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Is It Essential Tremor or a Parkinsonian Syndrome? Diagnostic Considerations in Primary Care CMETanya Simuni, MD

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Is It Essential Tremor or a Parkinsonian Syndrome? Diagnostic Considerations in Primary Care CME

This article is a CME-certified activity.To earn credit for this activity visit:

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CME/CE Released: 6/7/2013Valid for credit through 6/7/2014

Target AudienceThis activity is intended for primary care providers, family medicine specialists, internists, and neurologists.

GoalThe goal of this activity is to improve the recognition and diagnosis of patients with essential tremor, Parkinson disease, or both.

Learning ObjectivesUpon completion of this activity, participants will be able to:

1. Outline challenges to the accurate and timely diagnosis of Parkinson disease in the primary care setting

2. Compare clinical signs and symptoms of Parkinson disease, other parkinsonian syndromes, and essential tremor

3. Recognize when neuroimaging is appropriate in the diagnostic workup of patients with suspected parkinsonian syndromes

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Faculty and Disclosures

FacultyTanya Simuni, MDAssociateProfessorofNeurology,NorthwesternUniversity,Chicago,Illinois;Director,Parkinson’sDiseaseandMovementDisordersCenter,NorthwesternMemorialHospital,Chicago,Illinois

Disclosure:TanyaSimuni,MD,hasdisclosedthefollowingrelevantfinancialrelationships:Servedasanadvisororconsultantfor:TevaNeuroscience,Inc.;NovartisPharmaceuticalsCorporation;Ipsen;MerzPharmaceuticals;GEHealthcare;GlaxoSmithKline;UCBPharma,Inc.;IMPAXLaboratories,Inc.;SynPharmaTechInc.;EMDSerono,Inc.;Phytopharm

Servedasaspeakeroramemberofaspeakersbureaufor:TevaNeuroscience,Inc.;NovartisPharmaceuticalsCorporation;Ipsen;Allergan,Inc.;GEHealthcare;GlaxoSmithKline

DrSimunidoesnotintendtodiscuss off-label uses of drugs, mechanical devices, biologics, or diagnostics approvedbytheFDAforuse in the United States.

DrSimunidoesnotintendtodiscussinvestigational drugs, mechanical devices, biologics, or diagnostics not approvedbytheFDAfor use in the United States

EditorPriscilla Scherer, RNScientificDirector,Medscape,LLC

Disclosure:PriscillaScherer,RN,hasdisclosednorelevantfinancialrelationships.

CME Reviewer Nafeez Zawahir, MDCMEClinicalDirector,Medscape,LLC

Disclosure:NafeezZawahir,MD,hasdisclosednorelevantfinancialrelationships.

Peer ReviewerThis activity has been peer reviewed and the reviewer has disclosed no relevant financial relationships


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Hello.MynameisDrTanyaSimuni.IamthedirectoroftheParkinson’sDiseaseandMovementDisorderCenteratNorthwesternUniversityinChicago,Illinois.WelcometothisMedscapeaudiolecturetitled“IsItEssentialTremororaParkinsonianSyndrome?DiagnosticConsiderationsinPrimaryCare.”

AttheendofthispresentationyouwillbeabletooutlinechallengestoaccurateandtimelydiagnosisofParkinsondisease(PD)intheprimarycaresetting,compareclinicalsignsandsymptomsofPDandotherparkinsoniansyndromeswiththoseofessentialtremor (ET), and recognize when neuroimaging is appropriate in the diagnostic workup of patients with suspected parkinsonian syndromes.

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Parkinsondiseaseisacommonneurologicdiseaseofaging.Itaffects1millionpeoplelivingintheUnitedStates,andisthesecond most common neurodegenerative disease after Alzheimer disease.[1] Becauseitisadiseaseofaging,itisexpectedthattheprevalenceofthediseasewilldoubleby2040.[1,2]

ThediagnosisofPDisbasedontheclinicalassessment.WeroutinelyapproachitinastepwisefashionthatreflectstheUnitedKingdom(UK)Parkinson’sDiseaseSocietyBrainBank(PDSBB)ClinicalDiagnosticCriteria.[3] Let us walk through these criteria.

WewillnowreviewoftheprevalenceofPDandthediagnosticcriteriaforPD,discussthedifferentialdiagnosisofparkinsonisms,discuss the diagnostic criteria for ET, and then describe a clinical vignette that will illustrate the diagnostic challenges you may encounter in your clinical practice.

ThefirststepindiagnosingPDistoidentifytheclinicalfeaturesofparkinsonismasaclinicalsyndrome.Thesefeaturesinclude3cardinalmanifestations.Bradykinesia,orslownessofmovement,isacardinalfeatureandhastobepresentineverypersondiagnosed with parkinsonism. The second feature is rigidity, which is a specific type of increased tone that frequently includes acogwheelproperty.Thethirdcardinalmanifestationisthecharacteristicrestingtremor.Bydefinition,inordertomeetthediagnosticcriteriaofparkinsonism,apersonshouldhave2ofthe3cardinalmanifestations.Inaddition,anothercommonfeatureof parkinsonism is postural instability, which is frequently present as the syndrome progresses.


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At that point, with those features, you can make the diagnosis of the clinical syndrome of parkinsonism without alluding to any specificetiologyorevent.Ifrequentlytellmyresidentsthatatthepointofidentificationofparkinsonismyoudonotneedtoknowthepatient’shistorynordoyouneedtoknowanyofthepatient’smedications;itisstrictlyasyndromaticdiagnosis.Butadditionalinformation is necessary to proceed from the diagnosis of parkinsonism as a clinical syndrome to identifying the potential underlying etiology.

ThenextstepinthediagnosticcriteriaofPDisacarefulascertainmentofthepatient’smedicalhistoryandphysicalexamination,whichmaypointoutatypicalfeaturesthatwouldleadyoutoconsideranotherentityratherthanidiopathicPD.Youmustcarefullydeterminethepatient’shistory,lookingforanysymptomaticcauses,specificallydrugexposure,headinjury,historyofmultiplestrokes, and so on. This is also the time to look for any atypical features on the neurologic examination outside of the clinical syndromeofPDthatmightleadyoutosuspectanalternativediagnosis.

Accurate 90% of the time



Inconsistent

The third and final part of the diagnostic criteria relies on a compendium of historical information and neurologic examination toimproveyourdiagnosticaccuracy.Alongerdurationofthepatient’ssymptomsincreasesthediagnosticaccuracy.PresenceofasymmetrictremorismuchmorecharacteristicofPDthanofotheretiologiesofparkinsonism.ExcellentandsustainedresponsetomedicationsforPD,primarilylevodopareplacement,butalsoresponsetoanydopaminergicreplacementtherapy,isastrongindicatorthatitisPDratherthanaparkinsonismwithanalternativeetiology.Therefore,a3-stepapproachleadsyoutotheclinicaldiagnosisofPD.

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Clinical diagnostic accuracy is also supported by the results of imaging studies.[5] These have demonstrated that the greatest challenge in diagnosis is during the early stage of the disease, when the typical syndrome has not yet developed; with longer follow-up,thediagnosticaccuracyimproves.

Whatisthediagnosticaccuracyofthesecriteria?Thesediagnosticcriteriaweredevelopedusingtheclinical-pathologicalcorrelation of 100 patients who ultimately came to autopsy. Clinicians were correct in 76% of these cases.[3] Basedonthatexperience,thediagnosticcriteriawereappliedprospectivelyandasecondclinical-pathologicalserieswaspublished10yearslater, demonstrating a diagnostic accuracy to 90%.[4] The diagnostic accuracy remains at approximately 90% today.


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Whatotherneurodegenerativediseasescanpresentwithparkinsoniancharacteristicsaspartoftheclinicalpresentation?Hereis a long list of what we frequently refer to as atypical parkinsonian syndromes. They are included under that umbrella because allofthemshareparkinsonianfeatures.TheyalsousuallyincludeatypicalmanifestationsthatdifferfromclassicPD.Themostcommonofthesenon-PDparkinsoniansyndromesincludeprogressivesupranuclearpalsy(PSP),multiplesystematrophy(MSA),corticobasal degeneration syndromes, as well as a number of entities that share a combination of parkinsonism and dementia. The most common of these is diffuse Lewy body disease.

Fortoday’sdiscussion,wewillrefertoparkinsoniansyndromesastheentitiesthatareassociatedwithdopaminedeficiencyandlossofdopaminergicneuronsinthepresynapticspace.ThemostcommonoftheseclinicalentitiesisPD,whichisresponsiblefor85% of cases of parkinsonism; MSA is responsible for approximately 5% of the cases; and PSP is responsible for 5% of cases.[6] On the other end of the spectrum are the entities associated with clinical signs of parkinsonism but not associated with presynaptic dopaminergicdenervation.Themostcommonoftheseisdrug-inducedparkinsonism,whichischaracterizedbyablockadeofdopamine transmission rather than degenerative process.[6-8]Vascular parkinsonism[9] and psychogenic parkinsonism[6-8]are among the other common entities that will be encountered in clinical practice.

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Let us switch the discussion to the diagnostic criteria for ET. Essential tremor is a specific neurologic disorder, also known as familialtremor.Thecardinalmanifestationisintentionoractiontremorthatinvolveshandsandfrequentlythehead.Itcanaffectthe voice and sometimes the trunk and legs. There are no other neurologic findings on the clinical examination and no other symptomaticorothercausesfortremor.Itmaybehereditaryinsomepatients,althoughaspecificgenehasnotbeenidentified.

Tremorcanbecommoninpatientsandthelistofsymptomaticcausesislong.Thelistonthisslideisnotall-inclusive.Whenyouseeapatientwithrecentonsetoftremor,alwaysconsiderthepatient’smedications.Recentinitiationofmedicationcanresultintremor. Providing a catalog of drugs that may be associated with tremor is beyond the scope of this discussion. For patients with new-onsettremor,alwayschecktheprescribinginformationforeachofthepatient’smedicationstoseewhethertremoriswithinthespectrumofdrug-inducedadverseeffects.

Metabolic abnormalities, electrolyte imbalance, and thyroid dysfunction can all be the symptomatic causes of tremor. Patients with head injury or multiple sclerosis can develop tremor. Other neurologic conditions can be associated with tremor, and patients withPDhavetremoraswell.


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HowdoyoudistinguishtremorassociatedwithETfromtremorassociatedwithPD?ThecardinalmanifestationofETisthetypically symmetric tremor. Patients with ET have tremor as the single manifestation of the syndrome, and it is an action or posturaltremor,whereasapatientwithPDtypicallyhasarestingtremor.

ET is the most common movement disorder,[1,10] andisfrequentlyunder-recognizedorhidden,aspatientsdonotseekthephysician’sattentionforETuntilitbecomesbothersome.About5%ofpeopleage>65yearshaveETand,asIhaveindicated,frequently they will not be diagnosed and will not seek medical attention.

ThetypicalageoftheonsetofETisthe40s.However,thespectrumofonsetcanbewide,fromyoungadulthoodandevenchildhood to a much older age of onset. The onset is typically slow and insidious with a slowly progressive course. The patient shouldbereassuredthatETisnotaneurodegenerativedisease.Itisnotlife-threatening,itdoesnotleadtoachangeinlifeexpectancy, and the impact of the tremor is proportional to the degree of functional impairment associated with the tremor manifestation.

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PatientsfrequentlyaskwhetherthereisanyrelationshipbetweenETandPD.Theanswertothatquestionisthatthereisnorelationship.AsIhaveindicated,thepatternoftremorisdifferentinETvsPD.PatientswithETdonot“growinto”ordevelopparkinsonian syndromes, as the pathology of the conditions is different. The mechanism of development of tremor is different. On theotherhand,onemustrecognizethatPDandETarethe2mostcommonmovementdisordersofaging,soasubsetofpatientsmay have both diagnoses.

Now that we have reviewed diagnostic criteria for these 2 common movement disorders, let us talk about the importance of accuraterecognitionofsymptomsofonevstheother.TheaccuratediagnosisofPDandETisimportantformanagement,forcommunicating the prognosis to patients, for selection of appropriate therapy, and at some point in the future, when we do develop neuroprotective therapies, for screening of the population at risk. For all of these reasons it is important to establish an accurate diagnosis as much as possible.

Whatistheroleofdiagnosticimaginginthediagnosisofthese2commonmovementdisorders?Aswehaveindicated,bothdiagnoses are based on clinical diagnostic criteria and, in the majority of cases, physicians will make the correct diagnosis based on the clinical presentation.[11-17]PatientswithaclassicpresentationofeitherPDorETdonotrequirediagnosticimaging.DiagnosticimagingwillbehelpfulinpatientswithatypicalfeaturesthatarebeyondthescopeofaclassicpresentationofETorPDor who have poor response to appropriate therapy when the question arises of potential alternative diagnosis.


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On one end of the diagnostic spectrum is a large group of patients with parkinsonian manifestations.[11] You have no questions withregardtotheetiologyofparkinsonisminthisgroupandcanmakeareliablediagnosisofPDorotherparkinsoniansyndromes based on the clinical assessment and history. On the other end of the spectrum are patients with ET who have the classic presentation of postural or action tremor with no other findings on neurologic examination.[17] InthemiddleisasubsetofpatientswhohaveoverlappingsymptomsordonothavethatclassicpresentationforeitherETorPD,whowillpresentadiagnostic challenge.[12-16]

Howcommonisthatdiagnosticchallenge?Eveninthehandsofexperiencedclinicians,basedonanumberofpublishedreviews,apreviousdiagnosisofPDwasrejectedin15%ofpatientsusingstandardizedcriteria--onestudyfounda15%misdiagnosisrate,[18] another found a 26% rate.[19] Another study, looking at patients diagnosed with ET, found a 37% misdiagnosis rate.[20]

Certainly, these statistics provide an argument for improving our diagnostic certainty.

Letusillustratethatwithacasevignette.Thepatientisa60-year-oldwomanwhocomesforevaluationoflong-standingtremor.She reports having a history of bilateral symmetric hand tremors that occur with activity. The tremors are especially bothersome whenshewritesandwhensheholdsacup,andimproveaftershehasaglassofwine.Herfatherhadsimilartremors.Thetremordid not bother her until a couple of months ago, when she started experiencing an increase in the magnitude of the tremor and more recently when she noticed occasional spontaneous tremors in her right arm even at rest.

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On examination, she has a bilateral action tremor when she holds a cup. She also has a slight rest tremor component in the right arm and a trace of increased tone in the right wrist. She has normal balance and gait and she has no other pertinent neurologic or medical history.

ThinkaboutthiscaseaswediscusstheroleofdopaminergicimaginginthediagnosisofPD.

Biomarkersusedindopaminesystemimagingcanassistinthediagnosisofconditionsassociatedwithdopaminedysfunction.Severaldopamine-relatedimagingagentscanassesstheintegrityofdopaminergicneuronsusingeitherSPECTorpositronemission tomography (PET) imaging modalities. These radioligands image presynaptic targets such as the dopamine transporter, vesicularmonoaminetransporter,or3,4-dihydroxyphenylalanine(DOPA)decarboxylaseactivity;thesearebasicallystepsintheconversionofdopamineinthepresynapticsystem.Whatisimportanttorecognizeisthatallthepresynapticimagingmodalitieswill assess the functional integrity of the presynaptic dopaminergic system. Results of presynaptic imaging will be abnormal with any condition associated with presynaptic dopamine deficiency and normal with conditions that have a preserved presynaptic dopaminergic system.


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This slide presents a visual image of different levels of the presynaptic or postsynaptic system, where the specific tracer is much less relevant than the conceptual understanding of the role of establishing either normal presynaptic dopaminergic function or abnormal presynaptic dopaminergic functioning.[21] IoflupaneI123 is the only radiopharmaceutical that is currently approved by the USFoodandDrugAdministration(FDA)andiscommerciallyavailableforuseindopaminetransporterSPECTimaging.Thisagentisusedtovisualizestriataldopamine,toassistintheevaluationofadultpatientswithasuspectedparkinsoniansyndrome.Itmaybe used to help differentiate ET from tremor related to a parkinsonian syndrome.

DopaminetransporterSPECTscanswillbeabnormalnotonlyinpeoplewithPDbutinthosewithanyconditionsassociatedwith presynaptic dopamine deficiency, including MSA, PSP, and other atypical parkinsonian syndromes that we discussed earlier.DopaminetransporterSPECTimagingdoesnotestablishthediagnosisofPDandisnotrequiredforeverypatientwediagnose, but is used for the differential diagnosis of more challenging cases when the physician is not sure whether the clinical presentation is associated with presynaptic dopamine deficiency.

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Let us discuss the clinical diagnostic features that will be associated with presynaptic dopamine deficiency vs what is not associated.WetalkedaboutPD,thefoundationofwhichislossofdopaminergicneurons.Bythetimethesepatientshaveclinicalsymptoms, they have already lost up to 60% of dopaminergic neurons.[22] Thus,patientswithPD,nomatterhowearlytheyareinthe course of the disease, will have abnormal results on their scans. Patients with ET have no dopaminergic loss and therefore will have a normal presynaptic dopamine function, so the scan results will be normal.[21] Patientswithdrug-inducedparkinsonismhaveproblems with transfer but not production of dopamine so the scan will be normal. Patients with psychogenic parkinsonism will have no alteration of dopamine function. Vascular parkinsonism is a more complicated entity. A majority of patients with vascular parkinsonism will have normal results of the scan, but if the vascular lesion is strategically located in the striatal system the scan may be abnormal. Patients with Lewy body dementia will have abnormal results of the scan and patients with Alzheimer disease, in the majority of cases, will have normal results.[21]

Again, let us conceptually separate the 2 groups of patients. The group with abnormal presynaptic dopaminergic function includespatientswithPD,atypicalparkinsoniansyndromessuchasMSAandPSP,andthesepatientswillhaveabnormalresultsonthescan.Patientswithnormaldopaminergicorpresynapticdopaminergicfunction,includingpatientswithET,drug-inducedparkinsonism, and psychogenic parkinsonism will have normal results on the scan.[21]


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Letusreturntothecasevignette.Thepatient’sclinicalpresentationwasconsistentwithalongstandinghistoryofposturalandactiontremor,positivefamilyhistory,alcoholresponsiveness,allsupportingtheclinicaldiagnosisofET.However,herclinicalexamination also demonstrated features of possible early parkinsonian syndrome. The diagnostic uncertainty was discussed with the patient and the clinical question was whether this patient has ET with some atypical manifestations or whether the patient withlongstandingETnowhasdevelopedfeaturessuggestiveofearlyPD.

The patient elected to undergo SPECT imaging, which demonstrated normal dopamine transporter uptake, thus excluding theconditionsassociatedwithpresynapticdopaminedeficiency,suchasPD,andsupportingtheimpressionthatherclinicalpresentation was within the spectrum of ET.

Thisslidedemonstratesascanofapersonwithnormaltransporteruptake,whichisontheleft,vsapersonwithearlyPD,whichshows reduced uptake on the left side in the left striatum, corresponding with early clinical manifestations on the right side, and slightly reduced uptake in the right striatum.

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Inconclusion,PDandETarethe2mostcommonmovementdisorderswesee.Bothareclinicaldiagnoses,andrelyonthecarefulcollection of history, the physical and neurologic examinations, and the established diagnostic criteria. A subset of patients will have overlapping syndromes, however, or more challenging symptoms. Timely and accurate diagnosis of both conditions is importanttoadvanceappropriatetreatmentandimprovethepatient’squalityoflife.

Patients with atypical symptoms will benefit from dopamine transporter SPECT imaging, which differentiates between a parkinsonian syndrome and ET as adjunctive diagnostic testing.

Ihopethatthisdiscussionwillassistinyourfuturediagnosisofpatientswiththesecommonneurologicconditions.Thankyou.

This transcript was edited for style and clarity.


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References1.WattsRL,StandaertDG,ObesoJ.Movement Disorders: Neurologic Principles and Practice.3rded.NewYork,NY:McGraw-Hill;2012.

2.WrightWillisA,EvanoffBA,LianM,etal.Geographicandethnicvariationin Parkinson disease: a population based study of US Medicare beneficiaries. Neuroepidemiology.2010;34:143-151.

3.HughesAJ,DanielSE,KilfordL,LeesAJ.AccuracyofclinicaldiagnosisofidiopathicParkinson’sdisease:aclinico-pathologicalstudyof100cases.J Neurol Neurosurg Psychiatry.1992;55:181-184.

4.HughesAJ,DanielSE,LeesAJ.ImprovedaccuracyofclinicaldiagnosisofLewybodyParkinson’sdisease.Neurology.2001;57:1497-1499.

5.SeibylJ,JenningsD,TabamoR,MarekK.TheroleofneuroimagingintheearlydiagnosisandevaluationofParkinson’sdisease.Minerva Med. 2005;96:353-364.

6.RajputAH,RajputA,RajputM.EpidemiologyofParkinsonism.In:PahwaR,LyonsKE,KollerWC,eds.Handbook of Parkinson’s Disease. 3rd ed. New York, NY:MarcelDekker,Inc.;2003:17-42.

7.KägiG,BhatiaKP,TolosaE.TheroleofDAT-SPECTinmovementdisorders.J Neurol Neurosurg Psychiatry.2010;81:5-12.

8.ThanviB,TreadwellS.Drug-inducedparkinsonism:acommoncauseofparkinsonism in older people. Postgrad Med J.2009;85:322-326.

9.ThanviB,LoN,RobinsonT.Vascularparkinsonism--animportantcauseofparkinsonism in older people. Age Ageing.2005;34:114-119.

10.LouisED.Essentialtremors:afamilyofneurodegenerativedisorders?Arch Neurol.2009;66:1202-1208.

11.LeesAJ,HardyJ,ReveszT.Parkinson’sdisease.Lancet.2009;373:2055-2066.

12.HauserRA,GrossetDG.[123I]FP-CIT(DaTscan)SPECTbrainimagingin patients with suspected parkinsonian syndromes. J Neuroimaging. 2012;22:225-230.

13.PahwaR,LyonsKE.EarlydiagnosisofParkinson’sdisease:recommendations from diagnostic clinical guidelines. Am J Manag Care. 2010;16(suppl):S94-S99.

14.HauserRA,AuingerP,OakesD;ParkinsonStudyGroup.LevodoparesponseinearlyParkinson’sdisease.Mov Disord.2009;24:2328-2336.

15.SolidaA,GhikaJ,VingerhoetsF.Acutedopaminergicchallengeteststo assess postural/kinetic tremor of different origin: a case report. J Neurol Neurosurg Psychiatry.2002;73:206-207.

16.MarshallV,GrossetDG.Roleofdopaminetransporterimaginginthediagnosis of atypical tremor disorders. Mov Disord.2003;18(suppl7):S22-S27.

17.BhidayasiriR.Differentialdiagnosisofcommontremorsyndromes.Postgrad Med J.2005;81:756-762.

18.SchragA,Ben-ShlomoY,QuinnN.HowvalidistheclinicaldiagnosisofParkinson’sdiseaseinthecommunity?J Neurol Neurosurg Psychiatry. 2002;73:529-534.

19.MearaJ,BhowmickBK,HobsonP.AccuracyofdiagnosisinpatientswithpresumedParkinson’sdisease.Age Ageing.1999;28:99-102.

20.JainS,LoSE,LouisED.Commonmisdiagnosisofacommonneurologicaldisorder:howarewemisdiagnosingessentialtremor?Arch Neurol. 2006;63:1100-1104.

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22.MarekK,JenningsD.CanweimagepremotorParkinsondisease?Neurology.2009;72(7Suppl):S21-S26.

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Abbreviations

ALS = amyotrophic lateral sclerosis

CALM-PD=ComparisonoftheAgonistPramipexoleWithLevodopaonMotorComplicationsofParkinson’sdisease

CT = computed tomography

DAT=dopaminetransporter

DOPA=3,4-dihydroxyphenylalanine

ELLDOPA=EarlierversusLaterLevodopaTherapyinParkinsonDisease

ET = essential tremor

FDA=USFoodandDrugAdministration

MPTP=1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine

MRI=magneticresonanceimaging

MS = multiple sclerosis

MSA = multiple system atrophy

PCP = primary care provider

PD=Parkinsondisease

PDSBB=Parkinson’sDiseaseSocietyBrainBank

PET = positron emission tomography

PSP = progressive supranuclear palsy

REAL-PET=RopiniroleinEarlyParkinson’sDiseaseversusL-dopa

SPECT=single-photonemissioncomputerizedtomography

SWEDD=scanwithoutevidenceofdopaminergicdeficit

UK=UnitedKingdom

VMAT-2=type2vesicularmonoaminetransporter

DisclaimerTheeducationalactivitypresentedabovemayinvolvesimulatedcase-basedscenarios.Thepatientsdepictedinthesescenariosarefictitiousandno association with any actual patient is intended or should be inferred.

The material presented here does not necessarily reflect the views of Medscape, LLC, or companies that support educational programming on medscape.org.ThesematerialsmaydiscusstherapeuticproductsthathavenotbeenapprovedbytheUSFoodandDrugAdministrationandoff-labelusesofapprovedproducts.Aqualifiedhealthcareprofessionalshouldbeconsultedbeforeusinganytherapeuticproductdiscussed.Readers should verify all information and data before treating patients or employing any therapies described in this educational activity.

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Is It Essential Tremor or a Parkinsonian Syndrome ...img.medscape.com/images/805/072/805072.pdf · University in Chicago, Illinois. Welcome to this Medscape audio lecture titled “Is