[PSYCHIATRY

AND

NEUROLOGY]

Extrapyramidal
Examinations in Psychiatry
by RICHARD D. SANDERS, MD, and PAULETTE MARIE GILLIG, MD, PhD
Dr. Sanders is Associate Professor, Departments of Psychiatry and Neurology, Boonshoft School of
Medicine, Wright State University, and Dayton VA Medical Center, Dayton, Ohio; and Dr. Gillig is
Professor of Psychiatry and Faculty of the Graduate School, Department of Psychiatry, Boonshoft
School of Medicine, Wright State University, Dayton, Ohio.
SERIES EDITOR: Paulette M. Gillig, MD,
PhD, Professor, Department of Psychiatry,
Boonshoft School of Medicine, Wright State
University, Dayton, Ohio
FUNDING: No funding was received for the
development of this article.
FINANCIAL DISCLOSURES: The authors have
no conflicts of interest relevant to the content
of this article.
ADDRESS CORRESPONDENCE TO: Paulette
Gillig, MD, Professor, Dept. of Psychiatry,
Boonshoft School of Medicine, Wright
State University, 627 S. Edwin C. Moses
Blvd., Dayton, OH 45408-1461; E-mail:
paulette.gillig@wright.edu
KEY WORDS: Extrapyramidal signs,
parkinsonian signs, tremor, rigidity, motor
retardation, neurologic examination

Innov Clin Neurosci. 2012;9(78):1016

In this series, Drs. Sanders and Gillig explain

how aspects of the neurological examination
can aid in differential diagnosis of some
common (and some uncommon) disorders
seen in psychiatric practice.

ABSTRACT
Extrapyramidal signs include
increased motor tone, changes in the
amount and velocity of movement,
and involuntary motor activity. They
include two groups of signs and
related disorders: hypokinetic
(similar to Parkinsons disease) and
hyperkinetic (similar to Huntingtons
disease). This article covers some of
the neuroscience behind
extrapyramidal disorders, the
relevance of extrapyramidal signs in
the major psychiatric disorders, the
major extrapyramidal movement
disorders, and how to elicit
extrapyramidal signs.

importance of the basal ganglia in

psychiatric conditions has long been
appreciated.1,2 Also, extrapyramidal
signs and symptoms are very
commonly affected by psychiatric
medications, and monitoring these
effects of treatment is essential in
clinical psychiatry.
Extrapyramidal is a traditional
term that refers to impaired motor
control, usually referable to
dysfunction of the basal ganglia.
Extrapyramidal symptoms consist of
two broad groups of signs and
disorders: hypokinetic (as found in
Parkinsons disease and after shortterm exposure to dopamine-blocking
drugs) and hyperkinetic (as found in
Huntingtons disease and after
chronic exposure to dopamineblocking drugs). Most extrapyramidal
signs are revealed by observation,
and the rest by brief direct
examination.

INTRODUCTION
Of all the parts of a neurologic
examination, nothing is more
essential to daily psychiatric practice
than extrapyramidal motor
functioning. Extrapyramidal function
can affect many aspects of the
mental status examination, such as
speech, affect, and spontaneous
motor activity. Extrapyramidal
disorders (both iatrogenic and
idiopathic) are common in
psychiatric patients, and psychiatric
syndromes are quite common in
patients with extrapyramidal
disorders. Accordingly, the central
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RELEVANT ANATOMY AND

PHYSIOLOGY
Extrapyramidal function refers to
control of motor tone, the amount
and velocity of movement, and the
suppression of undesirable motor
activity. Motor systems other than
the pyramidal (corticospinal) tract
are understandably termed
extrapyramidal, but we should note
that the term was never anatomically
meaningful and has become more
anomalous. Motor coordination,
planning, sequencing, and inhibition,
which we tend to link with the

cerebellum and the frontal lobes, are

not routinely considered
extrapyramidal, but do involve the
basal ganglia as well as cerebellum
and neocortex. Also, the pyramidal
tract is now known to be only one of
several tracts subserving voluntary
motor activity.3
The forebrain basal ganglia are
the brain structures most
responsible for extrapyramidal
control. As discussed in our review
of the voluntary motor system,3
several parallel circuits or loops help
control motor planning and control,4
decision-making, and behavioral
reinforcement.5 These circuits
involve mostly frontal cortex,
cerebellum, thalamus, and limbic
structures in addition to basal
ganglia. They also communicate with
each other, with other limbic
structures to link with motivation,
and with other cortical areas to link
with other planning activities.6
Extrapyramidal control is effected by
gamma motor neurons activating
intrafusal muscle fibers. If we need
an anatomically rational name for the
systems controlling extrapyramidal
motor function, it might be basal
ganglia motor system or intrafusal
motor control system.
Although we touched on basal
ganglia anatomy in a previous
Psychiatry and Neurology series
article,3 we will delve a bit further
here. Anatomic terms for the basal
ganglia can be confusing and bear
repeating. The basal ganglia consist
of several functionally related nuclei.
Basal ganglia circuitry is
topographically and functionally
organized. The basal ganglia include
the caudate, putamen, nucleus
accumbens, globus pallidus and
subthalamic nucleus of the forebrain,
and the substantia nigra and ventral
tegmental area of the midbrain. The
striatum (sometimes called the
neostriatum) refers to the caudate
and putamen. The globus pallidus
(sometimes called the
paleostriatum) is the third major
basal ganglion (nucleus). Corpus
striatum is sometimes used to refer
to the caudate, putamen, and globus
pallidus together. Although not

included in basal ganglia, the

pedunculopontine nucleus and
several thalamic nuclei are highly
integrated in basal ganglia motor
control circuits.4 The ventral
striatum, consisting of the olfactory
tubercle and part of the nucleus
accumbens, is quite distinct and part
of the limbic system.7,8
Because extrapyramidal motor
control involves widely distributed
circuits, it is difficult to assign roles
to particular anatomic locations.
However, naturally occurring and
neurosurgical lesions do occur in
particular locations, so we still care
about the roles of these nodes in the
broader circuits controlling
movement. The caudate nucleus is
involved in the more cognitive tasks
of motor planning and goal
selection.9 The putamen enhances
sensorimotor coordination and plays
a role in habit learning.10 The globus
pallidus is involved in
communication among nuclei of the
basal ganglia. The subthalamic
nucleus receives inputs from
thalamus, pedunculopontine nucleus,
and cerebral cortex, and projects to
substantia nigra, pedunculopontine
nucleus, and globus pallidus. The
nucleus accumbens and striatum
(caudate and putamen) receive most
of their connections from the
cortex.11 The striatum receives
glutamatergic, dopaminergic, and
serotonergic input. Striatal neurons
predominantly use gammaaminobutyric acid (GABA), but
acetylcholine and others are
involved.
Neurosurgical treatment of
parkinsonism involves placing
stimulating electrodes in one of four
sites. Deep brain stimulation (DBS)
of the ventral intermediate thalamic
nucleus improves tremor.
Stimulation of the pedunculopontine
nucleus helps with gait freezing. DBS
of the subthalamic nucleus and
globus pallidum can be helpful with
any parkinsonian signs and
symptoms, and are currently the
preferred sites. Electrodes are
usually placed bilaterally. In
Parkinsons disease, the movement
disorder to which the technique has

been most applied, DBS plus

medication is more effective than
medication alone, but the
combination also increases the risk
of serious adverse events.12,13

SIGNS AND SYMPTOMS

MOVEMENT DISORDERS
Parkinsons disease and
related disorders. Many are misled
by the terms parkinsonian,
parkinsonism, and Parkinsons
disease. Parkinsons disease refers to
a specific disease, the most common
form of idiopathic parkinsonism. The
other two terms refer to the broader
syndrome, with similar signs and
symptoms but different causes. The
most common other parkinsonian
syndrome is drug-induced
parkinsonism. Along with Parkinsons
disease, idiopathic parkinsonism
includes the Parkinson-plus or
atypical Parkinsons diseases, which
include multiple system atrophy,
progressive supranuclear palsy,
corticobasal degeneration, and Lewy
body dementia. Ischemic lesions can
also cause parkinsonism.1416
Parkinsons disease often is
heralded by autonomic symptoms
(orthostatic hypotension,
constipation), sleep changes (REM
behavior disorder), and olfactory
deficits,17 but typically the first
symptom is a rest tremor of one
hand. Cardinal signs of Parkinsons
disease follow the mnemonic TRAP:
tremor (rest), rigidity (lead-pipe),
akinesia (or bradykinesia), and
postural instability.18 Other
parkinsonian signs include
hypophonia, micrographia, blunted
affect, low spontaneous blink rate,
stooped posture, short-stepped gait,
motor restlessness (akathisia), and
dystonia. If the presentation is
typical and there is nothing in the
history pointing to another possible
cause, the diagnosis is very likely to
be Parkinsons disease. If there is
cerebellar ataxia, prominent early
autonomic dysfunction (e.g., falls
due to orthostatic hypotension),
early dementia, pyramidal tract
signs, myoclonus, supranuclear gaze
palsy, and prominent apraxia, the
other parkinsonian diseases should

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be more closely considered.14,18

Dystonia. Idiopathic dystonia
(sustained unwanted contraction of
a muscle or muscle group) is easily
missed and misdiagnosed. It presents
with a variety of complaints,
including cramping, inability to
perform some task (particularly
when it involves repetitive, fine,
manual movements), or unsightly
movements. Dystonic movements
can take on a cyclic pattern and can
be difficult to distinguish from
tremor, and the peculiar movements
(in the absence of localizing
neurologic findings or abnormal test
results) are often mistaken as
psychogenic. The affected muscle
group may be rigid, but parkinsonian
signs are usually not prominent.
Exposures to dopamine-blocking
drugs (even metoclopramide or
prochlorperazine) can precipitate
dystonia.19
Chorea and athetosis. The
most important hyperkinetic
movement disorders in psychiatry
feature chorea and athetosis. These
movements are frequently combined
into choreoathetotic movements, in
which an abrupt irregular movement
(chorea) seems to launch a writhing
or stretching movement (athetosis).
Most prominent choreoathetotic
movements are attributable to
chronic exposure to dopamineblocking drugs (tardive dyskinesia)
or diphenyhydantoin (Dilantin) or to
acute exposure to stimulants
(sometimes called crack dancing).
However, they can also be caused by
Huntingtons disease (distinguishable
by family history and genetic
testing), Sydenhams chorea
(associated with a history of
streptococcal infection), Wilsons
disease (a disorder of copper
metabolism, usually of adolescent
onset), vascular lesions,15 and
numerous other rare disorders.20, 21
Tic disorders. The tic disorders
are another type of hyperkinetic
movement disorder, dominated by
motor and vocal tics. These are
named Tourettes disorder or simply
tic disorder, according to whether or
not the patient has ever had vocal
tics. These are often comorbid with
12

obsessive-compulsive disorder; in
fact, some consider tics to be a form
of compulsion. They are a feature of
pediatric autoimmune
neuropsychiatric disorder associated
with streptococcal infection
(PANDAS).22 They also tend to be
found in attention deficit
hyperactivity disorder, even without
exposure to stimulants. Stimulants
can precipitate tics, which may or
may not remit after the stimulants
are stopped.23

DEMENTIA AND MOVEMENT

DISORDERS
Any of the major dementing
illnesses can include parkinsonian
signs. Lewy body dementia tends to
show early parkinsonian signs, which
are among its diagnostic criteria.24
Vascular dementia may include early
parkinsonian signs.25 Although not
famous for it, extrapyramidal
movement disorders can precede the
emergence of frontotemporal
dementia.26 Later in its course,
Alzheimers dementia often includes
prominent parkinsonian signs.27

SCHIZOPHRENIA AND MOVEMENT

DISORDERS
Consistent with a long history of
clinical observation, recent studies
show that up to a third of patients
with recent-onset, never-medicated
schizophrenia have parkinsonian
signs.28,29 Extrapyramidal signs in
first-break schizophrenia patients
previously untreated with
antipsychotics predict a lower
response to typical30 and atypical
antipsychotic drugs.31,32
Dyskinesia or tardive-like
dyskinesia may be observed in mild
form in never-medicated
schizophrenia,28,33 and more
prominently in older and more
chronic (but still never-medicated)
patients,3436 as well as some normal
persons, especially the immature37
and elderly.38 Diagnostically, such
movements (particularly chorea)
raise the possibilities of Huntingtons
disease (distinguishable by family
history and genetic testing),
Sydenhams chorea, PANDAS,
cerebrovascular disease,39 and

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numerous other uncommon

entities.20,21

DEPRESSION AND
PARKINSONISM
Depression and parkinsonism are
statistically related and share clinical
features. Depression affects nearly
half of those with Parkinsons
disease.18 Also, idiopathic major
depression and parkinsonism share
certain signs and symptoms, such as
psychomotor retardation/
bradykinesia, blunted
affect/abulia/hypomimia, sleep
disturbances, and apathy. Patients
with melancholic40 or catatonic41
depression in particular may have
parkinsonian signs. Sometimes these
patients are in an early phase of
idiopathic parkinsonism, but often
the parkinsonism resolves with the
depressive episode.

DRUG-INDUCED MOVEMENT
DISORDERS
Dopamine-blocking drugs, such as
the antipsychotics (both typical and
atypical) and some anti-emetic
drugs, are the most recognized
causes of secondary extrapyramidal
movement disorders. Parkinsonian
side effects almost always arise
within one week of reaching the
necessary dose or concentration of
the drug, are reversible, and can
include any of the motor signs and
symptoms of Parkinsons disease.
When parkinsonian side effects are
caused or aggravated by dopamine
blocking drugs, dyskinesia rarely
emerges before four months on the
drug, but the effects often persist
after dopamine blocking drugs have
been discontinued. Tremor and
postural instability are less
prominent in drug-induced
parkinsonism than in Parkinsons
disease.42 Dopamine-depleting drugs,
such as reserpine and tetrabenazine,
can have the same side effects.
Stimulant drugs, such as cocaine
and amphetamines, also can have
similar effects, but via opposing
mechanisms. In acute withdrawal, a
stimulant user can have a
parkinsonian presentation,
presumably caused by dopamine

depletion. While intoxicated and

often persisting into withdrawal,
stimulants can cause dyskinesia
similar to tardive dyskinesia.43
Antidepressants are known to
occasionally cause both parkinsonism
and dyskinesia. This has little to do
with dose or duration of treatment.
Duloxetine is over-represented
among case reports of
antidepressant-associated movement
disorders, but there are no
systematic comparisons.44 Serotonin
syndrome, another side effect of
some antidepressants, can include
prominent dyskinetic movements, so
it is important to look for other
serotonin syndrome findings, such as
unstable vital signs and delirium.45
Also it should be noted that
antidepressants often induce
postural or action tremors, which
should be distinguished from rest
tremor.
Calcium channel blockers may
reduce the risk and slow the
progression of Parkinsons disease,46
but occasionally appear to have
caused (or precipitated)
parkinsonism.47
Many other drugs also can have
parkinsonism effects, including some
antihistamines, antiarrythmics,
anticonvulsants, and
cholinomimetics.42

EXAMINATION METHODS
Poverty of movement may present
to simple observation as diminished
gesturing, diminished arm swing
while walking, or diminished facial
expression (blunted affect or
hypomimia, which is a reduced
degree of facial expression).
Hypophonia (soft, thin speech)
also shows itself in the interview. If
asked to speak louder, the patient
usually does so only temporarily. Of
course, patients sometimes
deliberately speak softly, but the
distinction is almost always obvious.
Micrographia is evident in almost
any writing sample. It becomes more
pronounced after the first few
letters, so very brief samples may fail
to capture the effect.48,49 Some
healthy people are habitually
micrographic, but in parkinsonism

the writing becomes smaller and less

legible with continuation.
Posture is stooped and unstable.
Stooped posture is evident while
standing or sitting, with relative
flexion throughout the spine. The
chin may rest on the chest while
seated. While standing comfortably, a
light shove to the chest or back
(sufficient to displace the trunk an
inch or two) causes the patient to
step backwards or forwards
(respectively) or even to lose
balance.
Gait is notable for short steps,
diminished arm swing, and
festination. Watch the patient walk
casually, and/or ask the patient to
walk five steps, turn around, and
walk back to you. If the leading foots
heel strikes less than a foot-length
before the trailing foots toe, stride
length is short. If the heel does not
land beyond the tip of the other foot,
stride length is markedly shortened.
Festination is a tottering forwardleaning gait, in which fairly rapid but
short steps fail to keep up with the
center of gravity. To execute a 180degree turn, several steps are
required. The patient often looks
unable to rotate at the waist,
sometimes called en bloc turning.
The rigidity of parkinsonism is of
the lead-pipe variety. The relaxed
limb (or neck), moved passively,
gives a constant level of resistance
throughout the range of motion,
hence the term lead pipe.
Sometimes the rigidity can only be
appreciated with reinforcement, in
which the patient is simultaneously
engaged in some other motor task
with the other hand. One often hears
talk of cogwheel rigidity, which
refers to a ratcheting sensation
produced by palpable tremor. Leadpipe rigidity reflects parkinsonism,
with or without cog-wheeling.
Lead-pipe rigidity is distinct from
clasp-knife rigidity (initial
resistance that gives way at a certain
point in the range of motion). Claspknife rigidity, as well as velocitydependent rigidity (less resistance
when the imposed movement is
slower), reflects spasticity (e.g.,
stroke, multiple sclerosis, cerebral

palsy) rather than parkinsonism.

Finally, cognitively impaired patients
often seem to have difficulty relaxing
as requested. Active but involuntary
resistance to all movement is called
gegenhalten; this tends to improve
with distraction.
The tremor of parkinsonism is of
the rest variety. Rest tremor is noted
in a limb or other body part at rest,
particularly with distraction (patients
often attempt to quell the tremor). It
can be intensified by anxiety. When
the patient extends the hands
unsupported, rest tremor ceases, but
it may resume after several seconds
maintaining the posture. Rest tremor
is slow (about 46 cycles per
second). When rest tremor is
prominent in the second digit, so
that it rubs against the palmar
surface of the thumb, this is called
pill-rolling. There are several other
tremors that can be confused with
rest tremor, but only two other types
of tremor are seen with any
frequency. Postural tremor appears
promptly with unsupported posture
(such as hands extended), and is
more rapid than rest tremor. This is
the most common tremor in
psychiatry (and in general) and
might be attributed to essential
tremor, anxiety, caffeine,
theophylline, lithium, valproate, betaadrenergic agonists, and/or
withdrawl from alcohol,
benzodiazepines, or barbituates.
Postural tremor is often mislabeled
intention tremor. Intention tremor is
seen when a body part (usually a
finger) approaches a target and
consists of rhythmic shifting from
one side to the other of the target
(dysmetria).
The glabellar (Myerson) reflex is
found in parkinsonism of various
etiologies, as well as in diffuse
degenerative brain diseases. After
explanation and request to look
forward and to try not to blink, tap
firmly on the glabella (mid-line low
forehead) six times about once every
1 to 2 seconds. A blink or partial
blink is expected on the first 1 to 3
taps, but continuing to blink
thereafter is abnormal. Approach in
such a way that your hand is out of

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the patients view (to avoid the blink

response to visible threat). It may
have high sensitivity for Parkinsons
disease50 but some studies find
similar prevalence among the
parkinsonian disorders.51 It is not
uncommon for patients with other
parkinsonian signs to show no
response at all to even the first tap.
Patients with dyskinesia sometimes
blink early, as if anticipating the next
tap.
Blink rate is a rough indicator of
dopaminergic tone.52 A very low rate
of spontaneous blinking (<10 per
minute) is found in the hypokinetic
(parkinsonian) movement disorders,
shortly after beginning dopamineblocking drugs and in some other
cases of psychomotor retardation.
Rapid blinking (>30 blinks per
minute) can be elicited by dopamine
agonist drugs and is sometimes
found in hyperkinetic movement
disorders, including Tourettes
disorder, tardive dyskinesia, and
withdrawal dyskinesia. Numerous
other factors, including ocular
irritation, anxiety, hostility, and
speaking, can also influence blink
rate.
Motor restlessness (akathisia)
may seem an odd companion to the
other hypokinetic motor signs, but it
frequently accompanies both the
idiopathic parkinsonian disorders and
drug-induced parkinsonism. It
consists of a subjective urge to move
and an objective excess of movement
(usually walking). The patient may
complain of anxiety, being unable to
rest or relax, or may report simply
enjoying walking, but will usually
endorse feeling more comfortable
walking than sitting. Any excess of
movement, as long as the excess
movement does not consist of
tremor, chorea, athetosis, or tic,
could be akathisia. The most
convincing sign of akathisia is pacing
so persistent that the patient
marches in place when required to
stand still.
Dystonia, the unintended,
sustained contraction of a muscle
group, can accompany hyperkinetic
or hypokinetic syndromes. Thus,
dystonia can follow a particular
14

exposure to antipsychotic (acute

dystonia), but it can also be a part of
tardive dyskinesia (tardive dystonia).
Writers cramp and charley horse are
common types of dystonia. In serious
psychiatric and neurologic conditions,
dystonia more often affects the axial
muscles, causing torticollis or
rotation of the lower spine. The
extraocular muscles may also be
involved (oculogyric crisis).
Movement tends to elicit dystonia,
and anxiety often intensifies it.
Huntingtonian signs (dyskinetic
signs, abnormal involuntary
movements) are those characterizing
Huntingtons disease, several other
rare hyperkinetic movement
disorders, or resulting from either
acute exposure to dopamine agonist
drugs or chronic exposure to
dopamine-blocking drugs (tardive
dyskinesia). These signs include
chorea, athetosis, tic, and ballistic
movements. Specific examination
protocols, such as the Abnormal
Involuntary Movement Scale,53 consist
of observation with some distraction
procedures. They are important to
use routinely, particularly when the
patient has or is at risk for these
abnormalities.
Chorea is a sudden, quick,
involuntary movement that can affect
any skeletal muscle (including the
diaphragm). It is not rhythmic like
tremor and not as purposeful-looking
or patterned as tic. Athetosis is a
slower movement, often called
writhing or undulating, that
resembles deliberate stretching of a
muscle group. It is most noticeable in
the shoulders, fingers, and lower face.
Tic is also sudden, quick, and not
rhythmic, but more patterned and
purposeful in appearance. Common
tics include throat clearing, vigorous
blinking, sniffing, shaking the head as
if to reset the hair, and vocalizing.
Vocal tics, characteristic of Tourettes
syndrome, more often consist of
humming and meaningless syllables
than the famous blurting of
expletives. Tics are sometimes seen
in tardive dyskinesia, but much less
often than chorea.54
Hemiballism is sometimes seen
alone or in combination with other

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involuntary movements. These are

abrupt, large movements of the arm
and/or leg, typically including
extension and abduction of the limb
as if throwing. Sometimes these are
precipitated by similar deliberate
movements (e.g., a ballistic arm
movement triggered by deliberate
reaching). Basal ganglia lesions, not
limited to the subthalamic nucleus of
tradition, cause ballistic movements,
but they are also associated with
hyperglycemia and human
immunodeficiency infection (HIV).55
Spontaneous abnormal
movements, such as tremor,
dystonia, chorea, tic, and athetosis,
are often more evident when the
patient is distracted. Structured
examinations of movement (such as
the Abnormal Involuntary Movement
Scale) may include specific
instructions for distraction, but a
psychiatric interview or unobtrusive
observation are at least as effective.

MOVEMENT DISORDER
ASSESSMENT SCALES
Movement disorder assessment
scales are widely available and often
used in clinical as well as research
settings. For hypokinetic or
parkinsonian signs, these include the
Unified Parkinsons Disease Rating
Scale motor exam section,56 and the
Simpson-Angus scale.57 For
hyperkinetic or tardive-like signs,
these include the Unified
Huntingtons Disease Rating Scale58
and Abnormal Involuntary Movement
Scale.53 The Extrapyramidal
Symptoms Rating Scale59 attempts to
cover both hyperkinetic and
hypokinetic signs.
These assessments can be
sharpened with the use of some
fairly simple instruments. Tremor
measurement can be facilitated with
an iPhone app.60 Scaling of movement
velocity exploits the fact that healthy
people moving between two targets
have a maximal velocity
proportionate to the distance
between the targets, but that in
parkinsonism there is no such
relationship.61 Several aspects of
parkinsonism can be assessed using a
windows-based system.62 Writing on a

digitizing pad produces sensitive data

relative to subtle parkinsonism.49
Chorea can be quantified sensitively
and accurately with instruments
measuring force instability, or the
ability to maintain a constant amount
of motor force.63

12.

13.

CONCLUSION
The extrapyramidal examination,
which consists of observation and
very simple tests, is important in
understanding the mental status,
making psychiatric diagnosis,
selecting medication, and monitoring
of the effects of medications.

14.

15.

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