ArticleAnnals of neurosciences2018
Assessment of Sleep Spindle Density among Genetically Positive Spinocerebellar Ataxias Types 1, 2, and 3 Patients.
Article in Annals of neurosciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Respiratory Evaluation in Spinocerebellar ataxia Type 2.Cerebellum (London, England) · 2025Article
- Article
- Communication from the cerebellum to the neocortex during sleep spindles.Progress in neurobiology · 2021Article
- Pathogenesis of SCA3 and implications for other polyglutamine diseases.Neurobiology of disease · 2020Review
- Molecular Mechanisms and Therapeutics for Spinocerebellar Ataxia Type 2.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- Sleep Disorders in Hereditary Ataxias.Current neurology and neuroscience reports · 2019Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe effect of thalamic degeneration in patients with spinocerebellar ataxias (SCA) and sleep spindle (SS) abnormalities has not been studied so far, although there is a strong association between these disorders. This study was done to evaluate and compare the SS densities (SSDs) of genetically proven autosomal dominant SCA1, SCA2 and SCA3 patients with controls.
methodsProspectively and genetically confirmed cases of SCA and controls were recruited. Patients were assessed clinically, were evaluated with sleep questionnaires and an overnight polysomnography was performed. SSDs were analyzed using neuroloop gain plugin of Polyman version 1.15 software.
resultsEighteen patients of SCA1 (
conclusionSSDs were significantly decreased in patients with SCA, which is a novel finding. This is likely due to the "thalamic switch" disruption, observed as reduced SSDs in SCA2 and SCA3. Sleep spindle deficits could act as one of the biomarkers of ongoing neurodegeneration in the thalamic circuitry of SCA patients.
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