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Clinical and electrophysiological evaluation of myasthenic features in an alpha-dystroglycanopathy cohort (FKRP-predominant)
Journal article   Open access   Peer reviewed

Clinical and electrophysiological evaluation of myasthenic features in an alpha-dystroglycanopathy cohort (FKRP-predominant)

Paloma Gonzalez-Perez, Cheryl Smith, Wendy L Sebetka, Amber Gedlinske, Seth Perlman and Katherine D Mathews
Neuromuscular disorders : NMD, Vol.30(3), pp.213-218
03/2020
DOI: 10.1016/j.nmd.2020.01.002
PMID: 32115343
url
https://doi.org/10.1016/j.nmd.2020.01.002View
Published (Version of record) Open Access

Abstract

•Fatigue is a common symptom in α-dystroglycanopathy muscular dystrophies.•Fatigue did not predict abnormal NMJ transmission on electrodiagnostic studies.•NMJ defect was not found outside of the GMPPB α-dystroglycanopathy subgroup.•NMJ defect associates with mild GMPPB phenotypes and treatment response is variable. A postsynaptic dysfunction of the neuromuscular junction has been reported in patients with alpha-dystroglycanopathy associated with mutations in guanosine diphosphate (GDP)-mannose pyrophosphorylase B gene (GMPPB), some of whom benefit from symptomatic treatment. In this study, we determine the frequency of myasthenic and fatigue symptoms and neuromuscular junction transmission defects in a fukutin-related protein (FKRP)-predominant alpha-dystroglycanopathy cohort. Thirty-one patients with alpha-dystroglycanopathies due to mutations in FKRP (n = 25), GMPPB (n = 4), POMGNT1 (n = 1), and POMT2 (n = 1) completed a six-question modified questionnaire for myasthenic symptoms and the PROMIS Short Form v1.0-Fatigue 8a survey, and they underwent 3 Hz repetitive nerve stimulation of spinal accessory nerve-trapezius and radial nerve-anconeus pairs. Results showed that fatigue with activity was common; 63% of the cohort reported fatigue with chewing. A defective postsynaptic neuromuscular junction transmission was not identified in any of the patients carrying FKRP mutations but only in one mildly affected patient with GMPPB mutations (c.79 G>C, p.D27H and c.402+1G>A, splice site variant). We conclude that symptoms of fatigue with activity did not predict abnormal neuromuscular junction transmission on electrodiagnostic studies in this cohort and that, unlike GMPPB subgroup, a defective neuromuscular junction transmission does not appear to be present in patients with FKRP-associated muscular dystrophies.
Fatigue Myasthenia Fukutin-related protein (FKRP) Neuromuscular junction

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