论文标题
配对的联想刺激表明肝性脑病患者运动皮质突触可塑性的改变
Paired associative stimulation demonstrates alterations in motor cortical synaptic plasticity in patients with hepatic encephalopathy
论文作者
论文摘要
目的：肝性脑病（HE）是由肝衰竭引起的潜在可逆脑功能障碍。突触可变的改变应该在HE的病理生理中起主要作用。在这里，我们使用了与经颅磁刺激（TMS）方案的刺激间隔为25 ms（PAS25）的配对缔合刺激，以测试具有明显HE患者的运动皮层的突触可塑性。方法：研究参与了23名HE患者和23个健康对照。 Motor evoked potential (MEP) amplitudes were assessed as measure for cortical excitability.在两组之间比较了PAS25干预后MEP振幅变化的时间课程。结果：PAS25在对照组的PAS25后增加，表明PAS25诱导的健康对照中的突触可塑性如预期的。相比之下，HE组内的MEP膨胀没有变化，并且比对照组低，表明没有诱导可塑性。结论：我们的研究表明，HE原发性运动皮层的突触可塑性降低。意义：HE中的突触可塑性降低提供了分子水平的病理变化与疾病早期临床症状之间的联系。由于HE患者的已知高症血症，这种减少可能是由于谷氨酸能神经传递的障碍引起的。
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. Conclusion: 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.
