Bradykinesia in cirrhotic patients with early hepatic encephalopathy is related to a decreased glucose uptake of frontomesial cortical areas relevant for movement initiation

Abstract

Bradykinesia is one of the first symptoms of hepatic encephalopathy (HE). Recently it has been suggested that bradykinesia in HE is due to disturbances in movement initiation. Areas involved in self-initiated movement are the motor- and premotor cortex, the supplementary motor cortex, the motor areas of the cingulate gyrus, and part of the frontomesial- and parietal cortex. The present study aimed to test the hypothesis that bradykinesia in HE is due to a functional disturbance of these areas. Fourteen cirrhotics with grade 0-I HE were examined. Patients with alcoholic cirrhosis or concomitant cerebral disorder were excluded. Patients underwent a 3-dimensional computer-assisted movement analysis for forearm pronation and supination, hand tapping and finger tapping and a (18)F-fluorodesoxy-glucose-PET-examination during rest, analysed with statistical parametric mapping (SPM99). The frequency of finger- and hand tapping was significantly correlated to the glucose metabolism of the motor area of the cingulate gyrus and frontomedial, frontodorsal and parietal cortical areas known to be activated with self-initiated movements. A decrease of movement frequency was associated with a reduction of glucose metabolism within these areas. These data support the hypothesis that bradykinesia in cirrhotics with HE is caused by an alteration of movement initiation.