Butz, M., Timmermann, L., Gross, J., Pollok, B., Suedmeyer, M., Kircheis, G., Haeussinger, D. and Schnitzler, A. (2014). Cortical activation associated with asterixis in manifest hepatic encephalopathy. Acta Neurol. Scand., 130 (4). S. 260 - 268. HOBOKEN: WILEY-BLACKWELL. ISSN 1600-0404

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Abstract

ObjectivesSevere hepatic encephalopathy gives rise to asterixis, a striking motor symptom also called flapping tremor, which is characterized by a sudden ceasing of muscle tone in all muscles of a limb. In this study, we aimed at scrutinizing the cortical activation associated with asterixis and unraveling the underlying pathophysiological mechanisms. Material and methodsWe recorded simultaneously neural activity with magnetoencephalography (MEG) and muscle activity with surface EMG in nine patients with manifest hepatic encephalopathy showing asterixis. Asterixis events were detected semiautomatically and served as triggers for averaging MEG signals. Evoked responses averaged time-locked to asterixis events were subjected to equivalent current dipole (ECD) modeling. Additionally, we localized the strongest cortico-muscular coherence in the frequency of the co-occurring tremulousness. ResultsEvoked fields averaged time-locked to asterixis events were best explained by a single dipolar source in the contralateral primary motor cortex (M1, Talairach coordinates of mean localization: -40, -20, and 64; Brodmann area 4). This dipole showed a twofold field reversal, that is biphasic wave, with frontal dipole orientation at 49ms before flap onset and 99ms after flap onset. Conversely, two maxima with occipital dipole orientation were observed 2ms and 160ms after flap onset. Cortico-muscular coherence for the tremulousness was likewise localized in the contralateral M1 confirming earlier findings in the present patient cohort. ConclusionsOur results reveal an involvement of M1 in the generation of asterixis. As also tremulousness, also called mini-asterixis, was shown to originate in M1, asterixis and mini-asterixis may share common pathophysiological mechanisms.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Butz, M.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Timmermann, L.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Gross, J.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Pollok, B.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Suedmeyer, M.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Kircheis, G.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Haeussinger, D.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Schnitzler, A.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-427784
DOI: 10.1111/ane.12217
Journal or Publication Title: Acta Neurol. Scand.
Volume: 130
Number: 4
Page Range: S. 260 - 268
Date: 2014
Publisher: WILEY-BLACKWELL
Place of Publication: HOBOKEN
ISSN: 1600-0404
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
TRANSCRANIAL MAGNETIC STIMULATION; HUMAN MOTOR CORTEX; NEGATIVE MYOCLONUS; MINI-ASTERIXIS; SILENT PERIOD; HUMAN BRAIN; PATHOPHYSIOLOGY; QUANTIFICATION; INHIBITION; LESIONSMultiple languages
Clinical NeurologyMultiple languages
URI: http://kups.ub.uni-koeln.de/id/eprint/42778

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