Hippocampal volumes and diffusion-weighted image findings in children with prolonged febrile seizures

Natsume, Jun; Bernasconi, Neda; Miyauchi, Masaharu; Naiki, Misako; Yokotsuka, Taro; Sofue, Ayako; Bernasconi, Andrea

doi:10.1111/j.1600-0404.2007.00806.x

Cited by 32 publications

(28 citation statements)

References 19 publications

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“…Of importance, while the epileptic seizures resulting from the 20-minute FS were mild (stage 1, Racine 1972; average duration approximately 8 seconds), the spontaneous seizures in rats that experienced "febrile SE" (60-minute FS) lasted more than 2 minutes on average and were more severe (stages 2-5 with head bobbing, alternating or bilateral clonus, rearing, and falling; 13). These experimental data support the hypothesis that the duration of FS is an important predictor of the severity of the TLE that develops after FS (59)(60)(61)(62).…”

Section: Do Prolonged Fs or Febrile Se Cause Temporal Lobe Epilepsy Isupporting

confidence: 82%

Inflammatory Processes, Febrile Seizures, and Subsequent Epileptogenesis

et al. 2014

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Febrile seizures (FS) are the most common type of seizures in infants and preschool children. Inflammatory mediators, which are known triggers of fever, have also been implicated as contributors to the onset of these seizures. Evidence that inflammation is present following FS and during established epilepsy suggests that it could also influence epileptogenesis. However, the potential involvement of inflammatory mediators to the epileptogenic process that may follow prolonged FS has yet to be fully determined. This article reviews the current state of our knowledge and major gaps that remain by focusing on four questions: Does inflammation contribute to the generation of FS? Does prolonged FS or febrile status epilepticus (SE) cause temporal lobe epilepsy in the absence of predisposing factors? Does inflammation contribute to the process by which febrile SE causes limbic epilepsy? And finally, can inflammation be a foundation for biomarkers and therapy for FS-induced epileptogenesis?

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Section: Do Prolonged Fs or Febrile Se Cause Temporal Lobe Epilepsy Isupporting

confidence: 82%

Inflammatory Processes, Febrile Seizures, and Subsequent Epileptogenesis

et al. 2014

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“…These acute changes are reversible [83] and thought to be secondary to cytotoxic or vasogenic edema. Concurrent EEG background abnormalities and focal spikes have also been reported [82]. Increased T 2 signal and hippocampal volume changes, in this setting, are the most predictive indicators of subsequent development of mesial temporal sclerosis (MTS) [7,81,84].…”

Section: Signal Changesmentioning

confidence: 95%

“…In children, immediately after complex FS or prolonged status, increased T 2 /DWI signal has been reported in the hippocampus [80,81], ipsilateral thalamus, and anterior cingulate gyrus [82]. These acute changes are reversible [83] and thought to be secondary to cytotoxic or vasogenic edema.…”

Section: Signal Changesmentioning

confidence: 99%

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Neuroimaging the Epileptogenic Process

et al. 2014

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Epilepsy is one of the most common chronic neurological conditions worldwide. Anti-epileptic drugs (AEDs) can suppress seizures, but do not affect the underlying epileptic state, and many epilepsy patients are unable to attain seizure control with AEDs. To cure or prevent epilepsy, disease-modifying interventions that inhibit or reverse the disease process of epileptogenesis must be developed. A major limitation in the development and implementation of such an intervention is the current poor understanding, and the lack of reliable biomarkers, of the epileptogenic process. Neuroimaging represents a non-invasive medical and research tool with the ability to identify early pathophysiological changes involved in epileptogenesis, monitor disease progression, and assess the effectiveness of possible therapies. Here we will provide an overview of studies conducted in animal models and in patients with epilepsy that have utilized various neuroimaging modalities to investigate epileptogenesis.

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“…Prolonged febrile convulsion in childhood is associated with unilateral diffusion restriction in the hippocampus contralateral to the focal seizure and increase in T2 relaxation time on MR imaging performed early after the convulsion, with resolution on follow-up imaging, indicating that these changes probably are caused by transient hippocampal edema. 4,5 Prolonged ictal activity causes increased glucose requirements in the neuronal and glial cells, which, in combination with the glucose deprivation, causes severe energy failure, resulting in cytotoxic edema and restricted diffusion on DWI imaging. It is likely that the combination of hypoglycemia and prolonged seizure in our patient caused severe cytotoxic edema and neuronal injury in the hemispheric neuronal cells and was responsible for severe injury and poor outcome in this case.…”

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confidence: 99%