Catatonia and the neuroleptics: psychobiologic significance of remote and recent findings

Abstract

The previously common occurrence of catatonic schizophrenia and catatonic symptoms among schizophrenic patients has diminished sharply; catatonic symptoms now occur more frequently in association with severe affective disorders or with general medical conditions. Catatonia is generally viewed as a peculiar and puzzling syndrome and attracts limited attention. Yet significant catatonic symptoms tend to be present in close to 10% of patients admitted to psychiatric inpatient facilities. The dynamic significance of catatonia can be recognized by considering the original biologic role of catatonia in schizophrenia as an opposite to the paranoid disorder. Szondi viewed catatonia as an attempt at self-healing of the paranoid psychosis with its threatening total expansion, by extreme constriction of the ego. The previously predominant primary association of catatonia with schizophrenia has been eclipsed as neuroleptics have supplanted the endogenous self-healing attempt of catatonia, preventing the occurrence of catatonic symptoms in schizophrenia. Neuroleptics in fact duplicate or approximate the symptoms of catatonia by producing mental immobilization, hypokinesis (parkinsonism and dystonia), hyperkinesis (akathisia), and pernicious catatonia in the modern guise of the neuroleptic malignant syndrome (NMS). Patients with past or present catatonic symptoms are particularly vulnerable to NMS, and treatment of catatonia requires avoidance of neuroleptics and the use of benzodiazepines or electroconvulsive therapy (ECT). The extreme negativism and constriction of consciousness in catatonia suggest a primary role of the frontal lobes, with secondary involvement of the extrapyramidal system and its movement disorders. In an attempt to integrate clinical, psychologic, neuropharmacologic, and neurochemical findings, a modern dynamic neuropsychiatry must appreciate the major significance of catatonia.