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 h
istopathological studies. We investigated the effect of intravenous high-do
se methylprednisolone ( MP) on myelooptic 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 norma
l control group. In the MP-treated group, increased recovery of onset laten
cy, 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 th
e 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 sh
owed a significant difference in peak latency at all observation periods wh
en 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 th
e normal control group. Histopathological findings of the myelin sheath in
the MP-treated group generally showed less severe damage than in the aconit
e only-injected group. The true benefits of high-dose MP were clear within
two weeks. The authors conclude that treatment with intravenous high-dose M
P immediately after aconite injection may have some beneficial effects on t
he aconite-induced myelo-optic neuropathy, although such treatment does not
show a definite recovery.