Tardive dyskinesia in schizophrenia and other disorders: Associations with ageing, cognitive dysfunction and structural brain pathology in relation to neuroleptic exposure

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Abstract
Little is known of the processes which confer vulnerability to the emergence of involuntary movements (tardive dyskinesia) in only a proportion of patients receiving long‐term treatment with neuroleptic drugs. There is no consistent evidence that patients with involuntary movements have received either longer or more vigorous pharmacotherapy, and it has proved difficult to demonstrate any general relationship between increasing neuroleptic exposure and the emergence of the syndrome. Advancing age may be associated more with deleterious changes in the central nervous system within individual patients that can raise vulnerability to the emergence of involuntary movements, than with particular predisposing patterns of neuroleptic exposure. The literature in schizophrenic patients reveals that two indirect and putative indices of ‘organicity’, namely cognitive dysfunction and negative schizophrenic symptoms, together with several CT indices of structural brain pathology, show similar and robust associations with the presence of involuntary movements. In schizophrenia, predisposition to the emergence of involuntary movements during long‐term neuroleptic therapy appears intimately related with particular features of the illness, especially those associated with clinical deterioration. It is argued from clinical and animal studies that neuroleptics may hasten the appearance of dyskinetic movements in individuals with the greatest likelihood of ultimately having such movements spontaneously as cerebral deterioration proceeds.