ReviewJournal of neurology2014
The genetics of ataxia: through the labyrinth of the Minotaur, looking for Ariadne's thread.
Review in Journal of neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 35 citations in OpenAlex.
- The genetic basis of early-onset hereditary ataxia in Iran: results of a national registry of a heterogeneous population.Human genomics · 2024Article
- Ataxia with Ocular Apraxia Type 1 (AOA1) (APTX, W279* Mutation): Neurological, Neuropsychological, and Molecular Outlining of a Heterogenous Phenotype in Four Colombian Siblings.Molecular neurobiology · 2022Article
- Mitochondrial Ataxias: Molecular Classification and Clinical Heterogeneity.Neurology international · 2022Review
- Objective Assessment of Cerebellar Ataxia: A Comprehensive and Refined Approach.Scientific reports · 2020Article
- Genetic T-type calcium channelopathies.Journal of medical genetics · 2020Review
- Therapy of episodic ataxias: case report and review of the literature.Drugs in context · 2019Review
- Mitochondrial disorders and drugs: what every physician should know.Drugs in context · 2019Review
- Incidentalome in Neurogenetics: Pathogenic Variant ofFrontiers in genetics · 2018Article
- A SINE Insertion inG3 (Bethesda, Md.) · 2017Article
- Pure Cerebellar Ataxia with Homozygous Mutations in the PNPLA6 Gene.Cerebellum (London, England) · 2017Article
- Consensus Paper: Cerebellar Development.Cerebellum (London, England) · 2016Review
- Identifying Niemann-Pick type C in early-onset ataxia: two quick clinical screening tools.Journal of neurology · 2016Article
- Pain in Neurodegenerative Disease: Current Knowledge and Future Perspectives.Behavioural neurology · 2016Review
- Disruptive SCYL1 Mutations Underlie a Syndrome Characterized by Recurrent Episodes of Liver Failure, Peripheral Neuropathy, Cerebellar Atrophy, and Ataxia.American journal of human genetics · 2015Article
- Induced pluripotent stem cell technology for modelling and therapy of cerebellar ataxia.Open biology · 2015Review
- A variant of Nesprin1 giant devoid of KASH domain underlies the molecular etiology of autosomal recessive cerebellar ataxia type I.Neurobiology of disease · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Among the hereditary cerebellar ataxias (CAs), there are at least 36 different forms of autosomal dominant cerebellar ataxia (ADCAs), 20 autosomal recessive cerebellar ataxias (ARCAs), two X-linked ataxias, and several forms of ataxia associated with mitochondrial defects. Despite the steady increase in the number of newly discovered CA genes, patients, especially those with putative ARCAs, cannot yet be genotyped. Moreover, in daily clinical practice, ataxia may present as an isolated cerebellar syndrome or, more often, it is associated with a broad spectrum of neurological manifestations including pyramidal, extrapyramidal, sensory, and cognitive dysfunction. Furthermore, non-neurological symptoms may also coexist. A close integration between clinical records, neurophysiological, neuroradiological and, in some instances, biochemical findings will help physicians in the diagnostic work-up (including selection of the correct genetic tests) and may lead to timely therapy. Some inherited CAs are in fact potentially treatable, and the efficacy of the therapy is directly related to the severity of the cerebellar atrophy and to the time of onset of the disease. Most cases of CA are sporadic, and the diagnostic work-up remains a challenge. Detailed anamnesis and deep investigation of the family pedigree are usually enough to discriminate between acquired and genetic conditions. In the case of ADCA, molecular testing should be guided by taking into account the main associated symptoms. In sporadic cases, a multi-disciplinary approach is needed and should consider the following points: (1) onset and clinical course; (2) associated features; (3) neurophysiological parameters, with special attention to the occurrence of peripheral neuropathy; (4) neuroimaging results; and (5) laboratory findings. A late-onset sporadic ataxia, in which other possible causes have been excluded by following the proposed steps, might be attributable to metabolic disorders, which in some instances may be treatable. In this review, we will guide the reader through the labyrinth of CAs, and we propose a diagnostic flow chart.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.