Show simple item record

dc.contributor.authorBATTALOĞLU, ESRA
dc.contributor.authorParman, Yesim
dc.contributor.authorCandayan, Ayse
dc.contributor.authorTekgul, Seyma
dc.contributor.authorDurmus, Hacer
dc.contributor.authorBasak, Ayse Nazli
dc.contributor.authorCakar, Arman
dc.contributor.authorInci, Meltem
dc.contributor.authorAcarli, Ayse Nur Ozdag
dc.contributor.authorComu, Sinan
dc.date.accessioned2022-02-18T10:17:14Z
dc.date.available2022-02-18T10:17:14Z
dc.identifier.citationCakar A., Inci M., Acarli A. N. O. , Comu S., Candayan A., BATTALOĞLU E., Tekgul S., Basak A. N. , Durmus H., Parman Y., "Phenotypical spectrum of SACS variants: Neuromuscular perspective of a complex neurodegenerative disorder", ACTA NEUROLOGICA SCANDINAVICA, 2022
dc.identifier.issn0001-6314
dc.identifier.othervv_1032021
dc.identifier.otherav_8df0371b-5263-43df-8013-1d65954e5444
dc.identifier.urihttp://hdl.handle.net/20.500.12627/178955
dc.identifier.urihttps://doi.org/10.1111/ane.13592
dc.description.abstractObjectives Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is caused by the SACS gene variants. Main clinical features include early-onset and progressive cerebellar ataxia, spasticity, sensorimotor polyneuropathy. However, the phenotypic spectrum expanded with the increased availability of next-generation sequencing methods. Materials and Methods Herein, we describe the clinical features of nine patients from seven unrelated families with SACS variants from the cohort of the Neuromuscular Disorders Unit of the Neurology Department of the Istanbul University, Istanbul Faculty of Medicine. Results Seven patients were male. Seven patients in our cohort had disease onset in the first decade of life. Eight patients were born to consanguineous marriages. Distal weakness in the lower limbs was a prominent feature in all of our patients. Seven patients had ataxia, and six patients had spasticity. Interestingly, one patient showed an isolated Charcot-Marie-Tooth-like phenotype. Five patients showed sensorimotor demyelinating polyneuropathy in the nerve conduction studies. Linear pontine hypointensity was the most frequent cranial magnetic resonance imaging (MRI) abnormality. Two patients with a later disease onset had a homozygous c.11542_11544delATT (p.Ile3848del) variant. The rest of the identified variants were scattered throughout the SACS gene. Conclusions Atypical clinical features in our patients highlight that the phenotypic spectrum of ARSACS can be observed in a wide range.
dc.language.isoeng
dc.subjectNeurology
dc.subjectNeurology (clinical)
dc.subjectLife Sciences
dc.subjectHealth Sciences
dc.subjectDahili Tıp Bilimleri
dc.subjectNöroloji
dc.subjectSağlık Bilimleri
dc.subjectTıp
dc.subjectKlinik Tıp (MED)
dc.subjectKlinik Tıp
dc.subjectKLİNİK NEUROLOJİ
dc.titlePhenotypical spectrum of SACS variants: Neuromuscular perspective of a complex neurodegenerative disorder
dc.typeMakale
dc.relation.journalACTA NEUROLOGICA SCANDINAVICA
dc.contributor.departmentAfyon Kocatepe Üniversitesi , ,
dc.contributor.firstauthorID3390461


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following Collection(s)

Show simple item record