AI Article Synopsis

  • Episodic ataxia type 1 is linked to mutations in the KCNA1 gene, affecting potassium channels and leading to symptoms like brief cerebellar dysfunction, persistent neuromyotonia, and an increased risk of epilepsy.
  • Axonal excitability studies on patients with confirmed KCNA1 mutations showed they had significantly higher superexcitability and altered threshold electrotonus compared to normal controls, indicating pronounced abnormalities in nerve function.
  • The findings suggest that nerve excitability tests could serve as a reliable diagnostic tool for differentiating episodic ataxia type 1 patients from healthy individuals, helping to identify the condition effectively.

Article Abstract

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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2995887PMC
http://dx.doi.org/10.1093/brain/awq318DOI Listing

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