Classification of Tremor and Update on
Treatment
- P. DAVID CHARLES, M.D., GREGORY J. ESPER, B.S.,
THOMAS L. DAVIS, M.D., ROBERT J. MACIUNAS, M.D., and
DAVID ROBERTSON, M.D.
- Vanderbilt University School of Medicine
- Nashville, Tennessee
Tremor is a symptom of
many disorders, including Parkinson's disease,
essential tremor, orthostatic tremor, cerebellar
disease, peripheral neuropathy and alcohol
withdrawal. Tremors may be classified as postural,
rest or action tremors. Symptomatic treatment is
tailored to the tremor type. Combination therapy
with carbidopa and levodopa remains the first-line
approach for parkinsonian tremor. Essential tremor
may be amenable to propranolol or primidone.
Propranolol may be useful in treating alcohol
withdrawal tremor, and isoniazid may control the
cerebellar tremor associated with multiple
sclerosis. Clonazepam may relieve orthostatic
tremor. Other agents are also available for the
treatment of tremor. When medical therapy fails to
control the tremor, surgical options such as
thalamotomy, pallidotomy and thalamic stimulation
should be considered in severe cases. Thalamic
stimulation, the most recent of these surgical
approaches, offers the advantage over ablative
procedures of alleviating tremor without the
creation of a permanent lesion.
Tremor is the
involuntary, rhythmic oscillation of reciprocally
innervated, antagonistic muscle groups, causing
movement of a body part about a fixed plane in
space.1,2 Effective
treatment of tremor requires distinguishing this type
of movement disorder from other movement disorders.
Rhythmicity distinguishes tremor from disorders in
which tremor may be a component, such as
choreoathetosis and dystonia, and its biphasic nature
distinguishes tremor from clonus.1 The frequency and
amplitude of a tremor vary to the degree that the
tremor may be hardly noticeable or severely disabling.
Frequency can be divided into three categories of
oscillations per second: slow (3 to 5 Hz),
intermediate (5 to 8 Hz) or rapid (9 to 12 Hz).3 Amplitude may be
classified as fine, medium or coarse, depending on the
displacement produced by the tremor about the fixed
plane.3 A coarse
tremor has a large displacement, whereas a fine tremor
is barely noticeable. Tremor may be unifocal,
multifocal or generalized, and may affect the head,
face, jaw, voice, tongue, trunk or extremities.
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TABLE
1 Classification of Tremors, and Their
Characteristics and Treatment
|
Type of tremor
|
Frequency
|
Occurrence
|
Etiology
|
Treatment*
|
Postural tremor |
5 to 9 Hz |
When limb is positioned against gravity
|
Physiologic tremor, essential tremor,
alcohol or drug withdrawal, metabolic
disturbances, drug-induced tremor, psychogenic
tremor |
Beta blockers, primidone (Mysoline),
acetazolamide (Diamox), clonazepam (Klonopin),
botulinum toxin, brain gabapentin (Neurontin),
deep stimulation, thalamotomy |
Rest tremor |
3 to 6 Hz |
When limb is fully supported against
gravity and the muscles are not voluntarily
activated |
Parkinson's disease, multiple- systems
atrophy, progressive supranuclear palsy,
drug-induced tremor, rubral tremor, psychogenic
tremor |
Levodopacarbidopa (Sinemet),
anticholinergics and other antiparkinsonian
agents, deep brain stimulation, pallidotomy,
thalamotomy |
Action tremor |
3 to 10 Hz |
During any type of movement |
Cerebellar lesions, rubral tremor,
psychogenic tremor |
Wrist weights,
isoniazid |
*--Drugs and other treatments
are generally listed in the order in which they
should be tried. An adequate trial of each
medication must be tried before the agent is
judged to be ineffective. Many of these drugs
are not specifically labeled for the treatment
of tremor or have not undergone extensive
studies to support their use in the treatment of
tremor.
--Action tremor includes
intention tremor (exacerbation toward the end of
goal-directed movement), kinetic tremor (during
any type of movement) and task-specific tremor
(only during performance of highly skilled
activities, such as writing or playing a musical
instument). |
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Classification:
Postural, Rest and Action Tremors
Tremor is primarily classified on the basis of when
it occurs, either with a certain posture, at rest or
during action (Table 1). A resting tremor
occurs when the patient is attempting to maintain the
position of a body part at rest (e.g., when the
patient's hands exhibit a tremor as they are resting
in the patient's lap). Postural tremor is observed
when the patient tries to maintain a posture against
gravity, such as holding the arms out in front of the
body. An action tremor (kinetic or intention tremor)
occurs during movement of the affected body part from
one point to another. A task-specific tremor occurs
only when the patient begins to perform a highly
skilled activity, such as writing or speaking.2
Tremor may be either physiologic or pathologic.
Physiologic tremor is a normal variant, occurring at a
frequency of 8 to 12 Hz in the hands yet as slow as
6.5 Hz in other body parts during maintenance of a
posture.2,4 It can be
increased by emotions such as anxiety, stress or fear,
by exercise and fatigue, hypoglycemia, hypothermia,
hyperthyroidism and alcohol withdrawal. When such an
increase occurs, physiologic tremor is then called
enhanced or exaggerated physiologic tremor.1,4 Certain drugs can also
exacerbate physiologic tremor5
(Table 2). Pathologic tremor is
either idiopathic or occurs secondary to some
disorders (Table 3). Essential tremor and
parkinsonian tremor are two common types of pathologic
tremor.
Identification of the type of tremor depends on
keen observation. The location of the tremor or the
patient's position when it occurs should be identified
first, and special attention must be paid to other
signs of illness. Careful observation will reveal if
the tremor occurs at rest, during posture maintenance
or during movement. The patient should be asked what
produces or modulates the amplitude and frequency of
the tremor.2,3 A
correct diagnosis is essential for proper treatment of
the disorder, because different types of tremor
require different treatments.
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TABLE
2 Commonly Used Agents That Exacerbate
Physiologic Tremor
|
Caffeine
Fluoxetine (Prozac) Haloperidol
(Haldol) Lithium Methylphenidate
(Ritalin) |
Metoclopramide
(Reglan) Phenylpropanolamine
Pseudoephedrine Theophylline Valproic
acid |
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TABLE
3 Selected Secondary Causes of Tremor
|
Alcohol or drug
withdrawal Brain abscess Brain
tumor Multiple sclerosis |
Peripheral
neuropathy Pheochromocytoma
Psychogenic disorders
Thyrotoxicosis |
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Tremor Types Based on
Etiology
Parkinsonian Tremor
The tremor in
Parkinson's disease occurs at rest and is
characterized by a frequency of 4 to 6 Hz and a medium
amplitude. It is classically referred to as a "pill
rolling" tremor of the hands but can also affect the
head, trunk, jaw and lips.2,3 Although rare, a rest
tremor may also be found in patients with other
neurodegenerative diseases, such as multiple-systems
atrophy and progressive supranuclear palsy. The tremor
associated with these disorders is usually symmetric
and not as prominent as the tremor that accompanies
Parkinson's disease.
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A
physiologic tremor occurs in the hands at a
frequency of 8 to 12 Hz during maintenance of a
posture. |
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Parkinson's disease results from a slow
degeneration of a small area in the midbrain, called
the substantia nigra. Specifically, excitatory and
inhibitory dopaminergic neurons degenerate in the
substantia nigra pars compacta. These neurons project
to the striatum and then to the globus pallidus. From
there, multiple connections in the basal ganglia
project to one another, to the thalamus and, finally,
to the cortex, which makes up the extrapyramidal
system. This system regulates the initiation and
control of movement, and dysfunction of any of these
connections can lead to various types of movement
disorders.6 As a
consequence of neuronal degeneration in the substantia
nigra pars compacta, the ventral intermediate nucleus
of the thalamus becomes overactive, possibly producing
the tremor of Parkinson's disease. The neurons in the
ventral intermediate nucleus of the thalamus fire at a
rate that matches the tremor.7
Essential Tremor
Essential tremor is the
most common movement disorder.2,3,8 This postural tremor
may have its onset anywhere between the second and
sixth decades of life and its prevalence increases
with age.8 It is
slowly progressive over a period of years.3
The specific pathophysiology of essential tremor
remains unknown. Essential tremor occurs sporadically
or can be inherited. While the exact genetic defect
has not been identified, familial transmission seems
to be autosomal dominant with variable
penetrance.4
The frequency of essential tremor is 4 to 11 Hz,
depending on which body segment is affected. Proximal
segments are affected at lower frequencies, and distal
segments are affected at higher frequencies.3 Although typically a
postural tremor, essential tremor may occur at rest in
severe and very advanced cases.2 It most commonly affects
the hands but can also affect the head, voice, tongue
and legs.2,3,9 In some
patients essential tremor is alleviated by small
amounts of alcohol, an effect not found in Parkinson's
disease.
Cerebellar Tremor
The most common type
of cerebellar tremor is kinetic, or goal directed.
Cerebellar tremors are due to lesions of the lateral
cerebellar nuclei or superior cerebellar peduncle, or
its connections. Classically, a lesion within a
cerebellar hemisphere or nuclei leads to an action
tremor on the ipsilateral side of the body. Midline
cerebellar disease may cause tremor of both arms, the
head and the trunk.2
Lesions in the location of the red nucleus produce a
wing-beating type of tremor (called rubral tremor),
which is also present to a lesser degree with rest and
posture.
During examination, a cerebellar tremor increases
in severity as the extremity approaches its target.
Other signs of cerebellar pathology, such as
abnormalities of gait, speech and ocular movements,
and the ability to perform rapidly alternating
movements, may be present and may help to confirm the
diagnosis of cerebellar tremor.3
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Propranolol (Inderal) and primidone
(Mysoline) are both effective in the treatment
of essential tremor. |
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Another type of tremor may also be associated with
damage to the cerebellum. Termed "cerebellar postural
tremor," it is prominent with both action and
posture.4 In its most
severe form, cerebellar postural tremor has a
frequency of 2.5 to 4 Hz and may wax and wane in
amplitude, increasing progressively with prolonged
posture. It persists and worsens with goal-directed
movement.4 The milder
form of the tremor has a more rapid frequency,
approaching 10 Hz, and appears more distally, making
it harder to identify than the severe type.4
Multiple sclerosis is the most common cause of the
cerebellar postural tremor.4 Other causes of this
tremor include tumors and strokes, as well as neural
degeneration in the cerebellum.
Alcohol Withdrawal Tremor
Alcohol
withdrawal tremor is similar to essential tremor on
examination but with subtle differences. Alcohol
withdrawal tremor has a frequency between 6 and 10.5
Hz. In one study,10 74
percent of the patients with alcohol withdrawal
tremors had tremors at a frequency above 8 Hz. In this
same series, tremors in all of the patients who had
essential tremor were at a frequency below 8 Hz. Thus,
the tremor of alcohol withdrawal tends to be more
rapid than essential tremor.
A family history of tremor was found in only 1
percent of the patients with alcohol withdrawal
tremor, as compared with almost one half of the
patients with essential tremor.10 In addition, severity and
degree of functional disability were less with alcohol
withdrawal tremor.
Only the hands are affected in patients with
alcohol withdrawal tremor, but multiple sites of
involvement are possible in patients with essential
tremor. Overactivity of the sympathetic nervous system
is thought to be responsible for alcohol withdrawal
tremor, and prolonged alcohol abuse can result in a
chronic tremor disorder.10
Psychogenic Tremor
Psychogenic tremor is
a complex tremor that can occur at rest, during
postural movement and during kinetic movement. The
etiology and pathophysiology of psychogenic tremor are
likely to differ from patient to patient, and the main
focus of treatment should be psychotherapy, not
medication.
Clinical features of psychogenic tremor include an
abrupt onset, a static course, spontaneous remission
and unclassifiable tremors.11 Unresponsiveness to
antitremor drugs, an increase in frequency and
amplitude with attention and a decrease in frequency
and amplitude with distraction, responsiveness to
placebo, absence of other neurologic signs and
remission with psychotherapy are also signs of
psychogenic tremor.11
Clinical inconsistencies, such as being able to write
words yet not being able to draw a spiral, and
changing characteristics, such as direction and
affected body part, are also representative of
psychogenic tremor.11
Other Tremors
Other types of tremor
occur much less commonly than the previously described
tremors. Orthostatic tremor is defined as a postural
tremor of the legs, occurring at a frequency of 13 to
18 Hz, initiated on standing and alleviated by walking
or sitting.12 It is
more readily noticeable during palpation than by sight
and is not influenced by peripheral feedback.13 Unsteadiness, feelings of
imbalance or weakness, and trembling and shaking in
the lower limbs are associated features of orthostatic
tremor.14 The etiology
of orthostatic tremor is unknown, but it is currently
regarded as an entity separate from essential
tremor.12-14
Tremor associated with peripheral neuropathy is
clinically similar to essential tremor. Its etiology
is diverse. Not only can it be idiopathic, it can also
be caused by demyelination from immunoglobulin M
paraproteinemic neuropathies.2 Tremor in association with
peripheral neuropathy can also result from
Charcot-Marie-Tooth disease, diabetes mellitus, uremia
and porphyria.2
Drug Treatment of
Tremor
Parkinsonian Tremor
Treatment of
Parkinson's disease includes both medical and surgical
intervention. Dopamine replacement therapy by means of
levodopa clearly revolutionized the treatment of
Parkinson's disease. Levodopa is almost exclusively
given in combination with the peripheral decarboxylase
inhibitor carbidopa (Sinemet). Carbidopa blocks the
peripheral metabolism of levodopa to dopamine,
decreasing the peripheral adverse effects of levodopa,
such as nausea and vomiting, while increasing
levodopa's availability in the brain.15,16 In addition to
modulating the tremor associated with Parkinson's
disease, levodopa improves bradykinesia, rigidity and
other commonly associated symptoms.
Carbidopalevodopa is available in formulations of
10/100 mg, 25/100 mg and 25/250 mg. It is advantageous
to begin treatment of mild disease with the 25/100-mg
dosage, one tablet three times a day, and then
increase the dosage as symptoms become less
manageable.
When tremor is the predominant presenting symptom
of Parkinson's disease or when tremor persists despite
adequate control of other parkinsonian symptoms with
low dosages of levodopa, an anticholinergic agent such
as trihexyphenidyl (Artane) or benztropine (Cogentin)
may be the treatment of choice. In most patients,
however, anticholinergics do not significantly improve
bradykinesia and rigidity. Trihexyphenidyl dosages
necessary to improve tremor are between 4 and 10 mg
per day (maximum: 32 mg), and useful benztropine
dosages range from 1 to 4 mg per day. The side effects
of these agents are their limiting factor,
particularly in the elderly. Side effects include
memory impairment, hallucinations, dry mouth, urinary
difficulties and blurred vision.15
Other antiparkinsonian drugs--for example,
amantadine (Symmetrel), tolcapone (Tasmar) and
dopamine agonists such as pergolide (Permax),
bromocriptine (Parlodel), ropinirole (Requip) and
pramipexole (Mirapex)--are most helpful in patients
whose tremor responds poorly to levodopa alone.
Essential Tremor
As with other tremors,
effective treatment of essential tremor is not found
in a single, universal agent. Some therapies may be
satisfactory in some patients and ineffective in
others. The most widely used drugs for essential
tremor are the beta-adrenergic blocker propranolol
(Inderal) and the anticonvulsant primidone (Mysoline).
The typical dosage range for propranolol is 80 to 320
mg per day and for primidone, 25 to 750 mg per
day.3 Other
beta-adrenergic receptor antagonists used in the
treatment of essential tremor include metoprolol
(Lopressor) and nadolol (Corgard).2 Alcohol is also effective
in relieving essential tremor, but abuse may be an
adverse consequence.3
In our experience, propranolol and primidone are
equally effective in the treatment of essential
tremor. Patients who do not respond to one medication
after a few weeks of therapy should be tried on the
other one. Primidone may be preferred, because of the
exercise intolerance associated with high-dose beta
blockade. Patients who have a very-low-amplitude rapid
tremor are generally more responsive to these agents
than those who have a slower tremor with greater
amplitude. Patients who have tremor of the head and
voice may also be more resistant to treatment than
patients with essential tremor of the hands.
Other Tremors
There is no established
treatment for cerebellar tremor.2 In patients with multiple
sclerosis, severe cerebellar tremor may be improved
with isoniazid, in a dosage of 600 to 1,200 mg per
day, given together with pyridoxine.4
Propranolol in a dosage of 160 mg per day is very
effective in reducing the tremor associated with
alcohol withdrawal.10
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Thalamic stimulation by means of an
implanted electrode may effectively control
tremor in patients with essential tremor or
Parkinson's disease. |
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Treatment of orthostatic tremor should first be
attempted with clonazepam (Klonopin). In one small
study,14 eight of nine
patients responded to clonazepam in dosages ranging
from 0.5 to 2.0 mg per day. The patient who did not
respond to clonazepam responded to chlordiazepoxide
(Librium), in a dosage of 30 mg twice a day. In
another study,12 10 of
18 patients had sustained improvement with clonazepam,
and valproic acid was effective in the remaining eight
patients. However, propranolol in daily dosages of up
to 320 mg had no effect on controlling orthostatic
tremor.
Tremor due to peripheral neuropathy may be
ameliorated with propranolol, primidone,
benzodiazepines or baclofen (Lioresal), but the
underlying cause of the neuropathy itself should be
treated as well.2
Other medications have been shown to be helpful in
the management of tremor but should probably only be
tried in consultation with a neurologist, when the
previously mentioned drugs have failed to control the
tremor.
Surgical Treatment of
Tremor
Thalamotomy
Surgical therapy for tremor
should only be considered if drug therapy fails to
produce adequate relief. Stereotactic thalamotomy is
the surgical procedure most often used to quell
essential tremor. Before the introduction of levodopa,
thalamotomy was an often-selected option in the
treatment of Parkinson's disease. Because the benefits
of levodopa wane after four to seven years of therapy,
this procedure remains an option in some patients with
severe parkinsonian tremor refractory to drug therapy.
However, problems associated with bilateral
thalamotomy, such as dysphagia and dysarthria, limit
its use. Thalamotomy is usually only considered in
patients with severe, drug-resistant essential tremor
and in a very small subset of patients with
Parkinson's disease who have severe, disabling,
predominantly unilateral tremor.
In one study of the use of stereotactic thalamotomy
in the treatment of tremor,17 86 percent of the 42
patients with parkinsonian tremor and 83 percent of
the six patients with essential tremor had cessation
of tremor or moderate to marked improvement in tremor
after the procedure. Follow-up in some patients was as
long as 13 years (mean follow-up: 53.4 months). The
investigators used three criteria for patient
selection: (1) predominantly unilateral, severe and
incapacitating tremor, (2) a poor response to or
intolerance of optimal medical therapy and (3) no
potentially serious risk factors for surgery.
Postoperative complications included weakness,
dysarthria and confusion, but these problems subsided
with time.
Catastrophic complications in the perioperative
period include bleeding in the thalamus or the
subdural or epidural area, which can lead to death,
paralysis, aphasia or significant cognifive deficits.
Pallidotomy
Producing lesions in the
globus pallidus by means of pallidotomy is an
alternative to thalamotomy in the treatment of
parkinsonian tremor. Pallidotomy also improves other
symptoms of Parkinson's disease, such as bradykinesia
and levodopa-induced dyskinesias.18 As with thalamotomy,
pallidotomy should only be considered in cases of
severe tremor unresponsive to medical treatment.
In a series of 259 patients who underwent
pallidotomy for parkinsonian tremor,18 complete relief of all
symptoms on the side contralateral to the procedure
occurred in 212 patients (81.9 percent). Of the
remaining 47 patients, 36 experienced substantial
improvement and 11 had only minor or no improvement.
In many of the patients, pallidotomy also produced a
significant reduction in bradykinesia, rigidity and
levodopa-induced dyskinesias. The side effects
associated with the procedure were similar to those of
thalamotomy and included visual field defects, such as
lower central visual field scotomas, and hemiparesis.
Cognitive deficits, dysarthria and foot apraxia
occurred in less than 1 percent.
If the pallidal lesion is large enough and placed
at the posteroventral margin of the lateral pallidum,
it abolishes the tremor as often as thalamotomy.
However, because of theoretic concerns that bilateral
pallidotomy may cause cognitive deficits, this
approach must be explored before it is comonly used in
the treatment of tremor.
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 |
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FIGURE 1. Thalamic stimulation,
showing position of the electrode within the
thalamus and path of the wire to the pulse
generator in the subclavicular
pouch. | |
Thalamic Stimulation
During physiologic
localization in preparation for thalamotomy, the
observation that high-frequency stimulation of the
ventral intermediate nucleus of the thalamus abolished
tremor led to investigation of thalamic stimulation as
a treatment for tremor. The first study of this
technique as a long-term therapy for tremor was
reported in 1993.19
Thalamic stimulation involves implanting an
electrode in the thalamic area found to be responsible
for the tremor. After the wire of the electrode leaves
the skull, it is tunneled under the scalp and down the
neck to a purse generator located in the subclavicular
pouch (Figure 1). The implanted stimulating
device is much like a modified pacemaker, and its
electrical impulses can suppress tremor indefinitely.
The stimulator can be reprogrammed by using a small
portable computer that communicates with the device by
radio frequency. Moreover, the patient can turn the
device on and off with a magnet. Patients usually turn
the device on in the morning, leave it on during
waking hours and turn it off at bedtime, since most
tremors cease during sleep.
In the first study of this technique,19 as many as 88 percent of
the patients with Parkinson's disease had either good
or excellent relief of tremor. The operative risk of
implanting the device is proving to be similar to that
of thalamotomy; death, paralysis, aphasia and
significant cognitive deficits are possible
complications.
Tremor recurrence after placement of the electrode
can be controlled by adjusting the stimulation
parameter rather than by reoperation.20 The U.S. Food and Drug
Administration has approved thalamic stimulation as an
accepted therapy for unilateral suppression of
uncontrolled essential tremor or parkinsonian tremor
in an upper extremity. As with the other surgical
techniques, thalamic stimulation is an option that
should be chosen only after medical therapy has
failed.
Promising Surgical Approaches
At the
forefront of new surgical therapies for tremor are
pallidal stimulation and subthalamic nucleus
stimulation.21-23 With
new advances in deep brain stimulation, procedures can
be performed bilaterally to relieve tremor in patients
with bilateral involvement. Either a combination of
thalamotomy and stimulation or bilateral stimulation
without ablation is now a possibility.23 Targets in the brain that
are too dangerous to approach for producing a lesion
by means of thalamotomy may be treated with
stimulation instead, and electrical stimulation can be
modified to alleviate tremor as it progresses.22 Thus, deep brain
stimulation has become a promising option for
abolishing tremors that cannot be controlled by
medical therapy.
The authors have
received honoraria from Allergen, Inc., Medtronic,
Inc., Roche Laboratories, SmithKline and Beecham
Pharmaceuticals, and Upjohn Company, and research
support for clinical trials from Allergen, Inc.,
Roche Laboratories and Medtronic, Inc.
The authors thank
Dominick Doyle, Medical Arts Group, Vanderbilt
University, Nashville, Tenn., for providing the
drawing in Figure 1.
The Authors
P. DAVID CHARLES, M.D.,
is assistant professor
of neurology and director of the movement disorders
clinic at Vanderbilt University School of Medicine,
Nashville, Tenn. Dr. Charles received a medical degree
from Vanderbilt University School of Medicine, where
he also completed a residency in neurology and a
fellowship in movement disorders and neurophysiology.
GREGORY J. ESPER, B.S.,
is currently a
fourth-year medical student at Vanderbilt University
School of Medicine. He completed a bachelor's degree
in neuroscience at the University of Pittsburgh,
Pittsburgh, Pa.
THOMAS L. DAVIS, M.D.,
is associate professor
of neurology at Vanderbilt University School of
Medicine. Dr. Davis graduated from the University of
Mississippi School of Medicine, Jacksonville, and
completed a residency in neurology at Vanderbilt
University and a postdoctoral fellowship in
neuropharmacology at the National Institutes of
Health, Bethesda, Md.
ROBERT J. MACIUNAS, M.D.,
is professor of
neurosurgery at Vanderbilt University School of
Medicine. Dr. Maciunas graduated from the University
of Illinois, Abraham Lincoln School of Medicine,
Chicago, and completed an internship in general
surgery and a residency in neurosurgery at the Mayo
Graduate School of Medicine, Rochester, Minn.
DAVID ROBERTSON, M.D.,
is professor of
medicine, neurology and pharmacology, and director of
the General Clinical Research Center at Vanderbilt
University School of Medicine. Dr. Robertson graduated
from Vanderbilt University and completed a residency
in internal medicine at Johns Hopkins Hospital,
Baltimore.
Address correspondence
to P. David Charles, M.D., Director, Movement
Disorders Clinic, Vanderbilt University Medical
Center, 2100 Pierce Ave., Suite 352, Nashville, TN
37212. Reprints are not available from the authors.
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