Episodic ataxia type 1 is a neuronal channelopathy caused by mutations in the KCNA1 gene encoding the fast K(+) channel subunit K(v)1.1. Episodic ataxia type 1 presents with brief episodes of cerebellar dysfunction and persistent neuromyotonia and is associated with an increased incidence of epilepsy. In myelinated peripheral nerve, K(v)1.1 is highly expressed in the juxtaparanodal axon, where potassium channels limit the depolarizing afterpotential and the effects of depolarizing currents. Axonal excitability studies were performed on patients with genetically confirmed episodic ataxia type 1 to characterize the effects of K(v)1.1 dysfunction on motor axons in vivo. The median nerve was stimulated at the wrist and compound muscle action potentials were recorded from abductor pollicis brevis. Threshold tracking techniques were used to record strength-duration time constant, threshold electrotonus, current/threshold relationship and the recovery cycle. Recordings from 20 patients from eight kindreds with different KCNA1 point mutations were compared with those from 30 normal controls. All 20 patients had a history of episodic ataxia and 19 had neuromyotonia. All patients had similar, distinctive abnormalities: superexcitability was on average 100% higher in the patients than in controls (P < 0.00001) and, in threshold electrotonus, the increase in excitability due to a depolarizing current (20% of threshold) was 31% higher (P < 0.00001). Using these two parameters, the patients with episodic ataxia type 1 and controls could be clearly separated into two non-overlapping groups. Differences between the different KCNA1 mutations were not statistically significant. Studies of nerve excitability can identify K(v)1.1 dysfunction in patients with episodic ataxia type 1. The simple 15 min test may be useful in diagnosis, since it can differentiate patients with episodic ataxia type 1 from normal controls with high sensitivity and specificity.
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http://dx.doi.org/10.1093/brain/awq318 | DOI Listing |
Brain Commun
December 2024
Dipartimento Universitario di Neuroscienze, Università Cattolica del Sacro Cuore, 00168 Roma, Italy.
Familial hemiplegic migraine type 2 results from pathogenic variants in the gene, which encodes for a catalytic subunit of sodium/potassium ATPase. This extremely rare autosomal dominant disorder manifests with a spectrum of symptoms, most commonly pure hemiplegic phenotype, epilepsy, and/or intellectual disability. In this study, we detail the clinical features and genetic analysis of nine patients from a large family spanning four generations, with all carrying a previously unreported likely pathogenic variant, p.
View Article and Find Full Text PDFJ Vet Intern Med
December 2024
Small Animal Hospital, School of Veterinary Medicine, University of Glasgow, Glasgow, United Kingdom.
Background: Episodic ataxias (EAs) are a rare group of paroxysmal movement disorders (PMD) described in human medicine with only one suspected case described in veterinary literature.
Hypothesis/objectives: This study aimed to provide clinical description of a suspected primary EA in working Cocker Spaniel (WCS) dogs.
Animals: Seven WCS dogs with suspected primary EA.
Mov Disord Clin Pract
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Service de Neuropédiatrie, CHU Montpellier, Montpellier, France.
Cell Commun Signal
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Department of Physiology, College of Medicine, National Taiwan University, Taipei, 100, Taiwan.
Loss-of-function mutations in the human gene encoding the neuron-specific Ca channel Ca2.1 are linked to the neurological disease episodic ataxia type 2 (EA2), as well as neurodevelopmental disorders such as developmental delay and developmental epileptic encephalopathy. Disease-associated Ca2.
View Article and Find Full Text PDFJ Clin Neurol
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Biomedical Research Institute, Seoul National University Bundang Hospital, Seongnam, Korea.
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