Researchers in the FEBSTAT Study Team at centers in New York, Durham, Virginia, and Chicago, IL report MRI findings in their prospective study of the acute effects of febrile status epilepticus (FSE) in 199 children age 1 month to 5 years. Patients presenting with FSE (>30 minutes) were enrolled in FEBSTAT within 72 hours of the FSE episode. Mean duration of FSE was 71.7 minutes; 129 (68%) were focal, and 37 (19%) had prior FS. A group of 96 children with first simple FS were imaged as controls, using a similar protocol. MRI was performed within 3 days of FSE in 129 (67.5%) cases, and within 1 week in 165 (86%) cases.

Twenty-two (11.5%) children had definitely abnormal (n=17) or equivocal (n=5) T2 signal increase in the hippocampus following FSE compared to none in the control group. (p<0.0001). Developmental abnormalities in the hippocampus were revealed in 20 (10.5%) of FSE patients compared to 2 (2.1%) of the controls (p=0.0097); hippocampal malrotation was the most common abnormality (15 FSE cases and 2 controls). Extrahippocampal imaging abnormalities occurred with equal frequency in the FSE group and controls (15.7% and 15.6%, respectively); temporal lobe abnormalities, including amygdala and insula, were more common in the FSE group (7.9%) than in controls (1.0%)(p=0.015). Ongoing follow-up of cases should determine whether the presence of a concurrent developmental anomaly might increase risk of hippocampal sclerosis following FSE. [1]

COMMENT. The FEBSTAT study shows that FSE in young children is associated with a risk of acute hippocampal injury, and 10% of cases also have a developmental anomaly of the hippocampus that may increase susceptibility to complex seizures. Earlier reports of an association between prolonged febrile convulsions and mesial temporal sclerosis were confirmed at surgical excision in adults with refractory temporal lobe epilepsy [2]. However, Falconer may have used a liberal definition of a febrile convulsion that included patients with acute encephalopathy [3]. A provocative editorial comment [4] draws attention to results of viral studies reported by FEBSTAT [5]. Viremia with HHV-6 was identified in 32% cases of FSE and with HHV-7 in 7%. The findings support the role of viruses in the etiology of FSE and mesial temporal lobe epilepsy and the use of antiviral agents and vaccines in prevention. The FEBSTAT study findings rekindle the debate on the mechanism and definition of the febrile seizure. Is the febrile seizure triggered solely by fever and a threshold convulsive temperature or by a viremia and a transitory encephalitis or encephalopathy?

A case report of a 21-month-old boy who presented with fever and right-sided focal seizure lasting 10 hours and followed by persistent hemiparesis illustrates a possible outcome of a complex febrile seizure and febrile status epilepticus [6]. A pre-existing structural lesion is not ruled out in this case, but more effective therapies for febrile status epilepticus might prevent the development of cerebral edema, brain atrophy, and persistent hemiplegia.