The aim of this investigation was to determine the incidence of seizur
e activity in the acute phase following traumatic brain injury. Compre
ssion contusion trauma was produced in the right parietal cortex in 19
artificially ventilated rats. Electroencephalographic recordings were
carried out in 17 of the animals for 2 h following the impact. The ex
tracellular levels of neuroactive amino acids were simultaneously moni
tored in 9 of the experiments using microdialysis. In 14 of the 17 ani
mals a generalized seizure activity with an average duration of 59s (r
ange 30-101s) was recorded. The mean time lag between trauma and seizu
re onset was 67s (range 26-90 s). The seizure activity was consistentl
y followed by post-ictal depression. The trauma was accompanied by a t
ransient increase of aspartate, taurine, glutamate and glycine, in dec
reasing rank order. The seizure activity occurred when the levels of t
hese neuroactive amino acids were elevated. It is concluded that the h
igh incidence of seizure activity observed may be an important factor
contributing to secondary ischemia after traumatic brain injury. Aspar
tate and glutamate, potentiated by glycine, may play a role in post-tr
aumatic seizure activity.