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More than a quarter century has passed since the initial descriptions of tardive dyskinesia (Schonecker, 1957; Sigwald et aI., 1959). The earliest epidemiologic study of this disorder was carried out in Roskilde, Denmark, by Uhrbrand and Faurbye (1960); the term tardive dyskinesia was first used a few years later in a subsequent paper (Faurbye et aI., 1964). Despite 25 years of intensive investiga tive scrutiny, the syndrome persists, and approaches to its prevention and treat ment continue to have limited efficacy. It is thus fitting to evaluate what has already been learned and consider future directions for research. . Tardive dyskinesia is generally dermed as an involuntary movement disorder, mainly involving the mouth, which attends long-term neuroleptic exposure. Beyond these simple facts, however, there has been relatively little consensus about this disorder. A desire to address the controversies associated with tardive dyskinesia prompted the organization of an international symposium at Kolle kolle, just outside Copenhagen. This publication comprises all 26 presentations.
List of contents
Preclinical Aspects.- Brain Dopamine Receptors in Schizophrenia and Tardive Dyskinesia.- Receptor-Binding Profiles of Neuroleptics.- Functional Classification of Different Dopamine Receptors.- Pharmacological Properties of Presynaptic Dopamine Receptor Agonists.- Influence of GABA Mimetics and Lithium on Biochemical Manifestations of Striatal Dopamine Target Cell Hypersensitivity.- New Aspects on the Role of Dopamine, Acetylcholine, and GABA in the Development of Tardive Dyskinesia.- Discussion Section.- Differential Effects of Dopamine D-1 and D-2 Agonists and Antagonists in 6-Hydroxydopamine-Lesioned Rats.- Clinical Aspects.- Is Tardive Dyskinesia a Unique Disorder?.- Tardive Dyskinesia: Prevalence, Incidence, and Risk Factors.- Involuntary Disorders of Movement in Chronic Schizophrenia - The Role of the Illness and Its Treatment.- Tardive Dyskinesia: Reversible and Irreversible.- Pathophysiological Mechanisms Underlying Tardive Dyskinesia.- Chemical and Structural Changes in the Brain in Patients with Movement Disorder.- Medical Treatment of Dystonia.- The Effect of Dopamine Antagonists in Spontaneous and Tardive Dyskinesia.- GABA Dysfunction in the Pathophysiology of Tardive Dyskinesia.- Clinical Activity of GABA Agonists in Neuroleptic- and L-Dopa-Induced Dyskinesia.- Tardive Dyskinesia: Nondopaminergic Treatment Approaches.- Pathophysiology of L-Dopa-Induced Abnormal Involuntary Movements.- Discussion Section.- Prevalence of Tardive Dyskinesia in a Clinic Population.- Animal Models.- Differential Alteration of Striatal D-1 and D-2 Receptors Induced by the Long-Term Administration of Haloperidol, Sulpiride or Clozapine to Rats.- Pharmacological Differentiation of Dopamine D-1 and D-2 Antagonists After Single and Repeated Administration.- Pathophysiology ofTardive Dyskinesia.- Intermittent Treatment with Droperidol, a Short-Acting Neuroleptic, Increases Behavioral Dopamine Receptor Sensitivity.- Induction and Reversal of Dopamine Dyskinesia in Rat, Cat, and Monkey.- Behavioral Effects of Long-Term Neuroleptic Treatment in Cebus Monkeys.- Induction of Tardive Dyskinesia in Cebus apella and Macaca speciosa Monkeys: A Review.- List of Contributors.
