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.

中文翻译：

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肝性脑病患者运动皮质可塑性改变：配对联想刺激研究

客观的

肝性脑病（HE）是一种由肝功能衰竭引起的潜在可逆的脑功能障碍。突触可塑性的改变应该在 HE 的病理生理学中起主要作用。在这里，我们使用了 25 ms (PAS25) 刺激间隔的配对关联刺激，这是一种经颅磁刺激 (TMS) 协议，以测试明显 HE 患者运动皮层的突触可塑性。

方法

23 名 HE 患者和 23 名健康对照者参加了该研究。运动诱发电位 (MEP) 振幅被评估为皮质兴奋性的量度。比较两组 PAS25 干预后 MEP 振幅变化的时间进程。

结果

对照组中 PAS25 后 MEP 振幅增加，表明健康对照中 PAS25 诱导的突触可塑性，正如预期的那样。相比之下，HE 组内的 MEP 幅度没有变化，并且低于对照组，表明没有诱导可塑性。

结论

我们的研究揭示了 HE 中初级运动皮层的突触可塑性降低。

意义

HE 中突触可塑性降低提供了分子水平上的病理变化与该疾病的早期临床症状之间的联系。这种减少可能是由于 HE 患者已知的高氨血症导致谷氨酸能神经传递紊乱所致。