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Bradykinesia in minimal hepatic encephalopathy is due to disturbances in movement initiation
Authors:Joebges E Michael  Heidemann Melanie  Schimke Nicole  Hecker Hartmut  Ennen Jochen C  Weissenborn Karin
Affiliation:Department of Neurology and Clinical Neurophysiology, Medizinische Hochschule, Hannover, Germany. jiebges@sachsenklinik.de
Abstract:BACKGROUND: One of the predominant symptoms of early stages of hepatic encephalopathy (HE) is bradykinesia. AIMS: To further analyze the pathophysiology of bradykinesia in HE. METHODS: A three-dimensional computer-assisted movement analysis was performed in 36 cirrhotics with grade 0-I HE compared to 18 controls selected with regard to sex and age and 16 patients with Parkinson's disease (PD). Four types of movement were studied: finger tapping, hand tapping, pronation/supination of the forearm and flexion/extension in the hip joint. RESULTS: The patients with PD presented with a decrease of the maximal movement velocity (VMAX) and a prolongation of the time needed to reach VMAX (VTIME). In patients with minimal or grade I HE, the VMAX of all movements was unchanged compared to controls while the VTIME was significantly prolonged. This was caused by a delay before the beginning of each new part of the diadochokinetic movement cycle. CONCLUSIONS: The data suggest an impairment of movement initiation as main cause of bradykinesia in early HE.
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