Cerebellar inhibition in hepatic encephalopathy

Shady Safwat Hassan; Thomas J Baumgarten; Anwar M Ali; Nur-Deniz Füllenbach; Markus S Jördens; Dieter Häussinger; Markus Butz; Alfons Schnitzler; Stefan Jun Groiss

doi:10.1016/j.clinph.2019.02.020

Cerebellar inhibition in hepatic encephalopathy

Clin Neurophysiol. 2019 Jun;130(6):886-892. doi: 10.1016/j.clinph.2019.02.020. Epub 2019 Mar 30.

Authors

Shady Safwat Hassan¹, Thomas J Baumgarten², Anwar M Ali³, Nur-Deniz Füllenbach⁴, Markus S Jördens⁴, Dieter Häussinger⁴, Markus Butz², Alfons Schnitzler⁵, Stefan Jun Groiss⁶

Affiliations

¹ Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich Heine University Düsseldorf, Germany; Department of Neurology, Medical Faculty, Assiut University Hospital, Assiut, Egypt.
² Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich Heine University Düsseldorf, Germany.
³ Department of Neurology, Medical Faculty, Assiut University Hospital, Assiut, Egypt.
⁴ Department of Gastroenterology, Hepatology and Infectiology, Medical Faculty, Heinrich Heine University Düsseldorf, Germany.
⁵ Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich Heine University Düsseldorf, Germany; Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Germany.
⁶ 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.

PMID: 30981173
DOI: 10.1016/j.clinph.2019.02.020

Abstract

Objective: 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.

Methods: 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).

Results: 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.

Conclusion: 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.

Significance: The results support previous animal experiments showing increase of GABA-ergic neurotransmission in the cerebellum and decrease in the motor cortex in HE.

Keywords: 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).

Publication types

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

MeSH terms

Aged
Cerebellum / physiology*
Evoked Potentials, Motor / physiology
Female
GABAergic Neurons / physiology
Hepatic Encephalopathy / diagnosis
Hepatic Encephalopathy / physiopathology*
Humans
Male
Middle Aged
Neural Inhibition / physiology*
Transcranial Magnetic Stimulation / methods*