Status epilepticus in adults: From etiology to treatment response

This study explored the association between etiology of status epilepticus (SE) and treatment responsiveness. Consecutive episodes of nonhypoxic SE in patients ≥14 years old were included. Etiology was classified into acute, remote, progressive, defined electroclinical syndromes, and unknown. Four subcategories of acute etiologies were then considered based on the recent proposal: (1) triggering factors in patients with pre‐existing epilepsy; (2) acute insults to central nervous system (CNS; “acute‐primary CNS”); (3) CNS pathology secondary to metabolic disturbances, systemic infection, or fever (“acute‐secondary CNS”); and (4) drug/alcohol intoxication or withdrawal (“acute‐toxic”). Multinomial logistic regression models were fitted using a backward stepwise selection. Age, sex, consciousness before treatment, SE semiology, SE etiology, SE recurrence, level of disability, and year of presentation were independent variables. The etiological categories of acute‐primary CNS ( p < .001), acute‐secondary CNS ( p = .002), progressive ( p = .010), and unknown ( p = .018) SE were associated with increased odds of refractory SE. Acute‐primary CNS ( p < .001), progressive ( p = .009), and unknown ( p = .048) SE etiologies were associated with increased odds of superrefractory SE, whereas no association was found with acute‐secondary CNS etiology ( p = .948). Patients with SE showed different responsiveness to medications according to the underlying cause. Heterogeneity exists within the spectrum of acute symptomatic causes; distinct etiological subcategories may carry different risks of refractoriness and superrefractoriness.