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Bradykinesia in minimal hepatic encephalopathy is due to disturbances in movement initiation
E Michael Joebges1, Melanie Heidemann, Nicole Schimke
1Department of Neurology and Clinical Neurophysiology, Medizinische Hochschule, Hannover, Germany. jiebges@sachsenklinik.de
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.