Asymmetry of pathology in Alzheimer's disease.

of various aetiologies. The hypometabolism of the striatum, visually appreciated in four patients and present on quantitative analysis in the fifth, was used to support their conclusion that dysfunction of the striatum is the common pathophysiological disturbance in chorea ofdiverse causes. By inference, one is left to assume that all patients with chorea would be expected to show hypometabolism of the striatum on 18F fluorodeoxyglucose (FDG) positron emission tomography (PET). We have recently reported our experience with FDG PET scanning in four patients with chorea secondary to systemic lupus erythematosis (SLE).2 In contrast to the findings of Hosokawa et al,' we found no reduction in striatal LCMRglc; indeed there was a slight increase in the ratio of striatal to cortical glucose metabolism. The pathophysiology of chorea in SLE remains uncertain. Pathological study in a small number of SLE chorea patients has not revealed a consistent distribution of potential causative lesions and the striatum has not been invariably involved in these cases. This does not exclude the possibility that primary or secondary striatal dysfunction is the cause of SLE chorea. Nor does normal LCMRglc exclude a disturbance in function of striatal neurons. However, our results do indicate that striatal FDG hypometabolism is not the PET correlate of chorea. ANTHONY E LANG* ES GARNETTt Movement Disorder Clinic, *Toronto Western Hospital, Toronto, Ontario, Canada MST 2RZ McMaster University Medical Centre,i Hamilton, Ontario, Canada