Abstracts

Rationale: The hippocampus has been the primary focus of most studies investigating the sequelae of febrile status epilepticus (FSE). However, little is known about acute FSE-induced injury to extra-hippocampal structures. Previously, we encountered a boy in whom transient cortical hyperintensity was apparent in diffusion weighted magnetic resonance imaging (DWI) performed immediately after FSE offset, followed by hippocampal hyperintensity two days later. He was discharged with no neurological symptoms. In the present study, we investigated DWI data collected immediately after prolonged febrile seizure (PFS) offset to clarify the presence of acute extra-hippocampal injuries, and their neurological outcomes. Methods:  Between January 2013 and October 2018, PFS children who visited the emergency rooms of two hospitals were included. We excluded children who had neurological complications prior to PFS. PFS was defined as a febrile (>38.0°C) seizure persisting for 15 minutes or longer. Brain DWI was performed within six hours after PFS offset. When initial DWI detected any abnormality, follow-up DWI was performed a few days later. We also assessed demographic and clinical data including outcome, and compared these clinical features between with and without signal abnormalities on initial DWIs. Results: We included 55 PFS patients. On initial DWI, reduced cortical diffusion was evident in nine (16%) patients, of whom six also exhibited ipsilateral reduced diffusion of the connected thalamic nucleus. Reduced cortical diffusion was associated with the male sex (8/9 cases, 89%), asymmetrical PFS symptoms (6/9 cases, 67%), and shorter duration between seizure offset and MRI (median duration: 40minutes) but not with seizure duration. Such cortical lesions were observed in only the right hemisphere in seven patients and bilaterally in two. In the seven patients with right-sided cortical signal changes, six exhibited asymmetrical seizure manifestation, while both patients with bilateral signal changes exhibited symmetrical seizure manifestation. On follow-up DWI (13 to 72 hours after PFS) of these patients, all cortical abnormalities disappeared, but ipsilateral hippocampal hyperintensity appeared in one patient. The median (range) follow-up period was 36 (3 to 41) months. At the last follow-up, no patients exhibited epilepsy, but one patient was diagnosed as autism spectrum disorder with attention-deficit/hyperactivity disorder. Conclusions: Some of children with PFS exhibited reduced, regional cortical diffusion on DWI performed within six hours after PFS offset. The transient cortical hyperintensity seems not to be associated with an unfavorable clinical course, at least in the short term. Funding: No funding