Comparative analysis of patients with new onset refractory status epilepticus preceded by fever (febrile infection-related epilepsy syndrome) versus without prior fever: An interim analysis. | Semantic Scholar (2024)

Investigation of inflammation using cerebrospinal fluid and serum cytokines/chemokines in patients with new‐onset refractory status epilepticus (NORSE) to better understand the pathophysiology of NORSE and its consequences.

It is found that the majority of adult and pediatric patients continue to experience recurrent seizures and suffer from refractory epilepsy, a hallmark of chronic NORSE signifying the major public health importance of this disorder.

A systematic review of animal and human research findings since 2000 found altered innate immunity in sepsis shows early hyper-reactive response, prolonged inflammatory activity, and fever response contributing to cardiovascular and neurological morbidity, not temperature elevation.

The pathophysiology and unique cytokine profiles seen in these disorders and their links with diagnosis, prognosis, and treatment decision‐making are discussed.

No specific therapy for FIRES and NORSE currently exists; high doses of barbiturates and ketogenic diet can be used with some effectiveness, and anakinra and tocilizumab, targeting interleukin pathways, have emerged as potential specific therapies.

It is shown that treatment with the recombinant interleukin‐1 (IL1) receptor antagonist anakinra results in down-regulation in the production and function of endogenous IL1RA in patients with FIRES.

The strategy to unravel the cause of these disorders and to improve patient care is presented and standardized consensus definitions and a multidisciplinary multicenter strategy are presented to improve clinical care for patients with NORSE and FIRES.

There is a higher incidence of status epilepticus in the older adult population, and it commonly has a nonconvulsive presentation, so it is important to take into account the specific aspects related to the pharmaco*kinetic and pharmacodynamic changes in older critically-ill adults.

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