Cerebellar inhibition in hepatic encephalopathy.

Aged Cerebellum / physiology Evoked Potentials, Motor / physiology Female GABAergic Neurons / physiology Hepatic Encephalopathy / diagnosis Humans Male Middle Aged Neural Inhibition / physiology Transcranial Magnetic Stimulation / methods
Cerebellar inhibition (CBI) Critical flicker frequency (CFF) Gamma Aminobutyric Acid (GABA) Hepatic encephalopathy (HE) Score for assessment and rating of ataxia (SARA) Transcranial magnetic stimulation (TMS)

Journal

Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology
ISSN: 1872-8952
Titre abrégé: Clin Neurophysiol
Pays: Netherlands
ID NLM: 100883319

Informations de publication

Date de publication:
06 2019
Historique:
received: 17 01 2018
revised: 29 01 2019
accepted: 18 02 2019
pubmed: 14 4 2019
medline: 4 3 2020
entrez: 14 4 2019
Statut: ppublish

Résumé

Previous animal work reported that hyperammonemia leads to opposing changes of GABAergic neurotransmission in terms of increase in the cerebellum and decrease in the cerebral cortex. In this study, we investigate GABAergic tone in the cerebellum in patients with hepatic encephalopathy (HE) at different stages of the disease and its relation to critical flicker frequency (CFF) and ataxia. Cerebellar inhibition using transcranial magnetic stimulation was investigated in 15 patients with different stages of HE and 15 healthy controls. All patients were assessed using CFF and the score for assessment and rating of ataxia (SARA). Decreased cerebellar inhibition (CBI) was observed in manifest HE at interstimulus interval from 5 to 7 ms. However, the degree of CBI at 7 ms correlated significantly with disease severity measured with SARA and with CFF by trend. Reduced CBI in HE patients indicates affection of the cerebellar efferent pathway. The disease severity dependent increase of CBI magnitude supports the notion of disease stage dependent increase of GABAergic neurotransmission in Purkinje cells. The results support previous animal experiments showing increase of GABA-ergic neurotransmission in the cerebellum and decrease in the motor cortex in HE.

Identifiants

DOI: 10.1016/j.clinph.2019.02.020 PMID: 30981173
pubmed: 30981173
pii: S1388-2457(19)30102-6
doi: 10.1016/j.clinph.2019.02.020
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

886-892

Informations de copyright

Copyright © 2019 International Federation of Clinical Neurophysiology. Published by Elsevier B.V. All rights reserved.

Auteurs

Shady Safwat Hassan (SS)

Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich Heine University Düsseldorf, Germany; Department of Neurology, Medical Faculty, Assiut University Hospital, Assiut, Egypt.

Thomas J Baumgarten (TJ)

Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich Heine University Düsseldorf, Germany.

Anwar M Ali (AM)

Department of Neurology, Medical Faculty, Assiut University Hospital, Assiut, Egypt.

Nur-Deniz Füllenbach (ND)

Department of Gastroenterology, Hepatology and Infectiology, Medical Faculty, Heinrich Heine University Düsseldorf, Germany.

Markus S Jördens (MS)

Department of Gastroenterology, Hepatology and Infectiology, Medical Faculty, Heinrich Heine University Düsseldorf, Germany.

Dieter Häussinger (D)

Department of Gastroenterology, Hepatology and Infectiology, Medical Faculty, Heinrich Heine University Düsseldorf, Germany.

Markus Butz (M)

Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich Heine University Düsseldorf, Germany.

Alfons Schnitzler (A)

Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich Heine University Düsseldorf, Germany; Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Germany.

Stefan Jun Groiss (SJ)

Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich Heine University Düsseldorf, Germany; Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Germany. Electronic address: groiss-js@umin.net.

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Classifications MeSH

questionsmedicales.fr › Personnes › Tranches d'âge › Adulte › Sujet âgé › Cerebellar inhibition in hepatic encephalopathy.
questionsmedicales.fr › Système nerveux › Système nerveux central › Encéphale › Tronc cérébral › Rhombencéphale › Métencéphale › Cervelet › Cerebellar inhibition in hepatic encephalopathy.
questionsmedicales.fr › Phénomènes physiologiques de l'appareil locomoteur et du système nerveux › Phénomènes physiologiques du système nerveux › Excitabilité corticale › Potentiels évoqués › Potentiels évoqués moteurs › Cerebellar inhibition in hepatic encephalopathy.
questionsmedicales.fr › Cellules › Neurones › Neurones GABAergiques › Cerebellar inhibition in hepatic encephalopathy.
questionsmedicales.fr › Maladies métaboliques et nutritionnelles › Maladies métaboliques › Encéphalopathies métaboliques › Encéphalopathie hépatique › Cerebellar inhibition in hepatic encephalopathy.
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Primates › Haplorhini › Catarrhini › Hominidae › Humains › Cerebellar inhibition in hepatic encephalopathy.
questionsmedicales.fr › Personnes › Tranches d'âge › Adulte › Adulte d'âge moyen › Cerebellar inhibition in hepatic encephalopathy.
questionsmedicales.fr › Phénomènes physiologiques de l'appareil locomoteur et du système nerveux › Phénomènes physiologiques du système nerveux › Inhibition nerveuse › Cerebellar inhibition in hepatic encephalopathy.
questionsmedicales.fr › Thérapeutique › Magnétothérapie › Stimulation magnétique transcrânienne › Cerebellar inhibition in hepatic encephalopathy.