Factors predicting optic nerve axonal degeneration after methanol-induced acute optic neuropathy: a 2-year prospective study in 54 patients
Abstrakt
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 muV and for left eyes (LEs) were 6.56 +- 1.00/8.30 +- 1.40 muV. 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 muV, LEs 6.40 +- 1.10/9.30 +- 1.60 muV; 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).
