335
Clinical Pearls in Tremor and Other Hyperkinetic
Movement Disorders
Howard D. Weiss, MD1
1 Department of Neurology, Johns Hopkins University School of
Medicine, Baltimore, Maryland
Semin Neurol 2016;36:335–341.
Abstract Hyperkinetic movements, such as tremor, myoclonus, chorea, and dystonia, occur in
Keywords many neurologic and medical conditions. Accurate clinical evaluation is the important
► tremor first step for the proper diagnosis and treatment of patients with abnormal movements.
► chorea
► dystonia
► myoclonus
► athetosis
► tics
► essential tremor
► Parkinson disease
Familiarity with the clinical evaluation of patients with hyper-
kinetic movement disorders is relevant to every neurologist,
regardless of subspecialty interest. The most common hyper-
kinetic movement disorder is tremor. Approximately 5% of the
population develops either Parkinson’s disease (PD) or essen-
tial tremor (ET) by age 70.1 Other frequent causes of tremor,
such as enhanced physiologic tremor and medication-induced
tremors, affect every age group. Tremor is also seen in several
less common but important neurologic disorders, such as
dystonias, neuropathies, and Wilson’s disease. Chorea, dysto-
nia, myoclonus, tics, and other hyperkinetic movements occur
in a wide spectrum of disorders.
No specific biologic marker or test is available to diagnose
most of the conditions that cause hyperkinetic movement
disorders. The critical first step in evaluating patients with
excessive involuntary movement is knowledge of the clinical
phenomenology of the specific syndromes.
Phenomenology of Hyperkinetic Movement
Disorders
Tremor is the rhythmic oscillation of a body part (e.g., hand,
foot, tongue, head). In most disorders, the rhythmic oscilla-
tions recur with the same number of cycles/s, but the ampli-
tude may vary at different times.
Issue Theme Pearls and Pitfalls, Part 1;
Guest Editors, Justin C. McArthur, MBBS,
MPH, FAAN, FANA, and Nicoline Schiess,
MD, MPH
Address for correspondence Howard D. Weiss, MD, Department of
Neurology, Johns Hopkins University School of Medicine, 2411 W.
Belvedere Ave, Suite 201, Baltimore, MD 21215
(e-mail: howdyweiss@aol.com).
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Chorea is characterized by spontaneous brief, irregular,
randomly flowing involuntary movements that are not rhyth-
mic. Patients might be unaware of the movements, and
appear to be “fidgety” or restless. Patients with chorea often
incorporate the involuntary movement into a voluntary
movement (e.g., crossing and uncrossing the legs, rubbing
the chin), a phenomenon referred to as parakinesis.
The “dance-like” movements of chorea are sometimes
accompanied by athetosis, which refers to twisting and
writhing components that resemble dystonia. When chorea
is severe and affects proximal muscles, it creates a flinging
movement referred to as ballismus.
Dyskinesia is the term used to describe the intermittent
choreiform movements affecting the face, limbs, or trunk that
occur in some PD patients as a complication of treatment with
levodopa. Tardive dyskinesia refers to the persistent chorei-
form movements, especially affecting the mouth or tongue,
associated with prolonged exposure to dopamine-blocking
medications (e.g., neuroleptics, metoclopramide).
Dystonia is characterized by sustained or intermittent
muscle contraction, causing abnormal movement, postures,
or both. Dystonia is often initiated or worsened by voluntary
muscle action. Sometimes, dystonic movements affecting the
hands, head, or other body parts are very brief, resembling
myoclonic jerks or causing tremor (the latter referred to as
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336 Clinical Pearls in Tremor and Other Hyperkinetic Movement Disorders Weiss

Table 1 Subcategories of hyperkinetic movement disorders The most useful classification of tremor is based on observing
the position of maximal activation of the tremor: at rest, with
Rhythmic movements voluntary movement, or with maintenance of posture.3
Tremor Rest tremor refers to tremor in a body part that is not
Dystonia undergoing voluntary muscle contraction (e.g., tremor in the
fingers when the patient is sitting still with hands in lap, or
Jerky movements
hand tremor while walking with hands at the side).
Chorea Action tremor refers to tremors provoked with voluntary
Ballismus muscle contraction. Action tremors can be further
Dyskinesias subcategorized:
Postural tremor occurs when holding a body part motionless
Myoclonus
against gravity (such as tremor seen in the outstretched hands).
Tic disorders Kinetic tremor refers to tremor during active voluntary
Abnormal postures movements. This includes task-specific tremors such as when
Dystonia writing, and intention tremor, which is tremor with goal-
directed movements (such as pouring water from cup to cup
or on finger-nose-finger testing). Intention tremors worsen as
the body part (e.g., finger) nears the target.
dystonic tremor). Depending on the etiology, dystonia can be This classification of tremors provides clues to the etiology
a focal, segmental, or generalized phenomenon. Dystonia of the tremor (see ►Table 2).
patients might also develop tremor in regions not affected
by dystonia (referred to as tremor-associated dystonia).
Physiologic Tremor and Enhanced

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Myoclonus produces rapid, brief shock-like movements
Physiologic Tremor
caused by sudden muscle contraction (positive myoclonus)
or a sudden decrease in muscle tone (negative myoclonus) as Physiologic tremor is present in healthy people of all ages. The
occurs in asterixis. The distribution of the myoclonic jerks can amplitude of this tremor is so small that it is generally unnoticed,
be focal, multifocal, segmental, or generalized depending on or only seen when required to make very precise movements,
the underlying cause. Myoclonus can be isolated or repetitive, such as when threading a small needle or performing microsur-
and in some situations might be confused with tremor, gery. However, the amplitude of physiologic tremor intensifies
chorea, myokymia, or fasciculations. Myokymia and fascicu- and becomes clinically apparent under periods of great anxiety
lations are of lower amplitude, and do not cause movement or stress. This phenomenon, known as enhanced physiologic
across a joint as is likely to occur in myoclonus. tremor, is what causes individuals to tremble when speaking in
Tics are repetitive, rapid, stereotyped, unwanted muscle public or when taking an important test.4
contractions causing abnormal movements (motor tics) or Enhanced physiologic tremor (EPT) is usually a postural
sounds (phonic tics). Motor tics may be simple (resembling tremor in the outstretched hands, and is bilateral and sym-
myoclonus or choreic jerks) or complex (coordinated sequen- metrical with a frequency of 8 to 12 Hz. Enhanced physiologic
ces of movement such as head shaking). Phonic tics may be
simple (e.g., clearing the throat) or complex (e.g., identifiable
verbalizations including coprolalia). Premonitory sensory Table 2 Activating conditions of tremor in neurologic disorders
urges often precede the tics, and are alleviated after the tic
Underlying cause: Rest Postural Intention
release. This is a feature that distinguishes tics from other
tremor tremor tremor
disorders such as myoclonus, chorea, or dyskinesia. Tics may
be suppressed volitionally to some extent. Over time, tics may Parkinson’s disease þþ  
come and go or change in character. Tics are to be distin- Parkinson’s-plus disorders þ þ þ
guished from stereotypies, which are repetitive, ritualistic, Rubral (Holmes) tremor þ þ þ
suppressible, coordinated movements (e.g., body rocking)
Drug-induced þþ þ þ
that recur without change over time (►Table 1). parkinsonism
Essential tremor  þþ þþ
Clinical Phenomenology of Tremor Enhanced physiologic  þþ þ
tremor
Tremor can be classified on the basis of its frequency (oscil-
lations/s) and amplitude. Parkinsonian rest tremors usually Cerebellar tremor  þ þþ
range from 3 to 6 Hz, whereas the postural tremors seen in Dystonic tremor þ þ þ
essential tremor are usually in the range of 4 to 12 Hz, and Neuropathic tremor þ þ þþ
enhanced physiologic tremor is usually 8 to 12 Hz. However,
Psychogenic tremor þ þ þ
it is the amplitude of tremor rather than the number of
oscillations/s that correlates with patient embarrassment or Abbreviations: -, not noted;  , infrequently noted; þ, sometimes noted;
disability.2 þþ, characteristically noted.

Seminars in Neurology Vol. 36 No. 4/2016

 Clinical Pearls in Tremor and Other Hyperkinetic Movement Disorders
tremor might also affect voice, handwriting, and other fine
motor skills. The amplitude of EPT is proportional to the
degree of stress and anxiety.
Physiologic tremor is caused by the sum of several
“peripheral” interacting mechanisms in conjunction with
a central nervous system oscillator. Under stress, the
neurons in the central oscillator become entrained, which
amplifies the tremor, causing EPT. The clinical manifesta-
tions of EPT resemble ET, but physiologically the two
conditions are not the same. For example, limb weights
reduce both the amplitude and frequency of EPT, but
reduce the amplitude without altering the frequency
in ET.5,6
Patients with PD, ET, and other hyperkinetic movement
disorders (e.g., chorea, dyskinesia) often note that their
involuntary movements are more intense from time to
time. An important factor in causing an increase in the
severity of symptoms is the role of EPT in augmenting and
exacerbating involuntary movements in patients with under-
lying movement disorders (see ►Table 3).
For example, patients with mild PD or ET and relatively
subtle tremors are likely to shake very noticeably in the
setting of fever or when being interviewed for a new job.
Dyskinesia, chorea, tics, and other hyperkinetic movements
may also become much more prominent in stressful
situations. Patients are not always aware of the role of
stress in accentuating involuntary movements. It is useful
to discuss the role of emotional factors and other triggers
for increased tremor with patients, as this insight will help
them better understand and manage their symptoms.
Certain medications and medical conditions might also
trigger EPT.7 These too can induce tremor in patients with
no underlying neurologic disorder, or greatly magnify
shaking in patients with underlying movement disorders
(see ►Table 4). In most cases, the tremor-inducing effect of
these substances is a dose-related phenomenon. For exam-
ple, someone might tolerate a cup or two of caffeinated
coffee without problems, but become shaky after four or
more cups.
Table 3 Factors that induce enhanced physiologic tremor
(causing tremor in normal individuals or exacerbating
involuntary movements in patients with movement disorders)
Stress
Anxiety
Fever
Cold (shivering)
Excitement
Anger
Fear
Fatigue
Mental activity
Weiss 337
Table 4 Medications and medical conditions that cause
enhanced physiologic tremor
Lithium
Sodium valproate
Bronchodilators (e.g., theophylline, terbutaline)
Psychostimulants (e.g., cocaine, amphetamines, MDMA
(“ecstasy”)
Amiodarone
Mexiletine
Cyclosporine
Hypercaffeinism
Hypoglycemia
Hyperthyroidism / excessive thyroid replacement therapy
Alcohol or drug withdrawal syndromes
Toxins (e.g., mercury, lead)
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Acute or Subacute Onset of Tremor and Other
Involuntary Movements
Most of the neurologic disorders associated with tremor are
chronic conditions. The abrupt onset of bilateral tremor postural,
kinetic tremor, multifocal myoclonus, and asterixis (alone or in
isolation) should immediately bring to mind the likelihood of
intoxications, withdrawal syndromes, and metabolic disorders
(e.g., hepatic encephalopathy, renal failure). Myoclonus-inducing
drugs in the setting of renal insufficiency include amantadine,
acyclovir, dobutamine, gabapentin, meperidine, and antibiotics
(ciprofloxacin, penicillins, cephalosporins).
Abnormal movements induced by intoxication with psychos-
timulants (e.g., cocaine, amphetamines, methylenedioxyme-
thamphetamine [MDMA] or “ecstasy” and some of the
synthetic cannabinoids known on the street as “Spice” or “K2”
and “Bath Salts” or synthetic cathinones) are familiar to physi-
cians working in the emergency room. Symptoms might include
combinations of tremor, agitation, hyperactivity, dyskinesias,
dystonias, choreoathetosis, myoclonus, and stereotypies.8 Spice
and Bath Salts can also cause seizures, extreme swings in heart
rate and blood pressure, kidney and respiratory failure, psychotic
behavior, and hallucinations.
An acute dystonic reaction due to dopamine-blocking
medications (e.g., prochlorperazine for nausea or neurolep-
tics) should be considered in patients developing sudden
abnormal posturing or movements (e.g., opisthotonos, buc-
colingual spasms, oculogyric crisis). This phenomenon is
often misdiagnosed as a seizure disorder or psychogenic.
Another important consideration in patients with sub-
acute onset of tremor is serotonin syndrome. There are many
medications that can interact to trigger excessive agonism of
central and peripheral serotonin receptors. In full-blown
cases of serotonin syndrome, patients not only have tremor,
but also diaphoresis, agitation, hyperreflexia, clonus, and
potentially life-threatening autonomic dysfunction. Milder
Seminars in Neurology Vol. 36 No. 4/2016
338 Clinical Pearls in Tremor and Other Hyperkinetic Movement Disorders
cases are often overlooked, and misdiagnosis of this prevent-
able disorder is common.9
Rest Tremor
Rest tremor is associated with PD, and to a lesser extent some
Parkinson’s-plus disorders (e.g., multiple system atrophy,
progressive supranuclear palsy, dementia with Lewy bodies).
In PD, the rest tremor starts unilaterally, usually affecting the
distal limbs (e.g., fingers, hand, toes, foot), progressing over
the years to become bilateral.
Some PD patients do not have tremor, and in other cases the
PD rest tremor is not only intermittent, but may be quite subtle. If
the rest tremor is not appreciated on initial examination, it is
useful to have the patient perform a mental task (such as “serial
7s”) or discuss an unpleasant life event while sitting in a chair
with arms relaxed half pronated in the lap. Distraction and stress
exacerbate tremor and often will elicit rest tremors in the fingers,
hand, or foot that might otherwise be overlooked (see ►Table 5).
Rest tremors that are bilateral and symmetrical from the
onset are less common in PD, and raise the suspicion of other
diseases known to mimic PD or drug-induced parkinsonism.
Drug-induced parkinsonism is frequently misdiagnosed as
PD or is not diagnosed at all (particularly in akinetic rigid
patients without prominent tremor). The parkinsonian side
effects of neuroleptics and other dopamine-blocking agents
(e.g., metoclopramide, prochlorperazine) often persist for
6 months or longer after the offending agent is eliminated.
Consequently, the patient history must include inquiries
about not only current but also past medication intake if
one is to detect drug-induced parkinsonism.10
Patients with early PD often report that tremor is their
initial or only symptom. Although tremor is a symptom that
might promptly bring people to seek medical attention, it is
rarely the only finding on examination. The experienced
clinician is often struck by manifestations of bradykinesia
such as masked facies, decreased blink frequency, micro-
graphia, unilaterally decreased arm swing while walking,
body bradykinesia (sitting still without squirming), and fin-
gers that are held in flexion and adduction while seated.
Questioning the patient about loss of sense of smell, and
asking the spouse about dream-enactment behaviors (which
might suggest rapid eye-movement [REM] sleep-behavioral
disorder) are additional clues to establish a likely diagnosis of
early PD in patients with subtle clinical signs.11 A diminished
sense of smell and REM sleep-behavioral disorder are known
to precede motor manifestations of PD by many years in a
substantial number of patients.12
Table 5 Tricks to activate subtle parkinsonian rest tremors
Performing mental tasks (e.g., “serial 7s”) with hands,
feet at rest
Discuss emotionally charges issues
Observing hands and fingers while patient is walking
Observing hand or foot while contralateral limb is being
moved (the contralateral tapping test)
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Dystonia and Rest Tremor
The initial clinical diagnosis of PD is not always accurate. Early
in their course, multiple system atrophy, progressive supra-
nuclear palsy, corticobasal syndrome, and vascular parkin-
sonism can easily be confused with PD. In clinical trials of
neuroprotection, 10 to 15% of patients diagnosed with early
PD by expert clinicians were found to have scans without
evidence of dopaminergic deficits (“SWEDDs”), on functional
imaging studies. The normal scans mitigate against the
diagnosis of PD.13 In the subgroup of SWEDDs patients
with asymmetric rest tremors, many have been subsequently
diagnosed with a previously underrecognized disorder, adult-
onset dystonic tremor, rather than PD.14,15
In long-term follow-up, the SWEDDS patients with dystonic
tremor experienced very mild clinical progression, and did not
develop true bradykinesia, which is the true sine qua non of PD.
One-half of the SWEDDs patients had a positive family history
(much higher than found in patients who actually had PD). The
dystonic signs were subtle and easily overlooked in the
SWEDDs patients with adult-onset dystonic tremor.16
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Shaky Heads and Trembling Faces
Patients with shaky heads and trembling facial movement are
often a source of diagnostic confusion between ET, PD, dyskine-
sia, and dystonia (see ►Table 6). For example, tremulous head
movements occur in some patients with cervical dystonia. If the
dystonia is mild, dystonic tremor of the head can be easily
misdiagnosed as the head tremor associated with ET.
Parkinson’s disease seldom causes head tremor, but is
associated with tremor of the tongue, chin, or mouth, none
of which are common features of ET. Levodopa-induced
dyskinesias in PD often affect the face, with peculiar grimac-
ing, head bobbing, or bruxism. The patient may be unaware of
the facial dyskinesias, but the peculiar movements might
distress other family members. Chewing, lip smacking, and
abnormal tongue movements are signs of tardive dyskinesia
in patients receiving long-term neuroleptic therapy or other
dopamine-blocking drugs.
Severe bilateral disease of the cerebellum or cerebellar
peduncles can cause titubation, a slow (2–3 Hz) rhythmic
oscillation of the head that is usually accompanied by postural
and intention tremors of the limbs.
All of these movements need to be distinguished from
rabbit syndrome, the fine rapid mouth movements that
resemble a rabbit’s chewing movements, which is a dyskine-
sia associated with the use of neuroleptics and other dopa-
mine-blocking drugs.17
Postural and Action Tremor
Patients with ET have chronic bilateral postural tremors in the
hands, often accompanied by kinetic and intention tremor.
Head tremor and voice tremor occur in 10 - 30% of ET cases.
There may be some asymmetry, but ET seldom causes unilat-
eral hand tremor as is seen in PD. Patients with ET might have
mild cogwheel rigidity, but there should be no gait disorder,
 Clinical Pearls in Tremor and Other Hyperkinetic Movement Disorders
Table 6 Differential diagnosis of shaky heads and trembling faces
Head tremor Lip, chin, tongue tremor
Essential tremor þ 
Cervical dystonia þ 
Neuroleptic therapy  þ
Parkinson disease  þ
Levodopa-induced dyskinesias in PD  
Abbreviations: -, not noted;  , seldom noted; þ, occasionally noted; þþ, characteristic; PD, Parkinson’s disease.
bradykinesia or other signs that would suggest a parkinso-
nian disorder. Obtaining a writing sample (including drawing
a spiral, drawing the face of the clock, and writing a lengthy
sentence) is informative in evaluating every tremor patient.
Handwriting and spiral drawing is large and shaky in ET
(unlike the small cramped micrographia of PD).
Essential tremor can begin at any age, but becomes more
prevalent in later life and is the most common movement
disorder, affecting perhaps 3 to 4% by age 70. A positive family
history suggesting autosomal dominant inheritance is
obtained in 50 to 75% of cases of ET.18
There are many specific activities that are likely impaired by
ET and other disorders causing action tremor (see ►Table 7).
Although the diagnosis of ET seems straightforward, it is
often misdiagnosed as PD or overdiagnosed.19,20
Intention tremor without postural tremor should suggest
an alternative diagnosis (such as cerebellar disease or fragile
X tremor ataxia syndrome). Peripheral neuropathies (partic-
ularly demyelinating polyneuropathies) occasionally cause
postural and kinetic tremors that mimic ET.21 Some of the
many important conditions to be considered in the differen-
tial diagnosis of ET are listed in ►Table 8.
The postural tremors associated with ET and enhanced
physiologic tremor appear immediately when the hands are
held in the outstretched position. However, there is a variant
of postural tremor referred to as re-emergent tremor that
appears after a latency of one or more seconds. Re-emergent
tremor occurs in some patients with prominent parkinsonian
rest tremors, and does not suggest that the PD patient also has
essential tremor or another movement disorder.22 A small
number of PD patients will have prominent postural and
kinetic tremors in addition to rest tremor, but this combina-
Table 7 Activities often affected by essential tremor or other
action tremors
Drinking water from a full cup
Drinking soup with a spoon
Threading a needle
Writing
Applying make-up
Using a computer keyboard or mouse
Weiss 339
Facial dyskinesia Rabbit
syndrome
 
 
þþ þþ
 
þþ 
tion of signs should lead the physician to consider the
possibility of medication-induced parkinsonism or other
disorders mimicking PD.
Sometimes, tremor only occurs in certain positions (posi-
tion-specific tremors), for example, only when hands are held
behind the head, or when the arms are in the “bat wing”
position. Other patients might develop kinetic tremors that
occur only when performing certain tasks (task-specific
tremors) such as writing or playing a musical instrument.
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Task-specific tremors are often dystonic tremors.23
Alcohol reduces tremor in many patients with ET, but
should not be interpreted as a diagnostic marker for this
condition. The sedative effects of alcohol can decrease
enhanced physiologic tremor. Consequently, anxious patients
with PD or other tremor-inducing disorders might also find
that alcohol reduces their tremor to some extent.
Although ET and PD are generally viewed as distinct
disorders with vastly different prognoses, the relationship
is complex. Patients with long-standing ET might develop
mild rest tremors and rigidity without bradykinesia, gait
disturbance, or other signs of PD. However, having ET does
increase the risk of eventually developing full-blown PD,
particularly in younger-onset ET. Patients with ET have an
increased incidence of PD in other family members, and
vice versa.24
Table 8 Differential diagnosis of essential tremor
Enhanced physiologic tremor
Medication-induced tremor (see ►Table 2)
Metabolic tremors (e.g., hyperthyroidism, serotonin
syndrome)
Dystonia with tremor
Re-emergent tremor
Parkinson’s disease and parkinsonism
Cerebellar tremor
Fragile X tremor ataxia syndrome
Wilson’s disease
Neuropathic tremor
Psychogenic tremor
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340 Clinical Pearls in Tremor and Other Hyperkinetic Movement Disorders
Functional /Psychogenic Movement
Disorders
Not all movement disorders are caused by dysfunction in the
central or peripheral nervous system, and clinicians occasion-
ally encounter patients with “functional” or “psychogenic”
symptoms. The diagnosis of a functional or psychogenic
movement disorder is not merely a diagnosis of exclusion or
the failure to find an organic cause, but should be based on
positive findings in the history and clinical examination.
Never having seen strange movements before and pro-
nouncing them to be “psychogenic” is inappropriate. For
example, orthostatic tremor is a condition affecting middle-
aged patients who develop peculiar unsteadiness and fear of
falling due to leg tremor that occurs only while standing. The
high frequency of the leg tremor (14–16 Hz) causes a subtle
rippling in the leg muscles that is barely visible. Consequently,
misdiagnosis is common, and patients are often inaccurately
suspected of having a functional gait disorder.25 Clinicians
familiar with orthostatic tremor know that it can be detected
by palpation of the calf muscles or surface electromyographic
recordings. Another interesting feature in orthostatic tremor
is the “helicopter sign”: Auscultation of the thigh or calf
muscles while the patient is standing produces a sound
resembling a distant helicopter.26
Many movement disorders have signs that can fluctuate
dramatically, sometimes with symptoms triggered by stress
(e.g., tremors, motor fluctuations in PD, paroxysmal dyskinesias).
Other movement disorders, such as dystonia, can be alleviated
by sensory tricks (geste antogoniste). These disorders might
appear to be psychogenic to the patient’s family or an inexperi-
enced clinician. In fact, many hyperkinetic movement disorders,
including the dystonias, Tourette’s syndrome, hemifacial spasm,
blepharospasm, and Meige’s syndrome were initially believed to
be psychogenic conditions.27
Table 9 Positive criteria to help support the diagnosis of
functional/psychogenic tremor and movement disorders
Movements are not suggestive of a known
movement disorder
Abrupt onset of symptoms
Spontaneous remissions
Movements are inconsistent over time (e.g., symptoms
change at different examinations)
Patient is free of symptoms when left alone or not
knowingly observed
Movements disappear with distraction
Suggestibility
Entrainment of tremulous movements into a single rhythm
Tremor varies in frequency and direction
Incongruous movements and postures
Multiple somatizations
Deliberate slowness, fake weakness, bizarre gait
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Some of the positive criteria that help define psychogenic
tremor and other functional movement disorders are listed
in ►Table 9.28
Functional tremors are often entrainable (brought to a
specific rhythm). This can be demonstrated by having the
patient tap the hand or flex and extend the wrist of the
opposite hand at various frequencies. The affected hand will
become entrained to a frequency similar to the voluntary
repetitive hand movements.29
None of these criteria alone unequivocally establishes the
diagnosis of functional disease. Unfortunately, some patients
with organic illness will embellish their symptoms, making
them appear to have purely functional problems. To further
complicate matters, not all patients with functional or
psychogenic movement disorders will have obvious underly-
ing psychiatric illnesses, and not all patients with major
emotional disorders will necessarily have psychogenic
symptoms.30
We live in an era of amazing technological advances in
imaging, genetics, and physiological monitoring, all of which
can advance our diagnostic and therapeutic capabilities.
Asking the patient to bring a video clip of their movement
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disorder is particularly useful, especially when the symptoms
are variable or intermittent. The need for obtaining a detailed
history supplemented by careful clinical observation, com-
mon sense, and experience remains paramount in the evalu-
ation of patients with hyperkinetic movement disorders.
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