There is a well-documented correlation between epilepsy and sleep deprivation. For decades, preclinical and clinical studies have shown that sleep deprivation can lead to an increased risk of epileptic seizures. Additionally, sleep deprivation has been used clinically as a diagnostic tool for epilepsy by triggering epileptiform activity. However, an underlying mechanism for this relationship is yet to be confirmed. Interestingly, a decrease in gamma-aminobutyric acid (GABA)-mediated tonic inhibition has been shown in both epilepsy and sleep deprivation. This review focuses on the role of sleep deprivation in the induction of epileptic seizures and the possible role of reduced GABA receptor expression in the sleep-deprived state.

For decades, phenytoin has been the drug of choice for the treatment of epilepsy but also the second-line treatment for status epilepticus (SE). However, newer antiepileptic drugs (AEDs) have emerged as safer alternatives for the suppression of seizures. Consequently, phenytoin has recently fallen under scrutiny in the research world, prompting many studies to compare its efficacy to these other drugs, most notably levetiracetam. Levetiracetam is a second-generation AED, which is gaining wide clinical use as the second-line agent in treating SE patients. This review focuses on several clinical studies that have directly compared the effectiveness of phenytoin and levetiracetam in suppressing SE seizure activity. Additionally, this review highlights several advantages of using levetiracetam over phenytoin in this clinical context.