pemeriksaan extrapiramidal

Innovations in CLINICAL NEUROSCIENCE [ V O L U M E 9 , N U M B E R 7 – 8 , J U L Y – A U G U S T 2 0 1 2 ]10

In this series, Drs. Sanders and Gillig explainhow aspects of the neurological examinationcan aid in differential diagnosis of somecommon (and some uncommon) disordersseen in psychiatric practice.

ABSTRACTExtrapyramidal signs include

increased motor tone, changes in theamount and velocity of movement,and involuntary motor activity. Theyinclude two groups of signs andrelated disorders: hypokinetic(similar to Parkinson’s disease) andhyperkinetic (similar to Huntington’sdisease). This article covers some ofthe neuroscience behindextrapyramidal disorders, therelevance of extrapyramidal signs inthe major psychiatric disorders, themajor extrapyramidal movementdisorders, and how to elicitextrapyramidal signs.

INTRODUCTIONOf all the parts of a neurologic

examination, nothing is moreessential to daily psychiatric practicethan extrapyramidal motorfunctioning. Extrapyramidal functioncan affect many aspects of themental status examination, such asspeech, affect, and spontaneousmotor activity. Extrapyramidaldisorders (both iatrogenic andidiopathic) are common inpsychiatric patients, and psychiatricsyndromes are quite common inpatients with extrapyramidaldisorders. Accordingly, the central

importance of the basal ganglia inpsychiatric conditions has long beenappreciated.1,2 Also, extrapyramidalsigns and symptoms are verycommonly affected by psychiatricmedications, and monitoring theseeffects of treatment is essential inclinical psychiatry.

Extrapyramidal is a traditionalterm that refers to impaired motorcontrol, usually referable todysfunction of the basal ganglia.Extrapyramidal symptoms consist oftwo broad groups of signs anddisorders: hypokinetic (as found inParkinson’s disease and after short-term exposure to dopamine-blockingdrugs) and hyperkinetic (as found inHuntington’s disease and afterchronic exposure to dopamine-blocking drugs). Most extrapyramidalsigns are revealed by observation,and the rest by brief directexamination.

RELEVANT ANATOMY ANDPHYSIOLOGY

Extrapyramidal function refers tocontrol of motor tone, the amountand velocity of movement, and thesuppression of undesirable motoractivity. Motor systems other thanthe pyramidal (corticospinal) tractare understandably termedextrapyramidal, but we should notethat the term was never anatomicallymeaningful and has become moreanomalous. Motor coordination,planning, sequencing, and inhibition,which we tend to link with the

ExtrapyramidalExaminations in Psychiatry

[ P S Y C H I A T R Y A N D N E U R O L O G Y ]

by RICHARD D. SANDERS, MD, and PAULETTE MARIE GILLIG, MD, PhD

Dr. Sanders is Associate Professor, Departments of Psychiatry and Neurology, Boonshoft School ofMedicine, Wright State University, and Dayton VA Medical Center, Dayton, Ohio; and Dr. Gillig isProfessor of Psychiatry and Faculty of the Graduate School, Department of Psychiatry, BoonshoftSchool of Medicine, Wright State University, Dayton, Ohio.

Innov Clin Neurosci. 2012;9(7–8):10–16SERIES EDITOR: Paulette M. Gillig, MD,PhD, Professor, Department of Psychiatry,Boonshoft School of Medicine, Wright StateUniversity, Dayton, Ohio

FUNDING: No funding was received for thedevelopment of this article.

FINANCIAL DISCLOSURES: The authors haveno conflicts of interest relevant to the contentof this article.

ADDRESS CORRESPONDENCE TO: PauletteGillig, MD, Professor, Dept. of Psychiatry,Boonshoft School of Medicine, WrightState University, 627 S. Edwin C. MosesBlvd., Dayton, OH 45408-1461; E-mail:[email protected]

KEY WORDS: Extrapyramidal signs,parkinsonian signs, tremor, rigidity, motorretardation, neurologic examination

[ V O L U M E 9 , N U M B E R 7 – 8 , J U L Y – A U G U S T 2 0 1 2 ] Innovations in CLINICAL NEUROSCIENCE 11

cerebellum and the frontal lobes, arenot routinely consideredextrapyramidal, but do involve thebasal ganglia as well as cerebellumand neocortex. Also, the pyramidaltract is now known to be only one ofseveral tracts subserving voluntarymotor activity.3

The forebrain basal ganglia arethe brain structures mostresponsible for extrapyramidalcontrol. As discussed in our reviewof the voluntary motor system,3

several parallel circuits or loops helpcontrol motor planning and control,4

decision-making, and behavioralreinforcement.5 These circuitsinvolve mostly frontal cortex,cerebellum, thalamus, and limbicstructures in addition to basalganglia. They also communicate witheach other, with other limbicstructures to link with motivation,and with other cortical areas to linkwith other planning activities.6

Extrapyramidal control is effected bygamma motor neurons activatingintrafusal muscle fibers. If we needan anatomically rational name for thesystems controlling extrapyramidalmotor function, it might be “basalganglia motor system” or “intrafusalmotor control system.”

Although we touched on basalganglia anatomy in a previous“Psychiatry and Neurology” seriesarticle,3 we will delve a bit furtherhere. Anatomic terms for the basalganglia can be confusing and bearrepeating. The basal ganglia consistof several functionally related nuclei.Basal ganglia circuitry istopographically and functionallyorganized. The basal ganglia includethe caudate, putamen, nucleusaccumbens, globus pallidus andsubthalamic nucleus of the forebrain,and the substantia nigra and ventraltegmental area of the midbrain. Thestriatum (sometimes called theneostriatum) refers to the caudateand putamen. The globus pallidus(sometimes called thepaleostriatum) is the third majorbasal ganglion (nucleus). Corpusstriatum is sometimes used to referto the caudate, putamen, and globuspallidus together. Although not

included in basal ganglia, thepedunculopontine nucleus andseveral thalamic nuclei are highlyintegrated in basal ganglia motorcontrol circuits.4 The ventralstriatum, consisting of the olfactorytubercle and part of the nucleusaccumbens, is quite distinct and partof the limbic system.7,8

Because extrapyramidal motorcontrol involves widely distributedcircuits, it is difficult to assign rolesto particular anatomic locations.However, naturally occurring andneurosurgical lesions do occur inparticular locations, so we still careabout the roles of these nodes in thebroader circuits controllingmovement. The caudate nucleus isinvolved in the more cognitive tasksof motor planning and goalselection.9 The putamen enhancessensorimotor coordination and playsa role in habit learning.10 The globuspallidus is involved incommunication among nuclei of thebasal ganglia. The subthalamicnucleus receives inputs fromthalamus, pedunculopontine nucleus,and cerebral cortex, and projects tosubstantia nigra, pedunculopontinenucleus, and globus pallidus. Thenucleus accumbens and striatum(caudate and putamen) receive mostof their connections from thecortex.11 The striatum receivesglutamatergic, dopaminergic, andserotonergic input. Striatal neuronspredominantly use gamma-aminobutyric acid (GABA), butacetylcholine and others areinvolved.

Neurosurgical treatment ofparkinsonism involves placingstimulating electrodes in one of foursites. Deep brain stimulation (DBS)of the ventral intermediate thalamicnucleus improves tremor.Stimulation of the pedunculopontinenucleus helps with gait freezing. DBSof the subthalamic nucleus andglobus pallidum can be helpful withany parkinsonian signs andsymptoms, and are currently thepreferred sites. Electrodes areusually placed bilaterally. InParkinson’s disease, the movementdisorder to which the technique has

been most applied, DBS plusmedication is more effective thanmedication alone, but thecombination also increases the riskof serious adverse events.12,13

SIGNS AND SYMPTOMSMOVEMENT DISORDERS

Parkinson’s disease andrelated disorders. Many are misledby the terms parkinsonian,parkinsonism, and Parkinson’sdisease. Parkinson’s disease refers toa specific disease, the most commonform of idiopathic parkinsonism. Theother two terms refer to the broadersyndrome, with similar signs andsymptoms but different causes. Themost common other parkinsoniansyndrome is drug-inducedparkinsonism. Along with Parkinson’sdisease, idiopathic parkinsonismincludes the “Parkinson-plus” oratypical Parkinson’s diseases, whichinclude multiple system atrophy,progressive supranuclear palsy,corticobasal degeneration, and Lewybody dementia. Ischemic lesions canalso cause parkinsonism.14–16

Parkinson’s disease often isheralded by autonomic symptoms(orthostatic hypotension,constipation), sleep changes (REMbehavior disorder), and olfactorydeficits,17 but typically the firstsymptom is a rest tremor of onehand. Cardinal signs of Parkinson’sdisease follow the mnemonic TRAP:tremor (rest), rigidity (lead-pipe),akinesia (or bradykinesia), andpostural instability.18 Other“parkinsonian” signs includehypophonia, micrographia, bluntedaffect, low spontaneous blink rate,stooped posture, short-stepped gait,motor restlessness (akathisia), anddystonia. If the presentation istypical and there is nothing in thehistory pointing to another possiblecause, the diagnosis is very likely tobe Parkinson’s disease. If there iscerebellar ataxia, prominent earlyautonomic dysfunction (e.g., fallsdue to orthostatic hypotension),early dementia, pyramidal tractsigns, myoclonus, supranuclear gazepalsy, and prominent apraxia, theother parkinsonian diseases should


be more closely considered.14,18

Dystonia. Idiopathic dystonia(sustained unwanted contraction ofa muscle or muscle group) is easilymissed and misdiagnosed. It presentswith a variety of complaints,including cramping, inability toperform some task (particularlywhen it involves repetitive, fine,manual movements), or unsightlymovements. Dystonic movementscan take on a cyclic pattern and canbe difficult to distinguish fromtremor, and the peculiar movements(in the absence of localizingneurologic findings or abnormal testresults) are often mistaken aspsychogenic. The affected musclegroup may be rigid, but parkinsoniansigns are usually not prominent.Exposures to dopamine-blockingdrugs (even metoclopramide orprochlorperazine) can precipitatedystonia.19

Chorea and athetosis. Themost important hyperkineticmovement disorders in psychiatryfeature chorea and athetosis. Thesemovements are frequently combinedinto choreoathetotic movements, inwhich an abrupt irregular movement(chorea) seems to launch a writhingor stretching movement (athetosis).Most prominent choreoathetoticmovements are attributable tochronic exposure to dopamine-blocking drugs (tardive dyskinesia)or diphenyhydantoin (Dilantin) or toacute exposure to stimulants(sometimes called “crack dancing”).However, they can also be caused byHuntington’s disease (distinguishableby family history and genetictesting), Sydenham’s chorea(associated with a history ofstreptococcal infection), Wilson’sdisease (a disorder of coppermetabolism, usually of adolescentonset), vascular lesions,15 andnumerous other rare disorders.20, 21

Tic disorders. The tic disordersare another type of hyperkineticmovement disorder, dominated bymotor and vocal tics. These arenamed Tourette’s disorder or simplytic disorder, according to whether ornot the patient has ever had vocaltics. These are often comorbid with

obsessive-compulsive disorder; infact, some consider tics to be a formof compulsion. They are a feature ofpediatric autoimmuneneuropsychiatric disorder associatedwith streptococcal infection(PANDAS).22 They also tend to befound in attention deficithyperactivity disorder, even withoutexposure to stimulants. Stimulantscan precipitate tics, which may ormay not remit after the stimulantsare stopped.23

DEMENTIA AND MOVEMENTDISORDERS

Any of the major dementingillnesses can include parkinsoniansigns. Lewy body dementia tends toshow early parkinsonian signs, whichare among its diagnostic criteria.24

Vascular dementia may include earlyparkinsonian signs.25 Although notfamous for it, extrapyramidalmovement disorders can precede theemergence of frontotemporaldementia.26 Later in its course,Alzheimer’s dementia often includesprominent parkinsonian signs.27

SCHIZOPHRENIA AND MOVEMENTDISORDERS

Consistent with a long history ofclinical observation, recent studiesshow that up to a third of patientswith recent-onset, never-medicatedschizophrenia have parkinsoniansigns.28,29 Extrapyramidal signs infirst-break schizophrenia patientspreviously untreated withantipsychotics predict a lowerresponse to typical30 and atypicalantipsychotic drugs.31,32

Dyskinesia or “tardive-likedyskinesia” may be observed in mildform in never-medicatedschizophrenia,28,33 and moreprominently in older and morechronic (but still never-medicated)patients,34–36 as well as some normalpersons, especially the immature37

and elderly.38 Diagnostically, suchmovements (particularly chorea)raise the possibilities of Huntington’sdisease (distinguishable by familyhistory and genetic testing),Sydenham’s chorea, PANDAS,cerebrovascular disease,39 and

numerous other uncommonentities.20,21

DEPRESSION ANDPARKINSONISM

Depression and parkinsonism arestatistically related and share clinicalfeatures. Depression affects nearlyhalf of those with Parkinson’sdisease.18 Also, idiopathic majordepression and parkinsonism sharecertain signs and symptoms, such aspsychomotor retardation/bradykinesia, bluntedaffect/abulia/hypomimia, sleepdisturbances, and apathy. Patientswith melancholic40 or catatonic41

depression in particular may haveparkinsonian signs. Sometimes thesepatients are in an early phase ofidiopathic parkinsonism, but oftenthe parkinsonism resolves with thedepressive episode.

DRUG-INDUCED MOVEMENTDISORDERS

Dopamine-blocking drugs, such asthe antipsychotics (both typical andatypical) and some anti-emeticdrugs, are the most recognizedcauses of secondary extrapyramidalmovement disorders. Parkinsonianside effects almost always arisewithin one week of reaching thenecessary dose or concentration ofthe drug, are reversible, and caninclude any of the motor signs andsymptoms of Parkinson’s disease.When parkinsonian side effects arecaused or aggravated by dopamineblocking drugs, dyskinesia rarelyemerges before four months on thedrug, but the effects often persistafter dopamine blocking drugs havebeen discontinued. Tremor andpostural instability are lessprominent in drug-inducedparkinsonism than in Parkinson’sdisease.42 Dopamine-depleting drugs,such as reserpine and tetrabenazine,can have the same side effects.

Stimulant drugs, such as cocaineand amphetamines, also can havesimilar effects, but via opposingmechanisms. In acute withdrawal, astimulant user can have aparkinsonian presentation,presumably caused by dopamine


depletion. While intoxicated andoften persisting into withdrawal,stimulants can cause dyskinesiasimilar to tardive dyskinesia.43

Antidepressants are known tooccasionally cause both parkinsonismand dyskinesia. This has little to dowith dose or duration of treatment.Duloxetine is over-representedamong case reports ofantidepressant-associated movementdisorders, but there are nosystematic comparisons.44 Serotoninsyndrome, another side effect ofsome antidepressants, can includeprominent dyskinetic movements, soit is important to look for otherserotonin syndrome findings, such asunstable vital signs and delirium.45

Also it should be noted thatantidepressants often inducepostural or action tremors, whichshould be distinguished from resttremor.

Calcium channel blockers mayreduce the risk and slow theprogression of Parkinson’s disease,46

but occasionally appear to havecaused (or precipitated)parkinsonism.47

Many other drugs also can haveparkinsonism effects, including someantihistamines, antiarrythmics,anticonvulsants, andcholinomimetics.42

EXAMINATION METHODSPoverty of movement may present

to simple observation as diminishedgesturing, diminished arm swingwhile walking, or diminished facialexpression (blunted affect orhypomimia, which is a reduceddegree of facial expression).

Hypophonia (soft, thin speech)also shows itself in the interview. Ifasked to speak louder, the patientusually does so only temporarily. Ofcourse, patients sometimesdeliberately speak softly, but thedistinction is almost always obvious.

Micrographia is evident in almostany writing sample. It becomes morepronounced after the first fewletters, so very brief samples may failto capture the effect.48,49 Somehealthy people are habituallymicrographic, but in parkinsonism

the writing becomes smaller and lesslegible with continuation.

Posture is stooped and unstable.Stooped posture is evident whilestanding or sitting, with relativeflexion throughout the spine. Thechin may rest on the chest whileseated. While standing comfortably, alight shove to the chest or back(sufficient to displace the trunk aninch or two) causes the patient tostep backwards or forwards(respectively) or even to losebalance.

Gait is notable for short steps,diminished arm swing, andfestination. Watch the patient walkcasually, and/or ask the patient towalk five steps, turn around, andwalk back to you. If the leading foot’sheel strikes less than a foot-lengthbefore the trailing foot’s toe, stridelength is short. If the heel does notland beyond the tip of the other foot,stride length is markedly shortened.Festination is a tottering forward-leaning gait, in which fairly rapid butshort steps fail to keep up with thecenter of gravity. To execute a 180-degree turn, several steps arerequired. The patient often looksunable to rotate at the waist,sometimes called “en bloc turning.”

The rigidity of parkinsonism is ofthe lead-pipe variety. The relaxedlimb (or neck), moved passively,gives a constant level of resistancethroughout the range of motion,hence the term lead pipe.Sometimes the rigidity can only beappreciated with reinforcement, inwhich the patient is simultaneouslyengaged in some other motor taskwith the other hand. One often hearstalk of “cogwheel” rigidity, whichrefers to a ratcheting sensationproduced by palpable tremor. Lead-pipe rigidity reflects parkinsonism,with or without “cog-wheeling.”Lead-pipe rigidity is distinct from“clasp-knife” rigidity (initialresistance that gives way at a certainpoint in the range of motion). Clasp-knife rigidity, as well as velocity-dependent rigidity (less resistancewhen the imposed movement isslower), reflects spasticity (e.g.,stroke, multiple sclerosis, cerebral

palsy) rather than parkinsonism.Finally, cognitively impaired patientsoften seem to have difficulty relaxingas requested. Active but involuntaryresistance to all movement is calledgegenhalten; this tends to improvewith distraction.

The tremor of parkinsonism is ofthe rest variety. Rest tremor is notedin a limb or other body part at rest,particularly with distraction (patientsoften attempt to quell the tremor). Itcan be intensified by anxiety. Whenthe patient extends the handsunsupported, rest tremor ceases, butit may resume after several secondsmaintaining the posture. Rest tremoris slow (about 4–6 cycles persecond). When rest tremor isprominent in the second digit, sothat it rubs against the palmarsurface of the thumb, this is called“pill-rolling.” There are several othertremors that can be confused withrest tremor, but only two other typesof tremor are seen with anyfrequency. Postural tremor appearspromptly with unsupported posture(such as hands extended), and ismore rapid than rest tremor. This isthe most common tremor inpsychiatry (and in general) andmight be attributed to essentialtremor, anxiety, caffeine,theophylline, lithium, valproate, beta-adrenergic agonists, and/orwithdrawl from alcohol,benzodiazepines, or barbituates.Postural tremor is often mislabeledintention tremor. Intention tremor isseen when a body part (usually afinger) approaches a target andconsists of rhythmic shifting fromone side to the other of the target(dysmetria).

The glabellar (Myerson) reflex isfound in parkinsonism of variousetiologies, as well as in diffusedegenerative brain diseases. Afterexplanation and request to lookforward and to try not to blink, tapfirmly on the glabella (mid-line lowforehead) six times about once every1 to 2 seconds. A blink or partialblink is expected on the first 1 to 3taps, but continuing to blinkthereafter is abnormal. Approach insuch a way that your hand is out of


the patient’s view (to avoid the blinkresponse to visible “threat”). It mayhave high sensitivity for Parkinson’sdisease50 but some studies findsimilar prevalence among theparkinsonian disorders.51 It is notuncommon for patients with otherparkinsonian signs to show noresponse at all to even the first tap.Patients with dyskinesia sometimesblink early, as if anticipating the nexttap.

Blink rate is a rough indicator ofdopaminergic tone.52 A very low rateof spontaneous blinking (<10 perminute) is found in the hypokinetic(parkinsonian) movement disorders,shortly after beginning dopamine-blocking drugs and in some othercases of psychomotor retardation.Rapid blinking (>30 blinks perminute) can be elicited by dopamineagonist drugs and is sometimesfound in hyperkinetic movementdisorders, including Tourette’sdisorder, tardive dyskinesia, andwithdrawal dyskinesia. Numerousother factors, including ocularirritation, anxiety, hostility, andspeaking, can also influence blinkrate.

Motor restlessness (akathisia)may seem an odd companion to theother hypokinetic motor signs, but itfrequently accompanies both theidiopathic parkinsonian disorders anddrug-induced parkinsonism. Itconsists of a subjective urge to moveand an objective excess of movement(usually walking). The patient maycomplain of anxiety, being unable torest or relax, or may report simplyenjoying walking, but will usuallyendorse feeling more comfortablewalking than sitting. Any excess ofmovement, as long as the excessmovement does not consist oftremor, chorea, athetosis, or tic,could be akathisia. The mostconvincing sign of akathisia is pacingso persistent that the patientmarches in place when required tostand still.

Dystonia, the unintended,sustained contraction of a musclegroup, can accompany hyperkineticor hypokinetic syndromes. Thus,dystonia can follow a particular

exposure to antipsychotic (acutedystonia), but it can also be a part oftardive dyskinesia (tardive dystonia).Writer’s cramp and charley horse arecommon types of dystonia. In seriouspsychiatric and neurologic conditions,dystonia more often affects the axialmuscles, causing torticollis orrotation of the lower spine. Theextraocular muscles may also beinvolved (“oculogyric crisis”).Movement tends to elicit dystonia,and anxiety often intensifies it.

Huntingtonian signs (dyskineticsigns, abnormal involuntarymovements) are those characterizingHuntington’s disease, several otherrare hyperkinetic movementdisorders, or resulting from eitheracute exposure to dopamine agonistdrugs or chronic exposure todopamine-blocking drugs (tardivedyskinesia). These signs includechorea, athetosis, tic, and ballisticmovements. Specific examinationprotocols, such as the AbnormalInvoluntary Movement Scale,53 consistof observation with some distractionprocedures. They are important touse routinely, particularly when thepatient has or is at risk for theseabnormalities.

Chorea is a sudden, quick,involuntary movement that can affectany skeletal muscle (including thediaphragm). It is not rhythmic liketremor and not as purposeful-lookingor patterned as tic. Athetosis is aslower movement, often calledwrithing or undulating, thatresembles deliberate stretching of amuscle group. It is most noticeable inthe shoulders, fingers, and lower face.

Tic is also sudden, quick, and notrhythmic, but more patterned andpurposeful in appearance. Commontics include throat clearing, vigorousblinking, sniffing, shaking the head asif to reset the hair, and vocalizing.Vocal tics, characteristic of Tourette’ssyndrome, more often consist ofhumming and meaningless syllablesthan the famous blurting ofexpletives. Tics are sometimes seenin tardive dyskinesia, but much lessoften than chorea.54

Hemiballism is sometimes seenalone or in combination with other

involuntary movements. These areabrupt, large movements of the armand/or leg, typically includingextension and abduction of the limbas if throwing. Sometimes these areprecipitated by similar deliberatemovements (e.g., a ballistic armmovement triggered by deliberatereaching). Basal ganglia lesions, notlimited to the subthalamic nucleus oftradition, cause ballistic movements,but they are also associated withhyperglycemia and humanimmunodeficiency infection (HIV).55

Spontaneous abnormalmovements, such as tremor,dystonia, chorea, tic, and athetosis,are often more evident when thepatient is distracted. Structuredexaminations of movement (such asthe Abnormal Involuntary MovementScale) may include specificinstructions for distraction, but apsychiatric interview or unobtrusiveobservation are at least as effective.

MOVEMENT DISORDERASSESSMENT SCALES

Movement disorder assessmentscales are widely available and oftenused in clinical as well as researchsettings. For hypokinetic orparkinsonian signs, these include theUnified Parkinson’s Disease RatingScale motor exam section,56 and theSimpson-Angus scale.57 Forhyperkinetic or tardive-like signs,these include the UnifiedHuntington’s Disease Rating Scale58

and Abnormal Involuntary MovementScale.53 The ExtrapyramidalSymptoms Rating Scale59 attempts tocover both hyperkinetic andhypokinetic signs.

These assessments can besharpened with the use of somefairly simple instruments. Tremormeasurement can be facilitated withan iPhone app.60 Scaling of movementvelocity exploits the fact that healthypeople moving between two targetshave a maximal velocityproportionate to the distancebetween the targets, but that inparkinsonism there is no suchrelationship.61 Several aspects ofparkinsonism can be assessed using awindows-based system.62 Writing on a


digitizing pad produces sensitive datarelative to subtle parkinsonism.49

Chorea can be quantified sensitivelyand accurately with instrumentsmeasuring force instability, or theability to maintain a constant amountof motor force.63

CONCLUSIONThe extrapyramidal examination,

which consists of observation andvery simple tests, is important inunderstanding the mental status,making psychiatric diagnosis,selecting medication, and monitoringof the effects of medications.

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