Abstract
Studies in animals indicate that aconitine or aconite has toxic effects on the visual system of a rabbit model. The toxic effects include myelo-optic neuropathy, as proven in the visual evoked cortical potentials (VECP) and histopathological studies. We investigated the effect of intravenous high-dose methylprednisolone (MP) on myelo-optic neuropathy caused by aconite. The group treated with MP (30 mg/kg, twice a day, for 3 days followed by 15 mg/kg for 3 days) in addition to aconite (1.5 ml/kg, equivalent to 0.7 mg/kg of aconitine) was compared with an aconite only-injected group and a normal control group. In the MP-treated group, increased recovery of onset latency, peak latency, and amplitude in VECP was recorded at two weeks (p<0.05) when comparied with the aconite only-injected group. In comparison with the normal control group, the MP-treated group showed a significant delay in onset latency at one and two months (p<0.05). The MP-treated group also showed a significant difference in peak latency at all observation periods when compared with the aconite only-injected group. However, the amplitude in both the MP-treated group and the aconite only-injected group increased at two months and did not show a significant difference when compared with the normal control group. Histopathological findings of the myelin sheath in the MP-treated group generally showed less severe damage than in the aconite only-injected group. The true benefits of high-dose MP were clear within two weeks. The authors conclude that treatment with intravenous high-dose MP immediately after aconite injection may have some beneficial effects on the aconite-induced myelo-optic neuropathy, although such treatment does not show a definite recovery.
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