Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Department of Neurology and Geriatrics, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Muscle Nerve. 2019 Dec;60(6):739-744. doi: 10.1002/mus.26683. Epub 2019 Aug 30.
Hereditary motor and sensory neuropathy with proximal dominant involvement (HMSN-P) is characterized by adult onset, a slowly progressive course and autosomal dominant inheritance. It remains unclear whether myopathic changes occur histopathologically.
We encountered 2 patients in a family with a heterozygous p.P285L mutation in TRK-fused gene (TFG), which is known to cause HMSN-P. The affected individuals developed proximal-dominant muscle weakness in their 40s, which slowly progressed to a motor neuron disease-like phenotype.
Muscle biopsy showed myopathic pathology including fiber size variability, increased internal nuclei, fiber splitting, and core-like structures, associated with neurogenic changes: large groups of atrophic fibers and fiber type-grouping. Immunohistochemistry revealed sarcoplasmic aggregates of TFG, TDP-43, and p62 without congophilic material.
The present study demonstrates myopathic changes in HMSN-P. Although the mechanisms underlying the skeletal muscle involvement remain to be elucidated, immunohistochemistry suggests that abnormal protein aggregation may be involved in the myopathic pathology.
遗传性运动感觉神经病伴近端优势受累(HMSN-P)的特征为成人起病、缓慢进行性病程和常染色体显性遗传。其是否存在肌病的组织病理学改变尚不清楚。
我们在一个携带有 TRK 融合基因(TFG)杂合 p.P285L 突变的家系中遇到 2 例患者,该基因已知可导致 HMSN-P。受累个体在 40 多岁时出现以近端为主的肌无力,缓慢进展为类似于运动神经元病的表型。
肌肉活检显示肌病病理学改变,包括纤维大小变异性、内核增加、纤维分裂和核内包涵体样结构,并伴有神经源性改变:大簇萎缩纤维和纤维类型分组。免疫组化显示 TFG、TDP-43 和 p62 的肌浆聚集,无嗜刚果红物质。
本研究显示 HMSN-P 存在肌病改变。尽管骨骼肌受累的机制仍有待阐明,但免疫组化提示异常蛋白聚集可能参与肌病病理学。