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Abstract Details
Altered motor cortical plasticity in patients with hepatic encephalopathy: A paired associative stimulation study
Clin Neurophysiol. 2021 Aug 13;132(10):2332-2341. doi: 10.1016/j.clinph.2021.07.019.Online ahead of print.
Petyo Nikolov1, Thomas J Baumgarten2, Shady S Hassan3, Sarah N Meissner4, Nur-Deniz Füllenbach5, Gerald Kircheis5, Dieter Häussinger5, Markus S Jördens5, Markus Butz6, Alfons Schnitzler1, Stefan J Groiss7
Author information
1Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany; Department of Neurology, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany.
2Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany; Neuroscience Institute, New York University School of Medicine, New York, USA.
3Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany; Department of Neurology, Medical Faculty, Assiut University Hospital, Assiut, Egypt.
4Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany; Department of Health Sciences and Technology, ETH Zürich, Switzerland.
5Department of Gastroenterology, Hepatology and Infectious Diseases, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany.
6Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany.
7Institute 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@uni-duesseldorf.de.
Abstract
Objective: Hepatic encephalopathy (HE) is a potentially reversible brain dysfunction caused by liver failure. Altered synaptic plasticity is supposed to play a major role in the pathophysiology of HE. Here, we used paired associative stimulation with an inter-stimulus interval of 25 ms (PAS25), a transcranial magnetic stimulation (TMS) protocol, to test synaptic plasticity of the motor cortex in patients with manifest HE.
Methods: 23 HE-patients and 23 healthy controls were enrolled in the study. Motor evoked potential (MEP) amplitudes were assessed as measure for cortical excitability. Time courses of MEP amplitude changes after the PAS25 intervention were compared between both groups.
Results: MEP-amplitudes increased after PAS25 in the control group, indicating PAS25-induced synaptic plasticity in healthy controls, as expected. In contrast, MEP-amplitudes within the HE group did not change and were lower than in the control group, indicating no induction of plasticity.
Conclusions: Our study revealed reduced synaptic plasticity of the primary motor cortex in HE.
Significance: Reduced synaptic plasticity in HE provides a link between pathological changes on the molecular level and early clinical symptoms of the disease. This decrease may be caused by disturbances in the glutamatergic neurotransmission due to the known hyperammonemia in HE patients.