Susceptibility of immature and adult brains to seizure effects

Haut, Sheryl R.; Velı́šková, Jana; Moshé, Solomon L.

doi:10.1016/s1474-4422(04)00881-6

Cited by 175 publications

(118 citation statements)

References 137 publications

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“…Interestingly, these epileptologic characteristics are similar to those of young brains (Haut et al, 2004), and FGF-2 expression during postnatal development is highest in the first weeks of life (Monfils et al, 2006).…”

Section: Hyperexcitability and Epileptic Phenotypementioning

confidence: 67%

FGF-2 Overexpression Increases Excitability and Seizure Susceptibility but Decreases Seizure-Induced Cell Loss

Zucchini¹,

Buzzi²,

Barbieri³

et al. 2008

J. Neurosci.

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Fibroblast growth factor 2 (FGF-2) has multiple, pleiotropic effects on the nervous system that include neurogenesis, neuroprotection and neuroplasticity. Thus, alteration in FGF-2 expression patterns may have a profound impact in brain function, both in normal physiology and in pathology. Here, we used FGF-2 transgenic mice (TgFGF2) to study the effects of endogenous FGF-2 overexpression on susceptibility to seizures and to the pathological consequences of seizures. TgFGF2 mice display increased FGF-2 expression in hippocampal pyramidal neurons and dentate granule cells. Increased density of glutamatergic synaptic vesicles was observed in the hippocampus of TgFGF2 mice, and electrophysiological data (input/output curves and patch-clamp recordings in CA1) confirmed an increase in excitatory inputs in CA1, suggesting the presence of a latent hyperexcitability. Indeed, TgFGF2 mice displayed increased susceptibility to kainate-induced seizures compared with wild-type (WT) littermates, in that latency to generalized seizure onset was reduced, whereas behavioral seizure scores and lethality were increased. Finally, WT and TgFGF2 mice with similar seizure scores were used for examining seizure-induced cellular consequences. Neurogenesis and mossy fiber sprouting were not significantly different between the two groups. In contrast, cell damage (assessed with Fluoro-Jade B, silver impregnation and anti-caspase 3 immunohistochemistry) was significantly lower in TgFGF2 mice, especially in the areas of overexpression (CA1 and CA3), indicating reduction of seizure-induced necrosis and apoptosis. These data suggest that FGF-2 may be implicated in seizure susceptibility and in seizure-induced plasticity, exerting different, and apparently contrasting effects: favoring ictogenesis but reducing seizure-induced cell death.

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Section: Hyperexcitability and Epileptic Phenotypementioning

confidence: 67%

FGF-2 Overexpression Increases Excitability and Seizure Susceptibility but Decreases Seizure-Induced Cell Loss

Zucchini¹,

Buzzi²,

Barbieri³

et al. 2008

J. Neurosci.

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“…When cognitive decline, recognised as particularly rare in childhood epilepsy, does occur, it is explained by pre-existing structural brain damage 22 , the adverse effect on an immature brain of early onset seizures, especially when frequent and resistant to treatment 22,23 or the side effects of antiepileptic drugs AED 24 . These children had received virtually no AED, apart from herbal remedies, and the possible adverse affects of traditional medicine or absolute lack of treatment cannot be discounted.…”

Section: Discussionmentioning

confidence: 99%

Epilepsy and its effects on children and families in rural Uganda

Mb¹

2013

Afr H. Sci.

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Background: This report aims to assess the impact of childhood epilepsy in an isolated rural area in Western Uganda, with little access to medical care, via its effect on children and families. Basic information on 440 affected children, clinically examined at 19 rural centres, was collated and data on seizure pattern and duration analysed, together with information on school attendance of older children. Objective: To publicise the consequences of undertreated illness, and to encourage improved management of this condition. Results: Distribution by seizure type was: generalised 61%, focal 33%, and miscellaneous 6%. When information on all seizure types was combined, a 'typical seizure' lasted < 1 hour, followed by coma. The typical age of onset and duration of illness approximated 2½ and 4 years respectively. Modal frequency and duration of seizures suggested that ~96 hours might be 'lost' to seizures over 4 years.Twenty four children had delayed global or motor development; a further 93 were reported to have 'poor understanding'. Information on school attendance available on 162 of 231 school aged children indicated that 92 were attending and 70 not attending school. Fifty eight percent of children >10 yrs old attending school and 68% of non-attendees, had never progressed beyond the entry class. Conclusion: The unexpected prevalence of apparent cognitive delay is discussed, together with strategies for prevention and management of epilepsy at community level.

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“…Tendensen til feberkramper synker kraftig med økende alder både hos mennesker og dyr (2). Det kan altså se ut til at den umodne hjernen gjør spedbarn og barn i førskole-alder mer sårbare for feberutløste kramper.…”

Section: Alderunclassified