Watson C P N, Morshead C, Van der Kooy D, Deck J, Evans R J
Irene Eleanor Smythe Pain Clinic, Toronto General Hospital, Toronto, Ont. M5G 2C4 Canada Neurobiology Research Group, Department of Anatomy, University of Toronto, Toronto, Ont. M5S 1A8 Canada.
Pain. 1988 Aug;34(2):129-138. doi: 10.1016/0304-3959(88)90158-3.
The morphological and biochemical substrates of the severe pain in post-herpetic neuralgia (PHN) are unclear. This report is an autopsy study of a 67-year-old male with severe PHN during the last 5 years of his life over the right T7-8 dermatomes. The dorsal horn of the thoracic spinal cord of the affected side was atrophic from T4 to T8, with loss of both myelin and axons. Despite this, only the T8 ganglion was affected by fibrosis and cell loss and only the nerve roots at that level appeared affected. Markers of unmyelinated afferents (substance P), substantia gelatinosa neurons (opiate receptors), glial cells (glial fibrillary acidic protein), and descending spinal projections (dopamine-beta-hydroxylase and serotonin) were not different at affected versus non-affected spinal cord levels. The pain of PHN may result from the uninhibited activity of unmyelinated primary afferents as a result of the loss of myelinated afferent fibers and the possible presence of hypersensitive neurons in the dorsal horn.
带状疱疹后神经痛(PHN)中严重疼痛的形态学和生化底物尚不清楚。本报告是对一名67岁男性的尸检研究,该男性在生命的最后5年患有右侧T7 - 8皮节严重的PHN。患侧胸段脊髓背角从T4到T8萎缩,伴有髓鞘和轴突丧失。尽管如此,仅T8神经节受到纤维化和细胞丧失的影响,且仅该水平的神经根似乎受到影响。无髓传入纤维(P物质)、胶状质神经元(阿片受体)、神经胶质细胞(胶质纤维酸性蛋白)以及脊髓下行投射(多巴胺-β-羟化酶和5-羟色胺)的标志物在患侧与未患侧脊髓水平并无差异。PHN的疼痛可能是由于有髓传入纤维丧失导致无髓初级传入纤维的无抑制活动以及背角中可能存在的超敏神经元所致。