Tzourio C, Said G, Millan J
Institut de Léprologie, Dakar, Senegal.
J Neurol. 1992 Aug;239(7):367-74. doi: 10.1007/BF00812152.
In order to learn more about early nerve lesions observed in leprosy, we performed a clinical, electrophysiological and morphological study in seven patients with untreated lepromatous leprosy, palpably enlarged radial cutaneous nerve and preserved sensation in the corresponding territory. The conduction velocity of the cutaneous radial nerve, which was decreased in all patients, did not significantly differ from that of a group of patients with lepromatous leprosy, hypertrophy of the radial cutaneous nerve and sensory loss. In contrast, the sensory action potential was significantly lower in patients with sensory loss, which demonstrates that axon loss is more important than demyelination in producing sensory loss. In all patients nerve enlargement was due to thickening of the epineurium and of the perineurium subsequent to inflammatory infiltrates and proliferation of fibroblasts and perineurial cells. In several fascicles, the inflammatory infiltrates and the infected cells infiltrated endoneurial connective tissue septa and blood vessels. Mycobacteria leprae were abundant in perineurial cells, fibroblasts, macrophages, Schwann cells and endothelial cells, and lymphocytic vasculitis present in all cases. The average density of myelinated fibres was 2600 SD 880 fibres/mm2 (control: 7700 fibres/mm2), with marked differences between individual fascicles, versus 420 fibres/mm2 in patients with nerve hypertrophy and sensory loss (range 0-2080 fibres/mm2). Single fibre preparations showed that segmental demyelination predominated in two patients, axonal degeneration in one, while inflammatory infiltrates and proliferation of connective tissue adhering to individual fibres were prominent in the others.(ABSTRACT TRUNCATED AT 250 WORDS)
为了更深入了解麻风病早期出现的神经病变,我们对7例未经治疗的瘤型麻风患者进行了临床、电生理及形态学研究。这些患者的桡神经皮支可触及增粗,而相应区域感觉保留。所有患者的桡神经皮支传导速度均降低,与一组瘤型麻风、桡神经皮支肥大且伴有感觉丧失的患者相比,差异无统计学意义。相反,感觉丧失患者的感觉动作电位显著更低,这表明轴突丧失在导致感觉丧失方面比脱髓鞘更为重要。在所有患者中,神经增粗是由于炎性浸润以及成纤维细胞和神经束膜细胞增殖后神经外膜和神经束膜增厚所致。在几个神经束中,炎性浸润和受感染细胞浸润了神经内膜结缔组织间隔和血管。麻风杆菌在神经束膜细胞、成纤维细胞、巨噬细胞、施万细胞和内皮细胞中大量存在,且所有病例均存在淋巴细胞性血管炎。有髓纤维的平均密度为2600±880根/平方毫米(对照组:7700根/平方毫米),各神经束之间存在显著差异,而神经肥大和感觉丧失患者的有髓纤维平均密度为4根/平方毫米(范围为0 - 2080根/平方毫米)。单纤维标本显示,两名患者以节段性脱髓鞘为主,一名患者以轴突变性为主,而其他患者中炎性浸润和黏附于单个纤维的结缔组织增生较为突出。(摘要截选至250字)