ArticleBMC neurology2019
Spinocerebellar ataxia type 31 associated with REM sleep behavior disorder: a case report.
Article in BMC neurology, 2019. 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, 11 citations in OpenAlex.
- Ataxin-3 Overexpression via Adeno-associated Viral Vector Injection in the Primate Cerebellum: A Novel Model of Spinocerebellar Ataxia Type 3.Experimental neurobiology · 2025Article
- Predictive clinical factors for the progression from idiopathic late-onset cerebellar ataxia to multiple system atrophy cerebellar type.Journal of neurology · 2025Article
- Purkinje cell dysfunction causes disrupted sleep in ataxic mice.Disease models & mechanisms · 2024Article
- Dream enactment behavior: review for the clinician.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2020Article
- Sleep Disorders in Hereditary Ataxias.Current neurology and neuroscience reports · 2019Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSpinocerebellar ataxia type 31 (SCA 31) is a slowly progressive neurodegenerative disorder characterized by pure cerebellar ataxia. Unlike other CAG repeat diseases, sleep-related problems have not been reported in patients with SCA 31 so far. CASE PRESENTATION: A 67-year-old woman was admitted to our hospital with dysarthria and gait disturbance after onset age of 62 years. Neurological examination revealed pure cerebellar ataxia. Genetic analysis detected expansion of a TGGAA repeat in the coding region of the BEAN/TK2 gene on chromosome 16p22.1, confirming the diagnosis of SCA 31. One year later, her husband noticed the patient talking loudly during sleep once or twice a week. Overnight polysomnography showed rapid eye movement sleep without atonia. Cardiac scintigraphy with iodine-123-labeled meta-iodobenzylguanidine revealed a low heart/mediastinum ratio, indicating reduced uptake, and a high washout rate.
conclusionTo our knowledge, this is the first report of a patient with SCA 31 associated with rapid eye movement sleep behavior disorder (RBD). In the future, evaluation of autonomic function, assessment of the frequency of RBD, and performance of cardiac iodine-123-labeled meta-iodobenzylguanidine scintigraphy in a larger number of SCA 31 patients could be useful to resolve important issues regarding the mechanism of RBD.
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