Prevalence, dynamics, and biochemical predictors of optic nerve remyelination after methanol-induced acute optic neuropathy: a 2-year prospective study in 54 patients

Abstract

We conducted a prospective study in 54 patients with a median age of 48 years (range 23–73) to determine the prevalence and dynamics of optic nerve remyelination after methanol-induced optic neuropathy. Methanol was measured by a gas chromatographic method with flame ionization detection. Formate was measured enzymatically. Measurement of full-field visual evoked potential with monocular checkerboard pattern-reversal stimulation was performed 3–8 and 24–28 months after discharge. The latency of the positive peak (P1) was used for the analysis of remyelination dynamics. Twenty-seven patients had abnormal P1 latencies. Mean P1 latency for right eyes (REs) was 115.3 ± 2.1 ms and for left eyes (LEs) was 117.4 ± 3.2 ms. The group with abnormal latency had lower arterial pH (p = 0.017), higher anion gap (p = 0.013), methanol (p = 0.027), base deficit (p = 0.033), and lactate (p = 0.048). At the second examination, shortening of P1 latencies was registered (REs/LEs 98.3 ± 2.4/102.7 ± 4.5 ms; p < 0.001). The dynamics of latency shortening for REs/LEs were 17 ± 1.3/15.1 ± 3.1 ms, with insignificant inter-eye difference (p = 0.271). The dynamics of remyelination correlated with serum methanol (r = −0.588; p < 0.001), arterial pH (r = 0.339; p = 0.040), and concentration of carbohydrate-deficient transferrin (r = −0.411; p = 0.011). Remyelination occurred in cases of mild or moderate damage of myelin sheaths; no improvement of conduction was found in severe cases. The dynamics of remyelination correlated with the degree of acidosis and severity of poisoning. Chronic alcohol abuse had a negative effect on remyelination dynamics.