About 2.5% of patients treated with
neuroleptic drugs develop acute
dystonia within 48 h of commencing
therapy. The symptoms remit on
drug withdrawal or following
anticholinergic therapy. Acute
dystonia can also be reliably induced in many primate species by
neuroleptic treatment with comparable time course, symptomatology and pharmacological characteristics to those observed in man. In general, New World monkeys appear more susceptible to acute
dystonia than Old World primates. It is at present not clear whether all primates, including man, would exhibit
dystonia if a sufficiently high dose of
neuroleptic was administered. Alternatively, some unknown, possibly species-specific or even genetic, factors may determine an individual's susceptibility to develop
dystonia. Use of a rodent model of
dystonia might enable more detailed analysis of biochemical correlates of dystonic behaviour. Whilst rodents do not exhibit overt dystonic behaviour after
neuroleptic treatment, they may develop
oral dyskinesias which bear a close pharmacological similarity to
dystonia in man and primates. However, it is not known whether chewing induced by
neuroleptic drugs in rats resembles acute
dystonia in primates or whether this is another
movement disorder possibly unique to rodent species. The pathophysiology of acute
dystonia remains unknown, but may involve striatal dopaminergic and
cholinergic function. In view of the close similarity between
dystonia in man and other primates, studies on the mechanisms whereby
neuroleptic drugs cause acute dystonic reactions in monkeys may give some clues to the pathogenesis of spontaneous
dystonia in man.