Congenital myasthenia syndrome in a Chinese family with mutations in MUSK: A hotspot mutation and literature review

J Clin Neurosci. 2020 Jun:76:161-165. doi: 10.1016/j.jocn.2020.03.036. Epub 2020 Apr 3.

Abstract

Congenital myasthenic syndrome (CMS) caused by mutations in MUSK is very rare and the genotype-phenotype relationship in MUSK related CMS is still unclear. Here we identified two patients carrying a homozygous hotspot mutation, c.308A > G in MUSK from a Chinese family. Both of them presented predominant bulbar weakness and atrophy of bilateral temporalis and masticatory muscles. To address the phenotype-genotype relationship, a total of 27 MUSK related CMS patients were reviewed. Patients with nonsense, frameshift or splicing mutations showed earlier onset (10/13 vs 2/14 neonatal onset, p = 0.0018) and more occurrence of vocal cord paralysis or stridor (8/13 vs 0/14, p = 0.0006), indicating a more severe phenotype. Comparing with patients carrying other missense mutations, the four patients carrying a homozygous c.308A > G mutation showed the female predominance (4/10 vs 4/4) and dramatic exacerbation after emotional or physiological stresses (2/10 vs 4/4) like pregnancy, menstrual periods and infection. All these indicated a genotype-phenotype relationship in MUSK-related CMS.

Keywords: Congenital myasthenia syndrome; Hotspot mutation; Muscle-specific tyrosine kinase.

MeSH terms

  • Asian People
  • Family
  • Female
  • Frameshift Mutation
  • Genetic Association Studies*
  • Homozygote
  • Humans
  • Male
  • Mutation*
  • Mutation, Missense
  • Myasthenic Syndromes, Congenital / etiology
  • Myasthenic Syndromes, Congenital / genetics*
  • Myasthenic Syndromes, Congenital / pathology
  • RNA Splicing / genetics
  • Receptor Protein-Tyrosine Kinases / genetics*
  • Receptors, Cholinergic / genetics*
  • Risk Factors

Substances

  • Receptors, Cholinergic
  • MUSK protein, human
  • Receptor Protein-Tyrosine Kinases