Mechanisms of pain modulation in chronic syndromes
Mechanisms of pain modulation in chronic syndromes
复制标题
DOI：
10.1212/wnl.59.5_suppl_2.s2
复制
发表时间：
2002-09-10
期刊：
影响因子：
9.9
通讯作者：
Moskowitz, MA
中科院分区：
文献类型：
--
作者：
Bolay, H;Moskowitz, MA
疼痛从外周到皮质的传递依赖于脊髓、脑干和前脑内的整合和信号处理。敏感化是持续性或慢性疼痛的一个组成部分，可能通过外周机制发展，也可能是脊髓或前脑生理改变的结果。一些分子和生物物理机制导致了敏感化和持续性疼痛现象，包括感觉神经元特异性钠通道和香草素受体的上调，大的有髓轴突的表型转换，在背角内发芽，以及由于细胞凋亡而失去抑制神经元。最近，前脑结构被认为与持续性疼痛的病理生理学有关。尽管使用了许多治疗方案，但不幸的是，药物治疗神经性疼痛往往无效。解开慢性疼痛的谜团可能会带来更好的治疗选择，比如专门作用于感觉神经元特异性钠通道的药物，或者作为NR2B亚单位选择性N-甲基-D-天冬氨酸受体拮抗剂。
Transmission of pain from the periphery to the cortex depends on integration and signal processing within the spinal cord, brainstem, and forebrain. Sensitization, a component of persistent or chronic pain, may develop either through peripheral mechanisms or as a consequence of altered physiology in the spinal cord or forebrain. Several molecular and biophysical mechanisms contribute to the phenomenon of sensitization and persistent pain, including upregulation of sensory neuron-specific sodium channels and vanilloid receptors, phenotypic switching of large myelinated axons, sprouting within the dorsal horn, and loss of inhibitory neurons due to apoptotic cell death. Recently, forebrain structures have been implicated in the pathophysiology of persistent pain. Although a number of treatment options are used, unfortunately pharmacotherapy for neuropathic pain is often ineffective. Unraveling the mysteries of chronic pain may lead to better treatment options, such as drugs that act specifically on sensory neuron-specific sodium channels or as NR2B-subunit-selective N-methyl-D-aspartate receptor antagonists.