Lidocaine has a concentration-dependent effect on seizures. At lower concen
trations it has anticonvulsant properties, whereas concentrations above 15
mu g/ mt frequently result in seizures in laboratory animals and man. Seizu
res induced by lidocaine in experimental conditions invariably start in the
amygdala. Despite the clear focal onset in these experimental models, the
seizures emerging in patients given intravenous (i.v.) lidocaine are almost
invariably generalized and without any clear signs of focality. Given the
prevalence of partial seizures and the frequent use of lidocaine, a higher
incidence of partial seizures would be expected with its use. Yet this is c
learly not the case. These facts suggest that a history of partial seizures
is not a major risk factor fur the precipitation of partial seizures in pa
tients treated with intravenous lidocaine.