Hayashi Kentaro, Mochizuki Yoko, Koide Reiji, Kawata Akihiro, Homma Taku, Shimizu Toshio, Komori Takashi, Isozaki Eiji
Department of Neurology, Tokyo Metropolitan Neurological Hospital.
Department of Pathology, Tokyo Metropolitan Neurological Hospital.
Neuropathology. 2016 Dec;36(6):551-555. doi: 10.1111/neup.12303. Epub 2016 Apr 18.
We describe a Japanese man with familial amyotrophic lateral sclerosis (ALS) associated with a p.Cys146Arg mutation in the copper/zinc superoxide dismutase gene (SOD1). The patient developed bulbar signs followed by rapidly progressive limb muscle weakness. The prominent clinical feature was orthostatic hypotension due to autonomic failure, which occurred after he underwent tracheostomy 1 year and 3 months after the onset. Thereafter, he required mechanical ventilation and progressed to communication stage V (totally locked-in state) 7 years after the onset. Neuropathology showed ALS with posterior column degeneration and multiple system degeneration. Severe neuronal loss in the intermediolateral nucleus was also observed. Two previously reported cases of ALS patients with autonomic failure showed severe neuronal loss in the intermediolateral nucleus in addition to degeneration of the motor neurons. Thus, autonomic failure due to neuronal loss in the intermediolateral nucleus could present in patients with ALS associated with certain mutations in SOD1.
我们描述了一名患有家族性肌萎缩侧索硬化症(ALS)的日本男性,其与铜/锌超氧化物歧化酶基因(SOD1)中的p.Cys146Arg突变相关。患者出现延髓症状,随后肢体肌肉迅速进行性无力。突出的临床特征是自主神经功能衰竭导致的体位性低血压,这在发病1年零3个月后进行气管切开术后出现。此后,他需要机械通气,并在发病7年后进展到交流阶段V(完全闭锁状态)。神经病理学显示为伴有后柱变性和多系统变性的ALS。还观察到中间外侧核严重神经元丢失。另外两例先前报道的伴有自主神经功能衰竭的ALS患者除运动神经元变性外,中间外侧核也有严重神经元丢失。因此,中间外侧核神经元丢失导致的自主神经功能衰竭可能出现在与SOD1特定突变相关的ALS患者中。