POSITRON-EMISSION TOMOGRAPHIC LOCALIZATION OF ABNORMALITIES OF BRAIN METABOLISM IN PATIENTS WITH MINIMAL HEPATIC-ENCEPHALOPATHY

Many patients with compensated cirrhosis without overt hepatic encepha lopathy have deficits in visual-spatial perception, a condition we cal l minimal hepatic encephalopathy. Five patients with alcohol-induced c irrhosis and nine control subjects underwent positron-emission tomogra phic imaging of the brain with F-18-fluorodeoxyglucose. Patients also underwent neuropsychological and clinical chemistry tests. The patient s had mild arterial hyperammonemia (62 +/- 13 mumol/L, range = 11 to 3 5 mumol/L) and other abnormalities typical of patients with cirrhosis. The patients' mean percentile scores on the digit symbol and block de sign subtests, from the Wechsler Adult Intelligence Scale (revised), a nd Purdue pegboard test were 11 +/- 7, 24 +/- 7 and 7 +/- 8 (right han d). Tests of vocabulary, memory, and new learning were normal. The tec hnique of statistical parametric mapping was used to identify regions where cerebral F-18-fluorodeoxyglucose uptake and metabolism were abno rmal. We noted significant reductions in the cingulate gyrus, a center mediating attention, target analysis and response formulation and sig nificant increases in visual associative regions subserving motion and color perception and object orientation. We suggest that minimal hepa tic encephalopathy is due to a deficit in the detection and formulatio n of responses to visual stimuli, a function of the cingulate, which i s a part of the anterior attentional system of the brain. Increases in F-18-fluorodeoxyglucose metabolism may be compensatory. These studies show that brain regions differ in their sensitivity to the agents tha t cause hepatic encephalopathy and that positron-emission tomography i s useful in studying the pathophysiology of this disorder.