Тремор

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]).

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

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

• For action (including postural) tremors: Essential tremor

• For resting tremors: Parkinson disease

• For intention tremors: Cerebellar dysfunction (eg, due to a stroke, trauma, or multiple sclerosis)

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 suppress some tremors (eg, essential and physiologic tremor); higher doses may cause or exacerbate tremor.

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

• Multiple episodic neurologic problems: Multiple sclerosis

• Recent sudden onset of motor weakness, language difficulties, or dysarthria: Stroke

• Confusion and fever: Meningitis, encephalitis, brain abscess, or brain tumor

• Muscle rigidity, gait and postural problems, and slowness of movement: Parkinson disease or other forms of parkinsonism

• Weight loss, increased appetite, palpitations, diarrhea, and heat intolerance: Hyperthyroidism

• Sensory deficits: Peripheral neuropathy

• Agitation and hallucinations: Alcohol withdrawal or drug toxicity

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).

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.

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

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 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).

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 or another sedative or use of 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 blood urea nitrogen 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, especially if tremor has a wing-beating quality (with or without parkinsonism and dystonic features) and no family history of benign tremor. (Wing-beating is a low-frequency, high-amplitude, posture-induced arm tremor, elicited by sustained abduction of the arms, with flexed elbows and palms.)

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.

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).

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.

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

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, rotigotine), MAO type B inhibitors (selegiline, rasagiline), catechol O-methyltransferase (COMT) inhibitors (entacapone, tolcapone—used only in combination with levodopa), and amantadine.

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.

For patients with psychogenic tremor, tremor entrainment may help. This treatment refers to the change or elimination of tremor as the patient performs a voluntary rhythmical movement by the unaffected limb (1).

1. 1.Espay AJ, Edwards MJ, Oggioni GD, et al: Tremor retrainment as therapeutic strategy in psychogenic (functional) tremor. Parkinsonism Relat Disord 20 (6):647–650, 2014. Epub 2014 Mar 20. doi: 10.1016/j.parkreldis.2014.02.029