The neuropharmacology of tardive dyskinesia, spontaneous dyskinesia, and other dystonias

Stephen M. Stahl, Kenneth L. Davis, Philip A. Berger

Research output: Contribution to journalArticlepeer-review

30 Scopus citations

Abstract

Most classifications of movement disorders emphasize their differential diagnosis and epidemiol-ogy according to clinical history and neurological examination. This review of movement disorders is organized according to the hypothesis of basal ganglia neurotransmitter imbalance in order to emphasize current research based on the pharmacology of these disorders. Specifically, dopamine (DA) excess and acetylcholine (ACh) deficiency may characterize part of the pathology of several hyperkinetic movement disorders including tardive dyskinesia, Huntington disease, Gilles de la Tourette syndrome, l-dopa dyskinesias, tardive Tourette syndrome, and toxic Tourette syndrome. The mirror image of this paradigm, namely DA deficiency and ACh excess, may characterize several rigid-dystonic movement disorders including Parkinson disease, drug-induced dystonias, and dystonia musculorum deformans. Finally, the unique combination of DA excess with ACh excess may characterize idiopathic orofacial dyskinesia (also known as Meige dystonia, Brueghel syndrome, and blepharospasm-oromandibular dystonia). Evidence supporting this formulation of movement disorders is reviewed, the limitations of this hypothesis are discussed, and new data from our own studies are presented.

Original languageEnglish
Pages (from-to)321-328
Number of pages8
JournalJournal of Clinical Psychopharmacology
Volume2
Issue number5
DOIs
StatePublished - Oct 1982
Externally publishedYes

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