Abstract
Neurological abnormalities during early stages of hepatic encephalopathy (HE) include cognitive deficits,1 irregular jerky lapses of posture, termed asterixis, and an almost rhythmical tremor which is only present during a maintained posture and starts after a latent period of 2–30 sec.2,3 This tremor varies in frequency between 6 and 12 Hz and decreases during movements.2 Classically termed “metabolic tremor” it was proposed that it is a manifestation of the same phenomena that underlie “gross asterixis flaps” rather than a different type of abnormal movement.2 Accordingly, this tremulousness has been termed “mini-asterixis”.4 However, the origin and nature of central mechanisms involved in the generation of “mini-asterixis” remain unclear.4 Assessment of asterixis is a part of the routine staging of HE.5 We studied mini-asterixis in HE with simultaneous whole-head magnetoencephalography (MEG) and surface EMG-recordings in six patients with HE complicating cirrhosis and clinically visible tremulousness, as well as in two control groups. Our findings provide evidence for involvement in mini-asterixis of the primary motor cortex and a pathologically slowed and synchronized corticospinal oscillatory drive. Data from this study have been published previously6 and were the subject of an editorial.7
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© 2003 Springer Science+Business Media Dordrecht
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Timmermann, L., Gross, J., Kircheis, G., Butz, M., Häussinger, D., Schnitzler, A. (2003). Cortical origin of mini-asterixis in hepatic encephalopathy. In: Jones, E.A., Meijer, A.J., Chamuleau, R.A.F.M. (eds) Encephalopathy and Nitrogen Metabolism in Liver Failure. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-0159-5_11
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DOI: https://doi.org/10.1007/978-94-010-0159-5_11
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