1991
DOI: 10.1136/adc.66.10.1173
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Use of antiepileptic drugs in childhood epilepsy.

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Cited by 6 publications
(2 citation statements)
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“…It is thought to act by reducing the excitability of individual neurons and inhibiting the release of glutamate, an excitatory neurotransmitter, via inhibition of voltage-sensitive sodium channels. [10][11][12][13][14][15] While it does not block or reduce the rate of development of kindling, it does decrease the number of kindled responses and the duration of kindled seizures. 16 Further evidence that lamotrigine inhibits glutamate release is exhibited in the rat model, in which kainic acid neurotoxicity, mediated by glutamate release, is inhibited, while quinolinic acid and ibotenic acid neurotoxicity, mediated by N-methyl-D-aspartate (NMDA) receptor excitation, is not.…”
Section: Mechanism Of Actionmentioning
confidence: 99%
“…It is thought to act by reducing the excitability of individual neurons and inhibiting the release of glutamate, an excitatory neurotransmitter, via inhibition of voltage-sensitive sodium channels. [10][11][12][13][14][15] While it does not block or reduce the rate of development of kindling, it does decrease the number of kindled responses and the duration of kindled seizures. 16 Further evidence that lamotrigine inhibits glutamate release is exhibited in the rat model, in which kainic acid neurotoxicity, mediated by glutamate release, is inhibited, while quinolinic acid and ibotenic acid neurotoxicity, mediated by N-methyl-D-aspartate (NMDA) receptor excitation, is not.…”
Section: Mechanism Of Actionmentioning
confidence: 99%
“…It has been reported to be more effective in cryptogenic LGS than in symptomatic LGS. [47] Myoclonic, atypical absence and atonic seizures are the seizure types most effectively controlled by valproate in LGS. [48] Gastrointestinal upset and weight gain are common adverse effects but sedation is not a common problem.…”
Section: Valproatementioning
confidence: 99%