Leber Hereditary Optic Neuropathy (LHON) in Patients with Presumed Childhood Monocular Amblyopia

CONCLUSIONS: This report shows three different scenarios of presentation of LHON in patients with presumed uniocular amblyopia from childhood. In such cases, the diagnosis may be difficult, and detailed structural and functional evaluation of the optic nerve head is necessary to assess whether an earlier LHON episode was misdiagnosed as amblyopia or whether LHON presented bilaterally on both eyes whilst only being noticed in the previously good eye.

A rare, likely pathogenic variant causing Leber’s hereditary optic neuropathy in three-generation females of an African-American family

CONCLUSIONS AND IMPORTANCE: Our patients’ presentation stresses the importance of including LHON in the differential diagnosis in females presenting with unexplained bilateral, painless, severe visual loss. The OCT finding of profound GCC thinning with relatively preserved pRNFL thickness can be a red flag for LHON. A collaboration with genetic specialists to utilize expanded gene sequencing may greatly enhance our ability to identify rare pathogenic variants.

Leber hereditary optic neuropathy presenting as bilateral visual loss and white matter disease

Leber hereditary optic neuropathy (LHON) is a rare maternally inherited mitochondrial disorder that typically affects young male adults in their second and third decades of life. It usually manifests as painless, subacute, progressive, bilateral vision loss, with more than 90% of affected individuals losing their vision before age 50. Compared with other diseases that cause optic neuritis (multiple sclerosis or neuromyelitis optica spectrum disorders), LHON has worsening visual function in the…

Coenzyme Q10 trapping in mitochondrial complex I underlies Leber’s hereditary optic neuropathy

How does a single amino acid mutation occurring in the blinding disease, Leber’s hereditary optic neuropathy (LHON), impair electron shuttling in mitochondria? We investigated changes induced by the m.3460 G>A mutation in mitochondrial protein ND1 using the tools of Molecular Dynamics and Free Energy Perturbation simulations, with the goal of determining the mechanism by which this mutation affects mitochondrial function. A recent analysis suggested that the mutation’s replacement of alanine A52…