Essential tremor treatment

essential tremor treatment


Essential tremor (ET) is the most common adult movement disorder. Traditionally considered as a benign disease, it can cause an important physical and psychosocial disability. Drug treatment for ET remains poor and often unsatisfactory. Current therapeutic strategies for ET are reviewed according to the level of discomfort caused by tremor. For mild tremor, nonpharmacological strategies consist of alcohol and acute pharmacological therapy; for moderate tremor, pharmacological therapies (propranolol, gabapentin, primidone, topiramate, alprazolam and other drugs); and for severe tremor, the role of functional surgery is emphasised (thalamic deep brain stimulation, thalamotomy). The more specific treatment of head tremor with the use of botulinum toxin is also discussed. Several points are discussed to guide the immediate research into this disease in the near future. Dystonic tremor is a common symptom in dystonia. Diagnostic criteria for dystonic tremor and differential diagnosis with psychogenic tremor and ET are described. Treatment of dystonic tremor matches the treatment of dystonia. In cases of symptomatic dystonic tremor similar to ET, therapeutic strategies would be the same as for ET.


Basic algorithm of current drug treatment in essential tremor.

ET is characterised by the presence of postural and kinetic tremor. In classic ET, upper limbs (95% of patients) and less commonly the head (34%), lower limbs (30%), voice (12%), tongue (7%), face (5%), and trunk (5%) exhibit postural or kinetic tremor [Elble, 2006 ]. It has traditionally been considered a benign condition because of the perception that it does not reduce life expectancy or cause symptoms other than tremor and impaired tandem walking. However, this disorder may cause substantial physical and psychosocial disability. Tremor amplitude increases gradually over time and patients frequently face growing difficulties with writing, drinking, eating, dressing, speaking, and other fine motor tasks.


ET is a clinical diagnosis. Criteria for definite and probable ET include abnormal bilateral postural or kinetic tremor of the hands in the absence of other neurological signs. The clinical criteria were comprehensively reviewed by the Consensus Statement of the Movement Disorder Society on Tremor [Deuschl et al. 1998 ]. Six routine neurophysiological criteria (EMG and accelerometer) have recently been described [Gironell et al. 2004 ]: (1) rhythmic burst of postural tremor on EMG; (2) tremor frequency superior or equal to 4 Hz; (3) absence of rest tremor or, if present, frequency 1.5Hz lower than the postural tremor; (4) absence of tremor latency from rest to postural position; (5) changes of the dominant frequency peak

less or equal to 1 Hz after the weight load test; and (6) no changes in tremor amplitude after mental concentration.

There are several recent excellent reviews on ET treatment [Elble, 2006 ; Zesiewich et al. 2005 ]. This paper includes evidence-based medicine observations together with reviewer experience in this field. It is structured according to the severity of patient symptoms.

Management of pauci-symptomatic tremor

Neuroprotective therapy

There are to date no neuroprotective therapies for ET. A genetic locus will likely be found in the future. With the aid of genetic engineering, it will then be possible to replace the causative mutation into the wild-type allele. This would be a presymptomatic and curative therapy for the disease.

Nonpharmacological strategies

In milder cases of ET, drug treatment benefits are insufficient to justify continuous chronic treatment. Physicians should explain to patients that psychostimulants such as coffee, tea and cola drinks may have tremoric effects and that anxiety and stress also worsen tremor amplitude. Nonpharmacological anxiolytic measures may be beneficial in milder cases.


Ethanol is a potent suppressant of ET in many patients, but it has obvious limitations in the chronic treatment of the disorder. It has been reported that alcohol reduces tremor amplitude in 50–90% of cases, but tremor may temporarily worsen after the effects of alcohol have worn off [Koller and Biary, 1984 ]. The mechanism of ethanol in tremor suppression is uncertain. Other alcohols appear to have similar efficacy. Octanol and sodium oxybate were beneficial in pilot studies, but larger double-blind placebo-controlled trials are needed to test the safety, tolerability and efficacy of long-term treatment with these drugs. Sodium oxybate has been approved with restrictions in the United States and several European countries for the treatment of cataplexy [Frucht et al. 2005 ]. In mild cases of tremor, the physician may suggest an occasional alcoholic beverage (i.e. a beer) approximately 30 minutes prior to a tremor discomfort activity.

Pharmacological therapies

Another possibility in patients with mild tremor is the use of pharmacological treatment a short time prior to a concrete tremor discomfort activity. The drug should have a rapid absorption and antitremoric action. The most commonly used of such treatments is propranolol (the characteristics of which are discussed later). A dose of 20–40mg propranolol about 30–60 minutes prior to specific actions disrupted by tremor can be used.

Management of moderate tremor

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