Effect of fampridine on axonal excitability in multiple sclerosis

Publication date: July 2016
Source:Clinical Neurophysiology, Volume 127, Issue 7
Author(s): William Huynh, Hannah Pickering, James Howells, Jenna Murray, Christine Cormack, Cindy S.-Y. Lin, Steve Vucic, Matthew C. Kiernan, Arun V. Krishnan
ObjectiveTo investigate the effects of fampridine on nerve excitability, the present study utilized peripheral axonal excitability techniques in 18 MS patients receiving treatment with fampridine.MethodsStudies were performed at baseline and repeated 3months after institution of fampridine at standard dosing.ResultsFollowing treatment with fampridine there were significant changes in axonal excitability for those parameters associated with fast K⁺ channels that shifted towards normal control values. Specifically, increases were noted in the peak superexcitability of recovery cycle (fampridine, −25.6±1.6%; baseline −22.8±1.7%; p<0.004), peak depolarizing threshold electrotonus (fampridine, 69.1±1.0%; baseline 67.0±1.4%; p<0.004), and depolarizing threshold electrotonus between 40 and 60ms after onset of depolarization (fampridine, 52.8±1.3%; baseline 49.9±1.4%; p=0.02).ConclusionThe present study has established that fampridine at standard doses exerts effects on peripheral nerve function that may be mediated by reduction of fast K⁺ conductances.SignificanceModulation of fast K⁺ conductances by fampridine may contribute to the improvement observed in MS symptoms including motor fatigue.



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