Many patients with compensated cirrhosis without overt hepatic encephalopathy have deficits in visualspatial perception, a condition we call minimal hepatic encephalopathy. Five patients with alcohol-induced cirrhosis and nine control subjects underwent positron-emission tomographic imaging of the brain with 18F-fluorodeoxyglucose. Patients also underwent neuropsychological and clinical chemistry tests. The patients had mild arterial hyperammonemia (62 ± 13 μmol/L, range = 11 to 35 μmol/L) and other abnormalities typical of patients with cirrhosis. The patients' mean percentile scores on the digit symbol and block design subtests, from the Wechsler Adult Intelligence Scale (revised), and Purdue pegboard test were 11 ± 7, 24 ± 7 and 7 ± 8 (right hand). Tests of vocabulary, memory, and new learning were normal. The technique of statistical parametric mapping was used to identify regions where cerebral 18F-fluorodeoxyglucose uptake and metabolism were abnormal. We noted significant reductions in the cingulate gyrus, a center mediating attention, target analysis and response formulation and significant increases in visual associative regions subserving motion and color perception and object orientation. We suggest that minimal hepatic encephalopathy is due to a deficit in the detection and formulation of responses to visual stimuli, a function of the cingulate, which is a part of the anterior attentional system of the brain. Increases in 18F-fluorodeoxyglucose metabolism may be compensatory. These studies show that brain regions differ in their sensitivity to the agents that cause hepatic encephalopathy and that positron-emission tomography is useful in studying the pathophysiology of this disorder. (HEPATOLOGY 1993;18:1061-1068).