Remor, the most common movement disorder in the general population, is an involuntary

remor, the most common movement disorder

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.

1

Tremors can lead to social

and physical deterioration and may be a harbinger of a

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.

2

Many patients feel that tremors are a part of aging

and fail to report them to their physicians, which

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

3

showed that 25% of the

patients diagnosed by nonneurologists to have

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.

DIFFERENTIAL DIAGNOSIS FOR MOVEMENT DISORDERS

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

ruled out.

4

Athetosis constitutes slow writhing movements of

the arms and legs that commonly occur on movement.

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

syndrome.

4

Myoclonic jerks are sudden, brief, and shock-like

and lack the rhythmicity of tremors. In adults and the

elderly, myoclonus is rare and occurs in association

with Creutzfeldt-Jakob disease, uremia, hypomagne-

semia and liver failure.

4

Tics are brief contractions of a

muscle, which may be confused with tremors due to

their repetitive nature. Tics commonly occur in chil-

dren and can produce features such as sniffing, grunt-

ing, pouting, and grimacing. 

CLINICAL CLASSIFICATION OF TREMOR

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

T

Dr. Bhagwath is an internist at St. Louis Internal Medicine, St. Louis,

MO.

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31

C l i n i c a l   R e v i e w   A r t i c l e

Tremors in Elderly Persons: 

Clinical Features and Management

Gayathri Bhagwath, MBBS

of the skeletal muscle.

5

If the limb is not supported, its

muscles will be expending energy to maintain position;

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.

4

Action tremor includes postural, kinetic, and iso-

metric tremors.

6

Postural tremor occurs when a body

part is voluntarily held motionless against gravity—for

example, pointing at an object or protruding the

tongue.

7

Kinetic tremor occurs during voluntary move-

ment of a body part. An intention tremor is a kinetic

tremor that worsens during the completion of a visual-

ly guided, goal-directed movement (eg, pouring tea

into a cup).

6

Task-specific tremor occurs during com-

plex tasks such as writing or playing a musical instru-

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

stationary object.

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.

32

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Other tremor syndromes:

Dystonic tremor

Isolated chin tremor

Isolated voice tremor

Indeterminate tremor 

syndrome

Intention

tremor

Task-specific

tremor

Simple kinetic

tremor

Resting

tremor

Postural

tremor

Isometric

tremor

Figure 1. Clinical classification of tremor. (Data from Habib-ur-Rehman. Diagnosis and management of tremor. Arch Intern

Med 2000;160:2438–44.)

Table 1. Causes of Tremors in the Elderly

Action Tremor

Resting Tremor

Parkinsonism

Parkinsonism

Essential tremor

Alcohol withdrawal

Cerebellar disease

Essential tremor*

Holmes’ tremor

Neurosyphilis

Physiologic tremor

Drugs (except those 

causing parkinsonism)

*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.

Tremor

Action

tremor

Kinetic

tremor

CLINICAL FEATURES OF DISORDERS ASSOCIATED WITH

TREMOR

Essential Tremor

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.

7

Also

known as senile tremor, it constitutes a mixture of pos-

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%.

7

A con-

siderable number of patients with mild essential

tremor (up to 50%)

8

may be unaware of their tremor,

and it does not come to the attention of their physi-

cian. Some patients may present with only isolated

head tremor. 

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.

5

Typically, there is an absence of signs of other neuro-

logic disorders, although essential tremor may coexist

with Parkinson’s disease.

Etiology and pathogenesis.

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.

1

Autopsies of persons who had essential tremor revealed

no histologic abnormalities.

9

Routine computed tomog-

raphy and magnetic resonance imaging scans are typi-

cally normal.

1

It has been proposed that enhanced

oscillations in the olivocerebellar to rubrothalamic

pathways are the cause of essential tremor.

9

Increased

glucose metabolism in the olivary nuclei and increased

blood flow in the red nucleus, cerebellum, and thala-

mus have been observed bilaterally on positron emis-

sion tomography of patients with essential tremor.

10

In

animal models, a tremor similar to essential tremor was

produced on stimulation of olivary nuclei with the alka-

loid harmaline and serotonergic drugs,

11

lending fur-

ther support to the involvement of this site in the gene-

sis of tremor. 

Cerebellar 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.

12

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Table 2. Comparison of Essential Tremor and Parkinsonian Tremor

Characteristic

Essential Tremor

Parkinsonian Tremor

Type of tremor

Action, usually symmetrical

Rest and action, initially unilateral

Agents or states that improve

Alcohol, relaxation; voluntary

Sleep; voluntary suppression is

the tremor

suppression is possible

not possible 

Agents or states that worsen

Excitement, anger, fatigue, fear,

Emotional stress, excitement,

the tremor

caffeine, nicotine, 

β-agonists

fatigue

Other findings

Occasional cogwheel rigidity

Bradykinesia, cogwheel rigidity, 

gait disturbance, depression,

cognitive decline 

Head involvement

Titubation commonly present

Titubation is usually absent; chin,

jaw, and lip tremor may be 

present

Voice involvement

Tremulous voice

Low-volume voice

Involvement of the laryngeal muscles leads to an unco-

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.

4

The

cerebellum also receives sensory information from the

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

as tremors.

13

Vascular accidents, malignancy, and

chronic alcohol or drug abuse

4

may cause a lesion in

the deep cerebellar nuclei (ie, the dentate, globose, or

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

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.

14

The

same may hold true for drug-induced parkinsonism

(DIP).

4

Common causes of DIP include neuroleptic

agents, calcium channel blockers, valproic acid, tacrine,

bethanechol chloride, reserpine, and methyldopa.

15

Lower-potency neuroleptics or novel neuroleptics (eg,

clozapine) that lack prominent striatal receptor block-

ade are less likely to cause DIP.

16

Clinically, DIP cannot

be distinguished from idiopathic Parkinson’s disease;

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.

5,6

It must be

of 2-year duration to fit the diagnostic criteria and may

be a form of Parkinson’s disease.

Etiology and pathogenesis.

The anatomy of the

structures involved in production of parkinsonian

tremor is briefly described.

17

Subcortical grey matter

is grouped into nuclei known as basal ganglia, which

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

cerebral cortex.

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

2

recep-

tor blockade results in decreased dopamine activity.

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.

9

The

exact cause of the oscillations is unclear, however. The

cerebellum is involved in control of the parkinsonian

rest tremor.

18

Drug-Induced Tremors 

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.

6

Even short-term use

of intravenous high-dose haloperidol (> 240 mg) has

been associated with tremors, rigidity and dyskinesia.

19

Sympathomimetic agents, cyclosporine, lithium, and tri-

cyclic antidepressants are known to enhance physiolog-

ic tremor.

15

Lithium overdose produces ataxia, tremor,

34

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confusion, cardiac arrhythmias, gastrointestinal distress,

muscle twitching, and fasciculations. It can be diag-

nosed by measuring serum levels of lithium.

20

Tremors are one of the common clinical features of

serotonin syndrome, which is most commonly caused

by interaction between serotonergic agents and

monoamine oxidase inhibitors. Symptoms resolve after

the discontinuation of the serotonergic drugs.

21

Barbiturate withdrawal can produce anxiety, restless-

ness, delirium, seizures, and tremor.

22

Abstinence from

ethanol can produce similar symptoms within the first

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

(PCP) withdrawal.

22

Chronic exposure to metallic mercury produces an

intention tremor that can be accompanied by erethism

(memory loss, excitability, insomnia, and delirium).

This may be observed in workers in the felt-hat indus-

try and sometimes in dentists.

23

Acute exposure to mer-

cury or its vapors can also lead to tremors. 

Physiologic Tremor

Normal individuals can manifest an action tremor,

especially while fatigued or experiencing emotions

such as fear, anxiety, or stress.

6

Physiologic tremor can

also result from medical conditions such as hypother-

mia, hypoglycemia, pheochromocytoma, thyrotoxico-

sis, and alcohol withdrawal.

5

A characteristic feature of physiologic tremor is the

disappearance of the tremor on removal of the precipi-

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.

Dystonic Tremor

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.

1

If the voice is

affected, it is either crackling or breath-like in nature.

Psychogenic Tremor

Also called hysterical or functional tremor, psy-

chogenic tremor is characterized by sudden onset and

remission

5

and changes in severity over time. A history

of mental illness and unrelated neurologic signs may

be present. Tremor amplitude typically decreases with

distraction.

Other Tremors

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

speech.

4

Task-specific tremor is a type of action tremor associ-

ated with certain tasks, such as writer’s tremor.

5

Palatal

tremor includes symptomatic palatal tremor, which

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.

24

Certain neuropathies, including

chronic inflammatory demyelinating neuropathy,

Guillain-Barré syndrome, and dysgammaglobulinemic

neuropathy, are also associated with tremor.

6

The term

“indeterminate tremor syndrome” is assigned to a condi-

tion in which the patient has essential tremor along with

certain neurologic signs that are insufficient to make a

diagnosis of any neurologic syndrome.

6

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. 

Essential Tremor

β-Adrenergic blockers (eg, propranolol) and the

anticonvulsive agent primidone are the mainstays of

treatment for essential tremor (Table 3). 

β-Blockers

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-

essar y, 

β- blockers may be used to suppress the

tremor.

15

Primidone has a response rate of up to

75%

25

in patients with tremor and can be used in-

stead of 

β-adrenergic blockers. 

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Gabapentin is well tolerated by older patients.

1

Benzodiazepines may be used to control the anxiety that

enhances tremor. Severe drowsiness and confusion may

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.

1

The alternative agents acetazolamide

26

and metazo-

lamide

27

have not been shown to significantly improve

essential tremor. A double-blind placebo-controlled

study showed no benefits with acetazolamide but found

alprazolam effective in essential tremor treatment.

26

Patients may use alcohol to self - treat essential

tremor; however, this practice should be discouraged,

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

133 patients.

28

Although postural hand tremor was signifi-

cantly reduced, kinetic hand tremor showed no long-term

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.

1

Strength training programs have been shown to

decrease the magnitude of essential tremor but did not

improve functional ability.

29

Parkinsonian Tremor

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.

12

All anti-

parkinsonian drugs must be started at a small dose

and gradually increased in strength and frequency.

Anticholinergic agents constitute a reasonable first

line of treatment in Parkinson’s disease (Table 4).

12

Potential adverse effects include urinary retention,

confusion, and hallucinations; they also can worsen

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.

30,31

Drug-Related Tremor

While most drug-induced tremors disappear after

discontinuation of the drug, drug-induced parkinson-

ian tremor may persist for years after discontinuation.

15

Treatment of drug-induced parkinsonian tremor is

similar to that of Parkinson’s disease. 

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

treatment.

22

Antipsychotic agents should be avoided in

these patients because these agents lower the seizure

36

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Table 3. Pharmacologic Agents for Treatment of

Essential Tremor

β-Adrenergic blockers

Metoprolol 

Propranolol 

Benzodiazepines

Clonazepam 

Diazepam 

Botulinum toxin injection

Calcium channel blockers

Gabapentin 

Primidone 

Data from Habib-ur-Rehman. Diagnosis and management of tremor.

Arch Intern Med 2000;160:2438–44.

Table 4. Pharmacologic Agents for Treatment of

Parkinsonian Tremor

Amantadine

Anticholinergic agents

Benztropine mesylate

Biperiden 

Trihexyphenidyl

Bromocriptine mesylate

Levodopa-carbidopa

Data from Evidente VG. Understanding essential tremor. Differential

diagnosis and options for treatment. Postgrad Med 2000;108:

138–40, 143–6, 149. 

threshold. Hallucinogen and PCP users can be man-

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

dimercaprol.

23

Chronic mercury poisoning is treated

with  N- acetyl penicillamine.

23

Lithium intoxication is

treated with gastrointestinal decontamination, intra-

venous hydration, diuresis, urine alkalinization, and

supportive treatment. Hemodialysis may be required

for severe cases.

20

Treatment of Other Tremors

Cerebellar tremors are extremely difficult to treat.

Some progress has been reported with clonazepam and

ondansetron.

32,33

Holmes’ tremor has shown some

response to levodopa.

34

Physiologic tremor is best treated

by removal of the causative agent or resolution of the pre-

cipitating state. Small doses of 

β- blockers may also help.

6

Dystonic head tremors respond to botulinum toxin injec-

tions.

35

Propranolol, primidone, alcohol, and botulinum

toxin may be beneficial in the treatment of task-specific

tremor.

25

Neuropathic tremor does not always improve

with resolution of the underlying neuropathy and may

respond to propranalol.

5

Palatal tremors occasionally

respond to local botulinum toxin injection.

5

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.

6

These procedures, when performed on one side of the

brain, improve symptoms on the contralateral side.

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.

6

These procedures improve tremor in 80% to 90%

of patients with Parkinson’s disease. Although thalamo-

tomy improves essential tremor in 69% to 93% of

patients,

36

thalamic stimulation is preferred because of

the bilateral nature of the disease. One-year follow-up

of patients with disabling essential tremor treated with

bilateral thalamic stimulation showed reduced tremor

and better functional ability.

37

Thalamic surgery may be beneficial in Holmes’

tremor but is not usually performed because of the risks

involved and the possibility of spontaneous remission.

5

CONCLUSION

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.

HP

REFERENCES

1. Evidente VG. Understanding essential tremor. Differ-

ential diagnosis and options for treatment. Postgrad

Med 2000;108:138–40, 143–6, 149.

2. Louis ED, Wendt KJ, Ford B. Senile tremor. What is the

prevalence and severity of tremor in older adults? Ger-

ontology 2000;46:12–6.

3. Marttila RJ, Rinne UK. Epidemiology of Parkinson’s dis-

ease in Finland. Acta Neurol Scand 1976;53:81–102.

4. Patten JP, editor. Neurological differential diagnosis. 2nd

ed. London: Springer Publication; 1998.

5. O’Sullivan JD, Lees AJ. Nonparkinsonian tremors. Clin

Neuropharmacol 2000;23:233–8.

6. Habib - ur -Rehman. Diagnosis and management of

tremor. Arch Intern Med 2000;160:2438–44.

7. Elble RJ. Diagnostic criteria for essential tremor and dif-

ferential diagnosis. Neurology 2000;54(11 Suppl 4):S2–6.

8. Elble RJ. Tremor in ostensibly normal elderly people.

Mov Disord 1998;13:457–64.

9. Elble RJ. Central mechanisms of tremor. J Clin Neu-

rophysiol 1996;13:133–44.

10. Boecker H, Brooks DJ. Functional imaging of tremor.

Mov Disord 1998;13 Suppl 3:64–72.

11. Elble RJ. Animal models of action tremor. Mov Disord

1998;13 Suppl 3:35–9.

12. Miller JQ. Involuntary movements in the elderly. Parkin-

son’s disease and other causes. Postgrad Med 1986;79:

323–30.

13. Elble RJ. Origins of tremor. Lancet 2000;355:1113–4.

14. Nagayama H, Hamamoto M, Nito C, et al. Initial symp-

toms of Parkinson’s disease with elderly onset. Geron-

tology 2000;46:129–32.

15. Diederich NJ, Goetz CG. Drug - induced movement

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

(continued on page 49)

www.turner-white.com

Hospital Physician  December 2001

37

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

www.turner-white.com

Hospital Physician  December 2001

49

(from page 37)

disorders. Neurol Clin 1998;16:125–41.

16. Kompoliti K. Drug-induced and iatrogenic neurological

disorders. In: Goetz CG, editor. Textbook of clinical neu-

rology. 1st ed. Philadelphia: WB Saunders; 1999:1125.

17. Daroff RB, Martin JB. Nervous system dysfunction. In:

Fauci AS, et al, editors. Harrison’s principles of internal

medicine. 14th ed. New York: McGraw-Hill; 1998.

18. Deushl G, Wilms H, Krack P, et al. Function of the cere-

bellum in Parkinsonian rest tremor and Holmes’ trem-

or. Ann Neurol 1999;46:126–8.

19. Riker RR, Fraser GL, Richen P. Movement disorders

associated with withdrawal from high-dose intravenous

haloperidol therapy in delirious ICU patients. Chest

1997;111:1778–81.

20. Linden CH, Lovejoy FH Jr. Poisoning and drug over-

dosage. In: Fauci AS, et al, editors. Harrison’s principles

of internal medicine. 14th ed. New York: McGraw-Hill;

1998:2523–44.

21. Sternbach H. The serotonin syndrome. Am J Psychiatry

1991;148:705–13.

22. Brust JC. Acute neurologic complications of drug and

alcohol abuse. Neurol Clin 1998;16:503–21.

23. Hu H. Heavy metal poisoning. In: Fauci AS, et al, edi-

tors. Harrison’s principles of internal medicine. 14th ed.

New York: McGraw-Hill; 1998:2564–69. 

24. Deuschl G, Toro C, Valls-Sole J, et al. Symptomatic and

essential palatal tremor. 1. Clinical, physiological and

MRI analysis. Brain 1994;117:775–88.

25. Wasielewski PG, Burns JM, Koller WC. Pharmacologic

treatment of tremor. Mov Disord 1998;13 Suppl 3:90–100.

26. Gunal DI, Afsar N, Bekiroglu N, Aktan S. New alterna-

tive agents in essential tremor therapy: double-blind

placebo-controlled study of alprazolam and acetazo-

lamide. Neurol Sci 2000;21:315–7.

27. Busenbark K, Ramig L, Dromey C, Koller WC. Meth-

azolamide for essential voice tremor. Neurology 1996;47:

1331–2.

28. Brin MF, Lyons KE, Douchette J, et al. A randomized,

double masked, controlled trial of botulinum toxin type

A in essential hand tremor. Neurology 2001;56:1523–8.

29. Bilodeau M, Keen DA, Sweeney PJ, et al. Strength train-

ing can improve steadiness in persons with essential

tremor. Muscle Nerve 2000;23:771–8.

30. Hughes AJ, Lees AJ, Stern GM. Apomorphine in the di-

agnosis and treatment of parkinsonian tremor. Clin

Neuropharmacol 1990;13:312–7.

31. Friedman JH, Koller WC, Lannon MC, et al. Benz-

tropine versus clozapine for the treatment of tremor in

Parkinson’s disease. Neurology 1997;48:1077–81.

32. Trelles L, Trelles JO, Castro C, et al. Successful treatment

of two cases of intention tremor with clonazepam. Ann

Neurol 1984;16:621.

33. Rice GP, Lesaux J, Vandervoort P, et al. Odansetron, a 

5-HT3 antagonist, improves cerebellar tremor. J Neurol

Neurosurg Psychiatry 1997;62:282–4.

34. Findley LJ, Gresty MA. Suppression of “rubral” tremor

with levodopa. Br Med J 1980;281;1043.

35. Wissel J, Masuhr F, Schelosky L, et al. Quantitative assess-

ment of botulinum toxin treatment in 43 patients with

head tremor. Mov Disord 1997;12;722–6.

36. van Manen J. Stereotaxic operations in cases of heredi-

tary and intention tremor. Acta Neurochir (Wien) 1974;

Suppl 21:49–55.

37. Pahwa R, Lyons KL, Wilkinson SB, et al. Bilateral thala-

mic stimulation for the treatment of essential tremor.

Neurology 1999;53:1447–50.

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