Abstract
Tobacco-alcohol amblyopia, an acquired optic neuropathy, is now classified as toxic and nutritional optic neuropathy (TNON). A 40-year-old man presented with gradual, painless, symmetrical visual loss and central scotomas. Pupillary reactions were normal, with no relative afferent pupillary defect (RAPD), though colour vision was markedly reduced. Optic discs appeared normal with early temporal pallor in the left eye. Optical coherence tomography (OCT) revealed thinning of the peripapillary retinal nerve fibre layer (pRNFL) in the temporal quadrant and decreased macular thickness. The patient reported heavy alcohol consumption for five years and smoking two packs of cigarettes daily. Laboratory findings indicated vitamin B12 deficiency and low folate levels. Despite supplementation, visual recovery was limited due to longstanding retinal nerve fibre loss. Chronic alcoholism is indirectly toxic to the optic nerve, as vitamin B12 and folate deficiencies impair mitochondrial function. This leads to the selective injury of unmyelinated ganglion cell axons, particularly within the papillomacular bundle. Optic discs initially appear normal, but progressive thinning of the pRNFL results in temporal pallor later extending to all quadrants. The parafoveal ganglion cell-inner plexiform layer (GCL+IPL) and macular thickness may be reduced. Smoking further exacerbates nutritional deficiencies; however, cyanide in tobacco is also directly toxic to the optic nerve. Diagnosis relies on careful history-taking, the evaluation of macular and pRNFL thickness, visual field testing, and colour vision assessment. This case highlights the importance of early recognition of TNON, particularly when optic discs appear normal, to enable timely nutritional therapy and visual recovery.