An MFN2-related Charcot-Marie-Tooth Disease Patient with Optic Nerve Atrophy, Neurogenic Bladder Dysfunction, and Diaphragmatic Weakness

Intern Med. 2022 Jun 1;61(11):1743-1747. doi: 10.2169/internalmedicine.6487-20. Epub 2021 Nov 20.

Abstract

Charcot-Marie-Tooth disease (CMT) is a common hereditary peripheral polyneuropathy encompassing distinct monogenetic disorders. Pathogenic mutations in mitofusin 2 (MFN2) are the most frequent cause of its axonal type, CMT type 2A, with diverse phenotypes. We herein report a Japanese patient with a novel heterozygous MFN2 pathogenic variant (c.740 G>C, p.R247P) and severe CMT phenotypes, including progressive muscle weakness, optic atrophy, urinary inconsistency, and restrictive pulmonary dysfunction with eventration of the diaphragm that developed over her 60-year disease course. Our case expands the clinico-genetic features of MFN2-related CMT and highlights the need to evaluate infrequent manifestations during long-term care of CMT patients.

Keywords: Charcot-Marie-Tooth disease; diaphragmatic weakness; hereditary motor sensory neuropathy; mitofusin 2; neurogenic bladder; restrictive pulmonary dysfunction.

MeSH terms

  • Atrophy
  • Charcot-Marie-Tooth Disease* / complications
  • Charcot-Marie-Tooth Disease* / genetics
  • Female
  • GTP Phosphohydrolases / genetics
  • Humans
  • Hydrolases / genetics
  • Mitochondrial Proteins / genetics
  • Muscle Weakness / genetics
  • Mutation
  • Optic Atrophy* / genetics
  • Optic Nerve
  • Urinary Bladder, Neurogenic*

Substances

  • Mitochondrial Proteins
  • Hydrolases
  • GTP Phosphohydrolases
  • MFN2 protein, human