Gherardi R, Baudrimont M, Gray F, Louarn F
Acta Neuropathol. 1987;73(2):202-8. doi: 10.1007/BF00693790.
We report the quantitative and qualitative, light and electron microscopic studies, including teased fiber preparations of nerve biopsies obtained from eight patients, treated with almitrine, presenting with the characteristic association of a sensory peripheral neuropathy with a recent body weight loss. The data were consistent with an axonal damage affecting myelinated fibers, predominantly large ones and to a lesser degree unmyelinated fibers, some degree of segmental demyelination. Marked axonal regeneration was observed when the nerve biopsy was delayed after withdrawal of the drug, Micro-angiopathy secondary to the formation of concentric lamellae from the basement membrane was observed in five patients suffering from chronic hypoxemia. Almitrine is an agonist of the chemoreceptors. The pathogenesis of the toxic neuropathy induced by this compound remains obscure. Clinical features do not fit with a purely hypoxic mechanism at the origin of the neuropathy.
我们报告了定量和定性的光镜及电镜研究，包括对8例接受烯丙哌三嗪治疗的患者的神经活检进行的 teased fiber 制备。这些患者表现出感觉性周围神经病与近期体重减轻的特征性关联。数据表明存在轴突损伤，主要影响有髓纤维，尤其是大的有髓纤维，对无髓纤维的影响较小，同时存在一定程度的节段性脱髓鞘。在停药后延迟进行神经活检时，观察到明显的轴突再生。在5例慢性低氧血症患者中，观察到因基底膜形成同心板层继发的微血管病。烯丙哌三嗪是化学感受器的激动剂。该化合物所致中毒性神经病的发病机制仍不清楚。临床特征不符合神经病起源的单纯缺氧机制。
