Focal temporal lobe seizures in humans often cause loss of consciousness accompanied by cortical slow waves similar to deep sleep. Previous rat studies under anesthesia suggested that reduced subcortical arousal depresses cortical function, but could not link conscious behavior to physiology. In an awake mouse model, electrically induced hippocampal seizures impaired behavioral responses to sounds, triggered cortical slow waves, and reduced mean high-frequency cortical activity. Behavioral responses depended on cortical acetylcholine release at two timescales: slow state-related decreases correlated with overall impairment, while fast phasic release corresponded to variable spared or impaired responses per stimulus. These results establish a strong link between decreased cortical arousal and impaired consciousness during focal seizures.
Absence seizures cause sudden lapses in consciousness accompanied by spike-wave discharges, but how they impair sensory processing is unclear. In a rat model of absence epilepsy, behavioral performance on an auditory task collapsed during seizures, dropping from about 88% correct to less than 1%. However, electrical responses in the primary auditory cortex remained normal. Instead, a novel oscillatory signal in the anterior insular cortex was robust in healthy controls, reduced in epileptic rats between seizures, and nearly absent during seizures. This signal's reduction differed from that seen in satiated, unmotivated states, where waveform structure was preserved. The anterior insula appears to be a critical hub for gating auditory conscious awareness during seizures, offering a potential biomarker and intervention target.