To identify the timelines of magnetic resonance imaging (MRI) abnormalities and their relationships with the clinical outcomes of patients with new‐onset refractory status epilepticus (NORSE).
This retrospective observational study enrolled patients with NORSE who were admitted from March 2008 to July 2018. MRI abnormalities were analyzed visually with the readers blinded to the clinical characteristics of the patients. Poor functional outcome was defined as a Glasgow Outcome Scale score ≤ 3 at discharge. Subsequent pharmacoresistant epilepsy was defined as seizures not controlled by two or more anti‐seizure medications 6 months after discharge.
Among 39 patients with NORSE, 32 (82.1%) exhibited an MRI abnormality. The most common abnormalities were persisting mesial temporal lobe signal abnormality (51.3%); initial diffuse leptomeningeal enhancement within 16 days from seizure onset (15/35, 42.9%); and hippocampal atrophy, which started to appear 26 days after seizure onset (15/26, 57.7%). Only three patients had claustrum abnormalities. Patients with insular involvement had longer treatment delay than those without (24.0 vs 5.5 hours, respectively, P = .02). Duration of status epilepticus (SE) tended to have a linear association with hippocampal atrophy (P = .055). Patients with diffuse leptomeningeal enhancement were more likely to have a poor functional outcome and to develop subsequent pharmacoresistant epilepsy than those without this finding (93.3% vs 15.0%, P < .001; 75.0% vs 22.2%, P = .004, respectively); the results were significant even after adjusting for age, sex, and duration of SE. Hippocampal atrophy and diffuse cortical atrophy were also significantly associated with poor functional outcomes (P = .001 and P = .002, respectively), and patients with these conditions were more likely to develop subsequent pharmacoresistant epilepsy than those without these conditions, after adjusting for age and sex (P = .035 and P = .048, respectively), but not after adjusting for duration of SE.
Initial diffuse leptomeningeal enhancement and later hippocampal atrophy were associated with a poor functional outcome and subsequent pharmacoresistant epilepsy.