LHON is considered a common cause of blindness in young people, with an age range of 8-60 years reported in the literature, a male to female ratio of 3:1, and no family history in 40% of patients, characterized by subacute, painless bilateral vision loss with central dark spots in the visual field, color vision abnormalities, and optic nerve atrophy. visual impairment in LHON is usually bilateral, and several rare cases of unilateral optic nerve lesions have been reported. Visual acuity is at its worst 4-6 weeks after the onset of the disease and can drop to 6/60 or lower in severe cases. The typical visual field defect is a central dark spot. Other clinical features include early impairment of color vision, but the pupillary reflex to light is preserved and the patient’s eye movements are often painless. In the acute phase, ophthalmologic examination reveals central retinal vascular tortuosity, swelling of the retinal nerve fiber layer, and dilated capillary microangiopathy around the optic papilla; however, it is important to emphasize that approximately 20% of patients with LHON have an acutely normal-looking optic papilla. As the disease progresses, the retinal nerve fiber layer gradually degenerates and eventually the optic nerve atrophies after 6 months. If the patient presents only with optic nerve atrophy, especially if there is no clear family history, then it is difficult to exclude other causes (external forces, infiltration, inflammation) of bilateral optic neuropathy, in which case the patient must do neuroimaging of the previsual pathway before the results of molecular genetic testing are available. possible pathogenesis of LHON: respiratory chain dysfunction leading to axoplasmic stasis, swelling, and This blocks the function of ganglion cells and causes loss of vision. In some patients with LHON, a significant amount of functional damage to ganglion cells is reversible, but in other patients, apoptotic pathways are activated, followed by extensive degeneration of the retinal ganglion cell layer and optic nerve. In terms of diagnosis, the initial clinical diagnosis of LHON can be made if the patient has symptoms of vision loss and a clear family history. ophthalmic tests such as VEP can be used to rule out retinopathy, electrocardiogram is used to rule out cardiac affected diseases such as pre-excitation syndrome, and CT or MRI examinations are often normal. Blood DNA genetic testing is the gold standard for confirming the diagnosis and can identify patients carrying the type of mutation. There is no universally accepted method of preventing or delaying the disease, but nonetheless, smoking cessation and alcohol control are generally recommended for those patients who do not carry the mutation, and long-term follow-up is not necessary for asymptomatic carriers. To date there is no effective treatment to improve the prognosis of patients with LHON, and vitamin supplementation (B12 and C) may promote recovery of vision. Treatment options should be chosen carefully during the acute phase of the disease, and long-term management of patients with visual impairment is primarily supportive.