Regional cerebral glucose metabolism in SLE chorea: further evidence that striatal hypometabolism is not a correlate of chorea.
The pathophysiology of chorea in systemic lupus erythematosus (SLE) is uncertain. Pathologic examination has not identified a specific location for the causative lesion(s) and immunologic mechanisms have been suggested in its etiology. In other choreic disorders, such as Huntington's disease and benign hereditary chorea, glucose hypometabolism in the striatum has been demonstrated by positron computed tomography (PCT) using [18F]deoxyglucose. With this technique we have studied four patients with chorea secondary to SLE. In these patients the regional distribution of cerebral glucose metabolism was normal. In particular, striatal glucose metabolism was within the normal range, even though the ratio of striatal to cortical glucose metabolism was increased. Our results show that striatal hypometabolism, as seen in other disorders manifesting chorea, is not the PCT correlate of the dyskinesia.
D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D001921:Brain / Q000503:physiopathology*; D002819:Chorea / Q000503:physiopathology*; D003342:Corpus Striatum / Q000503:physiopathology; D003847:Deoxyglucose / Q000031:analogs & derivatives; D005260:Female; D019788:Fluorodeoxyglucose F18; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000503:physiopathology*; D008297:Male; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology; D013788:Thalamus / Q000503:physiopathology; D014055:Tomography, Emission-Computed
D001786:Blood Glucose; D019788:Fluorodeoxyglucose F18; D003847:Deoxyglucose