Treatment of catatonia with an anticholinergic agent.

Svejgaard A, Ryder LP (1¢)76): Interaction of HLA nmle-cules with non-immunological ligargls as an exp~ of HLA and disease. Lancet ii:547-549. To the Editor: In their recent overview, "'Benzodiazepines and Ca:atonia," Menza and Harris (1989) describe numerous theories regarding the response of catatonic symptoms to benzodi~zepines. Among these, they state that, "[Llow doses of GABA agonists reduce cholinergic activity in the basal ganglia," while, "[Hligher doses of GABA agonists reduce both do-paminergic and cholinergic activity." There is an analogy to the model of muscarinic-dopaminergic hy-peractivity in schizophrenia proposed by Tandon and Greden (1989), where increased muscarinic activity has been implicated in the production of negative schizophrenic symptoms. Panzer et al (1990) have suggested that it may account for catatonia in some cases as well. Although cholinergic activity has previously beel~ !inked to catatonia (Van Andel 1958), Panzer et al reported the first case of a patient with schizoaffective disorder in whom catatonia was treated with an anticholinergic agent. We report the first case of catatonia in a patient with schizophrenia that was successfully treated with a parenteral anticholinergic agent. Mr. A is a 24-year-old man whose psychiatric history began 9 months prior to his admission. His wife described him as becoming paranoid and increasingly hostile without provocation; he was afraid that his wife would take his two children away from him. The couple separated shoRly thereafter, and the patient remained a_m_.biva!ent about the marriage. Mr. A was a! ~o using cocaine, marijuana, and alcohol at that time. Two months prior to admission, the patient began experiencing auditory hallucinations, displayed loose associations and social withdrawal, and made a suicide attempt by pouring gasoline on his shi~, ~a. igniting it. Subsequent evaluation at a local hospital revealed normal laboratory values including electro-lyres, thyroid function tests, VDRL, EEG, and computed tomography of the head without contrast. He was transferred to the University of Michigan Hospital , but left against medical advice the following day. According to his family, Mr. A's psychotic symptoms cleared somewhat over the next several days. Shortly thereafter, however, his level of functioning again deteriorated. Mr. A quit his job of 2 years, and became more disorganized; he became withdrawn, his affect was flat, and his personal hygiene was poor. He had markedly decreased speech production with severe psychomotor retardation. Upon readmission Mr. A was noted to have increased rigidity, heightened startle response, and an absence of spontaneous movements; he …