THE VETERINARY CLINICSOF NORTH AMERICA lCOMPRAI SMALLANIMAL PRACTICE Lameness WALTERC.RENBERG,DVM, MS,AND JAMESK.ROUSH,DVM,MS SERVoI,OS DEEDE tXiEtlSA8 V.T.A.D. 2r;f65YO N . .....2........................... .... - .. Clus . .................................... VOLUME31NUMBER 1 W.B.SAUNDERS COMPANY AHarcourt Health SciencesCompany PHILADELPHIALONDONTORONTOMONTREAL JANUARY2001 W.B.SAUNDERSCOMPANY AHarcourtHealthSciencesCompany TheCurtis Center'Independence Square WestPhiladelphia,Pennsylvania19106 http: //www.wbsaunders.com THE VETERINARY CLINICSOFNORTHAMERICA: SMALLANIMALPRACTICE January2001 Editor:John Vassallo Volume31,Number 1 ISSN0195-5616 Copyright2001byW.B.SaundersCompany.Allrightsreserved.Nopartofthis publication may bereproduced or transmitted in any formor by any means,electronicor mechanical, includingphotocopy, recording,oranyinformationretrieval system,without written permissionfromthePublisher. 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LAMENESS GUESTEDITORS WALTERC.RENBERG,DVM,MS,Diplomate,American Collegeof Veterinary Surgeons;Assistant Professor,SmallAnimal Surgery, Department of Clinical Sciences,KansasStateUniversity,Collegeof Veterinary Medicine,Manhattan, Kansas JAMESK.ROUSH,DVM, MS,Diplomate,American Collegeof VeterinarySurgeons; Associate Professorand Section Head,Small AnimalSurgery,Department of Clinical Sciences,Kansas StateUniversity,Collegeof Veterinary Medicine,Manhattan, Kansas CONTRIBUTORS LEIGHA.CLAYTON,DVM,Department of Animal Health, Smithsonian National Zoological Park, Washington,DC JAMESL.COOK,DVM,PhD, Diplomate,AmericanCollege of Veterinary Surgeons; Assistant Professor,SmallAnimalOrthopaedics,Assistant Professor,Orthopaedic Surgery,andDirector,Comparative OrthopaediC Laboratory,University of Missouri-Columbia, Columbia, Missouri JAMES J.HOSKINSON, DVM, Diplomate,Al!lericanCollegeof VeterinaryRadiology; AssociateProfessor,KansasStateUniversity, Collegeof Veterinary Medicine, Manhattan, Kansas SPENCER A. JOHNSTON,VMD, Diplomate, AmericanCollegeof Veterinary Surgeons; AssociateProfessor,Department of Small AnimalClinical Sciences, Virginia-Maryland RegionalCollegeof Veterinary Medicine,VirginiaTech,Blacksburg, Virginia CYNTHIA ANNE LEONARD, DVM, Department of Small Animal Surgery,Veterinary Teaching Hospital, Ontario VeterinaryCollege,Universityof Guelph, Guelph, Ontario JOHN J.McDONNELL, DVM,MS, Diplomate,American Collegeof Veterinary Internal Medicine(Neurology); Assistant Professor,Department of ClinicalSciences,School of Veterinary Medicine,TuftsUniversity,NorthGrafton,Massachusetts RON M.McLAUGHLIN,DVM, DVSc,Diplomate,AmericanCollegeof Veterinary Surgeons;AssociateProfessorand Chief of Surgery,TheAnimal Health Center, Collegeof VeterinaryMedicine,MississippiState University,MississippiState, Mississippi iii SIMON R.PLATT,BVM&S, Diplomate,American Collegeof Veterinary Internal Medicine(Neurology);AssistantProfessor,The AnimalHealthTrust,Centre for Small Animal Studies,LanwadesPark,Kentford,Newmarket, Suffolk, England MARY ANN RADLINSKY,DVM, MS, Diplomate, American Collegeof Veterinary ASSIstant Professor,Small Animal Surgery,Department of Clinical SCIences,KansasStateUniversity,VeterinaryMedicalTeaching Hospital,Manhattan, Kansas WALTERC.RENBERG,DVM, MS,Diplomate, American Collegeof Veterinary Surgeons; ASSIstant Professor,Small Animal Surgery,Department of Clinical Sciences,KansasState University,College of VeterinaryMedicine,Manhattan, Kansas. JAMESKROUSH,DVM,MS,Diplomate,AmericanCollege of Veterinary Surgeons; Professor and SectionHead, Small Animal Surgery,Department of Clinical SCIences,KansasStateUniverSity,Cqllegeof VeterinaryMedicine, Manhattan, Kansas..KURTS.SCHULZ,DVM,MS,Diplomate,AmericanCollegeof VeterinarySurgeons; ASSIstant. and Chief of Small Animal Surgery,Department of Surgicaland RadlOlogIcalSCIences,Schoolof Veterinary Medicine,Universityof CaliforniaDavis California', MICHAELTILLSON,DVM,Diplomate, American Collegeof Veterinary Surgeons; ASSIstantProfessor, SmallAnimal Surgery,AuburnUniversity Collegeof Veterinary Medicine,Auburn, Alabama RUSSELL1. TUCKER,DVM:Diplomate, American Collegeof VeterinaryRadiology; ASSIstantProfessor,WashingtonStateUniversity,CollegeofVeterinary Medicine, Pullman, Washington iv CONTRIBUTORS LAMENESS CONTENTS Preface WalterC.Renbergand James K.Roush Evaluationof the LamePatient Walter C.Renberg Competenceinevaluatinglamenessisvitalfortheveterinary practitioner.Thisskill is becoming evenmore important withthe increasingpopularity of large-breeddogsandthecorresponding increaseinthenumberofdevelopmentalorthopedicproblems seen on aday-to-day basis.Aproper physical examination of the lamepatientisessentialtothemanagementofthecase.This article reviews the initial evaluation of the lame veterinary patient without dwelling on the specific differential diagnoses and corres-ponding treatments. Neurologic ConditionsCausingLameness in Companion Animals John J.McDonnell,Simon R.Platt,and Leigh A.Clayton Neurologicdiseasecancauselamenessmimickingorthopedic disease in companion animals. This article presents alogicalstep-wiseapproachtohelpdifferentiatebetweenorthopedicand neurologic causes of lameness.The neurologic examination, diag-nostictechniques,andtreatmentoptionsforthesechallenging casesarediscussed.Specificdiseasesexaminedincludemyopa-thies,neuropathies,intervertebraldiskdisease,lumbosacraldis-ease,peripheralnervesheathtumors,spinalcordtumors,and traumatic neuropathies. VETERINARY CLINICSOFNORTH AMERICA: SMALL ANIMAL PRACTICE VOLUME31 NUMBER1 JANUARY2001 xi 1 17 v Overview of Pain in theLamePatient Spencer A. Johnston Theexperienceofpainisoftenassociatedwiththestimulation of peripheralnociceptors.Theseneuroreceptorsareactivatedby stimulisufficienttopotentiallyoractuallycausetissuedamage. This articlereviewsthe types of neuroreceptors present in periar-ticulartissues,thechangesthat occurintheperiarticular tissues associated with joint injury,and how thosechanges can influence nociceptoractivityandsubsequently pain.Peripheralnociceptor activity,as well as the influence of nociceptive input on the spinal transmission of neural impulses, isdiscussed. ForelimbLamenessin the Young Patient JamesL.Cook Thisarticlediscussescauses offorelimblamenessindogs younger than 1year of age. The major categories covered include congenital, developmental, traumatic, infectious, nutritional,met-abolic,andneoplasticdisorders.Diagnosis,treatmentoptions, and prognosis are covered foreachdisorder. ForelimbLamenessin theAdult Patient Kurt S. Schulz Lamenessoftheforelimbmaybeoneofthemorefrustrating problemsinsmallanimalorthopedics.It islikelythat numerous causesofforelimblamenessarenotyetdefinedorwellunder-stood.Thecommonandsomelesscommoncausesofforelimb lamenessarediscussedaswellastheirmeansofdiagnosis.The applicationofnewdiagnostictoolsincludingarthroscopyand ultrasound arealsodiscussed. Hind LimbLamenessin the Young Patient Ron M. McLaughlin Thisarticlereviewsthe common causes of hind limb lameness in young dogs. Legg-Calve-Perthes, hip dysplasia, cruciate ligament injury,patellaluxation,osteochondrosis,hypertrophicosteodys-trophy,panosteitis,andcommongrowthplatefracturesarede-scribed.Emphasisisplacedontheclinicalsigns,diagnosis,and treatment optionsavailable foreach disease. Hind LimbLamenessin the MatureDog JamesK.Roush This article describesthe differential diagnosis of hind limb lame-ness in adult dogs withcommonclinicalpresentations and diag-nostic methodsoutlined. 39 55 85 101 125 viCONTENTS FelineLameness Cynthia AnneLeonardand Michael Tillson Felinelamenessisanincreasinglyrecognizedclinicalproblem. Today's veterinary practitionerwith his/her abilitytodiagnosethevarious forlam:-nessinthecatandbeabletodISCUSStheslgmflcanceoftherr findingswiththeclient.Diseaseofthe system can begroupedinto broadcategones,. mcludmg:trauma, arthritis,infectiouscauses,developmentaldIsorders,neoplasIa, andmuscularproblems.Specificdiseasesfromeach these categories will bediscussed, particularly those that dIffer mtherr presentationorclinicalbehaviorfromthatsamedIseasemthe canine patient. Diagnostic Imaging of LamenessinSmall Animals James J.Hoskinson and Russell L.Tucker Thedemandforadvanceddiagnosticimagingproceduressuch asnuclearscintigraphy,ultrasonography, computed and magnetic resonance imaging has over the past 10 .years. seeking to tic capabIlIties and clIents wIllmg to pursuebest medicmedriven this demand, resulting in installation of advanced Imagmg facilitiesatmostacademicandprivatereferralpractices.Knowl-edgeofpotentialbenefitsofvarious will. veterinariantooptimizehisorheruseofdIagnosticImagmgm hisorherown practice or in areferralpractice. Ancillary Diagnostic Techniquesfor theLamePatient Mary Ann Radlinsky Thecauseoflamenessisusuallyidentifiedthroughevaluation ofsignalment,history,andphysicalexamination.Radiographic evaluationprovidesadefinitivediagnosisin. manycases;hrkinghuntingdogs,whichonlydisplaytheirlamenesswhen achv.elyWhenthedog isexaminedintheveterinary no dIscomfort ISfound.Such patients usually have amild or early .theproblem mayor maynot showupon radiographseven Iftheto look.One solution istoexercisethe dog the clIme. ThIS bnng on the lameness and also gives the veterinar-IantheopportunItyto?bservetheanimalinmotion.Unfortunately, theremaynotbethehmeorspaceavailabletoproperlystressthe ammal tothe extent that the problem becomes visible. In those instances itisbesttohavetheownerreturntheanimalforexaminationas thedevelopduringworkortoproceedtoamoresensitive such .asnuclearscintigraphy.Alternatively,theowner can unhl. theleSIOnandthusbecomeseasier todiagnose. ObVIOusly,thISlattersolutIOn,althougheconomical,isnotideal.As inotherarticlesinthisissue,thereareabatteryofancillary dIagnosticprocedures that may be useful indifficult cases. Finally, the clinician should always remember that common diseases istosaythatbeforediagnosinganuncommon condItion(azebra),themorecommondiseases("horses")shouldbe ruledout.Suchanapproachusuallysavestimeandexpenseinper-formingthediagnosticworkup. 16RENBERG References 1.ArnoczkyS,TarvinG:Physicalexaminationofthemusculoskeletalsystem.VetClin North Am Small Anim Pract 11:575-593,1981. 2.BarrA,HoultonJ:Clinicalinvestigationofthelamedog.JSmallAnimPract29:695-703,1988fS11 An'1 3.LewisD,ParkerR,BloombergM:Self-AssessmentColorReview0mauna Orthopedics.Ames,Iowa StateUniversity Press,1998 .. 4.MuirP:Physicalexaminationoflamedogs. CompendContin EducPract Vet19.1149-1160, 1997. 5.NewtonC:Examinationoftheorthopaedicpatient.SectionOne:Evaluationofthe nonemergencypatient.InNewtonC,NunamakerD(eds):TextbookofSmallAmmal Orthopaedics.Philadelphia, JBLippincott, 1985,pp 1577-1586'.. 6.SchraderS,PrieurW,BruseS:DIagnOSIS:Histoncal,andancillaryexamma-tions InOlmstead M(ed):SmallAnimal Orthopedics. St Loms,Mosby,1995 7.Sumner-Smith G:Gaitanalysisandorthopedicexamination InSlatter D(ed): Textbook of Small Animal Surgery.Philadelphia, WBSaunders,1993 Addressreprintrequeststo Walter C.Renberg,DVM,MS Deparhnent of Clinical Sciences KansasState University College of VeterinaryMedicine 1800DenisonRoad Manhattan, KS66506-5606 e-mail:renberg@vet.ksu.edu LAMENESS0195-5616/01$15.00+.00 NEUROLOGICCONDITIONS CAUSINGLAMENESSIN COMPANION ANIMALS John J.McDormell,DVM,MS,Simon R.Platt,BVM&S, and Leigh A.Clayton,DVM Themost common causeof non-weight-bearinglamenessisortho-pediCdisease,butneurologiccausesshouldalwaysbeadiagnostic consideration. Distll1.guishing between orthopedic and neurologic causes oflamenesscanbedifficultbutiscriticalinformulatingadiagnostic andtherapeuticplan.Thediagnosticplanforneurologicdiseaseoften varies significantly from the workup foran orthopedicdisease.Thetwo mostcommoncategoriesofneurologicdiseasesthatareconfusedwith orthopedicdiseaseare myopathiesand spinal nerve pathologies. Thediagnosticevaluation of an animalwith the complaint of non-weight-bearinglamenessshouldll1.cludeacompleteandchronologie historytoidentifyonset,progression,andotherrelatedsymptoms.A physicalexaminationemphasizingtheorthopedicandneurologiccom-ponentsisalsorequiredtodifferentiatebetweenthesetwocausesof disease.Theneurologicexamination isasystem bywhichtheclinician can evaluate the functionalintegrity of the nervoussystem.The compo-nentsoftheneurologicexaminationcanbedividedintoobservation, palpation,posturalreactions,spinalreflexes,cranialnerves,andsensa-Fromthe Deparhnent of Clinical Sciences,Schoolof Veterinary Medicine,. Tufts University, NorthGrafton,MassachusettsGJM);TheAnimalHealthTrust,CentreforSmall AnimalStudies,LanwadesPark,Kentford,Newmarket,Suffolk,England(SRP);and the Deparhnent of Animal Health, Smithsonian National Zoological Park,Washington, DC(LAC) VETERINARYCLINICSOF NORTH AMEF1CA:SMALLANIMALPRACTfCE VOLUME31 - NUMBER1 JANUARY200117 18McDONNELL et al tion as shown in thebox on this page. Anunderstanding of the perform-ance and interpretation of the neurologic examination helps the clinician todifferentiate between neurologicandorthopedic causesof lameness. Abnormalitiesthatareorcanbeneurologicinoriginincludethe following: Seizures,convulsions,or fits Altered statesof consciousness(stupor,coma, rage,somnolence) Paresisor paralysiswith proprioceptive deficits. Vestibularataxia:headtilt,nystagmus,asymmetricataxia,roll-ing,falling Cerebellar ataxia:wide-based stance, intentiontremors,dysmetria Hyperesthesia,anesthesia(localized or generalized) Blindness Hearing deficit Incontinence Vomitingor regurgitation Observation Mentalstatus Posture Movement NeurologicExamination Triceps Biceps Gait,locomotion Palpation Muscleatrophy Hypertrophy Pain Posturalreactions Proprioceptivepositioning Wheelbarrowing Wheelbarrowingwithneck extended Hopping Extensorposturalthrust Hemistandingandhemiwalking Placing(tactile) Placing(visual) Spinalreflexes Quadricepsreflex Cranialtibialreflex Extensor carpiradialis Flexor(thoraciclimb) Flexor (pelviclimbreflex) Perinealreflex Cranialnerves Olfactory Optic Oculomotor Trochlear Trigeminal Abducent Facial Vestibulocochlear Glossopharyngeal Vagus Accessory Hypoglossal Sensation Dermatomalmapping Superficialpain Deeppain If these irregularities are noted to have commenced simultaneous to thepresenting complaint,theclinician should be awarethatother proc-NEUROLOGICCONDITIONS CAUSINGLAMENESSIN COMPANION ANIMALS19 esses besidesthose purely orthopedic in nature may be thecause of the animal'spresentation.Mentalstatusabnormalitiessuchaspersonality changes,seizures,rage,anddecreasinglevelsofconsciousnesscanbe causedbyprimarybrainabnormalities.It shouldberememberedthat individualsandbreedshavetheirownlevelofattentivenessandthat environmentalfactorscaninfluenceananimal'stemperament.Gaitab-normalitiesshouldbecarefullyinvestigatedinalargeopenareathat provides good traction.The clinicianshould have athorough knowledge ofthenormalgaitdifferencesbetweendifferentbreedsofdogsand cats.Awide-basedstance,ataxiawithnolossofstrength,dysmetria (particularlyhypermetria),andintention tremorsarehallmarksof cere-bellardisease.Nystagmus,strabismus,asymmetricataxia,falling,roll-ing, and headtilt are signs that the vestibular system is involved. Cranial nervedysfunctionsareindicationsthattheremaybeneurologicrather than orthopedic disease present in the patient. Posturalreactionsshouldbetestedinallanimalspresentedfor non - weight-bearinglameness.Animalswithonlyorthopedicdisease should not have deficits in proprioceptive placing,hopping, hemistand-ing,or placing Feactions.Support may be necessary if significant pain is acomponent of thepresenting complaint.Asanexample,adog with a femoralfracturemayattempttoreplaceitspaw tothe normal position afterthepawisknuckledoverif theanimalisgivenenoughsupport. Postural reactions that relyon muscle strength such as wheelbarrowing, extensorposturalthrustreaction,andhemiwalkingcanbeperformed, butresultsshouldnotbeoverinterpretedifsignificantpaincausedby orthopedic diseaseispresent. Lower motor neuron (LMN)disease isoften confused with orthope-dicdiseasessuch asarthritis or other joint abnormalities.If the clinician performs athorough neurologic examination, these perplexing signs can beeasilyrecognizedasneurologic.LMNsignsincludeplaccidparesis andparalysis,hypotoniaandatonia,hyporeflexiaandareflexia,and pronounced rapid muscleatrophy.Thesesigns developalmost immedi-atelyafterdisturbanceofthespinalnervesaffected.Muscleatrophyis detectable within1 week of serious nerve injuryand is severe.Weakness or paresiscan be recognized bygaitevaluation,and subtledisturbances can bedocumented by testing postural reactions.Hypotoniaand atonia arerecognizedbypalpationofthemusclesinnervatedbythespinal nervesaffected.Reflexesareevaluated by myotaticreflexessuchasthe quadricepsreflex(kneejerk)andcranialtibialreflexinthepelviclimb and theextensor carpi radialisreflexin.the thoracic limb. Flexor reflexes of the pelvic and thoracic limbs are easy to perform and can demonstrate weaknessearlier than other signsof LMN disease. Thesensorycomponentoftheneurologicexaminationistypically carried out last in theexamination toavoid losing the patient's coopera-tion.Pain or hyperesthesiamay have been detected during palpation, or duringthecranialnerveorspinalreflexesportionoftheexamination. During thesensory examination, areasof increased sensitivity(hyperes-20McDONNELLetal thesia),decreasedsensation(hypesthesia),orabsent sensation(anesthe-sia)are investigated and mapped out. Acareful sensory evaluation forparaspinal hyperpathia can discern areasof hyperesthesia.Beginning with L7and progressing cranially,the transverse processes are squeezed, or alternatively, the spinous processes arepressedfirmly.Thestimulusincreasesfromlighttouchtodeep palpation. Abehavioral reaction to what should be an innocuous stimu-lus can be interpreted as pain. Proper palpation should cause no reaction innormalareas.Placingonehandontheabdomenasthevertebral column is palpated allows detection of abdominal muscle splinting when pain is experienced.Flexing and extending the neck as well as palpation isused to examinethe cervicalarea.Cervical palpation isperformed by firmlypressing on the transverse processes fromC1through C7.During palpation,areasofhyperesthesiaarenotedandcomparedwiththe presentingnerve-rootsigns.Significantcorrelationfoundbetweenthe sensory examination and the nerve-root distribution of the limb-carrying lameness would indicate neurologic rather than orthopedicdisease.Ad-ministrationof anti-inflammatoryoranalgesicmedicationsandoverex-citement of the animal during the examination may influence the results of the sensory examination. Hypesthesiaandanesthesiaarehallmarksofneurologicdisease. Testingshouldbedonewiththeanimalinarelaxedsetting.Afoldof skin isgraspedgently,andasmallhemostatpinchestheskinfold;the stimulus intensity increases only until abehavioral response(vocalizing, escapebehavior,orturningofthehead)isnoted.Thisprocedureis repeated in asystematic way bilaterally fromeither adistaltoproximal or caudal tocranialdirection. Thereare individual and breed variations in theanimals tested.Remember that withdrawal of thelimb isareflex and does not indicate intact sensory function. Conditionsthatruleoutlamenesscausedbyneurologicdiseases shouldincludemusclediseases(myopathies),neuropathies,interverte-braldiskdisease(IVDD),lumbosacral(LS)disease,nerveroottumors, spinal cordtumors,andtraumatic neuropathies such as brachial plexus avulsion.Commonclinicalpresentationsaswellasusefulancillary diagnostics are discussed for these conditions. For a complete discussion, including treatment of these diseases, a review of the literature is encour-aged?11.14.24. 25.31.37. 38.43.50.60.63 MYOPATHIES Acquired,familial,and congenitaldisordersof skeletaland smooth musclearecalledmyopathies.In most cases,theyarecharacterizedby pain,generalized weakness,exerciseintolerance,fatigue,andastiff and stilted gait.376o The gait disturbance can present as shifting leg lameness. Musclepaincanbeelicitedwithpalpationofindividualmusclesor groupsofmuscles.Clinicalsignsthatcanhelptodistinguishbetween myopathiesandorthopedicdiseaseincludeagaitdisturbancethatis NEUROLOGICCONDITIONSCAUSINGLAMENESSIN COMPANION ANIMALS 21 often worsened by exercise, bilaterally symmetric distribution of affected muscles,localizedorgeneralizedmuscleatrophy,andlimitedjoint movement.3760 Common myopathiesinclude musculardystrophy,poly-myositis,endocrine myopathies,infectious myopathies,and myasthenia gravis. Ancillary tests helpful in diagnosing myopathies should be selected based on the resultsof the complete physical examination. Serum levels of muscleenzymeconcentrationssuch ascreatinekinase,lactatedehy-drogenase,and aspartate aminotransferase may be elevated in muscular dystrophyandmyositis.566o Urinalysismayshowthepresenceof myo-globinwithinflammatorymyopathies,whichisoftenincorrectlyre-ported as blood on urine dipsticks.There is ahigh likelihood that blood reportedonurinalysisisactuallymyoglobinifnoredbloodcellsare reportedon themicroscopicevaluation.Serum chemistryanalysismay showelevationsinalkalinephosphate,triglyceride,and cholesterol lev-els in cases of endocrine myopathies.34 Infectious myopathies may show elevation in totalserumprotein inassociationwith increasedf3- and "{-globulin fractions.56 60Definitivediagnosis of myasthenia gravis is made by detection of serum acetylcholine receptor antibodies or immune com-plexesattheneuromuscularjunction.51In patientswithsignsofvom-iting,regurgitation,dysphagia,orexcessivesalivation,thoracicradio-graphsareindicated toinvestigate megaesophagus.51 Electrodiagnostictestsdonot diagnose specific myopathies but can confirm myopathies suspected from the neurologic examination.Electro-myography(EMG),nerveconduction,f-waveanalysis,andrepetitive nervestimulationareelectrodiagnosticteststhataidinlocalizingthe abnormality to muscle or nerve.Specific distribution of nerve or muscle abnormalitiescanbemappedoutwiththesetestsY 53Thisaidsin guiding additional testssuch asnerve and muscle biopsies.Animals are typically anesthetized forelectrodiagnostic testing to eliminate volitional activityandmovementartifacts.Widespreaduseofelectro diagnosisis limited by equipment costsandavailabilityof trained personneL EMGisusefulforevaluatingspontaneouselectricactivitywithin musclescausedbymyopathiesandneuropathies.Thesediseases .have similarclinicalsignsandincludediseasesoftheventralhornnerve cell,nerveroot,peripheral nerve,neuromuscular junction,andmuscle. Electricallyevoked potentialssuchasmotor nerveconduction,sensory nerv.ef-waveanalysis,and repetitive nerve stimulation help todIfferentiatebetweenneuropathiesandmyopathies.Acompletere-view regardingtheperformanceand interpretation of thesetestscan be foundintheliterature.4253 Electrodiagnosticsignsofmyopathiesare abnormalelectromyogramswithnormal nervefunctionasrevealedby nerve conduction studies and f-waveanalYSis.Animals with myasthenia gravisandsomemyopathiesoftenhavedecreasedamplitudeandpro-longedlatencyafterrepetitivenervestimulation.53Thisdecremental responsecanbecorrectedwiththeadministrationoftheshort-acting anticholinesteraseedrophoniumchloride(Tensilon)atadoseof0.1to 0.2mg/kg.Electrodiagnostictestingformyastheniagravisdoesnot 22McDONNELL etal replacethedefinitivelaboratorytestingofthisdisease,becauseother diseases such aspolymyositis can show asimilar response.51 NerveandMuscleBiopsies Nerveandmusclebiopsiesarerequiredtoconfirmclinicaland electro diagnosticevidenceofneuromusculardiseaseandmaydiscern causativediagnosis.Methodsandcriteriaforobtainingthesebiopsies areavailable forvarious nerves and muscles.2, 5Although affected nerve andmuscleshouldbeselectedbasedontheresultsoftheclinical and electro diagnostic examinations, end-stagetissue should be avoided. Instead,tissuethatisonlymoderatelyaffectedmayprovideamore accuratediagnosis.Therearespecialized laboratoriesthatprovidemor-phologic, morphometric, histochemical,ultrastructural,and biochemical evaluation of muscleandnervesamples.*t It isstronglyrecommended thattheclinicianconsultwiththeselaboratoriessoastoselectand correctly processthe samples, Thetwomostcommonnervesthatarebiopsiedarethecommon peronealnerveasitpassesoverthelateralheadofthegastrocnemius musclenearthestiflejointandtheulnarnerveasitcoursesparallelto the medial head of the tricepsand superficial digital flexor muscles near theelbow.5 Generalanesthesiaisrequiredtoperformafasicularnerve biopsy.Nomorethan30%ofthetotaldiameteroftheparentnerve should be sampled so as to preserve the anatomic and electrophysiologic integrity of the nerve. Preparation of the surgical site should be the same asthatforanysterileprocedure.Aftertheskinincision,thenerveis isolatedfromthefatandconnectivetissue.A5-0or6-0monofilament suturewithaswedged-ontaperpoint needleisusedtoisolate30%of thediameterofthenerve.Theintended biopsysampleisthensharply excisedwithophthalmicsurgicalscissors.Usinggentletractiononthe suture,theophthalmicscissorsorscalpel isusedtodivideonethird of thenervefasciclesfromtheparentnerve.Atotallengthof2to4cm isrequiredtoprovidesamplesnecessaryforhistologic,morphologic, ultrastructural, and teased fiber studies. Fascial and subcutaneous tissues areclosedroutinelywithabsorbablesuture.Theskinclosureisper-formedusingnonabsorbablesuture.Thenervesampleisgently stretchedusingpinsorsuturematerialonapieceofwoodentongue depressorandplacedinfixative.Asolutionof2.5%glutaraldehyde fixativeispreferableto10%formalinforsomeofthenervestudies performed,s 'Comparative NeuromuscularLaboratory,Basic ScienceBuilding,Room1107,Univer-sityofCalifornia,SanDiego,LaJolla,CA92093-D612;telephone:(858)534-1537;http: // medicine.ucsd.edu/ vetneuromuscular / tDrKyleC.B r a ~ d ,c/oPeripheral 'NerveLaboratory,1476LakeviewRidge,Dade-ville,AL36853;telephone:(256)825-2624;fax:(603)676-2383;http:/ / www.lakemartin, net / - khbraund/ ner vepath.html NEUROLOGICCONDITIONS CAUSINGLAMENESSIN COMPANIONANIMALS23 Muscle biopsy is best performed under general anesthesia.Prepara-tionofthesurgicalsiteshouldbethesameasthatforanysterile procedure.Aftermakingtheskinincision,fatandconnectivetissue shouldbedissectedandretractedsothatthedirectionofthemuscle fiberscanbevisualized.Staysuturesof2-0or3-0monofilamentare placedat eachend ofthemuscletobe biopsied1to2cm apartandat right anglestothemuscle fibers.Thesuturesshould loosely encompass acylinderofmuscleapproximately0.5cmindiameterwithoutcom-pressing themuscle.Ascalpel oririsscissorsareusedtomakeparallel incisionsalongthelength of the biopsy specimen,While gentletraction is placed on the stay sutures, the blade or scissors are used to undermine thespecimenbetweentheincisions.Afterthelengthofthebiopsy specimenhasbeencompletelyundermined,theendsofthespecimen arecutwithascalpelorscissors.Afterspecimen removal,hemorrhage is controlled with direct pressure; in the case of arterial bleeding, ligation may be requiredto achieve hemostasis.After biopsy removal, the speci-menisplacedinagauzespongemoistenedwithphysiologicsaline solution and kept at refrigeration temperaturesunlessaparticular labo-ratory hasdifferent requirements.2,60 DISEASES OF NERVEROOTSANDPERIPHERAL NERVES Anydiseaseprocessthatcausesimpingement,entrapment,com-pression, or destruction of the nerve root or peripheral nerve may cause lamenessandpainsuggestiveofmusculoskeletaldisease(Fig.1),This non-weight-bearing lameness isalso referredto as nerve-rootsignature,a termthatdescribesdisturbancesofsensationinthedistributionofa nerve's sensory distribution.33 Pathology at the peripheral nerve or nerve rootmayoccuratanylevelofthespinalcolumn,butnon-weight-bearinglamenessispresentonlywhenitoccursatthecervicalor lumbar intumescences,Knowingthe common clinical presentationsand followingalogical plan in evaluating non-weight-bearing lamenesscan help the clinician todifferentiate between thesetwo causes of lameness. Diseasesofnerverootsandperipheralnervesthatcausenon-weight-bearinglamenessincludeIVDD,neoplasiaofthenerveroots, 'spinal cord tumors, and traumatic neuropathies. LMN disease can cause signsof afocalneuropathicsyndromeof themusclesinnervated,LMN disease ischaracterized by flaccid paresis or paralysis, reduced or absent reflexes,reducedorabsentmuscletone,andneurogenicatrophy.The presenceofthesesignsshouldalertthecliniciantothepossibilitythat thereisneurologicdisease involving the LMN unit. IntervertebralDiskDisease IVDDisoneofthemostcommoncanineneurologicdiseasespre-sentedtocompanionanimalveterinarians.n,12, 15,24,25, 48,49Thisdisease 24McDONNELL etal Figure1.Atransverseviewrepresentingcompressionoftheventralbranchofthespinal nerve(arrows).Pathologymayoccuratanylevelofthespinalnerveandmaycause lamenessandpainsuggestiveofmusculoskeletal disease. can occur anywhere in the vertebral column caudal to Cl to C2.Cervical IVDD can be seen between C2 and C3and C7 and T1intervertebral disk (IVD)spaces. Thoracolumbar IVDD is seen typically between IVD spaces T9and10and L5.Lumbosacral diseaseaffectsthevertebralcanal from L5toS3and isdiscussedinaseparate section. Whenan IVDimpinges directlyonthespinalcordwithinthevertebralcolumn,theresulting deficitsrange frommild back pain to paralysis. Nerve-root pain may be theprimarysignwhendiskmaterial impingeson thenerverooteither within thevertebralcolumn,at theintervertebral foramen,or along the course of the spinal nerve after it exits from the vertebral column.3 These lateralizeddiskscan causenon-weight-bearing lameness if theaffected nerve root iswithin thecervical or lumbar intumescences. Diagnosing alateralized IVD requires signalment evaluation, acom-pletephysicalexamination,andappropriatean.cillarydiagnostictests. In general, the chondrodystrophic or chondrodystrophic-like breeds such astheDachshund,CockerSpaniel,BassetHound,Beagle,Pekingese, and Poodle areprone todevelopthe kind of disk degeneration that can resultintheacutesevereonset ofclinicalneurologicsignsy,24Catsare rarelyaffectedbyIVDD,andtherehavebeennoreportsoflateralized diskscausingnerve-rootsigns.Physicalexamination,includingevalua-tionofthemusculoskeletalandneurologicsystems,oftenrevealsfocal paininadermatomaldistributionratherthanpainconfinedtoan anatomic region such as a joint or specific bone. The orthopedic examina-NEUROLOGICCONDITIONS CAUSINGLAMENESS INCOMPANIONANIMALS25 tionandancillarytestsfororthopedicdiseasesarecoveredmorethor-oughly in another article in this issue.Neurologic evaluation may reveal LMNdiseaseaffectingtheinvolvednerveroots.It maybedifficultto distinguish between neurogenic and disuse muscular atrophy. Conscious proprioceptiveorotherposturalreactiondeficitsmay be present inthe involvedlimb. If thenerverootsofC8throughT2areinvolved,there may beipsilateralHorner'ssyndromeandlossofthecutaneoustrunci (panniculus)reflex.TheHorner'ssyndromecanbeexplainedbythe interruptionofthesympatheticsupplytothepupil,whichexitswith spinal nerves Tl through T3.An ipsilateral cutaneous trunci reflex deficit iscaused by disruptionof the lateral thoracicnerve,amotor nervethat has acell body origin at the level of the C8 and Tl spinal cord segments. Acarefulsensoryevaluationforparaspinalhyperesthesiacould discernanareaofhypersensitivityassociatedwiththenerve-root involvement.Paraspinalpalpationisdonefromacaudaltocranial directionwiththestimulusincreasingfromlighttouchtodeeppalpa-tion.Abehavioralreactiontowhatshouldbeaninnocuousstimulus canbeinterpretedaspain.Placingonehandontheabdomenasthe vertebralcolumnispalpatedallowsdetectionofabdominalmuscle splinting when pain isexperienced.Cervicalpalpationisperformed by firmlypressingon thetransverseprocessesfromCltoC7.Thecervical areacanalsobeexamined by flexingandextendingtheanimal'sneck. Duringpalpation,areasof hyperesthesiaarenotedand compared with thepresentingnerve-rootsigns.If Significantcorrelationisfoundbe-tweenthesensoryexaminationandthenerve-rootdistributionofthe limb-carrying lameness, further diagnostic testing is warranted. Previous administrationof anti-inflammatory oranalgesicmedicationsand over-excitementoftheanimalduringtheexaminationmayinfluencethe resultsof the sensory examination. Diagnostictestingforsuspectednerve-rootimpingementfroma lateralizeddiskincludeselectro diagnostictestingandadvancedneuro-imaging.If theextrudeddiskmaterialiscalcified,radiopaquematerial may be seen within or adjacent to the intervertebral formina with routine surveyradiographs.Orthognicviews(perpendiculartoeachother)are needed to accurately localize an extruded IVD.Oblique views accentuat-ingtheintervertebralspacearehelpful indemonstrating whichsideof . thespinalcordthediskisaffecting.Myelographyandepidurography mayshowevidenceofIVDDsuchasaprotrudingdisk.Thesestudies can be normal,however, becausealateralizeddiskisoutside the verte-bral canal and cannot be seen readily with theseimaging techniques.s Electrodiagnostic testing that may be helpful in investigating lateral-ized disks includes EMG, nerve conduction, and f-waveanalysis.Herni-atedlateralizeddisksthatcausecompressioncancauseEMGchanges characterizedbydenervationpotentialsinatypicalperipheralnerve distribution pattern.42, 53, 54For example, compression at the L4 nerve root wouldresult indenervationpotentials in thequadriceps,iliopsoas,and sartoriusmuscles.Althoughspecificdiseasescannot bediagnosedwith eJectrodiagnostictesting,specificnervedistributioncan bemappedout 26McDONNELL et al withthesetests,whichaidinselectingadvancedneuroimagingand treatmentplanning.Itcommonlytakes5to7days?-e,nervation potentials to developafter nerve pathology occurs53; thus, It ISImportant to know when the signs first developed. Performance of an EMG evalua-tion before this 5-day window may result in false-negative results.Nerve conductionshouldbenormal,becauseonlytheperipheralportionsof thenervesareexamined.F-waveanalysismay beausefulelectrodiag-nostic technique to investigate the peripheral nerve proximal to the point of stimulation and ventral roots. Advancedimagingtechniquesreportedtobeusefulindiagnosing lateralized IVD include computed tomography (CT),magnetic resonance (MR)imaging,lineartomography,diskography,andultrasonograPI:y (US).Equipment costsandtrainingtypicallylm:uttheavail-abilityof these techniquestoreferraland other larger practIces.CT and MR imagingareadvantageous indiagnosingof thetransverse nature of theimages and theabIhty to VIewtheImage of interestin multipleplanes(Fig.2).27,45,59,62Thenormalanatomyand pathologicconditionsofthecaninespinehavebeen19, 35Mineralized disk material would appear hyperdense on CT Imagmg and T2-weighted MR imaging.Tl-weighted MR imaging of mineralized disk materialwouldbeiso- orhypointense.19, 35, 59 Thereisanadvantageto usingCTaftermyelographytopreciselylocalizethelesionwhenit occurs in thecervicaland thoracolumbar spine. 1, 19Figure 2.A soft-tissue window,transverse CT image at thelevel of theL7-S1intervertebral diskspaceina 4-year-oldmaleneuteredRottweiler presentingwitha3-yearhistory ofleft pelviclimblamenessunresponsivetononsteroidalanti-inflammatorydrugs .. Asoft-tissue mass(arrowhead)ispresentwithintheleftintervertebralforamen, compressingthenerve root.Surgical decompression showed a herniatedlumbosacral disk.Myelogram and epldur-ogram showed no abnormalities. After surgical decompressionanddiskremoval , allclinical signsresolved. (CourtesyofLeighGlerum, DVM, UniversityofGeorgia, Athens, GA) NEUROLOGICCONDITIONS CAUSINGLAMENESSINCOMPANION ANIMALS27 Linear tomographyanddiskography. offer littleadvantageover CT and MR imaging,but theequipment may bemoreavailablebecauseit islessexpensive.Lineartomography usesradiographicequipment that coordinatestheX-raytubeandfilmmovementaroundacentralpivot point. Objects within aspecific imaging plane are in sharp focus, whereas superimposedstructuresaboveandbelowtheimagingplaneare blurred.33Diskography involvesthe injectionof contrast material under fluoroscopicguidance through aspinal needle into the nucleus pulposus of the IVDY, 54 This technique may be quite sensitive, especially when it is interpreted with the results of radiographs, epidurograms, and EMG.54 In veterinaryandhumanmedicine,UShasbeenusedtoidentify herniateddiskmaterialoutsidethevertebralcolumnpreoperativelyas wellastoidentifydiskmaterialintraoperativelyl6,21, 46 Ultrasoundim-agesofperipheralnerveshavebeendescribedinthedog.22Herniated diskmaterialishyperechoic,allowinggoodcontrastbetvveenthedisk andthesurroundingtissueattheintervertebralforamenoralongthe spinal nerve.Ultrasound examination of the structures within the verte-bralcanalisrestrictedby thebonyencasementsurroundingthespinal cord, although. intraoperative US after ventral slot or dorsal laminectomy isextremelyhelpfulin identifyingdiskmaterialaswellasinassessing completeness of disk removal,16, 21, 46 The definitive diagnOSiSof alateralized IVD requires surgical explo-ration and sometimes histopathology of the disk,although most experi-enced veterinarysurgeonsreadilyrecognizenucleuspulposus.Surgical explorationisguidedbytheresultsoftheneurologic,radiologic,and electro diagnostictestsperformed.Accesstovarioussitesofthespinal cord, intervertebral foramen, and paravertebral area has been described.5. 36,61 Alternatively,prolongedconservativemanagementwithanti-inflanunatorydrugsmayreducethenerve-rootsignsinsomepatients. Thebenefitsofsurgicalexplorationshouldbeweighedagainstthe likelihood of treatment efficacy of the most likelydiagnosis. DegenerativeLumbosacralStenosis DegenerativeLSstenosis,alsoknownasLSinstability,LSdisease, . and cauda equina syndrome, is adisease of older large-breed dogs, with apredilection formale dogs.J4,31 The median age of affected animals has beenreportedtobe7years,withthemostcasesreportedinGerman Shepherd DogS. 13. 14,31 This isararecondition in cats.The most common disk space affected in dogsisL7to S1,although any disk space from L5 toS3maybeaffected.Inmostdogs,thespinalcordendsinthesixth lumbar vertebrae.Nerve rootsariseat the termination of the spinal cord andruninthevertebralcanaltoexitattheintervertebralforamina. When there is compression directly on these nerve roots, nerve-root pain anddysfunctionarethecommonresults.ThecauseofdegenerativeLS stenosisismultifactorial,but it isusuallycaused bydisk extrusion and stenosis,which often occur together. 28McDONNELL et al There isusually apresenting history of vague pain in most o.f dogs,withcommoncomplaintsofdifficultyrising,stairs, a reluctance to jump, and lamenessY14 Umlateral and mtermIttent shiftinglimblamenesssignsarecommon.Ahistryof arthri!isorhip dysplasiamayexist,andsomedogsimproveWIth .anti-inflammatorydrugsoranalgesics. Inabilitytoraisethetallurmary or fecalincontinence are usually later developments. On phYSIcal examI-nation, there isfocalpain over the LSjunction. Digital pressure over the LSjunctionorextensionoftheLSjunction?yliftingthepelviswhile pressingonthelumbarvertebraearespecIficmethodstoassessLS pain.Caremustbetakentohipfrom extension, as many of these dogs have hlp dysplasIa. Excellent palpation of the hips with assessment of pain is required of the clinician to identify hipdysplasiawithandwithoutLSdisease.Li!?htsedat.ionmay.be needed in performing hippalpation.If the dog obJects. to hlpandtherangeof motionispoor,thedog may have hipd;:splasla or without LSdegeneration.If thedog objectstoextreme hlp extenslOn, buttherangeofmotionisnormal,LSdiseaseshouldbesuspected. Paresis of the tail,limb, or sphincters isstronger evidence of LSdegener-ativedisease,although thesesignsarelesscommon now because of the increased knowledgeof the client and veterinarian. Neuroimaging and electro diagnosticsarethe most helpful ancillary diagnostictoolsforLSdegenerativedisease.Survey radiographsfsomebenefit.Spondylosisispresentinalmostallsuchcases,butItIS alsocommoninclinicallynormaldogsofthissizeandage.Manyof thesedogshavedegenerativeordevelopmentalabnormalitiesseenon plain radiographs.32,40 Narrowingof thevertebralcanal can beaccentu-atedbyextensionoftheLSjunction.Myelographycanbe to demonstrate compression at the LSjunction, although false-r,osltlvean.d false-negativeresultsarepossible,the. spac:IS absentin most large-breeddogsattheLSJunction.EpldurographyISa relativelyeasy procedureusefulindemonstratingLS is performed by injecting iohexa!- r a.lOdme solutlOn intheepiduralspace.ThemJectionIStypIcallymadecaudaltoS3 through Cdl and should not be made at the siteof the suspected lesion. FlexedandextendedviewsoftheLSjointduringepidurographymay demonstrate adynamic message.The interpretation and performance of epidurogramsrequiresomeexperience.Diskographyisanotherre.la-tivelyeasyproceduretoperform and mayd.lsk protrusionY 54Epidurogramsanddiskogramsaresnnplifiedbyusmg fluoroscopy.Myelography should precede .epidurograJ?hy and. diskogra-phy,asthepresenceofepiduralcontrastmterferesWIththemterpreta-tion of themyelogram. ImagesobtainedwithCTorMR ar:superior.tothose obtained using conventional radiography in dlagnosmg laterahzed dIsks intheLSarea,asdisksarecommonlylocatedinthelateralrecessesof the sacrum, causing compression of the nerve root.l,27, 28, 45. 59 The normal anatomy of the LSarea has been described.1.26 Mineralized disk material NEUROLOGICCONDITIONS CAUSINGLAMENESS IN COMPANION ANIMALS29 would appear hyperdense on CT imaging and T2-weighted MR imaging (seeFig.2).Tl-weightedMRimagingofmineralizeddiskmaterial wouldbeiso- orhypointense.1.26 Bloomartifactmaybeaproblemin CT-myelographyexaminationoftheLSspine.27.45Intravenouscontrast administrationhasbeenshowntobehelpfulindiagnosingLS stenosis.28, 45Electrodiagnostictestingisusefultoconfirmsuspectedcasesof LS degenerativedisease.Motor nerveconduction andf-waveanalysismay benormalinpatientswithLSpainastheonlysign.Thepresenceof EMG changes such as fibrillationpotentials and positive sharp waves in affectedmusclesofthepelviclimbs,paravertebralarea,tail,andperi-neumconfirmsthelocationofthelesion. 53, 54 Mappingthedistribution oftheabnormalityisusefulinestimatingtheextentandseverityof the lesion. 54 Prolongedmedicalmanagementwithstrictcagerestandanti-inflammatorydrugsmaybenefitfirst-episodepatientswithminimal signs.Animalswithrecurrentsigns,severeunrelentingpain,orLMN signs aregood candidates forearly surgical intervention.13, 14 Thedefini-tivediagnosis' ofLSdegenerativediseaserequiressurgicalexploration usually via aLSlaminectomy and diskectomy with or without foramin-ectomydependingonneurologic,radiographic,electrodiagnostic,and surgicalfindings.ThesurgicalapproachestotheLSareahavebeen described.61 Dogswithchroniccompressivelesionshaveanexcellent prognosis if treated surgically unlesstherearesevereLMN deficits. SpinalCordNeoplasia Thespinalcordmay beaffectedbymetastaticorprimarytumors arisingfromthesurroundingsupportingstructuressuchastheverte-brae, fibroustissue, cartilage, or blood vesselsassociated withthe verte-brae.38Primaryneuraltumorsalsoaffectingthespinalcordinclude astrocytoma,glioma,ependymoma,neuroepithelioma,menigioma,me-ningealsarcoma,malignantperipheralnervesheathtumor(MPNST), lymphosarcoma,and reticulum cell sarcoma.38Epidural lymphosarcoma isthemostcommonlyreportedspinaltumorincats.31, 43, 57MPNSTis discussedinthenextsectionofthisarticle.Clinicalsignstypically reflect the location of the tumor and usually result in slowly progressive neurologicdeficits.Spinalcordtumorsthatimpingeonspinalnerve roots or the cervical and lumbar intumescences may re:;;ultin nerve-root signsandlameness.lo. 35, 38 Spinalcordtumorsandlesionsdistantfrom theoriginof thespinal nerverootshavebeen reportedtocause nerve-rootsignsin human patients.23, 47 NewtonandRea41proposethatthese signsarecausedbytumor-induceddistortionanddemyelinationof cervicaldorsalsensoryaxons.Thisphenomenon has not been reported in animals. Diagnosingaspinalcordtumorcausinglamenessornerve-root signaturerequiressignalment evaluation,acomplete physicalexamina-30McDONNELL et al tion,andchoosingappropriateancillarydiagnostictests.Tumorsmore commonly occur in large-breed dogs older than 5 years of age.33,38Feline spinal lymphosarcoma ismore common in young animals.31, 43, 57 Nerve-rootsignsmaybeobviousonphysicalexamination,andneurologic evaluation may showLMNsigns.Muscleatrophymay bepresent ina spinalnervedistribution,althoughdistinguishingbetweenneurogenic and disuseatrophy may bedifficult.Postural reactionsmay bedelayed inthelimbsthatarecaudaltoorat thesiteofthetumor.If thenerve roots of the cervicothoracic spinal cord are involved, Horner's syndrome andabnormalitiesinthecutaneoustruncireflexmaybepresentas describedinthesectiononIVDD.Paraspinalhyperesthesiamaybe foundwith careful palpation.Extradural and intradural-extramedullary tumorscommonlyhavehypersensitivityassociatedwithaprocessin-volvingthenerveroots,thevertebrae,theIVD,orthemeninges.Intra-medullary tumorsarerarely associated with signs of pain in people and animals. Ancillary diagnostictestsmay includeradiology and myelography, electrodiagnostictesting,andadvancedneuroimaging(MRimagingor CT).Spinalcolumnradiographsmaydetectneoplasiainvolvingthe vertebralboneorcartilaginoussupportstructuresthatcompressthe spinal cord or nerve rootsexiting theintervertebral foramen. Myelogra-phycannotdefinitivelydiagnosespinalcordtumorsbutshouldallow identificationof thesiteof thetumorand itsrelationtothespinalcord and meninges(Fig.3).38 Tumorclassificationasextradural,intramedul-lary,or intradural-extramedullary may be difficult, because tumors may occupy more than one of thesecompartments.35Nevertheless,classifica-tionaidsinthedevelopmentofadifferentialdiagnosisandprOVides important information forprognosis and treatment planning. Figure 3.Lateral(AJandventrodorsal(B)myelogramofthecervicalspineina9-year,0Id maleneuteredLabradorRetrieverpresentingwithan8-weekhistoryofrightthoraciclimb lameness andinfraspinatus and supraspinatus muscle atrophy. Anintradural-extramedullary fillingdefect(arrowheads)isseenatthelevelofC6-C7.Surgicalexplorationrevealeda meningiomacompressingtherightC7nerveroot. NEUROLOGICCONDITIONS CAUSINGLAMENESSINCOMPANION ANIMALS31 Electrodiagnostictestingcandiagnoseneitherspecificdiseasesnor tumor types but aidsin identifying whetherabnormalities such asatro-phy,pain,andotherequivocalsignsoflamenessarecaused by neuro-logicor orthopedic disease.EMG, nerve conduction studies, and f-wave analysiscan defineandlocalizeperipheral or nerve-root disease,which aidsin the selection of advanced imaging and treatment planning. Elec-trodiagnostictests have been previously discussed in thisarticle, AdvancedneuroimagingsuchasCTandMRimagingcanaid inthediagnosisofspinalcordtumorsandisconsideredsuperiorto myelographyindetectingtheexactlocationofspinalcordtumors. Iodinatedcompoundsareusedtoenhancespinaltumorswhenexam-ined by CT,whereas gadolinium-DTPA(Magnavist; Beilex Laboratories, Wayne,NJ)isusedwhen spinaltumorsareexaminedby MRimaging. ReportsdescribethedifferentCTandMRimagingcharacteristicsof varioustumorsofthespineandspinalcord.1, 18, 29,35 IntraoperativeUS afterdorsallaminectomyhasbeendescribedindogswithspinalcord tumors,whichhelpedtodelineatetherelationtothespinalcordand theextent ofthetumor.16Tumor locationandappearancearecriticalin developinga'moreaccuratediagnosis,bettersurgicalplanning,and prognosis. Thedefinitivediagnosisofspinalcordneoplasiarequiressurgical biopsy and histopathology of thelesion.Biopsy isguided by theresults of theneurologic,radiologic,andelectro diagnostictestsperformed.Ac-cesstovarioussitesofthespinalcordhasbeendescribed.6, 36, 61The benefitsof surgicalbiopsyshould be weighedagainst thelikelihoodof treatment efficacy of the most likelydiagnosis. MalignantPeripheralNerveSheath Tumors MPNSTs,alsocalled neurofibromas, schwannomas,and neurofibro-sarcomas, arisefromthe myelin-producing cells(Schwanncells)or con-nectivetissuesurroundingnerves.4,7, 58 Theseareslow-growingtumors thatextendbylocalinvasionalonganyoftheperipheralnervesand their branches.They rarely invade surrounding tissue,andmetastasis is also rare.Although any peripheral nerve can be affected, more than 80% .ofthereportedcasesinvolvethebrachialplexusoritsnerveroots,58 Othersitesaffectedincludethepelvicplexus,thoracolumbarnerves, andcranialnerves.MPNSTsaffectmaturedogswithnosexorbreed predilectionand only rarely affect cats,58,64 Thetumorsthataffectthebrachialorpelvicplexusresultinslow but progressiveunilaterallamenessand muscleatrophyofthethoracic or pelvic limb, respectively.The initial presenting complaint is typically a chronic and progressive non-weight-bearing lameness that isminimally responsivetoanti-inflammatorymedications.SignsofLMNdisease affectingtheinvolvedlimbincludehypotonia,flaccidparesis,hypore-flexia,and muscle atrophy. The muscle atrophy, hyporeflexia, and hypo-toniausuallyhaveadistinctspinalorperipheralnervedistribution. Earlyinthecourseofthedisease,itmaybedifficulttodistinguish 32McDONNELLet al betweenneurogenicanddisusemuscularatrophy.Consciousproprio-ceptivedeficitsmay be present in the involved limb at an early stage in the disease. With involvement of the brachial plexus, MPNSTs may have axillarypainandapalpablemass.IpsilateralHomer'ssyndromeand abnormalities in the cutaneous trunci reflex may be present as described in the section on IVDD.MPNSTs can extend proximally along the nerve andcompressthespinalcord,causingdeficitsintheoppositelimb.If an MPNST of the brachialplexusinvadesthespinalcord,upper motor neuron signs may be present in the pelvic limbs. Diagnosisof MPNSTsrequiresahigh degreeof suspicion basedon the animal's signalment and choosing the appropriate ancillary diagnos-tictestes)basedontheresultsofacompletephysicalexamination. Helpfuldiagnosticaidsincludeplainfilmradiographs,myelography, electrodiagnosis,and advanced neuroimaging such asMR imaging, CT, or US.Radiographsof theinvolved limband associatedvertebral spine couldruleoutanMPNSTbydetectingosseousneoplasiaorother obviousmusculoskeletalabnormalities.Myelography can outlinespinal tumors,includingMPNSTsthat haveinvadedthevertebralcanal(Fig. 4).MPNSTsare typically classified as extradural or intradural-extramed-ullary tumors.Electrodiagnostic techniquesuseful in diagnosing periph-eralnervedisordersincludeEMGandnerveconductionstudies.JO 53Theelectrodiagnosticabnormalitiesaredenervationpotentials,nerve conductionslowingorblock,andf-waveslowingorblock.Although electrodiagnostictestingcannotdefinitivelydiagnoseMPNSTs,theab-normalities have atypical spinal or peripheral nerve distribution, which can aidin theselectionof advancedneuroimagingand treatmentplan-ning.If the contralateral limb hasdenervation potentials, there isahigh possibility that the MPNST has involved thespinal cord. CTandMRimagingdiagnosisofcanineMPNSTshavebeende-scribedandareadvantageous,becausethetransversenatureofthe imagesallowsvisualizationof nerveroots,spinalnerves,and proximal portionsoftheperipheralnerve.39, 44If theimagesarecenteredonthe vertebralcolumn,thecontralateralclinicallynormalnerverootand spinalnervesareavailableforcomparison.MPNSTsmayoccurany-wherealong thecourseofthespinal or peripheral nerve,however,and may not be seen adjacent tothe vertebral column.One recommendation istocenterthefieldofviewontheaffectedlimb,butthistechnique requiresadetailedknowledgeofthenormalanatomy.44Contrasten-hancementandsignalcharacteristicshavebeendescribedforhuman andcanineMPNST.9, 20,39,44CTvisualizationofthetumorisenhanced withtheintravenousadministrationofiodinecontrast.62 Nervesheath tumorsindogsandhumanbeingshaveintermediateSignalonTl-weightedimagesandhyperintensesignalonT2-weightedimages,and they show variable enhancement with the administration of gadolinium-DTPA(Magnevist). 1,35, 62 USdiagnosis of canine MPNSTs and human peripheral nerve sheath tumorshasbeendescribed.4,44,52 High-frequencyUSishighlysensitive in the detection of nervesheath tumorsof theextremities;nerve sheath NEUROLOGICCONDITIONS CAUSINGLAMENESS IN COMPANION ANIMALS33 Figure4.Lateral(A)andobliqueventrodorsal(B)myelogramofthelumbarspineofan 11-year-old femalespayed Labrador Retriever that presented witha10-month history of left pelvic limb lamenessunresponsive to nonsteroidal anti-inflammatory drugs, corticosteroids, .acupuncture,andchiropracticmanipulation.At thetimeofpresentation,therewassignifi-cant muscle atrophy of the biceps femoris,graCiliS,and cranial tibialmuscles.Anintradural-extramedullary fillingdefect(arrowhead) isseenat thelevelof L4.Electrodiagnostic testing suggestedthatthemasswascontiguouswiththeL6nerveroot.Asoft-tissuewindow, transverseCTimageat thelevelof theL5-L6intervertebraldiskspace(C)demonstrates asoft-tissuemassexitingtheleftintervertebralforamen.Surgicaldecompressionand debulkingrevealedamalignantperipheralnervesheathtumor oftheleftL6nerveroot. tumorsarerecognized ;3.S asolidhomogenousmassalongthe courseof the peripheral nerve. US has the advantage of allowing inspection of the distalperipheralnerveandwouldeliminateorreducetheneedfor anesthesia in veterinary patients.Ahigh degree of clinical suspicion and 34McDONNELLetal asuperiorknowledgeof theUSanatomyof theregionarerequiredto successfully diagnosethesetumors. ThedefinitivediagnosisofMPNSTrequiressurgicalbiopsyand histopathologyofthetumor.Biopsyisguidedbytheresultsofthe neurologic,radiologic,andelectrodiagnostictestsperformed.Accessto various sitesofthe spinal cord,brachial plexus,and lumbar plexushas been described.6, 36, 61 The benefitsof surgical biopsy should be weighed against the likelihoodof treatment efficacy of these tumors. TraumaticNeuropathies Traumatic injury to peripheral.nerves is a frequent cause of neuropa-thiesillanimals.30, 65 Commoncausesofnerveinjuryaremechanical blows,gunshotwounds,fractures,pressure,andstretching.Iatrogenic causesinclude trauma fromintramedullary pins(crushing,cutting,and spearingthenerve),castsorsplints(compression),injectionsintoor adjacenttothenerve,anddirecttraumacausedbymanipulation.65Traumatic neuropathies can often bediagnosed based purely on history andclinicalsigns,although if thetrauma wasnot witnessed, it may be difficulttodifferentiatebetweenneurologicandorthopedicdisease.A historyconsistent with trauma includesfree-roaminganimals,previous surgery, or concomitant orthopedic injury. Physical examination findings include abrasions, contusions, lacera-tions, abdominal organ injury, or chest wounds associated with vehicular traumaorgunshotwounds.Orthopedicinjuries,particularlyhumeral fractures, pelvic fractures, and femoral fractures, must be carefully evalu-ated to rule out peripheral nerve injuries that may affect the outcome of _ fracturerepair.It isanunfortunatesituationwhenaperipheralnerve injuryisoverlookeduntilaftermajororthopedicrepairhasbeenper-formed.Acompleteneurologicevaluationneedstobeperformedon thesecasestoprevent similar situations.Abnormalitiesdetected during theneurologicexaminationthatwouldindicatespinalorperipheral nerveinjurieswouldincludeLMNsignssuchasflaccidparesisor paralysis, hypotonia, hyporeflexia,and rapid neurogenic muscular atro-phy.Neurogenicatrophyshouldbeevidentwithin7to10daysofthe injury.Theotherhallmarksignofspinalnerveandperipheralnerve injuriesissensorydysfunction,whichisdetectedbymappingareasof decreased or absent superficial pain. This can be performed by grasping afoldof skin and pinching with asmall hemostat.Thethreeresponses thatwouldindicateproperfunctioningofthenerveareabehavioral, response,reflexwithdrawal of the limb,or twitchof theskin. Electrodiagnostictestingishelpfulinevaluatingtheextentand severity of traumatic neuropathies. Approximately 5 to 7 days must pass aftertheinjurybeforedenervationpotentialsaredetectedonEMG. Nerve conduction studies can be done proximal and distal to the injured sitetoassessnerveintegrity.Serialexaminationallowsformonitoring of regeneration after nerve injuryY,53 NEUROLOGICCONDITIONS CAUSINGLAMENESS IN COMPANION ANIMALS35 Althoughnotdescribedclinically,UShasbeenusedtoevaluate peripheral nerve degeneration and regeneration after experimental tran-section?2In thisreport,theproximaltransectednervewasconsistently visualized,whereasthedistal portion of thetransected nerve wasmore difficulttoidentify.Nerve regeneration wasdetected sonographically in threeof fourdogs in which regeneration was confirmed by histopathol-ogy.Thisstudy would suggest that US could be used to monitor degen-erationandregenerationofperipheralnervesindogsaswellasto precisely localize peripheral nerve injury. 22 The resultsof theneurologic evaluation and electro diagnostic testing would assist the US examination bylocalizingsectionsof peripheralnerveinjury.Adetailedknowledge of normal anatomy is essential in performing US examination of periph-eral nerves. MR imaging has not been described for evaluating peripheral nerve injuries.MR imaging might provideusefulinformation, but itsexpense may precludeitsusefulnessin serialexaminations.Assessmentof trau-maticneuropathiesusingMRimagingwouldalsorequireadetailed knowledge of normal anatomy. Exploratotysurgery has been advocatedtoassessperipheral nerve injury.The advantages of surgery would be direct evaluation of damage anddirect treatment either by surgical anastomosisorfreeingthe nerve from inflammatory adhesions.The obvious disadvantage to this surgery isthe requirement for precise localization of the site of injury; the results ofneurologic,electrodiagnostic,andUSexaminationsshouldhelpto guide the surgeon tothemost likelyareaof injury. SUMMARY Animalspresentedwithnon- weight-bearinglamenessareadiag-nosticchallenge forthe veterinarian. It isextremely importanttodistin-guishbetweenorthopedicandneurologiccausesoflameness,because thediagnosticandtherapeuticplanscan bequitedifferent.Myopathies canbeconfusedwithorthopedicdiseasebecauseofgaitabnormalities andassociatedmusclepain.Commonmyopathiesseenincompanion animalmedicineincludepolymyositis,musculardystrophy,endocrine . and infectious myopathies,and myasthenia gravis.Lameness caused by diseaseof thenerverootornerveisconfusedwithorthopedicdisease because of the disturbancesof anerve's sensory distribution(nerve-root signature)ordisruptionofthemotorinnervation.T h ~diseasesofthe nerve root or nervediscussed arelateralized intervertebral diskdisease, spinalcordneoplasia,malignantperipheralnervesheathtumors,and traumatic neuropathies. Thediagnosisofthesediseasesrequirescarefulattentiontothe signalment,acompletehistory,andathoroughphysicalexamination focusing on the neurologic and orthopedic components. Ancillary testing shouldbeselectedbasedontheseresultsandaminimumdatabase. Electrodiagnostictesting,radiography,and advanced imaging may help 36McDONNELL et al tolocalizethelesionmorepreciselyandsometimestoconfirmthe diagnosis.Surgicalexplorationandhistopathologyoftenprovidethe definitive diagnosis. Thesecasesofnon-weight-bearing lamenessareadiagnosticchal-lenge,but when successfulresolutioncan be reached,it isgratifyingto theclinician,client,andpatient. References 1.Adams WH:The spine. 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JAVMA202:1877- 1882,1993.. 41.NewtonHB,ReaGL:L'hermitte'ssignasapresentingsymptomofpnmaryspmal cord tumor. JNeurooncol29:183- 188,1996 42.NiederhauserUB,HollidayTA:Electrodiagnosticstudiesindiseasesofmusclesand neuromuscular junctions. SerninVetMedSurg (SmallAnim)4:116-125,1989 .43.Noonan M,Kline KL,Meleo K:Lymphoma of thecentral nervous system: Aretrospec-tivestudyof 18 cats.Compend Contin EducPractVet1997 44.Platt SR,Graham J,Chrisman CL, et al:Magnetic resonance rrnagmg and ultrasonogra-phy in the diagnosis of amalignant peripheral nerve sheath tumor in adog. 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VetImmunolImrnunopathol 69:239-249,1999 52.SimonovskyV:Peripheralnerveschwannomapreoperativelydiagnosedbysonogra-phy: Reportofthreecasesanddiscussion.Eur JRadiol25:47-51,1997 53.SimsMH:Electrodiagnostictechniquesintheevaluationof diseasesaffectingskeletal muscle.VetClinNorth Am Small Anim Pract 13:145--162,1983 54.SissonAF,LeCouteurRA,Ingram JT,etal:Diagnosisof caudaequinaabnormalities byusing electromyography, discography, and epidurography in dogs. J Vet Intern Med 6:253-263,1992 55.SmithMO:Idiopathicmyositidesindogs.SerninVetMedSurg(SmallArum)4:156-160,1989 56.Spodnick GJ,BergJ,MooreFM,et al:Spinallymphomain cats: 21cases(1976-1989). JAVMA200:373-376,1992 57.Summers BA,Cummings JF,deLahunta A:Diseases of theperipheral nervous system. InVeterinaryNeuropathology.St Louis,Mosby Yearbook,1995,pp 402-501 58.TagaA,TauraY,Nishimoto T,et al: Theadvantage of magnetic resonance imaging in diagnosisof caudaequinasyndrome in dogs. JVetMed Sci60:1345-1348,1998 59.TaylorSM:Selecteddisordersofmuscleandtheneuromuscularjunction.VetClin NorthAm SmallAnim Pract 30:59-75,2000 60.Tidwell AS:Advanced imaging concepts:Apictorialglossaryof CTand MRItechnol-ogy.Clin TechSmall AnimPract,14:65-111,1999 61.TomlinsonJ:Surgicalconditionsofthecervicalspine.SerrtinVetMedSurg(Small Anim)11:225-234,1996 62.Tomlinson J,Schwink KL:Surgicalapproaches tothe spine. InSlatter D(ed):Textbook of SmallAnimal Surgery,ed2.Philadelphia,WESaunders,1993,pp1038-1056 63.WatrousBf,LipscombTP,HeidelJR,etaI:Malignant peripheralnervesheathtumor inacat.VetRadiolUltrasound40:638-640,1999 64.Welch JA:Peripheral nerveinjury.SeminVetMed Surg (SmallAnim)11:273- 284,1996 Addressreprintrequeststo John J.McDonnell,DVM,MS Department of ClinicalSciences School of Veterinary Medicine TuftsUniversity 200WestboroRoad North Grafton,MA01536 LAMENESS0195- 5616/01$15.00+.00 OVERVIEWOFPAIN IN THE LAMEPATIENT Spencer A.Johnston, VMD Lamenesscanresultfromawidevarietyofconditions.Although lamenesscanoccurastheresultofapurelymechanicalabnormality suchasamalunionordiscrepancyinlimblength,lamenessismost frequently associated with acondition that causes pain either alone or in combination with amechanical alteration.Lamenessismost commonly associated with joint abnormalities as compared with long bone changes, because it isthecriticalfunctionof joints toallowtransfer of load from onebonetoanotherwhileallowingthesmoothmotionandangular changethatresultinsuccessful ambulation.Anyabnormalitythatpre-ventsthisfromoccurring,includingarticularandperiarticularchange, strainplacedonmusclesandtendons,andligamentsprains,can cause pain and lameness. The International Association for the Study of Pain has defined pain as"anunpleasantsensoryandemotionalexperienceassociatedwith actualorpotentialtissuedamage,ordescribedintermsofsuchdam-age.""OPain isdistinguished from nociception, which is the neurophysio-logicresponsetoastimulusthatactuallyorpotentiallycausestissue damage.Althoughhumanbeingscanreadilyexpressthesubjective experienceof pain,itisalwaysachallengetointegrate theconceptsof nociceptionand pain inanimals,which cannot verbalizethe experience ofpain.Despitethischallenge,asanycliniciandealingwithpatients experiencinglamenessisaware,exceptinunusualcircumstances,itis appropriatetoattributeatleastpart of theclinicalresponseof animals toactualor potentialtissuedamageaspain and not just asnociceptive reflexbehavior. FromtheDepartmentofSmallAnimalClinicalSciences,Virginia-MarylandRegional Collegeof Veterinary Medicine,VirginiaTech,Blacksburg,Virginia VETERINARYCLINICS OF NORTHAMERICA:SMALLANIMAL PRACTICE VOLUME31 NUMBER1 JANUARY200139 40JOHNSTON It is intuitively obvious why an animal with an acute fractureof the diaphysis of along bone or involving the articular surface is in pain and hasanalteredgaiteveniftheneurophysiologyisnotknownbythe casualobserver.Itislessobviouswhyananimalwithmoresubtle musculoskeletalchangesuchasthat occurringinosteoarthritis(OA)is in pain andlame.Thisarticleconcentratesonthemechanism by which painmaybeassociatedwithjointabnormalitiesandhelpstoidentify thepotentialcausesastowhythepatientsufferingfromOAorjoint injury experiencespain.Although OAisthefocusofthisarticle,many ofthetissuesandprocessesthatresultinpainwithOAaresimilarly affected in other acute or chronic musculoskeletal injury.Lameness isan avoidancebehaviortopreventstimulationofnociceptorspresentin these tissues. STUDY OFPAINMECHANISMS Painismosteasilystudiedinexperimentalmodelsinvolvingan acutenoxiousstimulus.Studiesofmorechronicpaintypicallyinvolve inductionofacuteinflammation,withsubsequentexaminationofthe sequelaetotheinflammatoryevent.Therearefewifanygoodstudies ofchronicpainmechanismssecondarytomechanicalchangeorthe combinationofmechanicalchangeandmildinflammationsuchasoc-curswith OA32Becauseofthelackof thesetypesof studiesaswellas theclinicalfindingoftemporalvariabilityof changesthatoccurinthe articular and periarticular tissues, the individual variability with respect to pain expression,27 and the frequent discrepancy between radiographic evidence of OA and the clinical expression of pain, it is difficult to make .definitive statements regardingOA pain that apply toallpatients. Despite knowledge of these limitations, it seems reasonable to glean informationfromthestudyofacuteandinflammatorypaintohelpus conceptualizewhy OA and other joint injury causepain,Knowledge of thetypesoftissuesinvolved,theneurallinkages,theresponsetome-chanicalandchemicalstimuli,andtheplasticityoftheneuralsystem may lead to improved understanding of OA, pain, and lameness, includ-ing therationale forvarious treatment methods and thedevelopment of arational expectation fortreatment outcome, OSTEOARTHRITIS OAcanbedefinedasaslowlyprogressivedisorderofmovable jointscharacterizedbydeteriorationofarticularcartilage,osteophyte formationandboneremodeling,changesinperiarticulartissues,anda low-gradenonpurulentinflammationofvariabledegreeYIt isconsid-ered to beacondition that istypically initiated by mechanical alteration of the joint but can also becaused bynormal forcesactingon abnormal cartilage.It isimportanttorecognizethatstabilityofthejoint,with OVERVIEWOF PAIN IN THE LAMEPATIENT41 appropriate transmission, dissipation, and absorption of forces generated duringmotion,occursonlywhenalltheconstituenttissuesfunction normally.2Articularcartilageismostfrequentlythefocusofstudyof thiscondition,withchangesoftheperiarticularstructuressuchassub-chondral bone, synovium, joint capsule, ligaments, and muscle receiving lessconsideration.Becauseof thecomplex natureof OA,it isrelatively easytofocusonthemorereadilydocumentablechangesofarticular cartilagethatoccur.Itismoredifficulttoevaluatetheperiarticular tissuesinvolved.Unfortunately, becausearticular cartilageisaneural,it isthechangesintheseperiarticulartissuesthat haveanintegral rolein the pain and dysfunction associatedwith thiscondition. ThespectrumofclinicalmanifestationsassociatedwithOAisless easily defined than are the pathologic changes. Pain is the clinical symp-tom most frequentlyassociatedwith OAs Thispainmay bequitevari-able,being present insomepatientswith relativelyminorradiographic changeof theaffected joint,although it isabsent in other patientswith muchmoredramaticevidenceofchange.9 Whenconsideringalarge populationofpatientswithOA,it ismostcommonlyrecognizedthat pain intensifies "and becomesmorepersistentasOA progresses.During theinitialstagesofOA,theconditionmaybeasymptomatic.AsOA progresses, pain may be present only during motion and weight bearing. As the condition progresses further,there may be continuous discomfort thatisexacerbatedbymotionandweightbearing.Ultimately,pain associated with OA can become pervasive and affect nearly all activities, includingsleep.Alleviationofthispainisthegoalofmosttreatments of OA Thesourceofpainassociatedwith OAismultifactorial.Although the discomfortcaused by thiscondition tothe patient affected with OA iseasily understood,tothe student studying OA,thephysiologic cause oftheacuteandchronicpain associatedwithOAismoreelusive.The situationiscomplicatedevenfurtherwhenconsideringthatitiswell recognizedin human beingsthat pain is influenced by nonarticular and supraspinalfactorssuchaspsychologicstate,pastexperience,gender, social status, and environmental factors .s, 28 Similar factorshave not been documentedasinfluencingOApainindogsandcats.Nevertheless, giventhedegreeof human andanimalinteraction thatoccurswith pet dogsandcats,itisreasonabletobelievethatsimilarnonarticularand supraspinal factors can contribute to an animal's ability to cope with OA NEURORECEPTORSANDNERVEFIBERS Jointsareinnervatedbyarticularbranchesfrommainperipheral nervesandbybranchesofnervesthatsupplynearbymuscles.These articular nervescontain myelinatedandunmyelinatedafferentfibersas well as unmyelinated sympathetic efferent fibers.3sIt has been estimated that20%ofthefibersofanarticularnervearemyelinated,and80% areunmyelinated.38Postganglionicsympatheticefferent fibersmakeup 42JOHNSTON approximately40%ofjointnervefibers,orapproximately50%ofthe unmyelinated fibers.I 738 Neuroreceptorsarespecialized neuralstructuresthat arenecessary toprovideinputfromtheperipheraltissuestothecentralnervous system. Many typesof specialized neuroreceptors exist, and their activa-tionprovidesrawinformationfortactile,thermal,andpain sensations. Jointstypicallycontainmechanoreceptorsandnociceptors.Mechanore-ceptorsaresensitivetomechanical stimuli such asstretch andpressure. Theiractivationisimportantinsensingstaticpositionanddynamic movement of the joint.Nociceptors areactivated by anoxiousstimulus, which is astimulus sufficient to potentially cause or actually cause tissue damage. Under normal circumstances, the activation of nociceptors often leads to the sensation of pain. Input fromperipheral mechanoreceptors travels to the dorsal spinal hornviamyelinatedafferentfibers,most ofwhichareclassifiedasA[3 fibers.Theserelativelylargemyelinatedfibersprovidefortherapid transmissionofimpulsestothespinalcord,wheretheysynapsewith second-orderneuronsandinterneuronsinthedorsalspinalhorn.Im-pulses originating from mechanoreceptors that then ascendtosupraspi-nal centers are processed to provide information regarding joint position andstatus.Nociceptiveimpulsestravelalongthinlymyelinated(Ao) and unmyelinated(C)fibers. These impulsestravel fromthe joint to the dorsalspinalhorn,wheretheycanconvergeandsynapseonmanyof thesamesecond-orderneuronstowhichthemechanoreceptorsproject. Once anociceptive impulse reaches the dorsal spinal horn, it can initiate areflex arc, sending asignal to periarticular muscle, or it can ascend the spinalcordtothebrain.Itmayalsobemodulatedbyinhibitoryin-terneurons or by descending neural mechanisms such as the endogenous opiates(enkephalinsanddynorphins)and be terminated.Impulsesthat originatefromnociceptorsthatascendtosupraspinalcentersareproc-essedtoformtheexperience known as pain. Postganglionic sympathetic efferent nerve fibersfound in the articu-larnervesterminatenearbloodvesselsandwithinthesynoviallining and subsynovial layers,24and are associated with control of the vascular toneofarticularvessels.38 Activationofthesesympatheticfibersisre-sponsibleforvasoconstriction.Somesympatheticfiberscontainneuro-peptide Y,a peptide that causes vasoconstriction and may also potentiate the action of other neurotransmittersYPostganglionic sympathetic fibers mayalsobestimulatedtoproduceprostaglandinsandinterleukin-l, whichthenmayacttosensitizetypeIVnociceptors.I 6Theroleofthe sympatheticresponseinarthritisisnotentirelyknown,althoughitis speculatedthatitmaybemoreimportantinrheumatoidarthritisthan inOAY Once a nociceptor is stimulated, it islikely to respond to subsequent noxious stimulation more vigorously and at a lower activation threshold. Thisphenomenonistermedhyperalgesia.Hyperalgesiaiscommonly associatedwiththepresenceof inflammatorymediatorsreleasedfrom damaged tissue.Inflammatory mediators that directly excite the nocicep-OVERVIEWOF PAIN IN THELAME PATIENT43 torarecalledalgogenicsubstances.Bradykinin,asubstanceproducedas part of theclottingcascade,isconsideredtobealgogenic.Otherdirect stimulators of primary nociceptor afferents include histamine, serotonin, and protons.I 6 Other inflammatory mediators contribute to hyperalgesia byloweringthethresholdfornociceptoractivation.Prostaglandinis consideredtoactinthismanner,althoughithasbeensuggestedthat prostaglandinsE2and12 canalsoactasdirectsensitizers.616 Thearea experiencingtissuedamageisconsideredtobetheregionofprimary hyperalgesia.Oncean inciting event occurs,however,it ispossible that the surrounding tissuesdemonstrate an exaggerated responseto further stimuli.Thisphenomenonistermedsecondaryhyperalgesia.Secondary hyperalgesiamayoccurasaresultofcollateralbranchesofafferent nerves being primarily stimulated,or it mayoccur asaresult of central sensitization,whichoccursbecauseof theafferentfibersprojectedover multiple segmentsof the spinal cord. Primaryafferent fibersdistributeoverarelativelylargeareaof the spinalcord.Thisresultsinpoorlocalizationofastimulusassociated withasomaticregionbecauseofoverlapofneuralinput,anditcan contribute to the sometimes relatively vague nature of joint pain. Within the dorsal spinal horn, there are two types of (second-order)dorsal horn neurons:nociceptive-specificandwidedynamic- range(WDR)neu-ronsYNociceptive-specificneuronsrespondonlytonoxiousstimuli, whereasWDRneuronsrespondtovariousstimuli,includingnoxious stimuli.ChronicactivationofprimaryafferentCfibersresultsinan increase in theexcitability of neurons in the spinal cord.This phenome-nonisknownascentralsensitization.43 Centralsensitizationoccursasa resultoftheactivityofglutamate,substanceP,andcalcitoningene-relatedpeptide(CGRP)withinthedorsalhorn.Releaseofthesesub-stancesoccursasaresultofstimulation fromsmallafferentfibers.The outcomeisanalterationinthereceptivefieldandadecreaseinthe activationthresholdofthedorsalhornneurons.Subsequently,thereis an increase in the magnitude and response of the postsynaptic ascending spinalneuronstofurthernoxiousstimuliaswellasanincreasedre-sponsetolow-thresholdstimulisuchasthoseoriginatingfromA[3 fibers.The expansion ofthereceptivefieldisconsistentwith secondary hyperalgesia,wheretheareasurroundingtheregionofprimarytissue injuryalsodemonstrates increasedsensitivity.In joint pain,thisprocess explains why tissues surrounding the injured joint are sensitiveto stim-uli. This phenomenon includes increased sensitivity of mechanoreceptors andnotjustnociceptors.Forexample,aninflamedandpainfuljoint may not only demonstrate increasedsensitivity toflexionand extension butevenlighttouchmayelicitanexaggeratedresponse,whereasit maynormallynoteven berecognized.Thephenomenonofanormally innocuousstimuluselicitingapainfulresponseistermedal/odynia.Al-though the stimulus would normally be considered innocuous, the mes-sagethatistransmittedtothesupraspinallevelsisconsistentwith stimulationofnociceptorfieldsandisinterpretedasbeingassociated with anoxious and painful event. 44JOHNSTON Thesechangesinnociceptivethresholdcanoccurwithacuteor chronic injury.The process explains why joint tenderness and sensitivity to motion or touch can occur after joint sprain or why muscle tenderness (sensitivitytopressureorstretch)followsmusclestrain.Avoidingjoint motionordecreasingtheforceplacedonalimbhelpstodecrease nociceptor activation and results in theclinical sign of lameness. TYPESOFNEURORECEPTORS FOUNDINJOINTS Much of the work describing the types of neuroreceptors present in jointshasbeenperformedincats.39Wyke44describedfourtypesof sensory receptors in joints.Type Iand II receptors are mechanoreceptors (receptororgansthat respondto mechanicalstimuli such aspressure or tension).Thesereceptorsarelocatedinthejointcapsule,withtypeI receptorslocatedinthesuperficiallayersandtypeIIreceptorslocated in the deeper layers.44 They are low-threshold receptors that are activated byjointmovementorpressureandareabletorapidlytransmitthis informationtothecentralnervoussystemviamyelinatedfibers.Both type IandIIreceptorsarethinlyencapsulatedorgans.TypeIreceptors areslowly adaptingandthusservestaticanddynamicfunctions .Type IIreceptorsaremorerapidlyadaptingandthushaveamoredynamic function.44The combination of input fromtype Iand IIreceptors as well asfromotherneuroreceptorslocatedin themuscleandskinallowsan individualtorecognizetheorientationofthelimband jointinspace.3, 32,39Theresponsepropertiesof typeII(mostly A(3)fibersaresimilar in thenormal and inflamedjoint,andthesefibersare not likelytohavea rolein nociception.39TypeIIIreceptorsarethinlyencapsulatedorgansfoundonthe surfaceofligaments.44Relativelylargemyelinatedafferentfibers(Aex) areattachedtotypeIIIreceptors,and these allow rapidtransmission of animpulse.44 TypeIIIreceptorshavearelativelyhighthresholdand thusrequireasubstantialstimulusforactivation.Theyareinactiveat restandwithinnormalandsaferangesof jointmotion.Theyareacti-vatedwhenastrongmechanicalstimulusapproachingthelevelthat may cause tissuedamage ispresent.Assuch,type IIIarticular neurore-ceptorsare considered to be nociceptors. Type IVreceptorsareactually freenerveendings.44 Thesereceptors differmarkedlyfromtypesIthroughIIIbecausetheyarenotspecific receptororgans.With theexceptionof articularcartilage,type IVrecep-torsarefoundinalltissuesofthejoint,includingsubchondralbone. Type IVreceptorsare nociceptors, They are high-threshold slowly adap-tive receptors that areconsidered to be polymodal.Polymodal receptors respondtomechanicalstimuliasdotypeIthroughIIIreceptors,and theyalsorespondtothermalandchemicalstimuliandarethusinti-matelyinvolvedinthepainassociatedwiththeinflammatoryprocess. Impulses from type IV receptors are transmitted toward the dorsal spinal horn viathinly myelinated ASfibersor unmyelinated Cfibers. OVERVIEWOFPAININ THE LAMEPATIENT45 ,SometypeIVreceptorsareconsideredtobesilentnociceptors.39Thesereceptorsareconsideredtobemechanoinsensitiveunder normal domechanosensitivityunder inflammatory condItI(:ms ..substancessuchasprostaglandin2,bradykinin, serotonm, hlstamme, nervegro,,:,thfactorcansensitize theserecep-tors.UndernormalClrcumstances,sIlentnociceptorsdonotcontribute any sensory information, afterinjury,they contribute tothe barrage of sensory Impulsesreachmg thedorsal spinal horn and contributing to central sensitization. MECHANICAL STIMULATIONOF ARTICULAR NOCICEPTORS TypeIVnociceptorsaretypicallystimulatedbytensionandpres-sure.can result in nociceptor stimulation, this may help toexplamwhymotIonmayexacerbatediscomfortassociatedwiththe osteoarthritic joint. Movement of ajoint results in tension on one side of the joint and co.mpression on the other.Intra-articular pressures mcreased m?tlOn,andthis inintra-articularpressure IScorrelatedWIthpam?IncreasedsynovIalfluidvolumealsocreates pressureand isfrequentlyrecognizedinosteo-suchasinthepatientwithchronicOAsecondaryto cruclate lIgament rupture.Increased fluidvolume may alsooccur in the earlystageof OA:ithasbeendocumentedwithhipdysplasia1s,19and mayalsooccurWIthanyacutejointinjurythatresultsin inflammation orhemorrhage.Anothersituationwherethereisarelativeincreasein intra-articularpressureoccurSwhenthereisadecreaseinatmospheric pressuresuch asthat occurring withthelow-pressuresystemstypically associated with bad weather.44 . st.imulationoftypeIandIIneuroreceptorsmayalso mfluencenOClceptIonbutinamanneroppositetodirectstimulationof typeIVnociceptors,Thisoccursthroughthegatetheoryoriginally by Melzack andWall.21 When allneuroreceptorsexperiencea stImul';ls .that exceedstheactivationthreshold,an impulse isgenerated, andthIStravelsvia theafferent nerve fibertothedorsal spinal horn, where Itsynapseson asecond-order neuron or an interneuron. At thissite,the impulse mayascendthespinal cord, initiate areflexarc,or be otherwise modified. The gate theory suggests that impulses generated by (mainly types Iand II)have the ability to stimulate aninhIbItorymterneuronordirectlyblockactivationofsecond-order neurons. byimpulsesgeneratedbynociceptiveafferents,therebypre- Impulsesby nociceptoractivation fromascending the spmalcord.If nOCIceptorImpulsesdonot reachsupraspinalsites,they cannot ?e interpretedascontributing tothepain response. . ThISbeusedasatherapeuticmodality.Forthe patIent wIth.Jomt mJ:-rry,stImulation of peripheral mechanoreceptors can beaccomplIshedWIthtranscutaneousnervestimulators,massageof 46JOHNSTON tissues,orcompressionofoverlyingtissueswithabandage.Inhuman beings,it has been speculatedthatrhythmicstimulationof mechanore-ceptorssuchasthatoccurringwhenthepatientusesarockingchair providesrelieffromjoint painassociatedwithOA.44It ispossiblethat thismechanismalsoprovidessymptomaticreliefindogsandcatsthat rest in a hammock type bed, where gentle movement along with redistri-butionofforceoveralargerareainsteadofonfocalpressurepoints may be beneficial. INFLAMMATIONANDSENSITIZATION Normaljointsarepainfulonlywhenanextremeforceisapplied suchasthatoccurringwhenthesaferangeofmotionofthejointis exceeded or whenthetissuescomprisingthejoint experienceexcessive pressure. Once disease or injury is present, however, pain may be experi-encedwithoutmotionorwithnormalmotion.Thisoccursprimarily through chemical mediation, which istypically associatedwith the pro-duction of inflammatory mediators.This occursthrough sensitization of joint afferents. AlthoughOAisconsideredtobeanoninflammatorycondition characterized by variabledegrees of mild inflammation,it isrecognized thatthelevelof inflammatory mediators suchasbradykinin,serotonin, histamine,lacticacid,prostaglandinE2,andsubstancePisincreasedat tim