Status epilepticus in adults: From etiology to treatment response.

Abstract

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.