Basal ganglia regional glucose metabolism asymmetry during a catatonic episode

Abstract

The pathophysiology of catatonic symptoms remains unknown, although several anatomical sites, including the basal ganglia (Kleist et al. 1960) and brainstem (Blasco et al. 1986), have been implicated. We have attempted to study the physiological substrate of these symptoms by employing positron emission tomography (PET) in the first PET study of a patient with catatonia. The patient was a 22-year-old black woman admitted to our research unit with a DSMIIf diagnosis of schizoaffect~ve disorder. She had a 4-year history of episodes of psychoses associated with auditory hallucinations and loose associations. She had been treated with antipsychotic medications during most of this period. On admission, she showed labile effect with racing thoughts, hypersexuality. and paranoid delusions. During a s-week drug-free period. she became increasingly psychotic and catatonic. Despite a subsequent week of lithium treatment (1200 mg daily, lithium level 0.8 mEqiliter), she continued to show mutism, posturing, waxy flexibility, and decreased psychomotor activity. In this state, she underwent a first PET scan. Seventeen days later, while on the same dose and blood level of lithium, she was retested in the PET procedure. At this time, there was no evidence of catatonia.