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Hector A. Gonzalez-Usigli

, MD, HE UMAE Centro Médico Nacional de Occidente

Last full review/revision May 2020| Content last modified May 2020
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Tremors are involuntary, rhythmic, oscillatory movements of reciprocal, antagonistic muscle groups, typically involving the hands, head, face, vocal cords, trunk, or legs. Diagnosis is clinical. Treatment depends on the cause and type of tremor and may involve avoidance of triggers (physiologic), propranolol or primidone (essential), physical therapy (cerebellar), levodopa (parkinsonian), and possibly deep brain stimulation or thalamotomy (disabling and drug-refractory).

Tremor may be

  • Normal (physiologic)

  • Pathologic

Physiologic tremor, usually barely perceptible, becomes noticeable in many people during physical or mental stress.

Tremors vary in

  • Pattern of occurrence (eg, intermittent, constant)

  • Severity

  • Acuity (eg, gradual, abrupt)

The severity of tremor may not be related to the seriousness of the underlying disorder. For example, essential tremor is generally thought of as benign and should not shorten life, but symptoms can be disabling, and cerebellar degeneration has been detected in some neuropathologic studies.

Pathophysiology of Tremor

Various lesions in the brain stem, extrapyramidal system, or cerebellum can cause tremors. Neural dysfunction or lesions that cause tremor may result from injury, ischemia, metabolic abnormalities, or a neurodegenerative disorder. Sometimes tremor is a familial condition (eg, essential tremor).


Tremor is classified primarily based on when it occurs:

  • Resting tremors are visible at rest and occur when a body part is completely supported against gravity. Resting tremors are minimal or absent during activity. They occur at a frequency of 3 to 6 cycles/seconds (hertz [Hz]).

  • Action tremors are maximal when a body part is moved voluntarily. Action tremors may or may not change in severity as a target is reached; they can occur at very different frequencies, but the frequency is always < 13 Hz.

Action tremors include kinetic, intention, and postural tremors.

  • Kinetic tremors appear in the last part of a movement toward a target; amplitude is low.

  • Intention tremors occur during voluntary movement toward a target, but amplitude is high and frequency is low during the complete movement, while the tremor worsens as the target is reached (as seen in finger-to-nose testing); they occur at a frequency of 3 to 10 Hz.

  • Postural tremors are maximal when a limb is maintained in a fixed position against gravity (eg, holding the arms stretched out); they occur at a frequency of 5 to 8 Hz. Sometimes they are modified by specific positions or tasks, which may indicate their origin; for example, dystonia may trigger a tremor (dystonic tremor).

Complex tremors can have components of more than one type of tremor.

Tremor can also be classified based on whether it is

  • Physiologic (within the range of normal)

  • A primary disorder (essential tremor, Parkinson disease)

  • Secondary to a disorder (eg, stroke)

Tremor is usually described based on frequency of oscillations (rapid or slow) and amplitude of movement (fine [low amplitude] or coarse [high amplitude]).

Etiology of Tremor

Physiologic tremor

Physiologic tremor occurs in otherwise healthy people. It is an action or postural tremor that tends to affect both hands about equally; amplitude is usually fine. It is often noticeable only when certain stressors are present. These stressors include

  • Anxiety

  • Fatigue

  • Exercise

  • Sleep deprivation

  • Withdrawal of alcohol or certain other central nervous system (CNS) depressant drugs (eg, benzodiazepines, opioids)

  • Certain disorders (eg, hyperthyroidism), when symptomatic

  • Consumption of caffeine or recreational drugs such as cocaine, amphetamines, or phencyclidine

  • Use of certain therapeutic drugs, such as theophylline, beta-adrenergic agonists, corticosteroids, and valproate

Pathologic (nonphysiologic) tremor

There are many causes (see table Some Causes of Tremor), but the most common are


Some Causes of Tremor


Suggestive Findings

Diagnostic Approach

Action tremor*

Alcohol or drug withdrawal (eg, of benzodiazepines or opioids)

Agitation and fine tremor starting 24–72 hours after the last use of alcohol or the drug (eg, a benzodiazepine)

Sometimes hypertension, tachycardia, or fever, especially in hospitalized patients

Clinical evaluation

History of drug use

Amelioration of tremor after stopping the drug

Endocrinologic, metabolic, and toxic abnormalities:

Tremor plus altered level of consciousness (suggesting encephalopathy) and an obvious underlying disorder (eg, renal or hepatic failure)

Exophthalmos, hyperreflexia, tachycardia, heat intolerance (suggesting hyperthyroidism)

Extreme, refractory hypertension (suggesting pheochromocytoma)

TSH level

24-hour urine collection to check for metanephrines

Ammonia level, BUN, glucose level, and calcium and PTH levels

Heavy metal testing

Essential tremor

Progressively persistent coarse or fine, slow (4–8 Hz) tremor, usually symmetric and affecting both upper extremities and sometimes the head and voice, particularly in patients with a family history of tremor

Clinical evaluation

Physiologic tremor

Fine, rapid (8–13 Hz) tremor that occurs in otherwise healthy people and may be enhanced by certain drugs or conditions (see above)

Usually suppression of tremor with low doses of alcohol and other sedatives

Clinical evaluation

Resting tremor

History of using drugs that block dopamine receptors or deplete dopamine reserves

Amelioration of tremor after stopping the drug

Low-frequency (3–6 Hz) alternating tremor, often of the thumb against the index finger (pill rolling) but sometimes also affecting the chin or a leg

Usually accompanied by other symptoms, such as micrographia, bradykinesia (slow movement), cogwheel rigidity, and shuffling gait

Often no family history of Parkinson tremor and no reduction in tremor after alcohol consumption

Specific clinical criteria

Good response to empiric trial of dopaminergic drugs

Intention tremor

Cerebellar lesions:

Low-frequency (< 4 Hz) tremor that usually occurs unilaterally with ataxia, dysmetria, dysdiadochokinesia (inability to perform rapid alternating movements), and dysarthria

In some patients, family history of the disorder (eg, Friedreich ataxia)

MRI of the brain

History of use of certain drugs

Amelioration of tremor after stopping the drug

Complex tremors

Holmes tremor (midbrain, red nucleus, rubral, or thalamic tremor)

Irregular, low-frequency (< 4.5 Hz) tremor predominantly in the proximal limbs

Combination of rest, postural, and intention tremors caused by midbrain lesions (eg, due to stroke or multiple sclerosis) near the red nucleus

Sometimes signs of ataxia and weakness

MRI of the brain

Neuropathic tremor:

Variable tremor type and frequency, usually postural and intention tremor in the affected extremities

Other signs of peripheral neuropathy


Psychogenic tremor

Abrupt onset and/or spontaneous remission of complex mixed-type tremor with changing characteristics

Increased by attention and lessened by distraction of patient

Clinical evaluation

Variable tremor type (usually in the proximal arm) in children or young adults, often with signs of hepatic failure, rigidity, clumsy gait, dysarthria, inappropriate grinning, drooling, and neuropsychiatric signs

24-hour urine collection to measure copper level; serum ceruloplasmin

Slit-lamp examination to check for Kayser-Fleischer rings around the iris (caused by copper deposition)

* Action tremors can be kinetic, intentional, or postural. Kinetic tremors appear in the last part of a movement toward a target part. Intention tremors occur during voluntary movement toward a target. Postural tremors are maximal when a limb is maintained in a fixed position against gravity.

BUN = blood urea nitrogen; Hz = hertz; PTH = parathyroid hormone; TBI = traumatic brain injury; TSH = thyroid-stimulating hormone.

Drugs (see table Some Causes of Tremor by Type) can cause or aggravate different types of tremor. Low doses of some sedatives (eg, alcohol) may relieve some tremors (eg, essential and physiologic tremor); higher doses may cause or exacerbate tremor.


Some Drug Causes of Tremor by Type


Postural Tremor

Resting Tremor (Drug-Induced Parkinsonism)

Intention Tremor



Amphotericin B

Beta-agonists (inhaled)*













MDMA (Ecstasy)















* More common cause of tremor.

MDMA = methylenedioxymethamphetamine; SSRI = selective serotonin reuptake inhibitor.

Data from Morgan JC, Sethi KD: Drug-induced tremors. The Lancet Neurology 4:866–876, 2005.

Evaluation of Tremor

Because the diagnosis of tremor is largely clinical, a meticulous history and physical examination are essential.


History of present illness should cover

  • Acuity of onset (eg, gradual, abrupt)

  • Age at onset

  • Body parts affected

  • Provoking factors (eg, movement, rest, standing)

  • Alleviating or exacerbating factors (eg, alcohol, caffeine, stress, anxiety)

If onset is abrupt, patients should be asked about potential triggering events (eg, recent trauma or illness, use of a new drug).

Review of systems should seek symptoms of causative disorders, including

Past medical history should cover conditions associated with tremor (see table Some Causes of Tremor). Family history should include questions about tremor in 1st-degree relatives. The drug profile should be reviewed for causative drugs (see table Some Drug Causes of Tremor), and patients should be asked specifically about caffeine intake and alcohol and recreational drug use (particularly recent discontinuation).

Physical examination

A complete and extensive neurologic examination is mandatory and should include evaluation of mental status, cranial nerves, motor and sensory function, gait, muscle stretch reflexes, and cerebellar function (with observation of finger-to-nose, shin-to-heel, and rapid alternating hand movements). The examiner should test muscles for rigidity by moving the limbs through their range of motion.

Vital signs should be reviewed for tachycardia, hypertension, or fever. General examination should note any cachexia, psychomotor agitation, and absence of facial expressions (which may indicate bradykinesia). The thyroid should be palpated for nodules and enlargement, and any signs of exophthalmus or eyelid lag should be noted.

Focused examination should note distribution and frequency of the tremor while

  • The affected body parts are at rest and fully supported (eg, in the patient’s lap).

  • The patient assumes certain postures (eg, holding the arms outstretched).

  • The patient is walking or doing tasks with the affected body part.

The examiner should note whether the tremor changes during mental distraction tasks (eg, serial subtraction of 7 from 100). The quality of the voice should be observed while the patient sustains a long note.

Red flags

The following findings are of particular concern:

  • Abrupt onset

  • Onset in people < 50 and with no family history of benign tremor

  • Other neurologic deficits (eg, change in mental status, motor weakness, cranial nerve palsy, ataxic gait, dysarthria)

  • Tachycardia and agitation

Interpretation of findings

Clinical findings help suggest a cause (see table Some Causes of Tremor).

Tremor type and onset are useful clues:

  • Resting tremors usually indicate Parkinson disease, particularly when they are unilateral or when tremor is isolated to the chin, voice, or leg.

  • Intention tremors suggest a cerebellar disorder but may result from multiple sclerosis or Wilson disease.

  • Postural tremors suggest physiologic or essential tremor if onset is gradual; it suggests a toxic or metabolic disorder if onset is sudden.

Severe essential tremor is often confused with Parkinson disease but can usually be distinguished by specific characteristics (see table Some Characteristics Differentiating Parkinson Disease From Essential Tremor). Occasionally, the two syndromes overlap (mixed essential tremor–Parkinson disease).


Some Characteristics Differentiating Parkinson Disease From Essential Tremor


Parkinson Disease

Essential Tremor

Tremor type

Resting tremor

Postural and intention tremors


Older age (> 60)

All age groups

Family history

Usually negative

Positive in > 60% of patients


Does not suppress tremor

Suppresses tremor

Tremor onset



Muscle tone

Cogwheel rigidity


Facial expression




Decreased arm swing

Normal or mild imbalance

Tremor latency

Longer (8–9 seconds)

Shorter (1–2 seconds)

The following findings may help suggest causes of tremor:

  • Sudden onset is most typical of psychogenic tremor after physical pathologic processes have been ruled out.

  • Stepwise progression suggests an ischemic vascular disorder or multiple sclerosis

  • Development of tremor after use of a new drug suggests that the drug is the cause.

  • Onset of tremor with agitation, tachycardia, and hypertension within 24 to 72 hours of hospitalization may suggest withdrawal from alcohol, a sedative, or an illicit substance.

Gait is observed. Gait abnormalities may suggest multiple sclerosis, stroke, Parkinson disease, or a cerebellar disorder. Gait is characteristically narrow-based and shuffling in Parkinson disease and wide-based and ataxic in cerebellar disorders. The gait may have histrionic or inconsistent qualities in patients with psychogenic tremor. In patients with essential tremor, gait is often normal, but tandem gait (placing heel to toe) may be abnormal.

Psychogenic tremor can be identified because psychogenic tremors decrease or disappear when the patient is mentally distracted and when tremor frequency synchronizes (entrains) to a volitional tapping rhythm by an unaffected body part. Maintaining different volitional movement frequencies simultaneously in two different body parts is difficult.


In most patients, history and physical examination are sufficient to identify the likely etiology of tremor. However, MRI or CT of the brain should be done if

  • Tremor onset is acute.

  • Progression is rapid.

  • Focal neurologic signs suggest a structural lesion (eg, stroke, brain tumor, a demyelinating disorder).

When the cause of tremor is unclear (based on history and physical examination findings), the following are done:

  • Thyroid-stimulating hormone (TSH) and thyroxine (T4) are measured to check for hyperthyroidism.

  • Calcium and parathyroid hormone are measured to check for hyperparathyroidism or hypoparathyroidism.

  • Glucose testing is done to rule out hypoglycemia.

In patients with toxic encephalopathy, the underlying condition is usually readily apparent, but measurement of BUN and ammonia levels can help confirm the etiology. Measurement of free metanephrines in plasma is indicated in patients with unexplained refractory hypertension. Serum ceruloplasmin and urinary copper levels should be measured to check for Wilson disease if patients are < 40 and have tremor with an unclear cause (with or without parkinsonism) and no family history of benign tremor.

Although electromyography (EMG) can differentiate true tremor from other movement disorders (eg, myoclonus, clonus, epilepsia partialis continua), it is rarely required. However, EMG may help establish peripheral neuropathy as a potential cause of tremor if a neuropathy is clinically suspected.

Treatment of Tremor

Physiologic tremors

No treatment is necessary unless symptoms are bothersome. Avoiding triggers (such as caffeine, fatigue, sleep deprivation, drugs, and, when possible, stress and anxiety) can help prevent or reduce symptoms.

Physiologic tremor is enhanced by alcohol withdrawal, by hyperthyroidism, and by use of drugs and by conditions that can cause tremor. The tremor responds to treatment of the underlying condition.

Oral benzodiazepines (eg, diazepam 2 to 10 mg, lorazepam 1 to 2 mg, oxazepam 10 to 30 mg) given 3 or 4 times a day may be useful for people with tremor and chronic anxiety, but continuous use should be avoided. Propranolol (20 to 80 mg orally 4 times a day) and other beta-blockers are often effective for tremor enhanced by drugs or acute anxiety (eg, stage fright).

Essential tremors

Propranolol 20 to 80 mg orally 4 times a day (or other beta-blockers) is often effective, as is primidone 50 to 250 mg orally 3 times a day. For some patients, a small amount of alcohol is effective; however, alcohol is not routinely recommended for treatment because abuse is a risk.

Second-line drugs are topiramate 25 to 100 mg orally 2 times a day and gabapentin 300 mg orally 2 or 3 times a day. Benzodiazepines may be added if other drugs do not control the tremor.

Cerebellar tremors

No effective drug is available; physical therapy (eg, weighting the affected limbs, teaching patients to brace the proximal limb during activity) sometimes helps.

Parkinsonian tremors

Parkinson disease is treated.

Levodopa is usually the treatment of choice for most parkinsonian tremors.

Anticholinergic drugs may be considered in certain cases, but their adverse effects (decreased mental concentration, dry mouth, dry eyes, urinary retention and the possibility that they enhance tau pathology) may outweigh their benefits, particularly in older patients.

Other drugs include dopamine agonists (eg, pramipexole, ropinirole), MAO type B inhibitors (selegiline, rasagiline), catechol O-methyltransferase (COMT) inhibitors (entacapone, tolcapone—used only in combination with levodopa), and amantadine.

Disabling tremor

For severe, disabling, drug-refractory essential tremor, surgical management with unilateral stereotactic thalamotomy or chronic unilateral or bilateral thalamic deep brain stimulation may be considered.

Dystonic tremor may respond better to functional neurosurgery targeting the internal portion of the globus pallidus.

In Parkinson disease, tremor substantially lessens after thalamic, internal globus pallidus, or subthalamic nucleus deep brain stimulation.

Although these techniques are widely available, they should be used only after reasonable drug therapy has failed and only in patients who do not have substantial cognitive or psychiatric impairment.

Geriatrics Essentials: Tremor

Many older patients attribute development of tremor to normal aging and may not seek medical attention. Although essential tremor is more prevalent among the older people, a thorough history and physical examination are required to rule out other causes and to determine whether the symptoms are severe enough to justify drug or surgical treatment.

Comparatively low doses of drugs may exacerbate tremor in older patients, and adjusting doses of chronically used drugs (eg, amiodarone, metoclopramide, selective serotonin reuptake inhibitors, thyroxine) to the lowest effective dose should be considered. Similarly, older patients are more vulnerable to adverse effects of drugs used to treat tremor; thus, these drugs should be used cautiously in older patients, usually at lower dosages than are otherwise considered optimal. If possible, anticholinergic drugs should not be used in older patients.

Tremor can significantly affect functional ability in older patients, particularly if they have other physical or cognitive impairments. Physical and occupational therapy can provide simple coping strategies, and assistive devices may help maintain quality of life.

Key Points

  • Tremor can be classified as resting or action (which includes intention, kinetic, and postural tremors).

  • The most common causes of tremor include physiologic tremor, essential tremor, and Parkinson disease.

  • History and physical examination can typically identify the etiology of tremor.

  • Consider Parkinson disease if patients have a resting tremor, consider essential or physiologic tremor if they have a postural or an action tremor, and consider cerebellar tremor if they have an intention tremor.

  • If tremor begins abruptly or occurs in patients who are < 50 and do not have a family history of benign tremor, evaluate them promptly and thoroughly with brain imaging and laboratory tests based on clinical presentation.

  • Treat according to the cause and type of tremor: avoidance of triggers (physiologic), propranolol or primidone (essential), physical therapy (cerebellar), usually levodopa (parkinsonian), and possibly deep brain stimulation (disabling and drug-refractory).

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