Tremor

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See related article Abnormal Involuntary Movements.

Tremor may occur as a symptom or sign of an underlying disease or as an exaggerated physiological phenomenon. It is not a diagnostic term. It can be defined as 'a rhythmic oscillatory movement of a body part, resulting from the contraction of opposing muscle groups'.[1]

The vast majority of tremor seen in the primary care setting is due to 'essential tremor' (ET). This condition has previously been termed as benign or familial essential tremor. The term 'benign' should be dropped, as although the majority of sufferers do not have significant sequelae as a result of the condition, it can be very troubling and in some cases disabling. 85% of sufferers report that it significantly affects their social and work lives, with 15% finding that it causes them serious disability.[2]

Essential tremor is thought to affect 0.4-6% of the population.[3] Men and women are equally affected. Approximately 50% of essential tremor (ET) cases are familial with autosomal dominant inheritance.

One study of 50-89 year-olds showed a prevalence of undifferentiated tremor of 14.5%.[4]

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Tremors can be initially classified as rest or action tremors.[3] Rest tremors occur when the body part is supported against gravity, eg hands at rest in one's lap. Mental stress or general movement makes rest tremors worse. Action tremors are further subdivided into static, postural or kinetic tremors:

  • Static - occurs in a relaxed limb when fully supported at rest. Causes include Parkinson's disease, Parkinsonism, other extrapyramidal diseases and multiple sclerosis.
  • Postural - occurs when a part of the body is held in a fixed position against gravity (it can also remain during movement). Types include physiological tremor, exaggerated physiological tremor (eg thyrotoxicosis), anxiety states, alcohol abuse, drugs (see below), heavy metal poisoning, neurological diseases, Wilson's disease, neurosyphilis, peripheral neuropathies, essential (familial) tremor, and task-specific tremors such as primary writing tremor.
  • Kinetic or action tremor - occurs during voluntary active movement of an upper body part. If action tremor worsens as goal-directed movement approaches its intended target, this is intention tremor (indicative of a cerebellar cause). Associated with brain stem or cerebellar disease, including multiple sclerosis, spinocerebellar degenerations, vascular disease and tumours.

It is often described by sufferers as a trembling or quivering movement or sensation.

Symptoms

  • Essential tremor (ET):
    • This is usually a distal symmetrical postural tremor of the upper limbs, usually of low amplitude with a fairly rapid frequency of 8-10 Hz.[5]
    • It may initially be transient but usually progresses to become persistent.
    • The neck muscles may be involved, causing tremor of the head (about 30% of cases), and voice, face and jaw muscles may be involved.
    • Frequency of the tremor tends to remain constant but amplitude is highly variable depending on emotional and physiological state.
    • Background tremor amplitude tends to progress over the course of years.
    • Some degree of control over the tremor, exerted by concentration on a task or via execution of a skilled manual repertoire, is common.
    • Tremor does not occur during sleep.
    • Most report improvement of tremor following alcohol ingestion.
    • It may be difficult to distinguish from exaggerated physiological tremor, that caused by hyperthyroidism/fever or tremor due to medications; these causes should always be borne in mind before diagnosing ET.
  • Physiological tremor:
    • Can occur in a state of normality or in an exaggerated form, due to a precipitant such as anxiety, hyperthyroidism, hypoglycaemia, caffeine excess, fever, medication-induced, etc.
    • It is usually associated with certain postures.
    • It is usually bilateral, symmetrical and non-progressive over time.
    • There may be a family history but this is less often than in ET.
    • Other motor symptoms should not accompany the tremor.
  • Secondary tremors due to neurological disease:
    • Individual presentation is highly variable depending on the underlying cause. Enquire about symptoms of specific diseases such as Parkinsonism, dystonias, cerebellar syndrome, symptoms in other parts of the body, constitutional symptoms and problems with gait and balance. Tremor is not usually the only motor symptom.
    • More than 70% of patients with Parkinson's disease have tremor as the presenting feature. This tremor is typically asymmetrical, occurs at rest and becomes less prominent with voluntary movement.
  • Psychogenic tremors are usually characterised by an abrupt onset, spontaneous remission, changing tremor characteristics and absence during distraction.[5]
  • Tremor may be worsened by lithium, antidepressants, bronchodilators, neuroleptics, amiodarone, procainamide, prednisolone, cinnarizine, flunarizine, ciclosporin, metoclopramide, methylphenidate and sodium valproate, caffeine (or other stimulants), sympathomimetics, eg salbutamol, L-dopa and associated anti-Parkinsonian drugs, theophylline, thyroid hormones and recreational drug use.
  • Withdrawal from medication may also cause tremor. Don't forget alcohol withdrawal.

Examination of the patient with tremor

The presence of any hard neurological signs suggests a secondary tremor due to underlying neurological disease.

  • Assess general appearance; does the face give any clues such as oromotor dystonia (may be tardive dyskinesia) or mask-like appearance (think Parkinsonism)?
  • Observe the symptomatic movements - is this tremor, chorea, dystonia or another movement disorder?
  • Ask the patient to hold their arms out in front of them with palms initially facing up, then down.
  • Ask the patient to adopt a posture or movement that they know brings on the tremor.
  • Look carefully at the hands and forearms. Is there a classical 'pill-rolling' Parkinsonian tremor?
  • Estimation of the frequency of the tremor is quite difficult without regular practice.
  • Perform a full screening peripheral neurological examination checking muscle tone, power, co-ordination, reflexes and sensation.
  • Observe gait, test for rigidity and bradykinesia indicating Parkinsonism.
  • Test cerebellar function by assessing speech (tongue-twisters), balance, finger-nose pointing and dysdiadochokinesia (inability to rapidly alternate movement, eg pronation and supination of hand at wrist held on outstretched contralateral palm).
  • A quick screening cranial nerve examination is useful in detecting neurological disease.

General points

  • Essential tremor (ET).
  • Physiological tremor.
  • Exaggerated physiological tremor due to illness, fever, hyperthyroidism, anxiety states, etc.
  • Post-traumatic/post-neurosurgical tremor.
  • Medication/drug-induced:
  • Multiple sclerosis.
  • Parkinsonism and Parkinson's-plus syndromes, eg multiple system atrophy, Shy-Drager syndrome.
  • Metabolic derangement, eg electrolyte disturbance, renal and hepatic failure.
  • Wilson's disease.
  • Cerebellar disease.
  • Basal ganglia lesions.
  • Dystonias.
  • Other movement disorders, eg tardive dyskinesia, cerebrovascular disease.
  • Writer's cramp or tremor.
  • Psychogenic tremor.
  • Arsenic, heavy metal, organophosphate or industrial solvent poisoning.
  • Vitamin deficiency (especially B12).

It is unusual to need to investigate patients with tremor if they appear to have a characteristic presentation of essential or physiological tremor.

  • Trials of reducing or stopping medication may be useful to determine an iatrogenic cause.
  • Electromyography (EMG)/accelerometry may be used as an objective neurophysiological measure of the tremor frequency, but should be used only occasionally to answer specific questions about a tremor.
  • If there is reason to suspect metabolic derangement then U&Es, LFTs and FBC may be helpful.
  • Check TFTs if there is a chance of thyroid disease.
  • Wilson's disease is diagnosed by measuring blood and urinary copper levels and caeruloplasmin assay. Suspect in people aged under 40 years with postural or kinetic tremor.[1]
  • If underlying CNS disease is suspected then CT/MRI imaging and/or neurological referral should be considered.
  • Vitamin B12 levels are unlikely to be helpful unless there is good reason to suspect a deficiency on the basis of dietary or alcohol history.

Essential tremor (ET)[6]

  • Propranolol and primidone are both effective.
  • Alprazolam, atenolol, gabapentin (monotherapy), sotalol and topiramate are probably effective.
  • Other agents such as clonidine, mirtazapine, gabapentin and benzodiazepines are sometimes used but there are little, or conflicting, data about their long-term efficacy and safety.
  • Thalamotomy or thalamic deep-brain stimulation have been shown to be possibly effective.
  • Levetiracetam, 3,4-diaminopyridine and flunarizine show little benefit and should not be considered.

Physiological tremor

  • Usually, this requires no active treatment.
  • If anxiety is a provoking factor then cognitive behavioural/relaxation therapy or antidepressant treatment may be helpful. See separate article on anxiety neurosis - Generalised Anxiety Disorder.
  • Other underlying causes should be excluded and the patient then reassured that the condition is non-pathological and non-progressive. Practical coping strategies utilising methods known by the patient to reduce the tremor should be encouraged.

Secondary tremor due to neurological disease

Treat as recommended for parent disease. See relevant individual articles, eg Parkinson's disease and multiple sclerosis.

NB: always bear in mind the effect that medication or other drug use may be having on tremor when deciding on an appropriate treatment strategy and consider trials of dose reduction or discontinuation of candidate medications before trialling new medication to treat tremor.

Essential tremor (ET) can lead to depression, anxiety states and social handicap or alcoholism. A small proportion of sufferers may be severely disabled by the condition, severely affecting their employment and social prospects.

  • Essential tremor (ET) tends to be progressive. Factors predicting likely progression include asymmetric tremor and unilateral onset of the initial tremor.[1]
  • It is of widely varying severity.
  • Physiological tremor is usually non-progressive and has an excellent outlook if underlying causes are treated or excluded.
  • Tremors due to primary CNS disease carry the prognosis associated with the parent disease.
  • Drug-induced tremors usually respond to withdrawal of the culprit medication, but those used for very long periods can occasionally cause persistent tremor even after their withdrawal.

Further reading & references

  1. Benito-Leon J, Louis ED; Clinical update: diagnosis and treatment of essential tremor. Lancet. 2007 Apr 7;369(9568):1152-4.
  2. Burke DA et al, Essential Tremor, Medscape, Oct 2009
  3. Crawford P, Zimmerman EE; Differentiation and diagnosis of tremor. Am Fam Physician. 2011 Mar 15;83(6):697-702.
  4. Wenning GK, Kiechl S, Seppi K, et al; Prevalence of movement disorders in men and women aged 50-89 years (Bruneck Study cohort): a population-based study.; Lancet Neurol. 2005 Dec;4(12):815-20.
  5. Alty JE et al. A practical guide to the differential diagnosis of tremor. Postgraduate Medical Journal. Jun 2011.
  6. Zesiewicz TA, Elble RJ, Louis ED, et al; Evidence-based guideline update: Treatment of essential tremor: Report of the Neurology. 2011 Oct 19.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Sean Kavanagh
Current Version:
Peer Reviewer:
Dr John Cox
Last Checked:
17/11/2011
Document ID:
1543 (v23)
© EMIS