Department of Pathology and Laboratory Medicine, Loma Linda University Medical Center.
Department of Pediatrics/Child Neurology, Loma Linda University Children's Hospital, Loma Linda, California.
J Neuropathol Exp Neurol. 2020 Apr 1;79(4):365-369. doi: 10.1093/jnen/nlaa011.
A 29-year-old man presented with rapidly progressive severe neck weakness, asymmetrical bilateral upper extremity weakness, bulbar dysfunction, profound muscle wasting, and weight loss. Within 1 year, his speech became unintelligible, he became gastrostomy- and tracheostomy/ventilator-dependent, and wheelchair bound. Electrophysiology suggested motor neuron disease. Whole exome sequencing revealed a heterozygous pathogenic variant in the fused in sarcoma gene (FUS), c.1574C>T,p. R525L, consistent with autosomal dominant amyotrophic lateral sclerosis. Autopsy revealed extensive denervation atrophy of skeletal musculature. Surprisingly, there was only minimal patchy depletion of motor neurons within the cervico-thoracic spinal cord anterior horn cells, and the tracts were largely preserved. TDP-43 inclusions were absent. Abnormal expression of FUS mutation product (cytoplasmic inclusions) was demonstrated by immunohistochemistry within anterior horn motor neurons. The most prominent finding was a disparity between profound neck weakness and relatively low-grade anterior horn cell loss or tract degeneration in the cervico-thoracic cord.
一位 29 岁男性以进行性严重的颈部无力、双侧上肢无力不对称、球麻痹、严重肌肉萎缩和体重减轻为表现。1 年内,他的言语变得难以理解,需要胃造口和气管切开/呼吸机辅助,并且只能坐轮椅。电生理学提示运动神经元疾病。全外显子组测序显示融合在肉瘤基因(FUS)中的杂合致病性变异,c.1574C>T,p. R525L,符合常染色体显性肌萎缩侧索硬化症。尸检显示广泛的去神经萎缩骨骼肌。令人惊讶的是,颈椎脊髓前角细胞中运动神经元仅出现最小程度的斑片状缺失,并且这些束基本保留。TDP-43 包涵体缺失。免疫组织化学显示前角运动神经元中 FUS 突变产物(细胞质包涵体)异常表达。最突出的发现是严重的颈部无力与颈椎脊髓前角细胞丢失或束变性程度相对较低之间存在明显差异。