Sir,

We report a case of tobacco–alcohol amblyopia (TAA) and correlate the improvement in visual function with changes in the thickness of peripapillary retinal nerve fibre layer (RNFL) measured by optical coherence tomography (OCT).

Case report

A 68-year-old man presented with bilateral reduced vision. He smoked a pipe and drank alcohol regularly for 30 years. The best-corrected visual acuities were 6/36 OD and 3/60 OS. Colour vision using the pseudoisochromatic plates was 3 of 17 in both eyes. Both optic discs showed pallor of the temporal neuroretinal rim. Static perimetry showed centrocaecal scotoma in the right eye and central scotoma extending to the periphery in the left eye. Serum vitamin B12 level was 187 μg/l (normal: 197–866 μg/l). Flash visual evoked response (VER) was reduced (Figure 1a) and OCT showed increased RNFL thickness in both eyes apart from thinning in the temporal quadrant (Figure 1b).

Figure 1
figure 1

At initial presentation the flash VER (a) showed a delayed, reduced, and negative waveform, and OCT (b) showed marked increase in RNFL thickness (solid arrows) apart from thinning in the temporal quadrant (hollow arrows).

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The patient ceased smoking; stopped drinking ethanol, and was prescribed hydroxocobalamin supplements. One year later, visual acuity improved to 6/9 OD and 6/12 OS. Flash VER was no longer delayed and pattern responses were present in both eyes with four cycles per degree checks (Figure 2a). The increased peripapillary RNFL thickness had normalised with persistent thinning temporally (Figure 2b).

Figure 2
figure 2

One year later, the VER (a) improved and was no longer delayed. OCT (b) showed resolution of RNFL thickness with persistent thinning temporally (hollow arrows).

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Comment

The preferential thinning of temporal peripapillary RNFL in our patient is similar to that reported in three cases of ethambutol-induced optic neuropathy.1 TAA belongs to the larger class of toxic/nutritional optic neuropathies in which the primary insult is to the mitochondria that disrupts the process of oxidative phosphorylation resulting in axonal loss, preferentially in the fast-firing, parvocellular neurons within the papillomacular bundle.1, 2, 3, 4 Increased RNFL thickness has been reported in TAA and may occur because of axonal swelling and intraretinal fluid accumulation in the acute phase of visual loss.4, 5 Normalisation of RNFL thickness following cessation of toxic insult and vitamin B12 supplementation correlated with improvement in visual function. The eye with the greatest increase in RNFL thickness showed the most improvement suggesting that axonal swelling precedes irreversible damage and optic atrophy. In patients with TAA, RNFL thickness measured by OCT may be useful to predict the visual prognosis.