Factors predicting optic nerve axonal degeneration after methanol-induced acute optic neuropathy: a 2-year prospective study in 54 patients

Abstract

Prospective cross-sectional study was conducted in 54 patients (mean age 46.7 ± 3.7 years) to determine the character of optic nerve axonal degeneration after acute methanol poisoning. 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 amplitudes of N1P1 and P1N2 components of evoked response were used for analysis of axonal loss. Altogether, 13 of 50 patients (26 %) had abnormal amplitudes at the first examination (including the patients with nonrecordable amplitudes), and 37 patients had normal amplitudes. Mean N1P1/P1N2 amplitudes for right eyes (REs) were 6.30 ± 1.10/8.70 ± 1.50 µV and for left eyes (LEs) were 6.56 ± 1.00/8.30 ± 1.40 µV. The group with abnormal amplitudes had lower arterial pH (p = 0.009), bicarbonate (p = 0.036), higher base deficit (p = 0.005), glucose (p = 0.015), and lactate (p = 0.018). At the second examination, insignificant amplitude changes were registered (REs 6.50 ± 1.10/9.80 ± 1.60 µV, LEs 6.40 ± 1.10/9.30 ± 1.60 µV; both p > 0.05). In 2 of 44 REs (5 %) and in 4 of 45 LEs (9 %) with 2 consecutive examinations the initially normal amplitudes deteriorated to abnormal values. In 3 of 45 patients (7 %) the abnormal amplitudes deteriorated in both eyes indicating the ongoing process of chronic neuronal degeneration. The dynamics of amplitude deterioration correlated with serum lactate (r = 0.533; p < 0.001), glucose (r = 0.462; p = 0.005), and formic acid (r = 0.380; p = 0.046) on admission to hospital. The correlation was present between the magnetic resonance signs of hemorrhagic brain lesions and the amplitude changes (r = −0.535; p < 0.001).