Aim. To study the features of the clinical symptoms of toxic optic neuropathy.
Methods. 21 patients (42 eyes) with toxic optic neuropathy were examined with the use of standard ophthalmic exam, computer visual field test, spectral optical coherence tomography of the retina and optic nerve.
Results. Toxic optic neuropathies were caused by the acute (4 patients) or chronic (10 patients) alcohol intake, drug abuse (6 patients) and medications (ethambutol, 1 patient). In all patients bilateral visual deterioration with central scotomas with various levels of light sensitivity reduction and prominent dyschromatopsia was revealed. The features of structural changes were reveled in patients with toxic optic neuropathy: the primary thinning of the retinal inner layers with further peripapillary retinal nerve fiber layer thickness loss. Severity of the structural changes ranged from the predominant damage of the retinal inner layers and minor decrease in the temporal peripapillary sector thickness to profound atrophy of the ganglion cell complex and optic nerve. In acute and chronic alcohol abuse after the treatment and complete alcohol cessation 43% of patients noted recovered visual function.
Conclusion. Severity of the symptoms of toxic optic neuropathy, intensity and the rate of atrophy development, and prognosis depend on the nature of the toxin, its dose and exposure time, genetic features in each case; such algorithm of the changes is probably connected to the pathogenesis based on mitochondrial dysfunction.
Ischemic optic neuropathy is an optic nerve disorder that requires thorough medical history taking and comprehensive assessment of the patient in order to identify the causes and risk factors of this disease as well as accompanying pathologies.
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