Mitochondrial DNA analysis in ocular myopathy. Observations in 29 Portuguese patients

Eur Neurol. 1998;39(3):148-53. doi: 10.1159/000007925.

Abstract

We analyzed 29 patients with progressive external ophthalmoparesis (PEO) either alone or as part of a multisystem disorder. Ragged-red fibers were very abundant (10-20%) in 15 patients, and many of them were also cytochrome c oxidase-negative. Biochemical analysis of the respiratory chain showed partial defects of single or multiple complexes in 18 patients (64%). Eleven PEO patients (38%) harbored single large-scale mtDNA deletions in muscle, which averaged 5.4 kb in size and 47% in relative abundance. One PEO patient harbored the A3243G mutation (MELAS mutation) in muscle (63%). Our findings, the first reported in Portuguese patients, confirm that single large-scale mtDNA deletions are a significant cause of PEO. Although ophthalmoparesis was the main clinical feature in the majority of patients, the clinical spectrum is broad, ranging from severe encephalopathy of childhood to a milder, though disabling, muscle weakness in adults.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Child
  • Child, Preschool
  • DNA, Mitochondrial / genetics*
  • Electron Transport Complex IV / metabolism
  • Female
  • Gene Deletion*
  • Humans
  • Infant
  • MELAS Syndrome / genetics
  • Male
  • Middle Aged
  • Oculomotor Muscles / enzymology
  • Oculomotor Muscles / pathology
  • Ophthalmoplegia / enzymology
  • Ophthalmoplegia / genetics*
  • Ophthalmoplegia / pathology

Substances

  • DNA, Mitochondrial
  • Electron Transport Complex IV