Objective: This study aimed to determine the frequency and factors associated with obesity in a cohort of children and adolescents with newly diagnosed untreated epilepsy.Methods: Body mass index (BMI) Z-scores and percentiles, both adjusted for age, were used as measures for obesity. Potential covariates associated with these BMI measures included age, etiology (cryptogenic, idiopathic, symptomatic), seizure type (generalized, partial, unclear), concomitant medications (stimulants, nonstimulants, none), and insurance status (privately insured, Medicaid). The primary analysis compared the epilepsy patients' BMI Z-scores to Centers for Disease Control and Prevention data for healthy children. The secondary analysis compared the epilepsy patients' BMI Z-scores to those of a regional healthy control group. Additional analyses incorporated the secondary outcome measure BMI percentiles indexed for age. Results:Children with newly diagnosed untreated epilepsy had higher BMI Z-scores compared to standard CDC growth charts (p Ͻ 0.0001) and the healthy control cohort (p ϭ 0.0002) specifically at both of the 2 tail ends of the distribution. Overall, 38.6% of the epilepsy cohort were overweight or obese (BMI Ն85th percentile for age). Differences in age, etiology, and concomitant nonepilepsy medications were significantly associated with variability in age-adjusted BMI Z-score. Patients in adolescence had higher adjusted BMI Z-scores than younger patients. Patients with symptomatic epilepsy had lower adjusted BMI Z-scores than patients with idiopathic epilepsy. Patients on stimulant psychotropics exhibited lower adjusted BMI Z-scores than patients on no medication. Conclusion:Obesity is a common comorbidity in children with newly diagnosed untreated epilepsy and correlates with increasing age, idiopathic etiology, and absence of concomitant medication. In 2007, the National Institute of Neurological Disorders and Stroke published updated epilepsy benchmarks aimed at guiding research directions toward, among multiple goals, improving safe and effective therapy for people with epilepsy. A new area of research was identified that focused on comorbidities. Several comorbidities in epilepsy have been previously addressed in some depth. However, obesity is a potential comorbidity which has been poorly examined. Obesity in childhood (Ն95th percentile of body mass index [BMI] for age) is increasingly identified as one of the premier public health concerns facing the pediatric population.2 National surveys show that 17.1% of children are obese with an increasing trend toward obesity for all children and adolescents.

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Although the piriform cortex (PC) has been previously implicated as a critical node for seizure generation and propagation, the underlying neural mechanism has remained unclear. Here, we found increased excitability in PC neurons during amygdala kindling acquisition. Optogenetic or chemogenetic activation of PC pyramidal neurons promoted kindling progression, whereas inhibition of these neurons retarded seizure activities induced by electrical kindling in the amygdala. Furthermore, chemogenetic inhibition of PC pyramidal neurons alleviated the severity of kainic acid‐induced acute seizures. These results demonstrate that PC pyramidal neurons bidirectionally modulate seizures in temporal lobe epilepsy, providing evidence for the efficacy of PC pyramidal neurons as a potential therapeutic target for epileptogenesis. imageKey points While the piriform cortex (PC) is an important olfactory centre critically involved in olfactory processing and plays a crucial role in epilepsy due to its close connection with the limbic system, how the PC regulates epileptogenesis is largely unknown. In this study, we evaluated the neuronal activity and the role of pyramidal neurons in the PC in the mouse amygdala kindling model of epilepsy. PC pyramidal neurons are hyperexcited during epileptogenesis. Optogenetic and chemogenetic activation of PC pyramidal neurons significantly promoted seizures in the amygdala kindling model, whereas selective inhibition of these neurons produced an anti‐epileptic effect for both electrical kindling and kainic acid‐induced acute seizures. The results of the present study indicate that PC pyramidal neurons bidirectionally modulate seizure activity.

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