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一例伴有多发挛缩的先天性肌无力患者继发性突触间隙稀少:一种发育障碍的超微结构形态学表现

Paucity of secondary synaptic clefts in a case of congenital myasthenia with multiple contractures: ultrastructural morphology of a developmental disorder.

作者信息

Smit L M, Jennekens F G, Veldman H, Barth P G

出版信息

J Neurol Neurosurg Psychiatry. 1984 Oct;47(10):1091-7. doi: 10.1136/jnnp.47.10.1091.

Abstract

A new form of congenital myasthenia is described. An infant whose foetal movements during pregnancy had been weak presented at birth with muscle weakness and multiple contractures of the lower limbs. The clinical course was characterised by myasthenic crises during febrile illnesses. Neurophysiological studies demonstrated a decremental response at 2-3 HZ stimulation; this effect was reversed by edrophonium iv. At the age of eight months, a biopsy from the soleus muscle showed a predominance of type I fibres and variation in fibre diameters was slightly increased. Ultrastructural studies of the motor endplates revealed a marked reduction of post-synaptic membrane lengths with paucity of secondary clefts. Signs of focal degeneration were absent. The picture was reminiscent of foetal neuromuscular junctions. A developmental disorder of the postsynaptic membrane was considered to be the basic cause of the neuromuscular transmission defect.

摘要

本文描述了一种新型先天性肌无力。一名胎儿在孕期胎动就很弱的婴儿,出生时表现为肌无力和下肢多处挛缩。临床病程的特点是发热性疾病期间出现肌无力危象。神经生理学研究显示,在2 - 3赫兹刺激下反应递减;静脉注射依酚氯铵后这种效应逆转。八个月大时,比目鱼肌活检显示I型纤维占优势,纤维直径变化略有增加。运动终板的超微结构研究显示突触后膜长度明显减少,次级裂隙稀少。未见局灶性变性迹象。此表现类似于胎儿神经肌肉接头。突触后膜的发育障碍被认为是神经肌肉传递缺陷的根本原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9fe/1028039/5e905f3022e5/jnnpsyc00126-0039-a.jpg

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