Clinical features
Acute dystonias are abnormal postures produced by sustained, contorting, twisting muscle spasms. The muscles of the head and neck are most commonly affected with a variety of conditions, including:

• trismus
• blepharospasm
• facial grimacing
• oculogyric crisis
• dysarthria, dysphagia
• torticollis.

Acute dystonic reactions are often painful and frightening, although more subtle forms may go unnoticed or be misinterpreted as hysterical symptoms or seizures. Two such subtle forms involve: tightness of the neck and shoulder muscles, and difficulties in speaking or chewing.

Epidemiology
The incidence of dystonic reactions among patients treated with antipsychotic drugs has variously been reported as 2-5³⁵, 16³⁶, 25³⁷, and 40%³⁸. This variability is probably attributable to differences among the populations studied, the types of antipsychotic medication employed, or the doses used³⁹.

A higher incidence of acute dystonia (60–94%) has been reported in children and young adult males^40,41.

The development of dystonia has been significantly correlated with younger age, severity of illness, and negative and positive symptoms at baseline^40,42. It has also been suggested that young, severely ill patients in their first psychotic episode who have never been treated with antipsychotics might be at higher risk of developing dystonia⁴⁰.

Acute dystonia is generally linked to the use of high-potency antipsychotics. Reactions usually occur within 24–48 hours of initiation of treatment, with 48% of cases occurring within the first 48 hours and 90% developing within 4–5 days of drug commencement⁴³. For these reasons, acute dystonia may contribute significantly to poor patient compliance, an important consideration in the management of schizophrenia.

Pathophysiology
The pathophysiological changes that characterize acute dystonias are related to compensatory increases in dopamine synthesis and presynaptic release, provoked by the acute administration of antipsychotic drugs, in association with acute supersensitivity of postsynaptic dopamine receptors.  Because the number of striatal D₂ dopaminergic receptors decreases with age, it is possible that a striatal hypodopaminergic status in older patients protects them from dystonia⁴⁰.

Treatment
Anticholinergic agents such as benztropine or diphenhydramine are the usual therapy for treatment-emergent dystonia.  If patients have specific contraindications (for example, narrow-angle glaucoma, prostatic hypertrophy, or cardiac conduction problems), benzodiazepines such as diazepam can be used.

Continued administration of anti-EPS drugs is usually necessary only if the patient remains symptomatic after 14 days.  If dystonia recurs, oral administration of anti-EPS drugs should continue for three months to prevent additional reactions.  The risk of dystonia decreases with continued use of antipsychotic drugs.

Prophylactic treatment with anti-EPS drugs at the beginning of antipsychotic treatment is controversial.  Those in favour of prophylaxis argue that dystonic episodes can be dangerous and that subtle forms of dystonia are often unrecognized.  Opponents argue that these anti-EPS drugs have their own side-effects, such as autonomic nervous dysfunction, memory impairment, and the risk of delirium.  Lower initial doses of antipsychotics or prophylactic anti-EPS drugs should be administered to patients that have a  high risk of EPS, predisposition to EPS, or detrimental sequelae of EPS.

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