Radboud University Nijmegen Medical Centre, Department of Neurology (935), Nijmegen 6500 HB, The Netherlands.
J Neurol Neurosurg Psychiatry. 2010 Sep;81(9):968-72. doi: 10.1136/jnnp.2009.177089.
Sandhoff disease is a lipid-storage disorder caused by a defect in ganglioside metabolism. It is caused by a lack of functional N-acetyl-beta-d-glucosaminidase A and B due to mutations in the HEXB gene. Typical, early-onset Sandhoff disease presents before 9 months of age with progressive psychomotor retardation and early death. A late-onset form of Sandhoff disease is rare, and its symptoms are heterogeneous. As drug trials that aim to intervene in the disease mechanism are emerging, the recognition and identification of Sandhoff disease patients-particularly those with atypical phenotypes-are becoming more important. The authors describe six new late-onset Sandhoff cases demonstrating cerebellar ataxia or lower motor neuron (LMN) involvement combined with, mostly subclinical, neuropathy. Two different mutations were found: IVS 12-26 G/A and c.1514G-->A. In patients with either progressive cerebellar ataxia or LMN disease in the setting of a possibly recessive disorder, Sandhoff disease should be suspected, even when the onset age is over 45 years.
沙夫病是一种脂质贮积疾病,由神经节苷脂代谢缺陷引起。它是由于 HEXB 基因突变导致功能性 N-乙酰-β-D-氨基葡萄糖苷酶 A 和 B 缺乏所致。典型的早发型沙夫病在 9 个月前发病,表现为进行性精神运动发育迟缓,早期死亡。晚发型沙夫病罕见,其症状呈异质性。由于旨在干预疾病机制的药物试验不断涌现,对沙夫病患者的识别和鉴定变得尤为重要,尤其是那些具有非典型表型的患者。作者描述了 6 例新的晚发型沙夫病病例,这些病例表现为小脑共济失调或下运动神经元(LMN)受累,伴有大多数亚临床神经病。发现了两种不同的突变:IVS 12-26 G/A 和 c.1514G-->A。在具有可能为隐性疾病的进行性小脑共济失调或 LMN 疾病的患者中,即使发病年龄超过 45 岁,也应怀疑沙夫病。