Altered motor cortical plasticity in patients with hepatic encephalopathy: A paired associative stimulation study
| Autor: | Nur-Deniz Füllenbach, Shady S. Hassan, Alfons Schnitzler, Petyo Nikolov, Dieter Häussinger, Gerald Kircheis, Thomas J. Baumgarten, Markus S. Jördens, Stefan Jun Groiss, Markus Butz, Sarah Nadine Meissner |
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| Rok vydání: | 2021 |
| Předmět: |
Male
medicine.medical_treatment Neurotransmission 03 medical and health sciences 0302 clinical medicine Physiology (medical) Neuroplasticity medicine Humans Evoked potential Hepatic encephalopathy Aged 030304 developmental biology 0303 health sciences Neuronal Plasticity business.industry Motor Cortex Middle Aged Evoked Potentials Motor medicine.disease Paired-Associate Learning Transcranial Magnetic Stimulation Sensory Systems 3. Good health Transcranial magnetic stimulation medicine.anatomical_structure Neurology Hepatic Encephalopathy Synaptic plasticity Female Neurology (clinical) Primary motor cortex business Neuroscience 030217 neurology & neurosurgery Motor cortex |
| Zdroj: | Clinical Neurophysiology |
| ISSN: | 1388-2457 |
| DOI: | 10.1016/j.clinph.2021.07.019 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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