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Abnormal cortical synaptic plasticity in minimal hepatic encephalopathy
Stefan Golaszewski1, Patrick B Langthaler1, Kerstin Schwenker1
1Department of Neurology, Christian Doppler Klinik, Paracelsus Medical University, Salzburg, Austria.
Abstract:
Minimal hepatic encephalopathy (MHE) represents the earliest stage of hepatic encephalopathy (HE). MHE is characterized by cognitive function impairment in the domains of attention, vigilance and integrative function, while obvious clinical manifestations are lacking. In the present study, we aimed at assessing whether subjects with MHE showed alterations in synaptic plasticity within the motor cortex. Previous findings suggest that learning in human motor cortex occurs through long-term potentiation (LTP)-like mechanisms. We employed therefore the paired associative stimulation (PAS) protocol by transcranial magnetic stimulation (TMS), which is able to induce LTP-like effects in the motor cortex of normal subjects. Fifteen patients with MHE and 15 age- and sex-matched cirrhotic patients without MHE were recruited. PAS consisted of 180 electrical stimuli of the right median nerve paired with a single TMS over the hotspot of right abductor pollicis brevis (APB) at an ISI of 25ms (PAS25). We measured motor evoked potentials (MEPs) before and after each intervention for up to 30min. In healthy subjects the PAS25 protocol was followed by a significant increase of the MEP amplitude. On the contrary, in patients with MHE the MEP amplitude was slightly reduced after PAS. These findings demonstrated that associative sensorimotor plasticity, an indirect probe for motor learning, is impaired in MHE patients.
Insights
Minimal hepatic encephalopathy (MHE) impairs motor cortex synaptic plasticity. This study found that MHE patients exhibit reduced associative sensorimotor plasticity, suggesting a deficit in motor learning mechanisms.
Area of Science:
- Neuroscience
- Clinical Neurology
Background:
- Minimal hepatic encephalopathy (MHE) is the earliest stage of hepatic encephalopathy (HE), characterized by subtle cognitive impairments without obvious clinical signs.
- Cognitive deficits in MHE affect attention, vigilance, and integrative functions.
- Motor cortex synaptic plasticity, particularly long-term potentiation (LTP)-like mechanisms, is implicated in motor learning.
Purpose of the Study:
- To investigate alterations in motor cortex synaptic plasticity in patients with MHE.
- To assess if MHE affects the ability to induce LTP-like effects in the motor cortex.
Main Methods:
- Utilized the paired associative stimulation (PAS) protocol with transcranial magnetic stimulation (TMS) to induce LTP-like effects.
- Recruited 15 MHE patients and 15 cirrhotic patients without MHE.
- Measured motor evoked potentials (MEPs) before and after PAS25 intervention (180 electrical stimuli of the median nerve paired with TMS over the abductor pollicis brevis hotspot at 25ms interstimulus interval).
Main Results:
- In healthy subjects, PAS25 significantly increased MEP amplitude, indicating successful induction of plasticity.
- In MHE patients, the PAS25 protocol resulted in a slight reduction of MEP amplitude.
- These results suggest impaired associative sensorimotor plasticity in MHE.
Conclusions:
- Associative sensorimotor plasticity, a measure of motor learning, is impaired in patients with minimal hepatic encephalopathy.
- The findings highlight a potential neurophysiological basis for motor deficits in the early stages of hepatic encephalopathy.
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