Failure of clonidine in tardive dystonia: Implications for nosology

Abstract

Tardive dystonia, a persistent dystonia of late onset associated with exposure to neuroleptic drugs, has been known for more than 2 decades (Harenko 1967; Keegan and Rajput 1973), but has recently been attracting increasing attention (Burke et al. 1982; GimenezRoldan et al. 1985; Lancer Editorial 1985). Various studies have found the prevalence of this rare disorder to be in the range of l.O%-2.0% (Crane and Naranjo 1971; Yassa et al. 1986; Friedman et al. 1987) among treated patients. It has been defined as a chronic dystonia with onset after a minimum of 2 months of neuroleptic treatment. It occurs in patients with no evidence of secondary dystonia (e.g., Parkinson’s disease, Wilson’s disease, Huntington’s chorea, cerebral tumors, stroke, cerebral lipidosis, etc.) and with no family history of dystonia (Burke et al. 1982). Though some authors did not think that tardive dystonia should be regarded as an entity separate from tardive dyskinesia (Burke et al. 1982; Gardos et al. 1987), this viewpoint has increasingly been questioned in recent years (Gimenez-Roldan et al. 1985; Yassa et al. 1986; Friedman et al. 1987; Ananth et al. 1988). In this article, we report a case of tardive dystonia that did not respond to treatment with clonidine. In view of this failure to respond to clonidine, we discuss the nosologic implications of the findings with regard to the predictive validity of tardive dystonia as a diagnostic entity.