Tremor

Tremors can be initially classified as rest or action tremors.² Rest tremors occur when the body part is supported against gravity e.g. 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.

A population-based Austrian survey of movement disorders among adults aged 50–89 found a prevalence of around 28% for all movement disorders, with approximately equal rates in men and women. The prevalence of movement disorders sharply increased with advancing age from 18% in 50–59 year olds to 51% in those aged 80–89. Tremor was the commonest of the movement disorders affecting 14.5% of the population. The next commonest were restless legs syndrome (10.8%), Parkinsonism (7%), primary and secondary dystonias (1.8%) and chorea/tics (<1%). A fifth of all movement disorders in this group were thought to be medication induced.³

Estimates of the prevalence of essential tremor vary widely depending on the methodology used to detect the condition and its definition. They range from 0.3 to 5.6% of the population.¹ A long-term prospective US study found a prevalence 305.6 per 100,000 and an annual incidence of 23.7 per 100,000.¹ It was estimated that 0.5–11% of those affected by essential tremor sought medical help.¹

Symptoms

Examination of the patient with tremor

• 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?
• Try and estimate the frequency of the tremor (quite difficult without regular practice):
  • Cerebellar tremor 2–3 Hz
  • Parkinsonism 5 Hz
  • ET normally about 7 Hz
  • Physiological ~10 Hz
• 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, e.g. pronation and supination of hand at wrist held on outstretched contralateral palm).
• A quick screening cranial nerve examination is useful in detecting neurological disease.
• In ET and physiological tremor there should be no hard neurological signs.
• In ET the tremor will have some postural and kinetic components.
• Physiological tremor is usually purely postural.
• Asymmetry may be found in ET but not usually in physiological tremor.
• The presence of any hard neurological signs suggests a secondary tremor due to underlying neurological disease.

• Essential tremor
• Physiological tremor
• Exaggerated physiological tremor due to illness, fever, hyperthyroidism, anxiety states e.t.c.
• Post-traumatic/post-neurosurgical tremor
• Medication/drug-induced:
  • Effect of caffeine or other stimulants
  • Antidepressants, especially tricyclics
  • Sympathomimetics e.g. salbutamol
  • Antipsychotics causing tremor or tardive dyskinesia
  • L-DOPA and associated anti-Parkinsonian drugs
  • Lithium
  • Sodium valproate
  • Metoclopramide and other dopamine antagonists
  • Theophylline
  • Thyroid hormones
  • Withdrawal from medication
  • Recreational drug use or withdrawal (don't forget alcohol)
• Multiple sclerosis
• Parkinsonism and Parkinson's-plus syndromes, e.g. multi-system atrophy, Shy-Drager syndrome
• Metabolic derangement (e.g. electrolyte disturbance, renal and hepatic failure)
• Wilson's disease
• Cerebellar disease
• Basal ganglia lesions
• Dystonias
• Other movement disorders, e.g. 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 physiologic tremor. Trials of reducing or stopping medication may be useful to determine an iatrogenic cause. 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. 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. Positron emission tomography (PET) and Single photon emission computed tomography (SPECT) scanning may become more useful in the future.²

• Essential tremor:⁴
  • Propranolol and topiramate have both proved effective in meta-analyses, but there is little data on long-term effectiveness and outcomes.
  • Botulinum-A toxin, phenobarbital and primidone have all been shown to be effective but side effects can complicate their use (hand weakness for botulinum-A toxin, depression and cognitive slowing for phenobarbital and primidone).
  • Other agents such as clonidine, mirtazapine, gabapentin and benzodiazepines are sometimes used but there is little, or conflicting, data about their long-term efficacy and safety.
  • Thalamotomy or thalamic deep-brain stimulation have been shown to be effective in severe, disabling cases of essential and post-traumatic tremor.^5,6

• Physiological tremor:
  • Usually 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.
  • 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 separate articles. Apomorphine appears to be particularly effective at treating troublesome tremor in Parkinsonian patients, and can be used as a diagnostic test to see if tremor is likely due to Parkinsonism.⁷

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.

ET tends to be progressive. It is of widely varying severity (probably reflecting a range of individual genetic aberrations causing the overall syndrome). 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. Tardive dyskinesia can be troublesome and deteriorate but is amenable to specialist intervention, use of prophylactic anti-dystonic medication and treatment with newer anti-psychotics where it seems to be less of a problem.