We read with great interest the recent paper from Brown and Marsden introducing new perspectives on basal ganglia functioning. 1 One of the outstanding fields in research opened up is the possible opposite linkage between psychosis and movement disorders through synchronisation dysfunction dependent on basal ganglia influence. We would like to report a clinical observation that could be regarded as a strong illustration of their hypothesis.

A 49-year-old-man, without family history of psychosis or neurological disorder, developed at the age of 25 years a recurrent brief psychotic disorder, according to the Diagnostic and Statistical Manual (DSM). After his last episode, which was followed by complete remission of the psychiatric manifestations under antipsychotic drugs, risperidone was introduced as monotherapy in June, 1997, because of extrapyramidal symptoms. Unfortunately, 3 months after introduction, tardive dystonia did appear consisting of rapid tonic movements involving mouth and neck muscles. Those movements were continuous but disappeared during sleep and while chewing gum. These symptoms persisted despite discontinuation of the drug and introduction of various therapeutic measures including anticholinergics, tetrabenazine, clozapine, NMDA blockers, and botulinum toxin.