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Abstract & Commentary
Source: Scott RC, et al. Magnetic resonance imaging findings within 5 days of status epilepticus in childhood. Brain. 2002;125:1951-1959.
Mesial temporal sclerosis (MTS) is the most common pathology found in surgical series of patients undergoing temporal lobectomy for pharmacologically intractable focal epilepsy. In fact, MTS with its classic MRI features (hippocampal volume loss, increased T2 signal, and loss of internal architecture) is the best predictor of a seizure-free surgical outcome, provided that MTS is concordant with the pre-operative electrographic ictal localization data. A better understanding of the mechanisms leading to this neuropathological substrate for temporal lobe epilepsy should provide fundamental insights into the pathophysiology of epileptogenesis.
Scott and colleagues describe the subacute effects of childhood status epilepticus (SE) on the hippocampus. They evaluated 35 children within 5 days of presentation with status epilepticus. They analyzed quantitative measures (T2 relaxometry and hippocampal volumetry) of MRI pathology. They also stratified the analysis according to whether the patients had prolonged febrile convulsions (PFC, 21 subjects) or afebrile status epilepticus (ASE). Nineteen PFC and all 14 ASE patients had never experienced SE previously.
This study found that hippocampal volumes were increased in all PFC patients vs controls (age-matched children undergoing cranial MRI to evaluate nonepileptic conditions, p = 0.004) but not in ASE patients (P = 1.0). T2 relaxation times were significantly increased for both PFC and ASE relative to controls if the scans were obtained within 2 days of SE. Scott et al concluded that PFC leads to hippocampal edema acutely and propose that this clinical presentation may eventually lead to MTS.
Gowers expressed the view that "seizures beget seizures." As demonstrated by Scott et al, a certain kind of seizure, ie, prolonged febrile convulsions, can beget acute edema in the hippocampus that may presage MTS and medical intractability.
Scott et al of course have not resolved the fundamental question of whether PFCs reflect an underlying predisposition to MTS and epilepsy or whether PFCs per se damage the hippocampus. They, in fact, acknowledge that there are genetic factors underlying complicated febrile seizures. Furthermore, hippocampal atrophy has been observed in 57% of patients with familial temporal lobe epilepsy (Neurology. 2001;56:166-172). Unfortunately, Scott et al did not repeat MRIs even less than a year later that might have revealed early signs of MTS exclusively in patients who had hippocampal edema. Such data would have extended the results of Van Landingham and colleagues (Ann Neurol. 1998;43:413-426). Those investigators demonstrated MTS in 4 of 15 children who had PFC with focal or lateralizing ictal findings. Of these, 2 of 4 patients showed MTS following acute edema caused by PFC. Moreover, PFCs are not the only answer, as suggested by the findings of Theodore and associates (Neurology. 1999;52:132-136) that hippocampal volume is inversely related to epilepsy duration, in support of Gowers’ dictum.
Other than the theoretical chicken-or-egg and nature-vs-nurture considerations, the implications of these data for the practicing pediatrician and pediatric neurologist are obvious: treat febrile convulsions aggressively and anticipate medical intractability and surgical referral early in children with a history of PFC. —Andy Dean
Dr. Dean is Assistant Professor of Neurology and Neuroscience, Director of the Epilepsy Monitoring Unit, Department of Neurology, New York Presbyterian Hospital—Cornell Campus.