Petit mal seizure spikes in olfactory bulb and cortex caused by runaway inhibition after exhaustion of excitation.

The olfactory bulb (OB), anterior olfactory nucleus (AON) and prepyriform cortex (PC) maintain 3 kinds of feedback among their populations of excitatory and inhibitory neurons: negative feedback, mutual excitation, and mutual inhibition. At normal levels of synaptic input these are balanced and give rise to chaotic and near-sinusoidal oscillatory EEG activity. Under intense repetitive electrical stimulation of the lateral olfactory tract (LOT), there is failure of the afferent excitatory terminals, perhaps due to transmitter depletion. In this circumstance there is deficient excitatory input under the condition of a high level of sustained activity among mutually inhibitory neurons. An instability develops in which some inhibitory neurons become more disinhibited (excited) and others more inhibited (less active) to the point of a paroxysmal discharge that is manifested in a massive compound IPSP of the excitatory neurons. The paroxysm terminates abruptly, but by mechanisms still unclear repeats at a rate of about 3/s for 10-70 s. It is accompanied by simultaneous ipsilateral twitching of the eyelids and muzzle, salivation, tearing, arrest, and lack of responding to sensory stimuli but without loss of posture, resembling absence in humans. It does not result from runaway mutual excitation, and it rarely culminates in full-blown convulsions. Similar spikes usually also occur in the OB and AON; the sequences of spikes appear to entrain. These normal and seizure EEGs are simulated with a network of non-linear differential equations, that is designed in conformance with the anatomy and physiology of the olfactory system. The seizure appears as an emergent property of the OB, AON and PC interactive system, that is due to an induced asymmetry in the feedback network that controls normal background activity.