ArticleJournal of neurology2009
Nerve conduction studies in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
Article in Journal of neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Persistent vessel wall enhancement and progression of cerebral microbleeds in CADASIL: a case report.Frontiers in radiology · 2026Article
- Article
- Review
- Effects of lacunar infarctions on cognitive impairment in patients with cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy.Journal of clinical neurology (Seoul, Korea) · 2011Article
- Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy: a genetic cause of cerebral small vessel disease.Journal of clinical neurology (Seoul, Korea) · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary cerebral microangiopathy linked to mutations in the Notch3 gene. The cerebral impairments of CADASIL are well-known, but peripheral nervous impairments such as polyneuropathy are less clear. Recently, peripheral neuropathy was proposed as one of the CADASIL phenotypes. We investigated peripheral nerve involvement in CADASIL patients. Forty-three CADASIL patients with confirmed Notch3 gene mutations underwent a nerve conduction studies using a conventional surface technique in 86 upper and lower extremities. Nerve conduction abnormalities were apparent in seven of the 43 patients. Of the seven patients, four displayed nerve entrapment syndromes (carpal tunnel syndrome, n = 3; ulnar neuropathy, n = 1), and three displayed sensorimotor polyneuropathy. Of the latter three, two patients had diabetes mellitus. We suggest that peripheral neuropathy may not be part of the CASASIL phenotype. However, genotype-phenotype heterogeneity can not be excluded.
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Registered trials
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