Dr. Hal Blumenfeld at Yale University has offered a testable hypothesis concerning the neural substrate of complex partial seizures. Blumenfeld postulates (2012): (1) that focal discharge arises somewhere in the brain, typically in the temporal lobes; (2) that the focal discharge spreads to subcortical structures that have strong inhibitory outputs, such as the septal nuclei; and (3) that the discharge in these structures suppresses activity in the arousal systems of the upper brain stem and diencephalon. Suppression of the arousal systems leads to unconsciousness, which is signaled by the onset of behavioural arrest and slow waves in the neocortical EEG.
Blumenfeld’s hypothesis has not yet been tested in the amygdala-kindling model – the most widely used and drug-validated animal model of complex partial seizures. Tests involving the Blumenfeld hypothesis and amygdala-kindled rats are now underway in our laboratory. We predict that behavioural arrest in kindled animals will correlate with the onset of slow waves in the rat neocortex. We also predict that the behavioural arrest will not be suppressed by anti-epileptic drugs (AEDs), since AEDs do not suppress complex partial seizures in patients or the kindled amygdala focus in rats (Albright and Burnham, 1980).