Abstract

Cortical dysplasia (CD) is a cerebral disorder caused by disruption of neuronal migration and disorganization of cortex development. The mechanisms of epileptogenicity in CD have been investigated yet still remain unknown. One of the possible reasons is the changes of expression of Nmethyl-D-aspartate (NMDA) receptors. Emerging evidences have shown that NR2A/B in the region of focal cortical dysplasia (FCD) cortex may play an important role in the risk of epilepsy and NR1 remains unchanged during epilepsy pathogenesis but recent published studies showed inconclusive results. This meta-analysis aimed to derive a more precise estimation of the associations between NMDA receptors and CD related epilepsy risk. A literature search of PubMed, Embase, Web of Science and China BioMedicine (CBM) databases was conducted on articles published before July 1st, 2013. Crude odds ratio (OR) with 95% confidence intervals (CI) were calculated. Ten studies were included with a total of 170 subjects. 104 of them were diagnosed with FCD and epilepsy while 66 resected specimen were non-CD cerebral tissue. The meta-analysis results showed that the expression of NR2B is increased in FCD cortex, which is indicated might be an important role in FCD related epilepsy pathogenesis. On the other hand, the expression of NR1 showed no significant difference between FCD group and controls, therefore the NR1 might not be a relevant factor. The function of NMDA receptors in development of FCD is not clear yet, a further explanation is still needed. We assume that NMDA receptors might interact with other substances in different signaling pathways to initiate and promote the epileptogenic process. Meanwhile we suggest more research to focus on the causal relationship between NMDA receptors and epileptogenisis.

Highlights

  • Cortical dysplasia is a cerebral disorder caused by disruption of neuronal migration and disorganization of cortex development

  • In accordance with the inclusion criteria, 10 randomized studies of patients with focal cortical dysplasia and epilepsy treated with surgical resection and post-operational pathological evidence versus other cerebral specimens without epileptiform discharges were selected for this meta-analysis

  • A total of 170 subjects were included in these studies, 104 of them were diagnosed with focal cortical dysplasia (FCD) and epilepsy while 66 resected specimen were non-Cortical dysplasia (CD) cerebral tissue nor with epilepsy

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Summary

Introduction

Cortical dysplasia is a cerebral disorder caused by disruption of neuronal migration and disorganization of cortex development. They are histologically characterized by changes in neocortical microarchitecture: disturbance of laminar organization, ectopic neurons, and cellular abnormalities such as cytomegalic or dysmorphic neurons [1]. One of the possible causes that may lead to abnormal neuronal discharges is an imbalance between the amount of excitatory and inhibitory neurotransmitter receptor such as glutamate Nmethyl-Daspartate (NMDA) receptor [9,10]. Several studies have reported differential changes in NMDA-receptor density and subunit composition in human epilepsy specimens [10,15,16,17]. The majority support the theory that the expression of NMDA receptors especially the subunit NR2A/B in epileptogenesis cortex is increased [10,15,17,18,19]

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