Background: The association between prenatal exposure to antiseizure medications (ASM) and autism spectrum disorder has been documented. This study sought to examine and synthesize evidence from studies that have eval...Background: The association between prenatal exposure to antiseizure medications (ASM) and autism spectrum disorder has been documented. This study sought to examine and synthesize evidence from studies that have evaluated these associations, with particular focus on the trimester of pregnancy and dosage of exposure. Methodology: PubMed, Embase, and PsycINFO databases were searched following strict inclusion/exclusion criteria. 10 studies were recruited involving children born to mothers with epilepsy who took ASM during pregnancy as cases, and those with epilepsy who did not take any ASM in pregnancy. Results: The relative risk of developing ASD among children exposed to valproic acid (RR, 3.90 [95% CI: 2.36 - 6.44], p < 0.006), was twice higher than that of carbamazepine (RR, 1.65 [95% CI: 0.62 - 4.37], p < 0.0001), or lamotrigine (RR, 1.60 [95% CI: 0.77 - 3.32], p = 0.006). The trimester of exposure and dosage of ASM administered were not significant. Conclusion: In summary, prenatal exposure to ASM increased the risk of developing ASD in children. The relative risk was twice as high in those exposed to valproic acid compared to those exposed to carbamazepine or lamotrigine. Trimester of pregnancy and dosage of ASM used by the mothers were not significant.展开更多
Epilepsy is a neurological disease characterized by excessive and abnormal hyper-synchrony of electrical discharges of the brain and a predisposition to generate epileptic seizures resulting in a broad spectrum of neu...Epilepsy is a neurological disease characterized by excessive and abnormal hyper-synchrony of electrical discharges of the brain and a predisposition to generate epileptic seizures resulting in a broad spectrum of neurobiological insults,imposing psychological,cognitive,social and also economic burdens to the sufferer.Voltage-gated sodium channels(VGSCs)are essential for the generation and propagation of action potentials throughout the central nervous system.Dysfunction of these channels has been implicated in the pathogenesis of epilepsy.VGSC inhibitors have been demonstrated to act as anticonvulsants to suppress the abnormal neuronal firing underlying epileptic seizures,and are used for the management and treatment of both genetic-idiopathic and acquired epilepsies.We discuss the forms of idiopathic and acquired epilepsies caused by VGSC mutations and the therapeutic efficacy of VGSC blockers in idiopathic,acquired and pharmacoresistant forms of epilepsy in this review.We conclude that there is a need for better alternative therapies that can be used alone or in combination with VGSC inhibitors in the management of epilepsies.The current anti-seizure medications(ASMs)especially for pharmacoresistant epilepsies and some other types of epilepsy have not yielded expected therapeutic efficacy partly because they do not show subtype-selectivity in blocking sodium channels while also bringing side effects.Therefore,there is a need to develop novel drug cocktails with enhanced selectivity for specific VGSC isoforms,to achieve better treatment of pharmacoresistant epilepsies and other types of epileptic seizures.展开更多
Background It has long been an interesting question of whether withdrawal seizures in epileptic patients differ from habitual seizures in terms of semiology and electrophysiology.Case presentation Here,we addressed th...Background It has long been an interesting question of whether withdrawal seizures in epileptic patients differ from habitual seizures in terms of semiology and electrophysiology.Case presentation Here,we addressed this issue in a 40 year-old woman with drug-resistant focal epilepsy monitored by presurgical intracranial EEG.As a part of this routine pre-operative investigation,anti-seizure medications(ASMs)were halted;as a result,multiple withdrawal seizures were recorded before ASM readministration.During 4 days of invasive monitoring,we noticed three different phases in seizure organization:Acute withdrawal seizure(AWS):The first recorded seizure 10h after the implantation;the stabilized withdrawal seizures(SWS):seven habitual seizures recorded from 24h post implantation to readministration of ASMs;and the Non-withdrawal seizures(NWS):ten seizures recorded 24h after readministration of ASMs.AWS and SWS had the same semiology and same epileptic network,but the propagation time from the temporal pole to the para-hippocampal gyrus(PHG)and hippocampus ranged from no latency in AWS to up to 50 s in SWS.NWS were electrographic seizures,without any apparent clinical manifestation.Seizure onset in this type of seizure,as in the first two types,was in the temporal pole.However,NWS could last up to 3 min without involving the PHG or hippocampus.Conclusions We concluded that in acute withdrawal seizures the propagation time of epileptic activity is significantly reduced without affecting ictal organization network or semiology.Furthermore,ASM in this case had a remarkable influence on propagation rather than initiation of epileptic activity.展开更多
文摘Background: The association between prenatal exposure to antiseizure medications (ASM) and autism spectrum disorder has been documented. This study sought to examine and synthesize evidence from studies that have evaluated these associations, with particular focus on the trimester of pregnancy and dosage of exposure. Methodology: PubMed, Embase, and PsycINFO databases were searched following strict inclusion/exclusion criteria. 10 studies were recruited involving children born to mothers with epilepsy who took ASM during pregnancy as cases, and those with epilepsy who did not take any ASM in pregnancy. Results: The relative risk of developing ASD among children exposed to valproic acid (RR, 3.90 [95% CI: 2.36 - 6.44], p < 0.006), was twice higher than that of carbamazepine (RR, 1.65 [95% CI: 0.62 - 4.37], p < 0.0001), or lamotrigine (RR, 1.60 [95% CI: 0.77 - 3.32], p = 0.006). The trimester of exposure and dosage of ASM administered were not significant. Conclusion: In summary, prenatal exposure to ASM increased the risk of developing ASD in children. The relative risk was twice as high in those exposed to valproic acid compared to those exposed to carbamazepine or lamotrigine. Trimester of pregnancy and dosage of ASM used by the mothers were not significant.
文摘Epilepsy is a neurological disease characterized by excessive and abnormal hyper-synchrony of electrical discharges of the brain and a predisposition to generate epileptic seizures resulting in a broad spectrum of neurobiological insults,imposing psychological,cognitive,social and also economic burdens to the sufferer.Voltage-gated sodium channels(VGSCs)are essential for the generation and propagation of action potentials throughout the central nervous system.Dysfunction of these channels has been implicated in the pathogenesis of epilepsy.VGSC inhibitors have been demonstrated to act as anticonvulsants to suppress the abnormal neuronal firing underlying epileptic seizures,and are used for the management and treatment of both genetic-idiopathic and acquired epilepsies.We discuss the forms of idiopathic and acquired epilepsies caused by VGSC mutations and the therapeutic efficacy of VGSC blockers in idiopathic,acquired and pharmacoresistant forms of epilepsy in this review.We conclude that there is a need for better alternative therapies that can be used alone or in combination with VGSC inhibitors in the management of epilepsies.The current anti-seizure medications(ASMs)especially for pharmacoresistant epilepsies and some other types of epilepsy have not yielded expected therapeutic efficacy partly because they do not show subtype-selectivity in blocking sodium channels while also bringing side effects.Therefore,there is a need to develop novel drug cocktails with enhanced selectivity for specific VGSC isoforms,to achieve better treatment of pharmacoresistant epilepsies and other types of epileptic seizures.
文摘Background It has long been an interesting question of whether withdrawal seizures in epileptic patients differ from habitual seizures in terms of semiology and electrophysiology.Case presentation Here,we addressed this issue in a 40 year-old woman with drug-resistant focal epilepsy monitored by presurgical intracranial EEG.As a part of this routine pre-operative investigation,anti-seizure medications(ASMs)were halted;as a result,multiple withdrawal seizures were recorded before ASM readministration.During 4 days of invasive monitoring,we noticed three different phases in seizure organization:Acute withdrawal seizure(AWS):The first recorded seizure 10h after the implantation;the stabilized withdrawal seizures(SWS):seven habitual seizures recorded from 24h post implantation to readministration of ASMs;and the Non-withdrawal seizures(NWS):ten seizures recorded 24h after readministration of ASMs.AWS and SWS had the same semiology and same epileptic network,but the propagation time from the temporal pole to the para-hippocampal gyrus(PHG)and hippocampus ranged from no latency in AWS to up to 50 s in SWS.NWS were electrographic seizures,without any apparent clinical manifestation.Seizure onset in this type of seizure,as in the first two types,was in the temporal pole.However,NWS could last up to 3 min without involving the PHG or hippocampus.Conclusions We concluded that in acute withdrawal seizures the propagation time of epileptic activity is significantly reduced without affecting ictal organization network or semiology.Furthermore,ASM in this case had a remarkable influence on propagation rather than initiation of epileptic activity.
