Generalised and focal to bilateral convulsive seizures are risk factors for Sudden Unexpected Death in Epilepsy (SUDEP). Postictal generalized EEG suppression (PGES), a generalized flattening of the scalp EEG, is a potential marker of increased seizure severity and risk of SUDEP. PGES has been variably linked to autonomic dysfunctions including loss of arousal. Risk of SUDEP may be increased in direct proportion to duration of PGES and loss of arousal. Convulsive seizures can co-exist with spreading depolarisation (SD), a slowly propagating wave of neuronal and glial depolarisation (typically lasting 30-120s). SD results in higher frequency activity suppression (spreading depression), which can take several minutes to recover. Whether seizure-associated SD contributes to PGES and loss of arousal is not known. We developed a novel transgenic rodent model of TLE (focal conditional-knockout of an astrocyte potassium channel, Kir4.1; Kir4.1-cKO) where seizures can be triggered on-demand by brief optogenetic stimulation. We used DC-coupled graphene micro-transistors to concurrently detect seizures and SD, and pupillometry as an indirect measurement of cortical state and arousal, in awake head-fixed mice. In 60% of Kir4.1-cKO mice (n=5), SD temporally co-existed with seizures resulting in longer post-ictal depression. Seizures were associated with pupil dilation, whereas there was a biphasic response to seizure-associated SD; initial dilation followed by pronounced pupil constriction, temporally correlated with the duration of neuronal activity suppression. Seizures associated with SD resulted in increased post-ictal depression and loss of arousal. Seizure-associated SD may be a risk factor for PGES and by consequence SUDEP; therefore warranting further investigation.