偏头痛病理生理解析.ppt

Key point: Central sensitization is a key event in the pathogenesis of migraine; sensitization within the brain places some portion of the disease in the CNS. 关键点:中枢敏化在偏头痛的发病机理中是一个关键性事件；脑内神经敏化是中枢神经系统疾病的一部分。 Central sensitization could be induced by peripheral sensitization through an escalating barrage of input from sensitized trigeminal primary afferents, possibly induced by CSD.1 CSD可以诱导三叉神经初级感觉纤维敏化，传入信号经过层级的放大由外周敏化又可进一步诱导中枢敏化。1 Alternatively, central sensitization may be a form of disinhibitory sensitization directly resulting from dysfunction of descending modulatory pathways within the brainstem.2 另外，中枢敏化可能是脑干和中脑下行调节通路障碍，而导致感觉信号失去抑制的一种形式。2 Central sensitization is associated with abnormal neuronal excitability in the TNC, possibly reflecting chemical disturbances that may include increased levels of calcium and glutamate, and elevated activity at NMDA receptors.1 中枢敏化与三叉神经尾侧核神经元的异常兴奋有关,可能反映出化学信号的紊乱,包括增加的钙和谷氨酸水平,以及提高门冬氨酸受体活性。1 In addition to its involvement in basal neurotransmission, CGRP also appears to contribute to the synaptic plasticity that underlies central sensitization in the TNC.3 除了参与基底神经传递，CGRP也加强了突触的可塑性，从而构成了三叉神经尾侧核的中枢敏化的基础。3 This effect of CGRP could be achieved by its regulation of the release of BDNF (brain-derived neurotrophic factor), a neurotrophin involved in synaptic plasticity at other sites of the CNS. CGRP的这种效应可以通过调控BDNF(脑源性神经营养因子)的释放来实现。这种神经营养因子在中枢神经系统的其他位点参与突触可塑性的生成。 In many respects, the activity-dependent plasticity of nociceptive spinal synapses producing central sensitization appears similar to long-term potentiation (LTP) of central excitatory synapses. LTP of nociceptive synapses in the TNC and/or alterations of endogenous central pain modulatory pathways, including PAG, are plausible hypothetical mechanisms for the maintenance of central sensitization of the TGS.4 在许多方面,脊髓痛觉突触活动依赖可塑性所产生的中枢敏化类似于中枢兴奋性突触长时程增强(LTP)。三叉神经尾侧核痛觉突触的长时程增强(LTP)和/或内源性中枢疼痛的调节途径的改变,包括PAG,为三叉神经系统中枢敏化的维持提供了合理的假设机制。4 Central sensitization could be the cause o