Abstract
In a study of 16 psychotic patients with neuroleptic-induced tardive dyskinesia and 16 patients with Parkinson's disease and l-Dopa-induced hyperkinesia kinesia it was found that (1) tardive dyskinesia, compared to l-Dopa hyperkinesia, was localized almost exclusively to the oral region (P), whereas the l-Dopa hyperkinesia was more pronounced in the neck (P) and the extremities (P); (2) l-Dopa hyperkinesia showed an increasing tendency to oral preponderance with age, irrespective of the severity of parkinsonism and extra-oral hyperkinesia, while tardive dyskinesia only itensified with age, without any change in distribution; and (3) extraoral l-Dopa hyperkinesia was related to the localization and severity of pretreatment parkinsonism, and more to bradykinesia than to rigidity and tremor. It is concluded that the irreversible neurotoxic effect of neuroleptic drugs may be associated with agerelated changes in the oral somatotopic region of the basal ganglia (to be given consideration in any future search for the pathogenetic process underlying irreversible tardive dyskinesia), and that the pathophysiology of involuntary hyperkinesia in neuroleptic-treated psychiatric patients and in l-Dopatreated Parkinson patients may consist of a primary dopamine deficiency (pharmacological or structural), and a secondary relative hyperactivity in the dopaminergic system (“dopaminergic hypersensitivity”) possibly corresponding to hypoactivity in the cholinergic system.