As discussed elsewhere in this book, several neurotransmitter systems have been implicated in the development of tardive dyskinesia. The most consistently cited abnormality is a disturbance in the dopaminergic–cholinergic balance at the nigrostriatal level (Klawans, 1973; Berger & Dunner, 1985). According to that hypothesis, dopaminergic overactivity can lead to an imbalance between dopamine and acetylcholine in the nigrostriatum and consequently can lead to the development of tardive dyskinesia (Klawans, 1973).

Since the early descriptions of tardive dyskinesia, anticholinergic drugs have been reported to be ineffective for treatment of this condition (Jeste & Wyatt, 1982). Indeed, that lack of efficacy has been considered an important diagnostic aspect of the condition (Jeste & Wyatt, 1982). In the ensuing years, two claims relating to increasing use of antiparkinsonian medications vis-à-vis tardive dyskinesia have been made:

• Antiparkinsonian medications increase the risk for development of tardive dyskinesia (Klawans, 1973).

• Antiparkinsonian medications may aggravate existing tardive dyskinesia (Chouinard, DeMontigny, & Annable, 1979).

To test those claims, we have reviewed the pertinent literature, seeking to discern the importance of prescribing antiparkinsonian medications for patients with tardive dyskinesia and the effects of such drugs on tardive dyskinesia. This review does not deal with animal models.

Do Anticholinergic Drugs Increase the Risk for Tardive Dyskinesia?

Klawans, Goetz, and Perlik (1980) recommended avoidance of anticholinergic drugs, because those medications potentiate anew the development of tardive dyskinesia.