INTRODUCTION — Tremor is defined as an involuntary, rhythmic, and oscillatory movement of a body part . It is caused by either alternating or synchronous contractions of antagonistic muscles. Tremor is the most common of all movement disorders, occurring from time to time in many normal individuals in the form of exaggerated physiologic tremor .
This topic will provide an overview of the classification, clinical features, diagnostic evaluation, and treatment of tremor, including essential tremor (ET), which also is discussed in greater detail separately. (See "Essential tremor: Clinical features and diagnosis" and "Essential tremor: Treatment and prognosis" and "Surgical treatment of essential tremor".)
CLASSIFICATION — Tremors have been variably defined and categorized over time, and classification is made difficult by overlapping clinical characteristics and etiologies. The most common distinction is based on the activating conditions (ie, at rest versus action), but other clinical characteristics, such as frequency and body distribution, also guide the evaluation and etiologic diagnosis.
A clinical and etiologic classification scheme has been proposed by the International Parkinson and Movement Disorder Society . It provides a framework upon which currently recognized and new tremor syndromes can be defined.
Clinical characteristics — Clinical classification of tremor is based on history, tremor characteristics, associated neurologic and systemic signs, and, in some cases, additional testing.
Rest versus action — The activating conditions that give rise to a tremor are a key distinguishing feature (table 1).
Rest tremor occurs in a body part that is fully supported, relaxed, and not voluntarily activated.
Action tremor occurs with voluntary muscle contraction and is further subdivided into three types:
●Kinetic tremor occurs during any voluntary movement. Kinetic tremors include:
•Simple kinetic tremor, in which tremor is roughly the same throughout the course of a voluntary movement
•Intention tremor, characterized by a crescendo increase in tremor as the affected body part approaches its target
•Task-specific kinetic tremor, which occurs during a specific task such as writing
●Postural tremor occurs when a specific posture or position, such as holding the arms outstretched or while standing, is voluntarily maintained.
●Isometric tremor occurs during muscle contraction against a stationary object, such as making a fist or squeezing an object.
Tremor frequency and body distribution — Tremor frequency (oscillations per second) is used to describe tremor, although it is not particularly helpful in diagnosis as most pathologic tremors have a frequency of 4 to 8 Hertz (Hz) . The most common subdivisions used for descriptive purposes are <4, 4 to 8, 8 to 12, and >12 Hz. Tremor frequency is typically estimated clinically but can be accurately measured using a motion transducer or electromyography (EMG).
The anatomic distribution of tremor can be classified as:
●Focal (only one body region is affected, such as voice, head, jaw, or one limb)
●Segmental (two or more contiguous body parts in the upper or lower body are affected, such as head and arm)
●Hemitremor (one side of the body is affected)
●Generalized (upper and lower body are affected)
Isolated versus combined — Tremor syndromes are specific combinations of clinical signs and symptoms that commonly coexist. Syndromes can help narrow the search for an etiologic diagnosis. Syndromes may be isolated, when tremor is the only neurologic manifestation, or combined, when other systemic or neurologic signs coexist with the tremor (table 2) . Importantly, syndromes may have multiple etiologies, and a particular etiology may produce multiple clinical syndromes.
Etiology — A vast number of diseases, disorders, medications, toxins, and substances cause tremor. Etiologies can be broadly classified as genetic, acquired, and idiopathic.
Some of the more common etiologies of resting and action tremors are listed in the table (table 3). In addition to these, there are many uncommon or rare conditions that may be associated with tremor; most are action tremors .
REST TREMORS — Parkinson disease (PD) and other parkinsonian syndromes are the most common causes of rest tremor (algorithm 1).
General features — Rest tremor is evident with the affected body part fully supported against gravity and completely at rest. It is temporarily dampened or abolished during voluntary activity. Rest tremors usually fluctuate in amplitude and may appear and disappear depending upon the degree of patient repose, whether the patient feels that they are under observation, and other factors, including stress, excitement, or recent exercise.
Rest tremor is typically less disabling than postural or kinetic tremors because of its absence during voluntary activity. However, a rest tremor may quickly reappear as soon as the body part assumes a new resting or antigravity posture (a phenomenon referred to as "re-emergent tremor"), and in this case will interfere with the use of eating utensils, handwriting, typing, and other purposeful postures or movements. Rest tremor with these postural features is more of a handicap or disability than pure rest tremor, which is of mainly cosmetic concern.
Dystonic tremor is usually postural or task specific but it can occur at rest, in which state it tends to be jerky and irregular, unlike the smoother, more rhythmic pattern of the tremor of parkinsonism. (See 'Dystonic tremor' below.)
On examination, when rest tremor is absent or minimally apparent, it usually can be activated or enhanced by having the patient walk, perform repetitive movements of the opposite limb, or perform a cognitive task, such as naming the months of the year backwards.
Idiopathic Parkinson disease — The rest tremor in PD typically appears first in one hand or less commonly in one leg. As the disease progresses, tremor may spread from one hand to involve the ipsilateral leg and/or the contralateral arm. Tremor of the leg or foot is more commonly due to PD than to essential tremor (ET). The face, lips, and jaw may be involved but, unlike ET or cerebellar disease, PD only occasionally produces tremor of the entire head. (See "Clinical manifestations of Parkinson disease", section on 'Tremor'.)
When the tremor in PD is limited to distal muscles of the hand, it may produce a characteristic "pill-rolling" pattern, with a frequency of 4 to 6 Hertz (Hz). With increasing severity, the tremor may become more continuous, larger in amplitude, and more proximal in distribution, but the frequency remains constant.
Postural tremor may coexist with rest tremor or may be present by itself in some patients with PD, sometimes leading to an incorrect diagnosis of ET. (See 'Essential tremor' below.)
Tremor-dominant Parkinson disease — A low-amplitude rest tremor of the hand or jaw, unaccompanied by other manifestations of parkinsonism, sometimes occurs as an isolated finding and may not progress to more generalized PD. However, tremor is such a common first sign of PD that it most often is followed by progressive and more disabling symptoms such as generalized bradykinesia, gait disturbance, and postural instability.
Patients can go many years into their disease with tremor as the only or the most prominent sign of their disorder. When this happens, this is referred to as "tremor-dominant PD," although this designation is most reliably applied in retrospect, when the relatively benign course has already been charted.
Isolated rest tremor (SWEDD) — The radiographic term "SWEDD" (Scans Without Evidence of Dopaminergic Deficit) has been used to designate patients with relatively isolated rest and action tremors of the arms, resembling those of early PD, that have failed to evolve over time into more generalized PD . Unlike patients with PD, these individuals lack evidence for nigrostriatal dopamine deficiency with dopamine transporter imaging (DaTscan). Patients with SWEDD sometimes exhibit reduced arm swing and mild focal dystonia on the affected side, and may have jaw or head tremor or facial hypomimia, but no signs of parkinsonian bradykinesia . They are therefore to be distinguished from individuals with tremor-dominant PD. (See "Diagnosis and differential diagnosis of Parkinson disease", section on 'Scans without evidence of dopaminergic deficit (SWEDD)'.)
Others — Other disorders associated with rest tremor include drug-induced parkinsonism secondary to dopamine receptor blocking agents; the atypical parkinsonian syndromes such as dementia with Lewy bodies, multiple system atrophy, and progressive supranuclear palsy; Wilson disease; non-Wilsonian hepatocerebral degeneration; and thalamic or midbrain injury due to stroke, trauma, or demyelinating disease. Rest tremor may also occur as a "spillover" phenomenon in a variety of disorders in which very severe action tremors predominate, such as Wilson disease, multiple sclerosis, severe forms of ET , and other cerebellar or extrapyramidal syndromes.
Rubral tremor and dystonic tremor are combined tremor syndromes in which the tremor can have a rest component but is often mixed with postural and kinetic features as well. (See 'Rubral tremor' below and 'Dystonic tremor' below.)
ACTION TREMORS — Action tremors are the largest group of tremors. They include postural tremors, elicited during examination with the arms suspended against gravity in a fixed posture, and kinetic tremors, which emerge during the course of goal-directed activity (eg, drinking from a glass of water, pouring water from one cup into another, writing, and drawing of a spiral).
Physiologic tremor — Normal individuals have a very low-amplitude, high-frequency physiologic tremor of approximately 10 to 12 Hertz (Hz). Physiologic tremor is usually not visible under ordinary circumstances, although some people have a natural proclivity to demonstrate mild, nondisabling physiologic tremulousness. Many factors can enhance the tremor to the point of detection, most often by increasing sympathetic activity .
●Medications – Common drugs that increase adrenergic activity include beta-adrenergic agonists such as terbutaline, albuterol, isoproterenol, epinephrine, amphetamines, selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants, levodopa, nicotine, and xanthines such as theophylline and caffeine (table 4).
●High adrenergic state – Anxiety, excitement, fright, muscle fatigue, hypoglycemia, alcohol and opioid withdrawal, thyrotoxicosis, fever, and pheochromocytoma also enhance adrenergic activity. (See "Neurologic manifestations of hyperthyroidism and Graves' disease", section on 'Tremor'.)
Enhancement of physiologic tremor is the most common cause of action tremor. Thus, a medical rather than primary neurologic cause for action tremor should be considered first in most cases.
Drug-induced tremor — Drugs and toxins that commonly increase physiologic tremor or induce tremor by other means include lithium, antidepressants, corticosteroids, sodium valproate, tacrolimus, bromides, mercury, lead, and arsenic (table 4).
Essential tremor — Essential tremor (ET) is reviewed here briefly and is discussed in detail separately. (See "Essential tremor: Clinical features and diagnosis" and "Essential tremor: Treatment and prognosis" and "Surgical treatment of essential tremor".)
ET is the most common neurologic disorder that causes action tremor, with an estimated prevalence worldwide of up to 5 percent of the population. The incidence of ET increases with age, although it often affects middle-aged individuals, especially when it is familial. A family history is present in 30 to 70 percent of cases, and evidence suggests an autosomal dominant pattern of inheritance with reduced penetrance. (See "Essential tremor: Clinical features and diagnosis", section on 'Pathogenesis and genetics'.)
ET varies from a low-amplitude, high-frequency postural tremor of the hands to a much larger-amplitude, and at times lower-frequency, postural and action tremor that is activated by particular postures and actions. ET most often affects the hands and arms and can be asymmetric. Less often, it may involve the head, voice, trunk, and legs. ET becomes immediately apparent in the arms when they are held outstretched; it typically increases at the very end of goal-directed movements such as drinking from a glass or finger-to-nose testing. Tremor in the legs is unusual in ET. Tremor of the head may be vertical ("yes-yes") or horizontal ("no-no") and is usually associated with tremor of the hand or voice. ET is typically relieved by small amounts of alcohol. Caffeine can worsen the tremor, although this effect is much more commonly seen with physiologic tremor.
The diagnosis of ET is based upon clinical features (table 5). (See "Essential tremor: Clinical features and diagnosis", section on 'Evaluation'.)
The main considerations in the differential diagnosis of ET are enhanced physiologic tremor, drug-induced tremor, parkinsonian tremor, tremor caused by cerebellar disorders, and dystonic tremor (algorithm 1).
A frequent entity on the differential diagnosis of ET is parkinsonian tremor (table 6 and table 7 and table 8). Differentiation from classic resting tremor should be straightforward; however, some patients with Parkinson disease (PD) also have an action tremor indistinguishable from ET. In fact, it is not unusual for patients with PD to present with a postural tremor before they display other signs of PD. Likewise, patients with severe ET may have a rest component to their tremor, and some patients with ET exhibit mild nonprogressive parkinsonism.
Primary writing tremor — Many action tremors are particularly severe during the act of writing. Tremor that occurs exclusively while writing, and not during other voluntary motor activities, is referred to as "primary writing tremor" . This tremor is limited to the hand and causes relatively large-amplitude supination-pronation movements at a frequency of 5 to 6 Hz. The low frequency and large amplitude of the tremor, its frequent occurrence in writer's "cramp" or writer's dystonia, its relative resistance to propranolol, and its occasional response to anticholinergic drugs suggest a closer relationship to dystonia than to ET. (See "Etiology, clinical features, and diagnostic evaluation of dystonia", section on 'Task-specific dystonia'.)
Orthostatic tremor — Orthostatic tremor is a postural tremor limited to the legs and trunk that occurs exclusively while standing [7-10]. In two reports of 184 and 68 patients, there was a female predominance (64 and 77 percent, respectively) [11,12]. The mean age of onset was between 54 and 59 years (range 13 to 85 years). Both high- and low-frequency orthostatic tremors have been described; their relationship to ET is uncertain. In cases of high-frequency tremor, movements of the legs may be so low in amplitude that they initially escape clinical detection.
Cerebellar tremor — "Cerebellar tremor" is the term used to describe a tremor that is caused by known cerebellar pathology. It can be postural, simple kinetic, intention, or any combination of these features. In severe cases, cerebellar tremor, like ET, can spill over and also occur at rest. Tremor frequency is typically low (3 to 4 Hz) and can be associated with ataxia and dysmetria.
Cerebellar tremor is due to disturbances anywhere along the path of the cerebellar outflow projection system from the dentate nucleus of the cerebellum to its termination in the ventral lateral nucleus of the thalamus. The most common causes are multiple sclerosis, midbrain trauma, and stroke (table 3). Degenerative and inflammatory diseases of the cerebellum, severe forms of ET, Wilson disease, hepatocerebral degeneration, and mercury poisoning may also produce this tremor.
Cerebellar tremor typically has a component of intention tremor in that the tremor increases in severity, either gradually or abruptly, as the hand moves closer to its target. Intention tremors are usually very large in amplitude due to involvement of proximal muscles and are sometimes difficult to distinguish from severe cerebellar ataxia. The frequent association with ataxia, dysmetria, titubation, and other cerebellar signs serves to identify the cerebellar origin of intention tremor.
Titubation of the head and neck ("to and fro" movements) may be associated with cerebellar tremor; it is distinguished from essential head tremor by the presence of other cerebellar findings.
Rubral tremor — Rubral tremor, sometimes called Holmes tremor after the early 20th century English neurologist who described it, is a subtype of cerebellar tremor with a greater degree of proximal, high-amplitude movement. Rubral tremor is caused by midbrain, thalamic, cerebellar, or pontine injury . In many cases of rubral tremor, there are combined lesions that interrupt the outflow pathway from the cerebellum to the motor thalamus, often involving the superior cerebellar peduncle, substantia nigra, or red nucleus.
Rubral tremor is present at rest but tends to have a slower frequency (3 to 5 Hz) than typical Parkinson rest tremor (5 to 7 Hz). It also persists unchanged or increases with postural changes or goal-directed activity. It may produce a combination of rest, postural, simple kinetic, and intention tremors.
Neuropathic tremor — Postural or kinetic tremors are sometimes associated with large fiber peripheral neuropathy. This association is most commonly observed in hereditary neuropathies, during the recovery phase of some cases of Guillain-Barré syndrome, and in chronic inflammatory demyelinating polyneuropathy (CIDP). Muscle weakness and loss of proprioceptive or muscle spindle inputs may account for the tremor. The frequency and amplitude of neuropathic tremor may vary greatly when associated with a proprioceptive deficit. (See "Overview of polyneuropathy".)
Dystonic tremor — Dystonic tremor refers to tremor in a body part that is affected by dystonia. Because of the association with dystonia, dystonic tremor is an example of a combined tremor syndrome . Common examples include dystonic head tremor and segmental tremulous dystonia of the head and upper limbs, which occur due to cervical dystonia. (See "Etiology, clinical features, and diagnostic evaluation of dystonia".)
Dystonic tremors are usually postural or task specific but sometimes occur at rest, in which state they tend to be jerky and irregular. The use of an alleviating maneuver (geste antagoniste, sensory trick) can be helpful in distinguishing dystonic tremor from other tremor syndromes, such as ET. In dystonic head tremor, for example, moving an arm to the face or head in a specific plane can alleviate cervical dystonia symptoms, including head tremor. Exacerbation of dystonic tremor by an attempt to maintain certain postures can also be helpful in the examination.
FUNCTIONAL TREMORS — Functional tremor, previously known as psychogenic tremor, is typically characterized by complex rest, postural, and kinetic tremor with abrupt onset, a static course, changeable features, functional disability out of proportion to tremor magnitude, and resistance to treatment. Any body part may be involved, but, remarkably, the fingers are often spared, with much of the tremor of the arm occurring at the wrist.
Other features of functional movement disorders are often present, such as distractibility, variability of symptoms, and clinical features that are incongruous with known tremor syndromes. Examination usually shows variable tremor direction and frequency, distractibility (attenuation or elimination of tremor with distraction maneuvers such as repetitive tapping tasks with an uninvolved opposite hand or foot), and/or tremor entrainment (ie, shift of tremor frequency to the speed of a distraction maneuver) (movie 1 and movie 2). (See "Functional movement disorders", section on 'Clinical features'.)
EVALUATION — The diagnostic approach to patients with tremor involves the history, physical examination, and selected laboratory studies . Action tremor is most common and, of these, essential tremor (ET) and enhanced physiologic tremor are the most frequent causes (algorithm 1) . Patients with tremor due to other disorders such as hyperthyroidism, Parkinson disease (PD), dystonia, Wilson disease, or medications frequently have additional signs or symptoms that help point to the diagnosis, although this is not always the case. The criteria for ET (table 5) and methods for distinguishing it from other tremors are shown in the tables (table 1 and table 3 and table 6 and table 7 and table 8).
History — The history concerning the age of onset and evolution of tremor is usually straightforward, since it is a highly visible symptom that is readily evident to the patient and family members. Examination of previous handwriting samples may be useful in determining the precise time of onset.
Body parts that are affected and symmetry can be helpful clues to the likely diagnosis. Head tremor is common in ET but unusual in PD; conversely, jaw tremor and resting leg tremor are common in PD and rare in ET. Jaw or chin tremor at rest should be distinguished from lower lip tremor that occurs with activation, as facial tremor with activation may be seen in ET. Vocal tremor is strongly suggestive of ET. Asymmetry or unilaterality is typically more characteristic of PD tremor than ET. Any involuntary posturing that occurs with tremor should raise the possibility of a dystonic tremor.
Precipitating, aggravating, or relieving factors such as caffeine, alcohol, medications, exercise, fatigue, or stress should be elicited; a complete list of all medications should be reviewed to exclude the possibility of enhanced physiologic tremor and drug-induced tremor (see 'Physiologic tremor' above). Mitigation of tremor by alcohol is classically described in ET but is not highly sensitive or specific.
Patients should also be questioned about any associated neurologic symptoms that would assist in diagnosis, including loss of dexterity, stiffness, stooped posture, voice softness, shuffling gait, acting out of dreams (all suggestive of PD), cognitive changes, and visual hallucinations (suggestive of dementia with Lewy bodies). Lack of any of the above features along with a predominantly action tremor would be suggestive of ET.
Family history in ET reflects an autosomal dominant pattern of inheritance in approximately half of all patients. Parkinsonian tremor is usually sporadic, but a family history of PD is present in approximately 15 percent of cases; the disease affects first-degree relatives (parents, siblings, or offspring) in approximately half of the familial cases. Autosomal PD affecting three or more generations is rare.
Examination — A detailed neurologic examination is important to identify specific features of the tremor (including its frequency, amplitude, pattern, and body distribution), activating conditions, and other neurologic findings, if present [1,16].
Examination begins with observations of the tremor during the interview. Due to stress, many patients with tremor are more symptomatic during the early part of the examination than after they become acclimated to the doctor-patient encounter. Patients should be observed sitting and walking. Horizontal or vertical head tremor is usually associated with tremor elsewhere. Isolated head tremor should raise the possibility of cervical dystonia or midline cerebellar syndromes. Localized jaw tremor is more commonly a manifestation of parkinsonism, while localized face or lip tremor may occur in ET. Essential voice tremor is readily audible and may be further enhanced by having the patient hold a prolonged note.
Tremor in the arm is observed with the affected limb fully supported on the patient's lap or the arm of a chair, with the limb elevated against gravity, and during goal-directed movements. Most resting tremors cease with changes in limb posture but may reappear following repositioning to another fixed posture, especially when held outstretched against gravity, referred to as "re-emergent tremor." Parkinsonian tremor, in contrast with ET, is usually activated by repetitive movements of the opposite hand, during walking, and during mental distraction such as reciting the months of the year backwards.
Postural and kinetic tremors are best elicited with the arms held outstretched; with the shoulders abducted, elbows flexed, and index fingers held an inch apart in front of the face (to elicit any "wing-beating" tremor); during finger-to-nose maneuvers; and while drinking from or pouring from a paper cup. Writing and drawing may demonstrate the large, tremulous, angulated loops of ET or the micrographia of parkinsonism. A drawing sample of a spiral is commonly used to evaluate ET severity and can be repeated to be compared over time. Having the patient draw a spiral with the hand suspended above the table increases the sensitivity of this test.
While examining for postural tremor and kinetic tremor, careful observation for abnormal posturing of the tremulous fingers, hand, or upper limb is required to rule out a dystonic tremor. Dystonic posturing can also be elicited during examination of repetitive movements of the opposite limb, writing, and walking.
Tremor of the leg should be assessed with the limb at rest, during heel-to-shin testing, and while standing and walking. Leg tremor is more commonly due to parkinsonism than ET.
Frequency of tremor should be estimated at rest and during postural and action maneuvers. Frequency varies depending on cause:
●High for enhanced physiologic tremor (10 to 12 Hertz [Hz]) and orthostatic tremor (14 to 20 Hz)
●Medium to high for ET (6 to 12 Hz)
●Low to medium for the resting tremor of parkinsonism (4 to 6 Hz)
●Low for rubral (Holmes) tremor (3 to 5 Hz)
Functional tremors tend to vary in frequency as well as amplitude and direction from moment to moment and either become more irregular or subside entirely when the patient is distracted by performing a complex, repetitive motor task with the contralateral limb. The tremor may also entrain to the frequency of the repetitive movement being tested in another limb. For this reason, it can be helpful to test for entrainability by asking patients to tap their fingers at the same rhythm as the examiner, and then slowly increase or decrease the frequency of the taps, looking for associated changes in the rhythm of the tremor. (See 'Functional tremors' above.)
The gait is almost always normal in patients with ET, while it is characteristically narrow-based and shuffling in PD and wide-based and ataxic in cerebellar disorders. The gait may have histrionic (nonphysiologic) qualities in patients with functional tremors.
Laboratory studies — The routine laboratory evaluation of tremor should include tests of thyroid function, diagnostic studies to exclude Wilson disease, and, rarely, screening for heavy metal poisoning such as mercury or arsenic if an environmental cause is suspected. Wilson disease should be suspected in anyone under age 40 who has tremor or other involuntary movements or postures  (see "Wilson disease: Clinical manifestations, diagnosis, and natural history"). Hypoglycemia and pheochromocytoma may need to be ruled out in patients with enhanced physiologic tremor.
Brain imaging is usually not indicated in patients with classic presentations of ET, PD, enhanced physiologic tremor, or drug-induced tremor, although normal pressure hydrocephalus (NPH) or stroke can rarely produce a parkinsonian phenotype. In cases where there is clinical uncertainty as to whether a patient has ET or isolated PD tremor, striatal dopamine transporter imaging (DaTscan) will detect striatal dopamine deficiency even very early in PD but will be normal in ET. (See "Diagnosis and differential diagnosis of Parkinson disease".)
Magnetic resonance imaging (MRI) can be useful in patients thought to have rubral or Holmes tremor, which is typically due to a lesion in the cerebellar outflow network; in those with Wilson disease; and in those with a pure hemidystonic tremor, which may be due to a contralateral structural lesion.
Quantitative computerized analysis of tremor is available in some tertiary care facilities, but its ability to reliably distinguish between tremor types has not been established.
TREATMENT — The treatment of tremor is symptomatic, and some forms lack any useful pharmacologic therapy. Even medications known to have some benefit for certain tremor syndromes usually have only partial effect. For combined tremor syndromes, treatment of the underlying disorder is the primary approach.
Physical and occupational therapy may be of benefit to help identify coping mechanisms and compensatory strategies. In patients with refractory or disabling tremor, the approach should be individualized according to the underlying cause. In addition to medications, some patients may be candidates for surgical therapies.
●Rest tremor – Rest tremor associated with Parkinson disease (PD) or other parkinsonian disorders is managed by treatment of the underlying disorder, typically with antiparkinson agents such as anticholinergic drugs, amantadine, dopamine agonists, levodopa, and zonisamide. Deep brain stimulation (DBS) is an option for some patients with refractory tremor due to PD, but not due to other parkinsonian disorders. This topic is discussed separately. (See "Initial pharmacologic treatment of Parkinson disease" and "Device-assisted and lesioning procedures for Parkinson disease".)
●Enhanced physiologic tremor – Physiologic tremor is best managed by reduction or removal of the responsible offending medication or toxin (table 4); diagnosis and treatment of possible associated endocrine disorders; and dealing with stress, anxiety, or fatigue (see 'Physiologic tremor' above). Single doses of propranolol, a short-acting beta blocker, taken in anticipation of social situations that are likely to exacerbate tremor (eg, as with tremor associated with public speaking or having dinner with friends) are useful in some patients.
●Essential tremor (ET) – ET can be treated pharmacologically with partial symptomatic benefit. Propranolol and primidone are the preferred, evidence-based drugs to use as initial monotherapy, and when used in combination they can sometimes offer additive benefit (algorithm 2). Second-line medications for ET include agents such as topiramate and gabapentin. Botulinum toxin injections can be effective for head tremor and vocal tremor in ET, and in selected cases for upper extremity tremor. Both DBS and unilateral thalamotomy, which can now be performed via focused ultrasound with MRI guidance, are effective for the treatment of medically refractory ET. (See "Essential tremor: Treatment and prognosis" and "Surgical treatment of essential tremor".)
●Orthostatic tremor – Orthostatic tremor involves the legs and trunk and occurs exclusively while standing (see 'Orthostatic tremor' above). In one retrospective case series of 184 patients with orthostatic tremor, treatment with benzodiazepines, mainly clonazepam, was associated with moderate or marked relief in approximately one-third of the patients . Other classes, such as antiseizure medications (eg, gabapentin, primidone, valproate) were associated with lower rates of improvement, and lack of a placebo control was a major limitation. Limited evidence suggests that some patients with medically refractory orthostatic tremor show modest improvement with DBS of the ventral intermediate nucleus of the thalamus .
●Cerebellar tremor – Cerebellar tremors lack any useful pharmacotherapy. The rare patient with severe intention tremor and little or no ataxia, such as sometimes occurs in multiple sclerosis, may be helped by DBS of the ventral intermediate nucleus of the thalamus. (See "Surgical treatment of essential tremor".)
●Rubral tremor – Rubral tremor sometimes responds to levodopa therapy [13,18]. Other medications that may have some benefit are levetiracetam and trihexyphenidyl; thalamic DBS has been used with some success for medically refractory patients but requires more study .
●Dystonic tremor – Dystonic tremor of the head related to cervical dystonia can be improved with botulinum toxin injections into bilateral cervical muscles. If sternocleidomastoid muscles are injected bilaterally, small doses should be used to avoid dysphagia. (See "Treatment of dystonia in children and adults", section on 'Focal dystonia'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Essential tremor".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Tremor (The Basics)")
●Beyond the Basics topics (see "Patient education: Tremor (Beyond the Basics)")
PATIENT PERSPECTIVE TOPICS — Patient perspectives are provided for selected disorders to help clinicians better understand the patient experience and patient concerns. These narratives may offer insights into patient values and preferences not included in other UpToDate topics. (See "Patient perspective: Essential tremor with onset in childhood" and "Patient perspective: An artist with essential tremor".)
SUMMARY AND RECOMMENDATIONS
●Classification – Clinical classification of tremor is based on history, tremor characteristics, associated neurologic and systemic signs, and, in some cases, additional testing. A vast number of diseases, disorders, medications, toxins, and substances cause tremor. Etiologies can be broadly classified as genetic, acquired, and idiopathic. (See 'Classification' above.)
●Rest versus action – The activating conditions that give rise to a tremor are a key distinguishing feature (table 1). Rest tremor occurs in a body part that is fully supported and not voluntarily activated, whereas action tremor occurs with voluntary muscle contraction. Action tremors can be further characterized as kinetic, postural, and isometric. (See 'Rest versus action' above.)
●Causes of action tremor – Examples of isolated tremor syndromes in which action tremor can be the sole neurologic symptom include (table 2):
•Task-specific tremors (eg, writing tremor) (see 'Primary writing tremor' above)
•Orthostatic tremor (see 'Orthostatic tremor' above)
Examples of combined tremor syndromes in which action tremor may be seen in association with other neurologic or systemic signs and symptoms include:
•Cerebellar tremor (see 'Cerebellar tremor' above)
•Neuropathic tremor (see 'Neuropathic tremor' above)
•Dystonic tremor (see 'Dystonic tremor' above)
•Functional tremor (see 'Functional tremors' above)
●Evaluation – A detailed neurologic examination is important to identify specific features of the tremor (including its frequency, amplitude, pattern, and body distribution), activating conditions, and other neurologic findings, if present. (See 'Evaluation' above.)
The routine laboratory evaluation of tremor should include tests of thyroid function, diagnostic studies to exclude Wilson disease, and, rarely, screening for heavy metal poisoning such as mercury or arsenic if an environmental cause is suspected. Brain imaging is usually not indicated in patients with classic presentations of ET, PD, enhanced physiologic tremor, or drug-induced tremor (algorithm 1). (See 'Laboratory studies' above.)
●Treatment – Physical and occupational therapy may be of benefit in patients with limb tremor to help identify coping mechanisms and compensatory strategies. Some forms of tremor are responsive to symptomatic pharmacotherapy. (See 'Treatment' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Daniel Tarsy, MD, who contributed to earlier versions of this topic review.
آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟