Inflammation in new-onset refractory status epilepticus

Aurelie Hanin, PharmD, PhD, Yale University, New Haven, CT, discusses her work investigating inflammation in new-onset refractory status epilepticus (NORSE). Patients with NORSE experience refractory seizures, and do not respond well to antiseizure medications. Research has suggested that the mechanisms underlying the pathology of NORSE are inflammatory, however this research is limited. Therefore, Dr Hanin and her group wanted to better understand the pathophysiology of NORSE and the outcomes of the condition. In this study, inflammation was assessed using cerebrospinal fluid (CSF) and serum cytokines/chemokines in patients with NORSE, and compared to patients with other refractory status epilepticus (RSE) and control patients. There was a significant increase in the levels of several proinflammatory cytokines and chemokines in patients with RSE compared to those without, in both serum and CSF. Futhermore, in patients with NORSE, there was a significant increase of proinflammatory cytokines in comparison to patients with RSE. When comparing those with cryptogenic NORSE (cNORSE) to those with non-cryptogenic RSE, there were higher levels of serum cytokines in those patients with cNORSE. From these results, the group concluded that proinflammatory cytokines may be the reason why SE is difficult to manage in NORSE patients. The group also investigated if patients with higher levels of chemokines and cytokines had worse outcomes. Overall, patients with higher levels had worse outcomes at both discharge and several months after SE had ended. Dr Hanin comments on the implications of these data, which suggest the importance of specific anti-inflammatory therapies in NORSE. This interview took place at the International Epilepsy Congress 2023 in Dublin, Ireland.

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