Clinical, pathological and genetic characterization of hereditary sensory and autonomic neuropathy type 1 (HSAN I)

被引:93
作者
Houlden, H
King, R
Blake, J
Groves, M
Love, S
Woodward, C
Hammans, S
Nicoll, J
Lennox, G
O'Donovan, DG
Gabriel, C
Thomas, PK
Reilly, MM
机构
[1] Natl Hosp Neurol & Neurosurg, Ctr Neuromuscular Dis, London WC1N 3BG, England
[2] Natl Hosp Neurol & Neurosurg, Dept Mol Neurosci, London WC1N 3BG, England
[3] Natl Hosp Neurol & Neurosurg, Dept Clin Neurophysiol, London WC1N 3BG, England
[4] Natl Hosp Neurol & Neurosurg, Div Neuropathol, London WC1N 3BG, England
[5] UCL Royal Free & Univ Coll Med Sch, Neurol Inst, Dept Clin Neurosci, London, England
[6] Frenchay Hosp, Dept Neuropathol, Inst Clin Neurosci, Bristol BS16 1LE, Avon, England
[7] Southampton Gen Hosp, Wessex Neurolog Ctr, Southampton SO9 4XY, Hants, England
[8] Addenbrookes Hosp, Dept Neurol, Cambridge, England
[9] Addenbrookes Hosp, Dept Neuropathol, Cambridge, England
[10] St Marys Hosp, Dept Neurol, London, England
[11] Norfolk & Norwich Hosp, Dept Clin Neurophysiol, Norwich NR1 3SR, Norfolk, England
基金
英国医学研究理事会; 英国惠康基金;
关键词
phenotype; peripheral nervous system; neuropathology; mutation; hereditary neuropathy;
D O I
10.1093/brain/awh712
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Hereditary sensory and autonomic neuropathy type I (HSAN I) is the most frequent type of hereditary neuropathy that primarily affects sensory neurons. The genetic locus for HSAN I has been mapped to chromosome 9q22.1-22.3 and recently the gene was identified as SPTLC1, encoding serine palmitoyltransferase, long chain base subunit-1. Sequencing in HSAN I families have previously identified mutations in exons 5, 6 and 13 of this gene. We analysed the SPTLC1 gene for mutations in 8 families with HSAN I, 60 individuals with sporadic sensory neuropathy, 6 HSAN II families, 20 Charcot-Marie-Tooth type I families and 20 families with Charcot-Marie-Tooth type II. Six HSAN I families and a single sporadic neuropathy case had an identical SPTLC1 mutation. No mutations were found in the other groups. Genetic haplotyping across the HSAN I critical region in 5 families and the sporadic case suggested a common founder. Several characteristics, previously not widely recognized were identified, including lack of penetrance of the SPTLC1 mutation in some individuals, variability in age of onset along with an earlier age of onset in younger generations, in some patients surprisingly early and often severe motor involvement and an earlier onset characterized by motor involvement with demyelinating features in males compared to females in 4 families. The sensory findings were often disassociated with prominent pain and temperature loss. Neurophysiology mainly showed a sensory axonal neuropathy but in many individuals there was electrical evidence of demyelination. Sural nerve biopsies from six affected individuals and the post-mortem findings in 1 case showed mainly axonal loss. This in depth study on the phenotype of HSAN I in 6 families and a single sporadic case with a common founder identifies a number of poorly recognized features in this disorder and highlights the clinical heterogeneity both within and between families suggesting the influence of other genetic and acquired factors.
引用
收藏
页码:411 / 425
页数:15
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