痉挛性睑内翻的临床与病理

目的：通过10例痉挛性睑内翻患者临床和眼轮匝肌的病理学研究，探讨其发病机理。方法：用眼轮匝肌缩短术矫正睑内翻，术中切除的眼轮匝肌进行肌活检常规、酶组织化学和电镜检查。结果：染色显示部分肌纤维萎缩和代偿性肥大，有肌细胞核内移、肌纤维透明变性、肌纤维断裂等现象，肌纤维间及肌束周均见多量纤维结缔组织增生，小血管数量增多。酶组织化学：ATPase、NADH—TR、SDH染色部分肌纤维酶活性增高，SDH／CCO双重染色见蓝纤维。电镜下肌纤维排列较正常，肌膜、基底膜无异常，灶性肌原纤维断裂、丢失，脱失处见髓小体及无定形物质，部分Z线漂移、消失，肌原纤维间可见较多无膜包绕的大小不等的脂滴。结论：证实了痉挛性睑内翻是由于患者的眼轮匝肌存在着肌源性肌病的病理改变，肌肉加强术治疗可以改善功能。

Pathologic changes and clinic study of senile entropion

Objective:To study the entropion mechanism by analyzing of clinical characteristics and the pathological findings of biopsied orbicularis oculi muscle from 10 cases of senile entropion. Methods:The orbicularis oculi muscle were shortened to correct the position of the lower eyelid,and the excised muscle were biopsied including histological examination,enzyme histochemistry and EM. Results:Parts of myofibers showed atrophy,hypertrophy,internal nuclei,hyaline degeneration,break and so on.There were amount of connective tissue and small blood vessels around muscle fibers and bundles.ATPase,NADH-TR and SDH stains demonstrated increase of enzyme activities of parts myofibers.SDH/CCO double stains showed single blue fiber.Electron microscopic observation showed that parts of muscle fibrils broken,lost,replaced by amorphous material and myelin-like figures;Focal Z lines streamed or lost.A few fat droplets without membrane were observed on muscle fibril. Conclusions:Pathologic changes of myogenic muscle diseases existed in entropion patients with orbicularis oculi muscle.Clinic therapy can improve the muscle function by operation of muscle shorten.