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莫顿神经瘤——发病机制与超微结构

Morton's neuroma--pathogenesis and ultrastructure.

作者信息

Ha'Eri G B, Fornasier V L, Schatzker J

出版信息

Clin Orthop Relat Res. 1979 Jun(141):256-9.

PMID:477115
Abstract

In an attempt to clarify the pathogenesis of Morton's neuroma, 106 documented cases were analyzed by multiple staining techniques and electron microscopy. The lesion was found to consist of a progressive fibrosis which enveloped and disrupted nerves and arteries. No evidence of a nerve proliferation nor of a specific inflammatory process was encountered. Based on these observations, it is concluded that repeated trauma in the connective tissue elements, including nerves and arteries in the interdigital clefts, lead to a reactive overgrowth of connective tissue (scarring) that disrupts the nerves and the arteries. Sclerosis of the arteries and the narrowing of their lumen contributes to ischemia and further nerve atrophy. The nerves and arteries caught in this reactive scar become more sensitive to pressure and cause characteristic pain.

摘要

为了阐明 Morton 神经瘤的发病机制,采用多种染色技术和电子显微镜对 106 例记录在案的病例进行了分析。发现该病变由渐进性纤维化组成,其包裹并破坏神经和动脉。未发现神经增生或特定炎症过程的证据。基于这些观察结果,得出结论:包括趾间裂中的神经和动脉在内的结缔组织反复受到创伤,会导致结缔组织反应性过度生长(瘢痕形成),从而破坏神经和动脉。动脉硬化及其管腔狭窄会导致局部缺血和进一步的神经萎缩。陷入这种反应性瘢痕中的神经和动脉对压力变得更加敏感,并引起特征性疼痛。

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