in the general population, is an involuntary,
rhythmic, oscillatory movement of a body part.
It is produced by activation of reciprocally
innervated, antagonistic muscle groups, which leads to
their repeated contractions.
Tremors can lead to social
complex medical syndrome. Although many forms of
tremor may begin earlier in life, they progress with
time and often do not come to the attention of a physi-
cian until a patient is elderly. In one study, 98% of a
multiethnic cohort of normal older adults had a mild
detectable tremor on testing; in one third of the cases,
the tremor worsened with activity.
Many patients feel that tremors are a part of aging
denies them adequate treatment. Under the current
health care system, most patients with tremors are like-
ly to initially present to their primary care physician. A
study by Marttila et al
showed that 25% of the
Parkinson’s disease actually had essential tremor. This
illustrates the importance of clinicians recognizing
tremors and their underlying causes in order to man-
age them successfully.
The 3 most common forms of tremor in the elderly
population are essential tremor, parkinsonian tremor,
and cerebellar tremor. This article reviews the clinical
characteristics, etiology and pathogenesis, and treat-
ment of these types of tremor. The clinical features and
management of several other types of tremor are
addressed, as well.
It is important to differentiate tremor from other
involuntary movements, including choreiform move-
ments, athetosis, dystonia, myoclonic movements, and
tics. Choreiform movements are involuntary and
rapid but jerky in nature, rather than rhythmic. They
are prominent in the face and distal extremities and
give the patient a fidgety appearance. Chorea present-
ing in elderly patients is generally either senile chorea
(which is not an inherited disorder) or, rarely, chorea
following a cerebrovascular accident. Although Syd-
enham’s chorea and Huntington’s chorea are rare in
older persons, Huntington’s chorea always must be
Athetosis constitutes slow writhing movements of
It may be associated with hemiplegia and often occurs
in children secondary to birth trauma.
Dystonic movements are slow, prolonged move-
ments of either the trunk muscles or a distal muscle
group. They may be associated with tremors of the
affected part (dystonic tremor). Examples of dystonia
include spasmodic torticollis involving the neck mus-
cles, writer’s cramp due to spasm of the shoulder mus-
cles, and blepharospasm, a form of dystonia that con-
sists of involuntary, repeated eye closure and is seen in
elderly women. Blepharospasm is worsened by stress
and can be confused with early Parkinson’s disease.
Patients with blepharospasm may also have twitching
of oral or facial muscles, which is known as Meige’s
Myoclonic jerks are sudden, brief, and shock-like
elderly, myoclonus is rare and occurs in association
with Creutzfeldt-Jakob disease, uremia, hypomagne-
semia and liver failure.
Tics are brief contractions of a
their repetitive nature. Tics commonly occur in chil-
dren and can produce features such as sniffing, grunt-
ing, pouting, and grimacing.
Tremors may be classified based on their clinical fea-
tures (Figure 1). Most tremors can be characterized as
either a resting tremor or an action tremor. Resting
tremor occurs in a limb or body part that is completely
supported against gravity with absolutely no contraction
If the limb is not supported, its
the tremor present in such a condition is an action
tremor. For example, essential tremor is a type of action
tremor that may be mistaken for a resting tremor if the
affected limb is not completely at rest during examina-
tion. Resting tremor is best observed when the patient
is distracted. In Parkinson’s disease, the physician may
observe mild tremor in the arm contralateral to the one
he or she has asked the patient to swing, even if the
patient is unaware of the tremor.
Action tremor includes postural, kinetic, and iso-
Postural tremor occurs when a body
example, pointing at an object or protruding the
Kinetic tremor occurs during voluntary move-
tremor that worsens during the completion of a visual-
ly guided, goal-directed movement (eg, pouring tea
into a cup).
Task-specific tremor occurs during com-
ment. Simple kinetic tremor occurs with acts such as a
simple turning of the wrist or foot. Isometric tremor
occurs when a voluntary muscle contraction is op-
posed by a stationary force. It can be elicited by having
the subject make a fist or push against a wall or other
EVALUATION OF THE PATIENT WITH TREMOR
A wide range of disorders cause resting and action
tremor (Table 1), and some can manifest both types of
tremor activity. As laboratory tests are not available for
the diagnosis of many common causes of tremor, a de-
tailed physical examination is a physician’s best diag-
nostic tool. Information regarding the patient’s cur-
rent and past medical history, as well as any family
history of tremors, should be obtained. All medications
used currently and in the past must be listed. A
detailed neurologic examination to evaluate motor
and sensory nervous systems, the extrapyramidal sys-
tem, and cerebellar function is required.
Careful observation during the performance of
each neurologic test can yield invaluable information.
For example, during a finger-to-nose test, a cerebellar
action tremor manifests during the terminal part of
the test, just before the finger touches the nose. In con-
trast, a parkinsonian tremor may either disappear with
the onset of finger-to-nose testing or may remain con-
stant throughout the range of motion.
Hospital Physician December 2001
B h a g w a t h : T r e m o r s i n E l d e r l y P e r s o n s : p p . 3 1 – 3 7 , 4 9
Other tremor syndromes:
Isolated chin tremor
Isolated voice tremor
Figure 1. Clinical classification of tremor. (Data from Habib-ur-Rehman. Diagnosis and management of tremor. Arch Intern
Drugs (except those
*Although essential tremor is predominantly an action tremor, rarely,
in advanced conditions, it may have a resting component. (Elble RJ.
Diagnostic criteria for essential tremor and differential diagnosis.
Neurology 2000;54[11 Suppl 4]:S2–6.)
Data from Patten JP, editor. Neurological differential diagnosis. 2nd ed.
London: Springer Publication;1998.
Essential tremor is the most common cause of
tremor in elderly patients. It has a bimodal peak of
onset in the second and sixth decades of life.
tural and kinetic tremors. It is generally bilateral and is
gradually progressive. It affects upper limbs in 95% of
cases, the head in 34%, lower limbs in 20%, the voice
in 12%, the face in 5%, and the trunk in 5%.
tremor (up to 50%)
may be unaware of their tremor,
cian. Some patients may present with only isolated
Although benign, essential tremor in its severe form
can cause functional and social impairment, titubation,
and a tremulous voice. Severe essential tremor may be
accompanied by cogwheel rigidity. If the postural form
of essential tremor is mistakenly characterized as rest-
ing tremor, the patient’s condition may be wrongly
diagnosed as Parkinson’s disease, especially if cogwheel
rigidity is present. However, in essential tremor, muscle
tone and strength are normal. The clinical features of
essential tremor and parkinsonian tremor are com-
pared in Table 2.
Essential tremor has been observed to be precipitat-
ed and alleviated by several factors (Table 2). It
improves with alcohol consumption but is generally
not suspected to cause alcoholism in patients.
Typically, there is an absence of signs of other neuro-
with Parkinson’s disease.
The etiology and patho-
physiology of essential tremor have not been elucidat-
ed. At least 50% of patients with essential tremor have a
positive family history. The familial form is an autoso-
mal dominant disease with variable penetrance.
Autopsies of persons who had essential tremor revealed
Routine computed tomog-
It has been proposed that enhanced
pathways are the cause of essential tremor.
blood flow in the red nucleus, cerebellum, and thala-
mus have been observed bilaterally on positron emis-
sion tomography of patients with essential tremor.
animal models, a tremor similar to essential tremor was
loid harmaline and serotonergic drugs,
sis of tremor.
Cerebellar tremor is a pure action tremor that is
absent at rest. On examination, a combination of termi-
nal intention tremor and some postural tremor can be
seen. Dysmetria (ie, difficulty alighting on the target
during voluntary movement) also characterizes cerebel-
lar lesions. This manifests in the finger-to-nose test as
“past-pointing.” Other features include ataxia (uncoor-
dinated or inaccurate movement), nystagmus, muscular
hypotonia, decreased reflexes, and dysdiadochokinesia
(ie, an inability to perform rapid alternating move-
ments). Titubation (head nodding) may be present
when the patient is upright but not on supination.
B h a g w a t h : T r e m o r s i n E l d e r l y P e r s o n s : p p . 3 1 – 3 7 , 4 9
Type of tremor
Action, usually symmetrical
Rest and action, initially unilateral
Agents or states that improve
Alcohol, relaxation; voluntary
Sleep; voluntary suppression is
suppression is possible
Agents or states that worsen
Excitement, anger, fatigue, fear,
Emotional stress, excitement,
Bradykinesia, cogwheel rigidity,
gait disturbance, depression,
Titubation commonly present
Titubation is usually absent; chin,
jaw, and lip tremor may be
ordinated voice, but unlike in parkinsonism, the voice is
of normal volume.
Etiology and pathogenesis.
The cerebellum receives
input from the motor cortex regarding the next
intended movement of the limbs and the trunk.
peripheral nerves regarding limb position and move-
ment. Under normal circumstances, the cerebellum
uses the information from these sources to anticipate
and prevent the occurrence of movement errors, such
Vascular accidents, malignancy, and
may cause a lesion in
emboliform nuclei) or in their connections to the con-
tralateral thalamus via the brachium conjunctivum.
Such a lesion disrupts the sensorimotor feedback loop
between the limb and the motor cortex, which is oscil-
latory in nature, and tremor results.
Parkinsonism is a movement disorder that can lead
to severe physical and emotional disability. Although
tremor is a hallmark of parkinsonism, it is not the
cause of physical limitation in patients with the disease.
Rather, functionality is severely limited by the bradyki-
nesia, rigidity, and postural instability that are also char-
acteristic of the disease.
Both resting and action tremor (kinetic type) can be
present in this disease, and it is commonly unilateral in
the early stages (Table 2). In Parkinson’s disease of
elderly onset (idiopathic Parkinson’s disease), resting
tremor may be an uncommon initial symptom.
Common causes of DIP include neuroleptic
agents, calcium channel blockers, valproic acid, tacrine,
bethanechol chloride, reserpine, and methyldopa.
Lower-potency neuroleptics or novel neuroleptics (eg,
ade are less likely to cause DIP.
Clinically, DIP cannot
however, DIP develops subacutely within the first weeks
of drug introduction or an increase in drug dosage.
Tremor may be a simple oscillatory movement or it
may be compound, such as a pill-rolling movement.
The tremor affects the distal extremities (especially the
hands) and the facial, jaw, and tongue muscles.
Anxiety, emotional upset, and fatigue exacerbate the
tremor, and it disappears during sleep. Cogwheel rigid-
ity may be present and the voice volume is low.
Monosymptomatic resting tremor is a predominant-
ly resting tremor (occasionally with a postural compo-
nent) that occurs in the absence of other parkinsonian
features such as bradykinesia and rigidity.
It must be
be a form of Parkinson’s disease.
The anatomy of the
structures involved in production of parkinsonian
tremor is briefly described.
Subcortical grey matter
include the striatum, globus pallidus, subthalamic
nucleus, and substantia nigra. Nerve cells in the sub-
stantia nigra pars compacta of the midbrain produce
dopamine. Dopamine is transported along the axons
to the caudate nucleus and the putamen, which col-
lectively form the striatum. Dopamine helps modu-
late the inhibitory output of the striatum to the
globus pallidus interna and substantia nigra pars
reticulata. These 2 nuclei, in turn, inhibit certain thal-
amic nuclei that have a stimulatory influence on the
In patients with Parkinson’s disease, dopamine is
depleted as a result of the death of dopaminergic cells
in the substantia nigra. In patients with neuroleptic
drug–induced parkinsonism, dopaminergic D
Both conditions can lead to disinhibition of the globus
pallidum, causing suppression of the thalamic nuclei,
which results in reduced excitation of the motor cor-
tex. Because the motor cortex depends on the basal
ganglia to facilitate movements generated by the cor-
tex, the outcome of this depletion or underactivity of
dopamine is a movement disorder.
This pathway does not explain the origin of the rest
tremor seen in parkinsonism. In Parkinson’s disease, it
is known that the death of nigrostriatal neurons leads
to abnormal intermittent oscillations in the neurons of
the motor cortex, basal ganglia, and thalamus and that
these abnormal oscillations can produce tremor.
cerebellum is involved in control of the parkinsonian
Drugs are associated with other types of tremor
besides DIP. Long-term use of antipsychotic agents can
also cause a postural tremor called tardive tremor. It is a
low frequency murmur that is usually postural but may
occur at rest or with movement.
Even short-term use
been associated with tremors, rigidity and dyskinesia.
Sympathomimetic agents, cyclosporine, lithium, and tri-
Lithium overdose produces ataxia, tremor,
muscle twitching, and fasciculations. It can be diag-
nosed by measuring serum levels of lithium.
Tremors are one of the common clinical features of
by interaction between serotonergic agents and
monoamine oxidase inhibitors. Symptoms resolve after
the discontinuation of the serotonergic drugs.
Barbiturate withdrawal can produce anxiety, restless-
few days; when severe, this can lead to delirium
tremens, which consists of gross tremor, altered senso-
rium, fever, and tachycardia. Benzodiazepine withdraw-
al leads to anxiety, nausea, vomiting, tremor, hallucina-
tions, and seizures. Tremors may also be caused by
hallucinogen use and may accompany phencyclidine
Chronic exposure to metallic mercury produces an
(memory loss, excitability, insomnia, and delirium).
This may be observed in workers in the felt-hat indus-
try and sometimes in dentists.
Acute exposure to mer-
Normal individuals can manifest an action tremor,
especially while fatigued or experiencing emotions
such as fear, anxiety, or stress.
Physiologic tremor can
mia, hypoglycemia, pheochromocytoma, thyrotoxico-
sis, and alcohol withdrawal.
A characteristic feature of physiologic tremor is the
tating agent or resolution of the underlying state. In a
patient with alcoholism, physiologic tremor should be
differentiated from asterixis (repetitive partial flexion
of the wrists during sustained wrist extension). Asterixis
is a sign of metabolic encephalopathy and accompa-
nies other signs of liver failure in these patients.
Patients with dystonia may have a localized tremor
that can occur in a part affected by dystonia (eg, tremu-
lous writer’s cramp) or in an unaffected part (eg, pos-
tural arm tremor in a patient with cervical dystonia).
This tremor is irregular in nature and is accompanied
by abnormal posturing. When it involves the head, dys-
tonic tremor may be confused with titubation (senile
tremor). It may be distinguished from titubation by hav-
ing the patient turn the head opposite to the direction
of the dystonic pull; worsening of the tremor indicates
dystonic tremor rather than titubation.
If the voice is
Also called hysterical or functional tremor, psy-
chogenic tremor is characterized by sudden onset and
and changes in severity over time. A history
be present. Tremor amplitude typically decreases with
Holmes’ tremor (red nuclear tremor) presents as a
terminal intention tremor or resting tremor that is vio-
lent in nature. Even a slight attempt to move a limb
can lead to severe jerking movements that may lead to
injury. Voice involvement can lead to inarticulate
Task-specific tremor is a type of action tremor associ-
manifests as rhythmic movements of the soft palate and
is usually associated with a brainstem or cerebellar
lesion, and essential palatal tremor, which manifests as
rhythmic ear clicks and is not associated with the pres-
ence of a brain lesion.
Certain neuropathies, including
Guillain-Barré syndrome, and dysgammaglobulinemic
neuropathy, are also associated with tremor.
tion in which the patient has essential tremor along with
certain neurologic signs that are insufficient to make a
diagnosis of any neurologic syndrome.
PHARMACOLOGIC MANAGEMENT OF TREMOR
Control of tremor is not always essential. Many
patients with mild essential tremor do not feel the
need to bring the tremor to the attention of their
physicians, let alone get treatment for it.
β-Adrenergic blockers (eg, propranolol) and the
anticonvulsive agent primidone are the mainstays of
treatment for essential tremor (Table 3).
can cause confusion and dizziness in elderly patients.
Furthermore, they must be used cautiously in patients
with asthma, heart failure, or diabetes. When essen-
tial tremor is induced by a drug that is medically nec-
β- blockers may be used to suppress the
Primidone has a response rate of up to
in patients with tremor and can be used in-
Benzodiazepines may be used to control the anxiety that
occur in the elderly with their use. Calcium channel
blockers are not very effective for the treatment of
tremor, but they may be tried if other agents fail.
The alternative agents acetazolamide
have not been shown to significantly improve
study showed no benefits with acetazolamide but found
alprazolam effective in essential tremor treatment.
Patients may use alcohol to self - treat essential
and the patient should be monitored because of the
potential risk of alcoholism. Long-term use of alcohol
is not beneficial because of the development of toler-
ance. In older patients, alcohol use can lead to falls,
drowsiness, and drug interactions.
Botulinum toxin is a new treatment mode that is cur-
rently under investigation. A randomized, double-blind
trial evaluated the use of botulinum toxin type A in
Although postural hand tremor was signifi-
improvement. Improved functional ability was not ob-
served, probably owing to the dose-dependent hand weak-
ness caused by the toxin itself. Botulinum toxin type A has
produced a modest response in patients with head and
voice tremor but carries the risk of producing dysphasia.
Strength training programs have been shown to
improve functional ability.
In patients with early Parkinson’s disease in whom
tremor is the only manifestation, there is no function-
al limitation; the use of medication is thus essential
only when other symptoms are present.
and gradually increased in strength and frequency.
Anticholinergic agents constitute a reasonable first
line of treatment in Parkinson’s disease (Table 4).
Potential adverse effects include urinary retention,
glaucoma in older patients. When anticholinergic
agents are inadequate, amantadine can be added. If
maximum tolerable dosages of both drugs are unsuc-
cessful in treating the patient, they are discontinued
and levodopa-carbidopa is begun. One of the prob-
lems of using levodopa-carbidopa is the fluctuation
between high and low blood levels of the drugs, lead-
ing to on-off phenomenon and dyskinesia. To avoid
this, smaller doses can be given at regular intervals.
Bromocriptine can help in the management of on-off
phenomenon and decrease the dose of levodopa.
Recent studies have found apomorphine and clozap-
ine useful in the treatment of parkinsonian tremor.
While most drug-induced tremors disappear after
discontinuation of the drug, drug-induced parkinson-
ian tremor may persist for years after discontinuation.
Treatment of drug-induced parkinsonian tremor is
Withdrawal symptoms produced by sedatives such as
barbiturates and benzodiazepines are treated by substi-
tuting related shorter-acting drugs given in tapering
doses. Alcohol withdrawal symptoms can be treated with
benzodiazepines. Delirium tremens is best managed by
adequate sedation of affected patients and supportive
Antipsychotic agents should be avoided in
Botulinum toxin injection
Calcium channel blockers
Data from Habib-ur-Rehman. Diagnosis and management of tremor.
Arch Intern Med 2000;160:2438–44.
Data from Evidente VG. Understanding essential tremor. Differential
diagnosis and options for treatment. Postgrad Med 2000;108:
138–40, 143–6, 149.
aged with supportive care and benzodiazepines. Frank
psychosis can occur with PCP use and requires treat-
ment with antipsychotic agents.
Acute inorganic mercury exposure is treated with
Chronic mercury poisoning is treated
Lithium intoxication is
venous hydration, diuresis, urine alkalinization, and
supportive treatment. Hemodialysis may be required
for severe cases.
Treatment of Other Tremors
Cerebellar tremors are extremely difficult to treat.
Some progress has been reported with clonazepam and
Holmes’ tremor has shown some
Physiologic tremor is best treated
cipitating state. Small doses of
β- blockers may also help.
Dystonic head tremors respond to botulinum toxin injec-
Propranolol, primidone, alcohol, and botulinum
Neuropathic tremor does not always improve
with resolution of the underlying neuropathy and may
respond to propranalol.
Palatal tremors occasionally
SURGICAL MANAGEMENT OF TREMORS
Surgical treatment is considered only for severe dis-
abling tremors after medical treatment has failed. Two
procedures used in the treatment of Parkinson’s dis-
ease and essential tremor are thalamotomy and thala-
mic stimulation targeting the ventralis intermedius
nucleus of the thalamus. Thalamotomy is performed
via thermocoagulation. Thalamic stimulation is per-
formed by local implantation of a pulse generator.
These procedures, when performed on one side of the
Thalamic stimulation has the advantage of being feasi-
ble bilaterally; however, a bilateral thalamotomy may
lead to bulbar neurologic deficits (ie, dysphagia and
dysarthria) and cognitive neurologic deficits, as well as
visual field defects and hemiparesis.
These procedures improve tremor in 80% to 90%
tomy improves essential tremor in 69% to 93% of
thalamic stimulation is preferred because of
of patients with disabling essential tremor treated with
bilateral thalamic stimulation showed reduced tremor
and better functional ability.
Thalamic surgery may be beneficial in Holmes’
involved and the possibility of spontaneous remission.
Because of their frailty and coexistent medical prob-
lems, geriatric patients are at high risk of morbidity
and mortality when afflicted by a movement disorder
such as tremor. Elderly patients may also be at risk of
developing multiple forms of tremor (eg, resting and
action). Because the presence of tremors is often con-
sidered a part of aging, many patients may not benefit
from the treatment opportunities available.
In the evaluation of tremor, particular attention
must be paid when the tremor is sudden in onset,
occurs in uncommon sites (eg, the lower extremities,
tongue, or chin), is preceded by a neurologic event, or
is associated with other signs of neurologic dysfunc-
tion. Careful assessment and the judicious use of med-
ication, when needed, will help these patients retain
their physical independence longer.
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Copyright 2001 by Turner White Communications Inc., Wayne, PA. All rights reserved.