| Literature DB >> 30460542 |
Katharina Vill1, Wolfgang Müller-Felber2, Dieter Gläser3, Marius Kuhn3, Veronika Teusch4,5, Herbert Schreiber6, Joachim Weis7, Jörg Klepper8, Anja Schirmacher9, Astrid Blaschek2, Manuela Wiessner10, Tim M Strom11, Bianca Dräger9, Kristina Hofmeister-Kiltz12, Moritz Tacke2, Lucia Gerstl2, Peter Young9, Rita Horvath13, Jan Senderek10.
Abstract
Mutations in the SACS gene have been initially reported in a rare autosomal recessive cerebellar ataxia syndrome featuring prominent cerebellar atrophy, spasticity and peripheral neuropathy as well as retinal abnormalities in some cases (autosomal recessive spastic ataxia of Charlevoix-Saguenay, ARSACS). In the past few years, the phenotypic spectrum has broadened, mainly owing to the availability and application of high-throughput genetic testing methods. We identified nine patients (three sib pairs, three singleton cases) with isolated, non-syndromic hereditary motor and sensory neuropathy (HMSN) who carried pathogenic SACS mutations, either in the homozygous or compound heterozygous state. None of the patients displayed spasticity or pyramidal signs. Ataxia, which was noted in only three patients, was consistent with a sensory ataxia. Nerve conduction and nerve biopsy studies showed mixed demyelinating and axonal neuropathy. Brain MRI scans were either normal or revealed isolated upper vermis atrophy of the cerebellum. Our findings confirm the broad clinical spectrum associated with SACS mutations, including pure polyneuropathy without characteristic clinical and brain imaging manifestations of ARSACS.Entities:
Mesh:
Substances:
Year: 2018 PMID: 30460542 DOI: 10.1007/s00439-018-1952-6
Source DB: PubMed Journal: Hum Genet ISSN: 0340-6717 Impact factor: 4.132