammation. In LeadbetterWB, BuckwalterJA,Cordon SL,eds:SponslnducedInflammauon, Park fudge, IL, 1990, American Academyof OrthopaedicSurgeons. Irvin T: Collagenmetabolismin rnfectedcolonicanastomoses,SurgCyxecolObstet143:220-224, 1976. CanicoT, Mehrhof A, CohenI: Biologyofwound healng, SurgClinNonhAn 64:721-733,l9B4. Woo SL, GelbermanRM, Cobb NC et a1:The importanceof controlledpassivemobilization on flexor tendon healing: a biochemical study,Acta OnhoVScatd 52:61,5-622,1,981.
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52. CelbermanRH, Woo SL,LothringerK et al: lffects of early intemittent passiveimmobilization on healing canineflexor tendons,l HandSurgT:170-175, 1982. 53. Lau SK, Chiu KY Use of continuouspassivemohon after total knee arthroplasty,/ AnhtoylastyApr;16(3): 336-339, 2001. 54. McCar*ry M\ Yates CK, Anderson MA et al: The eff€cts of immediate continuous passivemotion on pain duringthe inflammatoryphaseof soft tissuehealcruciare IigamentreconsuucEion, ing followingancerior 1993. IOSPT 17(2\:96-101, 55. Thomas DR: Age-relatedchangesin wound healing, -620,2001. DrugsAging18(8):607 56. Holm-PetersonP,Viidik A: Tensilepropertlesand morphologyof healingwounds in young and old rats,Scand Surg6:24-35,!972. I PlastReconstr 57. van de Kerkhoff PCM, van BergenB, Spruijt K et al: Age-related changes in wound healing, Cln Lrerc 4, 1994. Dernatol1,9:369-37 58. Goodson W, Hunt T: Studies of wound healing in experimentaldiabetesmellitus,/ SurgRes22:22L227, 1997. 59. PetersonM, Barbul A, BreslinR et al: Significanceof T-lymphocytesin wound healing, Surgery2:300-305, 1987. 60. Cogia PP: The biology of wound healtLng,Ostomy 38(9):12-22, 1992. 61. LeadbetterWB: Corticosteroid injection therapy n sports injuries. ln Leadbetter SE, Buckwalter JA, GordonSL,eds:Spo*-lxducedl(lannation, Parkfudge, IL, 1990,AmericanAcademyof OrthopaedicSurgeons. 62. Behrens TW, Coodwin JS: Oral corticosteroids.ln Leadbetter\48, BuckwalterJA,Gordon SL,eds:SportsIxducedlaflannation, Park fudge, IL, 1990, American Academyof OrthopaedicSurgeons. 63. EhlrichH, Hunt T: The effectof cortisoneand anabolic steroidson the tensilestrengthof healingwounds,A tl Sutg 170:203-206 , 1969. 64. BakerB, Whitaker W: Interfercncewith wound healing by the local ac on of adrenocorticalsterolds. 46.544-551, Eudoctixology 1950. 65. Howes E, Plotz C, Blunt J et al: Retardationof wound healingby cortisone, Surgery 28:177-1,81,,1,950. 66. StephensF, Dunphy J, Hunt T; The effect of delayed administration of corticosteroidson wound contracture,Ann Surg173:214-218 , 1971. 67. Abramson SB:Nonsteroidalanti-inflammatorydrugs: mechanismsof action and therapeuticconsiderations. In LeadbetterWB, Buckwalter JA, Cordon SL, eds: SVons-lxduced lnflammatlox,Park fudge, IL, 1990, AmericanAcademyof OrthopaedicSurgeons. 68. fuley CP,Cox M, HarrallRL et al: Inhibition of tendon cell proliferatronand matrix glycosaminoglycansynthesis by non-steroidal anti-inflammatory drugs in vitro,J HandSurg[Brl]rn;26(3):224-228, 2001.
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2 . Iaflamnation and TissueRepair
69. Albina JENutrition in wound heaLng,/Parnter E4teul
-376, 1,994. Nutr18(4):367 70. PollackS:Wound healing:a revtew.III. Nutritional factors affectrngwound healing,J Dernatol Sutg Onco! 1,979. 5:615-619, 7 1 . FreimanM, SerfterE, Connerton C: Vttamin A defiSutg,Forutt21t81-82,1'970. cienry andsurgicals:rress, 72. AlverezOM, GrlbreathRL:Thramrneinfluenceon collagen during granulation of skin wounds, J Surg Res 32:24-31, 1982. 73. GrenierJF,AprahamianM, Cenot C et al: Pantothenic acid (vitamin Br) effioency on wound healing, Acta . VtaminolEnzymol4:81-85, 1'982 74. Pollack S: Systemicdrugs and nutritional aspectsof wound healing,C/laDernatol2:68-80,7984. 75. Sandstead HH, HenriksenLK, GreferJLet al:Zinc nutri' ture in the elderly rn relauonto taste acuiry immune response,and wound healng, An J Cln Natr 36(Suppl 1982. 5):1046-1059, 76. Maitra AK, Dorani B: Roleof zinc m post-injurywound 1992. heahtg,Arch EmergMed Jut;9(2):122-124, 77. AthanasrouKA, ShahAR, HernandezRJet al; Basicsci' ence of arttcular cartilage repatr, Clin Spons Med Ap420(2):223-247,2001. 7 8 . GelbermanR, GoldbergY An K-N et al: Tendon ln Woo SL-l Buckwalter JA, eds: It4ury and Repar of Soft Tssues, Park fudge, IL, 1988, Musculosheletal AmericanAcademyof OrthopaedicSurgeons. 79. CaplanA, CarlsonB, FaulknerJet al: Skeletalmuscle.In Woo SL-Y Buckwalter JA, eds ltlury and Repai of Soft Tissues,Park fudge, IL, 1988, Musculosheletal AmericanAcademyof OrthopaedicSurgeons.
80. Strickland JW: Flexor tendon injuries, Otthoy Ret 15(10):21, 1986.
8 1 .LmdsayWK: Cellularbrologyof flexor tendonhealing ln Hunter JM, SchnerderLH, Mackin EJ, eds Tendon Sutgeryof theHand,St Louis, 1987,Mosby. AkesonWH, FrankCB,Amiel D et a1:Lrgamentbrology and biomechanics. In Frnnerman G, ed: Ameticax Symyostuwor Syons Surgeon's Acadenyof Onhoyaedrc M eddne, SrLours,1985,Mo sby. 83. KetchumLD: Primarytendonhealing:a revie:w, J Haxd 1977. Surg,2:428'435, 84. Goldfarb CA, Harwood F,Silva MJ et al: The effect of vanatlons rn applied rehab rtation force on collagen concentration and maturation at t}le intrasynovial flexor tendon repair slte, J Hatd Sutg lA,:tt] Sep;26(5):B4 I -846, 2001. 85. PeacockEE Jr: Brologicalprinciples in the healing of long tendons,Srrg Cln NonhAn 45:46L-476,1965 86. Potenza AD: Tendon healng wthin the flexor digital sheathin the dog,J Boxelont Sutg44A:49-64, 1,962. 87. FrankC, Woo SL-l Amiel D et al:Medial collateralligarn rabbits, ment healing:a multrdrscrplnaryassessment Med 1L.379'389,1983 AnJ Spons BB. FronekJ,FrankC, Amiel D et aLThe effectsof intermittent passlvemotron (lPM) in the healingof medial collateralligaments,Ir4 nsOrthoVResSocS:31,1983. 89. Long M, Frank C, SchacharN et al: The effects of motion on normal and healingirgaments , TMnsOfthol ResSocT:43,1982. 90. McKibben B: The brology of fracturehealing in long bones,J BoneI ont Surg(Bk) 60:150'162, 1978.
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S U A4A/A I R Y O F 1 , ^ / FO R M A T I O N C O V E R E D Typesof Pain -Mechanismsof PainReceptionand Transmission PainModulation and Control -\4easuringPain
PainManagementApproaches Clinical CaseStudies Chapter Review
rof
ong
OB]ECTIVES ofthis chayter,thereaderwill beableto: Uponcompletion L Differentiate acute,chronic, and referredpain.
2 . Discussthe peripheraland central mechanisms of nociception and pain transmission. Appraisecurrent theories ofpain control. 1 . Selectand apply appropriatemethods and tools to quantify and quali$r pain.
5. Compareand contrastvarious medical and usedto concrolpain. physicaltherapies 6. Evaluatethe use of physicalagentsfor ^^-+-^lt:-^
-^t-
4l
42
3 . Paitr
Painis an experiencebasedon a complex interaction of physical and psychologicalprocesses.it has beendefinedasan unpleasantsensoryand emotional experienceassociatedwith actual or potential tissue damageor describedin terms of suchdamage.l-3Pain usuallyservesas a warning to protect the body from damage and thus, although unpleasant,serves an essentialfunction in survival.aIt is important to realize that pain is not just the activationof receptorsof but also d:re noxious stimuli, known as nociceytion, sensoryexperiencesassociatedwith such activation, as well as the suffering and alterationsin behavior with suchactivation. associated Pain is the most common symPtom prompting patientsto seekmedical attention and is also a predominant D,mptom leadingpatientsto receiverehabilitation.s Many patients with musculoskeletalor neurologicalimpairmentspresentwith compiaintsof pain,andmostof theseindividualsconsiderpaincontroi or relieFto be the primary goalof treatment.oPain may also contribute to physicalimpaiment and disability, limiting participation in home, work, and recreationalactivities./The pain complaintsencountered 6y rehabilitation professionalsare generally relatedto inflammation of musculoskeletalor neurologicalstructurescausedby injury trauma,or degenerativedisease.Thesestructurescan be sourcesof of peripheral the responsiveness painandcanincrease pain recepto$to other painful stimuli.B-10 The goalsof pain treatmentinclude resolvingthe underlying pathology causingthe pain, when possible; modifying *re patient'sperceptionof the discomfort; and maximizing function within the limitations imposed by the source of pain, whether or not the sourceof pain can be modified. The final goal of treatment is resolution of the underlying condition. However,evenwhen the sourceof paincanbe modified by treatment,for example,in the caseof strucrural malalignmentbecauseof poor posrure or imbalancedmusclelength,or when the pain is caused by a self-limiting condition such as inflammation after an acutesoft tissueiniury it is beneficialto control pain during recovery so that the patient can participatemore fully in a rehabilitationprogram to correct the underlying deficit. When the pain is causedby a conditionthat cannotbe direcdymodified, suchasphantomlimb painor rheumatoidar*rritis,pain controlmay facilitateincreasedparticipationin a rehabilitation program, increasedpatient function, and decreased disabiliry
TYPES OFPAIN Pain can be categorizedaccordingto its duration or Acutepain is generor referred. sor:rceasacute,chronic, allv definedaspain oflessthan 6 mon*rs'duration for which an underlying pathology can be identified.ll Acute pain is felt in responseto actualor Potentialtissue damagethat resolveswhen tissuedamageor the threat of damagepasses.Chronic pain,alsoknown as persistentpain, persistsbeyond the normal time for tissue healing.l0Chronic pain conditions are generally the result of activation of dysfunctionalneurological or psychological responsesthat cause the individual to continueto experiencethe sensationof pain evenwhen no damagingor threateningstimulus is present.Referredpain is the experienceof pain in oneareawhen the actualor potentialtissuedamageis in anotherarea.Krowing whether a patient'spain is acute,chronic,or referredwill help the cliniciandeterthat may be conmine the mechanismsandprocesses tributing to the sensationand facilitate selectionof the most appropriateinterventionto controlor relieve this sFnptom.
AcutePain Acute pain consistsof a complex combination of unpleasantsensoryperceptual,and emotionalexpedences with associated autonomic, psychological, emotional, and behavioral reactions that occur in responseto a noxious stimulus provoked by acute Acute pain is generallyviewed injury or disease.l2'13 as biologically meaningful,useful, and timelimited. Acute pain is mediated through rapidly conducting pathways and is associatedwith increasesin muscle rone,heart rate. blood pressure.skin conductance, and other manifestationsof increasedsympathetic nervoussystemactivity.l4The intensity and location of the pain are usually relatedto the degreeof tissue inflarnmation.damage.or destructionin the areain which the pain is felt. Acute pain is generallywelllocalizedand defined,althoughits degreeof localization vades to some extent with the type of tissue involved. Pain sensationsfrom the skin are localized wirh grear accuracy.whereasmuscle pain is [requentlymorediffuse.l5l6 Acutepain lastsas longas the noxious stimulation persists.Acute pain servesa protective function foilowing an injury by Limiting activity to preventfunher damageandpromotetissue healingand recovery;however,it may alsoadversely
Ore . PATHOLOGY AND PATIENTPROBLEMS
,iect an individual's quality of life and impair the ,:,iry to function. Treatment of acute pain resulting from muscu:,.<eletalinjury generallyattemptsto facilitatereso,:on ofthe underlyingdisorder,reduceinflammation, .:-: modify the transmissionof pain from the periph::. ro the centralnervoussystem.
Pain - hronic
e ,f 5
n t5
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rf te
of rial. in Ite 'ed ed. cie rce. ?ttc 10n sue iin 'eLlisue zed iegas .ring SSUC
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-,:onic pain starts as acute pain. Most authors and ::anizations define chronic pain as pain that does -:: :esolvein the usualtime it takesfor the disorder :: :eal or that continuesbeyond the durationof nox: -s stimulation.lT However, some authors and :::anizations use time-based definitions, defining : :rnic pain asany pain lastinglongerthan 3 months The useof time-based definitionsis : i months.18'19 - : recommendedbecausethey do not take into .:-:trunt the variablecourseand duration of different :.=ologies and thereforedo not differentiatelong:.::: pain causedby chronic or progressivediseases : :athological states,such as rheumatoid arthritis, ftom painthat persists -:':er, or neuralentrapments, Chronic pain generpathology has resolved. the :'-:: stimuliareno longer ,-. :ontinuesevenatternoxious : :--'.'eandwhen thereis no longerany tissuedamage : -rreatof tissuedamage,whereaspain from a long::= disorderis generallyassociatedwith a long-term - rous stimulus.It has beenestimatedthat approxi-::ely one third of the American population has . -.::nic pain and 1,47ool the U.S. population suffers := chronicpain relatedto the joints andthe muscu: :ieletalsystem.20'21 with Jhronic persistentpain is generallyassociated -...;ical, psychological,and social dysfunction (see : - :.: . Patientswith chronicpain generallyhave been : - . :ically inactivefor a prolongedperiod,resultingin ;. of strength,skiil, and enduranceand thus progres: disability.They often dramatizetheir complaints, -,::ting that their pain is unbearableor incapacitattreatment,which - = andftequentlyreceiveexcessive , :-effective but can result in drug misuseor abuse -: progressivedependenceon others, including ':. -,i carepractitionersand family members.These including :::ents alsooften show signsof depression, : =,:r'edsleeponset and frequentawakening,altered The painbehavior , :--;rghabits,andsocialisolation.22 : -::epatientwith chronicpersistentpainmay be per-- ,tp..l hw Fin:nri:l o,in 23,24
43
Common Features of Patients with Ghronic Pain Have pain of several months' or years' duration. Have pair similar to the initial pain that is associatedwith a medical problem or injury. History of many treatment failures provided in great detail. Many medications tried, with a minimal to poor response. Continuous use of analgesics and tranquiJizets, despite patients' testimony that the medications offer no notable or long-lasting relief. Pain described as being unbearable and incapacitating. Strong belief that pain has an unidentified organic cause. Desire and willingness expressed to undergo "any treatrnent" for pain relief, Claim that everything will be fine if only the "doctor would treat my pain." Pain not relieved by any medical or surgical treaknent. Sqbstantial psychosocial changes present, especially depression, although patients vehemendy deny the label; they hequendy do admit to feeling frustated, angry, and iffitable, with disturbed sleep, altered moods, weight changes, decreased energy, decreased physical, social, recreational, and sexual activities, and increased family stresses and economic difEculties. From Cildenberg PL, DeVaul M: The ChrcnicPain Patient: andManagemeat, New York, 1985,Karger. Evaluatiotl
Chronic persistent pain may be the result of changesin sympatheticnervoussystem and adrenal activity, reducedproduction of endogenousopioids, or sensitizationof primary afferent and spinal cord neurons. Decreasedlevels of enkephalinsand increasednumbers and sensitivity of nociceptors have been observed in individuals with chronic pain.25These individuals frequendy have increased sensitivity to both noxious (hyperalgesia)and nonnoxious (allodynia)stimuli.26These changesin pain perceptionmay be the result of a processknown as wherebythe pathwind-uyor centralhyyersensitizatiaq ways that transmit pain continue to dischargeafter the discontinuationof intense or repeatedstimulation. Then, evena small additional stimulus exceeds Thus the threshold that is perceivedas painful.2T-3o for an individual with a painful condition that is severeor long-lasting,the noxious stimulation may
44
3 . Pait
resultin increasedpain receptoractivity and a consequentreducedtolerdnce for othernoxiousor nonloxious stimuli. Understanding of this sensitization mechanismhasled to increasedstudy and use of preemptive analgesiabeforeproceduresthat are known to be painful in an attempt to reducepostprocedural painandreducerecoverytime.31-33 Psychologicaland social factors have also been implicated in the etiology and maintenance of chronic pain.3aThe disturbedsleepassociatedwith depression may causemusculoskeletal pain,and the decreased activirymdy perpetuatepain by causing '2 weakness i".on'diiiorring. lndiuidualswiti "nd chronicpain alsofrequentlyadopt the dependentsick patient role and behaviors of the chronic invalid, which result in progressively reduced functional activiryto These behaviors may be unintentionally encouragedby the individual'sfamily members,who, i n a n . a t r e m p rh t oe l p a . c c u a l lpyr o m o t e* r e d e p e n d e n t
tissue include the pain associatedwith myocardial infarctionor anginacausedby cardiacischemiathat is felt in the upperchest,left shoulder,iaw and arm, and pain originating from the central portion of the diaphragmthat is frequently felt in the lateraltip of either shoulder.The gallbladderalsofrequendyrefers pain to the dght shoulderor the inferior angleof the right scapula,and the spleenrefers pain to the left shoulder It is proposedthat pain is refered in one of three ways: from a nerye to its area of innervation,from one area to another derived from the same dermatome, or from one area to another derived from the sameembryonicsegment,becausethe peripheral neuralpathways from thesedifferent areasconverge on the same or similar areasof the spinal cord and synapse with the same second-orderneurons to ascendthe spinalcord and reachthe centralcortex.39 For example,pain is referredfrom the diaphragmto role za the tip of the shoulder becauseboth of these areas Ideally,the developmentof chronicpain shouldbe initially developin the neck regionduring embryonic prevented by early identification of individuals at development, causing drem both to have efferent risk. Patientswith prolonged, severe,or very disinnervationfrom the phrenicnerveand afferentinnerabling acute pain are at increasedrisk of developing vation to the secondthroughfourth levelsof the cervichronic pain. Therefore, to reduce this risk, paincal spine.When pain that may be of eithervisceralor controlling interventions,such as physical agentsor musculoskeletalorigin convergeson the sameneuron medications,shouldbe appliedduring the acutestage in the spinal cord, it is usually interpreted to be of of an iniury and during the later recovery phases, musculoskeletalorigin. This may be becausemuscuw h e n .p a i ni ' s r i l lr h e r e s u l ro f p a i n r e c e p t oar c c i v a - loskeletal injuryandpainareso much morecommon tion.Jo S h o u l dc h r o n i cp a i nd e v e l o ps. u c c e s s ftur e l a t - that the brain "learns"that activity arrivingalongthat ment usually requires that all components of the pathway is associatedwith pain stimulusin a particudysfunction be addressed.Multidisciplinary treatIarmusculoskeletal area. ment programsbasedon a biopsychosocialmodel of Clinicians who treat neuromusculoskeletaldyspain have been specificallydevelopedto address functionmust be awareof the potentialfor pain referthese problems.a These treatment programs are ral and be familiar with common pain referral described beiowin the sectionon painmanagement. patternsto determinethe sourceof a patient'scomplaints and select appropriate treatment methods. Thereforewhen a patienrwith pain in a muscuReferred Pain loskeletalarea seekstreatment, the clinician should Referred pain is felt at a location distant from its first determineif the sourceof the pain is locatedin source. Pain may be referred ftom one joint to the areaof this sensation.Painof musculoskeletal orianother,from a peripheralnerve to a distal area of gin generallyvarieswith position or movementof the innervation.or from an internal organ to an area painful area,whereaspain causedby dysfunction in of musculoskeietal tissue.For example,hip joint other systemsgenerallyvaries with stresson those pathologyoccasionallyreferspain to the knee,particsystems.For example, shoulder pain that is aggraularly in children,and compressionofthe spinalnerue vated by raising the arm is likely to originatein the rootsat the L5 S1 level asthey exit throughthe spinal shoulder,whereas left shoulder pain that is aggraforamenmay causepain in the lateralleg becausethis vated by all forms of strenuousexercisemay be is the areaof sensoryinnervation.37.38 Common refercausedby a cardiaccondition.When assessing pain ral patternsfrom internal organsto musculoskeletal that is determinedto be of musculoskeletal origin, it is
Oqe . PATHOLOCY AND PATIENT qROBLEMS
:iso important to accurately determine the struc:.rre(s)at fauit to provide the most effective treat:rent. This can.be done by performing provocative :ests to reproduce the patient,s chief complaint. ?hysicalagentsmay effectivelyrelievereferrej pain; :.oweverthey shouldnot be usedas a ,ubstituti for :etermining the true sourceof the pain or for treatins := underlyingcause.They may be usedfor pain reliei '.';hilethe sourceofthe pain is beinginvestigated,dur_ :rg the recoveryprocess,and for conuollinq referred :arn where rhe underlyingcausecannorbe direcrly :eated.
MECHANISMS OFPAIN RECEPTION AND IRANSMISSION Specificity and pattern theories Pain receptors Peripheral nerve pathways Central pathways Sympathetically mediated pain The role ofsubstance P iain is generally felt in response to stimulation of :eripheral nociceptive structures. The stimulus is :ansmitted along peripheral nerves to the central ---ervoussystemJ from where it can reach the cortex .rd consciousness. The sensation of pain and the tdividual's response to the sensation are influenced .....a variety of factors, including the physiological ::echanisms of the pain receptoff, the anatomy of :ain transmitting structures, neurotransmitter levels, ::rd the motivation, behavior, and physiological -rd emotional state of the individual. Variations in ::ry of these factors can alter the individual,s :3rception of pain severity, type, location, and :lIatlon.
Specificity andPattern Theories Jver the years,varioustheoriesregardingthe nature :: peripheralpain receptionand transmissionhave ::en proposed.The primary early theorieswere the .:ecificity theory and the patterntheory Currentthe_ ::1es ntegrate componentsof both of these with :::orerecentfindings and obsewations.Accordingto -:respecificirytheory, as describedby Von lrey ind :-hers,the sensation of pain dependson the stimula_ - rn of specificnerveend,ings thar arespecialized for 42Thus a specrficrype :ch rype of sensarion.40 of
45
nerve fiber will always transmit the samesensation. no matrerhow intenselyor trequentlyir rssrimulared. According to *ris theory specific pain fibers are responsiblefor the transmissionof the sensationof pain (Iig. 3-1,.,1). Von lrey supportedthis theory with his identificationof freenerveendingswidely distributed in the skin that causeda sensationof pain when stimulated.He proposedthat thesefreenewe endinss were specificpain receptors.l2 Although rhe ,peJi_ ficity theory is consistentwith Von lrey,s findings,it has sincebeen found that the sensationof pain ioes not havethe preciseone-to-onerelationshipwith the type of receptorstimulatedthat would be predicted by-the specificitytheory The specificitytheory also failsto accountfor the fact that many qypesof siimuli are perceivedas painful and that pain can be modu_ Latedby input from the spinal cord or brarn.The limitations of the specificitytheory led to the devel_ opment of an alternativeexplanationof pain percep_ tion, the patterntheory According to the pattern theory the sensation . or pam re-sultsftom an appropriateintensity or fre_ quency of stimulation of receptorsthat also respond to other stimuli such as touch, pressure,or tem_ perature.'3Neural impulsesFromcheperipheryare combined and modified to summate in central nervous system structures,where the pain is then iocalizedand inrerprered. Accordingto rhe patrern theory and spatial summation of impulses _temporal along the pathways from the skin to the cerebral levels determinesthe individual,ssensationof pain (Iig. 3-1, B). This theory accountsfor the fact that a wide variety of stimuli cause the sensation of pain and also suggestsa role for centralinfluencebv pain summacion:however,ic [ar]sto considerthe roleo[ the idenLified specialized pain receprorsrruc_ tures and to account for affective or central pain modulation. theodesintegratecomponentsof the speci_ .. .Cuffent ficity theory and the pattem theory with other,more recent findings neuralanaLomyand Lhe ,regarding runcflonsot endogenous neurotransmiEters. currenf findings indicate that specific nerve endings called uociceprors respondro all painfulstimuli.anj specific nerve ryoes. small myelinatedA-delta tibers and unmyelinatedC fibers,transmitthe sensationof oain from these nerve endings to the spinal cord and thence,within specifictracts,to the brain.The quali$ of the pai,ndependson the type of tlssuefrom whicL the stimulusoriginatesand on which ofthe tvvonerve
46
3 . Ptritt
SPECIFICITY THEORY
Specialized heat receptor
PATTERNTHEORY
,il'il*l1ll-l l'il-11il*l{ll-l lil*l{1 |, Action potentials
-1,,,*1,*1,*1.*"1*l* Actionpotentjals
Figu]e3-1. Specificigz versuspattem theory of pain.A, Specificreceptorsfor eachrype of sensation.B, Patternof actionpotentialsresultingin sensation of pain. rypes transmitsthe pain; the intensiry of the pain is cles,and bareareasof axolemmathat are not covered relatedto the fidng rate of *re nerves.Painfrom cutaby Schwanncellprocesses.46 Nociceptors arepresent neous noxious stimulation is usuallv oerceived as in almostall typesof tissue.However,no nociceptors sharp.pricking.or tingling and is eisy to localize. are presentin the nucleuspulposusand the inner part 50 whereaspain from musculoskeletalstructuresis usuof the annulusfibrosusof the spinaldiscs.aT ally dull, hear,y,or achingand is harderto localize.aa Nociceptorscan be activatedby intense*rermal, Visceralpain has an aching quality similar to that of mechanical,or chemicalstimuli from exogenousor musculoskeletalpain but tends to refer superficially endogenoussources.Ior example,intensemechanirather than deeply.15Pain transmittedby C fibers is cal stimulation,suchas that causedby a brick falling usually dull, long-lasting,and aching,whereas pain on someonersfoot or a piece of broken bone comtransmittedby A-delta fibers is generallysharp.The pressinga nociceptor,will resultin nociceptoractivaintensity of the pain and the responsesto it are tion. Chemicalstimulation by exogenoussubstances thought to be more severewhen the relativeintensity suchas acid or bleach,or by endogenouslyproduced of nociceptive receptor stimulation is greater than substances suchasbradykinin,histamine,and arachithat of nonnociceptivereceptor stimulation, when donic acid, which are releasedas part of the inflamlevels of endogenousopioids are low, and with matory Iesponseto tissuedamage,can also activate certain vadations in *re individual's psychological nocic€ptors.Because thesechemicalmediatorsremain state.45 after the initial physical stimulus has passed,they generallycausepain to persist beyond the duration of the initial noxious stimulation. It is important PainReceptors to note that chemical mediators of inflammation Nociteytors are free, noncorpuscularperipheralnerve also sensitizenociceptors,reducing their activation endingsconsistingof a seriesof spindle-shaped, *rick thresholdto other stimuli.51,s2 This is the reason*rat, segments linked by thin segments to produce a clinically, many activities and stimuli to recendy injured areasare perceivedaspainful evenwhen they "string-of-beads"appearance.The beads and end :re nnt d:ma oino bulbs contain mitochondria,glycogenparticles,vesi-
Ote . PATHOLOGY AND PATIENT PROBLEMS
When nociceptors are activated, they releasea variery of neuropeptides from their peripheral terminals, including substanceP and a number of breakdown products of arachidonic acid such as prostaglandinsand leukotrienes.25 Nociceptorsalso convert the initial stimulus into electricalactivitv. in the form oI actionpotenrials. by a processknown as (Fig.3-2).It is thoughtrhat the released t'an,ductionzr neuropeptidesmay initiate or participatein transduction becausethey sensitizenociceptors.53 The action potentialsresultingfrom the processof transduction propagatefrom the nociceptorsalong afferentnerve pathwaystoward the spinalcord.
Peripheral NervePathways
47
C fibers,alsoknown asgroupIV afferexts, aresmall, unmyelinatednervefibersthat transmitactionpotentials quite slowly, at the rate of 1.0 to 4.0 meters/second.58They respondto noxiouslevelsof mechanical, thermal, and chemicalstimulation,causingpain that is generallydescribedas dull, throbbing, aching, or b:rgg^":d be reportedas tingling or rapry{."l= pingr"0o(Fig.3-3).The pain sensadons ffansmifted by these fibers have a slow onset after the initial painful stimulus, are longJasting,emotionally difficult for the individual to tolerate,and tend to be diffusely localized, particularly when the stimulus is intense.6l'62 They canbe accompaniedby autonomic responsessuch as sweating,increasedheart rate and blood pressure,or nausea.63 The pain associatedwith C-fiber activationcan be reducedby opiates,and this pain_rcliefis blockedby the opiate antagonistnalox-
Nociceptorsgive rise to two typesof first-orderafferent nervefibers,C fibersandA-deltafibers.The activone.oa ity in both rypes of fibers increasesin responseto A-delta fibers, alsoknown asgrouVIII afferexts,are peripheralnoxious stimulation,includingthat associ- also small-diameterfibers; however, they transmit atedwith acuteinflafirmationor muscleischemia.54-56 more rapidly than C fibers, at a rate of about 30 Eightypercentof afferentpain-transmittingfibersare meters/second,because they are myelinated.5S'65 C fibers,and the r ematnrng20%oare A-delta fibers.57 They are most sensitiveto high-intensitymechanical Cenerally,about 50% of the sensoryfibers in a cutastimulation,althoughthey canalsorespondto stimuneousnervehavenociceptivefunctions.45 lation by heat or cold and are capableof transmitting
Tissue
Mastcell 6---<4!)
Btood vesset ffi
/-\ =-'tfz\ Histamine (o o)*r( \-./
/,+
Substance P ,/
Leukotrienes
Arachidonicacid
\
Prostaglandins
Figule3-2. Pain transduction. (Modified with permission from lields HL, Levine JD: Pain-mechanisms and management fmedical p rogressl,WestJ Med 1.4I:347-357, 1984.)
3 . Pail
48
Stimuli
w
lvlechanical
0
il
Thermal
,n''
C fiber
Qltl) Chemical Stimuli
-
&t!
Yrxii
High intensity mechanical
Figure 3-3.Peripheral painpathways. nonnoxiousinformation.ooThe sensationsassociated with A-delta fiber activity are generallydescribedas sharp, stabbing, or pricking.asThe pain sensations transmitted by these fibers have a quick onset after the painful stimulus, last only for a short time, are generallylocalizedto the areafrom which the stimulus arose,and are not generallyassociatedwith emotional involvement.The pain associatedwith A-delta fiberactivationis generallynot blockedby opiates.6T Mechanicaltrauma usually activatesboth C and A-deltafibers.Takethe exampleof a brick landingon someone'sfoot. Almost immediately the individual feelsa sharpsensationof pain. The initial pain is followed by a deepachethat may last for severalhours or days.The initial sharp pain is transmittedby the A-deltafibersand is producedin responseto the highintensitymechanicalstimulationof the nociceptorsas a resultof the impact of the brick.The later,deepache is transmitted by the C fibers and is produced in responseto stimulationby chemicalmediatorsof inflammation releasedby the tissue after the initiai injury
either spinalcord.The C andA-deltafiberssynapse, direcdy or via interneurons,with second-orderneurons in the superficialdorsalhorn of the gray matter 7t SomeA-deltafibers (the substantiagelatinosa).58,68 penetratemore deeplyinto the dorsalhorn to terminate at the normal termination sites of A-beta afferents.The second-orderneuronsin the dorsalhorn are or T cells(Frg.3-4). known astransmission T cells make local connectionswithin the spinal cord,eitherwith efferentneuronsaspaft of spinalcord reflexesor with afferentneuronsthat oroiecttoward . o n L i n u eodr r e p e L i L iC v e- i i b e ra c t i v a L i o n t h ec o r t e xC can sensitizethe T cells,causingthem to fire more rapidly and to increasedreir receptorfield size, and input from other interneuronsoriginatingin the substantiagelatinosaof the spinalcord or from descending fibers originating in higher brain centers can inhibit T-ce1lactiviry72Inhibitory interneuronsin the substantia gelatinosaare activated by input from large-diameter,myelinated, low-threshold sensory neurons (primarily A-beta nerves) that respond to nonpainfu1stimuli.73,7a Theseinhibitory interneurons releasevarious neurotransmitters,including norepinephrine, serotonin, and enkephalins,to modulate rhe flow of t-heafferenrpainpar-hways.-sI hus t-he transmissioncellsreceiveexcitatoryinput from the C fibersand A-deltanociceptorafferentsand inhibitory
Thalamus C fiber (unmyelinated, slow;chronic parn)
Dorsal horn
Brainstem Spinothalamic tracts
Soutce of pain
@
Pathways Central
A-deltaliber (myelinated,last; acute pain)
The peripheral first-order C and A-delta afferents project from the periphery to the gray matter of the
Figure3-4. Ascendingneural pathway of pain via A-delta and C fibers.
Substantia gelatinosa
Fl :::
ai :tc :::l
O e . PATHOLOCYA^D PATIENTPROBLL\/IS
:.:tuf from large-diameter.nonnocicepror sensory ::rerenrs and- From fibers f rom hrgher ^d_"rTldi.ng. : - : r n c e n r e r s ' J( l ' i g .3 5 ) . T h e b a l a n c eo f t h e s ee x c r t a :,-ry and inhibitory inputs influences whether or not ---e individual feels pain and how severe the pain sen;:.rion is .73The inhibition of pain by inputs from non: rciceptor afferents is known as yain gatixg and rs :-scussed in greater detail below in dte section on : , i n m o d u l a t i o na n d c o n r r o lr h e o r i e ' . Transmission cell activation can also increasemus:-e spasm via a spinal cord reflex in which the trans-'-:ssioncell synapseswith anterior horn cells to cause :uscle contractions. The ongoing muscle contrac-rtrns can then cause accumulation of fluid and tissue ::itants. The contracting muscles may also directly :3come initiatorc of further nociceptive impulses by :.echanically compressing the nociceptors. In this .'.ay the combination of ongoing chemical and :echanical stimuli can set up a self-sustaining cycle : - pain causing muscle spasm, which then causes :-ore pain. This is known as the pain-syasm-yaincycle .ig. 3-6). Many interventions indirectly reduce pain, ..en after their direct analgesiceffect has passed, :ecause they reduce muscle spasms and thereby ::rerfere with this self-perpetuating cycle. Ascending second-order nerues carry stimuli ...'ithinthe spinal cord toward the higher brain centers - ig. 3-7). The second-order pathways that carry pain ::imuli are located primarily in the anterolateral , , p e c Lo f l h e c o r d . - 8T h i s a r e ao I t h e s p i n a lc o r d a J s o
49
Figure3-6. Pain-spasm-paincycle: nociceptor activation resultingin T cell activation stimulating an anterior hom cell to causea muscle fiber to contract,resulting in accumulation of fluid and tissue irritants and mechanical c o m p r e s . i oor Fr h er o c i c e p t o r a n idn c r e a s i rrgo c r c e p t o r acuvauon.
transmits information about temperature and touch. Most axons in the anterolateral system cross midline in the spinal cord to ascend contralaterally. Substantia '.cclceptive Information regarding pain is transmitted within the Cerebral gelatinosa :'deltaand C fibers cortex anterolateral cord via both the lateral spinothalamic {inhibitory tnlerneuron) tract and the larger anterospinothalamic tract to projI ...,/....... I ect to the thalamus. The lateral spinothalamic tract Thalamus projects direcdy to the medial area of the thalamus, whereas the anterospinothalamic tract separatesfrom the lateral spinothalamic tract in the brain stem to synapse with neurons in the reticular formation and the hypothalamic and limbic systems to then project to lateral, ventral, and caudal areas of the thalamus. The anterospinothalamic tract also relays information 'lonnociceptive to the periaqueductal gray matter, where there is a l.'betaandA-gammafibers large concentration of opiate recepto$, and is thought, : gure 3-5. Simple diagram showing the gate control thereby, to be associated with pain modulation. Impulses relayed via the lateral spinothalamic tract ::rechanismof pain modulation through the activation are involved in transmission of sharp pain and in :i A-delta and C-fiber input and gating/iniibition by locaiization of the painful stimulus, whereas those : lnnociceptor A-beta sensoryneruesand higher center :rput. sent via the anterospinothalamic tract are involved in
+
3 . Pail
of smooth and cardiacmusclesand with glandular Primary somatosensory secretion.This contrastswith most of the nervoussysconex
Thalamus
lnsula cortex
Hypothalamus
Midbrain
Reticular formation
Periaqueductal grey mater Lateralspinothalamic lract Anlerospinothalamic lracl
Nociceptor Spinal cord
Figure 3-7. Centralpainpathwaysfrom thespinallevelto the higherbraincenters. transmissionof more prolonged,achingpain and are thought to have stronger associationwith the disturbing emotionsthat accompanythe pain sensation. The second-orderneurons synapsein the thalamus with third-orderneuronsto projectto the cortex,from where the sensationof pain canreachconsciousness.
Sympathetic Nervous System Influences The sympathetic nervous system is a component of the autonomic nervous syslem.The autonomic nervous system consists of the sympathetic and parasympathetic svstems and is concerned with the activities
tem, which is concernedwith voluntary activationof the skeletalmusclesor with transmissionof sensory impulsesfrom the periphey'e,sO(Fig.3-8).The sympa*retic newous systemis consideredto be primarily involved in producingeffectstlLat preparethe body for "fight or flight," such as increasingheart rate and blood pressure,constdctingcutaneousblood vessels, and increasingsweating in the palms of the hands. Althoughit is normalfor the sympatheticneffous system to be activatedby acutepain or injury stimulation of the sympatheticnervoussystemefferentsdoesnot usuallycausepain.81HoweveEabnormalsy,rnpathetic activationrcausedby a hyperactiveresponseof the sympatheticnervoussystemto an acuteinjury or by a failure of its responseto subside,can increasepain signsandsymptomsof severityandcauseexaggerated vasomotoror sympatheric acrivirysuchas excessive sweating reactions.In patients with such signs and symptoms,pain relief can often be achievedby interruptingsympatheticnervoussystemactiviqyby chemical or surgicalmeans.B2-84 h addition, stimuli that evoke sympathetic discharges,such as the starde pain. reflexor emotionalevents,frequendyexacerbate sympaIt hascherefore beenproposedthat excessive thetic nervous system activation may increaseor maintainpain.Bo,79 Painthat is believedto involvesympa*reticnervous systemoveractivationhas a variety of names,including causalgia,reflex sympatheticdystrophy (RSD), shoulder-handsyndrome, posttraumaticdystrophy, Sudeck'satrophy, and sympatheticallymaintained pain.BsCurrently,the InternationalAssociationfor the Study of Pain(IASP)recommendsthe use of the term (CRPS).86 comylexregionalyainsyndrome CRPSinvolving tissuedamagewithout nervedamageis categorizedas tvoe I. and CRPSassociated with nerveinvolvementis caiegorizedastype IL86 CRPSgenerallyincludes the following signs and symptoms: severe pain that is out of proportion to the inciting injury or disease,hyperesthesia(excessive reaction to painful stimuli), and allodynia (the sensationof pain in responseto stimuli that are not usuallypainful).CRPSfrequendyalsoincludestrophic changessuch as skin atrophy and hyperhidrosis, edema,stiffness,increasedsweating,and decreased hair growth.86These symptoms generally result in decreased function and,if the syndromeis prolonged, sporryosteoporosis in the affectedarea.8Othersen-
o e.
PATHOLOCY AND PATIENTqROBLEI'\S
51
Eye
Superiorcervical gangron
Salivary granos
ch"d";;;h""'-'eyes,nose,mouth
r
J..",",
Svmoathetic cnatn
Parasympathetic nervoussystem Figure3-8. The autonomic nervous system.
sory vasomotot and skeletal motor abnormalities have also been associatedwith this syndrome.e8 CR.PScan occur in any areaof the body but is most common in the hand and, in suchcases,is frequently associatedwith ipsilateral restriction of shoulder motion. CRPS may develop as a consequenceof major or minor trauma,after visceraldiseaseor cen_ tral nervoussystem lesions,or without any known antecedentevent. The mechanismby which the sympatheticnerv_ ous systemaffectspain is not well understood;how_ ever,it may be the result of direct excitation of the nociceplor> by the sympathecic efferenrfibersor by the neurorransmifters releasedby rhe sympa*teric nerves.The normal activationof sympatheticactivity causedby pain may in some casesactivatethe affei_ ent C fibers,turther increasingpain,which couldthen
increase sympathetic activatioq creating a self_ zustaining vicious cycle. This cycle could amplify the sensationof pain and the signs of sympathetic activity, causingthem to^persistlong after an injury or diseasehas resolved./3 It has aiso b""n propos"i that faulty sympathetic effector mechaniims that cause inappropriate vasoconstriction,vasodilation, increasedcapillary permeabiliqz,or smooth muscle tone may indirectlycauseor exacerbatepain.45
p TheRoleofSubstance SubstanceP is a chemicalmediator that is thought to be involved in the transmissionof neuropathii and inflammatory pain. It is abundantin the centralnervous sy^s^tem and is found in approximately20% of C fibers.89It is alsoreleasedfrom'peripherainociceptors
3 . Pain
52
and has been detectedin inflammatory exudate.90-92 P release Substance has beenshown to excirepaintransmittingneuronsin the dorsalhorn of the spinal cord, and to be involved in nociceptiveprocessingat the spinal cord level.e3'9s Although less than 57o of the neurons in the dorsal horn expresssubstanceP receptors. the maioriryof pairr-transmirting neurons expressthese receptors.SubstanceP levels in the spinal cord increasein responseto induction of joint inflammation and in response to movement of inflamedjoints. Highly elevatedlevelsof substanceP have also been found in the cerebrospinalfluid of patients with persistentpain. SubstanceP receptor activationappearsto be invoived in the sensitization of pain-transmittingneuronsand in the development of hyperalgesia.95-98 Substance P release andreceptor to cissueinjury acLivation is thoughtro be a response andstress. A number of mechanismshave beenorooosedfor the action of substonceP on pain tiansmission. SubstanceP may facilitateexcitationof afferentpain fibers by activatingthe neurokinin-1receptorsin the spinal cord.99'100 When releasedinto the periphery substanceP increasesthe productionofthe inflammatory mediator prostaglandinE2 and the releaseof cytokines from macrophagesand neutrophils.l0l Both prostaglandins and cytokrnessensrtrze primary "Ff"r"^t.^.i.".t^'.
to explain pain control and modulation. These prooosed mechanisms attemDt to correlate what is lnown regardingpeople'seiperienceof pain with the structuresand physiologicalprocessesthought to be involved in pain transmission.Accordingto the gate control theory pain is modulated at the spinal cord level by inhibitory effects of nonnoxious afferent input. Accordingto the theory of endogenousopiates, pain is moduiatedat the peripheral,spinal cord, and corticallevelsby endogenousneurotransmitteffthat havethe sameeffectsasopiates.Psychologicalcentral control mechanismsare also thought to affect pain perceptionand control. Various physical, chemical, and psychological interventionshave beendevelopedbasedon the current understandingof the mechanismsunderlying painmodulation.Forexample,transcutaneous electrical nervestimuiationffENS) deviceswere developed basedon the gate control theory of pain modulation. AIso, the efficacy of a number of establishedtreatment aooroaches is now betterunderstoodbecause the unierlying mechanisms of pain control have becomeclearer.For example,it is now thought that themal agents,which havebeenusedto controlpain for centuries, may be effective for this purpose becausethey gate pain transmissionat the spinal cord.
t
{ l
;
i02
Treatmentsio control pain basedon the inhibition of substance P releaseor on the use of specificsubstanceP antagonistsare currentlybeingresearched.92 Opiates may in part exert an analgesiceffect by inhibiting *re releaseof substanceP from peripheral nervesl however, studies indicate that substanceP receptor-expressing neuronsare not the major site of actionof opiates.96'103
PAIN MOOULATION ANDCONTROL Gate control theory The endogenous opioid s;rstem
A number of observations make it apparent that pain transmission and perception are subject to inhibition and modification. for example, rubbing or shaking an area that hurts can relieve pain in that area, and stress can cause pain not to be felt at the time an injury occurs.Anumber of mechanismshave beenorooosed
Gate Control Theory The gate control theory of pain modulation was first According proporedby Melz.ck andWall in 1965.-3 to *Lis theory severityof the pain sensahonrs determined by the balanceof excitatory and inhibitory inDuts to the T cells in the spinal cord. These ce1ls receiveexcitatoryinput from a and A-delta nociceptor afferentsand inhibitory input, via the substantia gelatinosa,from large-diameter A-betanonnociceptor sensoryafferents.Increasedactivity of the nonnociceptorsensoryafferentscausespresynapticinhibition of the T cells,and thus effectively closesthe spinal the sensation sateto the cerebralcortexanddecreases ot parn(seefrg. 5-Jl. Many physical agents and rnterventrons are thoughtto controlpainin pan by activatingnonnociceptivesensorynerves,thereby inhibiting activation of pain transmissioncellsand closingthe gate to the For example,electrical transmissionof pain.1O4'tos stimulation,traction, compression,and massagecan ali activate low-threshold, large-diameter,nonnoci-
t
T
E
: I
One . PA|HOLOCY
AND PATIENT PROBLEMS
J5
:3Jtivesensorynervesandthereforemay inhibit pain by naloxone,an opiate antagonist.l13 Thesefindings :;rsmission by closingthe gateto paintransmission demonstratedthat these endogenouspeptides are '-.h"
Figule3-9. Indirect inhibition of pain by application of opiatesto opiate receptom.
54
3 . P/ritl
Electricalstimulation of areaswith hish levels of suchasrhePAGMandr-heraphenucleus, opiopeprins. hasbeenfound to stronglyinhibit the transmissionof pain messagesby some spinal dorsal horn neurons, therebycausinganalgesia.118,119 Electricalstimulation of theseareasof the brain can also relieveintractable pain in humans and increasethe amount of betaendorphinin their cerebrospinalfluid (CSI).120 Since these effects are reversedby the administrationof naloxone,they have beenattributedto *re releaseof opiopeptins.l2lThe concentrationof opiatereceptors and opiopeptinsin the limbic system,an areaof the brain largely associatedwith emotionalphenomena, also provides an explanation for the emotional responsesto pain, and for the euphoriaand relief of emotional stressthat is associatedwith use of morphine andthe releaseof opiopeptins.l22 The releaseof opiopeptinsis thought to play an important role in the modulation and control of pain during times of emotional stress. Levels of opiopeptinsin the brain and CSFbecomeelevated,and pain thresholdsincreasein both animalsand humans when stressis inducedexperimentallyby the anticipation of pain.r23'124 Experimentally,animals have been shown to expedencea diffuse analgesiawhen placed under stress.Humans demonstratea naloxone-sensitiveincreasein pain thresholdand a parallel depressionof the nociceptive flexion reflex when su6jectedto emotional s;ess.124,125 These findings indicatethat pain suppressionby stressis most likely causedby increasedopiopeptin levels at the spinal cord and highercentralnervoussystemcenters. The endogenousopiate system also provides an explanationfor the paradoxicalpain-relievingeffects of painful stimulationand acuouncture.Bearableleve1sof painful stimulation,suchastopicalpreparations that causethe sensationof burning,or noxiousTENS that causesthe sensationof pricking or burning,have been shown to reducethe intensity of less bearable preexistingpain in *re areaofapplicationand in other areas.125 Painful stimuli have also been shown to reduce the nociceptive flexion reflex of the lower limb.126Becausethese effectsof painful stimulation areblockedby naloxone,they arethought to be medi1 2 -1 2 8 aL e db y o p r o p e p t i in) .11 2 5 P a i nm a yb e r e l i e v e d becausethe applied painful stimulus causesneurons in the PACM regionsof the midbrain and thalamusto produceandrelease opiopeptins.l2s Placeboanalgesiais alsothought to be mediatedin paft by opiopeptins.This claim is supportedby the
observation that the opiate antagonist naloxone can reverse placebo analgesia and that placebos can also produce respiratory depression, a typical side effect of oPioids.l29'130
MEASURING PAIN Visual analog and numeric scales Comparison with a predeffned stimulus Semantic differential scales
To determine the most appropriatetreatment for a patient'spain and to assessthe efficacyof suchtreatment, it is helpful to assessthe natureand severiryof d:repatient'sexperienceof pain. Suchan assessment should attempt to ascertainthe causesand sourcesof pain, the intensity and duration of pain, and the degreeto which the pain resultsin disabilityor handicap.Variousmethodsand assessment toolshavebeen developedto quantifi/ and qualify both experimentally induced and clinical pain. These methods are basedon patientsrating their pain on a visual analog or numeric scale,comparingtheir presentpain with that experiencedin responseto a predefined,quantifiable pain stimulus, or selectingwords from a list to describetheir present expedenceof pain. Different tools providedifferentamountsand typesof information and requirediffering amountsof time and cognitive ability to complete.
Visual Analog andNumeric Scales Vsual analogandnumericscalesassess pain severiry by askingthe patient to indicatethe presentlevel of pain on a drawn line or to ratethe pain numericallyon a scaleof 1 to 10 or 1 to 100.131 With a visualanaloe scale.the patientmarksa positionon a horizonraloi verticalline, where one end of the line representsno pain and the other end representsthe most severe pain possibleor the most severepain the patient can imagine (Fig.3-10).With a numeric rating scale,0 is no pain and 10 or 100,dependingon the scaleused,is the mostseverepainpo'sibleor the mort qeverepain the patientcanimagine. Scalessimilarto the visualanalosor numericscales h a v eb e e nd e v e l o p e ldo r u s ew i t h i n d i v r d u a lws h o have difficulty using numeric or standard visual analogscales.lor example,childrenwho understand
Oqe . PATHOLOGY AND PATIENT PROBLEMS
Worstpain possible Pleaseplacaan X on thislineto indicat€ howsevereyourpainis now. Worstpain possible
f L
F .
f
tf
cc
Thesetypes of scalesare frequendyusedto assess the severiry of a patient's clinical pain because they are quick and easy to administer, are easily understood,and provide readily quantifiabledata.131 However, visual analog and numeric scalesprovide only a singlemeasureof the patient'spain complaint and fail to provide information about the patient's affectiveresponseto pain or the effect of the pain on his or her functionalactivity level.Also the reliability of visual analogand numeric rating vades between individuals and with the patient group examined, although the tr,vo scales have a high degree of agreementberween them.132These types of measures are most useful in the clinical setting when a quick estimate of a patient's perceivedprogressor change in symptoms over time, or ir responseto different activities or treatment interventions, is desired.
No pain
Figure3-10.Visual analogscalesfor rating pain severity.
witha Predefined Stimulus Gomparison
words or pictures but are too young to understand numericreDresentations of Daincan use a scalewith faceswith differentexpressions to representdifferent experiencesof pain, as shown in lig. 3-11.This type o[ scalecan also be used to assessoain in patients with limited comprehensionbecauseof linguage barriers or cognitive deficits. Pain scalesare also availablefor rating pain in very young children and infants. These are based on describingthe child's expressionand behavior[able 3-1).
Painquantificationmethodsthat involve comparison with a predefinedpainful stimulus are intended to provide a greaterdegree of intersubject reliabilit'y than visualanalogandnumericscales.Ior this rype of assessment, the individual comparesthe severity of his or her symptomswith the samepredefinedstimulus, causingtheir rating scalesto be more similar. Stimuli used for comparisoninclude the application of a toumiquet to the upper extremity to produce ischemiaand the applicationof electrical,thermal,or fingertip pressurestimuli.133,13a The toumiquet pain test is reported to correlatewell with pain assessMatching the ments using a visual analog scale.135
Which face shows how much hurt you have now?
/a\ /G\ /a\ \c/ a-Ar,;\ aA\ \7 !, 0 No hurt
1 Hurts littlebit
\r/
2 Hurts littlemore
\r/ \tY
3 Hurts evenmore
4 tlurls wholelot
5 Hurts worst
Figure3-11. Facescalefor rating pain severity in children age 3 years and older and others with limited numeric communication ability. The patient usesthis tool by pointing to eachface and using the brief word instructions under it to describepain intensiry from Wong DL, Peny SE,Hockenberry M} Matemal Child NursingCare,ed 2, St. Louis,2002, Mosby.)
56
p
3 . P/ril
f-t
*"orr"tal Infant Pain Scale(NIPS)Operational Definitions
Behaviorand score
Description
Facial Exqession 0 Relaxedmuscles 1 Cnmace
. Restfulface,neutralexpression . Tight facialmuscles,furrowedbrow, chin,jaw (negativefacialexpression n^<"
cty 0-Nocry I - Whimper 2 -Mgorouscry
-^,
'fh
".,1
h'^,-\
o Quiet, not crying o
Mild mnrnino
infPrmrrfPnr
. Loud screams,nsing,shrill,continuous(Note:Silentcry may be scoredif baby s ntubaced, a" evrdenced by obvrousmourh.lacialmovemenr.t
Breathing Patterns 0 - Relaxed 1 Changein breathrng
o Usualpatternfor thrsbaby o Indrawng. 'regular.tasterrhanusu"l.gaggrng. breachholding
Arrrrs 0 Relaxed/restraned 1 Flexed/extended
. No muscularrigidiry occasionalrandommovementsof arms . Tense,straightarms,rrgidor rapid extension,flexion
Legs 0 Relaxed/restrained 1 - Flexed/extended
. No muscularngidiry occasionalrandom1e8movement . Tense,straiShtlegs,rigid or rapid extension,flexion
Stateof Atorsal 0 - Sleeping/awake I Fussy
o Quret,peaceful, sJeeping, or alertandsettled o A1ert,resdess,and thrashing
NeonataiInfantParnScaleO 1989,Ch dren'sHosprtalof EasternOnrano.Usedwrth permrssron. Score0 = no parnhkely,maxlmum score7 = severeparnhkely.
intensity of clinical pain with electrical, thermal, or fingertip pressure stimuli has also been reported to correlate well with other measures of pain and has been reported ':r' to have a high degree of intrasubject reliability. lJ- gowever. I hese:ypes o[ pajn arressment tools also have a number of limitations. They require that the patient expefience clinical pain at the time at which the comparison stimulus is applied to make an accurate compadson. Also if a patient has severe pain, it may be both impractical and ethically unacceptable to induce a sufficiendy intense pain to provide a comparison with the clinical pain. For patients with pain that is different in quality from the pain of the expeimental stimulus; for example, burning or tingling rather d-ranthe ache of ischemic pain, a quantitative comparison may not be possible or meaningful. This type of pain measure also fails to
take into account, or report on, the emotional, behavioral, or motivational components of a patient's clinical condition. Thus although comparison pain measures may allow for a reliable gauge of some types of pain, particularly experimentally induced pain or clinical acute pain that is moderate or less severe, they are not well-suited for measuring clinical pain that is severe or chronic, or that has a quality different from that of the comparison stimulus.
Differenlial Semantic Scales Semantic differential scales consist of word lists and categories that represent various aspects of the patient's pain experience.The patient is asked to select, from these lists, words that best describe his or her present experienceof pain. These types of scales
One . PATHOLOGY AND PATIENTPROBLEMS
rre designedto collecta broad rangeof information :bout the patient's pain experienceand to provide ;uantifiable data for intra- and intersubiectcompar,,ons.The semanticdifterentialscaleincludedin rhe ,McGillpain questionnaire,or variationsof this scale, painl38-140 :re commonlyusedto assess Gig. 3-12). This scaleincludesdescriptorsof sensory affective, :nd evaluative aspects of the patient's pain and =roupsthe words into vadouscategorieswithin each rf these aspects.The categodesinclude temporal, ,.patial,pressure,and thermal to describethe sensory :spects of the pain; fear, anxret'4,and tension to jescribethe affectiveaspectsof the pain;and the cogitive experience ofthe painbasedonpastexpedence :nd learned behaviors to describe the evaluative .spectsof the pain. The patient circlesthe one word r eachof the applicablecategoriesthat bestdescribes :hepresentpain.13e,140 Semantic differential scales have a number of comparedwith other :dvantagesand disadvantages of pain measures. They allow assessment and rypes quantificationof various aspectsof the pain's scope, quality,and intensiry Counting the total number of '.vords chosen provides a quick gauge of the pain of pain severity severiryA more sensitiveassessment :an be obtained by adding the rank sums of all the '.vordschosento producea pair ratingindex (PRI).For sreaterspecificitywith regardto the mostproblematic area,an index for the three malor categoriesof the questionnairecan also be calculated.laO The primary of this scalearethat it is time-consuming 3isadvantages :o administer,and it requiresthe patient to have an ntact cognitivestateanda high levelof literacy.Civen -iese advantagesand limitations,the most appropriateusefor this type of scaleis when detailedinformaion about a patient's pain is needed,such as in a :hronic pain treatmentprogramor in clinicalresearch.
0therMeasures Other measuresor indicators of pain that may provide additionaluseful information about the individual's pain complaint and clinical condition include daily activiq/pain logs indicating which activities easeor aggravatethe pain, body diagramson which *re patient canindicatethe locationand natureof the pain (Iig.3-13), and open-ended,structuredinteru1"-r.141'1426physical examination that includes observationof posture and assessmentol strength, mobiliry sensation,endurance,responseto func-
J/
tional activity testing,and soft tissuetone and qualiry canalsoaddvaluableinformationto the evaluationof the severityand cause(s) of a patient'spain complaint. In selectingthe measuresto be used to assess pain, one should considerthe duration of the symptoms, the cognitive abilities of the patient, and the amount of time appropdateto assessthis aspect of the patient's compiaint. In many situations, a simple visual analogscalemay be sufficient to provide information regardinga progressivedecreasein pain as che parient recoversfrom an acute injury. However,in more complexor prolongedcases,more detailed measures such as semantic differential scalesor a combinationof severalmeasuresare more appropriate.
APPROACHES PAIN MANAGEMENT Pharmacological approaches Systemic aoalgesics Spinal analgesia Local injections to painful structrres Physical agents Multidisciplinary pain treatnent programs
Once the severity and nature of an individual's pain hasbeenevaluatedand, ideally,its sourceand nature determined,the goaiso[ treatmentinclude eliminating the cause of pain, controlling the nociceptor input, and reducing the degree of patient impairment. A wide rangeof pain managementapproaches may be used to help achievethese goals.These approachesare basedon our cuffent understanding of pain transmissionand control mechanisms,They may act by controlling inflammation, altering nociceptorsensitiviry increasingbinding to opiate receptors, modifying nerve conduction, modulating pain transmission at the spinal cord level, or altering higher-levelaspectsof pain perception.ln addition, some treatmentapproachesalso addressthe psychological and social aspects of pain. Different approachesare appropriate for different situations and clinical presentationsand are frequently most effectivewhen usedtogether The primary intervention used to alleviate pain is the administration of pharmacologicalagents. Although pharmacologicalagentsare often effective for this purpose, they can also produce a variety
3 . Paiq
58
Whaidoesyourpainteellike? Someof the words belowdescribeyour presentpain. Indicatewhich wordsdescribeit best. Leaveout any word group group-the onethatappliesbest thatis notsuitable.Useonlya singlewordin eachappropriate 1
2
'1Flickering 2 Quivering 3 Pulsing 4 Throbbing 5 Beating .6 Pounding
l Jumping 2 Flashing 3 Shooting
3 l Pricking 2 Boring 3 Drilling 4 Stabbling 5 Lancinating
4 1 Sharp 2 Cutting 3 Lacerating
5
6
7
8
'1Pinching 2 Pr€ssing 3 Gnawing 4 Cramping 5 Crushing
'! Tugging 2 Pulling 3 Wrenching
1 Hot 2 Burning 3 Scalding 4 Searing
l Tingling 2 ltchy 3 Smarting 4 Stinging
I
'10
11 l Tiring 2 Exhausting
l Sickening 2 Suffocating
14
15
16
1 Fearful 2 Frightful 3 Terrifying
1 Punishjng 2 Gruelling 3 Cruel 4 Vicious 5 Killing
1 Wretched 2 Blinding
17
18
19
1 Spreading 2 Radiating 3 Penetrating 4 Piercing
'1Tight 2 Numb 3 Drawing 4 Squeezing 5 Tearing
l Dull 2 Sore 3 Hurting 4 Aching 5 Heavy
1 Tender 2 Taut 3 Rasping 4 Splitting
I Cool 2 Cold 3 Freezing
1 Annoying 2 Troublesome 3 Miserable 4lntense 5 Unbearable 20 l Nagging 2 Nauseating 3 Agonizing 4 Dr€adful 5 Torturlng
Figure 3-12. Semantic differential scale from the McGill Pain Questionnaire. (Reprinted from Melzack R: The McGill Pain Questionnaire: major properties and scoring methods. In Pain, Amsterdam, 7975, Elsevter Science.)
ofadverseeffects.Thereforethe useofphysicalagents, which alsoeffectivelycontrolpainin many caseswhile producingfewer adverseeffects,may be more appropriate.Somepatients,particularlythose with persist-
ent pain,may needintegratedmultidisciplinarytreatment, which includespsychologicalaswell asphysiologicaltherapies,to achievepain relief or a retum to a morenormalfunctionalactivitylevel.
Ohe . PATHOLOCY AND PATIENT PROBLEITIS
59
Nonsteroid aI anti i nf Iam m atory dru gs NSAIDs have both analgesicand antiinflammatory properties and can therefore relieve pain from both inflammatory and noninflammatory sources. 4/7> shooringpain They inhibit peripheral pain and inflammation by inhibiting the conversion of arachidonic acid to prostaglandinsby cyclooxygenase;howeveq much X Sharppain lower doses and blood levels are required to NSAIDs reducepain than to reduceinflammation.143 been shown to reduce both spontaneous have Pleasemarkthetype and mechanicallyevoked activity in C and A-delta andlocationof your painon thesepictures fibers in acute and chronic models of joint inflammation. Evidencealso existsthat NSAIDSexert central analgesiceffects at the spinal cord and at the dtalamus.144-148 Front Back A.lthoughNSAIDs have excellentshort- to mediumFigure3-13. Body diagramsfor marking the location and term applicationfor the control of moderatelysevere nature ofpain. pain causedby musculoskeletaldisorders,particularly when the pain is associatedwi*r inflammation, sideeffectscanlimit their long-termuse.The primary long-term complicationof most NSAIDs is gastroinPharmacological Approaches testinal iritation and b1eeding.149,1s0 NSAIDs also cause decreased platelet aggregation and thus Pharmacologicalanalgesicagents control pain by modifying inflammatory mediatorsat the penphery, prolonged bleeding time. They can cause kidney damage, bone maffow suppression, rashes and alteringpain transmissionfrom the periphery to the anorexia,and decreasedrenal blood flow in dehycortex,or alteringthe centralperceptionof pain. The selection of a particular pharmacologicalanalgesic drared natienrs.lsll52 tlsins different NSAIDs togetherincreasesthe risk of sideeffects. agentdependson the causeof the pain, the length of The first NSAID was aspirin.Many other NSAIDs, time the individual is expectedto needthe agent,and the side effectsof the agent.Pharmacological agents such as ibuprofen (Motrin), naproxen sodium (Naprosyn,AJeve),and piroxicam (Feldene),are now may be administeredsystemicallyby mouth or injection, or locally by injection into sffucturessurround- availablebo*r over *re counter (OTC) and by preing the spinal cord or into painful or inflamed areas. scription. The principal advantagesof these newer NSAIDs over aspirin are that some have a longer These different routes of administrationallow conduration of action, allowing lessftequent dosingand centrationof the drug at different sitesof pain transbetter compliance,and some causefewer gastroinmission to optimize the control of symptoms with testinal side effects. However, for most patients, varyingdistributions. aspirin effectively relievespain at considerablyless expense,although with a slighdy higher risk of Systemicanalgesics gastrointestinalbleeding, than the newer NSAIDs. Administration of a systemicanalgesicis usuallythe Recendy, specific cyclooxygenaseq,?e 2 (COX?) primary me*rod of pain management.This type of inhibitor NSAIDs, such as celecoxib (Celebrex) treatmentis easyto administerand inexpensive,and can be an effective and appropdate pain-relieving and rofecoxib (Vioxx), have been developed.Prior NSAIDs inhibited both cyclooxygenasetypes 1 and interventionfor many patients.A wide rangeof analgesic medicationscan be systemicallyadministered 2. CyclooxygenaseLype 1, catalyzesthe production of prostaglandins associated with joint inflamorally or by other routes.Thesemedicationsinclude mation while cyclooxygenaseUtpe 2 catalyzes (NSAIDs), nonsteroidalantiinflammatorydrugs acetproduction tlte of prostaglandinsthat protect the aminophen,opiatesand opioids,andantidepressants.
fuIil,lo.n
60
3 t Pain
effects. They control pain that cannot be relieved by nonnarcotic agents and are most effective when the pain is dull and poorly Tocalized. The side effects of opiates, including nausea, vomiting, sedation, suppiession of cough, gastrointestinal mobility, and respiration, as well as their propensity to causephysicai iependence and depressionwith long-term use, limit their application for the long-term management of drugs. -,s.,rfoik"1eta1 pain. Respiratory depression also limits the dose that can be used even For short-term Acetaminophen administration. Tolerance causesdrug doses to mainAcetaminophen (Tylenol@) is an effective analgesic tain pain conlrol and to experience withdrawal, and for mild to moderately severe pain; however, unlike causesa consequent rebound increase in pain when an NSAID, it has no clinically significant antiinflamuse of the drug is decreased or discontinued after matory activity.lsa Taken in the same dosage as long-term use. Opiates are generally used clinically to aspirin, it has analgesic and - .antipyretic effects reliene postoperative pain or pain due to malignancy' comparable to those of aspirin.l5aAcetaminophen ts Unfortunately, concerns about tolerance and side administered primarily by the oral route, although effects frequently result in the administration of administration by suppository is effective for patients insufficient doses of these medications to patients who are unable to take medications by mouth. with severe pain, resulting in unnecessarilyhigh levAcetaminophen is useful Forpatients who cannot toiThe risk of psychological addiction els of pain.157,IsB erate NSAIDs because of gastric irritation or when or habituation should not prevent the appropriate use prolonged bleeding time causedby NSAIDs would be of opiate medications, particularly in the managea disadvantage.Prolonged use or large doses of acetament of terminal illness. minophen can causeliver damage;this risk is elevated Opiates can be delivered by mouth, intravenously, an occaalso are rashes Skin alcoholic. in the chronic 6 popular or by direct intraarticular iniection.159'160 sional side effect of this medication. particuiarly and effective means of administration, for hospitalized patients, is patient-controlled anaiOpiates a pump to Opiatesarenarcoticdrugsthat containopium,deriva- gesia (PCA). With PCA, patients use ielf-administer smali, rcpeated intravenous doses' dvesof opium,or any of severalsemisyntheticor synThe amount of medication delivered is limited by thetic drugs with opium-like activiqy. Morphine, preestablished dosing intervals and maximum doses hydromorphone, fentanyl, and meperidineare exama defined period. Pain control is more effective within appiicaclinical for used pies of opiatescommoniy eFfects are less common with this adverse and slightly have drugs tions. Although these opiate than with more convenadministration oF means opito all bind they differentmechanismso[ action, opiate administration tional,physician-controlled of them of all receptors,and the-effects
qut mucosa. Thus COX2 inhibitors have more speiific antiinflammatory effects and a lower risk of gastrointestinal irritation and bleeding. NSAIDs are primarily administered orally, although one, ketorolac fforadol@), is available for administration bv iniection.15311t" mode of administration does not aiter the analgesic or adverse effects of these
ate-specific methods.'"','"" are reversed by naloxone'1ssThe opiates differ and primarily in their potency, duration of action, restrictionof useasa resultof variationsin pharmaco- Antidepressants particularlythe tricyclicssuch as Antidepressants, dynamicsandpharmacokinetics' (Elavil@), have been found to be an amitryptiline It hasbeenproposedthat opialesprovideanalgesia of chronic pain treatcomponent adjunctive effective by mimicking the effectsof endorphinsand binding effective for this being doses with smaller ment, receptorsitesin the centralnervous to opiate-specific for the treatused typically those than application systlm.ls6'1heymay also relievepain by inhibiting these drugs o[ The efficacy depression.l63'164 of ment tire release of presynaptic neurotransmittersand to be thought pain is of chronic treatment the for inhibiting the activity of interneurons early in the and function, nerve on sleep, effects their to nociceptive pathways to reduce or block C-Fiber related with chronic patients that shown have Studies mood. inputsinto the dorsalhorn.116 pain who are also depressedreport much-higher levWhen givenin sufficientdoses,opiateswill control Lls of pain and show more pain-related behaviors even the most severeacutepain with tolerableside
One o PATHOLOGY AND PATIENT PROBLEMS
-j:an those who are not depressed.1'6s'1'66 Although it -i not certain if the higher 1evel of pain in such :arients is the cause or the product oF their depres::cn, the use of antidepressants in either situation ::ray prove beneficial. Spinalanalgesia :-ain relieFmay be achieved by the administration of irugs such as opiates, local anesthelics,and corlicos:eroids into the epidural or subarachnoid spaceof the ,rinal cord.167This route of administration provides ,nalgesia to the areas innervated by the segments of ::e cord receiving the drug and is therefore most =Jective when the pain has a spinal distribution, such .s a dermatomai distribution in a single limb. The :im.ary advantages of this route oF administration =:e that the ' ^ ^ - " .drus * D " . / | bvoasses the blood-brain barrier .:rd that high concentrations reach the spinal cord at :riate receptors at sites of nociceptive transmission, --:rusincreasing the analgesic effects while reducing :dverseside effects. Opiates administered spinally exert their effects by 'rimulating opiate receptors in the dorsai horn of -:'respinal cord.168When administered spinally, fatsoluble opiates have a rapid onset and a short dura=on of action, whereas water-soluble opiates have a slow onset and a more prolonged duration of .ction.169 Local anesthetics delivered spinally have --ne unique abilir,y to completely block nociceptive =ansmissionl however, with increasing concentra:on, these drugs also block sensory and then motor =ansmission, causing numbness and weakness.17o {igh dosesof these drugs can also causehypotension. These side effects of local anestheticslimit their appli;ation to the short-term control of pain and diagnostic rurposes. Catabolic corticosteroids, such as cortisone and dexamethasone, can be administered to the epidural or subarachnoid spaceto relieve pain due to nfiammation of the spinal nerve roots or surrounding strLlctures. These drugs inhibit the inflammatory :esponse to tissue injury; however, because of the side effects of repeatedor prolonged use, including fat and muscle wasting, osteoporosis, and symptoms of Cushing's syndrome, these drugs are not suitable for iong-term application.
Localinjection Local injection of a corticosteroid,opiate,or a local anestheticcan be particularlyeffectivefor relieving pain associatedwith local inflammation.ls9Such
67
injections can be administered into joints, bursae, trigger points, or around tendons and can be used for therapeutic purposes, to relieve pain, or for diagnostic purposes in identification of the structure(s) atfauh.l7l Although this type o[ treatment can be very effective, repeated local injections of corticosteroids are not recommended because they can cause tissue breakdown and deterioration. Local injections of corticosteroids directly after acute trauma are also not recommended because these drugs reduce the inflammatory response and may thus impair healing. Local injections of aneslhetics generally provide only short-term pain relief and are therefore used primarily during painFulprocedures or J:^^-^^+:^^11,, u r d S r r u ) L r L4 r r y .
PhysicalAgents Many physical agents effectively control or relieve pain. They are thought to exert these effects by moderatingthe releaseof inflammatory mediators, modulating pain at the spinal cord level, altering nerve conduction, or increasingendorphin levels. They may also indirectly rcducepain by decreasing the sensitivityof the musclespindlesystem,thereby reducingmuscle spasms,or by modifying vascular tone and the rate of blood flow, thereby reducing 4 lnaddition, physicalagents edemaor ischemia.172-17 may reducepain by helpingto resolvethe underlying causeof the painfulsensation. Different physical agentscontrol pain in different ways. For example, cryotherapy,the applicationof cold,controlsacutepain in partby reducingthe metabolic rate and thus reducing the production and reieaseof inflammatorymediatorssuchasserotonin, histamine,bradykinin, substanceP, and prostaglanThesechemicalscausepain direcdyby stimudins.17s iating nociceptors and indirectiy by impairing the local microcirculationand, in so doing, can damage tissueandimpair tissuerepair.Reducingthe releaseoF inflammatory mediatorscanthus direcdy reiievepain causedby acute inflammation and may indirectly limit pain by controllingedemaand ischemia.These short-termbenefitscan also optimize the rate o[ tissuehealingand recovery. Cry otherapy, thermotherapy, electrical stimulation, and traction, which provide thermal, mechanical, or other nonnociceptivesensory stimuli, are thought to alleviate pain in part by inhibiting pain transmissionat the spinalcord. Physicalagentsthat
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act by this mechanismcan be usedfor the treatment 'needed,and so becomesmore independentof the of acuteand cfuonic pain becausethey do not gener- health care practitionerand pharmacologicalagents. ally produce significant adverse effects or adverse The application of such physical agents at home interactions with drugs, and they do not produce can be an effective component of the treatment physical dependencewith prolonged use. They are of both acute and chronic pain.177This type of selfalsoeffectiveand appropriatefor pain causedby contreatment can also assistin containins the costs of ditions that cannot be direcdy modified, such as medicalcare. pain causedby malignancyor a recentftacture,and Physical agents.usedeitheraloneor in conjunction for pain caused by peripheral nervous system with other interventions, such as pharmacological pathology, such as phantom limb pain and periphagents,manual therapy, or exercises,can also help eralneuropathy.lT6 remediatethe underlying causeof pain while conElectrical stimulation is also thought to control trolling *re pain itself. For example, cryotherapy pain in part by stimulatingthe releaseof opiopeptins applied to an acute iniury controls pain; however, at the spinalcord and at higherlevels.l2BStudieshave this treatment also controls inflammation, limiting shown that pain relief by certain types of electrical further tissue damage and pain. In this case, the stimulationis reversedby naloxone.128 use of NSAIDs, rest, elevation, and compression, Physicalagentshave many advantagesover other in conjunction with cryotherapy,could also prove pain-modifying interventions. They are associated beneficial, although it may make assessmentof with fewe5 andgenerallylesssevere,sideeffectsthan the benefits of any one of these rnterventlonsmore pharmacologicalagents. The adverse effects from difficult. The selectionof physical agentsand their using physical agentsto control pain are generally specificmechanismsof action and modesof applicalocalized to the area of application and are easily tion for controlling pain are discussedin detail in avoidedwith care in applying the treatrnent.When Section2 of this book regardingthe differenttypes of usedappropriately,attendingto all contraindications . h - . ; " , 1 " " " . r . and doserecommendations,the risk of further injury ftom the useof physicalagentsis minimal. For examMultidisciplinary PainTreatment Programs ple, an excessivelywarm hot pack may causea burn in the areaof application,but this risk can be miniOver the past 2 to 3 decades,multidisciplinary prorntzedby carefully monitoring the hot pack's tempergramshave beendevelopedspecificallyfor the treatature, using adequate insulation between the hot ment of chronic pain.a,178 Theseprogramsare based pack and the patient, not applyinghot packsto indion a biopsychosocialmodel of pain and attempt to vidualswith impaired sensationor an impaired abiladdressthe multiple facets of chronic pain with a ity to report pain, and by checkingwith the patient multidisciplinary coordinated program of care.4'179 for any sensationof excessiveheat. Patientsalso do These programs attempt to addressnot only the not developdependenceon physicalagents,although physical and physiological aspectsof the patients' they may wish to continue to use them even after pain but also the behavioral,cognitive-affective,and they are no longer effective because they enjoy environmental factors contributing to their sympthe sensation or attention associatedwith their toms by the useof medical,psychological,and physiapplication.Ior example,patientsmay wish to concal interventions.lBo,lBl tinue to be treatedwith ultrasoundeventhough they Psychologicalintervention is focusedon improvhave reacheda stageof recoverywhere they would ing the coping skills of patients and modi$ring benefit more from active exercise.Physicalagents their behavior,whereasphysicalactivitiesarefocused also do not generallycausea degreeof sedationthat on reversing the adverse effects of the sedentary would impair an individual'sabiliry to work or drive lifesryle adopted by most patients with chronic sarery. pain. Coping skills can be improved with relaxation Many physical agents have the additional training, activity pacing,distractiontechniques,cogadvantageof being readily used independendyby nitive restructuring, and problem solving.1B2,1B3 patientsto treat themselves.Ior example,a patient Behaviormodificationusingthe principlesof operant can be educatedto apply a pain-controllingagent, conditioning can also alter the patient's perception such as heat, cold, or electricalstimulation, when of and responseto pain.184Graded activation and
ex di
ac AI
le th m m be to
th m Ie n(
One . PATHOLOGY AND PATIENT PROBLEMS
::.:3rciseprograms,in which the patient iearns the ---:erenceberweenhurt and harm, can help patients .,.-:ih chronic pain retum to a more functional, ,:ive lifestyle.l8s The patients' family members ::: generally involved in these programs by -::rning appropriatecopingskillsfor *remselvesand -:e patient. Such involvement can assistthe family :embers to help individuals with chronic pain :-.cre effectively rather than reinforce pain-related ::haviors. In contrastwith traditional treatment approaches :--,acutepain,in which the goal of careis to eliminate =e sensation of pain, the goals of care in most =ultidisciplinarypain treaffnentprogramsalsoinclude ::rning to cope and function with pain that may r rt resolve,although frequently patientsalso report
63
a reduction in pain after completing these proGoals of treatment also generally grams.186'187 include decreasingdependenceon health care per sonnel and pain relieving medications,particularly h a b i t - f o r m r nogp i a r e so r o t h e rn a r c o L i cisn:c r e a s i n g physical activities; and retuming patients to their usual social roles. If necessarynarcoticmedications are replacedwith non-habit-forming drugs or with nonchemicalmodes of pain relief such as exercise or physical agents.aMany studies have shown that multidisciplinary pain treatment programs do result in increasedfunctional activity levels while reducing pain behaviors and the use of medical i n c e r v e n t i o ni ns p a r i e n t sw i t h c h r o n i cp a i n . 8 8l q l These programs have also been shown to be cost elfe ctrve.rBI,I 92194
) Clinical CaseStudies a The following casestudiessummadzethe conceptsof pain discussedin this chapterBasedon the scenariopresented,an evaluationofthe clinicalfindingsandgoalsof ft€atmentareproposed.This is followed by a discussion ofthe factorsto be consideredin treatmentselection.
Case'l M? is a 45-year-oldfemale who has been referredto physicaltherapywirh a diagnosisoflow backpain and a physician'sorderto evaluateand fteat.MP complainsof severecentral low back pain that is aggravatedby any movement, particularly forward bending. Shereports no radiation of pain or other symptoms into her extremities.Paindisturbsh€r sleep,and sheis unableto work at her usualsecretarialjob or perform her usualhousehold taskssuchasgroceryshoppingand cleaning.Shereports that the pain startedabout4 daysago,whenshe reached to pick up a suitcase,and hasgraduallydecreasedsince its initial onset ftom a severity of 8, on a scaleof 1 to 10,to a severity of 5 or 6. Her only curent treatment is 600 mg ibuprofe4 which she is taking 3 times a day. The obiective exam is significant for resuicted iumbar range of motion in all planes. Forward bending is restricted to approximately 207o of norma| backward bending is resfticted to approximately 50% of normal, and side bendingis resriccedro approximately30qoof nonnal in both directions. Palpablemuscleguardingand tendemess in the lower lumbar areaoccur when the patient is standing o! prone. All neurological testing, including straight
leg raise and lower exftemity sensation, strength, aad reflexesarewithin normalLirnics. OF CLINICALFINDINGS EVALUATION This patient seeksmedical treatment for the impainrlents o[ low back pain and restricted lurnbar range of motion. These impairments have resulted in difficulties with her nomal functionalactivitiesof sleeping,working, shopping, and cleaning. A.lthough further analysis may help identify the speciticsffucturescausingthis patient'spain, its rccentonsetrelatedto a specificevent usingthe painful areaand its gradualresoludonover tl.re last few days indicatethat her pain is acute and is the result of local musculoskeletalinjury and probable inFlammadon. PREFERREDPRACTICEPATTERN Impaired Joint Mobility, Motor lunction, Muscle ?erformance, Range of Motion, arrd Reflex Integrity AssociatedWith SpinalDisorders,(4I). PLANOF CARE The goalsof treatmentat this time includecontrolling pain to allow MP to sleep and return to other functional activities as soon as it is safe for her to do so. The anticipated goals of treatment would also include regaining normai lumbar rante of motion and, ideally, preventing a recurtence of the present svmDtoms, Continued
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3. Pniu
) Clinical Case Stttdies-cottt'd ASSESSMENTREGARDINGSELECTIONOF THE OPTIMAL TREATMENT The optimal intervention would ideally address the acute s1'rnptomof pain and the underlying inflammation and, if possible,would help to resolveany underlying structural tissue damage or changes.Although a single ffeatxoentmay not be abie to addressall of theseissues, treafinentsthat addressasmany of theseissuesaspossib1eand that do not adverselyaffectthe patient'sprogress arerecommended. As is explainedingreaterdetailin Part 2 of this book, a number of physical agents, induding cryotherapyand electricalstimulation,may be used to control this patient's pain and reducethe probable acute inflammationof the lumbar structures,and lumbar traction may also help to relieve her pain while modifying the underlying spinal dysfuncrion.
Case 2 tj is a 45-year-oldfemalewho hasbeen referredfor therapy with a diagnosisof low back pain and an order to evaluate and treat, with a focus on developing a home program. TJ complains of stiffaess and generalaching of her lower backthat is aggravated by sittingformore than 30 minutes.she reportsoccasiorulradiationof pain into her left lateral leg but no other s;.rnptoms in her extremities. She states*rat the pain occasionallydisturbsher sleep,and she is unableto work at her usualsecretarial job becauseof her limited sitting tolerance.Shecanperform most ofher usualhouseholdtasks,suchasgrocery shopping and cleaning, although she ftequently receives help from her family. She reports that the pain started about 4 years ago,when she reachedto pick up a suitcase,and althoughit was initially severe,at a levelof 10 on a scaleof 1 to 10, and subsidedto somedegreeovel the first few weeks, it hasnot changedsignificandy in the past 2 to 3 years and is now usually at a level of 9 or greater Shehashad multiple diagnosticteststhat have not revealedany significaotanatomicalpathology,and she has received multipie treatments, including narcotic analgesicsand physicaltherapy consistingprimarily of hot packs,ultrasonography, andmassage, without significant benefit. Her only current treaftnent is 600 mg of ibuprofeq which sheis taking 3 times a day.The objective exam is significant for restricted lumbar range of motion in all planes.Forward bending is restrictedto approximately40% of normal, backward bending is restrictedto approximately50% of normal, and side bendingis resffictedto approximately507oof normalin both directions.?alpationrevealsstiffnessof the lumbar facetjoints at L3 throughL5 and tendemessin the lower lumbar area. All neurologicaltesting, including lower extremity sensation, strength, and reflexes are within
a
normal limits, although srraightleg raisingis limited to 40 degreesbilaterally by hamstring tightness and prone knee bending is limited to 100 degreesbilaterally by quadricepstighmess.T| is 5 leet 3 inchestall and reports her weight to be 180 pounds.She reportsthat she has gained 50 pounds sinceher initial back injury 4 years ago. EVALUATIONOF CLINICAL FINDINGS This patient seeksmedical ueatrnent for the impairments of low back pain and restricted lumbar range of motion. These impairments have resulted in difficulties widr her normal functional activities of sleeping, working, shopping, and cleaning. Although funher analysis may help identify the specificstructurescausingtJrispatient's pain, the long duration of the pain is well beyond t}re normal time neededfor a minor backinjury to resolve.The lack of changein her pain over the previous years and its lack of responseto multiple treatmentsindicatethat her pain may have a variety of contributory factors beyond local tissue damage, including deconditioning, psychological dysfunction,or socialproblems. PREFERREDPRACTICEPATTEFN Tmn:irarl
Pn
f/R\
PLAN OF CARE The proposed goals of treatrnent at this time may include controlling pain and regaining normal lumbar range of motion. However, the primary goals of treatment would be to retum fl to her maximal functional level and minirnize her dependenceon medicalpersonnel and further medical treatment. ASSESSMENTREGARDINGSELECTIONOF THE OPTIMAL TREATMENT The optimal intervention would ideally addressthe functional limitations causedby this patient's chronic pain and provide her widr independent means to manageher symptomswithout adverseconsequences. Thus the probablefocusof carewould be on teachingTJ coping skills and improving her physical condition, including strength and flexibiJity. The useof physical agentswouid probably be restricted to independent use for pain managementor asan adjunctto promoteprogressiontoward more functional goals-As is explained in greater detail in Section2 of this book, a number of physical agents, including cryotherapy, thermotherapy, and electrical stimulation,may be used by patientsindependentlyto conuol pain, while thermotherapy may also be used to help increasethe extensibiliry of soft tissuesto allow for more effective and rapid recovery of flexibiliry.
PreferedPhysicalTherapistPracticePaternssMl4Iand4Bl arecopynght2002AmericanPhysicalTherapy AIl rightsreserved. Association.
One . PATHOLOGy AND PATIENT PROBLE|S
CHAPTER REVIEW
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3. Merskey H, ed: Classificationof chronicpain: description of chronic pain syndromesand definition of pain terms,Parn(Suppl3)3(Suppl):S1, 1986. 4. Vasudevan SV, Llnch NT: Pain centers: organization and outcome, \YestJl\en $4F}532-535, t99t. 5. Vasudevan SV Rehabilitation of dre patient with chronic pain: is it cost effective?PainDigest2:99-L0L, 1992. 6. KazisLE,MeenanRI, AndersonJ:Painin the rheumatic diseases: investigationsof a key healt! statuscompo^er,t',Afthhk Rheum4(Suppl2):10-13,1983. 7. StrangP: Emotionaland socialaspectsof cancerpain, ActaOncol31(3):323-326 , 1992. 8. Stubble HG, Crubb BD: Afferent and spinal mechanismsof joint paiq Pah 55:5-54,1.993. 9. SlukaKA: Painmechanismsinvolved in musculoskeletai disorden,/ Onhop SVonPhys Ther24(4):240-254, 1,996. 10. Crigg B StubbleHC, SchmidtRI: Mechanicalsensitivity of group III and IV afferents from posterior articular nerve in normal and inflamed cat knee,J Newolhysiol 55635-643,7986. 11. BonicalJ: TheMaxagementof Pain, ed 2, Philadelphia, 1990,Lea& Iebiger 12. BonicalJ: Importanceof the problem.In Aronoff GM, ed: Evaluationand Treatmettof ChroxicPain, Baftinore, 1985,Urban & Schwarzenberg. 13. VasudevanSV Management of chronic pain: what have we achievedin the last 25 years?In Ghia JN, ed: The Muhidisciylinary Pain Cexter: Otgaxization and Petsoaxel Functions for Pait MaxagemetyBostoq 1988, Kluwer. 14. Melzack B" Dennis SC: Neurophysiologicalfoundations of pain. In StembachM, ed: ThePsychology of Pain,NewYork,1978, RavenPress. 15. KellgrenJH: Observationson referredpain arisingfrom muscle. Clin Sci3:175-190. 1938. 16. StaffPH: Clinicalconsiderationh referredmusclepain and tendemess-connectivetissuereactions,EutJ Appl Phvsiol57:369-372. 1988. 17. Black RC: Evaluationof the pain patrent,J Disabil 1,: 85-97,1990. 18. InternationalAssociationfor the Studyof ChronicPain, Sr.rbcommittee on Taxonomy:Classificationof Chronic Pain.Paiz(Suppl);3:SL-5225. 1986. 19. Crue BL, ed: Paix: Research axd Trcatment,New York, 1974,AcademicPress. 20. Osterweis M, Kleinman A, Mechanic D, eds Paix and Dkability - Clixlcal Behavioral axd Public Polky PersVectite:Coumittee on Paix, Dkability and Chrcnk References Illness Behavior,Washingto4 DC, 1987, National 1. SweetWH: In FieldJ, MagounHW, Hall \4' eds: AcademyPress. Haxdbook ofPhysiology. Section 4:NeuroVhysiology, Volume 27. Magni C, Caldieron C, Luchini SR et al: Chronic I Washington,DC, 1959,AmedcanPhysiological musculoskeletalpain and depressivesymptoms in Society. the generalpopulation:an analysisof the 1st national 2. BonicaJJrPain:what is sciencedoing abott \t? Paix health and nutrition examination survev data.Paix 43: 2:12-15,1975. 299-307. 1,990 .
?ainis the result of a complexinteractionof physical :nd psychologicalprocesses that occurwhen tissueis damagedor at risk of being damaged.The sensation -nd experienceof pain varieswith the duration and -.ourceof the painful stimulus to produce acute, :hronic, or referredpain. Pain is generallyperceived 'vhen specializedpain receptors(nociceptors)at the f,eripheryare stimulatedby noxious thermal,chemi:al, or mechanicalstimuli. Nociceptorscausetrans:nissionof the sensationof pain along C fibers and A-deltafibersto the dorsalhom olthe spinalcord and -Jrence,via *re thalamus,to the cortex. Pain trans:rission may be inhibited at the spinal cord level by activity of A-beta fibers that transmit nonnoxious sensations,or at the pedphery,spinal cord, or higher levelsby endogenousopiates.Painmay alsobe modiied indirecdy by disruption of the pain-spasm-pain cycle.The severiqrand quality of an individual'spain canbe assessed usinga variery ofmeasures,including visualanalogand numeric scales,comparisonwith a predefinedstimulus, or selection of words from a givenlist. Thesemeasurescan help to direct careand indicate patient progress.A number of approaches can be usedto relieveor control pain. Theseinclude pharmacologicalagents,physical agents,and multidisciplinary treatment programs. Pharmacological agentsmay alter intlammation or peripheralnociceptor activation or may act centrally to alter pain transmission.Physicalagentscan also modiflz nociceptor activation and may alter endogenousopiate levels. Multidisciplinary treatment programs integrate pharmacological,physical, and other medical approacheswith psychologicaland social interventions to address the multifaceted dysfunction of chronic pain. A good understandingof the mechanisms underlying pain transmissionand control, the tools availablefor measuringpain, and the various approachesavailablefor ffeating pain is required to selectand direct the use of physicalagentsappropriately within a comprehensivetreatment program for the patientwith pain.The readeris referredto the Evolve website http://evolve.elsevier.com/Cameron for study questionspertinentto *ris chapter.
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3 . Ptlilr
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3041985. 791. Keele IJ, Caidwell DS, Queen KT et aL Pain coping strategies in osteoarthdtis patients, / Cotsuh Cllx Psvchol55208-212.1987. 792. Mayer TC, GatchelRJ,Mayer H et aL A prospective two-year study of functional restoration in industrial low back injury-an objectiveassessment procedure, JAL4A 258t1763-1767, 1987. 193. Stieg RL, Williams RC, Timmermans-Williams G et al: Cost benefits of interdisciplinarychlonic pain fteatmenq Cli J Paih1t189-193,L986. 194. Simmons JW, Avant WS jr, Demski J et al: Determining successfulpain clinic treatrnent tlrough validation of cost effectiveness.Sdxe 1.3:342-344. 1988.
ToneAbnor lities DianeD. Allen,MS, PT, and Cail L. Widener,PhD, PT
SUMA,IARY
OF INFORMATI
-\luscleTone Defined Terminology for Tone Abnormalities -\leasuringMuscle Tone The Anatomical Basesof Muscle Tone and Muscle Activation
OT/ COVERED
Abnormal Muscle Tone and lt's Consequences Clinical CaseStudies Chapter Review
OBJECTIVES Uponcomyletionofthis chayte4the readerwill beable to: 1 . Define muscle tone and identify tone changesin
the normal adult. 2 . Use appropriateterminology to describe abnormalmuscle tone. Describequantitative and qualitative metrhods usedto measuremuscletone,determining when eachis appropriate. J . Identify the activeand passiveelementsof muscletlat contribute to muscle tone. J . Describethe function of the alpha motor neuron and its conduction of electrochemical signals. 6 . Idenri$rperipheral,spinal,and supraspinal sourcesofinput to the alpha motor neuron.
7. Describemuscle tone differencesresulting from changesin excitatory and inhibitory input to alpha motor neurons. 8. Discussvarious patholoSiesthat might result in abnormal muscle tone, including the q/pe of tone abnormality that is likely to occur. 9. Identifr clinically relevant consequencesof increased,decreased,or fluctuating muscle tone. 10. Determine appropriatemanagementof patientswith abnormal muscle tone, stating the expectedeffect ofvarious treatments.
/5
74
4 . ToneAbtormalities
Significantproblemsin both muscletone andmuscle activation severely limited Mrs. H's function. While she sat in her wheelchair, her thorax was kyphotic, her head was exaggeratedlyextendedforward, her left arm writhed, her left leg danced,and her right arm huggedher right knee to her chest.Her mouth and tongue worked continuously.The constant involuntary motion, or dyskinesia,was probably a result of large doses of medication used to control the lack of motion, or akinesia,typical of her Parkinson'sdisease.Her dyskinesiaalternatedwith a "freeze state" in which her left arm and les would slow and then stop:shewould let go of heriighc leg and becomestill in her chair, sitting with a masked faceand both feet on the floor like a sedatestatue.In the akineticfreezestate,eventhe simplestfunctional movementsbecamenearlyimpossiblefor her Mrs. H's dyskinesiaand freezesrepresentfluctuations in the tone and activation of her muscies. Muscle activation, or contraction,is readily understandablebecauseit is usuailyvisible through movements and can be measuredby the force or torque generatedarounda joint. ]n contrast,muscletone is a quality that is difficult to define or quantify. It is observablein its extremestatesand evenin its normal fluctuations. The difficulty lies in the perpetually changingnature of muscletone and in the many factors that affectit. This chapterdescribesaccepteddefinitions of muscletone and its relatedconceptsJ ways of measuringmuscle tone, the anatomic basesfor muscletone, and some of the issuesthat arisewhen tone is abnormal.Examplesand problemsare drawn from both neurorehabilitationand orthopedic settings.The focus,asin the rest of this text, is on problemsthacmay be affecredby physicalagenrs.
MUSCLE TONE DEFINED Muscle tone is variously describedas muscletension at rest,readinessto move or hold a position,priming or tuning of the muscles,lor the degreeof activation beforemovement.Muscletone is the underlyingtension in the muscle that servesas a backsroundfor To defineit moreconcrerely, contraccjon. musclerone is the passiveresistanceto the stretch of a muscle. The subjectmustbeinstructednot to resistthe stretch aoolied so that whatever resistanceis noted can be aitiibnt"d to the vadous components of muscle tone rather than to voluntary muscle contraction. The componentsof muscle tone include the active
resistancegenerated by neurally activated muscle fibers and the oassive.biomechanicaltension inherent in the connectivetissueand muscleat the leneth agentsuseJin atwhich the mu'cleis tested.2 Physical physicaltherapymay affect the neuralor the biomechanicalcomponents oI muscletone,or both. The following example may help clarify some concepts.A runner'squadricepsmuscleshave lower tone when tlte runner is relaxed and sitting, with feet propped up, than when those samemusclesare lengthenedover a flexedkneeand preparingfor imminent contractionat *re starting block of a race (Iig. 4-1).The differencebetrveenthe lower tone and the highertone canbe palpatedasa qualitativedifference in the resistanceto finger pressureover the musclein eachinstance.In the relaxedcondition,a palpatingfinger will sink into the muscleslightly becausethe muscle provides so little resistanceto that deforming pressure,which is a type ofstretchon the surfacemuscle fibers. The finger will register relative sofmess comparedwith the hardnessor resistance to deformation that is felt in the "ready' condition.In the ready condition, both the biomechanicaland the neural componenrscontrjbuteto a greater resistanceto deformatiorqor increasedmuscletone.Irom a biomechanicalstandpoint,the muscleis stretchedover the flexedknee,so any slackin the soft tissueis takenup, and the contractileelementsare positionedfor most efficientmuscleshorteningwhen the newessignalthe muscleto contract.Irom a neural standpoint.when the runneris poisedat the startingbloci, the neural activity increasesin anticipationof the beginningof the race.This neural activation of the quadricepsis greaterthan when the runnerwas sitting and relaxed; it presetsthe musclefor imminent contractron. Note that *re samequalitativedifferencein resistanceto fingerpressurecouldbe palpatedif the runner relaxedand then contractedthe quadricepsvoluntarily. One of the difficultieswith tone identificationand descriptionisthe overlapbetweenhow a musclelooks beingpreparedto and feelswhen it is subconsciously move or hold, and how it looks and feelswhen it is consciouslyorderedto contract.A key to the assessment of muscletone is that no activeresistanceto t}le musclestretchoccurs.If a subjectis unableto avoid actively resisting, then the tonal qualiqy assessed when the muscleis stretchedwill be a combinationof tone and voluntary contraction.Even people who have normal control over their musclessometimes have difficulty relaxingat will; therefore,one can see
Olrc . PATHOLOGY AND PATIENTPROBLEMS
Hightonein quadriceps muscle
Lowtonein quadriceps muscle
Figure4-1. Normal variations in muscle tone.
',vhythe differentiationbetween muscletone andvoluntarymusclecontractionmight be difficult. The continually changingnature of muscie tone can also lead to problems with its identification. Despitethe differencesin tone between the relaxed andimminent-contraction,or readystates,the runner in the exampledescribedaboveis consideredto have normal muscletone in bot! instances.Normal. then. rs a spectrumratherthan a precisepoint on a scale. Abnormal muscle tone may overlap normal muscle tone at either end of the span(Iig. 4-2), but it has the following distinction:with abnormal tone, the individual has a restrictedability to changethat tone to prepareto move readilyor to hold a position.In other words, slow movement is not abnormal unless an
Normalmuscletone
t_
Nol
muscre
i"" -.I__-Abnormaliy low muscletone
I
l
Excesstve I muscre I ,on: | t---_T__l Abnormallyhigh muscletone
Figure4-2. Normal muscle tone is a spectrum.
4 o ToneAbrormalities
76
individual can oflly move slowly. Lower tone is not abnormalunlessan individual cannotincreaseit sufficiently to preparefor movement or holding. Higher tone is not abnormal unless the individual cannot alter it at will, or unlessit occursuncomfortably as muscle spasms,cramps,or inefficient use of energy. Normal muscletone, then, is not a particularamount of passiveresistanceto stretch,but ratheris a controltensionsto supportnormal lablerangeof appropriace movementand posture.
FORTONE ABNORMALITIES TERMINOLOGY Flaccidityls the term used to denote lack of tone or zero resistanceto passivemovementwithin the middle rangeof the muscle'slength,andis usuallyconcuris rent with total paralysisof the muscle.Hyyotoniciry to resistance decreased to describe term used the stretchcomparedwi*r normal muscles.Ilaccidity is an extremecaseofhypotonicitY. Hyyenonicity,the term for high tone, may be ei*rer resistance to spastic,detinedas velocity-dependent in muscles like the (quick or rigid, stretch).3 siretch that to stretch are resistant Mrs. H's freezestate,which is applied quickly or slowly. A hypertonic or h)?otonic musclemay ormay not havesomedegreeof voluntary conffactility.Mrs. H, for example,hasboth rigidity and akinesiaduringa fteeze,which meansthat shealsohas difficulty initiating voluntary movement. The term sgasticitrhas had wide clinical use but causesconfusionunlessit is narrowly defined ffable 4-1).The termhassometimesbeenpairedwlth yaralysrs,which is the lossof voluntary movement,and has shared the blame for the loss of function noted in
patient conditions labeled syasticparalysisor syastic Muscle tone and voluntary muscleconhemiplegia.a,s traction,however,are distinct from eachother,as are spasticityand loss of function. Muscle tone and posture arealsodifferententities.Ior example,an individual who presentswith an adducted and internally rotatedshoulder,a flexedelbow,and flexedwrist and fingers,holdingthe hand closeto the chest,canbesaid to havea flexedpostureof the arm. He or she cannot be saidto havespasticityuntil the passiveresistanceto at differentvelocitiesfor eachof the stretchis assessed involved muscle groups. Spasticirycoexistswith hyperactivestretchreflexesin its qypicalclinicalpreseniationa,6but becausepatientswi*l rigidiry canalso the rwo terms have hyperactivesrrecchreflexes,7 should not be equated.In addition, some confusion becauseit has has arisenregardingthe term spasticity beenappliedto abnomal muscletonehavingdifferent underlying neural pathologies,such as spinal cord injury versusstrokeor cerebralpalsy To clari$zusein will be applied only to a particular this text, sl2asticiry qype of abnormal muscle response,whatever the pathology,in which quickerpassivemusclestretches than slowerstretches.r elicit sreaterresistance Clonusis the term usedto describemultiple rhythmic oscillationsor beatsin the resistanceof a muscle responding to quick stretch, observed particularly with stretchto ankle plantar flexors or wrist flexon. The claso-knifephenomenonconsistsof initial resistance followed by a sudden releaseof resistance responseto a quick stretch of a hypertonic muscle, much like the resistancefelt when closing a pock etknife.A musclespasmis an involuntary strong tractionof a muscle,typically asthe resultof a
P*'
What SpasticityIs and Is Not ts:
A type ofabnormal muscletone
Paralysis
One type of hypertonicity
Abnormalposturing
resistanceto passivemusclestr€tch Velocity-dependent
A particuiardiagnosisor neuralpathology HyPeractivestretchreflex MusclesPasm Voluntarymovementrestrictedto movementin flexor or extensorsynelSy
Note: Spasticity,when present,is not alwaysthe causeofmotor dysfunction.
O,,e . PATHOLOGY AND PATIENT PROBLEMS
stimulus.A client who has pain in the low back may have muscle spasmsin the paraspinalmusculature that cannotbe relaxedvoluntarily. For those who, like Mrs. H in the example describedearlier, have fluctuating abnormal tone, qualitative descriptionsare appl.ied.Mrs. H's tone variesbetweenrigidiry of the muscleson both sidesof her joints during a fteeze,and altematinghigher and iower tone in agonistsandantagonistsaboutthe joints duringher dyskineticstates.Muscletone is especially difficult to assesswhen it is fluctuatingwildly, so it is commonto describevisiblemovementratherthan the tone itself. The common term used to describeany type of abnormal movement that is involuntary and hasno purposeis /ysbixesia.Sornespecifictermsused to describevarioustypes of dyskinesiaarechorelform moveftteflts or chorea(dance-Iike,sharp, jerky movements), ballismus (ballistic or large throwing-rype movements),tremorQow-amplitude,high-frequenry oscillatingmovements),athetoidmovements (w orm'llke writhing motions), anddystonia (involuntarysustained musclecontraction).One exampleof dystoniais seen in the condition called spasmodic tonicollis,or wry necb, in which the individual'sneckmusculatureis continuously contractedon one side and the individualholds the headasymmetrically.E
MEASURING MUSCLE TONE Severalquantitative and qualitative methods have been used to assessmuscletone. Its variabiliry with subtle intrasubjector environmentalchanges,however,Iimits the usefulnessof staticmeasuresof muscle tone. In addition, measuringtone at one point in time during one movement ot stateof the muscle(at rest or during contraction)provideslittle information about how the muscletone enhancesor limits a differentmovementor state.9Thereforeexaminersmust be carefulto record*re specificstateof conffactionor relaxationof the musclegroup in questionwhen they assessmuscle tone, and not interpret the results as true for all other statesof the musclegroup. In other words, ankle plantar flexor hypertonicity assessed at rest cannotbe said to limit ankle dorsiflexiondurins che swing phaseof gait unlesste'ting is completeJ while the client is upright and moving the leg forward. The methods described in this section for measuringmuscle tone, then, should be used with two caveatsin mind. Iirst, the examinershouldavoid generalizingthe resultsof a singletest, or evenmulti-
77
ple tests,to all conditionsof the muscle.Second,the examinershould include measuresof movement or functionto obtaina more completepictureof the subject'sability ro usemuscletone appropriately.
Measures Quantitative Passiveresistanceto stretchprovided by muscletone can be measuredby tools similar to those used to measurethe forcegeneratedby a voluntarily contracting muscle.When a voluntary contractionis measured, a subjectis askedto "push againstthe device with all your strength.' When muscle tone is measured, a subjectis asked to nrelax,ar'd 1etme move you." Suchmeasuresare restrictedto the assessment of musclesthat are both reasonablyaccessibleto the examinerandeasyto isolateby the subjectto contract or relax on command.Muscles at the knee. elbow. wrist, and ankle, for example,are easierto position and to isolatethan trunk muscles. One protocol for quantifying muscle tone in the ankle plantar flexors was describedby Boiteau et al and utilizes a hand-held dynamometer or myometer.10The subjectswere seatedand positionedso that their feet were unsupported. The head of the dynamometerwas placedat the metatarsalheadsof the foot. The examiner passively dorsiflexed the ankle to a neutral position with pressurethrough the dynamometet severaltimes at different velocities. The examiner controlled the velocitiesby counting seconds:completingthe movementin 3 secondsfor a slow velocity and in less than half a second for a fast velocity.The authorsreportedhigh reproducibility (intraclasscorelation coefficients= .79 and .90) for both the high- and low-velocity conditions.l0 Comparinghigh- andlow-velociryconditionsenables the examinerto distinguishbetweenneuraland biomechanicalcomponentsof spasticity. A diagnostictool frequendy used for quantifying muscletone in researchis eiectromyography(EMC) (Iig. a-3). EMC is a record of the electricalactivity sampledfrom musclesat restand duing contraction, usingsurface,fine wire, orneedleelectrodes(Fig.4-4). During voluntary musclecontraction,the recordwill show deviationsaway from a straightisoelectricline €ig. a-O. The number and size of the deviations (peaksand valleys) give a measureof tlte amount of muscle tissue that is electrically active during the contraction.When a supposedlyrelaxedmuscle demonstrateselectricalactivity when stretched,that
4 . Tore Abnorualities
78
activity is a measureof the neurally derived muscle tone at that moment. to usingEMC to evalThereareseveraladvantages uate muscletone. One advantageis its sensitivityto low levelsof muscleactiviqythat may not be readily palpableby an examiner.In addition, precisetiming of muscleactivationor relaxationcanbe pickedup by EMG andmatchedto a commandto contractor relax. of thesebenefits,EMC can be usedto proBecause vide biofeedbackto a subjectwho is trying to leam how to initiate contractionor relaxationin a particular musclegroup.tl Another advantageof EMC is that
Figure 4-3. Setupfor performingsurfaceEMC
Figure4-5. Example of an EMC tracing from the extensor poilicis longus (uyyer ttacing) and flexor pollicis muscles (lower ttacing) dudng an isometdc contraction ofthe flexor pollicis longu. muscle.The nidJle na.ing is the force output produced with a 60% maximum voluntary contraction (MVC). (Reprintedwith permission from Basmajian fV, De luca CJ:Mu',|e, Alive:I hei,Funrio'1' byElectromyograyhy Revealed , ed 5, BaltLrnore, 1985,Williams & Wilkins.)
I
z=
in some casesit can differentiatebetweenthe neural and biomechanical components of muscle tone, which oaloation alone is unable to do. If a relaxed muscle-showsno electricalactivity via EMG when stretched, but still provides tesistanceto passive stretch,then its tone can be attributed to the biomechanical properties rather than the neural componentsof the muscleinvolved. Disadvantasesof EMC include its restriction to monitoring oJy a local areaof muscletissuedirecdy adiacentto the electrode.It also requiresspecialized equipment,and sometimestraining, that is beyond the budget of many clinical facilities. In addition, muscletone and activemusclecontractioncannotbe distinguishedfrom eachother by looking at an EMC record. A label of some kind must state when the subject was told to contract and relax and when the musclewas stretched.Although EMC is capable ofrecordingthe amount of muscleactivation,it measures force only indirectly via a complex relationship betweenactivitv and forceouttrrut.12
Figure4-4. Disposable (sma11),surface, and fine wire EMC electrodes.
One . PATHOLOGY AND PATIENT PROBLEMS
Somemeasuresof muscle tone have been develf,pedto test particulartypes of abnormalities,not just :one in general.One of these is calied the yexdulum :Jit,which is intendedto test spasticity.The test con-.istsof holding an individual'slimb so that when it is :ropped, gravity providesa quick stretchto the spasic muscle.The resistanceto that quick stretchwill :rop the limb trom falling beforeit reachesthe end of :s range.The measurement of spasticity, via an elec=ogoniometerl3 or isokineticdynamometer,14 is rhe Cifferencebetv,'eenthe angle at which the spastic ruscle "catches"the movement and the angie *re rmb would reachat the end of its normal range. 3ohannonreporredthe resr-rerest reliabiliryas hi-gh ivhen the quadricepsmuscle was tested consecuiveLy in 30 patientswho had spasticityafter experiencinga stroke or head injury.la A limitation of the cendulumtest is that somemusclegroups cannotbe :ested by dropping a limb and watching it swing, specifically,the musclesof the trunl
Measures Qualilative -\4uscletone is more often assessed oualitativelvthan quanticatively. Oneclinicalmeasure in commonusei, a s-point ordinal scalethat placesnormal tone at 2+. No tone and hypotonia are given scoresof 0 and 1+, respectively,and moderateand severehypertoniaare givenscoresof 3+ and4+, respectively.ls The clinician obtainsan impressionof the muscletone relativeto normal by passivelymoving the patient at varying
79
speeds.When muscle tone is normal, movement is light and easy.When muscletone is decreased, movement is still easy or unrestuictedbut the limbs are hear,y, as if they are dead weight. When tone is increasedfor a particularmuscle,the movementthat mechanicallystretches*rat muscleis stiff or unyielding. Various movementsmust be made at multiple joints to distinguishbetweenthe differencesin muscle tone of the flexorsversusthe extensors,for instance. Another common qualitativeway to assess muscle tone is to observethe responseelicitedby tappingon its tendon,activatingthe musclesftetchreflex.As with the clinicaltone scale,in this5-pointscale,2+is considerednormal,0is absentreflexes, 1+ is diminished,3+is briskerthan average,and4+ is very brisk or hyperactive.16The nonnai responses for differenttendonsdiffer For example,a tap on the patellar tendon will normally resultin a slight swing of the free lower leg from *re koee.In contrasqa bicepsor tricepstendon tap is still considerednormal if a small twitch of the musclebelly is observedor palpated;actualmovement of the whole lower arm would generallybe considered hyperactive.Normal responsesare determined by what is typicalfor that tendonreflex.In addition,symmetry ofreflexes,assessed by comparingthe responses to stimulationof the left and right sidesof rhe body, determinesthe degreeof normalcyofthe response. The Ashworth ScalelTand the Modified Ashworth ScaielBwere developedto specificallymeasurespasticity. Iive ordinal grades are defined, from 0 (no increasein muscletone)to 4 (rigidly held in flexion or
F*,
Modified Ashworth Scalefor Grading
Grade
Description
0
No increaseinmuscletone
1
Slightincreaseinmuscle tone,manifestedby a catchand releaseorby minimal tesistanceat the end of the rangeof motionwhen the affectedpart(s)is moved in flexion o! extension
1+
Slightincreaseinmuscle tone,manifestedby a catch,followed by minimal resistancethroughoutthe remainder(1ess than ha10ofthe ROM
2
More markedincreaseinmuscle tone throughmost of the ROM, but affectedpart(s)easilymoved
3
Considerableincreasein muscletone,passivemovementdifficuit
4
Affecredpan(s)rigidin flexionor extension
ROM, mngeof notion. Reprintedwith permissionof the American PhysicalTherapy Associaiion.From BohannonRW, Smirh MB: Interraterreliabiliry of a Modified Ashworth Scaleof MuscleSpastrcity, PhysThet67:207,1987.
80
4 . Tore Abnornalities
extension).An intermediategradeof 1+ distinguishes the original Ashworth Scale and the Modified Ashworth Scale,and is defined by a slight catch and continued minimal resistance through the range [able 4-2). Bohannon and Smith reported,867 o/o interrater agreementwhen testing 30 patientswho had spasticityin the elbow flexor muscles.lB
and its surrounding connective tissue. The practitioner must have an understandinsof the anatomical basestor both tone and accivatlonro determine appropriatephysical agentsto apply when either is dysfunctional.The anatomicalcontributionsto muscle tone and activationarereviewedin this section.
Muscular Contributions to Muscle Tone and General Considerations When Measuring Muscle Activation Tone The relativepositionsofthe limb, body,neck,andhead with respectto one another and to gravity canall affect muscletone. For example,the asymmetricand symmetric tonic neck reflexes(AfNR and STNR,respectively) are known to influence the tone of the flexors and extensorsof the arms and legs,dependingon the positionof the head(Iig. 4-Q, both duringinfanry and in subjectswho haveneurologicaldeficits.leSubdedifferencesin muscletonedueto thesereflexescanbepalpatedwhen the headpositionchangesevenin subjects with matureandintactnervoussystems.Likewise,the pull of gravity on a limb to stretchmuscles,or on the vestibularsystemto ffiggerresponses to keepthe head upright, will changemuscle tone accordingto the position of the headand body.The testingposition,therefore, must be reportedfor accurateinterpretationand replicationof any measurementof tone. Additional generalrulesformeasuringmuscletone includestandardizationof touch and considerationof the musclelengthat which a group of musclesis to be tested.The examinermustbe awaretlat touchinsthe subiect'sskin, eitherwith a hand or wirh an initrument, can influencemuscletone. The handholdsand inshument placementmust therefore be consistent for accurateinterpretationand replication.The length at which a specificmuscle'stone is testedmust also be standardized.Becausemuscle tone differs with passivebiomechanicaldifferencesat the extremesof range,and rangeof motion (ROM) canbe alteredasa result of long-tem changesin tone, the most consistent length to measuremuscletone is at the midrange of theavailablelengrhoI the muscletested.
THEANATOMICAL BASES OFMUSCLE TONE ANDMUSCLE ACTIVATION Muscle tone and muscleactivation originate from interactions between nervous system input and the biomechanicaland biochemicalpropettiesof the muscle
Muscleis composedof (1) contractileelementsin the musclefibers,(2)cellularelementsprovidingstructure, (3) connectivetissue providing coveringsfor the fibers andthe entiremuscle,and(4)tendonsattachingmuscle to bone.When neuralinput signalsthe muscleto contractor relax,biochemicalactivityof the contractileelements shortens and lengthens muscle fibers. As the conffactileelementswork, they slideagainsteachother, facilitated by the cellularelementsto maintain structure and the connectivetissuecovedngsto providesupport andlubricationwhile the musclechanges length. The myofilaments, actin and myosiq are the contractile elementsof muscle.With neurai stimulation of the musclefiber,storagesitesin the musclereleasecalcium ions that allow the actin and myosin moleculesto bind together.The bindingoccursat particularsitesto form cross-bridges Qlg. a-4. Breakingof thesecrossbridges,so that new bondscan be formed at different sites,is mediatedby energyderived from adenosine ffiphosphate(AT?).As bondsare formed,broken,and reformed, the length of the contractile unit, or sarcomere,changes.The cycle of binding and releasingcontinues as long as calcium ions and AT? are presenl Calcium ions are taken back into storasewhen activation of muscleceases.SourceswirlLin the musclesupply an adequateamount of AT? for short-duration activities,but themusclemustdependonfuel delivered by the circulatorysystemfor longer-duration activities. Actin and myosin myofilaments must overlap for cross-bridgeformation to occur (Iig.4-B). When the muscle is sftetchedtoo far, cross-bridges cannot be formedbecause thereis no overlap.Whenthe muscleis in its most shortenedpositiory actin andmyosin run into the stuctural elementsof the musclefiber andno further cross-bridges can be formed. In the midrangeof muscle,actin and myosin canform the greatest of cross-bridges.The midrange, then, is the length which that musclecan generatethe greatestamount force, or tension.This length-tensionrelationshipis of the biomechanical propertiesof muscles.
Ofte . PATHOLOGY AND PATIENT AROBLETIS
SYMMETRICAL TONICNECKREFLEX(STNR) STIMULUS RESPONSE Necktlexed Tonechangesso armsflex,legse)dend
STIIVULUS Neckextended
RESPONSE Armsextend,legsflex
ASYMMETRICAL TONICNECKREFLEX(ATNR) STIMULUS FESPONSE Neckrotationto oneside Tonechangesso jaw limbsextend andskulllimbsflex
SYMMETRICAL TONICLABYRINTHINE REFLEX(TLROR STLB) STIMULUS RESPONSE Proneor supineposition Tonechangestowardtotalflexion notedby labyrinths in head or totalextension
Figure4-6. Reflex responsesto head or nec.l(posrtion.
81
a2
4 o Tore Abnonralities
Midrange
Lengthenedsarcomere
Shortenedsarcomere
Sarcomere Figure4-7.Cross-bridge formationwithin musclefibers. Other biomechanicalpropertiesof musclesinclude friction and elasticiry lriction between connective tissuecovedngsas*rey slidepastoneanothermay be affectedby pressureon the tissuesand by the viscosity of the tissuesand fluids in which they reside. Elasticity of connective tissue results in varying to stretchat differentmusclelengths.When responses tissue becomestaut, as it is when a muscle is fully lengthened,corurectivetissuecontributesmore to the overallresistanceof the muscleto stretch.When connective tissue is slack,it contributesvery little to a muscle'stension.ln fact, when muscleis stimulated to contract while it is shortened,there is a delay beforemovementcanoccuror forcecanbe generated while the slackin d-reconnectivetissueis taken up. The runner'scrouch in lig. 4-1 takesup some initial slackin the quadricepsbeforethe start of the raceto reduceany delayin activation. Bodr activecontractileelementsand passiveproperties of the tissuescontribute to muscle tone and activation. Howeveq muscle tone can be generated from the passiveelements alone, whereas muscle activationrequiresboth activeand passiveelements.
Figure4-8. Relationshipbetweenactin and myosin at lengths. threedifferentsarcomere Physicalagents,such asheat and cold, can change both muscletone and activationby alteringthe accessibility of AfP to the myofilamentsthroughimproved circulationandby changingthe elasticityor friction of the tissues. Physical agents can aiso change the amountof neuralstimulationof the musclefibers.
toMuscle Tone and Neural Contributions Activation NeuralsourcesoI input that contributeto muscletone and muscleactivation come ftom the periphery the s p i n a cL o r d . supraspinb a rl a i nc e n t e r {' F : g . 4 9 ) . "nd Even though multiple areasof the nervous system may participate, all of them must work through the final common pathway, the alpha motor aeuron,
Orc I PATHOLOGY AND PATIENT PROBLEMS
83
major neurophysiologicaltext for a more complete descriptionof known input to alphamotor neurons.
Spinalcord
PeriPheral nerves(conlainbothsensory andmotorfibers)
Figure4-9. Schematic drawing of the nervous system, front view
which ultimately stimulatesmusclefibers to contract (Iig. 4-10).The generation,summation,and conduction of an activatingsignalin alphamotor neuronsare criticalcomponentsof muscletone and activation.In this section,discussionof nerve structureand function will be followed by an accountof some significant influenceson the alpha motor neuron. See a
Structureandfunctionof nerves Nerve cells,or neurons,include most of the components of o*rer cells,including cell bodieswith a cell membrane,nucleus,and multiple intemal organelles that keepthe cell alive.The distinguishingfeaturesof a neuron include the multiple projections,cal)edden drites,that recele stimuli-usually ftom other nerve cells-and the singleaxonalprojectionthat conducts stimuli toward a destination.The axon endsin multiple synapticboutons(Iig. 4-11).Theseboutonstransmit stimuli across the naffow gap, or synapse, betweena bouton and its targetmusclefibers,bodily organs,glands,or other neurons.Although a few specialized neurons can receive electrical,mechanical, chemical,or thermal stimuli, most neuronsrespond to and transmit signalsvia chemicalsknown as neura, tra smitters, Neurotransmittermoleculesaremanufacturedand storedin *re synapticboutons (ltg. a-n). An electrical signalconducteddown an axon causesthe release of thesemoleculesinto the synapticcleft. The molecules crossthe cleft and, if the postsl'napticcell is anotherneuron,bind to one of the chemicallyspecific receptor sites covering the dendrites,cell body, or axon(Fig.4-13). The neurotransmitterdopamine exemplifies the specificity of neurotransmittersand is significantto the study of muscletone and activation.Dopamineis normally found in high quantitiesin the neuronsof the substantianigra,oneofthe basalganglia,which is discussedlater in this chapter.Deficits in the production or use of dopamine result in rigidity, resting tremors.anddiFticulry initiacingandexecuting movement,luall manifesrarions of Parkinson's disease.2l The binding of a specificneurotransmitterwith its receptorsite tendseither to exciteor inhibit *re postsynapticcell.Whether the posts)mapticcell responds, by transmittingthe signalfrom the receptorsiteto the rest of the ce1l,dependson summation, or adding together,of many excitatory and inhibitory signals. Summation may be spatial or temporal (llg. a-M). Input to receptorsitesfrom many different synaptic boutonsat onetime resultsin spatialsummation,and sequential stimulation through the same receptor sitesresultsin temporalsummation.Excitatoryinput must exceedinhibitory input if the sum is to cause signal conduction down an axon. A single neuron
a4
4 . Tofle Abttorlfltlities
Neuronsin descendingiracts
Cellbody in spinalcord Sensoryneurons
:--------+ Spinal tnterneurons fromopposite sideof body
Spinalinterneurons Figure4-10.Alpha motor neuron: the final common pathway ofneural siSnalsto muscles.
ty-picallyreceivesinput from hundredsor thousands ot other neurons. Once excitatory stimulation reachesa particular threshold level, the signal is conducted down the axon in an action potential (having the potential to causean action).The action potential rapidly transforms the membraneof the neuron from its electrochemical state at rest. Membrane transformation occursin a wave of electrochemicalcurrentthat progressesrapidly from the cell body down the axon to the svnapticboutons.
Figure4-11. A typical alpha motor neuron.
At rest, the neuronal membrane separatesthe concentrationo[ sodium (Na+), chloride (Cl-), and potassium(K+)ions on the inside of the cell from the concentrationon the outside. Na+ and Cl are in greaterconcentrationoutsidethe cell,andK+andnegatively chargedprotein moleculesare in greatetconcentrationinsidethe cell.In addition to the chemical differenceacrossthe membrane,an overall electrical differenceexists immediately adjacentto the membraneof approimately -20 mV, with the insideof the membranemore negativethan the outside.Biological systemswith a differencein chargeor concenkation betweentlvo areaswill come to equilibriumif possible. Becauseof the electrochemicalditference,the membraneis saidto havea restingpotential,which is the potential for movement of ions toward equilibrium if the membraneallowed it. Channelsor holes in the membrane allow selective movement of ions from one side of the membrane to the other Allowing movement of only some ions Potassiumions makesthe membranesemipermeable. move fteely acrossthe membranewhen the neuronis at rest. Somemembranechannelsopen and closeat specific times to allow certain other ions to move gradieats.Still other accordingto their electrochemical ions are actively moved through the membrane from one sideto the other in a biochemicalpumping processThis processrequiresenergybecausethese ions are
85
O e. PATHOLOGY AND PATIENTPROBLEMS
P41. lvlultipledischargesfrom neuronA will activateneuron B temoorallv.or in time
NeuronD
2. Discharges fromneuronsA, C, andD willactivateneuronB spatially, or frommultiplespaceson neuronB Fiqure4-14. Temporal and spatial summation of input to Figwe4-12, Synapsebetween pre- and postsynapticneurons at rest.
Figure4-13. Synapsebetween pre- and postsynapticneurons when activated.
gradienqthat is, moved againsttheir electrochemical they move farther away from equilibrium of chargeor concentrationon the tvvosidesof tne memorane. When an action potential sweepsdown an axon, channelsin the membraneopen,allowing Na+ions to rush into the cell,therebyalteringboth the concentration and the electricaldifferencesbetweenthe inside and outside of the membrane. Durins the action pocenrial, the polardifferencebewveenthe electrical chargeinside and outside the membranechangesin that location; that is, that sectionof membranehas depolarrzed,with an increasein positive chargeon the inside. A sodium-potassium pump quickly restoresthe electrochemicaldifferencebetween the insideand outsideby transportingNa* ions back outsidethe cell andK* ions backinside.The endresultof the sodium-potassiumpump is repolarizationof that sectionof the cellmembrane. The successive depolarizationand repolarizationof membrane sections continues dovrm the axon until thosechangesstimulatethe reieaseof neurotuansmitters from all of the axon'ssynapticboutons(seeFig.4-13). The speedof conductionof an actionpotentialdepends on the diameterof the neuronandthe insulationavailable alons the axon. Neurons with smaller diameters have
4 . Tone Abnonnalities
86
slower conduction velocities. Larger-diameterneuronshavefasterconductionvelocities. Insulationspeedsthe ffansmissionof a depolarizing wave by increasing the speed with which the ions move across the membrane. A fatty tissue called myelin, provtded by Schwann cells in the peripheral in the cennervoussystem(PNS)andoligodendrog,tes tral nervoussystem(CNS),is the sourceof insulation for neurons.Myelin wraps around the axonsof neurons,leavinggapsat regularintervals(Iig. 4-15).When a depolarizing wave travels down an axon, it moves quickly down sectionswith myelin on them and slows at gapswhere no myelin is present,at the nodes of the signalslowsatthe nodesandtravRanvierBecause els very quickly between nodes,it appearsto jump all the ftom one node to the next in rapid succession This lumpway to the endof all the axonalbranches.z2 conductlon ing is refenedto assabatory Qi.g.4-1Q. The fastest conduction velocities recorded in human nervesare up to 70-80m/sec.23Temperature chanqescan alter these velocities.When axons are
Figule4-15. Myelin formed by Schwanncellson a periphetal neuton. Myelin
Node of ranvier
Figure4-16.Saltatoryconductionalong a myelin-wrapped axon.
cooled, as with the application of ice packs,nerve conductionvelocity slows by approximately2 m/sec for every 1"Cdecreasein temperature.24 Once the signalreachesthe synapticboutons and neurotransmittersare released,there is a slight delay for the moleculesto move acrossthe svnaptic cleft. Evenat 200Angst om units (200x 10-Ibm), it takes time for diffusion and then reception by the next neuronor targettissue.In addition,the receivingneuron must sum all of its input, both excitatory and inhibitory, before an action potential can develop. Therefore, larger numbers of connectionsbetween neurons take longer to transmit a signal than do smallernumbers.The shortestconnectionknown is connection of the musclestretch the singlemoxosynaptic reflex, observablewhen certain tendons are tapped (Ilg. 4-17).It is so called becausethere is only one synapsebetween the sensoryneuron receiving the stretch stimulus and the motor neuron transmitting the signalto the musclefibersto contract. Monorymapticffansmissiorlasrecordedftom muscle stretch (tap) to initiation of muscle stretchreflex contraction,hasbeenrecordedinas little as25 millisecondsat the arm.25The length of time betweenstimuareinvolved lus andresponsewhen multiple s1'napses is longer For example,when the arm is working to move a loadandvisualinputindicatesa suddenchange in the load,it takesapproximately300millisecondsfor the arm musclesto respondto that input.25[f a person unexpectedlysaw a ball begin to drop off a shelf 1 meter aboveher, the ball would fall approximately44 centimetersbeforeshecouldstartto move to catchit.
Stimulation ofMuscle Sources ofNeural Thealphamotorneuron Muscle tone and activationdepend on alpha motor neuronsfor neural stimulation.An alpha motor neurorq which is sometimescalled an axteriorhorx cell, hansmits signalsfrom the CNS to muscles.With its cellbody in the ventralor antedorgray matter or horn of the spinalcord (Fig.4-18),its axon exits *re spinal cord,andthusthe CNS,throughthe ventralnerveroot. Each axon eventually reaches muscle, where it branchesand imeruates benveen6 (in the eye muscle$ and 2000 (in the gastrocnemiusmuscle)muscle The musclefibers innerfibersat motor endplates.26 vatedby a singleaxonwith its branches,which is one motor unit (Iig. 4-19),all conffactat oncewheneveran actionpotentialis transmitteddown that axon.A sin-
Otre t PATHOLOCY
AND PATIENT PROBLEA"IS
87
Spinalcord (lrans\,€rsecross section) Peripheral nerye
Musclespindle
la afferentnerve
alphamotorneuron
Figure4-17. Monosynaptic muscle stretch reflex.
Ventral(anterior) horn Figure4-18. Alpha motor neuron: cell body in anterior horn of spinal cord, axon exiting spinal cord. gle action potential generated by the alpha motor neuron cannot provide its motor unit with a graded signal; each action potential is "all or none." When sufficient motor units are recruited, the muscle contracts. More forceful contraction ofthe muscle requires an increasednumber or rate of action potentials down the same axons, or recruitment of additional motor units. Activation of a panicular motor unit depends on dte sum of excitatory or inhibitory input to *rat alpha motor neuron (Fig. 4-20). Excitation or inhibition, in tun, depends on the sourcesand amounts of input via the thousands of neurons tlnt synapse on that one particu-
Figure4-19. One motor unit: alpha motor neuron and muscle fibers irLnervatedby it. lar alpha motor neuron. An understandingof the sources of input to alpha motor neurons is essential when atl-emptingto conffol motor unit activation or altermuscle tone via physical agentsor othermeans Clable4-3).
Inputfromtheperiphery The PNS includes all of the neurons that project outside of the CNS even if the cell bodies are locatedwithin the CNS.The PNSis composedof the alpha motor neurons,gamma motor neurons,some
88
4 . Tore Abtonnalities
Actionpotenlialpastthis line
Actionpolenlialpastthisline
Alphamotorneuron
Alphamotorneuron
MOTORUNITAT REST
MOTORUNITACTIVATED
Action potenlialpast this line
Alphamotorneuron OR
IV]OTOR UNITACTIVATED
Figure4-20. Balanceof excitatory and inhibitory input to the alpha motor neuron at rest and when activated.
p
l-S Irrp,r. ,o Alpha Motor Neu(ons (Simplified) From peripheral receptors
From spinal sources
From supraspina[ sources
Musclespindlesvia Ia sensoryneurons
Propriospinalinterneurons
Cortex, basalgangJiavia corticospinaltract
GTOs via Ib sensoryneurons
Cerebellum,red nucleusvia rubrospinal
cutaneousrecePtorsvia other sensoryneurons
Vestibularsystem,cerebellumvia ue(rih',1^<-ih,l
r.,.r"
Limbic system,autonomicnervous systemvia reticulospinaltracts
autonomic nervous system effectorneurons,and all of the sensoryneuronsthat carry information from *re periphery to the CNS. In this section,discussion will focuson sensoryinput from muscles,joints, and skin to alphamotor neurons. Sensory neurons can stimulate neurons in the spinal cord directly (Fig. 4-21), so they can have a quickerandlessmodulatedeffecton alphamotorneurons than some otlter sourcesof input that must traversethe brain. Quick, relatively stereotypedmotor responses, cal7edreflexes,commonly result from unmodulatedperipheralinput. At its simplest,a reflex involvesonly one synapsebetlveena sensoryneuron and a motor neuron;that is, the monosynapticstretch reflex definedpreviously(seelig. 4-12).In the monosynapticcase,for everyactionpotentialin the sensory neuron,the motot neuronreceivesthe sameunmodu-
lated input. Most reflexes,however,involve multiple inteneurons in ahespinal cord between the sensory and motor neurons.Becauseof the volume of input from multiple neuronsand sources,the actualmotor responseto a specificsensoryinput canbe modulated accordingto the contextof the action.27 The presumed objective of many peripheral sourcesof inpucin chenormallyfunctioningnervous system is to protect the body, counter obstacles,or adaptto unexpectedoccuffencesin the environment duringvolitional movement.Becauseof its directconnectionsin *re spinalcord,peripheralinput canassist function even before the brain has received or processedinformation about the successor failure of the movement.Peripheralinput also influencesmuscletone and is ftequentlythe medium throughwhich physicalagentseffectchange.
Ore . PATHOLOGY AND PATIENT PROBLEMS
89
Peripheral cutaneous receptor Figure4-21, Sensoryinput into spinal cord to alpha motor neurons.
Muscle spindle Insidethe muscle,lying parallelto musclefibers,are (Frg.4-22).When sVixdles sensoryorganscalledmuscle a muscleis stretched,asit is when a tendon is tapped to stimulatea stretchreflex, the musclespindlesalso arestretched.Receptorswrapped aroundthe equatorial regionsof the spindlessensethe lengtheningand send an action potential through sensoryneurons, specifiedas tyye Ia, rnto the spinal cord. A primary destinationof this signalis the pool of alpha motor neuronsfor the musclethat was stretched(homonymousmuscle).If the excitatoryinput of the Ia sensory neurons is sufficiendy greater than any inhibitory input from elsewhere,the alpha motor neuronswill generatea signalto contracttheir associatedmuscle fibers. Severaltaditional facilitation techniquesfor increasingmuscle tone use the stretch reflex: quick stretch,tapping,resistance, high-frequencyvibration, and positioning a limb so that graviry can provide stretchot resistance. Another destination for signals transmitted by type Ia sensoryneuronsfrom the muscle spindle is the pool of alpha motor neuronsfor the antagonist muscle to inhibit activity on the opposite side of the joint. In other words, signalsfrom the muscle spindlesin the bicepstend to excitealphamotor neurons of the bicepsand to inhibit those of the triceps (Iig. 4-23).This is an exampleof reciprocalinhibition,
which helps ensure that a muscle is not working againstits antagonistwhenit is activated. Becausemuscles shorten as they contract, and musclespindlesregisterlengtheningof musclesonly if they are taut, spindlesmust be continuallyresetto eliminate saggingin the center portion of the spindles. Camma motor neuronsinnervatemusclesoindlesat the end regionsand.when stimulated,ciuse the equatorial region of the spindle to tighten (see Iig. 4-22). In other words, gamma motor neurons sensitizethe spindlesto changesin musclelength.28 Gamma motor neurons are typically activated at tlre sametime as alpha motor neuronsduring voluncoactitary movement, a processcalledalVha-gamma vation.zgIn addition, gamma motor neurons can be activated separatelyfrom alpha motor neurons to preparethe musclespindleto senseexpectedchanges in length that might occur during voluntary movement. A good exampleof this occurswhen someone walks acrossan icy sidewalk, knowing that a slip is probable. Gamma motor neurons are activated to increase spindle sensitivity so that muscles respondvery quickly if one foot startsto slip on "an ure lce. Golgi tendon organs Colgi tendon organs (GTOs) are sensory organs located in the connective tissue at the junction
90
4 . TotrcAbuol
nlities
juncBecause of their locationat the musculotendinous tion, CTOs have been shown to signal a maximal stretchof the muscleand are thus thought to protect agairstmuscledamage.JU CTOshavealsobeenshown to be extremeiysensitiveto activecontraction,particularly small amounts of muscle tension.3lHouk and Hememan estimatedthat dresesensoryreceptorscan respondto activationof oneortwo singlemusclefibers thatareLn5efles with thatL I U. ' CTOsarelimitedin their ability to sensesteadyor larger1eve1s of muscular tension, however, so *rey must be supplemented by Ia sensory many other types of peripheral input in signaling overafferent neuron Encapsulated all musclecontraction.32 muscle spindle CTOs rransmit signals via type lb sensory neuronsto the alphamotor neuronpools o[ both the homonymous and antagonist muscles. The input to homonymousmusclesis inhibitory to stop signaiing the muscle fibers to contract.This spinai reflex responseis called autogenicinhibitiou.The input to alpha motor neuronsof antagonistmusclesis excitatory to signalcontraction.The purposeof the CTOs is regulatoryduring activemusclecontraction,possibly ro helppur on rhe brakesduringacrivarion. Note that musclestretchcanprovide contradictory input to an alphamotor neuron.Quick stretchstimuIatesthe spindlesto registera changein length,facilitating muscle contraction. Prolonged stretch may initially facilitate contractionbut ultimately inhibits contractionas the GTOs registertension at the tenFigure 4-22.Musclespindlewi*Lin a muscle. don and signalinhibition to the homonymous alpha betweenmusclefibers and tendons(Iig. 4-24).They motor neurons.Prolongedstretchis thus traditionally function in serieswith musclefibers,which is in conused to inhibit abnormally high tone in agonists trast to muscle spindies,which function in para1lel. and facilitate antagonist muscle groups. Inhibitory Figure4-23" Reciprocal inhibition: muscle spindle input excites agonist muscles and inhibits antagonistmuscles.
Peripheral neryes
Biceps
Ia afferentnerve
Peripheral
One . PAIHOLOCY AND PATIENTPROBLEMS
GTOs
Figure 4-24.CTOswithin a muscle.
pressureon the tendon of a hypertonicmuscleis also drought to stimuiate the CTOs to inhibit abnormal muscletone in the agonistswhile facilitatingantagonists.33 Thesetechniquesshouldbe consideredwhen positioning a patient for application of physical agentsor other modalities.
9l
Cutaneous receptors Stimulation of cutaneoussensoryreceptorsoccurswith every interaction of a person's skin wirh the extemal world. Temperature,texture, pressure,pain, and touch are all transmitted through these receptoff. Cutaneous reflex responsestend to be more complex than muscle and tendon responses, involving multiple muscles. Painful stimuli at the skin, like stepping on a tack or touching a hot iron, will ultimately facfitate alphamotor neuronsof wi*rdrawal musdes.In a flexor withdrawal reflex, the hip and knee flexors or elbow Bexorsare signaled to pull the foot or hand away ftom the painful stimulus.If the body is upright when the painful stimulus occurs, a crossedextension reflex is likely. Alpha motor neuronsof the oppositeleg'ship andkneeextensor muscleswill be facilitated so that when the foot is withdrawn ftom the painful stimulus, the other leg can supportthe individual's weight (Fig.4-25). Becausemusclesare linked to eachother neurally via spinalinterneuronsfor more efficientfunctioning, traditional antagonistson oppositesidesof joints are frequendy inhibited when a particular agonist is facilitated. Ior example, when the biceps muscle is facilitated during a withdrawal reflex, the triceps Figure4-25. Ilexor withdrawal and crossedextensionreflexes.
92
4 . ToneAbnorualities
muscle of the same arm is inhibited. Likewise, if a muscleis contractingstrongly,many of its synergists wiil alsobe facilitatedto contractto help the function of the orisinalmuscle. Treatrnent techniquesthat use cuaneous receptors to increase muscle tone include quic( light touch; manual contacts;brushing; and quick icing. Techniquesthat use cutaneousreceptolsto decrease muscletone include slow stroking,maintainedholding, neutralwarmth, and prolongedicing.33The facilitative techniquesprobablydirect attentionto the part of the body that the patient is about to activate,and the cutaneousreceptorsregisterchangesin input. The brain seemsto alert itselfwhen changesare occurring, preparingitself to respondwith movement, which necessitates increasesin muscletone. The inhibitory techniquesbegin in a similar way to the facilitative techniquesby directingatt€ntionto the relevantpart oI the body.Because o[ the slow repetitive.or maintained nature of the stimuli, however,the cutaneous receptorsadaptto the input. The brainignoreswhat it alreadyknows is there,andgeneralrelaxationis possible,with a diminution of muscletone. Becausecutaneousreceptorscan alter muscletone, any physical agent that touches the skin can change tone, whether the touch is intentional or incidental. Thus it is necessary to considerthe locationandtype of cutaneous input provided whenever using physical agents,especiailybecausethe effect on musde tone may be counterto the effectdesiredfrom the asentitself. Inputfromspinalsources In addition to the sensoryinformation from the periphery that signaisalphamotor neurons,circuitsof neurons within the spinal cord also contribute to excitation and inhibition. Thesecircuitsarecomposedof intemeurons, neuronsthat con-necthffo other neurons.Propriosoinal pathwaysareone rype of neuralcircuitthat iommunicate intersegmentdly, between different levels within the spinal cord. They receive input kom peripheral afferents,aswell asfi'om many of the descendingpathways that arediscussed below,andhelpproducerynergiesor particularpattemsof movements.34 Ior example,when a client flexesthe elbow forcefully againstresistance, propriospinalpathwaysassist in the communicationbetvveenneuronsat multiple spinallevels.The resultis coordinatedrecruitmentof synergisticmusclesthat add force to the movement. That same resistedarm movement also facilitates flexor muscleactivity in the oppositearm via the pro-
priospinal pathways. Both of these principleshave beenusedin therapeuticexercisesto increasethe tone and forceoutput from musclesin oersonswith neuroIogicaldysfunction.ss'3Supraspinal sourcesof input Suyrasyinalrefersto CNS areasthat originate abovethe spinal cord in the upright human (see Frg. 4-9). Ultimately these brain areasinfluence alpha motor neurons by sending signals down axons in a variety pathways.Any voluntary subconscious, of descending or pathologicalchangein the amount of input trom descending pathways alters the excitatory and bhibitory input to alphamotorneurons.Suchchanges, in tufl\ alter muscletone and activatiorl dependingon the individual and the pathway or tract involved. Severalof the major descendingpathways and their in relationto influenceon motorneuronsarediscussed the brainareasto which they aremost closelyrelated. Sensorimotor cortical contributions Volitional movement originatesin responseto a sensation,an idea,a memory or an extemalstimulus to move,act.or respond.The decisionro move is initiatedin tlre cortex,with signalsmoving rapidly among neurons in various brain areasuntil they reach the motor cortex.Axons ftom many of the neuronsin the motor cortex form a corticospinaltract (from cortex to spinal cord) that runs through the brain, mosdy crossesat the pyramidsat the baseof the brain stem, and descendsto synapseon appropriatealphamotor neuronson the opposite side of the spinal cord (Iig. 4-26. When the alphamotor neuronshave sufficient excitatoryinput,a;tion potentialssignalall the associated musclefibers to contract.Corticospinalinput to alpha motor neuronsin the spinal cord is primarily responsiblefor voluntary contractionand contributes lessto muscletone. Cerebellum Ior everyset of instructionsthat descendthrough the conicospinaltract to signalposture or movement,a copy is routed to the cerebellum(seelig. 4-2Q. The neuronal activity of the cerebellum functions to comparethe intendedmovementwith the sensoryinput it receivesabout the actualmovement.The cerebellum registersany discrepanciesbewveenthe signal from the motor cortex and the accumulatedsensoryinput from musclespindles,tendons,joints, and skin of the body during the movement.Cerebellaroutput helps
One . PATHOLOGY AND PATIENT PROBLEMS
Midlineof brain, brain stem, and spinal cord
Ehainstem
C€rebellum
Conispinal tract Peripheral nervesto right side of body
tract schematic pathwayfrom 4-26.Corticospinal Figure andspinalcord. Jortexro cerebeLlum co(ect for movement errorsor unexpectedobstacles io movementvia the cortex and the red nuclei in the brain stem.The red nuclei,in tum, cansendsignalsto *re alpha motor neurons through the rubrospinal nacts (RuSTs).Ongoing correctionis successfulonly it a movemenris comduring slower movemencs: pletedtoo quickly to alte5information about the suc-
93
cessor failure of the movement can improve subsequenttrials.Both corticospinaland rubrospinalinputs to alphamotor neuronsfunction primadly to activate musculature.Direct influencesof the cerebellumon muscletone and posture are mediatedthrough connectionswith the vestibulospinaltracts0/STr. Basal ganglia The basalgangliafunction asa movement-and tonemodulating system.Any volitional movement involves processingthrough connectionsin these five nuclei, or groups of neurons:putamen,caudate,globus pallidus, subthalamicnucleus,and substantianigra (Iig. 4-22). Multiple chains of neurons looping through thesenucleiandbackto motor corticalareasinfluence the planningand posturaladaptationof motor behavior. Dysfunction of any of the nuclei of the basalganelia is associatedwith abnormaltone and disordered movement.In the exampleftom the beginningof the chapter,Mrs. H's tone and movementpattemsexemplify wvo of the extremeforms of abnormaliryseenin basalgangliadisorders:the rigidity and akinesiaof a freezestateand the wildly fluctuatingtone and dyskinesia associatedwith high levels of the medication usedto treat Parkinson'sdisease. Other descending input The VSTshelp to regulateposture by transmitting signals ftom the vestibularsystem to the alpha motor neuronpoolsin the spinalcord.The vestibularsystem receivesongoinginformationaboutthe positionofthe head and the way it moves in spacewith respectto graviqy.The vestibularnucleialsointegrateand transmit responsesto information received about the movementof the headvia the joing muscle,and skin of rheheadandneck.The VSTsand related receptors tracts generally facilitate the extensor (antigraviry) alpha motor neurons of the lower extremity and trunk The to keepthe body andheaduprightagainstgraviqF. muscles tends to be higher tone of antigravity musde than the tone of other musclegroupswhen a person hasa neurologicaldeficit,partly becauseof the stretch that gravity placeson them and partly becauseof the increasedeffort requiredto stay upright. The reticulospinal tracts S.STs) transmit signals from the reticularsystem,which is a group of neuron cell bodies located in the central region of the brain stem, to the spinal cord. The reticular system receivesa rich supply of input from multiple sensory systems, including vision, auditory, vestibulaE and
94
4 o Tote Abtornalities
Putamen Globus pallidus Subthalamic nucleus
ANTERIOR CROSSSECTION LATERALVIEW
TRANSVERSE CROSSSECTION FiguJe4-21, Basal ganglia widrin the brain: side and cross-sectional views.
somatosensoryand the motor cortex.In additior\ it receivesinput from the auronomicnervoussysrem (ANS) and hypothalamus, reflecting the individual's emotions,motivation,andalertness. Muscletonedifferencesbetweensomeonewho is slumpeddueto sadness or lethargyandsomeonewho is happyandenergeticis mediated dlrough thesetracts. The RSTscan also help regulateresponses to reflexesaccordingto the context of the current movement. Ior example,whiie walking, someonemay stepona sharpobjectwith the nght foog noticing it only as the left foot is leaving the ground. Instead of allowing dre expected flexor withdrawal reflex on the right (which would causethe personto fall), the RSTshelp increaseinput to the alpha motor neuronsof extensormuscleson the right,momentarily permitting weight bearhg on that sharpobject until the left foot canbe positionedto bearweight. Limbic system The limbic systeminfluencesmovement and muscle tone via the RSTsand throush connectionswith the
basalganglia.Circuits of neuronsin the limbic system provide *re ability to generatememones and attachmeaningto them. Changesin muscletone or activation can occur as a result of emotions recalled with particularmemoriesof reai or imaginedevents. For example, fear may heighten one's awareness when walking into a dark parking lot, activatingthe s;,rnpatheticnervous system (SNS)to start planling for fight or flight. The SNS activatesthe heart and lungsto work faster,dilatesthe pupils,and decreases the amount of blood pulsing through the internai organs, diverting that blood flow to the muscles. Muscle tone is increasedto get ready to fight or flee from any potential dangerin the parking lot. Muscle tone may fur*rer increasewith a suddenunexpected noise, but then decreaseagain to an almost limp state when the noise is quickly identified as fwo good friends approaching from behind. Patients may have similar changes in muscle tone wi*r emotionalresponsesto fearsof falling or of increased pain.
One . PATHOLOGY AND PATIENT PROBLEMS
)ummary -Muscletone and muscle activation depend on the normal compositionand functioning of the muscles, *re PNS,and the CNS.Although both biomechanical neuandneuralfactorsinfluencemuscularresponses, ral stimulation through the alphamotor neuronsis a powerful influenceon both muscletone and activarion, especiallywhen the muscleis in the midrangeof its length.Multiple sourcesofneural input, both excilatory and inhibitory are required for normal funcrioning of the alpha motor neurons (seeTable 4-3). Ultimately the sum of all the input determinesthe amount of neurally derived muscle tone and activamuscles. don seenin the associated The assumptionin this sectionhas been that the body is intact. The motor units, with both the alpha motor neuronsand the muscle fibers, have all been functioning normally and receiving normai input ftom all sources.When pathologyor injury affectsthe muscles,alpha motor neurons,or any of the sources of input to the alphamotor neurons,abnormalitiesin muscletone and activationmay result.
MUSCLE TONE ANDIT'S ABNORMAL CONSEOUENCES canresultin abnorManytypesof injuriesor pathologies mal muscletone, some of which are corsidered in this section.One exampleof sucha pathology is depictedin
il V PRll\ilARYlMPAlRl\,1ENT
to muscletone Iie.4-28, with possibleconsequences (see \ t'"n present. also Fig. 1-1).383e unld fulr.tjon an impairmentthat abnormalmuscletoneis considered may or may not lead to functional changes.Evaluation of muscletone before and after a fteahnent canindicate the effectivenessof the treatrnentin reducingmuscle tone or in changing its precipitating condition. Treatrnent decisionswill dependon the role abnormal muscletone playsin exacerbatingfunctional limitations or disabfity, or whether it is lilely to result in future problemssuchasadverseshorteningofsofttissue. of muscle In this section,some of the consequences tone abnormalities are listed and rehabfitative treatof abnormaltone mentsarediscussed, The consequences depend on circumstances,each of which must be assessedalons with the evaluation of muscle tone. Circumstancescouldindude any additionalimpairments the patient has,aswell asthe psychologicalphysiological and environmentalresourcesavailableto the patient. A young, active, optimistic patient tends to have less severefunctional limitations than an older, sedentary depressedpatientwith the samedegreeof impairment. Note that any observedchangesin muscle tone consequentto a pathologicalcondition dependon the remaining input available to that muscle's alpha motor neurons.The remaininginput may includepartial or aberrantinformation from sourcesdamagedby the pathology,normal information ftom undamaged sources,and alteredinput from undamagedsourcesin
at Soine NerveRootComoression
PATHOLOGY
95
Figure 4-28.Classification scheme for pathologies and ih.i
&I
Hypotonicity in SensorydeficitsParesisin Pain thatnerve specificmuscles samemuscles
' .^^""^".-.""
95
4 . Tore Abronnaliries
units. If all the motor units of a particular muscle are involved, the muscle tone is flaccid and muscle activation is not possible;the muscleis paralyzed.Sometimes the :rrm flaccid?aralysris is usedto describesucha muscle'stone andlossof activation.When diseaseor iqury of the alpha motor neurons removes neuronal input from the muscle,denervationresults.Denervation of a muscleor group of musclesmay be whole or partial. Tone LowMuscle Examplesof processesthat may result in symptoms of denervation include poliomyelitis, which affects the Abnormally low muscletone resultsftom loss of the cell bodies;Guillain-Barr6rymdrome,which attacksthe normal alpha motor neuron input to otherwise normal Schwanncellsso that the axora areessentiallydemyelimuscle fibers.Although some muscle or motor endnated; crush or cutting types of trauma to the nervesl may alsoresultin low muscletone,this platediseases discussionis limited to neuronalpathologies.Losses andnerve compression. When poliomyelitis eliminatesfunctioning alpha may result kom damageto the alpha motor neurons motor neurons, recovery is limited by the number themselves,so that the relatedmotor units cannotbe activated.Lossof neuronalstimulationof the muscles of intact motor units remaining.Each remaining may also result from conditionsthat either increase alphamotor neuronmay increasethe numberof muscle fibers it innervatesby increasingits number of inhibitory input or prevent adequate excitatory input axonal branches,This processis known as rearboizfrom reachingthe alphamotor neurors Qig.a-29). ing- lntact neurons may thereby reinnervate muscle Low muscie tone means there is insufficient fibers that lost their innervationwith the desuuction activationof the motor units to preparefor holding or of associatedalpha motor neurons (Iig. 4-30). Such movement. Consequencesinclude (1) difficulty muscleswould be expectedto have larger-than-nordeveloping adequate force output for posture or malmotor units,with more musclefibersbeingir:nermovemengwith secondaryproblemsresultingfrom vated by a singlealpha motor neuron.40Denervated lack of movement,and (2)poor posturecausedby fremuscle fibers that are not closeenough to an intact quentsupportingof weight throughtaut ligaments,as alpha motor neuron for reinnewation will die, and in a hyperextendedknee.Poor postureresultsin cosmetically undesirablechangesin appearance,espe- loss of muscle bulk (atrophy) will be evident. Maintaining the length and viability of the muscle cially with a slumped spine or drooping facial fiberswhile any possiblerearborizationtakesplaceis muscles. Stretchedligaments cancompromisejoint advocated.4o,41 integriry andleadto pain flable 4-4). Recoveryafter injury to the axonsof alphamotor neurons includes the possibility of regrowth of Alphamolorneurondamage If alpha motor neuronsare damaged,electrochemical the axons from an intact cell body, through any remainingmyelin sheathstoward the musclefibers.zu impulseswill not reachthe musclefibers of thosemotor responseto the pathology.When an individual has a movementproblem,he or shewill usewhateverneural resourcesare most availableto solveit. For example,high muscletone may be usefulfor somepatients ifincreasedquadricepstone allows weight bearingon an otherwiseweak leg.
Figure4-29.Inhibition of alpha motor neuron:inhibitory input exceeds excitatoryirput.
Alphamolorneuron
Alphamotorneuron
97
O'E . PATHOLOCY AND PATIENT PROBLEMS
p
4-4
Consequences
of Abnormally
Low Muscle Tone
1. Difficulty developingadequateforceoutput for normalpostureand movement a. Motor dysfunction endurance b. Secondaryproblemsresultingfrom lack of movement,e.g.,pressuresores,lossof cardiorespiratory 2. Poorposture a. Relianceonligamentsto substituteformuscleholding-eventual stretchingof ligaments,compromisedjoint integriqy,pain b. Cosmeticallyundesirabiechangesin appearance, e.g.,slumpingof spine,droopingof facialmuscles c. Pain
Figure4-30. Rearborization of remaining axons to innervate orphaned muscle fibers after polio eliminates some alpha motorneurons.
Regrowth is slow, however, proceeding at a rate of I-8 rr:m/day,al and may not be able to continue if the distance is too far. Again, maintaining the viability of muscle fibers while regrow*r takes place is advocated.40Recovery following Guillain-Barr6 syndrome depends both on remyelination of the axons, which can be fairly rapid, and on regrowth of any axons that were secondadly damaged during the demyelinated pei.od.42
Rehabilitation following alpha motor neuron damage Rehabilitation of patients who have denervation hcludes treatmen* that faciiitateactivationof alpha motor neurons.In the past, physicalagentsincluded electricalstimulation to facilitatemusclefiber viabil-
ity while axonsregrewor rearborized.Electricalstimulation for this purpose has become controversial, with evidencethat the quiescence ofdenervatedmuscle may actually trigger regrowth of neurons (see Chapter B).Additional physicalagentsdrat are used after alphamotor neuron damageincludehydrotherapy and quick ice.33,a3 Becauseof buoyanry, hydrotherapy may be used to support the body or limbs and resist movement with range-of-motionexercisesin the water43 The combination of buoyancy and resistancecan help strengthenremaining or retuming musculature(see Chapter9). Quick ice (seeChapterQ or light touch on the skin over a particularmusclegroup adds excitatory input to any intactalphamotorneuronsvia cutaneoussensoryneurons.oo
9A
4 . Toqe Abqotmalities
Other treatment options include range-of-motion exerciseand therapeuticexerciseto maintain muscle length and joint mobiliqy and to strengthen the remainingmusculature.Treatmentalsoincludesfunctional training d:at teachespatients to compensate for the movement losses they have experienced. Orthotic devicesmay be prescribedto supporta limb tor function while the muscleis flaccid or to protect the nerveftom beingoverstretched. Note that excitatoryinput to an alpha motor neuron that is not intact will be ineffective.The alpha motor neuronthat is not intact cannottransmit information to its relatedmuscle fibers, either to change tone or to contract voluntadly. Also, if alpha motor neuronsare damagedin a cut or crush in1uryor by compression,local sensoryneuronsbringinginformation in the same nerve would also be damasedand unableto provide sensoryinput. Insufficientexcitationof alphamotorneurons If a pathologyaffectsperipheral,spinal,or supraspinal sourcesof input to alphamotor neurons,but doesnot affectthe alphamotor neuronsor musclefibersthemselves,low muscletone may result.The alphamotor neuronsmay be stimulatedto transmitinformationto muscle fibers to contract if excitatory input can be raisedto a higherlevelthan inhibitory input. Any condition, however,that prohibits alpha motor neurons ftom receivingsufficient excitatory input to activate the musclefiberswill resultin decreased muscletone. lmmobilization One condition that altersperipheralsourcesof input to the alpha motor neuron is applicationof a cast to maintain a position during healingof a ftacture.The cast applies a fairly constant stimulus to cutaneous receptorsbut inhibits receptionof the vadety of cutaneous input ordinarily encountered.The cast also inhibits movement at one or more joints. restricting lengtheningor shorteningof the local muscles.Alpha motor neurons are thus deprived of normal alterationsinmusclespindle,GTO, orjoint receptorinput. When the cast is removed, the result is typically a measurablelossof strengthin the musclesand a loss of ROM in the joints. Muscle tone is also affected, witl-r decreasedactivation of *re motor units and increasedbiomechanicalstiffness.Becausethe neural and biomechanical components of muscle tone counter one another in this case,the actual change in resistanceto passive sffetch must be carefully
assessed.The known effects of immobilization in decreasingmuscie tone have been used deliberately to lower hypertonicityin severecases.aa Stroke or head injury Other ways to affect supraspinalinput to the alpha motor neurons are through loss of blood supply or direct injury to cortical or subcorticalneurons/ as occurs with strokes or head injuries. The resulting muscletone changesdependon the remainingproportion of excitatory and inhibitory input to the alpha motor neurons.For example,if the descendingtracts are destroyedon one side,volitional movement and muscle tone may be lost in the associatedmuscles. However,most of the alphamotor neurongroupsthat receiveinput from multiple descendingkacts will not loseall descendinginput. Thosealphamotor neurons must adapt to a new proportion of excitatory and inhibitory input when the input from the damaged tractsis lost. The usualprogressionfrom flaccidityto increasedtone aftera stroke36 may be a resultof adaptation to new levelsof inhibitory and excitatoryinput. The predictionof muscletone changesin a particular individual after a strokeis complicatedby the fact that lesions within the supraspinalareas do not always completely eliminate the corticospinaltract. The portion of the tract that remainscan still be used to signalvolitional movement.In addition, although most of the fibers of the corticospinaltract crossto slmapseon the oppositesideofthe body ftom *re origin of those axons,some of the fibers do not cross. Therefore even if all of one corticospinaltract is destroyed,some fibers of the opposite corticospinal tract may provide enoughinput to alpha motor neurons for the tone in someof the musclesto remainrelativelynormal. Rehabilitation to increase muscle tone Physical agen* are not often associatedwith the rehabilitationofpatientswho havehad a stroke,head injury or other supraspinallesions.However, they canbe a valuableadjunctto the therapeuticexercises, orthotics, and functional training o[ traditional neurorehabilitation.s,36 Electrical stimulation, biofeedback,hydrotherapy,and quick ice may all be used.33 The intent of any treatment choice is to affect the alphamotor neuronsvia the remainingintact pedpheral, spinal,and supraspinalsourcesof input. Quick icing and tapping, for example,are facilitative techniquesthat can increasetone via cutaneousand mus-
Oqe . PATHOLOGY AND PATIENT PROBLEMS
99
ce spindlereceptors,respectively,and, when paired However, EMC studiesof patientswith hypertonic"r:d-r voiuntary movement, can increasefunctional ity haveshown essentiallyabsentactivity in the planscror output. Electricalstimulation might be comtar flexors during swing, as in normal gait.7Another t=ed with resistanceof the musclebeine stimulated study of upper extremity function found deficitsdue - of synergistic musclesto increase tone-andactiva- to inadequaterecruitment of the agonists,not by =3n via intemeuronsof the spinalcord.Many authors increasedactivity in the spasticantagonistmuscles.4T :;ve describedin much more detail the treatrnent Instead,voluntary movement is hindered by slowed =oices availableto the rehabilitation specialistfor and inadequate recruitment of the agonist and =creasingmuscletone and motor output in patients delayedterminationof agonistcontraction.4 a'tro havehad a strokeor head injury.s'33'36'45'a616" On the other hand, someresearchers have shown i:x below summarizes treatment suggestionsto that coactivation of spastic antagonists increases =crease low muscle tone for improved functional with faster movements, substantiating the claim r--dvation, that abnormal activation inhibits voluntary motor control.'8 Additionally, a review of multiple drug studies has revealedimproved function irt 607. to TreatmentSuggestionsfor Low Muscle Tone 707oof paients receivingintrathecallyadministered Ilydrotherapy baclofen,a drug that reducesspasticity.The authors Quick ice statetllat r/spasticiB/ rcductsoncakbe associatedwith (when Eectrical stimulation muscle Ebers are improved voluntary movement,' although it is also innervated) possiblethat a decreasein tone will haveno measuraBiofeedback ble effector evena negativeeffecton function.49 Eght touch Tapping Secauseof the controversy,it cannot be stated Resistive exercises unequivocally that hypertonicity itselt inhibits Range-of-motion orercises voluntary movement. However, other effects of Therapeutic exercises hypertonicity must not be ignored. These include Funcional training (1) muscle spasms that contribute to discomforq Orthotics (2) hypertonicity in a musclegroup on one side of a joint that canresultin contractures(shortenedresting Iength) or other soft tissue changes;(3) abnormal HighMuscle Tone posturesresulting from hypertonicity that can iead -\lany pathologicalconditions result in abnormally to skin breakdown ot pressureulcers;(4) resistance :igh muscletone.Any ofthe supraspinallesionsmento passive movement of a nonfunctioning limb ioned in the previoussectioncould ultimately result that results in caregiverdifficulties during assisted ::r hypertoniciry,eventhough they begin with some dressing, transfers, hygiene, and other activities; :orn of low muscle tone. Only the loss of alpha and (5) possibly a stereotypedmovement pattem rlotor neurons themselveswill be restricted to a that could hhibit alternative movement solutions :rypotonicpresentation;hypertonicity doesnot occur flable 4-5). asa result of lesionslimited to the alpha motor neu:ons.Instead,hypertoniciry is a result of abnormally Pain,eold,andstress righ excitatory input compared to the inhibitory An exampleof a peripheralsourceof input that might rnput to an otherwise intact alpha motor neuron, lead to hypertonicity is input from sensoryreceptors rvhateverthe sourceof that input (seelig.4-20). registeringpain. Cutaneousreceptionof painful stimResearchershave argued about the effects of uli, and the consequentwithdrawal or crossedextenhypertonicity, particularly spasticiry on function. sion reflexes,have already been discussed.Painful Somehave pointed out that spasticityof tlre antago- stimuli to the musclesor joints commonly result in nist does not necessarilyinterfere with voluntary increasedmuscle tension. This muscle tension is a movement of the agonist.a During walking, for form of hypertonicity and may be seen as muscle example,it has been assumedthat spasticiqyin the spasmsin *re paraspinalmusculatureof a person ankle plantar flexors preventsadequatedorsiflexion with back pain, for example.Suchmusclespasmsare during *re swing phaseof gait, resultingin toe drag. known asguardingandarethoughtto be a mechanism
ron. Abtot'rdlities Abtotndlnies 1 . To4' 1'
rO0 100
A B
I
Tone MuscleTone HighMuscle High Abnormally of Abnormally l-S Cottr"q.,.n.es Cor,r"r.,.n.esof 4-5
Par i:*-*il"-m'd
I I
I I
1. Discomfoltorpain lrommusclespasms
3. Abnormalposlure
rranslers dressing,rranslers wi$ bathing, dressing, assistwi$bathing, caregiversro assist effort by caregivers effort Iocreased 5. Iocreased
I
tives aLtema may inhibit developmenrof movementaltematives 6. Developmentof stereot/pedmovementpattemsthat mav -. i n h r b tfunction tru - b o n M a y or o - may m a . onot r inhibir 7. May
I I
4. Skin breakdown
I
I
usedtoavordfurrnerpain'Luardinsprobably\asaAntaSofustscdnbesdmula|edwl!,Llreslscede\erc (seeLhapleru) slimulatron co-n- elecrrical .omponelras wel' as a peripheral supraspinal I the limbic and n\us pon".ri, bec"u"" dte emotions I Spinalcordinjury ;ystem aresoheavilyinvolvedint'\e inlerpretationof I
;ii"ii::::'r'.,:;'".respondsrocodviapedp' ::*#i:':'Ji"J1:#?(i"JLH",i.",TilI is inhibitory and excitatory input trom supcsprnal systems.when homeostasis
I eral and supraspinil t hel saJJreceiveinput.kom propnosptnal sources. ard lhe body mry rhre.r.ned,nuscleron" increases I or rlle lesron l beeLnto shre:. Mu"cle lone also tends to increase and other neurons below Lhe le\el Immedialelyfo[owin8 the iniuly' f.oYev:I' lh: n:ry' I w;h otherttueals,r€gisteredas stress.Hypertonicitv ou' cysremic rr?ically trl a sta|f,called,tlt at ',ao'b,n I nay be palpablern various mu"cle Crouos such as tro.ern'rneshouLdersandneck'whenanindividua|whi(hitshutsdo\aa|a|andbelow|helevel may lasrtor\oursot weeksandI rniury I}e condrrion reeisrersmorpqeneralpanolperceivesdsrtuarionas -tf" tlaccid to.le ot *le alteLtedmuscles by the is marked .ell-esreem The nus body or ro '-hi.a,"n ne ,o I level reflexaclivity]ike the mus of spinal the loss and for fighl or fli8ht, and Lhereslofrhe clesareprelparing l
bodyi'""g'"g"di"oth;.sNSresponses. :fffi;*H,yJ."*:1fr1j,H,,',:"::;:,Hi:
LheSCIalows;lpha motoinelrons beLowthelewl ofl f4;atment for reducing high tone splllPadentswith hy?erlonicitydueto pai4 cold,or stress the injury to respondespecialyeasiLyto musd€ thusI The hypeftorurty input cutaneous dle, GTO, or can be treated-in severalways. The first and most I apparentis known as spaslicitysince.quickstretchl effective measr.rreis to remove the source of the elicits Sreaterlesistancethan slow stretch hvpertonicity; fteat the biomechanical cause of a\e l Oui.k stretchmay occurnof onl/ when $e mus-I *r-. lb. o"uenr,or :lleviare ti" sness Wlren "!i". for rone b-urak? u h:r.everl tesLed clesarespeciticallv not poss'be not appricableor ih""" '""r.rr..;r. the weight ot a limb sudd€rlyl otherwiseineffecdve,treatmentto decreasemuscle lhe patienlmovesand -e pull on the musdes-for exampleal exedsa differe.lt axdrionrechnique' tone md) ndude edJ(auon ir mayl level EMGbi;fe.dback,Lhcu"eofneurralwannmorhear patlentwhohasa complere-thora'ic ,n-ury
-t'j,i'j::' l:f,ilrfi[::Tru"': ili.ff i;: H: H:i'j " ":,1::::,ix'jniJ:?;;*'
relaxation ol a panicular muscle group$ Muscles ro 'e'axor dire.rl**rth ue:balcue" canb. aooroacl'ed rruscle relaxauon. ro elcit towels uooltl:r,onetrold indirectly,bv Aliematively,musclescanbe approached in reciprocal wiich results stimulating tire antagonists,
andlowersasonistmuscletone. inhibirionof asonists
tifted, the foot hangs down with Lhe an*]e, pLantar-I flexed when chelegis placedthe weiShrrandsool 3n'qlemovespdssively intol rneballofthefoorandc,he relativedorsiflexion lf the foot Placemenris qujc&l the piantar flexors are quickly stretched and cLonusl
mavbeseen
l
the hl,petdni.ity k geak on oneside Frequendy, oI a joint 6,n on L\e otAerbe.ase L\. loc of gnviqr' F unidn{tio.t on tAe ms of a linb. Bdu* n\. parlmi wiL\ scl bs m acri'e novenmr dr:t Gn romcr the h'"etun.iq, nusle shofreninsends $ o(ur in L\e tus.l* L6:r n rcbtivet noft hyp.donic.The bionechani.:l stiltrs of the hrpd 6ni. n$cls $us imres6, :d .oMctofts cn d.vdop Su.h.otuactofts mi.nibitturctios suchs di.$n$, tsfeB, andpositionnrsforpa$ure reliet r@th g ttw. rton ldtt loll owlng SCI nb.tive Gnse-of.nohon qeEises,5051prclorsed ;fteb,33 posirionins!r othoiie to mainbin nhcdonal m$.1e len8rh,lo.a1dr sy*ehi. oediatio$, trnd sucettl have beenlsd b .onEr ?ither L\e hypa&niciry or rAe ..ndadurcs ink&d.8 virh nnction. Heat couldbe usedb.for beloresEetchi.€ dI shonenedmuscles(seeChapEr O, blt t nu* be .aEtully nonit ied be.auseol L6epatieosspo@tial in*ditivig/ b painor dedeasd *tration SelowL\e GveloI dr spinalcoid injrry. orhe locrt applied one iiliSiti.€ L\.iapies, such as pnlongcd i.iry, lould tleoreti€Iy alleviak h),Tdoniciry in pati.ns lvirh scl Howeve! researchn hcki.€ eith{ to cor. am or to rejed ihe ustulnes of n\e* a8enbin this popdation.F$ctiml electial stinulation gEs) has alsobecru*d to intreasen\eircrion oI p{etic nus d* in L\is population (seeChaper 3) bui !o! for
d\ar afiecr hlrnission of neucl impulrs in the CNS,like nulriple slerosn (ILS)qn resultin hypq. tori.irr Hypeionicity in patienb lo11owin8all oI thef patholosts h the Esult oI a .hangein inpur b :lph,ndtorn rbns(s..FU a 20)Theexftntorthe paiholo&/ ddtrnines {hdh{ many mu*ld ChrPs ae affeded or ody a Gq and whei!- alphanotol neuoN b a pani.ular m$cle 96|plo* a1lor only sone of a paticular sourceoI srpraspinalinplt. nypertmbhy: Nin.ry inpaiment ot adaprne
The reuiophysiologi.:lne.hanisnof b,petuni.iq k in sob. disprE. A varieryof deahent appnches addresb,peibnici4' bafd on asunptiDns aboutlhe way $e neNoussysen fun.tions Ll one apprca.h, developedby Bobath,sthe nenoussFEm n duned to tunction as a hEcrchy in *hnh Lhes|praspitrl cnec .ontdl L\e sFiml ftnks ol nov.nat, and sbnom:l iotus' iesLftsnon los of mnibibry .on. tul fron hjghtr cenEn The csulbnt n\dapelti. *que.rt is 6 nomalEe n\e hypetoni.iq belon before fa.ilhting nomal novem.dt In ,noL\ei appGch, the tur.onentd apF6icn, whnh k bas.d on a sysEm ndd€l oI L\e neno's sy*en, each hoe€nent h 3 Frcdld oI smorinotor noriv*ional, bionechmi.:1, and enwomenhl input.e'* Ttr€ pimry goal ol the neFous q,*en id pod!.ing noenent r to aconpltuh i!€ d4ned bs! AIt* a lesiondevelopr,the neio's sysEn !*s its rcraining larimb with SCI nay alsonaw nusde spasm, resourc* to penom novenent bsk. Ht?doni.ir, then,n,y be L\e he* adaptiveepose $e nerous ge.*aUy adibubble b p,inhil sdmuli, exapt i\ar sy*.n .a mke Siven i6 aeailableresourcesafter patidb nay be mwar oI tAepainbedu* sffo9 injury nth{ dxn a ptmary Bult of L\einjrr/ i6elr. s€mlsa*mg hon below[\e kvel of nhei.jur/ donot An enmple of tul o enkd ft*oning h as 6tr1 e.h dreeEbral cotu. Mwcle spasm may a&obe lo{s: p,ti.nh with parsis m sonetlms ablcto use atubuEd b vbeGl stimuli su.h .s i urjftry tad tunk :id lowei dtemi./ .xftNor ht"etonidry b i.Gdior dhtend.! bladde(oi3de ot1relinEtul iri lold m upitlr posture In L\is cs, hyperbniciq n ation5t ldentifi.ationandrnoval oI the p:i.ftlstin an adaDtivcresDonse b a.comrfishthe hsk of Frn' uli aie rhe lisr seps in aleviari.3 nusci. spastr. einnis anupn;ht pstuE lrt irimimtiis the hyptr wh.n musdespasmsde penhEnt, teq!€nt, or i.nibit iunctron,and aE withou! idmtinabk and rcmovable bni.ity in sd.h a .as would d.deas luciion udes concumr inftass in .ontoled voluntary mov+ aE .au*s, 3y*enic or lo.aly qe.ad n.diotim m.nt arecliciEd On nlleoth{hand, conkolledmov* soi.tin spcscdh€dtd :Ieviah L\e.5r Getul ev:l mentis alwaysprelenbleb hypetoni.iq, iI i! en be u,tim ot nhesoure oI a nuscle spasn nu* o(!r clicited Contol inplies n\eabiliq,b makechang* in belon anyphtri.:l agdt oi reahenr isapplied a ftspose asodns to envnomenhl dem:ndsl whecas ihe hlp.6ni. exknsorftspore ne.tioned abdveis rclarivet $rcoryped The us of a ${eoLsioN Edn .eiebDl @dLi dnodes or seke, rypedhyperctu.respoBe lof hrchon*em! b bld.k ftrbr:l palst tunos, CNSi.fecriorr or hcadinj!ry r eo n d . o i m l 5 5 6 6ay i.sul! in hypetunicit In additioq .onditions s p o n b n e o s deeo p m e d o t m o n
l02
4 . Toflc Abnothralities
Evidencethat hypertonicity may be an adaptive includesrhe factthat it is not an immediate resDonse ,"qu"la of injury but instead develops over time Iollowing a cortical stroke, recoveryof muscle tone and voluntary movement follows a fairly predictable At first, musclesareflaccidand paralyzed course.36,44 on the side of the body oppositethe lesion,without eiicitablestretchreflexes The next stageof recovery by increasingresponseo[ the musis characterized clesto quick stretch and the beginningof voluntary motor output that is limited to movement in flexor Becausemuscle or extensorpatterns,calledsynetgies. tone and synergy patterns ot movement appear ar approximatelythe same time. clinicianstend to eguate the two, but spasticity and synergy are distinct from each other (seeTable 4-1). Furtherrecovery stages include progression to full-blown spasticity and ultimately the gradual normalization of muscle tone. At the same time, voluntary movement shows full-blown synergy dependence,progressing to the mixing of synergles,.and finally iesolvins to controlledmovementof isolatedmusculature.3i A particuiar patient's course of recovery may stall, skip, or plateauanywhere along the way, but it doesnot regress
anxiety is a criticaiadjunctto any treatrnentintended to reducemuscletone. It a patient has severehypenoniciryor if many that influence areaffected.techniques musclegroups -decrease individual the or calm arousal to ANS the include techniques Such be used. mighr generally warmrh, neutral rocking. slow music, or ioft lietrtine slo* i,roklng. maintajnedtouch,33rotation of the trunk, or hydrotherapy (see Chapter 9), as long as the patient feels safely supported For example, hydrotherapy in a cool water pool is particularly advocatedfor patientswith MS to reducespasticity' Stretchingand cold packsare also of benefit in temof MS, but they lack porarilvr-educing t}e spasciciry of allowing gende b"nefi, ivdroth"rupy t add.d a diminishedpull of wjth ,".rn"-ot--otion exercises gtavrty.""
Rigidity: a consequence of CNS pathology Some cerebrallesions are associatedwith rigidity insteadof spasticity.Head injuries,for example,may result in one o[ two specificpattems of riSidity that mav be eicherconstantor intermittentBothpatterns inciudehypertonicity in the neck and back extensors, the hip extensors,adductors,and internal rotators, the knee extensors,and the ankle plantar flexorsand invertors.The elbows are held rigidly at the sides, Rehabilitation to decrease muscte tone with the wrists and fingersflexed in both pattems, Rehabilitationto address hyperronicity after a elbows are flexed,and stroke depends on whether the clinician believes but in decorticaterigidiry the in decerebraterigidity they are extended.The rwo that hypertonicity inhibits function or instead is a rypesof rigidiryare thoughrto indjcatethe levelo[ nroduct of adaptivemotor control.In either case,the t'h"lesion'ibot e or belowthe rednucleusin the brai'n emphasis is on return of independent function, stem,respectively.In most patientswith head iniury the whether that necessitatestone reduction or however,the lesionis diffuse,and this desiSnationis reeducation of controlled voluntary movement unhelpfui. Two positioning principles can diminish pafiems. be consideredalong Treatmentto reducehypertoniciqyin preparatron rigidity in either caseand should the patient (1) reposition therapies: any other with icing' couldincludeprolonged tor functionalmovement with emphasis listed, posrures to those opposite in inhibitory pressure,prolonged stretch,33inhibrtory flexion hip and flexion trunk and neili slisht casting,sTor positioning. Reeducationof controlled on positiorq supine the (2) avoid and degrees, past 9b voluntary movement pattems could include weight which promotes extensionin the trunk and limbs bearing to facilitate normal postural responsesor via the symmetricaltonic labyrinthine response(see training with directed practice of functional moveTtg.a-Q. ment patterns.4sReductionof hypeftonicity may, irl canresultin biomechanical fugidity, like spasticiqy, fact, be a product of improved motor control in the placement in the long-term after following example.If a patientfeelsinsecurestanding muscle stiffness period of time the longer The position. uprjght, muscle Lone will increasecommensurate shortened positioning to or exercises witli the anxietylevel.If balanceand motor control without range-of-motion the biomechanigreater the group, elongatea muscle are improved such that the patient feelsmore confithe best cure for is Prevention occur. cal clanses that dent in the upright position, hypertonicity will also but of hypertonicity, be reduced.4sPositioningfor comfon and to reduce biomeclianical comPonents
One . PATHOLOGy AND PATIENT PROBLEMS
::-ioticss8 or serialcastingsT have alsobeenusefulin ::Jucing the musclestiffnessrelatedto hypeftonicity. ---:at may be used to increaseROM temporarily ::Iore applyinga castor orthotic. Parkinson's disease usually includes rigidity, .',-richoccurs throughout the skeletal musculature :.-jrer than being limited to a particular extensor ::tern. In addition to pharmaceuticalreplacement :: dopamine,bvtreatment can include temporary ::Cuction of hypeftonicity through heat and other .:neral inhibiting techniques to allow patients to :-complish particular functions. The following box ;':mmarizes treatment suggestionsto decreasehigh =uscletone.
TreatmentSuggestionstor High Muscle ToneAssociated with Pain, Cold, or Stress ReEove source r Eliminate pairr . Warm patient . Alleviate stress Relaxation techniques EMG biofeedback Neutral warrnth Heat Hydrotherapy Cold towels Stimulation of antagonists . Resisted exercise o Electrical stimulation .\ssociated with Spinal Cord Injury Selective range-of-motion exercises Prolonged stretch Positioning Orthotics Medication Surgery Heat Prolonged ice Associated with Ceretrral Lesions Prolonged ice Inhibitory pressure Prolonged stretch Inhibitory casting Positioning Reeducation of voluntary movement patteflrs Genetal relaxation t€chrdques o Soft lighting or music
o . . . . .
103
Slow rocking Neutral wa!:Erth Slow stroking Maintained touch Rotation of the trunk Hydroth€rapy
Associated with Ngidity Positioning Range-of-motion exercises Orthotics Serial casting following head injury Heat Medication General relaxation techniques (as listed above)
Fluctuating Muscle Tone Commonly, pathology of the basalgangliaresultsin disordersof muscletone and activation.Not only is voluntarymotor output difficultro initiare,execute. and control, but the variationsin muscletone seenin this population can be so extreme as to be visible with movement. The resting tremors of a patient with Parkinson'sdiseaseand the dyskinesiasseen in the examplewith Mrs. H while she is medicated are examples of fluctuating tone that result in involuntary movement. A child with athetoid-type cerebralpalsy, for whom movement is a series of involuntary writhings, also demonstratesfluctuating tone. When an individual has fluctuating tone that movesthe limbs through largerangesof motion, contracturesare usually not a problem, but inadveftent self-inflictedinjuries sometimesoccut As a hand or foot flails around,it will sometimesrun into a hard, immovableobject.Patientsand caregiverscanbe educated to alter the environment, padding necessary objectsor removingunnecessaryonesto avoid harm. Ifthe fluctuatingtone doesnot resultin movementof large amplitude, then positioning and range-ofmotion treatments should be considered.Neutral warmth has been advocated to reduce excessive movementresultinsfrom muscletone fluctuationsin athetosis.6o
to4
4 . ToneAbtonralities
) Clinical CaseStuilies I The following casestudiessummarizethe conceptsof tone abnormalitiesdiscussedin this chapterand are not intendedto be exhaustive.Basedon the scenariospresented,an evaluationof the clinicalfindingsand goalsof treatmentareproposed.Theseare followed by a discussion of the factorsto be consideredin treatrnentselection. Note that any technique used to alter tone abnormalitiesmust be followed with functionaluse of the musculatureinvolvedifthe patientis to improve the ability to hold ormove.
Case I CM is a 37-year-oldbusinessman who saidthat the first signs of his Bell's paisy appearedafter a long airplane flight when he slept with his head againstthe window. He'd had a cold, but whedrer or not this factor and his nap on the planeprecipitatedhis unilateralfacialparalysis,he did not know. A noticeabledroop was visible on the left sideof his face,and he was havingtroublewith lip closureto control salivaand eatproperly. Wat is thenuscletoxeln theleftfaclalmuscles? Wat techxi4ues *,ould be appropiau for changiagthe toae fot this EVALUATION OF THE CLINICALFINOINGS Bell's palsy is any disorderof the facial newe, usually only on one side, with varied etiologies.The sudden onset of GM's symptomsmay indeed have been instigated by the chilling of the side of his face while on the airplaneor by his cold virus. If the entire facialnerveis affectedon the left, then none of the muscle fibers on the left side of the face will be able to receivesisnals ftom any alphamotor neurons.and the muscleswill be flaccid. If the facial nerve is only partially affected, then some mssclesmight be hy?otonic. GM noted that the entire left side of his face felt as though it was being pulleddownward. PREFERREDPRACTICEPATTERN ImpairedMotor Functionand SensoryIntegriqyAssociaed With NonprogressiveDisordersof the CentralNervous System*Acquired in Adolescence or Aduithood, (5D). PLAN OF CABE Iortunately, reinnervationof tie muscle fibers is common following a facial palsy, usually within 1 to 3 months. Muscle tone can be expectedto normalizeas reinnervationoccursif the muscle and connectivetissueshave been maintainedso that secondarybiomechanicalchangesdo not intedere.Thereforeanticipated
goals of treatment would include prevention of overeyeprotection(while *re blink stretchingof soft tissuesJ reflex is lost), and strengtheningof musclesonce reinneNalion occurs. PROPOSEDTREATMENTPLAN AND RATIONALE Cendepassivemovementof the facialmusculaturemay be indicatedto countersofttissuechangesresultingfrom lack of active movement.Otherwise, CM may be Ieft with a cosmeticallyunacceptable facialdroop when the musclesare reionervated.A patch or other form of protection over the left eyemay be requiredto preventeye injury while the motorcomponentof the comealreflexis paralyzed.As the muscle fibers are reinnervated,the emphasiswill be on exercises to elicitvoluntarycontraction rattrerthan on improvingmuscletone. Quick icing or light touch on the skin over a panicularmusclethat is beginningto be innervatedmay help CM to isolatea muscleto move it voluntarily.Practiceof facial move' mentswhile looking in a miror may provideextrafeedbackforCMwhile he is attemptingto reestablish oormal activation of the facial muscles.Electricalstimulation with biofeedbackmay be used to help the patient resumefunctiononcemusclesarereiru:ervated.
Case2 ELwas young,only in her 40s,for the severiryof arthritic damageto herrighthip. The damagewas most likely the resultofabnormaluseof the right legfollowing a caseof polio when shewas an infant. Severalsurgeriesin childhood to stabilizethe foot andto transfera hamstrinetendon anreriorly to linction for rhe quadricepshad ailowed her independentambularion,but her limp had worsenedover the last severalyears.The head of the femur had slippedout ofthe acetabulumand moved fartLer up toward her trunt EL had to walk on her right toes sincethe right leg was functionallyseveralinches shorterthan the left. After a successfirl total hip replacementchatevenedtheleglengt-hs. ELwaslearning ro walk again.Her gait trainingwas more complexthan is typical following total hip replacementsurgerybecauseof her complications.During supinepassiveROM of her right leg (within the limits allowed by her postoperativetotal hip precautions),the ankle plaatar flexors resisted stretch.Her hip and kneemoved very easilybut the leg feit heary, almost like deadweight. Basedon theinformationyresented,howshauldEIls muscle nxe bedescibedix thehfu flexors? Thebaeeextensots? The aable ylannr flexors?\Y/hattteatmenttechxi4ueswould be aypropriateto ahet the muscletonelabeledix the yreceding
-fl
O e. PATHOLOGY AND PATIENTPROBLEMS
EVALUATION OF CLINICALFINDINGS Both the hip flexorsand kneeextensomarehypotonic,a 1 on the clinical tone scale,witJr decreasedactivation of the alpha motor neurons.The ankle plantar flexor would be expectedto have biomechanicalshortening,causing stiffnessand resistanceto musclestretchat ttre end of a diminishedROM, a resultof habitualtoe walking.If passive movement resultedin resistancein the middle of the available range, then the anlle plantar flexor would be labeledhypenonic,a 3 on the clinical tone scale.Neumlly mediated hypertoniciry is unlikely with this diagnosis sinceno spinalor supraspinal neurallesionsareevident. The hip flexor alphamotorneuronsmay be temporarily inhibited becauseof pain in the incisionarealateralto the hip. If this hypothesisis correct,normalization of muscletone and voluntary contractionwill progressas paln resolves. The quadricepsmuscle was presumablyaffectedby the polio since the hamstring tendon was transferred many yearsago.The quadricepswould havebeenhypotonic following loss of the affected alpha motor neurons: no activationwould have been possiblevia those neurons,eitherfor passiveresistance to stretchor for voluntary contraction. Efs present knee extensor, the hamstring muscle,is probably normal in tone, which will be apparentoncethe hip healsfurtherandpain resolves. Having no information about EIls muscle tone or strengthbeforethe totalhip replacementsurgerythe c1inicianmust palpatefor activationof the musclesduring voluntary contraction.EMC testing of the quadriceps, hip flexors, ankle plantar flexors, and hamstrings may aisoprovide information about the number and size of activemotor units in eachmusclegroup. Suchinformation could differentiate between muscles tl-rat were more or less affected by poliomyelitis. Muscles that wele mole affecteddo not have the samecapacityfor motor unit recruiffnent during strength training as musclesthat were lessaffected.The goalsfor strengthening would be reducedinmusclesthat were more affected.
105
PROPOSEDTREATMENTPLAN AND RATIONALE Pain control could be accompLishedwith physical ag€nts,soft tissuemobilization, and positioning. (See Chapter6 for instructionson the useof heat or cold, or see Chapter 8 for instructionson t}re use of electrical stimulation.) Gait training and functional training with appropiate feedbackand practice will be necessary Cait trailing in a pool will take advantageof buoyancy andthe resistance the waterprovidesagainstmovement and could begin as soon as the surgicalincision is weli healed(seeChapter9). The hypotonicity is expectedto becomelessapparenta6 EIJspain decreases and she is betterableto contractat will. Treatment of the ankle plantar flexors must include prolongedstretch,preferablywith priorheat or thermallevel ultrasound(seeChapters6 and 7) tor soft tissue remodeling.Stretchcould be accomplishedwith exerciseor weight bearingon the whole foot. Somewould advocateserialcastingiffunctional dorsiflexionrangeof motion cannotbe obtailredin any other way.
Case3 S?,a 24-year-oldfemale,had noticed intermittent back pain over the last severalmonths. Her lifestyle had changed significandy from that of an a*rlete, training regularly,to that of a studengsitting for long periods. The pain increaseddramaticallyyesterday,however, while she was bowling for the first time in a couple of years.On€ of her problemsat this point is the palpable musclespasmin the paraspinalmusclesat the lumbar level. \Vhat is theundetlyingst nuluscaus;flgthe ftusclesVasmi' Whattteatmentis ayproliate to alle\)latethespasm?
PREFERREDPRACTICEPATTERI\ Impaired Joint Mobiliry, Motor Functioq Muscle Performanceand Range of Motion AssociatedWith Joint Arthroplasry, (4H), or Impaired Motor Function andSensoryIntegrityAssociatedWith Acute or Chronic Po\meuropathies,(5C).
EVALUATION OF CLINICALFINDINGS Muscle spasmsgpically originate hom painful stimuli, evenif the stimuli aresubde.Possiblestimuli in SP'scase include injury to muscle ftbers or other tissue while engagingin vigorous but unaccustomedactivity, pain signals from a facet joint, or nerve root irritation. The consequenttensionin the musclemay hold or splintthe injured area to avoid local movement that could iritate and exacerbate the pain.Ifpersistengthe musclespasmitself can contribute to the pain and discomfon by inhibiting local circulation and setting up its ou'n painful feedback loop.
PLAN OF CARE Anticipated goals include pain alleviation at the hip, incision healing, and improvement of hip muscle activation, recruitrnent, and timing to improve functions such as gait and transfen, Increasingthe ROM at the ankle will alsobe necessary
POSSIBLEPREFEBREDPRACTICEPATTERNS Impaired Joint Mobility, Motor Function, Muscle Performance,and Range of Motion Associatedwith Connective Tissue Dysfunction, (4D), or lmpaired Joint Mobility, Motor lunctio4 Muscle Performance, and Ranse of Motion Associated with Localized Contirued
t06
4 . Tonc Abtonnnlitics
) Clinical CaseStudies-cont'd a Inflammatior:,(4E),or Impaired Joint Mobiliry, Motor Iunction, Muscle Performance,Rangeof Motion, and ReflexIntegrity Associatedwith SpinalDisorders,(4F), or ImpairedPosture,(4B). PLAN OF CARE The anticipatedgoalsof treatmentwould includeidentifying and removing the causeof the painful stimulus. Frequendy,temporarily easingthe muscle spasmfirst allows more accurateidentification of the underlying pathology. PROPOSEDTREATMENTPLAN AND RATIONALE Diagnosingthe sourceof the painful stimulusis beyond the scopeof this chapter,but many texts are devotedto the subject.6l-63Once stimulus identification and removaloccurs,the musciespasmmaydiminishbyitself or or ir may requireseparale treatment. Heat.uluasound, massagecan increaselocal circulation(seeChapters6 and 7).Prolongedicing,neutralwarmth, or slow stroking couldbe usedto diminishthe hypertonicitydirecdyand thus allow restorationof more normal local circulation. Once the painful feedbackloop of the musclespasmis Educationshould broken,patienteducationis necessary. includeinstructionson preventivestrengtheningof local musculatureand avoidanceof posturesand movements that reaggravatethe initial injury Other sretching and s[€ngtheningexercises havebeenidentifiedbutwill not be discussed in this text on physicalagents.
Case4 RB had a lefthemiplegiafollowing a stroke.He had progressedfrom an initial flaccidparalysisto his curent status of hypertonicity in the biceps brachii and ankle plantar flexors.When askedto lift fus left arm, he was unable to do so without elevating and retracting his scapula,abductingand externallyrotating his shoulder, arld flexing and supinatingat the elbow, all consistent with a flexor synergy. When standing, he tended to rotateintemally and adducthis left hip, with a retracted pelvis and a hyperextendedknee, consistentwith the lower extremity extensor synergy pattern. He was dependentin bed mobility and transfersbecauseof lack of controlledmovementofthe left sideofhis body.The hypertonicity in the arm and leg increasedwhen he attemptedto keep his balancein a standingposition or takestepswith a quad-cane. of muscletaneareaVqoyriatelx euluatittg Wat measures Mr. B? \Yhat trcatlne t is aVyroVriateconsideitg Mr B's
OF CLINICALFINDINGS EVALUATION usingstretch Muscletone would most likely be assessed reflexes,the clinical tone scaleor the Modified Ashworth Scale,andctnical observation.Mr, B was found to havea hyperactive sEetch leflex in both the biceps and the triceps,but muscle tone in t}le triceps was h'?otonic, wi*r a 1 on the clinicaltone scale.The bicepsandplantarflexors were given a 1+ on the Modified Ashworth Scale which equaleda 3 on the clinical tone scale,During quick stretchof the plantarflexors,clonuswas apparent,lasting for three beats. During clinical observation, Mr. B rested his left forearm in his lap while sitting with his back supponed, but when he stood, gravity quickstretchedhis bicepsoncethe weight of his foream was unsupported,and the elbow flexedto approximately80 degrees.During bed mobility, transfers,or standing,fuli elbow extension was never observed.His left anl-le bouncedwith plantarfledon clonuswhen he first stood up, ending with weight mostly on the ball of his foot unlesscarewas taken to position the foot beforestanding to facilitate weight bearing through the heel. Other possibletestsforMr B'smuscletoneinclude*re pendulum test for *re biceps,a dynamometer ol myometer test for the plantar flexors, or EMG studiesto compare muscle activity on the tlvo sidesof Mr. B's body. These quantitativemeasureswould be especiallyuseful for researchthat rcquiresmore pr€cisemeasurementthan describedabove. the qualitativemeasures PREFERBEDPRACTICEPATTERN ImpairedMotor lunction and SensoryIntegrity Associated With NonprogressiveDisorders of the Central Nervous System-Acquired in Adolescenceor Adulthood, (5D). PLAN OF CARE Coais are focusedon improving Mr. B's function and preventingsecondaryproblems. PROPOSEDTREATMENTPLAN AND RATIONALE Appropriate treatment techniques for Mr. B may come Only from multiple sources andtheoreticalbackgrounds. a few techniquesthat influencemuscletone will be discussedhere.Prolongedstretchof the bicepsor the plantar flexors may be incorporated into functional activities like standing or weight bearing on the hand to normalize musde tone. Prolongedicing (seeChapter 6) may be added if soft tissue shortening is inhibiting full passive ROM. Exercisesto facilitate activity of the antaSoniststo inhibit the biceps or plantar flexors may be used. Electical stimulation of the triceps and dorsiflexors would have the dual benefit of inhibiting hypertonic
Orc . PATHOLOCY AND PATIENT PROBLEMS
musculature and strengthening muscles ttrat are currendyweak (seeChapter8). EMC biofeedbackmight be usedduring a specifictask to train Mr. B in more appropriate activation pattems for the bicepsor plantar flexors. The hypertonicity increase seen during standing could be alleviatedwith techniquesto increaseMl B's alignment, balance,and confidencewhile standing. If he is better able to relax in this posture, his muscle tone will decrease aswell. Discussionof specifictherapeuticexercisesto enhanceMr B's balanceis bevond the scopeof this chapter
Case 5 Mrs. H was eagerto tell her story. Her Parkinson's diseasehad progressed, with increasingftemor and harder and longer freezes of her limbs between dyskinetic statesthatl€d to the graduallossof handwriting,reading ability, and other functions. She had taken increasing dosesof a dopaminereplacementdrug with deceasing benefit.Becauseof her good health otherwise,shewas deemeda good candidatefor a surgicalprocedurecalled a vallidonmv andhada 3- to 4-inch recentincision visible in the left sideofher scalp.Now shecouldsignher name with her right hand and read print on an exercisesheet. But shestill froze a few times eachday,when shewould find any movement difficult, although not impossible with sufficient effort, until her muscle tone diminished afteran hour orso. EVALUATIONOF CLINICAL FINDINGS Mrs. H, describedat the beginningof this chapter,is an example of a patient with fluctuating muscle tone during her dyskinetic periods and rigid hypertonicity during her freezestates.Her limbs have suchlarsemovements
l07
during her dyskinetic periods that loss of motion will probablynot be a problem.Her trunk and neckmuscles, routinely positioned with a thoracic kyphosis and forward-extendedhead.however,could righten. PREFERREDPRACTICEPATTERN Impaired Motor Function and Sensory Integrity AssociatedWitJr ProgressiveDisorders of the Central NervousSystem,(5E). PLAN OF CARE Anticipated goals of treatrnent include avoiding injury preventingsecondaryproblemslike soft tissueshortening,and promoringindependentfuncrjon. PROPOSEDTREATMENTPLAN AND RATIONALE Mrs. H's environment should be assessedand her wheelchairfootplatespaddedto avoid injury when her flailing limbs koock against objects. Posture training, active and passive RON4, locally applied heat, and supine positioning can help maintain her trunl< and necktissueintegrity.In Mrs. H's case,sinceher dyskinesia is a result of massivedosesof a dopanrinereplacement drug, one might ask why she does not have the dose reducedor the drug eliminated to decreasethe fluctuationofher muscletone. Her responseis that she prefers dyskinesiato a treeze: it is easier to initiate movement and therefore function in the former condition. The pati€nt's preference takes precedence, althoughreportsof specific,effectivetherapyfor dyskinesiaale ra!e. Neutral warmth, as is used in attretosis, and hydrotherapy,for its resistanceto limb movement but require inall directions,havepotentialeffectiveness further study.
ireferred PhysicalTherapistPraclicePattemssN4I4R, 4D,4L, 4F, 4l{, 5D,5E, and 5Gl are copyright 2002 AmericanPhysicalTherapy All riehtsreserved. .\ssociation-
REVIEW CHAPTER Muscletone is definedasa muscle'spassiveresistance :o stretch.The resistancehas both a neural compo:rent, from the activation of motor units via alpha :notor neurons,and biomechanicaland biochemical :omponents,from the propertiesof the musclefibers and conrrectivetissue surrounding them. NeurallyCerived tone abnormalities resuit from abnormal ;hangesin the inhibitory and excitatoryinput to the alphamotor neuron.Abnormal changesmay occuras a result of peripheral,spinal,or supraspinalpatholo3iesthat affecteither the alphamotor neuronitself or any of the sourcesofinput to the alphamotor neuron.
If the resultis hypotonicity, the goal of rehabilitation is to increase the muscletone to promoteeasieractivation of motor output, improve posture,and restore an acceptablecosmeticappearance.If the result of abnormalinput to the alpha motor neuron is hypertoniciqy,the goal of rehabilitationis to decreasethe muscle tone to decreasediscomfort, easeROM and caregivingactivities, a1low normal positioning, and preventcontractures.If the resultof abnormaiinput is an uncontrollablefluctuationof muscletone, the goal of physicaltherapyis to increasefunction asmuch as possibleand prevent injuries. Some treatment ideas have been suggestedthat make use of the structures
108
4 . ToneAbnonxalities
and neurophysiological principles described here. Later chapters in this text explain more fully how physical agents may be used to manage some of the problems presented when muscle tone is abnormal. ih" reader is referred to the Evolve website at http://evolve.elsevier.com/Cameron for study questions pertinent to this chapter
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One . PATHOLOGYAND PATIENTPROBLEMS
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Motion Rest cfions Linda C. Monroe,MPT, OCS
SUMl\IARY
OF INFORMATION
lntroduction Typesof Motion Patternsof Motion Restriction TissuesThat Can RestrictMotiorr PathologiesThat Can CauseMotion Restrictions Assessmentof Motion Restrictions
COVERED
Treatment Approachesfor Motion Restrictions The Role ofPhysical Agents in the Treatment of Motion Restrictions Clinical CaseStudies Chapter Review
OBJECTIVES Uyon comyletionof this cha2zter, the readerwill beable to: 1 . Define different b?es of motion. 6. Selectand apply appropriatemethods to 2 . Describedifferent patternsof motion determinethe structuresand restrictions. pathologiescontributing to motion 3 . Identify tissuestl.ratcan restrict motion. restrictions. Discusspathologiesthat can contribute to 7. When presentedwith a clinical caseinvolving a motion restrictions. motion restriction, evaluatethe clinical findings, 5 . Selectand apply appropriatetools and methods proposetreatment goals,and identi$zpossible to quantify and qualify motion restrictions. interventions.
ltl
lt2
5 . .Ilotiot
Re strittions
INTRODUCTION This chapter discussesmotion between body segments and the factorsthat can restrict such motion. The amountof motionthat occurswhen onesegment oI the body moves in relationto an adjacentsegment is known as rangeof motiox(ROM).1When a segment of the body moves through its. available ROM, all tissuesin that region, including the bones, strucligaments,tendons.intraarticular ioint capsule, tur"r. mrr.les, nerves,fascia,and skin may be affected.When all of thesetissuesfunction normally, ful1, normal ROM can be achieved;however, dysfunction of any of these tissuesmay contribute to a restriction of the avai.lableROM. Many patients in rehabilitationseekmedicaltreatmentwith an impairment of restricted ROM. To restore motion most effectively,the therapist must understandboth the factorsthat influencenormal motion and the factors thatmay contrjbuteto motionrestrictions.' fhe impairment of restricted motioh may contribute directly or indirecdy to patient functional limitation and disability.3-6lor example, restricted shoulderROM may stop an individual from raising the arm aboveshoulderheightandmay preventhim or her from performing a job that involvesoverhead lifting, This impairment may also contribute indirecdy b further pathology by causingimpingement of the rotatorcuff tendons,resultingin pain.weakoflifting capaciry. ness,andadditionalLimitation ROM is generaliyiimpathology, absence of In the of anatomior approximation ited by the lengthening of the sott flexibility and The integrity cal structures.T joint, and relationshape and the a tissuessurrounding o[ amount the affect structures. ship of the articular it joint midrange, is at a When motion that can occur. a small o[ application with the cangenerallybe moved force.This is becausethe collagenfibersin the connective tissuesurounding the joint are in a relaxedstate, loosely oriented in vadous directions, and only sparselvcross-linkedwith other fibers,allowingthem t; dist;nd readily.As *re joint approachesterminal motion, the collagenfibersbegin to align in the direction of the stressandstartto straightenMotion ceases at the normal terminal range when the fibers have achievedtheir maximum alignmentor when soft or bony tissuesapproximate.Ior example,ankle dorsiflexion normally ceaseswhen *re fibers of the calf muscles have achieved maximum alignment and the musclesarefully extended,whereaselbow flexion normally ceaseswhen the soft tissuesof the anterior
arm aonroximate with the soft tissuesof the antedor foreanl, and elbow extensionceaseswhen the olecranon processof the ulna approximateswith the olecranonfossaofthe humerus(Fig.5-1) The normal ROM for all human joints has been measuredand documented;howeveqthesemeasures vary wirh the individual'sage,sex,and health stawith age Rang"of -otion generallydecreases tur.B-10 and is qreaterin women than in men, althoughthese differeicesvary with differentmotions andjoints and are not consistentfor all individuals.ll-l9Becauseof this variabiliry normal ROM is generallydetermined bv comparisonwith the motion of the contralateral limb, if'available, rather than by comparisonwith notmative data. A motion is considered to be restrictedwhen it is less than that availablefor the samesegmenton the contralateralside of the same individual. When a normal contralateralside is not available-as occurs,for example,with the spinemotion is consideredto be restrictedwhen it is less than normal for the individual'sageand sex.
OFMOTION TYPES Motion ActiveandPassive The motion of body segmentscan be classifiedas ei,theractiveor yassiveActive motion is the movement producedby contractionof the musclescrossing a joini. Assessmentof activeROM can provide information about an individual's functional abilities' Active motionmay be restrictedby muscleweakness, abnormal muscle tone, Pain originating trom the musculotendinousunit or other local structures,an inability or unwillingness of the subject to follow directions,or as the result of restrictionsin passive ROM.20 Passivemotion is movementproducedentirely by an externalforce without voluntary muscle contraction by *re subiect.The externalforce may be produced by gravity, a machine,another individual, or another'pirt of the subiect'sown bodyl Passive motion may be restdctedby shorteningof the soft tissues,edema,adhesion,mechanicalblock, spinal disc neuraltension. or adverse herniarion, ROM is greaterthannormalactive Normalpassive ROM when motion is limited by *re distention or aooroximation of soft tissue, but both types of -otio.r ut" equalwhen motion is limited by approxiof passive a fewdegrees mationofbone.Forexample,
One c PATHOLOGY AND PATIENTPROBLEMS
113
' gure5-1. A, Ankle dorsiflexion limited by solt tissuedistension.B, Elbow flexion limited by soft tissueapproxima'-:n. C, Elbow extensionlimited by bone approximation.
,::kle dorsiflexion motion are available beyond the .::rit of active motion because the limiting tissues are - astic and may be extended by an external force that i greater than that of the active muscles when at ter:::inal active ROM. A few degrees of additional pas,. .'e elbow flexion are availabie beyond the limit of .:,ive range because the limiting ris'ues are com::essible by an external force greater than that of the ::iive muscles in that position and because the ::proximating muscles may be less bulky when ,"laxed. This additional passive ROM may protect ,iint structures by absorbing external forces during ::rivities, particularly those performed at or close to -- .-A ^t ,.ri,'" ."^."
Physiological andAccessory Molion :rysiological motion is the motion of one segment of ::re body relative to another segment. For example, :nysiological knee extension is the straightening of -:reknee *rat occurs when the leg moves away from re thigh. Accessory motion is the motion that occurs : . ' w e e n t h e ' o i n r , u r f a c e sd u r i n g n o r m a lp h y s o l o g i r l m o t i o n . T14 24 3F o re x a m p J ea. n c e r i ogr l i oi n g o f t } e
tibia on the femur is the accessorymotron that occurs d u r i n g p h y s i o l o g i c akl n e e e x r e n s i o nr l i g . 5 - 2 ) . Accessorymotions may be intraarticular,as in the prior example of anterior tibial gliding during knee extension,or extraarticular,aswith the upward rotation of lhe scapula during physiological shoulder flexion (Iig. 5-3). Accessorymotions cannot be performed actively in isolation from their associated physiologicalmovement;howeveSthey may be performed passivelyin isolation from their associated physiologicaimovement. Normal accessorymotion is required Ior normal active and passivejoint motion to occur.The direction of normal accessorymotion depends on the shape of the articular surfacesand the direction of physiologicalmotion. Concavejoint surfacesrequire accessoryglidingto be availablein the directionof the associatedphysiological motion of the segment, whereasconvexjoint surfacesrequireaccessorygiiding to be availablein the opposite direction of the associatedphysiologicalmotion of the segment.2llor example, the tibial plateau, which has a concave surface at the knee, glides anteriorly during knee extensionwhenthe tibia is moving anteriorly,and the
ll4
Figure5-2. Accessoryanterior gliding of the tibia on the femur during physiological kneeextension.
Figure5-3. Extraarticular accessory motior\ which is the upward rotation of the scapula that accompaniesshoulder flexton.
5 . Motion Restictions
Femur
O$e . PATHOLOGY AND PATIENT PROBLMS
:emoralcondyles,which have convexsurfacesat the
PATTERNS OFMOTION RESTRICTION Capsular andNoncapsular Patterns ofMotion Restriction l1le restrictionof motion at a joint canbe classifiedas :aving either a caysularor a noncaVsular pattern. A :apsularpattem of restrictionis the specificcombina:on of motion lossthat is causedby shorteningof the 'oint capsulesurroundinga joint. Eachsynovialjoint ras a unique capsularpattern of restriction.Capsular rattems generally include restrictionsof motion in ::rultipledirections.Ior example,the capsularpattern :or the glenohumeral joint involves restriction of 3xternal rotation, abduction, internal rotation, and lexion to progressivelysmaller degrees.Capsular f,attemsof restrictionmay be causedby the effusion, ibrosis, or inflammation commonly associatedwith legenerativejoint disease,arthritis, immobilization, fnd acutetrauma. A noncapsularpattern of restdctionis a combina:on of motion loss that doesnot follow the capsular eattem.A noncapsularpattem of motion lossmay be :ausedby ligamentousadhesion,an internalderange:rrent,or an extraarticularlesion.ligamentous adhe,ionwill limitmotion in the directions*lat stretchthe adheredligament. For example,an adhesionof the :alofibularligament after an ankle sprainwill restrict :nkle inversion because this motion olaces the :dheredligamenton srretch;however,thjs adhesion '.vill not alter the motion of the ankle in other direc:ons. Internal derangement,the displacement of .oose fragmentswithin a joint, will generallylimit :rrotiononly in the directionthat compresses the frag:nent. Ior example,a cartilagefragmentin the knee -,villgenerallylimit knee extensionbut will not limit klee flexion. Extraarticularlesions,such as muscle adhesions,hematomas, cysts, or inflamed bursae, nay limit motion in the directionof either stretchor .ompression,dependingon the nature of the lesion. For example,adhesionof the quadricepsmuscle to -rheshaftof the femurwill limit stretchinsof the mus;le, while a poplicealcyst will limit compression of -J-re popliteal area.Both of these lesionswill restrict irotion in the noncapsularpattern of restrictedknee Jexion.with fulJ.painless kneeexrension.
115
TISSUES THAT CANRESTRICT MOTION Contractile andNoncontractile Tissues Any of the musculoskeietaltissuesin the area of a motion restrictionmay contributeto that restriction. Thesetissuesaremostreadilyclassifiedascontractile or notlcontractile flable 5-1). Contractile tissue is composedof the musculotendinousunit, which includes *re muscle,the muscuiotendinousjunction, the tendon, and the tendon's interfacewith bone. Skeletal muscleis consideredto be contractilebecauseit can contractby forming cross-bridges of the myosin proteins with the actin proteins within its fibers.24 Tendonsand their attachmentsto boneareconsidered contractilebecausecontractingmusclesapply tension direcdyto thesestructures.When a muscleconftacts, it appliestensionto its tendons,causingthe bonesto which it is attachedand the surroundins tissuesto movethroughtheavailable accjveROM. *hen all the componentsof the musculotendinousunit and the noncontractiletissuesare functioning normall, the availableactiveROM will be within normal limits for the ageand sexofthe subject.Injury or dysfunctionof contractiletissuegenerallyresultsin a restrictionof active ROM in *re direction of movement oroduced by contraction of the m usculotendinousunit. Dysfunction of contractiletissue may also result in pain or weaknesson resistedtestingof the musculotendinousunit. For example,a tear in the anteriortibialis muscleor tendon can restrictactivedorsiflexion at the ankleandreducethe forcegeneratedby resisted testing of ankle dorsiflexion,but this lesion is not
Contractile tfusue
Noncontraatile tissue
Muscle
Skin
Musculotendinousjunction Ligament Tendon
Bursa
Tendinousinterface with bone
Capsule Articular cartilage Intervertebraldisc Peripheralnerve Dura mater
5 . Moriofl Resttictiotts
ll6
likely to alter passiveplantar flexion, dorsiflexion, ROM, or activeplantarflexion strength. A11tissuesthat are not componentsof the musculotendinous unit are considered noncontractile. Noncontractiletissuesincludeskin, fascia,scartissue, ligamenqbursa,capsule,articularcanilage,bone,intervertebraldisc,newe, and dura mater When the noncontractiletissuesin an areaare functioningnormally, the passiveROM of the segmentsin that areawill be within normallimits. Injury or dysfunctionof noncontractile tissue can causea restrictionof the passive in question ROM o[ the johcs in rheareaof the cissue oI actjveROM.2s to restriction andmayalsocontribure The direction,degree,andnatureof the motion restriction dependson the type of noncontractiietissue involved,the type of tissuedysfunction,andthe severiqyof involvement.Forexample,adhesivecapsulitisof *re shoulder,which involvesshorteningof the glenohumeraljoint capsuleand elimination of the inferior axiliaryfold, will restrictbothpassiveandactiveshoul(Iig. 5-4). derROM in a capsularpattem26-31
THATGANCAUSE MOTION PATHOLOGIES RESTRICTIONS Contracture Motion may be restrictedif any of the soft tissue structuresin an area have become shortened.Such
may soft tissue shortening,known as a contracturet noncontractile tissues.32,33 A occur in contractileor resuitcontracturemay be causedby immobilization ing from external splinting provided by a cast or splint, for example.Contracturesare also causedby imbalanceof musclepower resultingfrom weakness, ascouldbe causedby poliomyelitisor from spasticity from central, nervous system (CNS) damage, for It has been proposedthat immobilizaexample.33,34 tion results in contracturebecauseit allows anomalouscross-linksto form betweencollagenfibers and it causesfluid to be lost from fibrous connectivetissue,includingtendon,capsule,ligament,and fascia.34 36 Anomalous crosslinks can developwhen tissues remain stationarybecause,in the absenceof normal stressand motion, fibersremainin contactwith each otherfor prolongedperiodsand startto adhereat their points of interception.Thesecross-linksmay prevent normalalignmentof the collagenfiberswhenmotion is attempted.They also increasethe stressrequiredto stretchthe tissue,limit tissueextension,and resultin contracture(Iig. 5-5).Iluid losscanalsoimpair norrnal fiber gliding,causingcollagenfibrilsto haveclosercontactandlimitins tissueextension.32 The risk of contractureformauon rn responsero immobilization is increasedwhen the tissuehas been injuredbecausescartissue,which is formedduringthe proliferationphaseofhealing,tendsto havepoor fiber alignmentand a high degreeof cross-linkingbenveen
,:'.:ii.:'.,.\\
', \ ,:.,. } . ' . . . ' . , ] 1.',:
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r 1 1:.:.,.,.; f.r-.:. .,_
,"/
l\.'::,r,ll '.':i L\
li
J,/ \'::,1.'tl\ Normal inferiorjoint capsule HUmerus
Figure5-4. Joint capsuleshorteningand adhesionrestricting shoulder rangeof motion.
One . PATHOLOGY AND PATIENTPROBLEMS
CollagenFibersat Resl withCrosslinks
NormalCollagen Fibersat Rest
I t I I
I + 5-5. Normal collagenfibersandcollagenflberswith Figure cross-links.(FromWoo SL,Matthews [{ AkesonWH et to immobility.Correlative aLConnective tissueresponse study of biomechanicalmeasurementsof normal and Mayimmobilized rabbrtktrces,Anhitls andRheumatism, permission of 197 5. This material is used by 78(3):262, June of JohnWiley & Sons,Inc.) Wiley-Liss, Inc.,a subsidiary its fibers.Restrictionof motion after an irlury may be further aggravatedif a concurrentproblem, such as sepsisor ongoing trauma, amplifies the inflammatory scarring.33 responseand causesexcessive A persistentshort€ningof a musclethat is resistant A muscle to stretchis known as a musclecofltracture. contracturecanbe causedby prolongedmusclespasm, guarding, muscle imbalance, muscle disease, or ischemicmusclenecrosis,and by immobilization.33A musclecontracturemay limit both activeand passive motion of the joint(s)that the musclecrossesand can also cause deformity of the joint(s) normally cont'^ll.J
hv thp mr,vle
Edema Normally,a joint capsulecontainsfluid but is not fully distended.This allows the capsuleto fold or distend
tt7
when the joint moves, altering its size and shape as required for movement through fuI1 ROM. If excessivefluid forms inside a joint capsule,a condition known as ixtraatticularedema,the joint capsule becomesmore distended,limiting i* folding and further distention and potentially restrictingbo*r passive and activejoint motion in a capsularpattem.For example,intraarticularedema in the knee will producethe capsularpattern of knee flexion being more limited than kneeextension. Accumulation of fluid outside of the ioint, a condition known as extraarticularedema,may also restdctactiveand passivemotion by causingsoft tissue approximation to occur earlier in the range. Extraarticularedema generallyrestrictsmotion in a noncapsularpattem. Ior example,edemain the calf musclemay resffict knee flexion ROM while having no effecton kneeextensionROM.
Adhesion Adhesion is the abnormal joining of parts to each Adhesionmay occurbetvveendifferenttypes other.37 of tissue for various reasonsand ftequendy causes restriction of motion. During ttre healing process, scartissuecan adhereto surroundingstructures,and fibrofatty tissue may proliferate inside joints and adherebetweeninftaarticularstructuresas it matures into scartissue.38 Prolongedjoint immobilizatioq even in the absenceof local injury can also causethe synovial membrane sunounding the joint to adhereto the cartilageinside the joint. Adhesionscan affect both the quality and the quantity of joint motion. For example, with adhesivecapsulitis,not only doesthe joint capsuleshorten,it alsoadheresto the slmovialmembrane. This lirrli* motion andreduces,or evenobliterates,the space between the cartilage and the sl,novial membrane, thus blocking normal synovial fluid nutrition that can and causingarticular cartilage^d-egeneration alterthe qualityof joint motion.rr
Mechanical Block Motion canbe mechanicallyblockedby bone or ftagments of articularcartilage,or by tearsin intraarticular discs or menisci. Degenerativejoint diseaseor malunion of bony segmentsfollowing fracturehealing frequendy resultsin a bony block that restricts joint motion in one or more directions (Fig 5-Q This is becausethese pathologies cause bone to
tta
5 . Motiofl Restictioqs
length of the spinal column without interuption of transmission.au Adverseneuraltensionis the presence of abnormal responsesproduced from peripheral nervous system structures when their ROM and stretch capabilitiesare tested.arAdverseneural tension may resulcfrom majoror minor nerveinjury or may be causedindirecdy by extraneuraladhesions that result in tethering of the nerve to surrounding structures.Nerve injury may be the result of trauma due to friction, compression,or stretch.It may alsobe causedby disease,ischemia,inflammation, or a disFigure5-6. Osteophytesblocking metatarsophalangeal ruption in the axonaltransportsystem.42 ]schemiacan extenston. pressure extravascular fluid, blood, be causedby ftom discmaterial,or soft tissueswith decreased mobiliqy. joints. hypertrophy in or around the Loosebodiesor Adverseneural tensionis most commonly due to fragmentsof articular cartilage,causedby avascular restriction of nerve motion. A number of structural necrosisor ffauma,canalsoalterthe mechanicsof the features predispose nerve motion to restriction. joint, causing"lockingoin variouspositions,pain,and Nerve motion is commonly restrictedwhere nerves pass through tunnels, as, for example, where *re other dysfunctions.33 Tearsin intraarticularfibrocarti laginous discs and menisci caused by high-force median nerve passesthrough the carpal tunnel or traumaticinjury or by repetitivelow-force straingenwhere the spinal nervespassthrough the interuerteerallyblock motion in one directiononly. bral foramina.Peripheralnewe motionis alsolikely to be restrictedat points where the nervesbranch;for example,where the ulnar nerve splits at the hook of DiscHerniation Spinal the hammateorwhere the sciaticnervesplitsinto the pironeal and tibial nervesin the fiigh. Placeswhere Spinaldischerniationmay resultin direct blockageof sninal motion if a portion of *re discal material the systemis relativelyfixed arealsopoints of vulnerbecomestrapped in i facet joint or if the disc comability; for example,at the duramater at L4 or where pressesa spinal nerve root where it passesthrough the common oeronealnerve oassesthe head of the the vertebralforamen. Other pathologiesassociated fibula. The system is also ielatively fixed where with spinal disc hemiation, including inflammation, nervesare closeto unyieldinginterfaces;for example, hyp€ftrophic changes,decreaseddisc height, and where the cordsof the brachialplexuspassover the pain, may further limit spinal motion. Inflammation first rib or the greateroccipitalnerve passesthrough *re fasciain the posteriorskull.al about the spinalfacetjoint or herniatedsegmentcan limit motion by narrowing the vertebralforamenand compressingthe nerveroot. Hypertrophicchangesat Weakness the vertebral margins and facet joints, as well as decreaseddischeight, alsonarow the vertebralforaWhen musclesare too weak to seneratethe force men, making the nerve root more vulnerable to requiredro move a segmenL of the body throughits compression.Painmay limitmotion by causinginvolnormal ROM. activeROM will be restricted. untary musclespasmsor by causing*re individual to weakness may be the result of contractile restrictmovementsvoluntarily. changessuch as atrophy or injury poor along the motor nerves,or poor synaptic sion at the neuromuscularjunction. Osleophytes
Adverse Neural Tension
Under normal circumstances,the nervous system, including *re spinal cord and the peripheralnerves, must adapt to both mechanicaland physiological stresses.39 lor example,during forward flexion of the trunk, the newoussystemmust adaptto the increased
0therFactors Motion restrictions may also be causedby other factors, including pain, psychological and tone.Painmay restrictactjveor passive
O,te . PATHOLOGYAND PATIENTPROBLEMS
dependingon whether contractileor noncontractile sffucturesare the sourceof the pain. Psychological factorssuchasfeat poormotivatior! or poor compr€hension are most likely to causerestriction of only active ROM. Tone abnormalities,particularlyhypotonia or flaccidity, may also impair the control of activemusclecontractionsand may thus limit active ROM.
ASSESSMENT OFMOTION RESTRICTIONS When a patient seeksmedical treatment for complaints of limited motion. an examination of the mobility of all the structuresin the areaof the restriction, including the joints, muscles,intra- and exffaarticular structures. and newes. should be made. Evaluationof all these findings is required to determine the pathophysiology underlying the motion restrictioq identify the tissues limiting motioq and assessthe severity and irritability of the dysfunction.€ This comolete examination and evaluation will direct treatment to the appropriatestructure(s) and will facilitate selectionof the optimal intervention to meet goals.Ongoing assessment of outcomes is required to modify treatment appropriately in responseto changesin the dysfunction. This will accelerateand optimize progresstoward the treatment goals.22,23'42 A variety of tools and methodsare availablefor quantitativeand qualitative assessment of motion andmotion restrictions.
Measures 0uantitative Goniometers,tape measures,and various types of inclinometersare commonly usedin the clinical setting for quantitativeassessment of ROM. Thesetools provide objective and moderately reliable measures of ROM. and are oracticaland convenientfor clinical use. Radiographs,photographs,electrogoniometers, flexometers,and plumb linesmay be usedto increase the accuracyand reliability of ROM measurement. Theseadditionaltools areoften usedfor researchpurposesbut are not availablein most clinical settings. The different tools provide different information about the available or demonstratedROM. Most tools,includinggoniometers,inclinometers,and electrogoniometers,provide measuresof the angle, or changein angle, between body segments,whereas other tools, such as the tape measure,provide measuresof the changein lengthof bodysegments.aa
l19
Measures 0ualitative techniquessuchassoft tissue Qualitativeassessment palpatiorSaccessorymotion testing,and end-feelprovide valuableinformation about motion restrictions that canhelp to guidetreaunent.Soft tissuepalpation may be usedto assessthe mobility of skin or scartissue,local tendemess,the presenceof musclespasm, skin temperature,and the quality of edema.It is also usedto identify bony landmarksbefore quantitative measurementof ROM.
TestMethods andRationale Active, resisted,passive,and accessorymotion, and neuraltensiontestingcanbe usedto determinewhich tissuesare restrictingmotion and the nature of ttre pathologiescontributingto a motion restriction. Activerangeof motion Active ROM is testedby askingthe subjectto move the desiredsegmentto its limit in a given direction.The subjectis askedto reportany s)'mptomsor sensations, such as pain or tingling, experiencedduring this activity. The maximum motion is measuted,and the quality or coordination of the motion and any associated symptoms are noted. Testing of active ROM yields ' information regardingthe subjecCsability and willingnessto move functionally and is generally most useful for assessingthe integrity of contractile structures. The following questionsshould be noted when testingactiveROM: 1. Is the ROM symmetrical, normal, restricted,or excessive? 2. Whatis *re quality of the availablemotion? 3. Are any signs or symptoms associatedwith the motion?
Resisted muscle testing Resistedmuscle testing is performed by having the subjectcontracthis or her muscleagainsta resistance strong enough to prevent movement.45,46 Resisted muscletestsprovide information about the ability of a muscleto produceforce.This information may help detemine whether contractileor noncontractiletissuesare the sourceof a motion resffictionsincemuscleweaknessis commonly the causeof a lossof active ROM.47 Cyriax25has identified four possibleresponsesto resisted muscle testing and has proposed interpretations for each of these responses(able 5-2).
5 . Motiot Restrictiotts
120
Interpretation
1. Strongand painless
No apparentpathologyof contractileor neryoustissue
2. Strongand painful
trAinorlesionof musculotendinousunit
3. Weak and painless
Completeruptureofthe musculotendinousunit Neurologicallesion
4. Weak and painful
Partialdisruptionof the musculotendinousunit Inhibitionby pain due to pathologysuchasinflammation, f',.r"'" ^' -.^-1,.Concurrentneurologicaldeficit
lromCynaxJ: Textboab of Orthoyedic Medicine,ed 6, Baltimore,1975,Williams & Wilkins.
When the force is strong and there is no pain with testing,this indicatesno pathology of contractileor nervoustissues.When the force is strongbut pain is producedwith testing,this usuallyindicatesa minor structurallesionof the musculotendinousunit. When the force is weak and there is no pain with testing, this indicates a complete rupture of the musculotendinous unit or a neurologicaldeficit. When the force is weak but pain is producedwith testing,this indicatesa minor structurallesion o[ the musculotendinousunit with a concurent neuroloeicaldeficit or inhibition of conffacdon resultinglrom pain causedby pathology such as inflammation, fracture, or neoplasm. Passive rangeof motion PassiveROM is assessedby the tester moving the segment to its limit in a given direction. During passive ROM testing, the quantity of available motion is measured,and the quality of motion and symptoms associatedwith motion and the end-feel are noted. End-feelis the quality of the resistanceat the limit of passivemotion felt by the clinician.An end-feelmay be normal (physiological)or abnormal (pathological).A normal end-feelexistswhen passive ROM is full and the normal anatomyof the joint stops movement. Certain end-feelsare notmal for some joints but may be pathological at other joints or at abnomal points in the range.Other end-feelsare abnormal if felt at any point in the motion of any joint. Normal and abnormalend-feelsfor most joints arelistedinTable 5-3.20,42'47 PassiveROM is normally
limited by stretchingof soft tissuesor by the opposition of soft tissuesor bone and may be restrictedasa result of soft tissue contracture,mechanicalblock, or edema.The amount of passivemotion available and *re quality of the end-feel can assist in the determination of tlre structures at fault and the nature of the pathologiescontributingto the motion resffiction.4/ Combining the findings of active range of motion assessment, resrsted muscle testing, and passive range of motion Combining the findings of active ROM, resisted muscle testing, and passive ROM can assist in differentiatingbewveenrestrictionsoI motion caused by contractile and nonconffactile structures. For example, if active elbow flexion is restricted, the elbow flexors are weak and passiveelbow flexion rangeis normal, then the structureslimiting motion are most likely to be contractile. In contrast, if both active and passive elbow flexion ROM are restrictedand the strengthofthe elbow flexorsis normal, then noncontractile tissues are proba involved. Other combinations of abnormality may indicate muscle substitution durine active ROM testing, psychologicalfactors limiting motion, use of poor testing technique, or pain inhibi musclecontraction(lable 5-4).To definitelyimpli a particular pathology or a particular stuucturq the findings of thesenoninvasivetests may need to be correlatedwith the findinss of other
pf 5-3 Descriptions and Examplesof Different Types of End-Feels Type
Description
Exarnples
Comments
Hard
Abrupt halt to movement when two hard surfaces meet
Normal: elbow extension Abnormal:resuitof malunion fractureorheterotoPic ossification
May be normal or abnormal
Firm
Leathery firm resistance when rangeis limited by joint capsule
Normal: shoulderrotation Abnormal:resultofadhesive capsulitis
May be nomal or abnormal
Soft
Gradualonsetofresistance when softtissue approximatesorwhen rangeis limited by length of muscle
Approximation:kneeflexion Musclelength:cervicalside bending
May be normal or abnormal, dependingon tissuebulk andmusclelength
Empry
Movement stoppedby subjectprior to tester's feelingresjstance
Passiveshoulderabduction stoppedby subjectdue to pain
Always abnormal
Spasm
Movementstoppedabrupdy by reflexmuscle contraction
?assiveankledorsiflexionin subiectwith spasticitydue to uppermotor neuronlesion Active trunk fl€xion in subiect with acutelow backinjLrry
Always abnormal
Springyblock
Reboundfelt and seenat end ofrange
Causedby loosebody or displacedmeniscus
Always abnormal
Boggy
Resistance by fluid
Kneejoint effusion
Always abnormal
Extended
No resistancefeltwithin the normal rangeexpected for t-hepanicularjornt
Jointinstabiliryorhypermobility
Always abnormal
ed 3, New York, 1991, lrom Cote L, CrutcherMD: The basalganglia.In KandelERuSchwartzJH,fessellTM, eds:P/wiVlesofNeuralSciexce, :Lsevier.
h g
5-4 Combining the Findings of Active Rangeof Motion, ResistedMuscle Testing, and PassiveRange of Motion Assessment Active range of motion
Resisted testing
Passive range ofmotion
Int€rpretation
Normal
Normal
Normal
No pathologyrestrictingmotion
Normal
Normal
Abnomal
Pathologybeyondterminalactiverangeof motion Poortestingtechniquefor passiverangeof motion
Normal
Abnormal
Abnormal
Poortestingtechniqueforpassiverangeofmotion Strengthat least3/5butless*ran 5/5
Normal
Abnormal
Normal
Strengthat least3/5 butless*Ian 5/5
Abnormal
Normal
Abnormal
Nonconffactiletissuerestrictingmotion
Abnormal
Abnormal
Normal
Contractiletissueiniury resuictingmotion
Abnormal
Normal
Normal
Poorrestingtechniquesforactive rangeof motion or psychologicalfactorslimiting activerangeof motion
Abnormal
Abnormal
Abnormal
Conuactileandnoncontractiletissuesrest ctinSmotion
122
5 . Motiofl Restrictiofts
proceduressuch as radiographicimaging, diagnostic injection, arthroscopic exploration, and blood tests. motion Passive accessory Passiveaccessorymotion is testedusing joint mobiThe clinician can lization treatrnent techniques.s,13 to assess the motion use thesetreatmenttechniques joint surfaces and the extensibility of maior of ligamentsand portions of the joint capsule.During accessorymotion testing the clinician notes qualitatively if the motion felt is greatertharl lessthar5 or similar to the normal accessorymotion expectedfor that joint in that planein the particularindividual and Ac."ttory if pain is produced with testing.22,4e-50 motion testing may provide information about joint mechanicsnot availablefrom other tests.Ior example, a reduction of accessorygliding of the glenohumeral joint when passive shoulder tlexion is normal may indicatethat glenohumeraljoint motion is resfticted,and the motion of the scapulothoracic joint is excessive. Musclelength Muscle length is tested by passively positioning muscle attachmentsas far apart as possibieto elongate the muscle in the direction opposite to its action.4sThe testing of muscle length by this technique will producevalid resultsonly if pathology of the noncontractilestructuresor muscletone doesnot limit jointmotion. When testingthe lengthof muscles that crossonly one joint, the passiveROM available at that joint will indicatethe length of the muscle.Ior example, the length of the soleus muscle can be assessedby measurement of passive dorsiflexion ROM at the ankle.To test the length of a musclethat crossestwo or more joints, the musclemust first be elongatedacrossone o[ the joints and then that joint must be held in that position while the muscle is elongatedas far as possible acrossthe other joint that it crosses.4s The oassiveROM availableat the joint wiil indicate the length of the muscle. second the length of the gasrocnemiusmuscle For example, can be tested by first elongatingit acrossthe knee, by placingthe knee in full extension,and then measuring the amount of passivedorsiflexionavailableat the ankle. It is essentialthat multijoint musclesbe fully extendedacrossone joint before measurement
at the other ioint to obtain a valid test of muscle length. Adverseneuraltension Adverseneuraltensionis usuallytestedby passively placing neural structuresin their position of maximum length.Evaluationis basedon comparisonwith the contralateralside, comparisonwith norms, and of the symptomsproducedin the position assessment maximum length. of Adverse neural tension tests include the passive straight leg raise (PSLR"Lasegue'ssign), prone knee bend, passiveneck flexion, and upper limb tension tests.The PSLRis the most commonly used neural tension test and is intended to test for adverseneural tensionin the sciaticnerve. Becauseadverseneuial tensiontestsmay alsoprovoke s;rmptoms in the presence of pathologies associatedwith the muscles or joints, it is recommended that maneuversthat apply tension to the nervoussystembutdo not additionallystressthe muscles or joints be used to differentiatethe sourceof symptoms with this ty?e of test. Ior example,the PSLRtest can provoke symptomsin the presenceof pathologiesassociated with the hamstringmusclesor the sacroiliac,iliofemoral,orlumbarspinalfacetjoints. Therefore at the onset of s)'rnptomswith this test, additionaltensioncan be appliedto the nervoussystem by passivelydorsiflexingthe ankleto increasethe tension on the sciaticnerve distally or by passively flexing the neck to tighten the dura proximally. If these maneuversincreasethe patient'ss;'rnptoms,adverse neuraltensionratherthan joint or musclepat'hologyis probablythe causeof symptoms.al
toRange of andPrecautions Contraindications Techniques Motion when Rangeof motion techniquesarecontraindicated motion of a part may disrupt *re healing process. However, some controlledmotion within the range, speed,and toleranceof the patientmay be beneficial during the acute recovery stageor immediately following acute tearc, ftactures,and surgery Limited, controlled motion is recommendedto reduce the severity of adhesion,contracture,decreasedcirculation, and loss of strength associatedwith complete immobilization.33,aT
123
O e. PATHOLOGY AND PATIENTPROBLEMS
Contraindications techniquesare con-Lctiveand passiveassessment =aindicated: 1 In the region of a dislocation or an unhealed fracture. ?. Immediatelyfollowing surgrcalproceduresto tendons,ligaments,muscle,joint capsule,or skin.
F
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Precautions Caution should be obsewed when performing active or passiveROM techniqueswhen motion to -Jrepart might aggravatethe condition. This may SCCUr:
1. When there is an infection or an inflammatory processin or aroundthe joint. 2. In patientstaking pain medicationwho may not be ableto respondappropriately. 3. In the presenceof osteoporosisor any condition that causesboneftagiliry. 4. With hypermobile joints or joints prone to subluxation. 5. In painful conditionswhere the techniquesmight reinforcethe severityof the symptoms. 6. In patientswith hemophilia. 7. In the regionof a hematoma. 8. lf bonyankylosisis suspected 9. Immediatelyafter an injury where therehasbeen a disruptionof soft tissue. 10. In the presenceof myositis ossificans. In additioq neural tension testing should be per[ormedwith cautionin the presenceof inflammatory conditions;spinal cord symptoms; tumors; signs of nerveroot compression;unrelentingnight pain; neurologicalsymptomssuchasweakness,reflexchanges, or lossof sensationlrecentparesthesiaor anestltesial al a2 Detailed and reflex sympathericdystrophy.3q contraindicationsand precautionsfor each specific neuraltensiontest areprovidedin other textsdevoted to the assessmentand treatrnent of adverseneural rension.4l
APPROACHES FOR MOTION TREATMENT RESTRICTIONS Stretching Currendy,most noninvasiveinteruentionsfor reestablishing soft tissue ROM involve sffetching.Clinical
TIME
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and experimentalevidencedemonstratesthat stretching can increasemotion; however, the results may not be consistentand the recommendedprotocols vary51 When a stretch is applied to connectivetissues,within the elastic limit, over time the tissues may demonstratecreep,stressrelaxation,and plastic deformation.S2Creep is transient lengthening or deformation with the application of a fixed load. is a decreasein the amount of force Stress-relaxation required over time to hold a given length (Fig.5-7). Creepand stressrelaxationcan occurin soft tissuein a short time and are thought to be dependenton Plastic the viscous components of the tissue.53'55
124
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appliedfor a proiongedtime to causeplasticdeforma_ tjon. The Jengthof-timenecessary ro determinerhac no furcherROM gainsarepossibleis nor known and ] is probablydepe"ndent on rhe specificpoLhologyor j p at h o l o g i ecsau s i n gr h er e srr i c t i o a n n di L s d u r a t i oLnr . j additionLotime.the forcedirectionandspeedof the I
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rissueor cau,inghypermobiliry. I Many srretchingLechniques ro increasesoft tis_ | sue lengrbhave beendescribed. The mosLcommon I of stretching are passive sLrerching.pro. I to"r prioceptive neuromuscular facilitation (PNI), and I ballistic stretching(Table5-5). To perform a passive I
Fisure 5-8.plastic deformation versus elastic deformation.*[:'f';:" deformation is the,elongationproducedunder loading drat remainsafter the load is removed (Iig. 5-8). After plastic deformation,tissuewill have a permanent increasein length. A controlledstretchmust be
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77:1090-1096,1997.
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One c PAIHOLOGY AND PATIENT PROBLEMS
lathological tissueshave not been established,it is generally recommended that low-load, prolonged iorces be applied to minimize the risk of adverse effects. Manipulation of a joint while the subjectis anes-Jretizedalso involves passivestretchingof the soft dssuesto increaseROM. Manipulation under anesihesiacan producea rapid increasein ROM because high forcesthat would otherwisebe painful or cause musclesto spasmmay be applied.Thesehigh forces may cause greater increasesin soft tissue length andmay tear adhesionsto increasemotion; however, -fie risk of damaging structures or exacerbating inflammation may be greaterwith such techniques -.han with stretching while the subject is fully conscious. Proprioceptive neuromuscular facilitation techniques for muscle stretching inhibit contraction of rhe musclebeins stretchedand facilitate contraction This is achievedby having the o[ its opponent.5o subject actively contract and then voluntarily relaxthe musclesto be stretchedbefore the applicacion of the stretching force. PNF techniqueshave the advantageover other stretching techniquesof rncluding a motor leaming component ftom the repeatedactive muscle contractionslhowever, their use is frequendy limited by the requirement that a skilled individual help the patient perform the techruque. Ballisticstretchingis a techniquein which the subiect performsshort, bouncingmovementsat the end of the availablerange.Although somepeopleattempt to sffetch in this manner, ballistic stretchingis not generally used or recommended,becauseit may increasetissue tightness by activating the sketch reflex.5/
Motion The formation of conffactures is a time-related processthat may be inhibiredby motion.3sMotjon can inhibit contractureformation by physically disrupting the adhesions between gross structures and/or by limiting intermolecular cross-linking. Active or passive motion also stretches tissues, promotes *reir lubrication, and may also alter their metabolic activiqy,s4Becauseactive ROM may be
125
contraindicatedduring early stagesof healing,particularly when contractile tissue is damaged,passive motion may be usedto limit conEactureformation at this stage.For example,continuouspassivemotion (CPM) can be used to prevent motion loss after joint trauma or surgery.In addition to inhibiting the formation of contractures and adhesions, CPM has been shown to acceleratehealing, improve the orientation of collagen fibers, and inhibit edema formation.5s-61
Surgery Although the noninvasiveapproachesof stretching and motion frequently resolve or prevent motion restrictions,in some casesthese approachesare not effective and surgery may be required to optimize motion. Surgery will be necessaryif motion is restrictedby a mechanicalblock, particularly if the mechanicalblock is bony. In such cases,the surgical procedureremovessome or all of the tissueblocking motion. Surgerymay also be required'if stretching techniquescannotlengthena contractuleadequately due or if the functionallengthofa tendonis decreased procedures to hypertoniciqy.For example,Z-plasry arefrequentlyperformedto lengthentheAchillestendon in children with limited dorsiflexioncausedby congenitalplantar flexion contracturesor by hypertonicity of the plantarflexor muscles.Z-plasty is generally preformedwhen it canbe expectedto permit a more functional sait than is achievedwith noninvasive techniques alone.9 Surgical procedures to increase ROM are also frequently performed in adults. For example, surgical releasemay be performed to restoremotion limited by a Dupuytren's contracture,and tenotomy may be performedwhen tendonlengthlimits motion. Surgerymayalsobe performed to releaseadhesionsand lengthenscarsthat have formed after prolonged immobilization. Ior example, patients with extensivebums who have received limited medical intewention frequently develop contractures that cannot be stretched sufficiendy to allow fuIl function and therefore require surgicalrelease.Surgeryis more commonly requiredto releaseadhesionsthat form after injury if by prolongedinflammationor scarringis exaggerated infection.
126
5 . Motiott Restrictiotts
OFPHYSICAL AGENTS INTHE THEROLE TREATMENT OFMOTION RESTBICTIONS Although physical agents alone are generally not sufficient to revelse or prevent motion restdctions, they may be used as adjuncts to the treatment of such impairments. Physical agents combined with other appropriate treatment can enhance the functional recovery associatedwith regaining normal motion. Physicalagents are generally used as componentsof the treatment of motion restrictions becausethey can increasesoft tissueextensibility, control inflammation, contuolpain, and facilitate moUon.
Extensibility Increase SoftTissue Physicalagentsthat increasetissuetemperaturemay be used as componentsof the treatment of motion resftictionbecausethey canincreasesofttissueextensibiliry thereby decreasingthe force required to increasetissuelengthand decreasingthe risk of injury during the stretching procedure.62'64 Applying physical agentsto soft tissuebefore prolongedstretching can alter the viscoelasticityof the fibers, allowing 66 To achievethe plastic deFormationto occur.65 maximum benefit from the use of physical agents that increase soft tissue extensibility, agents that increasesuperficialtissuetemperature,such as those describedin Chanter6. shouldbe usedbeforestretching superficialtiisues, whereas agentsthat increase deep tissue temperature, such as ultrasound and diathermy,shouldbe usedbeforestretchingdeepsoft tissues.
Control lnflammation andAdhesion Formation A numberof physicalagents,panicularlycryotherapy and certain types of electricalcurrents,are thought
to control inflammation and its associatedsigns Controlling and symptoms after tissue injury.6z,6e inflammation may help to prevent the development of motion restrictions by limiting the formation of edema during the acute inflammatory stage and thereby limiting the degreeof immobilization. Controlling the severity and duration of inflammation alsolimits the durationand extentof the proliferative responseand may thus limit the formation of adhesionsduring tissuehealing.
PainDuring Stretching Control Many physical agents, including thermotherapy, cryotherapy,and electricalcurrents,can help to control pain. This effect may assistin the treatment of motion restrictionsbecause,if pain is well controlled, tissuesmay be stretchedfor a longer period, which may increasetissuelength more effectively.If pain is controlled,motion may also be initiated soonerafter inlury limiting the lossof motion causedby immobi lization.
Motion Facilitate Somephysicalagentsfacilitatemotion and thus assist in tlle treatment of motion restrictions. Electrical stimulation of the motor nervesof imervated muscles or direct electrical stimulation of denervated muscle can make muscles contract, These muscle contractionsmay complementmotion producedby normal physiological contractionsor substitute for such conffactionsif the subject does not or cannot move independently. Water may also facilitate motion since it provides buoyancy to an immersed body to assistwith motion againstgravity.The buoyancy of water may prove particularly beneficialin assisting patients with active ROM restrictions causedby contractiletissueweakness.
127
Ote . PATHOLOGY AND PATIENT PROBLEMS
) Clinical Case Studies I The following casestudiessummadzethe concePtsot motion restrictionsdiscussedin this chapter.Basedon the scenariopresented,an evaluation of the clinical findingsand goalsof treatmentareproposed.Theseare followed by a discussionof the factorsto be considered in treatmentselection.
Case 4 TR is a 45-year-oldmale who has been referred to physicaltherapywith a diagnosisof a right L5, Sl iadiculopathy. He complains of constant mild to moderatelysevereright low back pain that radiatesto his right buttock and lateral thigh after sitting for more than 20 minutes and that is relievedto some degreeby walking or lying down. He rcPortsno numbness,tingling, or weaknessof the lower extremities.The pain staltedabout 6weeks ago,the moming afterTR spenta day stackingfirewood, at which time he woke up with severelow backand rightlower extremitypain down to his lateral calf. He also had difficulty standing up sffaight.He has had similar problemsin the past;however,they have always ful1yresolvedafter a couple of daysofbed restand a few aspirins.TRfirct saw his doctor regardinghis presentproblem 5 weeks ago, and at that time he was prescribeda nonsteroidalantiinflammatory drug and a muscle relaxant and was told to take it easy.His symptoms improved to their current level over t}le following 2 weeks but have not changedsince that time. He hasalsonot beenable to retum to his job as a telephoneinstallersincethe onset of symptoms 6 weeks ago. An MN scan last week showed a mild posterol;teral disc bulge at L5-S1 on the right. The patient has had no prior physical*rerapy for his back problem. The objectiveexam is siSoificanttor a 50o/. restrictionof lumbar active ROM in folward bending and right sidebending.both of which causeincreased right low back and lower extremity pain. Left side bendthe patient'spain.Passivestlaight leg raising decreases ing is 35% (on rhe right, limited by right lower extremity pain),and 60% (on the left, limited by hamstringtiShtness).Palpationrevealsstiffnessand tendemessto right unilateral posterior-anteriorPressureat L5-S1 and no notableareasof hypermobility.All other tests,including lower extremity sensatlon,strength,and reflexes,are witlin normal limits. OF THE CLINICALFINDINGS EVALUATION This patientpresentswith the impairmentsof restricted lumbarforward-bendingand right side-bendingmotion,
pain, restrictedlumbar nerveroot mobiliry on the right, is indicatedby the restrictedpassivestraightleg raising test, and bul8ing of the L5-S1disc,TheseimPairments have resultedin a iimitation of sitting toleranceand ao inability to retum to work. PREFERREDPRACTICEPAfiERN lmpaired Joint Mobility. Motor Function, Muscle Peiformance,Range of Motion, and Reflex Integrity AssociatedWith SpinalDisorders,(4F) PLAN OF CARE The anticipated goals of ueatment at this time are to reducepain and increasesitting tolennce sufhciendy for the patient to be able to retum to limited duty wo*. The long-term goals of treatment are to fully alleviate pain, recumlumbar rangeo[ morion to normal,increase passivestraight leg raising and sitting toleraoceto within normal limits, and have ttre patient retum to his full work dutles. ASSESSMENTREGAFDINGSELECTIONOF THE OPTIMAL TREATMENT The optimal treatment for this patient would separate the disc spacesand/or reduce disc protrusion, thus decreasingcompressionon the nerveroot and aliowing improved,pain free motion. Thereforethe interyention of ihoice at this time is Eaction.The approPdatetype of of treatmentare discussed tractionand the parameters in Chapter10.
Case2
MP is a 40-year-oldfemale diagnosedwith adhesive capsuLitisof the left shoulder Shereportsthat her shoulder first beganto hurt about 6 months a8owithout any apParent cause. Although *rc pain has almost comPletely resolvedsince that time, her shoulder has also gradually become more stiff, preventing her from reaching up to brush her hair and from reachingbehind herself to zip up her skirts. The obiective evaluation is significant for restrictedROM of the left shoulderasfollows:
Left
Active Range of Motion
Right
Flexion Abduction Hand behindback
100" 170' 80' 170' Leftsacroiliac Central thoracolumlolnt barjunction Continued
728
5 . Motiot
Restrictiotts
) Clinical Case Swdies-cont'd PassiveRange of Motion Intemal rotation Extemalrotation
Right 90' B0'
Left 50' 10'
Glenohumeralpassiveinferior and posterior glide are both restrictedon the left. MP has had no pdor trcatmPnr
F^r rhi< n'^hl.-
EVALUATION OF THE CLINICALFINDINGS This patient presentsimpairments of testrictedactive and passivemotion of her left shoulderin a capsular pattem, reducing her ability to perform activities of daily living, including grooming and dressing. This patient's signs and symptoms and their duration indicate that the problem has probably progressedto t}le remodelingstageof healing,with some possibility of chronicinflammation,MP doesnot report significant pain at this time. No tone abnormalitiesarenoted. This patient's signs and symptoms are consistent with the diagnosis of adhesive capsulitis, which occursmost often in the shoulder.30,69,70 The onset of this problem is frequendy reported to be insidious, although it may be associatedwith other pathology such as local trauma, tendiaitis,cerebrovascular accident,or swgery of tlre neck and tl\ohx.27,29'30'69 Predisposingfactors include female gender,history of diabetes,immobilizatioq and ageover40 yea$.29's0,71 PBEFERREDPRACTICEPATTERN Impaired Joint Mobility, Moror Functioq Muscle Performance,and Range of Motion AssociatedWith ConnectiveTissueDysfunction,(4D) PLAN OF CARE The anticipated goals of treatment at dris time are to restore normal active and passive motion of the
I
left shoulder and to give MP the abiliry to perform all activities of daily living in t}le manner she used previously, using both upper extremities. Since her shoulderROM is probably restrictedby soft tissue shortening, interyention should be dilected at increasing dre extensibility and length of the shortened tissues, particularly the anterior inferior capsule of the glenohumeral joint. Other appropriate goals for this late stage of healing are to control scar tissue formation and to ensure adequate circulation. Although no strength abnormalities were noted on this initial evaluation, the patient's strength should be reevaluatedas she regains ROM since she may have strengtJrdeficits at these end rangesdue to disuse. Should strength deficits become appareng an additional goal of treaftnent would be to restore normal streneth to the left shoulder muscles. ASSESSMENTREGARDINGSELECTIONOF THE OPTIMAL TREATMENT Although there is disagreement conceming the optimal intervention for adhesivecapsulitis,it has been suggestedthat treatments that increasethe extensibfity and length of the restricted soft tissues around the glenohum€ral ioint and decreaselocal inflammation facfitate the resolution of this problem.3072,73 As is explained in greater detail in Section 2 of this book, a number of physical agene that provide localized deep heating may increase the extensibfity of the tissues, whereas other physical agents, such as ice or low-dose ultrasound, may facilitate resolution of the inflammation. Thermottrerapy could be used in conjunction with stretching and raoge-of-motion activities to lengthen the shortenedtissues.Joint mobfization and later strengthenlng may also be necessaryto regain full function of the should€r.
PrefenedPhysicalTherapistPatlemssMl4D and 4F]arecopyright2002AmericanPhysicaltherapyAssociation.A.llrightsreserued.
CHAPTER REVIEW The musculoskeletaland neural structures of the body are normally abie to move. Active movement occurs when muscles contract, and passivemovement occurswhen the body is actedon by an outside force.Physiologicaljoint motion is the motion of one segmentof the body relativeto another,while accessory motion is the motion that occursbetween the joint surfacesduring normal physiologicalmotion.
The amountof motion normally availabledependson the joint being consideredand may also vary wi& the subject'sage, sex, and health status; howeveq motion may be restrictedby a variety of pathologies including contractures,edema,adhesions,mechanical blocks,spinaldisc herniation,adverseneural teosiorq and weakness.Motion will be restrictedin a capsularpattern if the capsulesuffoundinga joint is affectedand otherwisecan be restrictedin a noncap
Ow c PATHOLOGY AND PATIENTPROBLEMS
129
13. SullivanMS, Dickinsin CE,Troup JD: The influenceof ageand genderon lumbar spinesagittalplanerangeof motion, Spine19682-686, 1994. 14. HolmesA, Wang C, Han ZH et al:The rangeandnature of flexion-extension motion in the cervical spine, Spine t9:2505-2510 , 7994. 15. Kublman KA: Cervicalrangeof motion in the elderly, AtchPhysMed Rehabil74:107t-1079, 1993. 16. EinkaufDK, GohdesMl, JensenCM et al: Changesio spinal mobility with increasingage in women, Plys Ther67:370-375, 1987. 17. Lind B, SihlbomH, Nordwall A et aL Normal rangeof motion of the cervical spine,Arch PhysMed Rehabil 70:692-695 , 1989. 18. DesrosiersJ, Hebert R, Bravo, et al: Shoulderrangeof motion of healthy elderly people: a nomative study, t995. PhysOccuVThetCetiatr73:101-11,4, Brown IM, Downed PA, 19. Iiebert J: Active shoulder References range of motion in personsaged 60 years and older, Foundations and Exercise: L KisnerC, ColbyLA: Therapeutic PhysOc.cup TherCeriatrt3:L15-128,1995. ed3,Phrladelphia, 1996,IA Davis. Tethni4ues, 20. Kessler RM, Hertling D: Managemeutof Commoa of muscleto othersofttisGS:Comparison 2. Cummings Disorders,PhysicalTheraVyPrillci7lesand Musculoskeletal suein limiting elbowextension, J OnhoySponsPhys Philadelphia, 1983,Harper & Row. Methods, 4, 1984 . 5(4):170-1,7 Ther 21. Kaltenborn FM: Mobllizatiax of the Extrenity Joints: 3. SofbergJO: The stiff elbow,Acta OnhoVScand67: ed 3, Oslo, Techni4ues, and BasicTreatmext Examination 626-631 , 1996. .1.CooperJE, Norwat 1980,Olaf Norlis Bokhandel. ShwedykE,QuanburyAOetal:Elbowjoint restriction:Effecton upperlimb motion duringper- 22. Maidand GD VenebtalManipulation,ed 5, London, 1986,Butterworths. formanceof three feeding acivities, Arch PhysMed 23. SaundersHD, SaundersR: Evaluation,Treatmettaad Rehabil7 4:805-809 , 1993. Disoders: Spine, ed 3, Pteventionof Musculoskeletal J. BadteyEM, WagstaffS, Wood ?H: Measuresof Saunders Group. MN, 1995, (disability) Chaska, arthritis in relation to in functionalability Phlladelphia, Dis 43:563-569, 24. Cuyton AC: TextboobofMedicalPhysiology, of jointmotion,AnnRheum impairment 1981,WB Saunders. 1984. PG,Engelke KA:Effectsof exercise 25. Cyri,ax J: Textbook of OnhoVaedicMedictue, ed 6, 6. Godges JJ,MacRae Baltimore,1975,Williams & Wilkrns. and on hip rangeof motion,trunt muscleperformance NeviaserJf:The ftozenshoulder:Diagnosis 26. NeviaserRJ, . 7 3:468-477 1993 gaiteconomy, PhysThet , andmanagement,C/lnOnhoV223:59'64,1987. of the 7. Nordin M, Irankel YH Basic Blomechaxics System,ed 2, Philadelphia,1989, 27. Andrews AW, Bohannon RW: Decreasedshoulder Musculosbeletal rangeof motion on pareticside aker stroke,PhysThel Lea& Febiger. 66:768-772, 7989. 8. American Academy of OrthopaedicSurgeons:Joint Edinburgh, 28. fuzk TE, Pinals RS: Irozen shoulder, Senin Athtitis Motiox:Methodsof MeasurixgandRecordittg 1982. Rheun11:440-452, 1965,ChurchillLivingstone. Scodand, 29. Bunker TD, Anthony ?P: The pathology of frozen 9 . ShinaburgerNI: Limited ioint mobility in adults with shoulder:a Dupuytrenlike disease,/BoreJoitttSurgBr diabetesmellitus,P, ys Ther67:2L5-218,1987. 77:677-683, 1995. Dudgeon BJ: Shoulder limitation AK, Sheny DD, 1 0 .Libby in juvenilerheumatoidarthritis,Atch PhysMed Rehabil 30. ParkerRD, Iroimson AJ, Winsberg DD et al: Irozen clinicalpicshoulder Part 1: chronology,pathogenesis, 72:382-384,1991,. nhopedics 1.2:869-873 ture, andtreatment,O , 7989. 11. RoachKI, Miles TP: Normal hip and knee activerange a review oflitersyndrome: N: Frozen shoulder 31. Grubbs Thet 7\: o[ rnotion: ttre relationship to age, Phys ature,JOfthol SlrottsPhysThert8:479-487 ,1993. 656-665, 1,99t. 32. AlesonWH, Amiel D, Woo SL-YImmobiliry effectson 12. Iilbert I, Iuhri JR,New MD: Elbow, forearm,and wrist synovial joints, the pathomechanicsof joint conftacpassiverangeof motion in personsagedsixry and older, -32 1795-Irc,1980 ture,Biorheology PhysOuup ThetCetiatr10:17 , 1992.
:Jlar pattern.Vadoustestsandmeasuresmay be used = determine the degreeof motion restdctioq the =sue involved, and the nature of the pathology :cntributing to a motion restdction.Motion restric:ons may be treated conservativelyby stretching :-rd morion or, in somecases.may requireinvasive :urgery Physical agents may seffe as adjuncts to :rese interventionsby increasingsoft tissueextensiiility beforestretching,controllinginflammationand -dhesionformation during tissuehealing,controlling :ain during stretchingor motion, or causingor assistrg with motion. The readeris referredto the Evoive -.vebsiteat http://evolve.elsevier.com/Cameron for :rudy questionspertinentto this chapter.
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5 . Motioft Restictioas
33. Salter RB: Textbaoleof Disorders and lnjuies of the Musculoskeletal System,ed.2,BaIamore,1983,Williams &wilkins. 34. Iranl C, AkesonWH, Woo SL-t et al: Physiologyand therapeuticvalue of passivejoint motion, Clin OnhoV 185113-125,1984. 35. Woo SL,Matthews JV,Akeson WH et al: Connective tissueresponseto immobiliry. Correlativestudy ofbiomechanicaland biochemicalmeasurementsof normal and immobilized rabbit knees, Anhitis Rheum 18: 257-264,1975. 36. Akeson WH, Amiel D, Abel MF et al: Effects of immobilization on joints, Clin Onhap 219:28-37, 1987. 37. Dorlaxds lllustatedMedicalDictioxary,ed 29, Philadelphia, 2000,WB Saunders. 38. EnnekingWI: The intraarticulareffectsof immobilization on the human knee,/ Boneloint Surg 54A:973,
52. Taylor DC, Dalton JD, SeaberAV et al: Viscoelastic propertiesofmuscle-tendonunits:the biomechanicsof stretching,AmJ SponsMed 18:300, 1900. 53. Fung YC: Biomechanics:Mechanical Properties of Living Tissues, ed 2. New York: Springer-Verlag 7993. 54. McClure PW, Blackbum LG, Dusold C: The use spLintsin the treatmentof stiffness:biologic rationale and an algorithm for making clinical decisions, Plys Ther74:1101-1 107.1994. 55. Norkin CC, Levatgie PK:Joint Structurcand Fuftctiott: Comprehexsive Analysis, ed 2, Philadelptta, 1990, Davis. 56. Voss Dt, ionra MK. Myers Neuromuscular Faciliation,ed 3, Philadelphia, Harper& Row 57. LamontagneA, Maloun F, fuchards CL: behavior of piantar flexor musde-tendonunit at r972. J OtthopSportsPhysTher26:244-252 , 1997. 39. SlaterH, Buder DS: The dynamic centralnervoussysSalterRB, SimrnondsDF,Malcolm BW et al: The ter:e.ln Cieve'sModetnMaxual ed,2,New York, 1994, logicaleffectofcontinuouspassivemotion on the /-L..--L:lr I :..:----^^ !L'ur!r,,! !rvuB urrc. ing of fulI thicknessdefectsin anicular cartilage: 40. Oliver J, Middle drtchA: Functional Anatomyof theSyine, experimentalinvestigatton in dtenbbit,J BoneI oiat London,1991,Butterworth-Heinemann. 62A:1232-1251, 1980. 4L. ButIerDS: Mobilizatiottof theNenous Systen,Edirtbvgh, 59. SalterRB, Bell RS,KeeleyIW: The protecriveeffect 1991,ChurchillLivingstone. continuous passivemotion on living anicular cartilage -fomberlin 42. acute septicarthritis: an experimentalinvestigation JP,SaundersHD: Evaluatiox, Tteatuext and Preventioxof MusculosbeletalDisorders:Ettremities,ed 3, rhe abbit, Clix Onhoy 159:223-247,198\. Chaska,MN, 1994,SaundersGroup. 60. FrankC, AkesonW, Woo S et al: Physiologyand 43. Creenman PE: PrinciVtesof Manual Medicine, ed,2, peutic value of passive joint motion, C/,, BalcJmore, 1996,Williams& Wilkins. 185t113-125, 1984. 44. Norkin CC, White DJ: Measurement of Joint 61. Covey MH, DutcherK MaryinJA etal: Efficacyof Motiot: A Cuide to Coaiometry, Philadelphia,1985,FA tinuous passive motion (CPM) devices with Davis. -400,I9BB. bws, J Burx CareRehabil9:397 45. Kendali Fl McCreary EK: Muscles:Testingaxd Futction, 62. LentellC, HetheringtonT, EaganJet al: The useof ed 3, Baltimore,1983,Williams & Wilkins. mal agentsto influencethe effectivenessof low 46. Daniels L, Worthrngham C: Muscle TestingTechaiques prolonged stretch, J Onhop Spon Phys Ther 1 of Manual Examixation,ed 4, Philadelphia, 1980, WB 200-207 ,1992. Saunders. 63. WarrenC, LehmarrnJ,KoblanskiJ:Elongationofrat 47. ClarksonHM, Cllewich CB:Musculosbeletal Assessmeat: tendon: effect of load and temperawre, Arch Phys Joixt Range of Motion aud Manual Muscle Streagth, Rehabil52:465-474, 484, 1971. Baltimore,1989,Williams & Wilkns. 64. WarrenC. Lehmam J, KoblanskiJ: Heacand 48. fuddle DL: Measurement of accessory motion: procedures:an evaluationusing rat tail tendon, cdtical issues and related concepts, Phys Ther 72: PhysMed Rehabil57:122-126 , 1976. 865-874, 1992. 65. CerstenJW: Effectof ultrasoundon tendon 49. .N4intsN, Dvir Z: Wrist complex mobility: a study of 1tr7, AnJ PhysMetl 34:362-369 , 1955. passive flexion and extension and accessorymove66. LehmannJ, MasockA, Warren C et al: Effect of ments, PhysiotherCaxada 40:282-285, t9BB. peutic temperatureson tendon extensibiliryArcl 50. Binlley J, StratfordPW, Cill C: Interraterreliability o[ A4edRehabil51:481-487 , 1970. lumbar accessorymotion mobility testrrLg, Phys Thet 67. Hocutt JE,Jaffe\ Rlplander CR: Cryotherapyin 75:786-795,1995. spratns.An J Syon: Med l0:3 | 6-319, 1982. 51. Bonutti PM, Windau JE: Static progressivestretch ro 68. Cote DJ, ?renticeWI, Hooker DN et al: reestabLishelbow range of motioq Clh OnhoV of three treatment proceduresfor minimizing 303:128-134,1994. sprainswelling,PftysTher68(7):1072-107 6, 1988.
Ore o PATHOLOGY AND PATIENT PROBLEMS
69. Patten C, Hillel AD: The 11th newe syndrome, Arch Onlaryngol Head Nec* Sutg 1!9:215-220, f993. 70. Emig EW, Schweitzer M!, Karasic D et al: Adheiive capsulitis ofthe shoulder: MR diagnosis,AmJ Roextgenol 164(Q:1457-1459,f995. 71. Kozin I: Two uniqueshoulders:adhesivecapsulitisand sympathetic dystrophy syndrome of r'j:otion, Postgrad Med73:207-216,1983.
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72. Rizk TE, Morris L, Gavant MI: Treatment of adhesive capsulitis(frozenshoulder)witharthrographiccapsular distension and rupture, Arch Phys Med Rehabil75: 803-807,7994. 73. RizkTE, PinalsRS,TalaiverASrCorticosteroid injections in adhesive capsulitis: investigation of their value and 1991. site,ArchPhysMed RehabilT2:20-22'
ThePhysicalAgents
ThermalAgents: ld andHeat SUMMARY
OF INFORMATIOIl
Physical Principles of Thermal Energy SpecificHeat -Vodesof Heat Transfer Cold-Cryotherapy Effectsof Cold Usesof Cryotherapy Contraindicationsand Precautionsfor Cryotherapy AdverseEffectsof Cryotherapy Application Techniques Clinical CaseStudies Heat-Thermotherapy EffectsofHeat
COVERED
Usesof SuperficialHeat Contraindicationsand Precautionsfor Thermotherapy AdverseEffectsof Thermotherapy Application Techniques Other Means of Applying Thermotherapy Clinical CaseStudies Choosing Between Cryotherapy and Thermotherapy Chapter Review
OBJECTIVES IJVonampletion of this chaytet,the readerwill beabk to: 1 . Identi$r the physicalpropertiesof and the physiologicalresponsesto, thermal agents. 2 . Analyze the physiologicalresponsesto thermal agentsnecessaryto promote particular treatment goals. 3 . Assessthe indications, contraindications,and precautionsfor the use of thermal agentswith respectto different patient management situations. ,| Evaluatedifferent gzpesof thermal agents with respectto their potential to produce
desiredphysical and physiological effects. 5 . Chooseand use the most apPropriatethermal agent to obtain desiredtreatment goals. 6 . Presentedwith a clinical case,evaluatethe clinical findings, proposegoalsof treatment, assesswhether a superficialthermal agent would be the best treatment, and, if so, formulate an effectivetreatment plan, including the most appropriatethermal agent,for achievingthe goalsof treatment.
133
134
6 c Thermal Aeents: Cold atd Heat
This chapter discussesthe basic physical principles and physiologicaleffects of transfering heat to or ftom patients by using thermal agents.The clinical applicationsof cold and superficialheatingagentsare also addressed.Superficialheating agentsare those that primarily increasethe temperatureof the skin andsuperficialsubcutaneous tissues.In contrast,deep heating agents also increase the temperature of deepertissues,includinglargemusclesand periarticular structures,and generallyreachto a depth of about 5 cm. The clinicalapplicationsof deep-heatingagents are not coveredin this chapter but are discussedin Chapters7 ard 1.2. The therapeutic application of themal agents resultsin the transferof heat to or ftom a patient's
body and bewveenthe variouscomponenttissuesand fluids ofthe body.Heattransfermay occurby conduction. convection,conversion,radiation, or evaporation. Heatingagentstransferheatto the body,whereas cooling agents transfer heat away ftom the body. Thermoregulationby the body also uses the above processesto maintain core body temperatureand to maintainequilibriumbetvyeenintemalmetabolicheat production and heat loss or gain at the skin surface. The following section of this chapter discussesthe physicalprinciplesofheat transferto or ftom the body and wittrin *re body. This sectionis followed by discussionsof the physiologicaleffects of cooling and heating and directionsfor the clinical applicationof superficialcoolingandheatingmodalities.
PHYSICAL PRINCIPLES OFTHERMAL ENERGY HEAT SPECIFIC Specificheat is the amount of energyrequiredto raise the temperatureof a given weight of a material by a given number of degrees.Different materialsusedas thermalagentsand differentbody tissueshave different specificheats (lable 6-1). For example,skin has higher specificheat than fat or bone,and water has a higher specificheat than air. Materials with a high specificheat requiremore energyto achievethe same temperatureincreasethan materialswith a low specilic heat.Materialswith a high specificheat alsohold more energythan materialswith a low specificheat when both are at the same temperature.Thermal agentswith a high specificheat, such as watet are therefore applied at lower temperaturesthan airbasedthermalagents,suchaslluidotherapy,to transfer the sameamount ofheat to a patient.The specific
p
e-t Sp."nc Heat of Various Materials Material
Water Averagefor human body Skin Muscle Iat Bone
Specificheat in /g/'C
4.19 1.01 3.56 3.77 3.75 2.30 1,.59
heat of a materialis generallyexpressedin joulesper gramper degreesCelsius.
MODES TRANSFEF OFHEAT Different physical agentstransfer heat by different modes.Theseincludeconducrion.convection.conversion, radiation, and evaporation,as discussedin detailin the following sections.
Conduction: HeatTransfer byDirect Contact SuchasHotPacks andColdPacks Heating by conduction is the result of energy exchangeby directcollisionbetweenthemoleculesof tlvo materialsat different temperatures.Heat is conductedfrom the materialat the highertemperatureto the material at the lower temperatureas the faster moving molecules in the warmer material collide with the moleculesin the cooler material and cause them to accelerate.Heat transfercontinuesuntil the temperatureand the speedof molecularmovementof both materials become equal. Heat may be transfered to or from a patientby conduction.If the physical agent used has a higher temperaturethan the patient'sskin, for example,a hot pack or warm paraffin, heat will be transferred ftom the agent to the patient,and the temperatureof the superficialtissues in contactwith the heatingagentwill rise.If the physical agent used is colder than the patient's skir5 for
Tgo . THE PITYSICAL ACENTS
:xample,anice pack,heatwill be transferredftom the :atient to the agent,andthe temperatureofthe super-cial tissuesin contactwith the coolingagentwill fall. Heat can also be transferredfrom one areaof the :ody to another by conduction.Ior example,when :ne areaof the body is heatedby an extemalthermal :gent,the tissuesadjacentto and in contactwith that :rea_will increasein temperaturedue to heating by :cnoucuon. Heat transferby conductionoccursonly between raterials of different temperaturesthat are in direct :cntact with eachother.lf there is any air berweena :cnductivethermal agentand the patient, the heat is :rst conductedfrom the thermal asent to the air and =en ftom the air to the patient. Rateot heattransferbyconduction -he rate at which heat is transferredby conduction :erween tvvo matedalsdependson the temperature :ifferencebetween the materials,their thermal con' iuctivity, and *reir areaof contact,and is expressed :y *re following formula. areaofcontactx thermalconductivityx remn."t"'"
iate of a-ea! :ansfer
li Ff"'"-."
tissuethickness
The thermal conductivity of a material describes -,\erateatwhich it transfersheat by conductionandis expressed x'C/cm) ffable in (callsec)/(cm2 .eneralJy 5-2).Note that this is not the sameasa material'sspe:ific heat. A number of guidelinescan be derived from the precedineformula.
p"
Thermal Conductivity of Various Materials
Material
Silver A.lumrnum Ice Waterat 20 "C Bone Muscle Fat Airat0'C
Thermal conductiviw (caVsec),1(cm2 x 'Clcrir)
1.01 0.50 0.005 0.0014 0.0011 0.0011 0.000s 0.000057
135
for heatlransferbyconduclion Guidelines 1. The greaterthe temperaturedifferencebetweena heating or cooling agent and the body part it is applied to, the faster the rate of heat transfer.For example,the higher the temperatureof a hot pack, the more rapidly the temperatureof the area of the patient's skin in contact with the hot pack will increase.Generally,the temperaturesof conductive physicalagentsare selectedto achievea fast but safe rateoftemperaturechange.Ifa heatingagentisonly a few degreeswarmer than the patient, heating will take too long; by contrast,if the temperaturedifference is large, heat transfer could be so rapid as to quickly burn the patient. 2. Materialswith high thermal conductivitytransfer heat more rapidly than those with low thermal conductivity.Metals have high thermal conductivity, whereas water has moderate thermal conductivity and air haslow thermalconductivity. Heating and cooling agents are generally composedof materialswith moderatethermal conductivitv to orovide a safeand effectiverate of heat transfer Materialswith low thermal conductivity canbe used as insulators to limit the rate of heat transfer For example,some types of hot packs are kept hot by soakingin and absorbingwater that is kept at approx'C 'F). (125 imately 70 The high temperature,high specificheat, and moderatethermal conductivity of the water allow efficientheattransfer:however.ifthe pack is applieddirecdy to a patient'sskin, the patient will probably soon feel uncomfortablyhot and could easilybe burned.Thereforetowels or terrycloth hot pack coversthat trap ai5 which has low thermal conductivity, areplacedbetweenthe packand the patient to limit the rate ofheat transfer.In general,six to eight layersof toweling are placedbetr,veena hot pack and a patienq however, if the patient gets too hot, additional layersof toweling can be addedto further limit the rate of heat conduction. Note that newer towels and coversare generally thicker and thereforeact asmore effectiveinsulators than older ones.Sincesubcutaneous fat haslow thermal conductivity,it also actsas an insulator,limiting the conductionofheat to or ftom the de€pertissues. Because metal has high thermal conductivity, metal jewelry should be removedfrom any areathat will be in contactwith a conductivethermal agent.If metal jewelry is not removed,heat will rapidly transfer to the metal, with the potential to burn the skin that is in contac!with it.
135 136
ThermalAgeflts:CoMandHeat 6. ThetmalAgerrts:ColdandHeat
Becauseice has higher thermal conductivity than water evenat thanwater it causesmore iapid coolingthan water, ,^/ater, th"ttti"l conductivitiesof Th" thermal the he sametemperature.ihe jifferent commercially available cold packs vary, different some somebeinghigher than water or ice and othersbeing the brand or type of Theiefo"re,when changing lower. tower.Theiefore, -assume not issume that th; new cold :old pack used,one should n"ot tor the same manner.for rhesamemanner, packcanbe packcanbe appliedin the layersof samenumber numberof layers orr with with the same of rime. time, o a-ount amountof insulatingmaterialasthe old pack. 3. Thi larger the areaof iontact between a thermal agent and the patient, the greaterthe total heat transfer.Ior example,when a hot pack is appliedto up to patient is immersed immersedup when a patient entire back, back,or when the entire the the neck in a whirlpool or a Hubbard tank, the total amount ofheat transferredwill be greaterthan ifa hot the calf. pack is appliedonly to a smailarea-overlying ' 4. The'rcte o[ iemperaturerise decreaslsin propottionto tissuetiickness.When a thermalagentisin contact with a patient's skin, the skin temperature increasesthe most and deeper tissuesale proglessively lessaffected.The deeperthe tissue,the lessits t"-p"rutur" wili change.Thereforeconductivethermal agentsarewell-suiledto heatingor coolingsuperficial tissuesbut should not be usedwhen the goal is to changethe temperatureof deepertissues.
I an areaof the body and producesa local changein tis- | temperature,the circulationconstandymovesthe I suetemperatufe, Sue heatedblood out of the areaand moves coolerblood I into t[]e areato returnthe localtissuetemperatureto a I convectionreduces normal level.This local coolingby convectionreduces I local rhe localth€ impact of superficialheating agentson the the | the rate of increasesq" tissuetemperature.Vasodilationincr..u::t I rare,at,whichthe tissue circulation,increasingthe rare,at.which circulation. I vasodilaIhus. the vasodllanormal.r Thus, Ieturns returnsto normal. temperatule cemPerature I plotects the tistion that occursin responseto heat protects I burning' risk of burning the suesby reducing l
Energy I Type of rype oreners from One One Conversion from Conversioni conversion trii::5;**r'':5?:fifi:1T:ff ".;f,1"}"tr conversioni and and Diathefmy, Diathefmy, Ultfa'Ound Ultfa'Ound SUChaS aS tOAn.thef An.thef SUCh I Metabolism Metabo'ism *.r*lrul;":ili"T;ft:?il*1t;f;ji:: I Heattransfer Heat transferby conversioninvolvesthe conversionof I a nonthermalform of energy,suchasmechanical,elec- | trical, or chemical energy, into heat. Ior example, I ultrasound,which is a mechanicalform of energy,is I converted into heat when applied at a sutlicient I intensity to a tissue that absorbsultrasoundwaves. I Ultrasoundcausesvibration of moleculesin the tiszue, I which generatesfriction between the molecules,I resultingin an increasein tissuetemperature.When I diathermy, an elecffomagneticform of energy,,is I applied to the body, it causes rotation of polar I
ofa bycirculation HeatTransfer convection: such as Temperature Different of a Medium
the between in friction whichalsoresults molecules, I teto*"T: intissue tncrease ::1"::1"-:""d "" "t-:T: I
Heattransferby convectionoccurs contact betwe;n a circulatingmedium and another This is in contrastto materialofa differenttemperature. is constantconthele heatingby conduction,i[which tactbJwveena stationarythermalagentandthe patient. During heatingor .ooltg by coniection the thermal agentis in moiion, so new pirts of the agentat the initi"altreatmenttempetature'keep coming into contact with the patient'sbodypart.As i resulqhiat transferby convectiontransfersmore heat in the sameperiod of time than heat transferby conductionwhen the same matedal at the same initial temperatureis used.For example,immersionin a whirlpool will heata patient's skinmorerapidlvthanimmersionina bowl o[water of the sametempeiature,and the fasterthe water moves, the morerapii the rateofheat transferwill be. Blood ciiculatingin the body alsotransfersheat by local changesin tissuetemperaconvectionto redu-ce ture. For example,when a therial agentis appf;d to
I causingit to become cold. Thermal energy is con- | vertedinto chemicalenergyto drivethis reaction. I Unlike heatingby conduction_orconvection,heat- | ing by conversionis not affectedby the temperature I of the thermal agent.When transferringheat by con- | rate of heat transfer depends on the version, I _the power of the energysource.The power of ultrasound I and diathermy is usuallymeasuredin watts, which is I the amount of energyin joulesoutput per secondThe I amount of enelgy output .by a chemical reaction I depends on the reacting chemicalsand is usually I measuredin joules.Jhe rate of tissue temperature I increasealso dependson the size of the area being treated,the size of the applicator,efficiencyof transmission ftom.the apPlicatorto-the Patient,and the type of tissuebeingtreated.Different t'?es of tissues absorbdifferent forms of energyto different extents and thereforeheat differently'2
Fruidotherapy,wtrirtpoot,etooiiii.uiu-tl* fi""'"".H]tltrn',"'"::5:ll:ftrtfi," I a chemicalreactionthat extractsheat from the pack, asthe resultofdirect
TTT'oC THE PHYSICAL AGENTS
Heattransferby conversiondoesnot requiredirect -':rtact betvveenthe thermal agent and the body; - ,.wever,it doesrequire any interveningmaterial to :. a good transmitter of that type of energy.For ,:':ample,a transmissiongel, lotion, or water must be ,-.ed between an ultrasound transducer and the ::rient to transmit the ultrasoundbecauseai1 which :-:ght otherwise come between the transducerand -- e patient,transmitsultrasoundpoorly. Physicalagentsthat heat by conversionmay also -:ve other nonthermal physiological effects. Ior .:.:ample,although the mechanicalenergy of ultra.:und and the electricalenergyof diathermy canpro:'ice heat by conversior5they are also thought to :ve direct mechanicalor electricaleffectson tissue. .- ful1discussionof absorptionand the thermal and :nthermal effectsof ultrasoundand diathermy can : e foundin Chapters7 and,12, respect:ely.
ladiation: Exchange ofEnergy Directly without :n Intervening Medium SuchasInfrared Lamp -:--eating by radiation involves the direct transfer of :rergy from a materialwith a higher temperatureto ne with a lower temperaturewithout the needfor an rtervening medium or contact.This is in contrastto -eat transfer by conversion,in which the medium :rd the patientmay be at the sametemperature.It is .-so different from heat transfer by conduction or :cnvection,which both requirethe thermal agentto :e in contactwith the tissuebeingheated.The rate of :emperatureincreasecausedby radiationdependson
the intensity of the radiation, the relative sizes of the radiation source and the area being treated, the distance of the source from the treatment area, and the angleof rhe radiarionro the ti"sue.
Evaporation: Absorption ofEnergy astheResult ofConversion ofa Material froma Liquid toa Vapor StateSuchasVapocoolant Sprays Sweating A materialmust absorbenergyto evaporateand thus change form from a liquid to a gas or vapor. This energy is absorbedin the form of heat, either from the matedai itself or from an adjoining material, resultingin a decreasein temperature.For example, when a vapocoolantsprayis heatedby the warm skin of the body, it changesfrom its liquid form to a vapor at its specific evaporationtemperature.During this process,the spray absorbsheat and thus cools the skin. Another exampleis the evaporationof sweat, which alsoactsto cool the body. The temperatureof evaporationfor sweatis a few degreeshigherthan the normal skin temperature;therefore,if the skin temperatureincreasesfrom exerciseor an extemalsource and the humidity of the environmentis low enough, the sweatproducedin responseto the increasedtemperature will evaporate,reducing the local body temperature.If the ambient humidiry is high, evaporation will be impaired. Sweating is a homeostatic mechanismthat servesto cool the body when it is overheatedto help return body temperaturetoward ule nolmal lange.
COLD-CRYOTHERAPY Jryotherapy,the therapeuticuse of cold, has clinical ipplicationsboth in rehabilitationand other areasof nedicine. The primary useof cryotherapyoutsideof :ehabilitationis for the destructionof malisnant and ronmal'gnanttissuegrowths, for which very lo:emperaturesare used and the cooling is generally :pplied directly to the tissuebeingtreated.In rehabil:tation,miid cooling is usedto control inflammatior! cain, and edema; to reduce spasticity; to control :ymptoms of multiple sclerosis;and to facilitate movement (Iig. 6-1). This type of cryotherapy is a p p l i e dr o r h e s k i nb u t c a nd e c r e a st ei s s u et e m p e r a ture deepto the areaof application,includingintraariicular areas.r Cryotherapy exerts its therapeutic
737
Figure 6-1. Cryotherapyagents.
138
6 . Tlrcrnal Ageflts: Cold awl Heat
effectsby influencinghemodynamic,neuromuscular, and metabolic processes,the mechanismsof which areexplainedin derailin the Following secrions.
EFFECTS OFCOLD Hemodynamic effects Initial decrease in blood flow Later increase in blood flow Neuromuscular effects Decreased nerve conduction velocitv Increased pain threshold Altered msscle strength Decreased spasticity Facilitation of muscle contraction Metabolic effects Decreased metabolic rate
Figure 6-2. How cryotherapydecreases bloodflow
Hemodynamic Eflects
the circulatory rate by increasing blood viscosirytherebyincreasing the resistance to flow. It is thought that the body reducesblood flow in immediate constriction of the cutaneous vessels responseto a decreasein tissuetemperatureto proand a reductionin blood flow. This vasoconstric- tecrotherareasfrom excessive decreases in temperation persists as long as the duration of the cold ture and stabilize core body temperature.The less applicationis limited to lessthan 15 to 20 minutes.a blood that flows through an area being cooled,the Studiesshow that repeatingice application after an smaller*re amount of blood that is cooledand thus initial 20-minute application for 2 repetitions of *re less other areas in the circulatory system are 10 minutes off and 10 minutes on lowers blood affected. Reducing circulation results in a greater flow significantly more than a single 20-minute ice decreasein the temperatureof the area to which a application.'The vasoconstrictionand reduction coolingagentis appliedbecausewarmer blood is not in blood flow producedby cryotherapyis most beingbroughtinto the areato raiseits temperatureby pronouncedin the areawhere the cold is applied convection,and lessof a decreasein temperaturein because this is where the rissue temperature otherareasof the body becauselittle of the cold blood decrease 1sgreatest. is circulatedto theseareas. Cold causescutaneousvasocorstrictionby both directand indirectmechanisms(Fig.6-2).Activationof Laterincreasein bloodtlow the cutaneouscold receptorsby colddirecdystimulates The immediatevasoconstrictionresponseto cold is a the smoodrmusclesof the blood vesselwalls to conconsistentand well-documentedphenomenonlhowtract.Coolingof the tissuealsodecreases the production ever,when cold is appliedfor longer periodsof time andreleaseof vasodilatormediators,suchashistamine or when the tissue temperature reachesless than and prostaglandins, resultingin reducedvasodilation. 10 'C (50 'F),vasodilationmay occur.This phenomeDecreasingthe tissuetemperaturealso causesa reflex non is known as cold-inducedyasodilation(CIVD) and activationof sympatheticadrenergrc neurons,resulting was first reported by Lewis in 1930.7His findings in cutaneousvasoconsftictionbo*r in the areathat is were replicatedin a number of later studies;810howcooledand,to a lesserextent,in areasdistantfrom the ever,vasodilationhas not beenfound to be a consissiteof coid application.6 Cold is alsothought to reduce tent responseto prolongedcold application.4,11
Initialdecrease inbloodflow Generally, if coldis appliedto the skin,it causes an
Two c THE PIIYSICAL ACEATS
Lewis reported that when an individual's fingers z-ereimmersedin an ice bath, their temperatureinihowever,after 15minutes,theirtem=lly decreased; -rature cyclicallyincreasedand decreased(Iig. 6-3). :avis cofielatedthis temperaturecycling with alter-dng vasoconstrictionand vasodilation and called It is proposedthat the huntis rhe huntingrespozse. rg responseis mediatedby an axonreflexin response = the pain of prolongedcold or very low tempera::res, or that it is causedby inhibition of contraction :i the smooth musclesof the blood vesselwalls by .{reme cold.12Maintained vasodilation, without --.'cling,has also been observedwith cooling human :orearmsat 1 "C (35"D for 15minutes.u Cold-inducedvasodilationis most likely to occur = the distal extremities,such as the fingers or toes, -arthaoolicationsof cold for more than 15 minutesat 'C. Although the amount of =-p"iutur"r below 1 rasodilation is usually small, in clinical situations :,,-here vasodilationshould be avoided,it is generally =commended that cold applicationbe limited to 15 srnutes or less,particularlywhen treating the distal r*remities. When vasodilationis the intendedgoalof :eatment, cryotherapy is also not recommended ':ecause it doesnot consistendyhavethis effect. Although the increasein skin rednessseenwith the :cplicationof coldmay appeartobea signof CIVD, it is :.-tually thought to be primarily the result of an increase = the oxyhemoglobin concentrationof the blood due
139
to the decreasein oxygen-hemoglobindissociation that occursat lower temperaturesl31Fig.6-4). Since cooling decreasesoxygen-hemoglobindissocialion, making less oxygen available to the tissues, coldto bean effective inducedvasodilationis not considered oxygendeliveryto an area. meansof increasing
Effects Neuromuscular Cold has a variety of effectson neuromuscularfunction, including decreasingnerve conduction velocity, elevating the pain threshold, altering muscle force generatior5decreasingspasticity,and facilitating muscle contraction. velocity oecreased neruec0nduction nerveconducWhen nervetemperatureis decreased, tion velociry decreasesin proportion to the degree and duration of the temperaturechange.laDecreased newe conduction velocity has been documentedin responseto the application of a superficialcooling agent to the skin for 5 minutes or longer.lc The decreasein nerve conduction velocity that occurs with 5 minutes of cooling fully reverseswithin 15 minutes in individuals with normal circulation. However,after 20 minutes of cooling,nerve conductionvelocitymay take30 minutesorlonger to recover dueto the greaterreductionin temperaturecausedby the longerdurationof cooling.l6
o
z
100
Lll
f
o
IE t!
56 zF
= H10 z
x<
Y o
E !,1
z ii0
Figure6-3. Hunting response,cold-induced vasodilation cf finger imrnersed in ice water, measuredby skin temoeraturechange.(Irom Lewis T: Observationsupon *re ieactionsof the vesselsof the human skjn to co\d,Hean 15177-208, I93Q.\
E{* 7Al =.t !J
f 0
Figure6-4. Effect of temperature on oxygen-hemoglobin dissociation curve- (Irom Barcrott J, King W: The effect of temperature on the dissociation curve of blood, J Physiol39.374-384, 1909.)
t40
6 o Thetmal Asents: Cold ard Heat
Cold can decreasethe conduction velocity of tion, thus conffolling post-injury edemaformation.19 both sensoryand motor nerves.It has the greatest Reducingedemacan aileviatepain that resultsfrom effect on conduction by myelinated and small compressionof nerves or other pressure-sensitive fibers and the leasteffect on conductionbv unmvelistructules. nated and large fibers.l6A-delta fibers,whicfr are small-diameter,myelinated,pain-transmittingfibers, Alteredmusclestrength demonstrate the greatest decreasein conduction Dependingon the durationof treatmentand the timvelociqyin responseto cooling.Reversibletotal nerue ing of measurement,cryotherapyhasbeenassociated conductionblock can also occurwith the aoplication with both increasesand decreases inmuscle strensdl of iceoversuperficially locaredma;ornervebranches ]sometricmusclestrensthhas beenfound to suchas *re peronealnerve at the lateralaspectof the direcdyafter the applicationof ice massagefor 5 mi Knee." utes or less;however the duration of this effect nor beendocumented.To The proposed painthreshold Increased for this response to brief coolinginclude The application of cryotherapy can increase the of motor nerve excitability and an increased pain thresholdand decrease the sensationof pain.The logicalmotivationto perform.In conrast,after proposed mechanisms for these effects include ing for 30 minutes or longer, isometric counter-iritation via the gate controlmechanismand strengthhas beenfound to decreaseinitially and the reductionof musclespasm,sensorynewe conduc- to increasean hour later, to reach greaterthan tionvelocity, or postinjuryedema.18 cooling strengthfor the following 3 hours or Stimulation of the cutaneouscold receptorsbv (Iig. 6-5).The proposedmechanismsfor the cold may providesufficienrsensoryinput io block strength after prolonged cooling include red the transmissionol painful stimuli fully or partially of blood fiow to the muscles,slowed motor alongthe spinalcord to the cerebralcortex,increasing conduction,increasedmuscleviscosity,and pain threshold or decreasingpain sensation.Such joint or soft tissuestiffness. gatingof the sensationof pain canalsoreducemuscle It is important to be aware of these changes spasmsby interrupting *re pain-spasm-paincycle, muscle strength in responseto *re application as describedin Chapter 3. Cryotherapy may also cryotherapysincethey canobscureaccurate, reduce the pain associatedwith an acute rnjury by assessmento! muscle strengthand patient reducingthe rate ofblood flow in an areaand decreas- It is therefore recommendedthat muscle ing the rate of reactionsrelated to acute inflammabe consistendymeasuredbefore the application Figure 6-5. Effectsof cold on stength of musclecontraction. @ata ftom Oliver RA, Jobnson DJ, Wheelhouse WW et al: Isometricmuscle contractionresponseduring recovery from reduced rntramuscular temp€rature, ArchPhysMedRehabil60:L261,29,1,979;JohnsonJ, Leider IE: Influenceof cold bath on maximum handgripstrength, PerceVt Mot Skills44:323-325, 1977;DaviesCTM, YoungK: Effectof temperatureon the contractile properties and musclepowerof tricepssurae in humans, J Aypl Physiol 55191-195 , 1983.)
Tgo . THE PIIYSICAL AGENTS
--:)'otherapyand that pre-cooling strength not be :rmpared with postcoolingstrengthwhen trying to paI.renrprogress. 5SeSS spasticity Decreased r,hen applied appropriately,cryotherapy can tem-,,crarilydecreasespasticity. Two mechanismsare ::oposed to act sequentiallyto produce this effect: ::st, a decreasein gammamotor neuronactivity and? ;ier, a decreasein afferentspindleand Colgi tendon ::gan activity. A decreasein the amplitude of the -r.chillestendon reflex and integratedelectromyogra--1y (EMC) activity have beenobservedwithin a few rconds of the application of cold to the skin.2a,25 -hesechangesarethought to be relatedto a decrease = the activity of the gammamotorneuronsasa reflex =action to stimulation of the cutaneouscold recep=rs. This fast responsemust be relatedto stimulation :j cutaneousstructuressincethetemperatureof the ruscles cannot decreaseafter such a brief period of :coling. After more prolongedcooling,lastingfor 10 to 30 ainutes, a temporarydecreaseor eliminationof spas:city and clonus, depressionof the Achilles tendon :eflex,and a reductionin resistanceto passivemotion :ave aisobeen observedin some oatientswith soasThesechangesare thou;ht to be causei by :city.25-2e in the dischargefrom the afferentspindles : decrease -rd Colgi tendon organs as a result of decreased :)uscle temperature.30 These later effects generally 1 to :ersist for 1.5 hours and can thereforebe taken :dvantageof in treatmentby applyingcryotherapyto lypertonic areasfor up to 30 minutes before other rterventions, to reducespasticityduring functional
741
MetabolicEffects Decreased metabolic rate Cold decreases the rate of all metabolicreactions, including those involved in inflammation and healing.Thus cryorherapycan be usedto control acute inflammation, because it is not recommended when healing is delayed becauseit may further impair recovery The activiry of cartilagedegradingenzymeq including coliagenase,elastase, hyaluronidase,and protease,is inhibited by decreases in joint temperature,almostceasingat joint temperatures of 30 "C (86 "I) or lower.3l Thus cryotherapyis recommendedas a ffeatment for the prevention or reduction of collagen destruction in inflammatory joint diseasessuch as osteoarthritisand rheumatoid arthritis.
USES OFCRYOTHERAPY Inflammation control Edema control Pain control Modifi cation of spasticity Sjmptom management in multiple sclerosis Facilitation Cryokinetics and cryostretch
lnflammation Control
Cryotherapycan be usedto control acuteinflammation and thereby acceleraterecovery ftom injury or trauma.32Decreasingtissue temperatureslows the rate of the chemical reactions that occur during -r rhprrncr rri. ,.ri0itiF< the acuteinflammatory responseand alsoreducesthe heat, redness,edema,pain, and lossof function assoFacilitation otmuscle contraction ciatedwith this phaseof tissuehealing.Cryotherapy -he stimulusof a brief applicationof cryotherapy directly reducesthe heat associatedwith inflamma:s thoughtto facilitatealphamotor neuronactivity tion by decreasingthe temperatureof the area to :o producea contractionin a muscle that is flaccid which it is applied.The decrease in blood flow caused jue to upper motor neuron dysfunction.25 by vasoconstrictionand increasedblood viscosiqy, This and the decreasein capillarypermeabilityassociated :ffect is observedin responseto a few secondsof with cryotherapy, impede the movement of fluid :ooling andalsolastsfor only a short time. With more :rolonged cooling of evena tew minutes, a decrease from the capillariesto the interstitial tissue,thereby controllingbleedingand fluid lossafter acutetrauma. .:r garnmamotor neuron activiq/ reducesthe force These effectsreducethe rednessand edemaassoci:f muscle contraction.This brief facilitation effect ated with inflammation. As describedin more detail :f cryotherapy is occasionallyused clinically when to stimulate production below, cryotherapy is thought to control pain by the of appropriate rying decreasingthe activity of the A-delta pain fibers and :notor pattems in patientswith upper motor neuron by gating at the spinal cord level. Controlling *re -esions.
142
6.
Thentt,rl Ageats: CoA 4t d Heat
edemaand pain associatedwith inflammation limits the loss of function associatedwith this phaseof tissuehealing. It is recommendedthat cryotherapy be applied immediately following an injury and throughout the acute inflammatory phase. Immediate application helpsto controlbleedingand edema;thereFore, the soonerthe treatmentis applied,the greaterand more irnmediate the potential benefit.33Clinically, local skintemperature canbe usedto estjmatethe itaeeof healingand tlus to determineiI cryorherapyis indicated.If the temperatureof an areais elevated,the area is probably still inflamed and cryotherapy is likely to be beneficial.Once the local temperature returnsto normal,tie acuteinflammaLion hasprobably resolvedand thereforecryotherapyshouldbe discontinued. Acute inflammation usually resolves within 48 to 72 hours of acute trauma but may be prolongedwith severetrauma. inflammatorydiseasessuch as rheumatoid arthritis, or with chronic recuffent injuries. If the temperature of an area remains elevated for longer than appropriate for the patient's condition, the possibility of an infection should be consideredand the patient should be referred to a physician for further evaluation. Cryo*rerapy should be discontinued when acute inflammationhas resolvedto avoid slowins chemical reactionsor impairing circuiationduring"the larer stagesof healing when these effectsof cryotherapy canimpederecovery The prophylacticuse of cryotherapyafter exercise has also been shown to reduce the severitv of delayed-onset muscle soreness(DOMS).34DOMS is thought to be the result of inflammation from muscleand connectivetissuedamagecausedby exercise.35'36 Clinically,the prophylactii use of cryotherapy after aggressivejoint or soft tissuemobilization, or,after lighr activiryin an areawith a preexisting inflammatiorS can effectively decreasepostactivity soreness. Although cryotherapycan help to control itflammation and its associatedsigns and symptoms, the causeof the inflammation must also be addressed direcdy to preventrecurence.Ior example,if inflammationjs causedby overuseof a tendon,*Lepadent's useof thar tendonmusrbe modifiedif recuirence of symptomsis to be avoided. When cryotherapy is applied with the goal of controlling inflammation, the treatment time is generally limited to 15 minutes or less because
longerapplicationhas beenassociatedwith vasodilation and increasedcirculation.T-1o However, since reflex vasodilationin responseto cold has not been shown to occur outside of the distal exffemitieslonger treatmentdurationsmay be used for areas other than the distal extremities.4,llTo limit the probability of excessivedecreasesin tissue temperatureand cold-inducedinjury cryotherapyapplications should be at least t hour apart so that the tissue temperature can retum to normal between tleatments.
Edema Gontrol
Cryotherapycan be usedto control the formation of edema, particularly when the edema is associated with acute inflammation.3TDuring acute inflammation, edemais causedby extrava;don of fluid into the interstitium caused by increasedintravascular fluid pressureand increasedvascularpermeabiliw. Cryotherapy reducesthe intravascularfluid pressuie by reducingblood flow inro the areavia vasoconstriction and increasedblood viscosity.Cryotherapy also controls increasesin capillary permeability by reducingthe releaseof vasoactivesubstances, suchas histamine. To minimize edema formation, cryotherapy should be applied as soon as possibleafter an acute trauma. The formation of edema associatedwith inflammation will be most effectively controlled if the cryotherapyis appliedin conjunctionwith compression and elevation of the affected area.38,39 Compressioncan easily be applied with an elastic wrap (Fig. 6-Q, and elevation should be above the level of the heart. Cornpressionand elevationreduce edema by driving extravascularfluid out of the swollen areainto the venousand lymphatic drainage systems.The combined treatment of rest, ice, compression,and elevationis frequendyreferredto bythe acronym RICE. Cryotherapy is not effective in controlling the formation of edema caused by immobiliw and poor circuladon.Itr such cases,increasedrather than decreasedvenous or lymphatic circulation is required to move fluid out of the affected area. This is best accomplishedwith compression,elevation, heat, exercise,and massage.40 The mechanisms of action of this combination of treatrnents are discussedin detail in Chapter 11 in the section on compression.
Tvo . THE PIIYSICAL AGENTS
743
Modification ofSpasticity
:gure6-6,Cryotherapy with compressionand elevation.
Cryotherapycan be usedto temporarilyreducespasticity in patients with upper motor neuron dysfunctions.As explainedabove, brief applicationsof cold, lasting for about 5 minutes, causean almost immediate decreasein deep tendon reflexes.Longer applications,for 10 to 30 minutes, also decreaseor eliminateclonusand decreasethe resistanceof musclesto passivestretch.24Becauselonger applications oI cryotherapycontrolmore of the signsof spasticiry cryotherapyshould be applied for up to 30 minutes when this is the treatmentgoal.The decrease in spasticity producedby prolongedcooling generallylasts for t hour orlonger afterthe treatment,which is sufficient to allow for a varietyof therapeuticinterventions, inciudingactiveexercise,sffetching,functional :ctiwitipc nr hwoienc
rainGontrol
Symptom Management inMuliiple Sclerosis
-1e decreasein tissue temperature produced by :notherapy may direcdyor indirectlyreducethe sen.:rion of pain.Cryotherapydirecdyand rapidly mod:es the sensationof pain by gatingpain transmission .'.-id:r activiqyof the cutaneousthermalreceptors.This rmediate analgesiceffect of cold is exploitedwhen .apocoolantspraysor ice massageare used to cool -':e skin before stretching the musclesbelow. The ::duced sensationol pain allows the stretch to be :ore forcefuland thus potentiallymore effective. Applyt.tg cryotherapy for 10 to 15 minutes or :nger cancontrol pain tor 1 or more hours.This pro.:nged effect is thought to be the result of blocking ::nduction by deep pain-transmittingA-delta fibers, :rd by gating of pain transmissionby the cutaneous -'ermal receptors.l6 fhe effectis rhoughrro be pro:nged becausethe temperatureof the arearemains wer than normal tor 7 or 2 hours after removal of =e coolingmodality. Rewarmingof the areais slow :ecausecold-inducedvasoconstrictionlimits the flow :i warm blood into the area,and subcutaneousfat :sulatesthe deepertissuesfrom rewarming by con:uction from the ambientair. The reduction of pain by cryotherapy can also -rterrupt the pain-spasm-paincycle, resulting in :educedmuscle spasmand prolongedalleviation of :ain evenafterthe temperatureof the treatedareahas :eturnedto nomal. Cryotherapycanalsoreducepain rdirectly by alleviatingthe underlying causeof this ,vmptomj suchasinflammationor edema.
The symptomsof somepatientswith multiple sclerosis are aggravatedby generalizedheating, such as occursin warm environmentsor with activity. This groupofpatientscanrespondwell to generalizedcooling, with improvementsin electrophysiological measuresand in clinicalsymptomsand function.alCooling with a vest has been shown to improve fatigue, muscle strength,and posturalstability in a group of patientswith heat-sensitivemultiple sclerosiswhen comparedwith a shamnoncoolingvest.42
Facilitation The rapid application of ice as a stimulus to elicit desiredmotor patterns,known as4lrrb icing rs a technique developedby Rood. Although this technique may be used effectively in the rehabilitation of patientswith flaccidity resulting from upper motor neurondysfunction,it tendsto haveunreliableresults and is thereforenot commonly used.43 The resultsof quick icing are unreliablebecausethe initial phasic withdrawal patternstimulatedin the agonistmuscles may lower the restingpotentialof the antagonists,so that a secondstimuluselicitsactiviqyin the antagonist musclesratherrhanin the agonists.r4 This produces motion first in the desireddirection. followed bv a reboundmovementin the oppo,itedirectjon.lc i.ras also been proposed*rat icing may adverselyimpact motor control causedby dysynchronizationof the cortexasa rerultof increased symparhetic tone.45
144
6 o Thennal Asents: Cold and Heat
andCryostretch Cryokinetics Cryokinetics is a technique that combinesthe use of cold and exercisein the treatment of pathology or disease.46This technique involves applying a cooling agentto the point of numbnessshordy after any injury to reducethe sensationof pain and thus allow *re patient to exercise and work toward regainingrangeof motion (ROM) as early as possible in the recovery process.4/This approach is most commonly used in the rehabilitation of athletes. Cold is applied first for up to 20 minutes, or until dre patient reports numbing of the area; then the patient performs strengthening and stretching exercisesfor 3 to 5 minutesuntil sensationretums.48 The coolirg agent is then reapplieduntil analgesia is regained.This sequenceof cooling, exercise,and recooling is repeated approximately five times. Because*re numbnessproducedby the cryotherapy masksthe pain relatedto the injury to avoid further trauma and tissuedamageit is essential*rat, before applyingthis technique,the exactnatureof the inlury is known and the therapistis certainthat it is safeto exercisethe areainvolved.
CONTRAINDICATIONS
fortheApplication of Cryotherapy o Coldhypersensitivity o Cold intolerance ' Cryoglobulinemia
The useof cryotherapyis contraindicated. . . . . . in patients with cold hypersensitivity, cold intolerance, cryoglobulinemia, paroxysmal cold hemoglobinuria, Ra1'naud's disease, or Ra1'naud's phenomenonso Cold Hypersensitivity (Cold-indtceil Urticaria). Someindividualshave a familial or acquiredhypersensitivityto cold that causesthem to developa vascular skin reacrionin responseto cold exposure.sl This reactionis marked by *re transientappearance of smooth, slightly elevatedpatches,which are redder or more pale than the surroundingskin and are often attended by severeitching. This responseis
Cryosftetchis dre applicationof a cooling agent beforestretching.The purposeofthis sequence oftreatmentsis to reducemusclespasmandthusallow greater !o range-of-motion increases with stretching.
CONTRAINDICATIONS ANDPRECAUTIONS FOR CRYOTHERAPY Although cryotherapyis a relatively safe treatment modality, its use is contraindicatedin some circumstancesand it should be applied with cautioo in others.Cryotherapymay be appliedby a qualified clinicianor by a properlyinstructedpatient.Rehabilitation cliniciansmay useall forms of cryotherapy are noninvasiveand do not desftoy tissue.Patients may use cold packsor ice packs,ice massage,or contrastbathsto treatthemselves. If *re patient's condition is worsening or is
improving within the period of two or three ments, the treatment approach should be
and chansedor the patient should be referredto physicianfor further evaluationevenwhen apy is not contraindicated.
o . o .
Paroxysmalcold cryoglobinuria Raynaud'sdiseaseor phenomenon Overa regeneratingperipheralnerve Overan areawi*r circulatorycompromise or peripheralvasculardisease
or cold-induced known as coldhyyersexsitivity These symptoms can occur only in the area of applicationor all over the body. Cold lrtolerance. Cold intolerance. in the form severe pain, numbness, and color changesin
to cold,canoccurin patientswith sometypesof matic diseasesor following severeaccidentalor -^l
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LU urc
l:-:--
ur6rLb.
CryogJobulinemia. Cryoglobulinemia is an mon disorder characterizedby the aggregation serumproteinsin the distalcirculationwhen the di extremities are cooled. These aggregatedproteins a precipitate or ge1that can impair circulatioq
Two o THE PHYSICAL A GENTS
r:':al ischemiaand then gangrene.This disordermay - idiopathic or may be associatedwith multiple :','eloma, systemiclupus erythematosus, rheumatoid ;:-:rritis,or other hyperglobulinemicstates.Therefore =e therapistshouldcheckwi*r the referringphysician :e;oreapplyingcryotherapytothe distalextremitiesof =,,' patientwith thesepredisposingdisorders. - troxysnal Cold Hemoglobituria. Paroxysmalcold ::inoglobinuria is the releaseof hemoglobininto the :::ae from lysedred blood cellsin responseto local or .-nerrlcvno
t^
"^
. . . over regenerating peripheral nerves Cryotherapy should not be applied directly over a regeneratingperipheralnervebecauselocal vasoconstriction or alterednerveconductionmay delaynewe regenelatron. ASK THE PATIENT: o Do you haveany nervedamagein this area? o Do you haveany numbnessor tingling in this limb? If so,where?
l,-l
:;vraud's Disease afld Phenomenon.Raynaud,s :iease is the primary or idiopathic form of paroxys=-aldigital cyanosis.Raynaud'sphenomenon,which -. more cofi)rnor\ is paroxysmaldigital cyanosisdue :: some other regional or systemic disorder.Both ::nditions are characterizedby sudden pallor and -.-anosislollowed by rednessof the skin of the digits ::ecipitated by cold or emotional upset and relieved :',-warm*r. Thesedisordersoccurprimarily in young .','omen. InRaynaud'sdiseasethe symptomsarebilat::ai and symmetricevenwhen cold is appliedto only :re area, whereas in Raynaud'sphenomenon,the :.rnptoms generallyoccuronly in the cooledextrem-'. Raynaud'sphenomenonmay be associatedwith =oracic outlet syndrome,carpaltunnel slmdrome,or
ASKTHE PATIENT o Do you have any unusual responsesto cold? If the patient answers"yes" to this question,ask for further details.Includethe following questions: . Do you developa rash when coldi (A sign of cold hyp ersensitivity) . Do you have severe pain, numhne<<
changes in your fingers*h"^';;;;i;;
ASSESS: . Testsensation In the presenceof sensory impairment or other signsof newe dysfunction,cryotherapyshouldnot be applieddirecdyover the affectednerve. . . . over an area with circulatory compromise or peripheral vascular disease Cryotherapy should not be applied over an area with impairedcircularionbecauseir may aggravate the condition by causing vasoconstriction and increasingblood viscosity. Circulatory impaiment may be the result of peripheralvasculardisease, trauma to the vessels,or early healing, and is often associatedwith edema.When edemais present,it is important that its causebe determined,sinceedema due to inflammation can benefit from cryotherapy, while edema due to impaired circulation may be increased.These causesof edema can be distinguishedby observationof local skin coloration and temperature.Edemadue to inflammation is characterized by warmth and redness,whereasedemadue to poor circulation is characterizedby coolnessand pallor.
en,l rnl^'
;;i;;
(Signiof Raynaudt dl"ur"zpheno-".ron1 . Do you geLblood in your urjn. .^tA) "+.. t -i-^ '"'"
rAsisnoiparoxysmut -ld h"-;;;,;;;;"
if the"responses'indicate that the"patient mayhave :oldhypersensitivity, coldintolerani",.t;gl;;ili"":nia,paioxysmal coij i,"-og1out.,uri;;ild;;ffi :ase,-or Raynaud's phenomlnon,;;;;i;;;;fu ' ' ror be applied.
145
lsl(rHEPArlENt ' lJo you havepoor circulationin this limb? fsj:ss: ' sf
146
6.
Thermal Aseflts: Cold qnd Heat
PRECAUTIONS
ol Cryotherapy fortheApplicati0n . Over the superficialmain branchof a nerve o Over an openwound
Applycryotherapywith caution, , . . . . over a superficial main branch ofa nerve Applying cold direcdy over the superficial main branch of a nerve, such as the peroneainewe at the lateral knee or the radial nerve at the posterolateral '52,53 elbow, may causea nerveconduction61ock.14,17 Therefore when applying cryotherapy to such an area,one shouldmonitor for signsof changesin nerve conduction,such as distal numbnessor tingling, and discontinuecryotherapyif theseoccur. . . . over an open wound Cryotherapyshould not be applieddirecdy over any deep open wound becauseit can delay wound healing by reducing circulation and metabolic rate.sa Cryotherapymay be appliedin areasof superlicialskin damagelhowever,it is important to realizethat *ris can reducethe efficary and safety of *re treatment becausewhen there is superficialskin damage,the cutaneousthermalreceptorsmay alsobe damagedor absent.These receptorsplay a part in activatingthe vasoconstrictio4pain control,andspasticityreduction producedby cryotherapy;therefore,theseresponses are likely to be lesspronouncedwhen cryotherapyis appliedto areaswith superficialskin damage,Caution should also be usedif cryotherapyis appliedto such areasbecausethe absenceof skin reducesthe insulatlayersandincreases ing protectionofthe subcutaneous coolinsto thesetissues. Llee riskof excessive
t Hypertension . In patientswith poor sensationor poor mentation . Very young andvery old patients ASSESS: . Inspectthe skin closelyfor deep wounds, cuts, or abrasions.Do not apply cryotherapyin the areaofa deepwound, and uselessintensecoolingif cuts or aoraslonsarepresen[. . . . when treating patients with hypertension Sincecold can causetransientincreasesin systolic diastolicblood pressure,patientswith should be carefullymonitored during the app of cryotherapy.55Treatmentshould be if blood pressureincreasesbeyond safelevels treatment. Guidelines for safe blood pressures individual patients should be obtained from physician. . . . when treating patients with poor or mentation Although adverseeffectswith cryothe:oPyarewe, the patient cannot sense or report discomfort the clinicianshould other abnormalresponses, tor the patient'sresponsedirectly.Check for responses to cold suchaswhealsor abnormal in color or strength,both in the areaof cold app tion and generally. . . . when treating very young and very old Caution should be usedwhen applying cryoth to the very young or the very old becausethese viduals frequendyhave impaired thermal and a limited ability to communicate.
ADVERSE EFFECTS OFCRYOTHERAPY Tissse death Frostbite Newe damage Unwanted vasodilation
A variety of adverseeffectshavebeenreported cold is applied incorrecdy or when The most severeadverseeffect ftom *re applicationof cryotherapyis tissuedeath caused prolonged vasoconstriction, ischemia, and
bosesin the smallervessels.Tissue death may result ftom freezingof the tissue.Tissuedamage
Two . THE PIIYSICAL ACENTS
:ccur when the tissue temperature reaches 15'C i9'I); however, freezing (frostbite)does not occur ':ntil the skin temperaturedropsto bewveen- 4" and -10 "C (39"to 14'F)orlower Excessive exposureto cold ray alsocausetemporaryor permanentnerve damage, :esultingin pairl numbness,tingling,hyperhidrosis,or ::erveconductionabnormalities.56 To avoid soft tissue :r nerve damage,the duration of cold application :tould be limited to under 45 minutes,and the tissue :emperature shouldbe maintainedabove15'C (59'F). Becausethe prolongedapplicationof cryo*rerapy :c the distalextremitiesmay causereFlexvasodilation :nd increasedblood flow, cryotherapy should be
Evaluatethe patientand set the goalsof treatment. Determineif cryotherapyis *re most appropdate treatment. Determinethat cryotherapyis not contraindicated for this patientor condition. Inspectthe areato betreatedfor openwoundsand rashesand assesssensation.Check the patient's chartfor any recordofpreviousadverseresponses to coldand for any diseases that would predisposethe patientto an adveneresponse. Ask the appropriate questionsof the patientasdescribed in the preceding sectionson contraindications andprecautrons. Selectthe appropriatecoolingagentaccordingto the bodypartto be treatedandthe desiredresponse. Selectan agentthat providesthe desiredintensity of cold treatment,best fits the locationand size of the area to be treated, is easily applied for the desired duration and in the desired nosition. is readily available.and is reasonablypriced. Ar agent that conforms to the contours of the area beingtreatedshouidbe usedto maintaingood contact with the patient'sskin. With agentsthat cool by conductionor convection,suchas cold packsor a cold whiripool, good contactmust be maintained bewveenthe agent and the patient's body at all times to maximize the rate of coolins. For brief coolingthe besrchoiceis an agentthaiis quickto apply and remove. Any of the cooling agents describedas follows may be availablefor use in a clinicalsetting,and the patient can readily use ice packs,ice cups,and cold packsat home. Ice packs and ice massageare the least expensivemeansof
147
applied for only 10 to 15 minutes when the goal of treatmentis vasoconstriction.
TECHNIQUES APPLICATION Cryotherapymay be appliedusinga vadety of materials,including cold or ice packs,ice cups,controlled cold compressionunits, vapocoolant sprays,f:,ozen towels,ice water,cold whirlpools,and contrastbaths. The following section gives details on application techniquesfor thesedifferent cooling agentsand the decisionsto be made when selectinga specificagent and an applicationtechnique.
providing cryotherapy,whereas controlled cold compression unitsarethemostexpensive. 5. Explainto the patientthe procedureand reasonfor applying cryotherapy and the sensations tlre patientcanexpectto feel. During *re application of cryotherapy by any means the patient will usually experiencethe tollowing sequenceof sensations:intensecold followed by burning,then aching,and finally analgesiaandnumbness.Thesesensationsarethought to correspondto increasingstimulation of the thermal receptors and pain receptors followed by blockingof sensorynerveconductionasthe tissue tpn^er^t-"ra
Ap.ra
)
SEOUENCEOF SENSATIONSIN BESPONSETO CRYOTHERAPY . Intensecold . Burning o Aching o Analgesiaandnumbness 6. Apply the appropriatecoolingagent. Seleafron thefollowinglist: Cold packsor ice packs Ice cupsfor ice massage Seeapplication Controlledcold compression methodsfor units Vapocoolant spraysor brieficing eachcooling agenton the Irozen towels following pages. Icewater immersion Cold whirlpool Contrastbath Continued
748
6.
Thennal Ase ts: Cold atd Heat
/. Assessthe outcomeof ffeatment. After completing cryotherapywith any of the precedingagents, reassessthe patient, checking particularly for progresstoward the set goals of treatmentand for any adverseeffectsof the treat-
ment. Remeasure quantifiable subjective conditions and objective limitations, and reassessthe impairments and disabilities. 8. Document the treatment.
Figure6-7. Cold packs. (Courtesy Chattanooga Croup, Inc., Hixson, TN.)
Figure6-8. Cooling units for cold packs. (Courtesy Chattanooga Group,Inc.,Hixson,TN.)
orlcePacks ColdPacks Cold packsare usually filled with a gel composedof silicaor a mixture of salineandgelatinandare usually coveredwith vinyl (Iig. 6-Z).The gel is formulatedto 'C (32'to 41 "I) for be semisoiidat between0' and5 the pack to conform to the body contourswhen it is within this temperaturerange.The temperatureof a cold pack is maintainedby stodng it in a specialized coolingunit (Fig.6-8)or in a freezerar 5 "C (23'I). Cold packsshouldbe cooledfor at least30 minutes betweenusesand for 2 hours or longer beforeinitial use.Patientscan useplasticbagsof frozenvegetables at home as a substitutefor cold packs,or they can make their own cold packs from plastic bags filled with a 4:1 ratio mixture of water and rubbing alcohol
cooledin a home freezer.The addition of alcohol to the water decreasesthe freezing temperature of the mixture so that it is semisolidand flexibleat -5 "C
(23'r).
Ice packsare made of crushedice placedin a plastic bag. Ice packs provide more aggressivecooling than cold packs at t'he same temperaturebecause ice has a higher specific heat than most gels and because ice absorbs a large amount of energy when it melts and changesfrom a solid to a liquid. 57 Both cold packs and ice packs are applied in a similar manrrer, as described below; however, more insulation should be used when applying a n i c e p a c k b e c a u s ei t p r o v i d e ' m o r e a g g r e s s i v coorng.
Tvo . THE PHYSICAL AGENTS
: quipment Required :ld Packs Cold packsin a variety of sizesand shapes appropriatefor differentareasof the body coolingunit Ereezeror spectalized Towelsor pillow casesfor hygieneand/or :nsula on
'ROCEDURE - Removeall jewelryandclothingfrom the areato be treated and inspect the area. ,. Wrap the cold pack or ice pack in a towel. Use a damp towel if a maximal rate of tissue cooling is desired. It is recommended that warm water be used to dampen the towel to allow the patient to gradualiy become accustomed to the cold sensation. A thin, dry towel can be used if slower, less intense cooling is desired. A damp towel is generally appropriate for a cold pack, whereas a dry towel should be used for an ice pack since ice provides more intense cooling. r. Position the patient comfortably, elevating the area to be treated if edema is present. :. Place the wrapped pack on the area to be treated and secure it well. Packs can be secured with eiastic bandagesor towels to ensure good contact with the patient's skin (Iig. 6-9).
t49
Ice Packs o Plasticbags o lce chips o Icechipmachineor keezer o Towels or pillow casesfor hygieneand/or insulatlon 5. Leavethe packin placefor 10 to 15minutesto conA recentsystrol pain, inflammation, or edema.58 cryotherapy on the research of review tematic is most time application a 1O-minute found that associswelling pain and the reducing effectivefor risk *re minimizing and injury atedwith softtissue 5e iniury further possible of sideeffectsand When cold is appliedover bandagesor a cast,the applicationtime should be increasedto allow the cold to penetratethroughtheseinsuiatinglayersto the skin.60In this circumstance,the cold pack shouldbe replacedwith a newly frozenpackif the originalpackmeltsduring the courseof treatment. If cryotherapyis beingusedto control spasticiry the pack should be left in placefor up to 30 minutes.With theselonger applications,check every 10 to 15 minutesfor any signsof adverseeffects. 6. Providethe patient with a bell or other meansto callfor assistance. Z. When the treatment is completed, remove the pack and inspectthe treatmentareafor any signs of adverseeffectssuchaswhealsor a rash lt is normal for the skin to be red or dark pink after icing. 8. Cold or icepackapplicationcanbe repeatedevery or 1 to 2 houm to controlpain and inflammation ADVANTAGES . EasYto use . lnexpensivematerialsand equipment . Shortuseof clinician'stime o L o w i e v eol f s k i Ur e q u i r e fdo r a p p l i c a t i o n . Coversmoderateto largeareas . Can be appliedto an elevatedlimb
6-9. A pplicationof a cold pack Figure
DISADVANTAGES o Packmust be removed to visualize the treatment areaduringtreatment . Patientmay not tolerateweight of the pack Continued
6 t Thernal Agents: Cold axd Heat
150
. Packmay not be able to maintain good contacton smallor contouredareas o Long duration of treatment comparedto massage with an ice cup
Figure 6-10.Icecup.
ICE PACKVEBSUSCOLD PACK o Ice packprovidesmore intensecooling o lcepackis lessexpensive o Cold packis quickerto apply
Figure 6-11.Wate(popsicle.
lceMassage
direct contact with the patient's skin. Water Ice cups (Fig. 6-L0) or frozen water popsicles62 clesaremadeby placinga stickor tonguedepre inro the water cup before freezing.When fro Irozenice (Fig.6-11)canbeusedto applyicemassage. cups are made by treezingsmall paper or Styrofoam the ice canbe completelyremovedfrom the cup the stick used as a handie for applying che icecupsof water.To use*rese,the therapistholds on to Patientscan easilymake ice cups or popsicles the bottom o[ *re cup and graduallypeelsback the home use. edge to exposethe surfaceof the ice and puts it in
Equipment Required o Smallpaperor Styrofoamcups . lteezel
or popsiclesticks(optional) Tonguedepressors water Towelsto absorb
Two . THE PIIYSICAL ACENTS
t5l
]ROCEDURE I Removeall jewelryand clothingfrom the areato be treated and inspect the area. - Place towels around the tueatment area to absorb any dripping water and to wipe awaywater on the r(!r
qurrrS
rrcdurrcrr(.
:. Rub the ice over the treatment area using small, overlapping circles (Fig. 6-12). Wipe away any water asit melts on the skin. r. Continueice massageapplicationfor 5 to 10 minutes or until the patient experiencesanalgesiaat thp
:. When the treatment is completed, inspect the treatmentareafor any signsof adverseeffectssuch as wheals or a rash. It is normal for the skin to be red or dark pink after the application of ice massage.Ice massagemay be appliedin the above mannerfor the local control of pain,inflammation, or edema.Ice massagecanalsobe usedasa stimulus for facilitatingthe productionof desiredmotor pattemsin patientswith impaired motor control. When appiiedfor rhjs purpose.t-heice is eicher rubbedwith pressurefor 3 to 5 secondsor quickly stroked over the muscle bellies to be facilitated. This techniqueis known asqukbicing. ADVANTAGES . Treatmentareacanbe observedduringapplication
ColdCompression Unit Controlled lontrolled cold compressionunits altematelypump :old water andairinto a sleeve*rat is wrapoedaround of che r par.ient s limb lErg.6-13 A.81.fhe temperature 'C 'I) .vatercanbe setat between10' and25 (50'to ZZ :o provide cooling.Compressionis appliedby internittent intlation ofthe sleevewith air.Controlledcold .ompressionunits are most commonly useddirectly after surgeryfor the control of postoperativeinflamnation and edema;however,they may alsobe usedto
Figuie6-12. Applicationof icemassage. o . o o
Can be usedfor smalland irregularareas Shortdurationof treatment Inexpensive Can be appliedto an elevatedlimb
DISADVANTAGES . Too time-consumingfor largeareas . Requires active participation by t'he clinician or patientthroughoutapplication
control inflammation and relatededemain other cirthe sleeve When appliedpostoperatively, cumstances. is put on the patient'saffectedlimb immediatelyafter completionof the surgerywhile the patient is in t'he recoveryroomJ and the unit is sent home with the patientso that it canbe usedfor a few daysor weeks after surgery The applicationof cold with compression in this mannerhas beenshown to be more effective dran ice or compressionalone in controlling swelling, pain, and blood loss after surgery and in assistingthe patientin regainingROM.63'64
152
6 o Tlrctnnl Agens: Cold awl Heat
A
Libertywille, IL).B, AutoChill@ Figure 6-13.A, Controlledcoldcompression unit. (CourtesyInCareMedicalProducts, System20B.(CourtesyAIRCAST@Inc,,Summit,NJ.)
Equipment Required o Controlledcold compressionunit . Sleevesappropriatefor area(s)to be treated . Stockinettefor hygiene PROCEDUBE 1, Removeall jewelry and clothing from the areato be treatedandinspectthe area. 2. Cover the limb with a stockinettebeforeapplying the sleeve. 3. Wrap the sleevearoundthe areato be treated(Fig. 6-14). 4. Elevatethe areato be treated. 'C 'I). 5. Setthe temperatureat 10' to 15 (50' to 59 6. Cooling can be applied continuouslyor intermittendy. For intermittent treatmentTapply cooling for 15minutesevery2 hours. Z. Cycling intermittent compressionmay be applied at all timeswhen the areais elevated. 8. When the treatment is completed, remove the sleeveandinspectthe treatmentarea.
ADVANTAGES o Allows simuitaneousapplicationof cold and compression . Temperatureand compressionforce are easilyand e m r rr e t ' c L r e n n t r n l l e r l
o Can be appliedto largejoints DISADVANTAGES . Treatment site cannot be visualized during treatment . Expensive o Usableonly for extremities o Cannotbe usedfor trunk or digits
Tg'o . THE PHYSICAL AGENTS
153
:!ure6-14. A, Application of controlled cold compressionunit. (Courtesy InCare Medical Products,Libertyville, IL.); .: C,B, I(nee CryolCuff@. (CourtesyAIRCAST@ Inc., Summit, NJ.)
Sprays andBrieflcing ,'apocoolant -e vapocoolant sprays ethyl chloride and lluori..'-ethanehave been used for many years to achieve :ief and rapid cutaneouscooling(Fig.6-15).These ::oducts cool by evaporation.Ethyl chloridewas first ;;ed for this purpose;however,sinceit is volatile, : . , mm a b J ea.n dc ap a b l eo f c a u s i negx c e s s i vt e m p e r a lluori-Methane, which also effec.rre decreases,65 -..'elycoolsthe skin but is nonflammableand causes -c redrrcrion rn lemDerature. was
incroduced.66
.--owever, FluoriMethane is a volatile chlorofluoro--arbon that can damage the ozone layer; therefore, .s use is not pemitted by a number of facilities, :-though it has been granted a nonessential class I ::oduct exemption from the Environmental Protection .-gency (EPA) to permit its use in a clinical setting.6T lue to these limitations of vapocoolant spray prod- . r r . m a n y c ' i n i c r a n sa p p l y b r i e f i c e m a s s a g eu. s i n g
ice cupsor popsicles,when rapid cutaneouscoolingis desired. Rapid cutaneouscooling is generally used as a componentof the treatmentof triggerpoints.Ior this application,the vapocoolantspray or brief icing is applied in parallel strokes along the skin overlying the muscleswith trigger points immediately before (Figs.6-16 and 6-1l). This stretchingthesemuscles6s type of treatmentis frequently applied directly after trigger point injection. The purpose of the rapid coolingis to provide a countedffitant stimulusto the cutaneousthermal afferents overlying the muscles to causea reflex reductionin motor neuron activity and thus a reduction in the resistanceto stretch69 This techrriquewas developedby JanetTravell,who describesthis combinationwith the phrase"Stretchis The "disffaction" the action;sprayisthe distraction."T0 of rapid cutaneouscooling is intended to promote
154
6 . Thennal Agents: Cold and Heat
greaterelongationof the musclewith passivestretching. The combination of sprayingwith vapocoolant spray followed by stretchingis known as "sprayand stetch."
or a contrastbath. Irozen wet towels are rarelyused becausethey are inconvenientand messy.The useof cold water, cold whiripools, and contrastbathsis discussedin detailin Chapter9 of thisbook.
Cryotherapy ofApplying 0therMeans Cryotherapymay also be applied using frozen wet towels,a bucketof ice or coldwater,a cold whirlpool,
Figure6-15,Vapocoolantsprays:ethyl chloride and lluori-Medune. (Courtesy GebauerCompany,Cleveland,OH.)
Figure6-16.Application of vapoc Figure6-17. Quick stroking with ice oolanr spray. r,Courtesy Gebauer cup Company, Cleveland,OH.)
PROCEDURE 1. Identifytriggerpointsanddreirrelatedtight muscles. 2. Position the patient comfortably, with all limbs and the back well supportedand the area to be Inspectthe areato treatedexposedand accessible. be treated.lf usingethyl chloridespray,protectthe surroundingareasof skin with petrolatumto avoid excessivecooling. Becauselluori-Methane produceslessintensecoolingthan ethyl chloride,the surroundingareasof skin do not need protection when Fluori-Methaneis beingused. 3. Apply tlvo to five parallelsweepsof the spray or 10cm ata speedof approximately brieficemassage muscle fibers. the direction of the per secondalong When using a spray,hold the bottle about 45 cm from the skin and angledso that the sprayhits the
skin at an angleof about30 degrees.If applying spraynearor aroundthe patient'shead,try to mj mize the patient's inhalation of the spray,
1arlywith ethyl chloride,sincethis substance producegeneralanestheticeffects. 4 . During the cooling, maintaingentle, smooth, tension on the muscle to take up any slack that develop.
5 . Immediately after the cooiing, have the take a deep brearh and then perform a gentJe sive stretch while exhaling. Contraction-/relaxa
techniquesmay alsobe usedto enhancethe RO increasesobtainedwith this procedure. 6 . Iollowing this procedure, the skin should rewarmed with moist heat, and then the m
shouldbe moved through their full activeROM
T$o . THE PITYSICAL AGENTS
155
. Limited to usefor brief, localized,superficialapplicationof cold beforestretching o Possiblenarcoticor generalanestheticeffectif ethyl chlorideis hhaled
ADVANTAGES ' Brief durationof cooling o Very localizedareaof application DISADVANTAGES r Fluori-Methanespraydamagesthe ozonelayer
Documentation locument the area of the body treated, dre type :f cooling agent used, the treatment duration, :atient positioning, and *le responseto treatment. locumentation is typically written in the SOAPnote Plan)fomat. The Subjective,Objective,Assessment, the modaliry sumrnarize only examples :cllowing to repintended are not and of treatment :omponent pian oI care. comprehensive :esenta
etaqhl' 0: 99 2 ante.trL*,,knzox | 5', M 4.: lttid.pafzuat Sjrlh dr4rraard pv*n | 6 lt t& | 5' Wil " tlr4t tA^444h" w,^Akq inlr^&4rd (^NL alahL, P: 9n '\l&L N, irL klm4 puatara aN 9? fu"I arltdtioa kluz, | 5', u A, 9 fE elztolzd', 3 X eath dat2 until nz'xl t'tzattnz* auaiolL
When applyingicemassage(lM) to the areaof dreright (R)lateralepicondyleto treatepicondylitis,document:
9: PLolapain in R talz.talell
!:
?t ela ! lqze fojn w4l*hq.
and' tuzUitrq
tAat ittt'tuen*-a' uilA'
) Clinical Case Stildies a The following casestudiessummarizethe conceptsof cryotherapy discussedin this chapter-Based on the scenariopresented,an evaluation of the clinical findings andgoalsof treatmentarepfoposed.Thesearefollowed by a discussionof the factors to be consideredin the selection of cryotherapy as tlr€ indicated ffeatment modality and in the selectionof the ideal cryotherapy agentto promoteprogresstoward the setgoals.
Case'l TF is a 20-year-o1dmale accountant.He injured his ght knee 4 months ago while playing footbail and was treated conservatively with nonsteroidal antiinflammatory drugs (NSAlDs) and physical therapy for I weeks, with moderate improvement in symptoms; however, he was not able to retum to sPots due to continuedcomplaintsof medial knee pain. A magneiic resonanceimaging (MRI) scan 3 weeks ago revealed a tear of the medialmeniscus,and the patient undelwent adhroscopic partial medial meniscectomy of his right knee 4 daysago.He has beenreferledto physical
therapv with an order to evaluate and ffeat TI in intencomplainsof paininhis kneerhat hasdecreased sit:y'komg /10 b7 /1'0sincethe surgerybut that increases with weight bearing on the right lower extremity. He also complainsof knee stiffness The objective exam revealsmoderate wannth of the skin of the right knee, panicularly at the anteromedial aspect, and RO{ restrictedto -10 degreesof extensionand 85 degreesof fiexion. The patient is ambulating without any assistive devicebut witb a decreasedstancephaseon the right lower extremity and with his right knee held stiffly in approximately 30 degreesof flexion tJrroughout the gait on rycle. Kneegirtb at the midPatellarlevelis l7 inches li2 left on the the righr and 15 inches EVALUATIONOF THE CLINICAL FINDINGS This patient presentswith the impainnentsof pain,loss of motion, and increasedgirth of the right k.nee,resultine in the disabilitiesof limited ambulationand sports activity. He is independent in his home environment witlout the useof adaptiveequipment Continued
756
6 . Tlrcrnal
Agcuts: Cold aul llcat
) Clinical Case Stttdies-cont'd PREFERREDPRACTICEPATTERI. impaired Joint Mobiliq/, Motor lunction, Muscle Performance,and Range of Motion AssociatedWith Bony or SoftTissueSurgery,(41) PLAN OF CARE The goalsof treatmentat this time are to control pain and edema,accelerateresolutionof the acuteinflammation phase of healing, and acceleratethe recovery of ROM and function. ASSESSMENTREGARDINGTHE APPROPRIATENESS OF CRYOTHERAPY AS THE OPTIMALTREATMENT Cryotherapyis an indicatedtreatmentfor the control of pain, edema,andinflarrmation.It cancontol the formation of edema,and compressionand elevationcanreduce edemaalreadypresentin the patienr'sknee.The application of cryotherapy early during the recovery from articular surgeryhasalsobeenassociated with an acceleration of functional tecovery.72Since the peronealnerve is superficialat the lateral knee, the patient should be monitored for signsof nerve conductionblock, such as tingling or numbnessin his lateralleg,during treab.nent. The presenceof any contraindications to the application of cryotherapy,suchasRaynaud'ssyndrome,shouldalso be ruled out before ttre application of cryotherapy. Cryotherapyalsoshouldnot be appliedifinfection is suspected.Although this patientdoeshave signsof inflammatiorl includingheat, rednessrpain, swelling,and loss of function, *re fact that his signs and symptoms have decreased sincesurgeryindicates anappropriatecourseof recoveryand *re probableabsenceof infection.A progressiveincreaseinthe signsandsymptomsof inflammation or complairts of fever and generalmalaisewould suggestthe presenceof infectioq requiring physician evaluationbeforethe initiationof rehabilitation. PROPOSEDTREATMENTPLANAND RATIONALE To obtain maximum cooling of the knee, cryotherapy shouldbe appliedto all the skinsurfacessurroundingthe kr.reejoint. A cold pack, ice pack, or controlled cold compressionunit could adequatelycover this area.In choosingamong theseagents,one should considerthe convenienceand easeof applicationof a cold pack, the low expenseand ready availabilityof an ice pack, and the additional benefits(althoughgreatercosr)of intermittent compressionprovidedby a controlledcold compressionunit. Ice massagewould not be an appropdate featment becauseit would take too long to apply to
a
sucha largearea.Immersionin iceor coldwaterwould also not be appropriate since this would require the swollen knee to be in a dependentposition, potentially aggravating the edema,and would required.readditional discomfortof imrne$ing *re entke distallower extremibTin coldwater Whetherusinga cold pack,ice pack,orcontrolledcold compression unit, cryotherapy should generally be applied for approximately 15 minutes to ensureadequate cooling of the tissuesand minimizing the probability ofexcessivecoolingor reactivevasodiiation.This treatment should be reappliedby the patient at home every 2 to 3 hours while signsof inflammationare still present(Fig.6-18).
Figure6-18. Application ofice pack to nght knee.
Case2 SC is a 4O-year-oldfemaleoffice worker Shehas been referredto therapywith a diagnosisoflateralepicondylitis and an order to evaluateand treat. SG complainsof constant moderate to severepain at her right lateral elbow that preventsher from playing tennis.The pain startedabout 1 month ago,the morningaftershespenta whole day pulling weeds, and remainedunchangedin severityor frequencyuntil3daysago.Shereportsa slight decrease in pain severiqyover the last 3 days,which she associates with startingto takean NSAID prescribedby her physician.Shehashad similarsymptomspreviously, aftergardeningor playingtennis,but thesehave always resolvedwithin a couple of days without any medical intervention.Objectiveexaminationrevealstenderness andmild swellingat the right lateraiepicondyleand pain witlout weaknesswith resistedwrist extension.All other tests,includingupper extremiry sensation,ROM, andstrength,arewithin normallimits.
TIyo C THE PHYSICAL
EVALUATION OF THE CLINICALFINDINGS This patientpresentswith the impairmentsof Paiq tenderness,and swelling of the right elbow resultingin an inabiliq' to participatein her normal sports activity of teffus.
PRACTICEPATTERN PREFERRED lmpaired Joint Mobility, Motor Function, Muscle Performance,and Range of Motion AssociatedWith I ^"'li'",1 T.Flrmm:rinn f4F\
PLANOF CARE The goals of ffeatment at this time are to resolvethe inflammation and control pain. The anticipatedlongterm goals of treatmentinclude the patient'sretum to playing tennis and prevention of recurrencesof this problem. REGARDINGTHE ASSESSMENT AS THE OF CRYOTHERAPY APPROPRIATENESS OPTIMALTREATMENT Cryotherapyis an indicatedtreatmentfor inflammation andpain,and canalsobe usedprophylacticailyafier exerciseto preventtie onset of inflammationand soreness. The advantagesof cryotherapyover other fteatments indicatedfor these applications,such as ultrasoundor electricalstimulation,are that it is quick, easy,and inexpensiveto apply,and the patient can apply it at home. Cryotherapyalone may not resolvethe Presentsymptomsandmay thereforeneedto beappliedin conjunction with otherphysicalagentsjactivitymodification,manual to achievethe protherapytechniques,and/or exercises posedgoalsoftreatment.Sincethe radialneweis superficialat the lateralelbow,the patientshouldbe monitored for signsofnerve conductionblockageduringtreamlent, suchastinglingor numbnessin her dorsalarm.The presence of any contraindicationsto the application of cryotherapy,such as Raynaud'ssyndrome, should be ruledoutbeforethe applicationof cryotherapy. PROPOSEDTREATMENTPLANAND RATIONALE Ice massage,an ice pack, or a cold pack can be usedto providecryotherapyto the areaoI the lateralepicondyle (Fig.6-19).Sinceice massagehasthe advantagesof taking little time to apply to tl|is smallareawhile allowing visualizationof the treatment area and assessmentof signs and symptoms throughout the treatment, this would be the most appropriateagent to use for this patient,althoughan ice pack or cold pack could aisobe used.An ice packor cold pack would be more appropriate if the symptomaticareawas larger;for example,if the areaextendedinto the dorsalforearm.Cryotherapy should be applied until the treatment area is numb,
tJ/
ACENTS
which usuallytakes5 to 10minuteswhen usingice massageorabout 15minuteswhen usinganicepackora coid pack.Tream-rent shouldbe discontinuedsoonerif numbness extendsinto the hand in the distribution of the radialnerve.Cryotherapytrealmentsshouldcontinueto be applieduntil the signsandsymptomsof inflammation haveresolved.Treatmentsshouldbe disconthuedthereproducedby cryotherapy aftersincethe vasoconstriction may retardthe later stagesof tissuehealing The patient shouldalso be instructedto apply cryotherapyprophylacticallyafter activitiesthat have previouslyresultedin elbow pain, such as terxis or gardening,to reducethe risk ofa recurrenceof her presentsymptoms.
Figure6-19. Application ofice massageto elbow.
Case 3 FBis a 60 year-oldmaletruck driver He hasbeenreferred to physicaltherapywith a diagnosisof osteoarthritisof the leftkneeandanorderto evaluateandtreat.He reports thathe hashadarthritisin thiskneefor the last5yearsand that he recendy started performing exelcisesthat have increasedthe strength,stability,andenduranceofhis Iegs but causeknee pain and thigh musciesorenessthe next day.His goalsin therapyare to controlthis postexercise program. of hisPxercise oiscomfonro allowcondnualion He performed his exercisesyesterday,and today the objectiveevaluationreveaisa mild increasein the temperofthe antedorthigh. atureof the leftkneeand tendemess Kneeginh andROM areequalbilaterally. OF THE CLINICALFINDINGS EVALUATION This patient presentswith the impairmentsof intelmittent left kneeand thigh pain resultingin the disabilityof '".f',.r".1
"'e'.i(c,.rivit'1/
PREFERREDPRACTICEPATTERN impaired Joint Mobility, Motor }unction, Muscle Perforrnance,and Range of Motion AssociatedWith LocalizedInflammation,(4E) Contmued
158
I |
I I I |
6 t Thennal Agefis: Cold antl Heat
I) Chnical Clinical v4rc Case Studies-contd Case Studies-eont'd t'"tttltEr-curtt t't I ||
PLANOF CARE PLANOFCARE goalsof treatmenr The goai" treatmentat this this time time areto eliminate eliminateposposrexercise rexercise thighmuscle joincsoreness. thigh muscleand knee kneejoinc soreness. -^^_^^ _ __ ASSESSMENTREGARDINGTHE llE OF CRYOTHERAPY AS THE OPTIMALTREATMENT TBEATMENT Cryotherapy Cryotherapyis an indicated indicatedtreatrnent treatrnentfor for delayed-onset delayed-onset muscle muscle.soreness sorenessand and joint in-0ammation:however, however,the t}le ioint inlammation; patient s exerciseprogram programshould shouldalso alsobe evaluated evaluated and Pacie.ntt,exercise modified as appropdate approPrjateto ro reducehis discomfort discomfon after ex€rcising. The exercrsmg. the presence presence of any contraindications otany contraindications ro the to the application of cryotherapy,such as Raynaud,sslmdrome, shouldbe ruledout beforetlle the application applicarionof cryotherapy.
I APPROPRIATENESS f:E_1Yf-tT_l!911?l!9
I I I I I I I I I
,
||
-
PROPOSEDTREATMENT PR6PoSED TREATMENTPLAN PLAN AND RATI9NALE RATIONALE II As in Cas€1. in Case 1, the *re application applicationof cryotherapy cryotherapyfor for 15 minmin- | | r-rres ut€s with an ice paci< packor cold packwould be b" appropriate upprop.iat" | | for treatment rreatmento[ of tlis this patient's pacJent,s knee. knee. The additional additional ll expense expense of a controlled of a controlled cold cotdcompression compression unit unitis isnotjusnotjus_ | | js no edema tified ciftedin this this case casesince sincethere thereis edemaand andtherefore th"reiore | | compr€s compression sionis not not n€eded. needed. patientshould The The patient shouldapply applythe rhe | | pack immediately after alrer completing his hi. exercisepro- | | "*",.i""'program.Sincethe peronealnerve nerveis is superficialat sup"erficial ar the lateral laieral | | knee, knee.the the patient patienishould shouldbe monitored monito;edfor for signs signsofnerve of nerve ll conduction conductionblockage. blockage.such suchastrnglhg trnglhg ornumbness ornum"bnes"inhis inhis | | lateral lateralleg. leg, during durjngtreatment. treatment. ll || ||
ll
PreferredPhysicalTherapistPraclicePatternssM[4] and4E]areCopyright2002AmericanPhysicalTherapisrAssociation. All rightsreserued. I
I
HEAT_THERMOTHERAPY
I Hemodynamic Effects
The therapeuticapplicationof heat is knownas thermothera7y. Thermotherapyis used clinically outside of rehabilitationprimarily to destroymalignanttissue growth or to treat cold-relatedinjuries.Wi*rin rehabilitation, thermotherapyis usedprimarily to control pain, increasesoft tissueextensibiliry_, increasecirculation, and acceleratehealing.Heat has these therapeutic effectsdue to its influenceon hemodynamic, neuromuscllar,and metabolicprocesses, the mechanismsof which areexplainedin detailfollowing.
I Vasodilation I Heat causesvasodilationand thus an increasein theI rate of blood flow.73When heat is appliedto one areaI of the body, there is vasodilation#h"r. the heat is I applied,and to a lesserdegree,systemically,in areasI disiant from the site of hJat application.SuperficialI heating agentsproduce mor. pionounc"d vasod a-l tion in thJ local'cutaneousblood vessels,where theyI causethe greatestchangein temperature,,nd l.ss I
EFFE'T' 0FHEAT
liffT'*,11:i:';iH'""fT"::'nt."i
Hemodynamiceffects Vasodilation
Neuromuscurar effects Changesin nerveconductionvelocityand Ering rate
3f::fi"*r"*:":l:$, Metaboliceffects Increasedmetabolicrate Altered tissueextensibility Increasedcollagenextensibility
changein temperature.Thermotherapyappliedto rheI whole body can also causegenenlized vasodilationI and may improve vascularendothelialfunction in theI
'"Til:,*:il:fi;'5jTi?l';l'"",.o,r"tion by u,,i_ | " ety of mechanisms,including direct reflex actlvation I of the smooth musclesof the blood vesselsbv rheI
;"i:ff.,::,*T:i*U'a:_,lm:
ceptors,or by increasingthe_!o_c-al releaseof chemicalI mediatorsof inflammation.7s,76 eig. 6_20).A recentI study demonstratedthat at least two independent! mechanismscontributeto the rise in skin blood flow I during local heating: a fast-respondingvasodilator systemmediated by the axonreflexes and -*. I
"
Two . THE PIIYSICAL AGENTS
Figure6-20. How heat causesvasodilation.
:lowly respondingvasodilatorsystem that relies on -ocalproductionof nitrous oxide.77 Superficial heating agents stimulate increased activity of the cutaneous *rermoreceptors. It is rroposedthat transmissionftom the cutaneoustherroreceptors via their axons direcdy to nearby cutareous blood vesselscausesthe releaseof bradykinin andnitrousoxide.Bradykininandnitrous oxide act as ','asoactivemediators stimulating relaxation of the ;mooth musclesof the vesselwalls to causevasodilaion.76-78This vasodilationoccurslocally,in the area -,vherethe heat is applied. Cutaneousthermoreceptorsalso project via the Corsalroot ganglionto synapsewith intemeuronsin *re dorsalhorn of the gray matter of the spinalcord. Theseinterneuronssynapsewith sympatheticneuronsin the lateralgrayhorn of the thoracolumbarsegmentsof the spinalcord to inhibit their firing andthus in symdecrease sympatheticoutput.79This decrease patheticactivity causesa reductionin smooth muscle contraction,resultingin vasodilationboth at the site ofheat aoplicationandin the cutaneousvesselsof the distalexirlmities.B0This distantvasodilativeeffectof thermotherapymay be used to increasecutaneous blood flow to an areawhere it is difficult or unsafeto apply a heating agent directly.BlFor example, if a patienthas an ulcer on his leg as the result of arterial insufficiencyin the extremity,thermotherapymay be aonliedto his lower backto increasethe circuiationto his lowet extremity and thereby facilitate wound
159
healing.This would be most appropriateif the ulcer was bandagedor did not toleratepressure,or if the arealackedsufficientcirculationor sensationto tolerate the direct applicationofheat. Becauseblood flow in the skeletalmusclesis primarily influencedby metabolicfactorsratherthan by changesin sympatheticactiviry,and superficialheating agents do not increasethe temperatureto the depth of most muscles,skeletalmuscle blood flow is much less affectedby superficialheating modaliThe use of exercise ties than is skin blood flow.82,8s or deep heating modalities, such as ultrasound or diathermy,or a combinationof theseinterventions,is thereforerecommendedwhen the goal of treatment is to increaseskeletalmuscleblood flow. Cutaneousvasodilation,and the resultingincrease in blood flow that occursin responseto increasedtissuetemperature,actsto protectthe body from excessiveheatingand tissuedamage.The increasedrate of blood flow increasestlte rate at which an area is cooled by convection.Thus when an areais heated with a thermal agent,it is simultaneouslycooled by circulatingblood, and as the temperatureof the area increases,the rates of circulation and cooling both increaseto reduce the impact of the thermal agent on tissue temperaturethereby reducing the risk of buming.
Effects Neuromuscular velocity andtiringrate in nerveconduction Changes ]ncreasedtemperaturehas long been known to increase nerve conduction velocity and decrease the conduction latency of both sensoryand motor nerves.84,85 Nerve conduction velocity has been to increase by approximately2 meters/secreported 'C (1.8'F) increasein temperature. for every I ond implications of theseeffectsare Although the clinical not well understood, they may contribute to the reducedpain perceptionor improved circulationthat occursin responseto increasingtissuetemperature. Newe firing rate (frequency)has also been found to change in responseto changesin temperature. 'I) 'C Elevationof muscletemperatureto 42 (108 has beenshown to resultin a decreasedfiring rate of gzpe II musclespindle efferentsand gamma efferentsand an increasedfiring rate of type Ib fibers from Golgi These changesin nerve firing tendon organs.86,87 rates are thought to contribute to a reduction in the firing rate of alpha motor neuronsand thus to a
160
6 . Thermal Aeents: Cold and Hcat
reductionin musclespasm.BB The decreasein gamma neuron activity causesthe stretch on the muscle spindlesto d-ecrease. reducingatferentfiring trom the spindles.ue The decreased spindleafferentacciviry resultsin decreasedalpha motor neuron activiqzand thus in relaxationof musclecontraction.
information, it is recommendedthat musclestrength and endurancealwaysbe measuredbeforeapplyinga hp.rtino mnri:linr
Metabolic Effects Increased metabolic rate
Increased oainthreshold Severalstudies demonstratethat the apolication of 9I The proiocal heat can increasepain threshold.eO posed mechanisms of this effect include a direct and immediatereductionof pain by activationof the spinal gating mechanismand an indirect, lateq and more prolonged reduction of pain by reduction of ischemiaand muscle spasm or facilitation of tissue healing. Heat increasesthe activity of the cutaneous thermoreceptors,which can have an immediate bhibitory gatingeffect on the transmissionof the sensationof pain at the spinalcord level.Stimulation of the thermoreceptorscanalsoresultin vasodilation, as describedabove, causing an increasein blood flow and thus potentially reducing pain causedby ischemia.Ischemiamay also be decreasedas a result of reductionof spasmin musclesthat compressblood vessels.The vasodilationproducedby thermotherapy may also acceleratethe recovery of the local pain thresholdto a normal levelby speedingtissuehealing. Changes in musclestrength Muscle strengthand endurancehave been found to decreaseduring the initial 30 minutesafter the application of deep or superficialheating agents.92-94 It is proposedthat this initial decreasein musclestrength is the result of changesin the firing rates of qfpe II musclespindleefferent,gammaefferent,and type Ib fibersfrom Golgi tendon organscausedby heatingof the motornerves.In tum, this decreases the firing rate of alphamotor neurons.Beyond30 minuresaftJrthe applicationof heat, and for the next 2 hours,muscle strength gradually recovers and then increasesto above pretreatmentlevels.This delayedincreasein strengthis thought to result in augmentationof the individual'spain threshold. Although changesin muscle strength produced by heating are not generallyused to modify a rehabilitation program, it is important to be aware of them when assessingmuscle strength as a measure of patient progress. Since comparing preheating strength with postheatingstrength from the same sessionor another sessioncan provide misleading
Heat increasesthe rate of endothermicchemicalreactions, includingthe rate of enzymaticbiologicalreactions.Increasedenzynnaticactiviqyhasbeenobserved 'C in tissuesat 39"to 43 (102"to 109'F),with the reaction rate increasingby approximately13% for 10'C (18'F) increasein temperatureand doubling for every 10'C (18 "F) increasein temperature.32 Enzymatic and metabolic activity rates continue 'C 'I). increaseup to a temperatureof 45 (113 this temperature,the protein constituentsof beginto denatureand enzymeactivity rates ceasing completelyat about50 "C (122'F).es Any increasein en4,'rnatic activity will result in increasein the rate of cellularbiochemical This can increaseoxygenuptakeand accelerate ing but may also increasethe rate of processes. Ior example,heat may acceleratethe ing of a chronic wound; however, it has also shown to increase*re activity of collagenase and thus acceleratethe destructionof articularcartilasei patientswith rheumatoid arthritis.3lTherefore motherapy should be used with caution in with acuteinflammacory disorders. Increasingtissuetemperatutealso shifts the gen-hemoglobindissociationcurveto the right, ing more oxygen availablefor tissuerepair (see 6-4). It has been shown that hemogiobin twice as much oxygen at 41 "C (106'F) as it does - 'rirh rhe rate of blood flow stimulatedby increased ture and the increasedenzymatic reaction rate, increasedoxygenavailabilirymay contributeto erationof tissuehealingby thermotherapy.
Altered Tissue Extensibility Increased collagen extensibility Increasing the temperature of softtissueincreases extensibility.9TWhen soft tissue is heated stretching, it maintains a gteater increase in
after the sketching force is applied, less force requiredto achievethe increasein length,andthe of tissueteadng is reduced.98,99 If heat is applied
T*o . THE PHYSICAI ACENTS
761
The indirect effects of thermo::llagenoussoft tissuesuchas tendor\ Iigament,scar nerve conduction.go and ischemiaare primarily tissue healing therapy on joint prolonged stretchinS, capsule before or :;sue, vasodilation and increasedblood flow. to attributable increases in whereby the tissue . -ascicde[ormation, proposed that the psychologicalexpebeen It has aiso coolincrease after most of the ."rsth and maintains and relaxingmay influas comfortable of heat dence if coilagenous In contrast, b" achieved.100,101 .-g]can pain. perception of patient s ence the prior elastic heating, without ,ssue is stretched Although thermotherapy may reduce pain of ::formation, whereby the tissueincreasesin iength etiology,it is not recommendedas a treatment any most o[ the applied but loses .'.'hilethe force is pain causedby acute inflammation becausean for generally occurs. ::creasewhen the forceis removed, in tissue temperaturemay aggravateother increase tissue 1e maintained elongation of collagenous -::at occursafter heating and stretchingis causedby signsand symptoms_ ^ofinflammationincludingheat, redness. and edema.LUa fibers and :rangesin the organizationof the collagen :: changesof the viscoelasticiqyof the fibers them:elvesratherthan to increasesin the number of fibers. Joint Range ofMotion andDecrease lncreased Forheat to increasethe extensibilityof soft tissue, --:e appropdate temperature range and sffuclures Stiffness ::ust be reached.A maximum increasein residual Thermotherapycanbe usedclinicallyto increasejoint :rgth is achieved when the tissue temperature ROM and decreasejoint stiffness. Both of these effectsare thought to be the result of the increasein : maintainedat 40"to 45'C (104'to 113"I) tor 5 to 101 -l minutes.B6 The superficialhearing agents soft tissue extensibility that occurswith increasing soft tissuetemperature.Increasingsoft tissueextensi:escribed in the following sectionscan cause this .:vel of temperatureincreasein superficialstruclures, bility contributesto increasingjoint ROM because :;ch as cutaneousscartissueor superficialtendons. it results in greater increasesin soft tissue length and less injury when a passivestretch is aPplied.A iiowever, to adequatelyheat deeperstructures,such :. the joint capsulesof large joints or deep tendons, maximum increasein length,with the lowest risk of injury is obtainedif the tissuetemperatureis main::ep-heatingagentssuchas ultrasoundor diathermy 'F) for 5 to 10 mintainedat 40"to 45 "C (104"to 1l3 ::ust oeuseo. utes and if a lowJoad, prolongedstretch i5 aPplied duringthe heatingperiodand while the tissueis coolHEAT OFSUPERFICIAL JSES that ing86l0l 1fig.6-21;.Thereforeit is recommended sffetchingbe performed during and/or immediately Pain control afterthe applicationof thermotherapy,sinceif the tisIncreased ROM and decreasedioint stifftress suesare allowed to cool before being stretched,the Accelerated healing effectsof the prior heatingon tissueextensibilitywill Infrared radiation for psoriasis and dermal ulcers be lost.
rainControl lermotherapy can be used clinically to control :ain. This therapeuticeffectmay be causedby gating :: pain transmission by activation of cutaneous --:rermoreceptors or may indirectly be the result of decreased muscle spasm, or healing, :::rproved ischemia.102 lncreasing skin temperature ::duced sensation of pain by altering ray also reduce the For examand/or transmission.l03 erve conduction produced in the senthe analgesia :le, it is likely that (the volar and nerue .cry distribution of the ulnar is applied when infrared radiation redial forearm), 'ver the ulnat nerveat the elbow,is causedby altered
Figure6-21. LowJoad prolonged stretchwith heat
162
6 o Theftnal Aeents: Cold atd Heat
joint stiffness,a qualThermotherapycandecrease iuy related to the amount of force and the time requiredto move a joint; as joint stiffnessdecreases, less force and time are required to produce joint For example,increasingtissuetempermotion.105-107 ature by placing the hands in a warm water bath or warm paraffin,orheatingthe surfacewith an infrared lamp, have all been shown to decreasefinger joint The proposedmechanismsof this effect stiffness.l0B are increasedextensibiliryand viscoelasticityof the periarticular stuuctures,including the joint capsule and surroundingligaments. When using a heatingagentto increasesoft tissue extensibilitybeforestretching,an agentthat canreach the shortenedtissuemust be used.Thus superficial agentssuch as hot packs,paraffin, or inftared lamps areappropriatefor usebeforestretchingskin, superficial muscle,joints, or fascia,whereas deep heating agents such as ultrasound or diathermy should be usedbeforestretchingdeeperjoint capsules,muscles, or tendons.
Healing Accelerated Thermotherapycanacceleratetissuehealingby increasing circulation and enzymatic activity rate and by increasingthe availability of oxygen to the tissues. Increasingthe rate of circulation acceleratesthe del.ivery of blood to the tissues,bringing in oxygen and other nutrients and removing waste products. The application of any physical agentthat increasescirculation can be beneficial during the proliferative or remodeling stagesof healingor when chronic inflammation is present.However,sinceincreasingcirculationcanincrease edema, the application of thermotherapy during the acuteinflammationphasecan prolongthis phaseand delayhealingandis thereforenot recommended. By increasingthe enzymatic activity rate, thermotherapy also increases*re rate of metabolicreactions, thus allowing the processesof inflammation and healing to proceedmore rapidly. Increasingthe temperatureof the blood also increasesthe dissociation of oxygen from hemoglobin,making more oxygenavailablefor the processes oI tissuerepair. Becausesuperficial heating agents increase the temperatureof only the superficialfew millimetersof the healingof tissue,they aremostlikely to accelerate only superficialstructures,suchasthe skin, or deeper tissuelayers exposeddue to skin ulceration.Deeper effects may also occur as the result of consensual
vasodilationin areasdistant ftom or deepto the of increasedtemperature.
lnfraredRadiation forPsoriasis Although the ultraviolet(U! frequencyrangeof tromagneticradiationis usedmost commonly in treatment of psoriasis,the infrared (IR) rangeis used occasionally for this application.109,110 increasedtemperatureof the upper epidermis dermisin the regionof psoriaticplaquesproduced IR radiationhas beenoroposedasthe mechanism the reductionin psoriaticplaquesthat occursin individualsexposedto IR radiation.110
for DermalUlcers lnfraredRadiation Infraredradiationhas beenusedfor the treatment dermal ulcers.The pumoseof such treatmentwas improve healing by increasingcirculation, bacterialgrowth, and dehydratingthe wound site. However, becausecurrent researchindicates wound healingis optimized with a moist ratler a dry environment,the applicationof IR radiation openwounds is no longerrecommended.l12
ANDPRECAUTIONS FOB CONTRAINDICATIONS THERMOTHERAPY Although thermotherapyis a relativelysate modaliw. its use is contraindicatedin some stances,and it should be appliedwith cautionin ers. Thermotherapyrnay be applied by a clinicianor by a properlyinstructedpatient. may useall forms of thermotherapy,andpatients be instructedto usehot packs,paraffin,or IR lamps home to treat themselves.When patientsare to use these modalities at home, thev should insftucted how to usethe modal.ity,including the tion it should be applied to, the temperatureto used, safety precautions,and the duration and quencyof treatment.Patientsmust alsobe taught to identify possibleadverseeffectsandmust be told discontinuetreatrnentshouldany ofthese occur. Evenwhen thermotherapyis not as with all treatments. if the patient's condition
worseningor not improving after tlvo to three ments, the treatrnent approach should be
or the patient should be refered to a physician reevaluation.
T\ro . THE PIIYSICAI
ACENTS
753
CONTRAINDICATIONS
fortheUseofThermotherapy o Acute injury or inflammation . Recentor potentialhemorrhage o Th'nmhnnhlphiti<
The use of thermotherapy is contraindicated. . . . . in the area of an acute iniury or acute inflamrration )o notapply heatto the areaofan acuteinjury or acute :Jlammation becauseincreasingtissue temperature :anincreaseedemaandbleedingasa resultofvasodila:on and increasedblood flow.11aThis may aggravate :re injury increasepain,andlordelayrecovery ASKTHE PATIENT: . When did this injury occur? Do not apply heat within the first 48 to 72 hours :lter an injury ASSESS: o Skintemperatureand colorand local edema Elevation of skin temperature, rubor, and local :dema demonstratethe presenceof acuteinflamma:on and indicate that heat should not be applied to -j]earea, . . over an area of recent or potential hemor:hage :leat causesvasodilation and an increasedrate of vasodilation maycausereopening :loodflow.Because increasingthe rateofblood flow in :ia vascularlesior5 ra areaof recenthemorrhagecanrestartor worsenthe :leeding.In addition,increasingblood flow in an area rf potential hemorrhagecan causehemorrhageto ::art. Thereforeit is recommendedthat heat not be :pplied to areasof recentor potentialhemorhage. ASKTHE PATIENT: . When did this inj!ry occtn? . Did you haveany bruisingor bleeding? ASSESS: r Visuallyinspectfor ecchymosis
o Imne itpd
. Malignancy o Infraredirradiationof the eyesllr Do not apply thermotherapyif the patient reports bruisingor bleedingin the previous48 to Z2 hours or if recentlyformed red, purple, or blue ecchymosisis presen[. . . . in areas with thrombophlebitis The vasodilation and increasedrate of circuiation causedby increasedtissuetemperaturemay causea thrombus or a blood clot to become dislodged ftom the areabeing treatedand to be moved to the vesselsof vital organs,resultingin morbidity or even death. ASK THE PATIENT o Do you havea blood clot in this area? ASSESS: o Check for calf swelling and tendemess(Homan's sign)before applyingheat to the leg. Do not apply thermotherapy if the patient says that there is a blood clot in the area.Do not apply thermotherapy to the leg if there is tendernessand swelling of the calf until the presenceof a thrombus in the lower extremityhasbeenruled out. . .. over areas with impaired sensation or to patients with impaired mentation A patient'ssensationand a report of heat or pain are used as the primary indicators of the maximum safe temperature for thermotherapy; therefore, a patientwho cannotfeeior reportthe sensationof heat can easilybe burnedbeforethe clinicianrealizesthat there is a probiem. Therefore heat should not be applied to areaswhere sensationis impaired or to patientswho may haveany other difficulty letting the therapistknow when they aretoo hot. ASK THE PATIENT o Do you havenormal feelingin this area? Colrhued
6 o Ther Ml Asents: Cold dttd Heat
164
DICATI0NS-cont'd C0NTRAIN ASSESS: o Sensationin the area Test tubes containing hot and cold water can be usedto teqgthermalsensation.Ifsensationis impaired only in the treatment area, heat may be applied proximally to increaseperipheralcirculationvia the soinalcord reflex,as describedabove.Note that sensation in the distal extremitiesis frequentlyimpaired in patientswith neuropathydue to diabetesmellitus. o Alertnessand orientation Do not applythermotherapyif the patient is unresponslveor conruseo. . . , over or near malignant tissue Thermotherapymay increasethe Srowth rate or rate of metastasisof malignanttissue,eitherby increasing circulationto the areaand/or by increasingmetabolic rate. ASK THE PATIENT Becausea patient may not know that he or she has cancer,or may be uncomfortablediscussingthis diagnosis direcdy, the therapist should first check the chart Fora diagnosisof cancer.Then askthe patient:
. Are you under the care of a physician for any major medicalproblem?lf so,what is the problem? . Have you experiencedany recent unexplained weight lossor gain? o Do you haveconstantpain that doesnot change? If the patient has experiencedrecent unexplained changesin body weight or hasconstantpain that does not change,deferthermotherapyuntil a physicianhas performed a follow-up evaluation to rule out malignancy.If the patient is known to havecancer,askr o Do you know ifyou havea tumor in *ris area? Thermotherapyshould generallynot be appliedin the areaof a known or possiblemalignanry;however,such treatmentmay be given,with informed consent,to provide relief of pain for the terminaLly ill patient.
Infraredirradiationof the eyes IR irradiation of the eyesshould be avoidedbecause such treatmentmay causeoptical damage.To avoid irradiation of the eyes,IR opaquegogglesshould be wom by the patientthroughouttreatmentusingan IR lamp, and by the therapist when near the lamp, as occurswhen settingup t]1etreatment
PRECAUTIONS
fortheUseofThemotheraPy o o o o
Pregnancy Impairedcirculation Poorthermalregulation Edema
Useheatwith caution. . ' ... during pregnanry A fetus may be damagedby maternalhyperthermia; however, since this is unlikely to occur with superticial heatingo[ the limbs. drermotherapymay be applied to such areas, but full body heating, as ociurs with immersion of most of the body in a whirlpool, should be avoided during pregnancy.
o o o o
Cardiacinsufficiency Metal in dre area Overan openwound Over areaswhere topical countedrritantshave recentlybeenapplied
Although matemal hyperthermia has not been demonsffatedwith application of hot packs to the low back or abdomen,suchapplicationis alsogenerally not recommended. ASK THE PATIENT . Are you pregnant? o Do you think you may be pregnant? . Are you trying to get pregnant?
r65
Tpo . THE PIIYSICAL AGENIS
-i -.hepatientis ormay be pregnant,do not aPplyheat l the abdomenor low back and do not immersethe :arient in a warm or hotwhirlpool . , over areas with poor circulation or in ratients with poor thermal regulation -.-:easwith poor circulation and patients wi*r poor :ermal regulation may not vasodilateto a nomal igree in responseto an increasein tissuetempera=re and thereforemay not have a sufficientincrease : blood flow when tissuetemperatureincr€asesto :--otect the tissues ftom buming. In general,poor =ermgl regulationis encounteredin the elderly and ';.ry yourlg. ASSESS: r Check skin temperatureand quality and nail qualiry, and look for tissue swelling or ulceration. Decreasedskin temperature,thin skin, poor nails, dssue swelling, and ulceration are all signs of rmpairedcirculation. Usemilder superficialheat in areaswith poor circu;:on or in elderlyor very young patients.Apply heat a: a lower temperatureor with more insulatiorSand c.eck thesepatientsftequently for any discomfortor ;3ns of burning. . . . in areaswith edema --ee application of thermotherapy to a dependent rruemiry has beenshown to increaseedema.loaThis ei:ct is thought to be the result of the vasodilation ;:d enhancedcirculationthat occurwith raisedtissue :errperatureand the increasein inflammationcaused F; increasedmetabolicrate. ASSESS: . -\4easurelimb girth in the area to be treated and comparethis with the contralateralside. Palpatefor pitting or brawny edema. Check for other signs of inflammation, including heat, redness,and pain. Do not apply heat with the area in a dependent srsition if edema is present.Heat may be applied -^rth cautionwith the areaelevatedif edemais presct and is thought to be a result of impaired venous ;:culation. . , . with patients with cardiac insufEcienry lleat can cause both local and generalizedvasodi;ion, which can contribute to increasedcardiac
demand.Because*ris may not be well toleratedby patients with cardiac insufficiency, such patients shouldbe monitored closelyif heat is applied,particularly if the heat is appliedto a Iargearea. ASK THE PATIENT o Do you haveany problemswith your heart? ASSESS: . In patientswith heart problems,check heart rate and blood pressurebefore,during, and after treatment. A slight decreasein blood pressureand an increase in heart rate are notmal consensual responsesto the application of heat. Discontinue heat treatment in a patient with cardiacinsufficiencyif the patient'sheart rate falls or the patient complains of feeling faint. . . . in areas with metal Metal has a higher thermal conductivity and higher specific heat than body tissue and therefore may becomevery hot with the applicationof conductive heatingmodalities.Ior this reason,jewelry shouldbe removedbeforethe applicationof superficialheating modalities,and cautionshouldbe appliedwhen there is metal, such as staplesor bullet fragments,in the superficialtissuesof the areabeingtreated. ASK THE PATIENT: o Do you have any metal in you in this area,suchas staplesor bullet fragments? . Pleaseremoveyour jewelryin the areato be heated. If there is metal present that cannot easily be removed,applyheatwith caution.Usemilder heat,at or intensiryor with moreinsulaa lower temperature tion, and checkthe areafrequently during treatment for any signs of buming. ASSESS: . Inspectskin for scarsthat may covermetal. . . . over any open wound Do not use paraffin over an open wound becauseit may contaminate the wound and is difficult to remove.All other forms of thermotherapyshouldbe appliedover open wounds with caution becausethe lossof epidermisreducesthe insulationof the subcutaneoustissues.If forms of thermotherapyo*rer than paraffin are usedin the areaof an open wound, they shouldbe appliedat a lower temperatureor intensity, Continued
r56
6.
Thetmal Aeents: Cold and Heat
PRECAUTI0NS-cont'd or with more insulation than would be used when treatins areaswith intact skin. One shouldalsocheck frequentlyduring treatmentfor any signsof burning. When applying a heating agent with the goal of increasingcirculationand acceleratingthe healingof an open wound, hydrotherapy with clean, warm water may be applieddirectly to the wound, or other superficialheatingagentsmay be appliedcloseto, but not diretdy over,dre wound to provide a therapeutic effectrihile reducingthe riskof cros'-conraminarion and burns. . . . over areas where topical counteriffitants have recently been applied Topical counterirritantsare ointmentsor creamsthat causea sensationof heat when applied to the skin. Suchpreparationsgenerallycontain substancessuch as men*rol that stimulate the sensationof heat by
EFFECTS OFTHERMOTHERAPY ADVERSE Bums Fainting Bleeding Skin and eye damage ftom IR irradiation
Burns Excessiveheating can cause protein denaturation and cell death.These effectsmay occur when heat is applied for too long, when the heating agent is too hot, or if heat is applied to a patient who does not have the appropriate protective vasodilation responseto increasedtissuetemperature.The effects viability are exploitedin the medical of heat on ce11 treatment of malignancies,where heat is applied with the goal of killing the malignantcells;however, in applicationof heat in rehabilitation,cell deadr is proteinbeginsto denatureat 45 to be avoided.Because 'C (113"F),andcelldeathhasbeenobservedwhen cells 'C were mahtained at 43 (109'F) for 60 minutesor at 46 "C (115"F)for only ZV2minutes,when applyingheat in rehabilitatioq the durationand tissuetemperature 116 shouldbe keptbelowtheselevels.l15
causing a miid inflammatory reaction in *re Thesepreparationsalsocauselocal superficial lation. If a thermal agentis appliedto an area*rat i already vasodilatedas the result of application of topical countedrritant, the vesselsin the area may be able to vasodilate furdrer to dissipate *Ie heat the thermal agent, and a burn may result.
ASK THE PATIENT . Have you applied any cream or ointment to areatoday? o If so,what type? If the patient has recently applied a topical terirritant to an area,do not apply a superficial ing agent. Tell the patient not to use this type oreparationbetorefuture treatmentsessionsand to apply a superficialheating agent at home usingthis type of preparation.
Overheating and tissue damage can be avoided
usingsuperficialheatingagentsthat get cooler their application,bylimiting the initial temperature the agent, and/or by using insulation between
agentand the patient'sskin. Ior example,hot that arewarmed in hot water beforebeine placed the patient start to cool as soon as they are from the hot water and applied, and are
unlikely to causeburns.In contrast,superficial ing agentssuch as plug-in electric hot packs or lamps that do not cool with use are more likely causeburns.The higher*re temperatureof a tive superficiaiheating agent,the greaterthe rate heat transfer to the patiencand thus the greater
risk of burns:thereforeit is important not to a conductive superficial heating agent and to use adequateinsulation.
To avoid bums,heatingagentsshouldbe applied the mannerrecommendedbelow.They shouldnot appliedfor longerperiods or at higher and the treatment time and temperature of the
agent should be reducedif the patient has circulation. Heating agents should not be where contraindicated, and all patients should be vided with a means of calling for assistance,such
bell. if the clinicianor anotherstaff memberis not
Two . THE PIIYSICAL A GENTS
167
rtheimmediatefteatmentarea.During the treabTrent, the brain to help the patient recover.Heating as small *eck to be surethat the patienthasnot fallenasleep, an areaasclinicallybeneficial,andremovingexcessive heavy clothing that insulates the whole body, may I]; instructthe patientto usea timer that ringsloudly jre also help to limit this consensualdecreasein blood a patient uses time if the *re treatment end of m and thusreducethe probabilityof fainting. pressure agent athome. heating srerficial may also feel faint when getting up after Patients be at home should agent used heating -\ superficial This is due to the additive hypotenthermotherapy. as a microwavable over time, such fe wpe that cools (orthostatic) hypotensionand postural effects of sive heating If an electric pick water botde. or a hot l,:i as describedabove. of the heat, effect hypotensive the type be the it should rad is usedby a patientathome, with a pillow durelevated patient's head the Keeping at all down a switch tar requiresthe patient to hold postdecrease help to can application the heat ing that ensures safety feature -es for it to stay on, This the by reducing postural hypotension ffeatment patient falls asleep if the ::e heatingpad will turn off of the completion at the change of positional extent cd stopsholding down the switch. patient the that is also recommended It treabarent. patient's skin be the It is recommended that remainin the positionusedduringt}le ffeatmentfor a s-.pecredfor bums beforeinitiating treatmentsincea minutes after the thermal agent is removed to few skin :;f,ent may have been burned previously.The allow blood pressureto normalizebeforerising. iculd alsobe inspectedduringand after thermother:cv. A recentsuperficialburn will appearred andmay -ve blistering.As the bumheals,the skinwill appear Bleeding :ale andscarred. The vasodilationand increasedblood flow causedby increasingtissuetemperaturemay causeor aggravate Fainting bleedingin areasof acutetraumaor in patientswith hemophilia.The vasodilationmay alsocausereopen3;casionally,a patient may feel faint when heat is ing of any recentvascularlesion. ::pLied. Iainting, a sudden, transient loss of con;-iousness,is generally due to inadequatecerebral :,ood flow and is most commonly caused by ltradiation lromInfrared SkinandEyeDamage :eripheral vasodilation and decreased blood with a decreased Inftaredradiationcanproduceadverseeffectsthat are ::essure,generallyin association ^-cartrate.llTHeatingan areaof rhe body generally not produced by other superficial thermal agents. These include permanent damageto the eyes and -uses vasodilationlocally and, to a lesserextent,in -eas distantfrom the siteof application.This distant, pemanent changesin skin pigmentation.Iniury to :r consensual,responsecan result in a sufficient *re eyes,including corneal burning and retinal and jecreasein cerebralblood flow to causea patient to lenticulardamage,is consideredto be the most likely ofIR radiationapplicationll3 andmost severe-hazard :aint during the application of thermotherapy.If a :atient feelsfaint while heatis beingapplied,lowering Prolongedexposureto lR radiationmay also cause epideriral hyperplasia.llB :\e headand raisingthe feet will bring more blood to
Evaluatethe patient problem and set the goalsof tleanneru. Determine if thermotherapy is the most appropriate treatrnent. Detemine that themotierapy is not contraindicatedfor this patient or Ihis condirion. Inspect the fteatment area for open wounds and rashes and assess sensation. Check the patient's
chart for any recordof previousadverseresponses to heat or for any diseasethat may predisposethe Ask the appropriate patientto an adverseresponse. questionsof the patient,asdescribedin the preceding sectionson contraindicationsand precautions. 4. Select the appropdate superficial heating agent accordingto the body Part to be treatedand the desiredresponse. Coainued
MA
b . Thenftal Agerts: Cold and Heat
When applying superficialheat, selectan agent that bestfits the iocationand sizeof the areato be treated,is easily applied in the desiredposition, allows the desired amount of motion during application,is available,and is reasonablypriced. Choose an agent that will conform to the area beingtreatedsothat itmaintainsgoodcontactwith *re body. If edemais present,an agentthat canbe appiied with *re area elevatedshould be used. When applying d-rermotherapywith the goal of increasingROM, it canbe beneficialto allow active or passivemotion while the treatment is being applied.Any of the heatingagentsdescribedbelow can be applied in the clinic; only hot packs and paraffinmay be appiiedby patientsat home. 5. Explainto the patientthe procedureandthe reason for applyingthermotherapy,and describethe sensationsthe patient canexpectto [eel. During the application of thermotherapy the patient shouid feel a sensationof mild warmth Dependingon the agentand the amount of insulation, the warmth may not be felt for the first few minutes of treatment.The patient should not feel
TECHNIQUES APPLICATION HotPacks Commerciallyavailablehot packsare usuallymadeo[ bentonite,a hydrophilicsilicategel, coveredwith canvas.Bentoniteis usedfor this applicationbecauseit can hold a largequantity of water for the efficientdelivery ofheat. Hotpacksaremadeinvarioussizesandshapes designedto fit differentareasof the body (Iig. 6-22) They arestoredin hot water kept at about70' to Z5"C thermostati(158'to 167'I) insidea purpose-designed, (Iig. stayson 6-23) *rat water cabinet cally controlled takes 2 hours q?e pack initially of hot at all times.This each use. betv/een to heatand30 minutesto reheat
excessivelyhot or feel any sensationof increased pain or burning.If the patient reportsany of these sensations,discontinuethe treatment or reduce the intensity of the heat. 6. AppIy the appropriate superficial agent. Selectfrom tltefollowinglist:
h
Hotpacks l Paraifin I Seeapplicationsfor Fluidotherapy I eachsuperficialheating on the following IR lamp I agent pug"t. Whirlpoolor I contrastbath ,l Z. Inspectthe treatedareaand assessthe outcome
pdrricularlyfor progressroward the ser g of treatment and for any adverse effects the treatment.Remeasurequantifiablesubj complaints and objective impairments and abilities. 8. Documentthe treatment.
Electric, plug-in heating pads are not mendedfor ciinicalusebecausethey do not cool ing applicationand thereforemay more easilybu patient.If patientsare usinga plug-in electrichea pad at home, advise them to use a pad that re( the "on" switch to be held down for the pad to
to use only the medium or low settings, to application at the medium setting to 20 minutes,
to discontinueuseif any sensationof pain, ov ing, or burning occurs. Patients should also advisedto inspect their skin for any signs of br direcdyafter the useof a hot pack and for the [o ing 24 hours.
Two C THE PHYSICAL AGENTS
-Jre 6-22.Hot packs of vadous shapes and sizes. ,uftesy ChattanoogaCroup, Inc., Hixson, TN.)
:::LripmentRequired . l-lot packsin a variety of sizesand shapes ,rpropriate for differentareasof the body . ,ipecializedheatingunit
169
Figure6-23.Thermostaticallycontrolled hot pack containers. (CourtesyWhitehali Manufacturing, City of Industry CA.)
. . . .
Towels Hot packcovers(optional) Timer Bell
: ?OCEDURE Removeclothing and jewelry from the areato be createdand inspectthe area. Wrap the hot packin six to eightlayersof dry towr l s .H o r p a c kc o v e r sw. h i c hc o m ei n v a r i o u s i z e s :o match the hot packs,can substitutefor two to rhree layers of towels Ffg. 6-2a). More layers shouldbe usedif the towelsor hot packcoversare o l d a n d h a v e b e c o m e- h i n o r i f t h e n a r i e n r :omplainsof feeling,oo*" rr" auring';;"Jrie;;. The towels can be preheatedto achievemore uniform heating throughout the treatment period. More layers of towels should be usedif ahebody part is on top of the hot pack than if the hot pack is piacedover the body part becausewhen the F i g u r6e- 2 4 H . o r p a c k c o v e r so f v d r i o u ss h a p e sa n d body part is on top of the packthe towels are comsizes.(CourtesyChattanooga Group,Inc.,Hixson,TN.) pressed,reducinginsulation of the body, and the underlying table providesmore insulation to the the increasedskin temperaturemay decreasethe pack, causing it to cool more slowly.llg If the patient's thermal sensitivity and the ability to patient complains of not feeling enough heat, judge the tissue'sheat toleranceaccuratelyand fewer layers of towels may be used for the next safely. treatmentsesslonjhowever,towels should not be 3. Apply the wrappedhot pack to the treatmentarea removed during heating with hot packs because and secureit weil (Frg.6-25).
6 c Tlrcrnol Agerts: Cold and Heat
170
4. Provide the patient with a bell or other means to cail for assistancewhiie the hot pack is on and j n s r r u c rt h e p a r i e n t r o c a l l i m m e d i a - e l yi f h e o r she experiences any increase in discomfort. If the patient feels too hot, extra towels should be placed berweer t-he hot pack and the patenr. I[ t]e p a L i e n rd o e s n o t F e e lh o L e n o u g h . f e w e r I a y e r s of towels should be used at the next treatment session. 5 . A f r e r 5 m i n u r e s .c h e c l
;1,r,nd
rrp:fmcnr
Paraffin Warm, melted paraffin can be used for thermother apy. For this application,the paraffin is mixed with mineraloil in a 6:1 or 7:1 ratio of paraffinto oil to reducethe melting temperatureof the paraffin from 'I) 'C 54 (129 to between45' and50 "C (113'to 122"I). Paraffincan safely be applied directly to dre skin at because of its low specificheat and this temperature 'h".-,T
.^^.1',.r,\/in/
F^r
th,<
ennl e:r,on
rhe
paraffin is heated and stored in a themostatically
F i g u r e6 - 2 5 .A p p l i c a . i o no f a h o t p a c k . ( C o u n e s ; Whitehall Manufacturing, City of Industry CA.) . Patient may not tolerate the weight of the hot pack o Pack may not be able to maintain good contac: with small or contoured areas . Acrive -notion noLpracricalduringtreaLmenL o Moderately expensive equipment (heated wate: cabinet)
controlled container Such containers are available in small portable sizes for home or clinic use ani in l.rger sizes oe.igned primari'y [or clinic use (lig. 6-26 4B). Paraffin is usually used for heatir: r h e d i s r a le x r r e m i r i e sb e c a u s er t c a n m a i n t a i ng o o C contact with these irregularly contoured areasPdr"[['n may also be applied to more proxima areai such a, r\e elbows and knee,, or even th. low back, by using the paint method describei following.
Ttro . THE PHYSICAL ACENTS
17l
: gure6-26. Thermostatically controlled paraffin baths. A, Small size for home or clinic use. (Counesy Chattanooga .roup, Inc., Hixson, TN). B, Largesize for clinic use.(CourtesyThermo-Electric,Imperial, PA.)
:quipment Required I Paraffin r Mineral oil (or commerciallyavailablepremixed paraffinintendedfor this application) PROCEDURE -here are three differentmethods by which paraffin ; commonly applied:dip-wrap, dip-immersion,and :aint. The dip-wrap and dip-immersionmethodscan rnly be used for treating the distal extremities.The :aintmethod canbe usedfor any areaof the body.For allthreemethods,do the following: i. Removeall jewelry from the areato be treatedand rnspectthe area. J. Thoroughly wash and dry the areato be treatedto minimize contaminationof the paraffin.
o Thermostaticallycontrolledcontainer o Ple
hro<
nr nrner
o Towels FortheDip-wrapMethad(forthewristaxd hand):
3. With fingersapart,dip the hand into the paraffinas far aspossibleand remove(Frg.6-27). Advise the patient to avoid moving the fingers during the treatment because this will crack the paraffin coating. Also, advise the patient to avoid touching the sides or bottom of the tank because these may be hotter than the paraffin. 4 . Wait briefly for the layer of paraffinto hardenand becomeopaque. Contiweti
172
6 . Thernnl Agehts: CoLl and Heat
Figure6-27. Application of paraffin by Figure6-28. Removing paraffin from a the dip-wrap method. (Courtesy The patient's hand. Hygenic Corporation,Akron, OH.)
5. Redip the hand, keepingthe fingersapart. Repeat steps3 through5 six to ten times. 6. Wrap *re patient'shand in a plasticbag,wax paperr or ueatment table paperand then in a towel. The plasticbag or paperpreventsthe towel from sticking to the paraffin,and the towel actsasinsulation to slow the cooling of the paraflin. Caution the patientnot to move the hand duringdippingor during the restperiodbecausethis may crackthe coating of paraffin, allowing air to penetrateand the paraffinto cool more raoidlv
7. E 1 . . , " i . + k . - - + " - - i k , L Leavethe paraffin in placefor 10 to 15 minutes or until it cools. 9. When the treatmentis completed,peelthe paraffin off the hand and either replacethe paraffin in the containerto melt or discardit (Iig. 6-28). FortheDip-immersion Method: 3. With fingersapart, dip the hand into the paraffin and remove. 4. Wait 5 to 15 secondsfor the layer of paraffin to hardenandbecomeopaque. 5 . Redipthe hand,keepingthe fingersapart. 6. Allow the hand to remain in the paraffin for up to 20 minutesand then removeit (Iig. 6-29). The temperatureof the paraffin should be at the lower end o[ the rangefor this method of application becausethe hand cools less during treat-
Figure6-29. Application of paraffin the dip-immersion method.
ment than with the dip-wrap method. The should be turned off durine the treatmentso the sidesand bottom of *re tan! do not too hot. ForthePaintMethad: 3 . Paint a Iayer of paraffin onto the treatment with a brush. 4. Wait for the layer of paraffinto becomeopaque. 5 . Painton anotherlayer of paraffinno largerthan first layer.RepeaLsteps3 through 5 six to ten times
6. Cover the area with plastic or paper and then wi toweling. As with the dip-immersionmethod, plasticor paperis usedto preventthe towel stickins to the paraffin and the towel acts as
fion to slow down the coolingof the parafft Caution the patient not to move the area duri treatment as this may crack the coating of paraffi allowing air to penetrate and the treatment area cool more rapidly.
7. Leavethe paraffinin placefor 20 minutesor until cools. 8 . When the treatment is completed, peel off paraffin and either replace it in the contalner melt or discard it. ForAll Methads: When the rreaunenris complere.inspeccthe ment area for any signs of adverse effects and ument the treatment.
Two . THE PHYSICAL AGENTS
'C Paraffinmay be sterilizedby heatingit to 80 ',176'F) andthen allowing it to cool overnight.Its temperature should be allowed to retum to 'C between45' and50 (773'to 122'I) beforeit is usedagainfor treatment. IDVANTAGES . -\4aintains goodcontactwith highly contouredareas . Easyto use .llexpensive . Bodypart canbe elevatedif usingthe dip-wrapmethod
:luidotherapy :-uidotherapy is a dry heating agent that transfers It consistsof a cabinetcontain::at by convection.l20 :g finely ground celluloseparticlesmade from corn ::bs (fig. 6-30).Heated air is circulatedthrough the ::rticles, suspendingand moving them so that they ::i like a liquid. The patient extendsa body part into
173
o Oil lubricatesand conditionsthe skin . Can be usedby patientat home DISADVANTAGES o Messyand time-consumingto apply . Cannot be usedover an open skin lesion as it may contaminatethe lesion o fusk of cross-contaminationif the paraffin is reused . Part in dependent position for dip-immersion method
the cabinet,where it floats, as if in water. There are also portalsin the cabinetthat allow the therapistto accessthe patient'sbody part while it is beingheated. Iiuidotherapy units comein a variety of sizessuitable for treating different body parts. Both the lemperature and the amount of particleagitationcan be controlled by the clinician.
:quipment Required . Iluidotherapy unit of appropriatesizeand shape for areasto be treated ) ROCEDURE l. Removeall jewelry and clothing from the areato be treatedand inspectthe area. i. Cover any open wounds with a plastic barrier to prevent the cellulose particles from becoming l^l--l
i - + 1 " .' " ' ^ , ' - J
:. Extend the body part to be treated through the portalof the unit (Fig.6-31). -. Securethe sleeveto prevent particlesfrom escapi^^ f,^*
rL.
""hi--r
: . S e t t h et e m p e r a t u raet 3 8 ' t o4 8 " C( 1 0 0 ' t o1 1 8 ' I ) . 5. Adjust the degreeof agitation to achievepatient comfort. -. The patientmay moveor exerciseduringthe treatrnent. :. Treatfor 20 minutes.
ADVANTAGES . Patientcan move during the treatmentto work on gainingactiveROM e Minimal pressureappliedto the areabeingtreated o Temperaturewell-controlledand constantthroughout treatment o
F,..'r^
"J-inictpt
DISADVANTAGES o Expensiveequipment o limb must be in dependentposition in someunits, increasingthe risk of edemaformation o The constantheat sourcemay resultin overheating o If the corn cob particlesspill onto a smooth floor, they will make the floor slippery Cafitfuued
174
6 . Tlrcrmal Aseflts: Cold atd Heat
Fluidotherapycontrols.(CourtesyChattanooga Figure6-30. Group, Inc., Hixson, TN.)
Figure 6-31. Application oF Fluidotherapy. ChattanoogaGroup, Inc., Hixson, TN.)
Lamps Infrared Infrared lamps emit elechomagneticradiation within the frequency range that gives rise to heat when absorbedby matter (Flg.6-32).lnfraredradiationhas a wavelengthof 770nm to I mm (106nm1.Iying bewveen visible light and microwaveson the electromagnetic spectrum(seelig. 12-1)andis emittedby many sources that emit visible light or W radiation, such as the sun. Infiared radiationis divided into threebandswith different wavelength ranges:IR-A" with wavelengthsof 770 to 1400nm; IR-B,with wavelengthsof 1400to 3000nm; and IR-C.with wavelengthsof 3000to 106nm. The IR sourcesusedin rehabilitationincludesunlighgIRlamps, andlow intensity lasers.Infraredlampsthat emit IR radiation in both the luminous (visible) and nonluminous (invisible) rangeswere availablefor clinical use in the pasq however, only those emitting luminous IR-A Figure6-32. Infrared lamp. (Courtesy Brandt radiation are currendy being manufactured.The lamps Inc., Brorx, NY.)
Two . THE PHYSICAL AGENTS
;'. ailable at this time generally emit IR radiation with '.'.avelengths of between780and 1500nm with a peak ::iensityat 1000nm. producedby IRradiThe tissuetemperatureincrease :ion is direcdyproportionaito the amountofradiation :-at penetratesthe tissue.This is relatedto the power --rd wavelengthof the radiatiorl the distanceo[ the :.diation sourcefrom the tissue,the angleof incidence ,: the radiationto the tissue,andthe absorptioncoeffi::nt of the tissue,Higher power IR will delivermore r=diationto the skin. Most lamps deliverIR radiation .'.ithpower inthe rangeof 50 to 1500watts.The wave.::rethof IR radiationusedclinically,which is beween -30 and1500nm, is absorbedwithin the first 1 to 3 mm :: humandssue.It hasbeenshownthat at least50% of beyond L radiationof 1200nm wavelengthpenetrates -.3mm andis thereforeableto passthroughthe skinto capillariesand cutaneous :,teract with subcutaneous Humanskinailowsmaxlmumpene::rve endings,l2l :ation of radiation with a wavelengthof 1200 nm radiation with a i'hile being virtually opaqueto "lR .r'aveiength of 2000.rmor gteater.113 The amount of energyreachingthe patientfrom an 3 radiation source is also related to the distance ::tween the sourceand the tissue As the distanceof ie sourceftom the target increases,the intensity of =diation reachingthe targetchangesin proportionto ie inversesquareof the distance.Ior example,if the :curceis movedfrom a posidon5 cm from the targetto : Dosition10 cm from the target,increasingby a factor :i 2, the intensity of radiationreachingthe targetwill 111to one-fourth of its prior level The amount of :rergy reachingthe targetis alsorelatedto the angle :i incidenceof the radiation.As the angleof incidence ::- the radiation changes,the intensiry o[ the energy ::achingrhe rargetchangesin proportionto the cosine -i the angleof incidenceof the radiation.For examPle, -'the angleo[ incidencechangesfrom 0 degrees(i.e.,
:quipment Required . IRIamp . IR opaquegoggles
175
perpendicularto the surfaceof the skin),wiLh a cosine with a cosineof f2rz, the intensity of i, to +Sdegrees, a factorofx/2r2.Thus,the intenwill fallby of radiation is greatestwhen the radiation the skin sity reaching sourceis closeco the parient'sskin and the radiadon beam is perpendicularto the skin surface,and, as the the intendistanceor *re angieof incidenceincreases, will diminish. the skin reaching the radiation sity of Infraredradiationis absorbedmost by tissueswith IR absorption Because coe[Ficients highIR absorption color.with primarily by skin affected aie .o-.[fi.i"n,t lighter than radiation more abiorbing darker skins positioning, and lamp radiation skins,with the same dark skin will absorbmore IR radiationand therefore increasemore in temperaturethan liSht skin A number of authorshave provided formulae for calculatingthe exactamount of heat being delivered or methodologies to a patiJnt by IR radiation,109'122 for measuringthe exacttissuetemperatureincrease;110 however,in clinicalpractice,the sensoryreport of the patient is usuallyusedto gaugethe skin temperature. The amount of heat transferis adjustedby changing the power output of the lamp and/or the distanceof the iamp from the patient so that the patient feelsa comfoftablelevel of warmth. Although the clinical use of IR lamps for heating superficialtissueswas popular during the 1940sand 19'50s,this practicehaswaned in recentyears.Its fall in populariry appearsto be the result of changesin practicestyle preferencesandlimitations in the quaniw of prblith.d tesearchdata ratherthan becauseof of excessiveadverseeffectsor lack of u.ry "uid"tl."efficacv. Most of the current use and theraoeutic recentliterature regardingclinical applicationsof IR radiationrelateto high-intensiryIR lasersintendedto rather producelocal burning and photocoagulation than to the lower-intensirylamps intendedfor gentle heatingduringrehabilitation
. Tapemeasureto measuredistanceof treatment areafrom IR source . lowe.Ls Continued
176
6 . Thermal Agants: Cold ard Hcar
PROCEDURE 1. Removeclothing and jewelry from the areato be treatedand inspectthe area.Drape the patient for modesty,leavingthe areato be treateduncovered. 2. PutIR opaquegoggleson the patientandthe therapist if there is a possibility of IR irradiation of the eyes. 3. Allow the IR lamp to warm up for 5 to 10 minutes soit will reacha stablelevel of output.109 4. Position*re patientwith the surfaceof the areato be treatedperpendicularto the IR beamand about 45 to 60 cm away from the source.Rememberthat the intensity of tJle IR radiation reaching the skin decreases, with an inversesquarerelationship,as *re distanceftom the sourceincreases, and in oroporcJon to thecosineof theangleof incidence oi the beam. Adjust the distancefrom the source and wattageof the lamp output so that the patientfeels a comfortablelevelof warmth. Measureandrecord the distanceof the lamp from the targettissue. 5. Providethe patient with a meansto call for assistance,and instruct the patient to call if discomfort occurs. 6. Instruct the patient to avoid moving closer to or farther from the lamp and to avoid touching the lamp since movement toward or away from the lamp will alter the amount of energyreachingthe patrent. 7. Setthelamp to treatfor 15to 30 minutes.Generally, treatment times of about 15 minutes are used for subacuteconditionsand up to 30 minutes for chronic conditions.Most lamps have a timer that
automaticallyshuts off the lamp when the rnpnt
timc
hrc
pLn
B. Monitor the patient'sresponsedudng treatment. maybe necessaryto move the lamp fardrer the patient becomestoo warm. Be cautious moving the lamp closerif the patient reports feeling warm enough as the patient may accommodatedto the sensationandmaynot the heatlevelaccuratelyoncewarm. 9. When the treatment is completed, tum off lamp and dry any perspirationfrom the area. ADVANTAGES . Does not require contact of the medium with patient. This reducesthe risk of infection and possiblediscomfort of the weight of a hor pack. alsoavoidsthe problemofpoor contactwhen ing highly contouredareas. o The areabeing treatedcan be observed the treatment. DISADVANTAGES o Lefraredradiationis not easilylocahzedto a treatmentarea. o It is difficult to ensureconsistentheatinsin all ment areasbecausethe amount of heat transfer affected by the distance of the skin from radiation source and the angle of the beam
the skin, both of which vary with tissue and may be inconsistent between sessions.
MEANS OTHER OFAPPLYING the distanceof THERMOTHERAPY Superficialheat may alsobe appliedby immersionin a walm whirlpool or a contrastbath, as describedin detailin Chapter9.
the agent from the patient, and patient's position or activity if these can be with the agentused.Documentationis typicaily ten in the SOAPnote format.The followins only summarize the modality component of
Documentation
ment and are noi intended to represent a sive plan of care.
Document the area o f tthe body treated,*re type of heating agent used, the treatment duration, and the
When applying a hot pack to the low back,
response to treatment. Also document treatment parameterssuch as the temperatureor power of the agent,the number and type of insulationlayersused,
Examples
9 : 9t,ela tu* Aa& pain al k4z4 7| | 0 0: NP tou* Ao&,,2A , N,t1^t'!14 LL,ebUuA <,4U'rrr!l
177
-1:9ain dsnza.azd, P,"!tu 7ll0 b.4ll0. 9i&lna U,lu,aruz ino*nzd. (,wn 30' to 60' . ?: 9ottlltuz uazol N? aL dlure W.\z 'tfulchihq anl, tla e'x lt^.qrL4lrr
,i,'l-renapplying paraffin to the right hand, document: !:?LcIatlhand, illnz,a.t ea.p*:al&pwitlL Pnar^ e lz.tatolr 1: 9aral$nllhand,, 50'e, l0', dipw^a'lt, Lzltendi'tta' ,+ 0enzalzn iolAf ili44n ,tL. 9+anlnal inlzt'pAalnnAzal e,^latian in 2aA2t |0 20 dzatu't, altzt atiw atn, pa,ttito tltlelchhq. AWekt tiz aAte ea"tt u A.blndaablan e. ?: &nlirulz u.tz o4 fa^a44in o,t al'arrz to" n hahd A4)42 ahekAinA dnd naliliynh& .r.hen applying lluidotherapy to the left leg, anlle, :rd foot, document:
9: ?tola 2 ot&teal|lfu,al I U, 42 "e, 2f . An*le .4n0m dt^irq 0 : ?A.addAz^a'pq hultnq
.,4: 1n*b.99 utavaun kwntuulAaXtlt 5 &yee.' P: oi'tanlbua (luifatAaaPa. P^aq&M' U, dAita dnd' P . dtte tl0IL anl. gait aajtuilia, in urddV Aqrn4' llotilt*a
When applyingIR radiationto the right forearm,document: 9: PLcla k fu'vatm pain wi& utitirry 0: 9k ll fu'rzatm,9R--41000nn', 10011)ol 50 cn fun 20ninulza., :1: tllili, uttali<'n o( untmth ol futza'vn; d*tendzd,50% 9: &alluz 9ll a't,ol'aw 2x Pztt
*^,itirrg
) Clinkal CaseStudies 1 The following casestudiessummarizethe conceptsof supedicialheat discussedin dris chapter.Basedon the scenariospresented,an evaluationof the clinical findingsand goalsof treatmentare proposed.Theseare followed by a discussionof the factorsto be consideredin the selectionof superficialthermotherapyas the indicatedtreatmentmodality and in the selectionof theideal thermotherapyagentto promote progresstoward the setgoals.
Case 4 MP is a 75-year-old female who has been referred for *rerapy with a diagnosis of osteoarthritis of the hands and an order to evaluateand treat with a focus on developing a home program. MP complains of stifftress and aching in all her finger joints, causingdifficulties in gripping cooking utensils and performing other household tasksand pain with w ting- Shereports that these s),rnptoms have gradually worsened over the last 10 years and have become much more severein the last month since she stopped taking ibuprofen due to gastric side effects. The objective exam revealsstiffrressand restrictedflexion ROM of the proximal interphalangealsto approximately 90 degrees,and mild ulnar drift at the carpometacarpal joints bilaterally. The joints are not warm or edematous, and sersation is intact in both hands. EVALUATIONOF THE CLINICAL FINDINGS This patient presentswiti the impairments of restricted finger RON! stifftiess and swelling of the finger joints, joints of andabnormalulnardrift of the carpometacarpal
the hands. These impairments have resulted in difficulties with the functional activities of cookine, household tasks,andwriting. PREFERREDPRACTICEPATTERN Impaired Joint Mobiiity, Motor Function, Muscle Performance,and Range of Motion AssociatedWith ConnectiveTissueDysfunction,(4D) PLAN OF CARE The goals of ueatment at this time are to increaseioint RON,I,leducejoint stiffrress,control pairl and increasethe patient's ability to grip cooking utensils, p€rform household usks, and write. Civen the chronic, progressive ruture of osteoartlritis, the treatment should focus on maintaining the patienCsstatus,optimizing her function, and slowing progressionof her disabfities if possible. ASSESSMENTREGARDINGTHE APPROPRIATENESSOF THERMOTHEBAPYAS THE OPTIMAL TREATMENT Superficialheating agentscanincreaset}re extensibfity of superficial soft tissue and are therefore indicated for the treatmentof ioint stif:frEssand restrictedROM. Superficial heating agentscanalsoreducejoint-r€lat€dpain. Reducing these impairments may also help decreasethis patienCs disabiliry. Thermotherapy is not conffaindicated for this patient at this time because,altlough shehas a diagnosis of osteoarthritis, which is an inflammatory disease,her hands do not show signs of acute in-flammationsuch as increasedtemperatureor edemaof the finger joints, Her Cantinued
17a
6 . Thernal Agents: Cold atd Heat
) Clinical Case Studies-cont'd Cautionshouldbe used, handsaisohaveintactsensation. however, since at the age oE 75 yeats she may have impaired circulation or impaired thermal regulation. Therefore the iatensity of the thermal agentshould be at the lower end of the rangegpically used PROPOSEDTREATMENTPLAN AND RATIONALE It is proposed that superficialheat be applied to the wrists, hands, and fingers of both hands. Paraffin, for or warerare approprjaleLreatments th-ridotherapy. these areas;however, a hot pack is not appropriate becauseit would not provide good contactwith these highly contoured areas. ?araffin has the additional advantageof allowing elevation while heat is being applied,thus reducingthe risk of edemaformation.It is aiso inexpensiveand safeenough to be used at home; ofnotallowing motion however,ithas the disadvantage during application. Therefore for optimal benefit, if paraffinis usedto treat this patient,sheshouldperform ictive ROM exercisesdirectly after removing the paraffin from her hands. Fluidotherapy and water Lave the advantageof aliowing motion during their application; however, Iluidotherapy is generally too expensiveand cumbersomefor useat home or in many clinics,and water immersion may result in edemaformationbecauset}Ie patient'shandsmustbe in a dependentpositionwhile beingheated.Civen *reseadvantages and disadvantages,walm water soaks together with if rhe parienrdoes would be most appropriare exercise and paraffinfof treatment, with this not developedema iowed by exercisewould be most appropriateif the patient developsedemawith soakingin warm water If paraffinis used,it shouldbe appliedusingthe dip-wraP methodratherthan the dip-immersionmethod sincethe former allows elevationof the hand and resultsin less intenseand prolongedheating.Thereforeit is lessiikely to result in edemaformation and is saferfor the older patientwho may have impairedcirculationand/or thermal regulation.
I
not letuned to his job as a carPenterbecauseof low by forward bending and back pain that is aSSravated Iow back stiffnesst}tat is most intenseduring $e first few hoursol the day.I(B reportsthar his pain is also by lyingsupinefor motethan5 minutesand aggravated to somedegreeby taking a hot shower'He alleviated is had beenmakinggood progress,with increasingIumbar ROM, strength,and endurance,until the last 2 weeks, when his progressreacheda Plateau The objective exam revealsspasmsof the lumbar Paraverteblalmuscles,a 507orestrictionof activeforward-bendingROM, and a 30% restrictionof sidebendingbilatelally,with a complaint of pulling of the 1ow back at the end of the range. Other objective measures,including activebackwardbendinS,passiveioint mobiliry, sensation, and lower extremity strengttr,are within oormal limits. OF THE CLINICALFINDINGS EVALUATION This patient presentswith impairments of resfficted trunk forward- and side-bendingROM, paravertebral musclespasms,and low back pain. He also has nor retumedto work sincehis injury' PREFERREDPRACTICEPATTERN lmpaired Joint Mobiliry, Moror Function, Muscle Performance, Range of Motion, and Refiex Integdty AssociatedWithSpinalDisorders,(4F) PLAN OF CARE The eoalsof ffeatment at this time are to decreaselow back pain and stifktess,to increaselumbar folwardbendingand side-bendingROM, and to havethe Patient tetumto worK.
ASSESSMENTREGARDINGTHE APPROPRIATENESSOF THERMOTHERAPYAS THE OPTIMALTREATMENT It is important to re alizethat 2 months after a soft dssue injury a patient's rehabilitation program should generallyfocus on activepartjciparionin a proSram Case 2 however the app{ipain. of srrerchingand strengtbening: back KB is a 45-year-oldmalepatientwi*r mild low activeexercisemay before physical agent a of suscation ladder and fiom a he fell 10 feet Two months ago, be indicated to improve performanceand accelerate tainedseveresoft tissuebruising;however,therewas no progress.Thermotheapy may be indicated for this evidence of a fracture or disc damagewith this tmuma. patient sinceit canreducepain, stiffness,and soft tissue KB was refered for physical therapy 1 month ago with optishorteningand becausethis patient has rePoftedthat a anorder to the diagnosisofa lumbarstrainandwith shower,which providessuperficialheating, helps hot to patient retuming goal of the with the function mize in dn dcriveexercise to alleviate his symptoms. There are also no conwork. KB i" currendypanicipating programto work on spinalflexibiligzand stabilization, traindications to the use of thermotherapy for this patient. but he often feelsstiff when surting to exerciseand has
TTyo . THE PHYSICAL ACENTS
PROPOSEDTREATMENTPLAN AND RATIONALE A deep or superficialheatingagentwould be appropriate for providingthermotherapyto this patient.A deep heating agent would be ideal since it could direcdy increasethe temperatureof both the superficialtissues and the musclesof the low back;however,a superficial heating agent would generally be used because diathermy, which can provide deep heating to large areas,is not available in most clinical setiings (see Chapter12)and ulhasoundcanonly provide deepheating to small areas(seeChapter 7). Superficialheating couldbe providedto the low backusingan lR lamp or a hot pack.A hot pack is most likely to be usedsinceIR lamps are aiso not availablein most clinical settings. to the useof thermotherThereareno contraindications apy for this patient. A hot pack could be applied with the patieot in a prone, side-lyingror sitting Positioq however, suplne positioningshouldbe avoidedsincehe reportsthat this agg(avateshis pain. More insulating towels may be n€ededin *re sitting position than in the prone or sidelying position due to compressionof tl.retowels and the insulatingeffectofthe backofthe chair.Treatmentwith any superficialheatiogagentwould generallybe applied for 20 to 30 minutes.Also, to optimize the ben€fit of increasedsoft tissue extensibilily, active or Passive stretchingshould b€ performedimmediately following the applicationofthe thermalagent.
Case3 BD is a 72-year-oldfemale with a 10-yearhistory of non-i.nsulin-dependent diabetes mellitus and a fullthickness ulcer on her lateral right ankle causedby aterial insufficiency.The ulcer has been presentfor 6 months and has been treated only with dressing changes.BD has poor arterial circulationin her distal lower extremities,but her physician has determined that she is not a candidatefor lower extremity bypass surgery Sensationis impaired distal to the patient's kneesand is intact proximal to the knees.The patientis alert and oriented.Shelives aloneat home and is independent in all activities of daily living; however, her walking is limited to approximately500 feet becauseof calf pain. BD has been referredto physicaltherapy for evaluationand treatmentof her ulcer.
179
EVALUATIONOF CLINICAL FINDINGS This patient presentswith the imPairmentsof loss of skin and underlying soft tissue on her right lateral ankle and reducedsensationin both lower extremities.Her ambulationtoleranceis limited, and she is requiredto change the dressing on her wound two or three times perweek. PREFEBREDPRACTICEPATTERN ImpairedIntegumentaryIntegdty AssociatedWith FullThicknessSkinInvolvementand Scarlormation,(7D) PLAN OF CARE The eoalsof treatmentat this time are to decreasethe achieve wound closure, and eliminate *o.rrrd "t"u, with openwoundsand risk associated high infection the the needfor dressingchanges. ASSESSMENTREGARDINGTHE APPROPRIATENESSOF THERMOTHERAPYAS THE OPTIMAL TREATMENT Thermotherapymay be indicated to achievethe proposed goals of treatment because it can improve circulationand thus facilitatetissuehealing Superficial heating agents can lncreasecirculation both in the areato which the heat is appliedand distally lncreasing tissuetemperatulecan also increaseoxygen-hemoglobin dissociation,increasingthe availability of oxygen for tissue healing. Becausethe application of thermotherapydirecdyto the distallowel exuemitiesof this patientis contraindicateddue to her impairedsensation in theseareas,proximalapplicationof thermotherapyto the patient'slow backor thighsmay be usedto increase the cilculation to her distal lower extremitieswithout excessive risk. PROPOSEDTREATMENTPLAN AND RATIONALE Thermotherapyusinga deeporsuperficialheatingagent would be appropriatefor this patient As with Case2, deepheatingwould be idealsincethis would affectboth deep and superficialtissue temperatuleslhowevet, a superficial heating agent is more likely to be used becauseofgreater availability.A hot pack or an IR lamp could be usedto heat this patient'slow back or thighs and shouldbe appliedfor about20 minutes.
All dghts ?referredPhysicalThempistPraclicePattemssM[4D, 4F and 7D] arc copyr\Eht2002AmericanPhysicalTherapy Association
6 t Thermal Aeerts: Cold and Heat
180
p
6-3 Effectsof Effect
and Thermotherapy Cryotherapy
Thermotherapy
Pain
Musclespasm Bloodflow Edemaformation Nerveconduction velocity Metabolicrate Collagenextensibiliry Jointstiffness
0 = decreases;+ = increases;0 = no effect.
CHOOSING BETWEEN CRYOTHERAPY ANDTHERMOTHERAPY Becausesome of the effectsand clinical indications for the useof cryotherapyand thermotherapyare the sameand othersare djfferent,thereare somesituations in which eithermay be usedand othersinwhich only one or the otherwould be appropriate.Table6-3 provides a summary of the effects of cryotherapy and thermotherapyto assistthe clinicianin choosing betweenthesetreatmentoptions.
blood flow,
increase nerve conduction
increasepain threshold, alter muscle strength, increase enzvmatic activitv rate. These effects thermotherapy are used clinically to control
increasesoft tissue extensibiliry.and healing. Thermal agents should not be applied situations in which drey may aggravate an
pathology,suchas a malignancy,or may cause age,suchas frostbite or burns.The readeris
Chapter Review
to the Evolve website at http://evolve.elsevier.
Thermal agentstransferheat to or from patientsby conduction, convection, conversiory or radiation. Cryotherapyis the transferof heat from a patient by use of a cooling agent, and thermotherapy is the transferof heat to a patientby useof a heatingagent. Cryotherapy has been shown to decreaseblood flow, decreasenerve conduction velociry increase pain threshold,alter musclestrength,decreaseenzymatic activity rate, temporarily decreasespasticiqy, and facilitate muscle contraction. These effects of cryotherapyare used clinically to control inflammation, pain, edema, and muscle spasml to reduce spasticirytemporarily; and to facilitate muscle conftaction.Thermotheraovhas beenshown to increase
Cameron for study questions pertinent to chapter
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Two . THE PITYSICAL ACENTS
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22. loLnson J, Leider FE:Influenceof cold bath on maximum handgrip strength, PerceVtMot Skills 44:323-325, 1977. 23. Davies CTM, Young K: Effect of temperature on the contractile properties and muscle power of triceps surae in humans,J Appl Physiol55:191-195, 1983. 24. Knuttsson E, Mattsson E: Effectsof loca1cooling oo monosynaptic reflexesin man, ScandJ RehabilMed 52:166-168,1969. 25. KnuttssonE: Topical cryotherapyin spaslciry,ScatldJ Rehabil Med2:159-L62 , 1970. 26. Hartvikksen K: Ice therapy in spasticity,Acta Neurol Scatrd38:79-83, 1962. 27. Mrghena O: Electromyographic characteristicsof donus and influence of cold, Arch Phys Med Rehabll 45:502-503 , 1964. 28. Miglietta O: Action of cold on spasticrty, AnJ PhysMed 52:198-205 , 1973. 29. PriceR, LehmannJl Boswell-Bassette S et al: Influence of cryotherapyon spasticityat the human ankle,Arr& PhysMed Rehabil7 4:300-304,1993. 30. Wolf SL,LetbetterWD: Effectof skin coolingon spontaneousEMG activity in fticeps suraeof the decerebrate cat,Braix Res91:151-155,1975. 31. Harris ED, McCroskery?A: The influenceof temperature and fibril stability on degradation of cartilagecollagen by rheumatoidsynovialcollagenase, N Eryl J Med 290:1,-6, 1,97 4. 32. Hocutt JE,JaffeR, RyplanderCR et al: Cryotherapyin arkle sprairs,AmJ SyonsMed 10(5):316-319, 1982. 33. Ohkoshi Y, Ohkoshi M, Nagasaki S: The effect of cryotherapyon intraarticulartemperatureand postoperativecareafter ante or cruciat€ligamentreconstntctton,An J SVotrs Med May-1v427(3):357-362,1999. 34. Meeusen\ Lievens?: The useof cryotherapyin sport injuries,SVotts Med 3:398-414 , 1,986. 35. Friden J, Sjostrom M, Ekblom B: A morphological study of delayed onset muscle sorctess,Erperiefitia 37:506-507 , 1981. 36. Jones D, Newhan D, Round J et al: Experimental human muscledamage:morphologicalchangesin relation to other indicesof damage,IPhysiolSTS:435-448, 1986. 37. Cote DJ,PrenticeWL, Hooker DN et al: Comparisonof threekeatment proceduresfor minimizing anklesprain swelltng,PhysTher68(71:1072-107 6, 1988. 38. Wilkerson GB: Treatment of inversion ankle sprain through synchronousapplicationof focai compression andcold,Athl Truia26220-225, 199L. 39. Quillen WS, Roullier LH: Initial management of acuteankle sprainswith rapid pulsedpneumaticcompressionand cold,J Onhop SponsPhys Ther4:39-43, 1982.
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Boris 44, Wiedorf S, Lasinski B et al: Lymphedema 60. MetzmanL, GambleJG,RinskyLA: Effectiveness of ice reductionby noninvasivecomplex lymphedematherpacksin reducing skin temperatureunder casts,Clir apy,Oncology -221, 1.996. 8(9):95-106, 1.994. OnhopSep;(330):217 4 T , BeenakkerEA, OparinaTI, HartgringA et al: Cooling 6r. Iarryr PJ,PrenticeNG: Ice treatment of injured ligaments:an expedmentalnod,el,NZ MedJ 9:12-14,1980. SarmentUeatment in MS: clinical improvement and decreasein leukocyte NO productioq NeutologySep 62. KrumhanslBR: Ice lollies for ice massage,Plys 11;57(5):892-894,2001. 49(10):1098 , 1969. 4 2 . CapelloE, GardellaM, LeandriM et al: Lowering body 63. SchroderD,PasslerHH:Combinationofcold and comtemperaturewitl a cooling suit as symptomaticfteatpressionafter knee sutgery:aprospectiv€ ment for thermosensitivemultiple sclerosispatients, study,KxeeSurgSyonsTtaumarol Anhrosc2B\:758-1 halJ NeurolSciNov;16(8):533-539, 1995. 1994. Umphred DA: NeurohgicalRehabllintiou,St. Louis, 64. Webb JM, Williams D, Ivory JP et al: The use of 1985,Mosby, compressiondressingsafter total knee replacement: 44. SelbachH: The principiesof relaxationoscillationas randomized coqtrolled tial, OnhoVedicsJat;21 a special instance of the law of initial value in 59-61,, 1998. cybemetic functions, Axn NY Acad Sci 98:1227-!228, 65. Travel J: Temporomandibularjoint pain referred 1962. musclesof the head and neck,J Ptosthetic Dent I0( 45. Celhom E: PirciVles of Autoaomic-Somatic htegration: 745,763,1960. Physialogical BasisandPsychololal and Clixiul Inpliutiotts, 66. Rubin D: Myofascial t gger point syndromes: Minneapolis, 1967,Universiry of MinnesotaPress. approach co marragement.A,ch Phys Med 46. Krright W: Cryothetapy:Theory Techxi4ue,Physiotogy, -I70, 1981. 62:107 Chattanooga,Tenn, 1985,ChattanoogaCorp. 67. Fluorimethaxe rcchxicalspeclfcatioxs, Cleveland, 47. Hayden CA: Cryokinetics in an early treatrnentpro1996,Cebauer Co. gram,JAn PhysTherAssoc44:990,1964. 68. TravellJC,SimonsDG:MyofascialPaiaand 48. BugajR The cooling analgesigand rewarming effectsof The Tigger PoinrManual, Baltrmore, 1983, ice massageon iocalizedskjn,PhysTher55(l):11-19,1975. Wilkins. 49. PrenticeWEr An electromyographicanalysis of the 69. Travell jC: Myofascialtrigger points: cljnical vjew. effectiveness ofheat or cold and stretchingfor inducing BonicaJJ,Albe-IessardD,ed.s: AAtaaces ln Pain relaxation in injured muscle,J Onhop SponsPhys Ther and Therapy, NewYork, 1976,RavenPress, 3tt33-137, 1982. 70. SimonsDC, TravellJC: Myofascialoriginsof low 50, Tiemey IM, McPheeSJ,lapadakis NM er al: Curett pain. 1: Priaciplesof diagnosisand treatment,P Medical Diagnosisand Treatwext.Norwalk, Cl 1998, Med73Q):70-77,1983. Appleton & Lange. 71. SimonsDC: Myofascialpain syndromedue to 51. Day MJ:Hypersensitiveresponseto ice massage: repolt points, Int RehabilMetl AssocMonogr 1, 7987. of a case,PhvsTher54t592-593 . 1974. ScarcellaJB, Cohr BT: The effect of cold therapv 52. PatkerJ! Smail NC, Davis DG: Cold-inducednerve the postoperativecourse of total hip and total palsy,Athl Traint876-77, 1.983. -852, arthroplastypatients, AnJ Onhop24(11):847 53. Creen GA, ZachazewskiJE,JordanSl: Peronealnerve 73. Bickford RH, Duff RS: Influenceof ultrasonic palsy induced by cryotherapy, Physician Sport Med tion on temperatureand blood flow in human 17(9)t63-70 , 1989. muscle,CrnRzs1:534-538,1953. 54. Lundgren C, Muren A, Zed.erfeldtB: Effect of cold Imamura M, Biro S, I(hara T et al: Repeated vasoconstrictionon wound healingin t}Ie rabbit,Acta therapy improves impaired vascularendothelial Chi Scand1,1,8:1, 1959. tion ir patientswith coronary rlsk factors,J Am 55. Boyer J! Iraser JRE,Doyle AE: The hemodlmamic CatdiolOcr;38(4):1083-1088, 2001. effects of cold imme rsiory Clix Sci 19:539-543,7980. 75. Crockford GW, Hellon M, ParkhouseJ:Thermal 56. CovingtonDB, BassettIH: When cryotherapyinjures, motorresponsein humanskin mediatedby local Physician SyonMed 2I(3)i 8-93, 1993. allusraes, 1.962. J Physiol161:1.0-L5, 57. Knight W: Cryotherayy in SFofi lniury Management, 76. Kellogg DL Jr, Liu I Kosiba II et al; Role of Champaign,IL, 1995,Human Kinetics, oxide in the vasculareffects of local warming of 58. BensonTB, Copp EP:The effectsof therapeuticforms skin in humans,J Ayyl PhysiolApr;86(4):1185-11 of heat and ice on the pain threshold of the normal 1,999. should.er, Rheumatol Rehabll13:101-104, 1974 . 77. Minson CT, Berry LI, Joyner MJ: Nirric oxide and 59. MacAuley DC: Ice therapy:how good is the evidence? rally mediated regulation of skin blood flow -384,2001. IxtJ SponsMerl.Jul;22(5)1379 -1626,2001. localheating,J AyyI PhysiolOc991(4):1619
Tso . THE PIIYSICAL AGENTS
-3.
Fox HH, Hilton SM: Bradykinin formation in human skin as a factor in heat vasodilation,/ Pltysbl142:219, 1958. -9. Guyton AC Textbaok of Medical Physiology,ed 8, Philadelphia,1991,WB Saunders. :4. AbramsonDl Indirect vasodilationin thermotherapy, ArchPhysMed Rehabil46:412-415 , 1965. !1. WessmanMS, Kottke FJ:The effect of indirectheating on peripheralblood flow, pulse rate, blood pressure and temperature,Atch PhysMed Rehabil48:567-576, 1967. .2. WWer DJ, McNiven DR: Effects of some physiotherapeutic agentson skeletaimuscleblood f1ow,Physiothetayy 6283-85, 1976. :3. Crockford GW, Hellon RF: Vascular responsesin human skin to infta-red radiation, / Physiol 149: 424-426,19s9. :-1. CurrierDP,IGamerJF:Sensorynerveconduction:heating effecs of ultrasound and infrared radiation, Caxada34:24I-246,1982. Physiothet :5. Halle JS, Scoville C\ GreathouseDGr Ultrasound effecton the conductionlatencyof t}Ie superficialradial rewe ln mar, PhysTher61:345-350,1981. :6. LehmannJF,Delateur BJ:Therapeutic heat. In Lehmann JF,ed TherayeuttHeat and CoA, ed 4, Baltimore, 1990, Williams & Wilkios. :7. Rennie GA, Michlovitz SL: Biophysicalprinciples of heating and superficialheating agents.In Michlovitz SL, ed: Thetnal Agents ix Rehabilitatior, Philadelphia, 1996,FADavis. 38. FountainIP, GerstenJW,SengerO: Decreasein muscle spasmproducedby ultrasound,hot packsand I\ Arcl PhysMed Rehabil41:293-299, 1960. !9. FischerM, SchaferSS:Temperatureeffectson the dischargefrequencyof primary and secondaryendingsof isolated cat muscle spindlestecorded under a rampand-holdstretch,Braix Res840(I-2):!'15, 1999. 10. Lehmann JF,Brunner GD, Stow RW: Pain threshold measurementsafter therapeuticapplication of ultrasound, mictowaves and nfrared, Arch PhysMed Rehabil 39:560-565,1'958. il. BensonTB, Copp EP:The effectsof therapeuticforms of heat and ice on the pain threshold of the normal 1974 Rehabil13:101-104, shoride4Rheumatol 92. Chastain PB: The effect of deep heat on isometric strengtt, PhysTher58:543-546,1978 93. Wickstrom R, Polk C: Effect of whirlpool on the strength and enduranceof the quadricepsmuscle in trained male adolescents,An J PhysMed 4091-95, 1961. 94. Edwards\ Harris \ Hultman E et al: Energymetabolism duringisometricexerciseat differenttemperatures of m. quadricepsfemoris in man, Acta PhysiolSand 80:I7-18,1970.
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95. tvtiller MW, Ziskin MC: Biological consequencesof -722, 1989. hyperrhermia, lJhtasoundMed Biol 1'5(8):707 96. BarcroftJ, King W: The effect of temPeratureon the dissociationcuwe of blood,I PhysiolS9:374-384,1909. 97. Lentell G, Hetherington T, EaganJ et al: The use of thermal agentsto iofluencethe effectivenessof lowload prolongedstretch,J OnhopSponPhysTher16(5): 200-207, 1992. 98. Waren C, LehmannJ, KoblanskiJ: Elongationof rat tail tendon:effect of load and temPeratwe,ArchPhys 4, 484' I971'. Med Rehabil52:465-47 99. Warren C, LehmannJ, KobianskiJ; Heat and stretch procedures:an evaluationusing rat tail tendon,Arch PhysMed Rehabil57:122-126 , 1976. 100. GerstenlW: Effectof ultrasoundon tendonextensibil1q',Afl l Phys'Med34:362-369,1'95s. 101. Lehmannl, MasockA, Waren C et al: Effectof therakch Phys peutictemperatureson tendonextensibilLty, Med Rehabil51:48I-487, 1970. 102. Kramer JI: Uitrasound:evaluationof its mechanical and thermaleffects,A rchPhysMed Rehabil6S:223-227, 1984. 103, SteilarJ,Habot B: Improvementof pain and disabiliry in elderlypatientswith degenerativeosteoarthritisof the knee treated with narrow band light th erapy,J An GeriatrSoc40(l):23-26,1992. j, Garett I Erickson D: Swelling of the Magness 104. upper extremity during whirlpool baths, Arch Phys Med Rehabil51:297-299, I970. 105. Wright V, JohnsR: ?hysicalfactorsconcernedwith the stiffnessof normai and diseasedjoints,/ohxsHoltblns HosyBull 706.215-229 , 1960. 106. Kik JA, Kersley GD: Heat and cold in the physical treaffnent of rheumatoid arthritis of the ktee, Axx PhysMed 9:270-274, 1968 107. BlacklungL, Tiselius P: Objective measurementof joint stiffness in rheumatoid arrhtitis, Acta Rheum . Scaad13:275, 1.967 108. Johns R, Wight V Relative impodance of various tissuesin joint stiffness,/ AVpl Physiol17:824-828, 1962. 109, Orenberg EK, Noodleman I\ Koperski JA et al: Comparisonof heat delivery systemsfor hyperthermia treatment of psoriasis,Int J Hypenhetn 2(3): 231-241 , 1986. 110. WesterhofW, SiddiquiAH, CormaneRH et al: Infrared hyperthermia and psoriasis,Arch Detmanl Res 279:209-210,1987. 111. Hyland DB, Kirkland VJ: Infra red therapy for skin 1801,1980. tlcers,AmJ Nuts80(10):1800112. Cummings J: Role of light in wound healing. In Kloth L, McCulloch JM, Ieedar JA, eds lYoundHeallxg Aheruativesifl Maftagenettt,Philadelphia, 1990, IA Davis.
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Thental Aeenrc:Cold aad Heat
113. Moss C, Ellis & Munay W et aI: hftated Radiatioq Nouioftkixg RadiationPlotectioft,ed 2, WHO Regional Publications,European Series, 25, Ceneva, 1989, World Health Organization. 114. Schmidt KL: Heag cold and inflammation, Rheunatology 38:391'404,1979. 115. SaparetoSA, Dewey WC: Thermal dose determinatron in cancer therapy, Iat I Radiol Oncol Biol Phys 1984. tQ787 -1QQ, 116. Homback NB: Hyyenherniaand Carcet Boca Raton, FL. 1984.CRC Press. II7. Canong Wl Revieu, of Mediul Physiology,ed 13, Norwalk, Cl 1987,Appleton & Lange. 118. KligmanLH: Intensificationof ultraviolet-induced dermal damageby infra-redradiation,ArchDermatolRes 272:229-238,1982.
119.Enwemeka CS,BoothCK,IisherSLet al:Decaytime of temperature of hot packsin two application positions,PhysThet76(5):596, 1996. 120.BorrellRM, HenleyES,PurvisH et al:lluidotherapy evaluationof a new heat modalty, Arch PhysMet Rehabil 58:69-71 , 1977. 121.HardyJD: Spectral transmittance and reflectance of excisedhuman skin, J AVyl Physiol9:257-264 1956. for physical 122.SelkinsKM, EmeryAF:Thermalscience medicine.In LehmannJF,ed:Therapeutic HeataudCokl" ed3, Baltimore, 1982,Williams& Wilkins.
SUMMARY
OF lNFORMATION
Jistory nrminology leneration of Ultrasound -ffects of Ultrasound Ilinical Applications of Ultrasound lontraindications and Precautionsfor Ultrasound
COVERED
AdverseEffectsof Ultrasound Application Technique Documentation Clinical CaseStudies Chapter Review
OBJECTIVES UVoncomyletionof this chayter,thereaderwill beable to: 6 . Chooseand use the most approPriate Recognizeand distinguishthe terminology used theraoeuticultrasound deviceand treatment ultrasound. therapeutic to describe parametersto obtain the desiredtreatment responses to physiological the Analyze goals. particular to promote necessary ultrasound 7. Evaluatedifferent therapeutic goals. treatment ultrasound deviceswith respectto their properties of, and the physical ) . Identify the for treating different patient potential to, therapeutic physiologicalresponses problems. ultrasound, Presentedwith a clinical case,evaluatethe J , Evaluatethe indications, contraindications,and clinical findings, proposegoalsof treatment' orecautionsfor the use of therapeutic assesswhether therapeuticultrasoundwould be patient ultrasoundwith respectto different the best treatment, and, if so, formulate an managementsituations. treatment plan, including the effective 5. Design appropriatemethods for selecting appropriatetreatment parameters,for achieving therapeuticultrasound treatment Parametersto the soalsof treatment. producedesiredphysical and physiological effects.
185
t86
7 o Ultrasound
HISTORY Methods to generate and detect ultrasound first becameavailablein the United Statesin the 19th century; however, the first large-scaleapplication of ultrasoundwas for SONAR (SoundNavigation and Ranging)during World War II. For this application,a short pulse of ultrasoundis sent from a submarine through the wate! and a detectoris usedto pick up the echo of the signal. Becausethe time required for the echo to reachthe detectoris nrooortional to the disrance o[ the detectortrom a refleciingsurface, the durationof this periodcanbe usedto calculatethe distanceto objectsunderthe wateg suchasother submarines or rocks. This pulse-echotechnology has sincebeen adaptedfor medicalimagingapplications, for "viewing" a fetus or other intemal masses,Early SONAR devicesused high-intensity ultrasound for easeof detection;however, it was found that these devicescan heat and thus damageunderwater life. Although this fact limited the intensity of ultrasound appropdatefor SONA\ it led to the developmentof clinical ultrasound devicesspecificallyintended for heating of biologicaltissue.Ultrasoundwas found to heat tissuewith a high collagencontent,suchas tendons, ligaments,or fasciaand, for the past 50 years or more, has beenwidely usedin the clinical setting for this purpose. More recendy, ultrasound has also been found to have nonthermal effects and, over the past 20 years, therapeuticapplicationsof these effects have been developed.Low-intensity pulsedultrasound,which producesonly nonthermal effects,has been shown to facilitate tissue healing, modify inflammation,and enhancetransdermaldrug delivery
WhatlsUltrasound? Ultrasoundis a type of sound,and all forms of sound consistof waves that transmit energy6y altemately compressing and rarefying material (Fig. Z-1). Ultrasoundis defined as sound with a frequencvof greaterthan 20,000cyclesper secondftlertz. Hz). ihls definition is based on the limits of normal human hearing.Humanscan hearsoundwith a frequencyof 16 to 20,000Hz; soundwith a ftequencygreaterthan this is known as uhrasound.Cenerally,therapeutic uitrasoundhas a ftequency of between 0.2 and 3.3 megahenz (MHz) in order ro maximize enery absorptionat a depth of2 to 5 cm ofsoft tissue.
Transducer
?
Compression
-----T----Rarefaction
Figure 7-1. Uitrasoundcompression-rarelaccionwave.
Audible sound and ultrasoundhave many properties.Ior example,asultrasoundtravels material, it gradually decreasesin intensity due attenuationin the sameway that the soundwe becomesquieter as we move farther from its (Frg 7-2). Ultrasound waves causea slight motion of material as they are transmitted, but
do not carry the material along with the Similarly,when someonespeaks,the audible waves of the voice reachacrossthe room. but the in front of the speaker'smouth is agitated slightly,not moved acrossthe room. Ultrasoundhasa variety ofphysicaleffectsthat be classiliedas thermalor flonthermaL Its ability increasetissuetemperatureis its thermaleffecqand ability to causeacousticstreaming, and cavitation.which mav alter cell membrane meability, are its nonthermal effects.This describesthe physicalpropertiesof ultrasoundand effectson the bodyin orderto deriveguidelinesfor optimal clinicalapplicationof therapeuticultrasoundThe followine sectionlists and definesthe used specificallyto describetherapeutic and its effects.Termsusedto describeuitrasound other physicalagentsaredefinedin the glossaryat end of this book.
Figure7-2. Decreasingultrasound intensity as tJ.re travelsthroueh tissue.
Two . THE PIIYSICAL AGEN'IS
TERMINOLOGY Transducer (sound head): A crystal that converts electricalenergyinto sound (Iig. Z-3).This term is alsousedto describethe part of an ultrasoundunit that containsthe crystal.
747
Power: The amount of acousticenergyper unit time. This is usuallyexpressedinWatts [V). Intensi$r: The power per unit area of the sound head. This is usuallv exoressedin Watts/centimeter squared 6vi.-2j. lh" World Health
FigureT-3.Ultrasound units:,A, transducer;B, frequency indicator; C, pulse duty cycle indicator; and D, power/intensiqy indicator. (Part one courtesy Rjch-Mar, Inola, Ok, Part Two courtesy Mettler Electronics, Anaheim, CA; Pan Three courtesy ChattanoogaGroup, Hixsoq TN.)
188
7.
Ultrasornd
Organizationiimits the averageintensity output by therapeuticultrasoundunits to 3 Wcm2.1 Spatial Average Intensiqz: The averageintensity of the ultrasoundoutput over the area of the transducer. Spatial Peak Intensity: The peak intensiry of the ultrasoundoutput over the areaof the transducer. The intensityis usuallygreatestin the centerof the beamandlowest at the edsesof the beam. Beam Nonunifoffiity Ratio (BNR): The ratio of the spatial peak intensity to the spatial average intensity(Fig.7-4).For mosr urirs rhis is usually berween5:1 and 6:1, althoughit can be as low as2:7,
= !1,
Time(ms)
EXAMPLEs Using a transducerwith a maximum BNR of 5:1,when the spatialaverageintensiryis set at 1 Wcm2, the spatialpeak intensiqrwithin the field couldbe ashigh as5 Wcm2. Using a transducerwith a maximum BNR of 6:1, when the spatialaverageintensiqyis set at 1.5Wcm2, the spatial peakintensitywithin the field couldbe ashigh as9 Wcm2. The IDA requires that the maximum BNR for an ultrasoundtransducerbe specifiedon the device. Continuous Ultrasound: Continuous delivery of ultrasound throughout the treatment period
(Iig.7-5). Pulsed LTltrasound: Delivery of ultrasoundduring only a portion of the treatmentpedod.Delivery of ultrasound is pulsed on and off throughout the
Figure 7-5.Continuous ultrasound.
= !D
Time(ms)
Figure 7-6.Pulsedultrasound. treatment period. Pulsing the ultrasound minimizesits thermaleffects(Iig.7-Q. Duty Cycle: The proportion of the total treatmeni time that the ultrasound is on. This can be expressedeitherasa percentageor a ratio.
'6
EXAMPLES
20okor 1.:5duty cycle,is on 20% of the time and off 80% o: rhe rjme. This is generallydelivered2 ms on.8 ms ol (Frg.7-7). 100% dury cycleis on 100% of the time and is tle same ascontinuousultrasound.
Figure7-4. Beamnonuniformify.
Spatial Average Temporal Peak (SAIP) Intensity The spatial averageintensity ofthe ultrasound during *re on time of the pulse (Iig. Z-8). Therapeutic
r89
Tgo . THE PHYSICAL ACENTS
=-
B
- SATP
!,
c
_ SATA Time(ms)
Time(ms)
Figure 7-8. SATPandSAIA intensiry Note that SAIA is equalto SAT?for continuous ultrasound. EXAMPLE
1wcm2 'ATP at 100%dutycycle= B
Tlme(ms)
7-7. Duty cycles:20okand5Ao/". Figure
ultrasoundunits displaythe SAIP intensityand the duty cycle. ln this chapter, all intensities are expressedas SAT| followed by the duty cycle, unlessstatedotherwise. Spatial Average Temporal Average (SAIA) Intensity: The spatial averageintensity of the ultrasoundaveragedover both the on time and the off time of the pulse. SAT?x duty cycle = SAIA ExAMPLE : w/cmz SAfP at 20% duty cycle =
i x 0.2= 0.2wcm2 SAIA
This is a measureof the amount of energydelivered to the tissue.SAIA units are frequentlyusedin the nonclinicalliteratureonultrasound.
1x 1 = 1wcmz 'ATA
Frequenry: The number of compression-rarefaction cyclesper unit of time, usually expressedin ryrles (Hertz, Hz) (Itg.7 -9).lncreasingthe freyer second in its depth quencyof ultrasoundcausesa decrease of penetrationand concentrationoI the ultrasound energyin the superficialtissues(Iig Z-10). Effective Radiating Area (ERA)r The area of the transducerfrom which the ultrasoundenergyradithe crystaldoesnot vibrate ates(Fig.7-11).Because uniformly, the ERAis always smallerthan the area of the treatmenthead.
trrftJttlfi
ifu'L,ru 1 and3 MHz. 7-9.Ultrasoundfrequencies: Figure
790
7 t Ulttasound
1 l\,4H2 3.3lvlHz
Transducer
Figure7-10. Frequencycontrols the depth of penetration of ultrasound; 1 MHz ultrasound penetrates approximately 3 times as far as 3.3 MHz ultrasound. (Courtesy Metder Electronics,Anaheim, CA.)
L______r________
L_____T_-___l
Nearlield
Far field
Figurc7-'12.Longitudinal cross-sectionof an ultrasouni oeam.
Transducer face Lengthof nearfield =
Wavelengthof ultrasound
In most human tissuethe majority of the ultrasound intensity is attenuatedwithin the first 2 to 5 cm oftissuedepth,which, fortransducersof mosr frequenciesand sizes,lieswithin the nearfield. Absorption: Conversionofthe mechanicalenergyor ultrasound into heat. The amount of absorptior that occursin a tissuetype at a specificfrequenc,is expressedby its absorption coefficient. The absorptioncoefficientis determinedby measririn3 the rate of temperaturerise in a homogeneous tissue model exposed to an ultrasound field oi known intensiry Absorption coefficientsare tissue and frequencyspecific.They are highest for r i s s u e sw i t h r h e h i g h e s rc o l l a g e nc o n t e n ta n d increasein proportion to the ultrasoundfrequencrSable 7-2). Reflection: The redirection of an incident bearn away from a reflecting surfaceat an angle equa. and oppositeto the angleof incidence(Frg.7-1?;.. Ultrasound is reflected at tissue interfaces,witl most reflectionoccurringwhere thereis the greaEest differencebetween the acousticimpedanceo:
Figure 7-11. Effectiveradiatingarea.
Near Field/Far Field: The ultrasoundbeam deliveredfrom a transducerinitially convergesand then diverges(Iig. 7'12). The near field, also klown as che Fresnelzone. js rhe convergentregion.and the far field, alsoknown asthe lraunhoter zone,is the divergentregion.In the nearfield thereis interferenceof the ultrasoundbeam.causingvariations in ultrasoundintensity.In the far field thereis little interlerence,resultingin a more uniform distribution of ultrasoundintensity.The length of the near field is dependenton the ultrasoundfrequencyand the EM of the transducerand can be calculated from the foilowing formula (Table7-1):
$ g
Radius oftransduce12
7-1 fength of the Near Field for Different Frequenciesof Ultrasound and Different Areas (ERA)ofultrasound Transducers Uttrasound frequency (MHz)
ERA (cm2)
Length ofnear field (cm)
3
5
33
I
1,
2.1,
3
1
6.3
1511
19l
Two . THE PHYSICAL AGENTS
g'-'
A bsorption Coefficients in Decibels/cm at 1 and 3 MHz lMHz
3MHz
llood
0.028
0.084
:at
0.14
0.42
\erve
0.2
0.6
tluscle (parallel)
0.28
0.84
(perpendicular) lr,!uscle
0.76
2.28
31oodvessels
0.4
I.2
ikin
0.62
1.86
Tendon
1.1,2
3.36
Cartilage
1.t6
3.48
throush tissue. Attenuation is the result of absorption, ieflection, and refraction, with absorption accountinq for about one-half of attenuation' Arrenuation coefficientsare Lissueand Frequency specific. They are higher for tissues with a higher collagen content and increase 1n proporlon to tne frequencv of the ultrasound flable Z-3) Half bepth' Ihe depth o[ tissue at which rhe ulrra7-4) sound inrensiryjs half irs initial intensity(lable at minima Standing Wave: Intensity maxima and apart fixed positions one-half waveleng*r -Standing ,r"ua, o..u, when tl-re uitrasound transducer and a reflecting surface are an exact multiple of wavelengths apart, allowing the reflected wave to
p
Z-t Oar"orrationof 1 MHz Ultrasound
Bone
Attenuation (dB/cm)
4.12
3
Iat
0.61
13
Nerve
0.88
Muscle
L2
24
Bloodvessels
\.7
32
Skin
2.7
39
Tendon
4.9
59
Cartilage
5.0
68
13.9
96
Bone
7-13.Ultrasoundreflectionandrefraction. Figure adjacent tissues. In the body, most reflection, about35T", occursat soft tissue-boneinterfaces There is 100% reflectiono[ ultrasoundat the airskin interface and only 0.1% reflection at the transmissionmedium-skin interface.There is no reflecdonat the transmissionmedium-soundhead interface,A transmissionmedium that eliminates the air bewveenthe sound head and the body is used in order to avoid an air-skin interfacewith hish reflection. Refriction: The redirectionof a wave at an interface occurs,rhe ultra(seeFig.Z-13).When refraccion angleand conat one tissue soundwave entersthe angle. a different rinuesdrroughthe tissueat in ultradecrease of the Attenuation: A measure wave travels 5ound intensityas che ulrrasound
BIood
p
z-o
oepthsin mmat 1 and3 MHz ""ff
Water
tt*lllz
3 MHz
11,500
3833
Iat
50
Muscle(parallel)
24.6
Muscle(perpendicular)
9
16.5 I 3
11.1
4
Tendon
6.2
2
Cartilage
6
2
Bone
2.1
Skin
7 . Ulttasouad
burst. With unstablecavitation,the bubbles over a number of cycles and then implode(Iig. Z-15).This implosionproduces brief, local pressureand temperaturerncreases causesfree radicalformation.Stablecavitation beenproposedasa mechanismfor the *rerapeutic effects of ultrasound,while cavitation is dlought not to occur at the i
of ultrasoundusedtherapeutically.2 Microstreaming: \4icroscaleeddying that takes near any small, vibrating object.
ilf:::' Figure 7-14.Formation of sranding waves. superimposeon *re incidentwave entedngthe dssue (Fig.7-14).Standingwaves can be avoidedby moving the soundheadthroughoutthe treatment. Cavitation: The formation,growth, and pulsationof gas-or vapor-filledbubblescausedby ultrasound. During the compressionphase of an ultrasound wave, bubbles present in the tissue are made smaller, and during the rarefaction phase they expand. Cavitation may be stable or unstable (transient).With stable cavitation, the bubbles oscillatein sizethroughoutmany cyclesbut do not
occursaround the gas bubblesset into oscilla by cavitation.3 Acoustic Streaming: The steady,circular flow of iularfluidsinducedby ultrasound. Thisflow is in scalethan with microstreamingand is thought alter cellularactiviry by transporringmatedal onepart ofthe ultrasoundfield to another3 Phonophoresis: The applicationof ultrasound a topical drug in order to facilitate
drugdehery$ig.7-1Q. In summary ultrasoundis a high-frequency wave that can be described by its intensity,
duqt cyd.e,EM, and BNR. It enters*re body and attenuatedin the tissueby absorption,reflection,a: refraction. Attenuation is ereatest in tissues with
high collagencontent and with the use of high
IVICFOCURRENIS '.:
;.'ful"':
| | ----) | \-./ \J
l----' t \_/
l
.V
STABLE cAVtrAloN( tv /-{ -----| | \_,/
)
|
\
^__ i^\
UNSTABLE ( ) CAVjTATION \__-,// \..
rveLostoru ! ; .,, i
:o, ",,,
I ,' Free
r!,, Badicals oH-.H*
'ii"#i:iiH'"
Figure7-15. Cavitation and mi.r^
Figure 7-16.Phonophoresis.
193
Ttvo . THE PIIYSICAL AGENTS
srnd frequencies.Ultrasoundcan generateheat, its ::rmal effect,and hasthe mechanicaleffectsof cavi =:on, microstreaming,and acousticstreaming.Both :e thermal and mechanicaleffects can be used to r:elerate the achievementof ffeatment goalswhen :-=asoundis appliedto the approprialepatholoSyat -e:nnr^hrrrfP
frrnP
OFULTRASOUND iENERATION ---=asoundis generatedby applying a high-ftequenry uemating electricalcurent to the crystal in the ffansr:er of an ultrasound unit. The crystal is made of a :;rerial with piezoelectricpropertiescausingit to =:-pond to the alternating current by expanding and =rtracting at the samefrequencyat which the current :-anges polarity. when the crystal expands it com=?ssest}Iematerialin front of it, andwhen it contractsit =efies the material in front of it. This altemating com:-ssion-rarefaction is the ultrasoundwav e Qtg.7-17). The property of piezoelectriciry,the abiliry to gensare electricityin responseto a mechanicalforce or = changeshapein responseto an electricalcurrent, 'r-asfirst discoveredby Paul-Jacques andPierreCurrie : :he 1880s.A varieryof marerialsarepiezoelectric, :;luding bone,natural quartz and synthetic plumbium =conium titanate(PZT),and barium titanate At this -jre, ultrasoundtransducersare usuallymade of PZT :ecausethis is the least costly and most efficient :::zoelectricmaterialreadilyavailable In order to obtain a pure singleftequencyof ultra-und from a piezoelectriccrystal,a singlefrequency :: alternatingcuffent must be applied to it and the -r'stal must be of the appropriatethicknessto res::rate with this frequency.Resonanceoccurswhen oi
cx
x
ooSoo 5o8o oH
the ultrasound frequency and the crystal thickness conformto the following formula: t-c '2t
where fis frequency,c is the speedof sound in the matedal, and t is the thicknessof the crystal.Thus thinner, more fragile crystals are generally used to generate higher frequenciesof ultrasound. These crystalsshouldbe handledwith care. Multiftequencytransducersusea singlecrystalof a thicknessoptimized for only one of the frequencies. The crystal is made to vibrate at other frequencies by application of those frequenciesof alternating electricalcurrents;however, this is associatedwith decreasedefficiency, variability in the output frequency,reduction of the EM, and increasedBNRa Recently,compositematerialshave been developed to deliver multiple frequenciesof ultrasound more accuratelyand eificiently.5 Pulsedultrasoundis producedwhen the high"frequencyalternatingelectricalcurrentis deliveredto the transducerfor only a limited proportion of the treatment time, asdeterminedby the selectedduty cycle.
OFULTRASOUND EFFECTS Ultrasoundhas a variery of biophysicaleffects lt can increasethe temperatureof deepandsuperficialtissues and has a range of nonthermal effects. Traditionally, although separately, theseeffectshavebeenconsidered both to some degree tha! should be aware the reader Continuous ultrasound. of with all applications occur uitrasoundhas the most effecton tissuetemperature; however, nonthermal effects can also occur with the use of continuousultrasound.Additionally, although pulsedultrasoundproducesminimal sustainedchanges in tissuetemperature,it probably doeshave a small brief heating effect during the on time of a pulse Althoush a number of studieshave demonsffatedthe biophyiical effectsof ultrasound,the degreeto which the findings canbe extrapolatedftom the exPedmental conditionsto specificclinicalapplicationsis still uncertain andrequiresfurtherstudy.o
^Xooo oo-o
I
\--//-
ll
Compression
ll:1 Rarefaction
igure 7-17, Ultrasound production by piezoelectric
EFFECTS THERMAL Affected Tissues The earliest studies demonstratingthat ultrasound can increasetissue temperaturewere published by
194
7 c Ufutasoutd
Hawey in 1930.7The thermal effectsof ultrasound, including accelerationof metabolic rate, reduction or confiol of pain and muscle spasm,alteration of nerve conductionvelocity, increasedcirculation,and increasedsoft tissue extensibility,are the same as those obtained with o*rer heating modalities, as describedin Chapter 6, except that the structures heated are different.s-10Ultrasound reaches more deeply and heats smallerareasthan most superficial heating agents.Ultrasound also heats tissueswith high ultrasound absorption coefficientsmore than those with low absorptioncoefficients.Tissueswith high absorptioncoefficientsaregenerallythosewith a high collagencontent,while tissueswith low absorp,tion coefficientsgenerallyhave a high water content. Thus, ultrasoundis pafticularlywell-suitedto heating tendons,ligaments,joint capsules,and fasciawhile not overheatingthe overlyingfat. Ultrasoundis generally not the idealphysicalagentfor heatingmuscletissue becausemuscle has a relativelv low absomtion coefficient;also.most musclesare much larger'than the availableultrasoundtransducers.
Factors Affecting theAmount ol Temperature lncrease The increasein tissuetemperatureproducedby the absorptionof ultrasoundvaries accordingto the tissueto which the ultrasoundis applied,aswell aswith the frequency,intensity, and duration of the ultrasound.The heatingrate is proportionalto the tissue's absorptioncoefficientat the applied ultrasoundfrequency.li Tissue absorption coefficients increase with increasedcollagencontent and in proportion to the ultrasoundfrequency.Thus, higher temperatures are achievedin tissueswith a high collagencontent and with the application of higher-frequencyultrasound.When the absorptioncoefficientis high, the temperatureincreaseis distributed in a smallervolume of more superficialtissuethan when the absorytion coefficientis low, sincechangingthe absorption coefficient alters the heat distribution but does not change the total amount of heat being delivered (Iig. Z-18).To increase*re total amount of heat being delivered to the tissue, the duration of ultrasound applicationor the averageultrasoundintensity must be increased.One MHz frequenry ultrasoundcan be usedto heat tissuesup to 5 cm deep,whereas3 MHz ftequenry shouldbe usedwhen the goalis to heat tissuesonlv 1 to 2 cm deep.Note that with 3 MHz ultra-
E
Depthot tlssue
Figure7-18.Temperaturedistributionfor 1 and 3 ultrasoundat the sameintensily. sound,althoughthe maximum temperature is higher,the depth of penetrationis lower theoreticalmodelspredictthat3 MHz ultrasound increasetissuetemperature3 timesmore than 1 ultrasound.an in vivo studv in which ultrasound applied to human calf muscle found an almost fold greatertemperatureincreasewith 3 MHz soundthan with 1 MHz ultrasoundannliedat 0.5 2.0 W/cm); therefore,clinically,an iniensity3 to times lower should be used when applying 3 ultrasoundthan when applying1 MHz ultrasound. During ultrasoundapplication,tissuetemp€ changeis also affected by factors other than sound absorption.Blood circulatingthrough the sue will cool the tissueswhile conductionfrom warmed area of rissueto another and reflection ultrasoundwavesin resionsof soft tissue-bonei faceswill heat the tissues.l3 On average, soft tissue temperature has shown to increasebv 0.2' C oer mrnutein vivo ultrasound delivered at 7 W/cm2 at 1 MHz. Nonuniformiw of the intensitv of ultrasound the variety of tissuetypes with different a coefficientsin a clinicaltreatmentarea,and at tissueboundaries,causethe temperature within the ultrasoundfield not to be uniform. The highesttemperatureis generallyproducedat soft sue-bone interfaces where reflection is sreat Moving the sound head throughout the appli helos to eoualizethe heat distribution and the incidenceof excessivelyhot or cold areas. The number of unknown variables, i the thickness of each tissue layer, the amount
Tvo . THE PHYSICAL AGENTS
-:ulation, and the distanceto reflectingsoft tissuer:re interfaces,makes it difficult to predict accu:e-:ly the temperatureincreaset}ratwill be produced ::::ically when ultrasound is applied to a patient. l:'-rs, initial treatmentparametersaresetaccordingto :ioretical and researchpredictions; however, the l.:ent's repoft of warmth is used to determinethe =-:l ultrasoundintensity.If the ultrasoundintensity -: :oo high, the patient will complain of a deepache =:n overheatingof the periosteum lf this occurs,the :r:asound intensity must be reduced in order to rcid burningthe tissue.If the ultrasoundintensity is =,: low, the patientwill not feel any increasein tem-:ature. More specificguidelinesfor selectionof the rjmal ultrasound ffeatment parametersfor tissue r:dng are given below in the sectionon application =:rrrique. Becausethe patientjs report is used to -:ermine the maximum safeultrasoundintensity,it s :ecommended*rat thermal-levelultrasoundnot be =:lied to patientswho are unable to feel or report =comfort causedby overheating
195
pendentlywhen consideringapplying a combination of agentseitherconcuffentlyor in sequence.
EFFECTS NONTHERMAL
Ultrasound has a variery of effects on biological processesthat are thought to be unrelated to any increasein tissuetemperature.These effectsare the result of the mechanicalevents Producedby ultrasound, including cavitation, microstreaming, and acousticstreaming.When ultrasoundis deliveredin a pulsed mode, with a 20y" or lower duty cycle, the heat generatedduring the on time of the cycleis dispersedduring the off time, resultingin no measurable net increasein temperatureThus, pulsedultrasound with a 20% ducy cycle has generallybeen used to apply and study the nonthermaieffectsof ultrasound. Somerecentstudieshavealsousedlow intensitiesof continuousultrasoundto study theseeffects'17 Ultrasoundwith a low averageintensity has been shown to increaseintracellular calcium,l8 increase increas.mast skinandcellmembranepermeabiliry,lo cell degranulation,increasechemotacticfactor and inConiunction PhysicalAgents Other lpplying increasemacrophageresponsivehistaminerelease,20 rith Ultrasound the rate of protein synthesisby increase and ness,21 -.'-ious have been demonstrated effects These fibroblasts.22 physicalagentscanbe appliedtogetherwith, and duty cyclesthat at intensities :.or to, or after the application of ultrasound. using ultrasound increasein temperaany measurable produce did not ,':plying a hot packprior to ultrasoundtreatmenthas to be nonthermal considered ture and are therefore :een shown to increasethe temperatureof only the to cavitation, been attributed tissue effects. They have ,;cerficial 1 to 2 mm of skin and subcutaneous 3".urt" -r;rile not affectingthe temPelatureof deepertissue acousticstreaming,and microstreaming.2l'23 compoessential processes are these cellularlevel Similarly,usinga warm conductionmedium ;-,'ers.15 processes in these '.:.i.1not affect the heating of deep tissues.Applyt"g changes nentsof tissuehealing,the producedby uitrasoundare thought to underlie the ,=asound in cold water coolsthe superficialskin by enhancedhealingobservedto occurin responseto the ::nduction and convection, thereby reducing the applicationof ultrasoundto a variety of pathologies. r;rease in superficialtissuetemperatureproducedby '-:asound. Applying ice prior to the application Ior example,increasingintracellularcalciumcanalter the enzymatic activity of cells and stimuiate their :i ultrasoundhasalsobeenshown to reduced:retemsynthesisand secretionof proteins becausecalcium :erature increase produced by ultrasound in the to :eeper gissues.l6Ice, or any other thermal ageng ions act as chemicalsignals