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• W2141444240 abstract "The immature brain is more prone to seizures than is the mature brain because of an imbalance between the development of excitation and inhibition and a variety of other physiologic and structural features 1, 2. Unfortunately, in addition to being common, seizures in young children often portend a poor prognosis for mental and motor development 3, 4. There are some suggestions that seizures during early development are worse in regard to cognitive impairment than are those occurring in the mature brain 5. Although the poor prognosis after seizures during early life is often related to the underlying cause of the seizures, there is concern that the seizures themselves may be detrimental. Results from animal studies parallel clinical studies, demonstrating that the immature brain is more susceptible to seizures than is the adult brain. Kindling, a process in which repeated electrical stimulations that initially result only in brief electrical discharges and mild behavioral changes but result progressively in more prolonged and intense electrical and behavioral seizures, occurs at all ages. Young animals kindle more rapidly than do mature animals 6. In addition, a shorter period of postictal refractoriness in young animals leads to a quicker progression through early stages of kindling and results in rapid generalization of seizures 7. Immature rats are more likely to develop seizures with hypoxia than are mature rats 8. Although the threshold for seizure generation is lower in immature than in adult brains, developing neurons are less vulnerable, in terms of cell loss, than are adult neurons to a wide variety of pathologic insults. For example, immature hippocampal neurons will continue responding to synaptic stimuli in a fully anoxic environment for longer durations than will adult ones; likewise, longer anoxic episodes are required to destroy the circuit irreversibly in young animals 9. Young animals are less vulnerable to cell loss after a prolonged seizure than are mature animals 10-16. Likewise, sprouting of mossy fibers is less prominent after prolonged seizures in young animals than after seizures of similar duration in older animals 17, 18. There is increasing evidence that the immature brain is more resistant to glutamate toxicity than is the mature brain 19-21. Marks et al. 21 found that the degree of Ca2+ entry into the hippocampal subfield CA1 and subsequent damage was directly related to age. In P1–3 neurons, glutamate increased [Ca2+]i minimally, whereas in P21–25 neurons, glutamate resulted in marked increases in [Ca2+]i and caused severe swelling of the cell and retraction of dendrites into the soma of the neuron. This relative resistance is thought to be due to the smaller density of active synapses, lower energy consumption, and in general, the immaturity of biochemical cascades that lead to cell death after insults. Despite this relative resistance of immature neurons to epilepsy-induced brain damage, seizures in the developing brain do produce a marked, and often, irreversible alteration of the developing brain. Kindling during the first weeks of life results in a life-long increase in seizure susceptibility 22. With two models of neonatal seizures, pentylenetetrazol and flurothyl, we recently demonstrated that recurrent seizures during the neonatal period result in subsequent increases in mossy fiber growth in both the supragranular region and CA3 hippocampal subfield (Fig. 1)23-25. Recurrent seizures also result in alterations of neuronal pathways activated during seizures 25; animals undergoing a series of seizures have a progressive increase in the extent of neuronal activation, as evidenced by early gene activation of c-fos. In addition to the anatomic changes, neonatal seizures also have been shown to result in impairment of visuospatial memory when the animals are tested as adults 23. Timm staining in a control rat (A) and in a rat with recurrent seizures (B). Note the differences in Timm staining in the stratum pyramidale staining (arrows) in controls and rats subjected to flurothyl-induced neonatal seizures. Bar = 100 μm. From reference 23, with permission. The aberrant networks set up by recurrent seizures also increase brain vulnerability to future injury. Schmid et al. 26 produced status epilepticus by using either kainic acid or perforant pathway stimulation in adolescent rats who had a history of flurothyl seizures during the neonatal period. However, animals that had neonatal seizures but had not been exposed to status epilepticus had no cell loss. Animals that had neonatal seizures had significantly more severe brain injury after both kainic acid and perforant pathway stimulation than did animals without a history of neonatal seizures. Although the mechanism by which this enhanced susceptibility to injury is not yet known, the study provides further evidence that neonatal seizures alter the brain in a maladaptive manner. Seizures may perturb a wide range of developmental phenomena that are activity dependent, including cell division, migration, sequential expression of receptors, formation, and probably stabilization of synapses 1. Indeed seizures can modify—slow down or accelerate—a wide range of unique processes that take place during development and are essential for the correct formation and wiring of the brain circuitry. The migration of neurons, the arborization of the neurites, the formation of synapses, or the removal of redundant processes are all essential processes that are activity dependent and may be disturbed by seizures. Thus, recurrent activation of N-methyl-D-aspartate (NMDA) receptors accelerates neuronal migration 27 and may lead to the formation of aberrant connections. In addition, as noted earlier, most of the receptor proteins or second-messenger cascades that have been studied are modified during development, and there are good reasons to believe that aberrant hyperactivity may alter the pattern and sequence of expression. Thus, the expression of AMPA receptors appears to be activity dependent, with synchronized activity being required to facilitate its expression, much as in the plasticity of adult synapses 28. Aberrant episodes of hyperactivity will modify this sequence. There is sufficient evidence from animal studies to conclude that early seizures may profoundly influence the development of the maturing brain, but also may increase the later vulnerability of the matured brain to the deleterious effects of seizures. These studies have relevance for understanding the associations between epilepsy, seizures, and learning disorders. Acknowledgment: This research was supported by the Emily P. Rogers Research Fund and a grant from the National Institutes of Health (NS27984) to G.L.H." @default.
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• W2141444240 date "2001-03-01" @default.
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• W2141444240 title "Pathogenesis of Learning Disabilities in Epilepsy" @default.
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• W2141444240 doi "https://doi.org/10.1046/j.1528-1157.2001.00504.x" @default.
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