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.