目的:皮质发育异常(MCD)是耐药性癫痫的常见原因。相关的癫痫发生和癫痫发生的潜在机制仍未阐明。EEG可以帮助理解这些机制。我们系统地回顾了报告MCD的头皮或颅内EEG特征的研究,以表征不同MCD类型的发作间期和癫痫发作的EEG模式。
方法:我们根据PRISMA指南进行了系统评价。MEDLINE,PubMed,在Cochrane数据库中搜索了描述MCD患者发作间期和癫痫发作脑电图模式的研究。实现了一个分类框架,将脑电图特征分组为20个预定义的模式,包括九个间期(五个,头皮脑电图;四,颅内脑电图)和11次癫痫发作(5次,头皮脑电图;六,颅内脑电图)模式。使用Logistic回归估计每种癫痫发作模式与特定MCD类型相关的比值比(OR)。
结果:我们的搜索产生了1682项研究,其中27例包括936例MCD患者。在九种发作间脑电图模式中,五(三,头皮脑电图;二,颅内脑电图)在≥2种MCD类型中检测到,而仅在局灶性皮质发育不良(FCD)中发现了四种(头皮脑电图上的1型和2型节律性癫痫样放电;颅内脑电图上的重复爆裂尖峰和零星尖峰)。在11种癫痫发作模式中,八(三,头皮脑电图;五,颅内脑电图)在≥2种MCD类型中发现,而仅在FCD(头皮脑电图抑制;颅内脑电图上的δ刷)或结节性硬化症(TSC;头皮脑电图上的局灶性快波)中观察到三种。在头皮脑电图发作模式中,与FCD相比,TSC发生阵发性快速活动(OR=0.13;95%CI:0.03-0.53;p=0.024)和重复性癫痫样放电(OR=0.18;95%CI:0.05-0.61;p=0.036)的可能性较小.在颅内脑电图发作模式中,在异位症中更可能检测到低电压快速活动(OR=19.3;95%CI:6.22-60.1;p<0.001),Polymicrogyria(OR=6.70;95%CI:2.25-20.0;p=0.004)和TSC(OR=4.27;95%CI:1.88-9.70;p=0.005)比FCD。
结论:不同的MCD类型可以共享相似的发作间期或癫痫发作的脑电图模式,反映共同的潜在生物学机制。然而,选定的脑电图模式似乎指向不同的MCD类型,表明他们的神经元网络存在某些差异。
Malformations of cortical development (MCDs) are common causes of drug-resistant epilepsy. The mechanisms underlying the associated epileptogenesis and ictogenesis remain poorly elucidated. EEG can help in understanding these mechanisms. We systematically reviewed studies reporting scalp or intracranial EEG features of MCDs to characterise interictal and seizure-onset EEG patterns across different MCD types.
We conducted a systematic
review in accordance with PRISMA guidelines. MEDLINE, PubMed, and Cochrane databases were searched for studies describing interictal and seizure-onset EEG patterns in MCD patients. A classification framework was implemented to group EEG features into 20 predefined patterns, comprising nine interictal (five, scalp EEG; four, intracranial EEG) and 11 seizure-onset (five, scalp EEG; six, intracranial EEG) patterns. Logistic regression was used to estimate the odds ratios (OR) of each seizure-onset pattern being associated with specific MCD types.
Our search yielded 1682 studies, of which 27 comprising 936 MCD patients were included. Of the nine interictal EEG patterns, five (three, scalp EEG; two, intracranial EEG) were detected in ≥2 MCD types, while four (rhythmic epileptiform discharges type 1 and type 2 on scalp EEG; repetitive bursting spikes and sporadic spikes on intracranial EEG) were seen only in focal cortical dysplasia (FCD). Of the 11 seizure-onset patterns, eight (three, scalp EEG; five, intracranial EEG) were found in ≥2 MCD types, whereas three were observed only in FCD (suppression on scalp EEG; delta brush on intracranial EEG) or tuberous sclerosis complex (TSC; focal fast wave on scalp EEG). Among scalp EEG seizure-onset patterns, paroxysmal fast activity (OR = 0.13; 95% CI: 0.03-0.53; p = 0.024) and repetitive epileptiform discharges (OR = 0.18; 95% CI: 0.05-0.61; p = 0.036) were less likely to occur in TSC than FCD. Among intracranial EEG seizure-onset patterns, low-voltage fast activity was more likely to be detected in heterotopia (OR = 19.3; 95% CI: 6.22-60.1; p < 0.001), polymicrogyria (OR = 6.70; 95% CI: 2.25-20.0; p = 0.004) and TSC (OR = 4.27; 95% CI: 1.88-9.70; p = 0.005) than FCD.
Different MCD types can share similar interictal or seizure-onset EEG patterns, reflecting common underlying biological mechanisms. However, selected EEG patterns appear to point to distinct MCD types, suggesting certain differences in their neuronal networks.