Intracranial electroencephalographic seizure-onset patterns: effect of underlying pathology
Intracranial electroencephalographic seizure-onset patterns: effect of underlying pathology
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DOI：
10.1093/brain/awt299
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发表时间：
2014-01-01
期刊：
影响因子：
14.5
通讯作者：
Gotman, Jean
中科院分区：
文献类型：
--
作者：
Perucca, Piero;Dubeau, Francois;Gotman, Jean
由于癫痫发作起源于不同的病理基质，因此出现了不同病理状态下癫痫发作产生的机制是否不同或相似的问题。更好地定义颅内脑电图的形态学模式在癫痫发作可以提高对这些机制的理解。为此，我们研究了与不同致痫性病变相关的颅内脑电图癫痫发作模式，并定义了每种模式的高频振荡相关性。我们分析了连续33例耐药局灶性癫痫和结构性磁共振成像病变（11例内侧颞叶硬化，9例局灶性皮质发育不良，6例皮质萎缩，3例室周结节性异位，3例多微脑回，1例结节性硬化症）患者的代表性癫痫发作类型，这些患者接受了深度电极脑电图记录（500 Hz滤波器，2000 Hz采样率）。仅当癫痫发作由位于病灶/病灶周围组织的接触引起，并且临床表现在电描记发作之后时，才纳入患者。癫痫发作模式由两名对临床信息不知情的审查者独立定义，并在讨论后达成共识。对于每次发作，选择发作前和发作切片进行高频振荡分析。在53次癫痫发作中确定了7种癫痫发作模式：低电压快速活动（43%）;低频高振幅周期性尖峰（21%）; 13 Hz的尖锐活动（15%）;尖峰和波活动（9%）;高振幅多尖峰的爆发（6%）;爆发抑制（4%）;和δ刷（4%）。每种模式都发生在几种病理中，除了周期性尖峰，仅观察到内侧颞叶硬化症和三角刷，仅限于局灶性皮质发育不良。然而，内侧颞叶硬化症并不总是与周期性尖峰或局灶性皮质发育不良与三角刷。与其他模式相比，低电压快速活动与更大的癫痫发作区相关（P = 0.04）。四种模式，在13 Hz，低电压快速活动，尖峰和波活动和周期性尖峰，也被发现在癫痫发作蔓延的地区，与周期性尖峰只出现从内侧颞叶硬化。七种模式中的每一种都伴随着癫痫发作时高频振荡的显著增加。总体而言，我们的数据表明：（i）生物学上不同的致痫性病变具有共同的颅内脑电图发作模式，表明不同的病理基质可以影响类似的网络或癫痫发作的机制;（ii）某些病理与癫痫发作时的颅内脑电图特征相关，例如周期性尖峰，可能反映了内侧颞叶硬化症特有的机制;（iii）在扩散区域中也可以发现一些癫痫发作模式，包括周期性尖峰，这提醒人们不要依赖于初始放电的形态来定义癫痫区;以及（iv）高频振荡在癫痫发作时增加，与模式无关。
Because seizures originate from different pathological substrates, the question arises of whether distinct or similar mechanisms underlie seizure generation across different pathologies. Better defining intracranial electroencephalographic morphological patterns at seizure-onset could improve the understanding of such mechanisms. To this end, we investigated intracranial electroencephalographic seizure-onset patterns associated with different epileptogenic lesions, and defined high-frequency oscillation correlates of each pattern. We analysed representative seizure types from 33 consecutive patients with drug-resistant focal epilepsy and a structural magnetic resonance imaging lesion (11 mesial temporal sclerosis, nine focal cortical dysplasia, six cortical atrophy, three periventricular nodular heterotopia, three polymicrogyria, and one tuberous sclerosis complex) who underwent depth-electrode electroencephalographic recordings (500 Hz filter, 2000 Hz sampling rate). Patients were included only if seizures arose from contacts located in lesional/peri-lesional tissue, and if clinical manifestations followed the electrographic onset. Seizure-onset patterns were defined independently by two reviewers blinded to clinical information, and consensus was reached after discussion. For each seizure, pre-ictal and ictal sections were selected for high-frequency oscillation analysis. Seven seizure-onset patterns were identified across the 53 seizures sampled: low-voltage fast activity (43%); low-frequency high-amplitude periodic spikes (21%); sharp activity at 13 Hz (15%); spike-and-wave activity (9%); burst of high-amplitude polyspikes (6%); burst suppression (4%); and delta brush (4%). Each pattern occurred across several pathologies, except for periodic spikes, only observed with mesial temporal sclerosis, and delta brush, exclusive to focal cortical dysplasia. However, mesial temporal sclerosis was not always associated with periodic spikes nor focal cortical dysplasia with delta brush. Compared to other patterns, low-voltage fast activity was associated with a larger seizure-onset zone (P = 0.04). Four patterns, sharp activity at 13 Hz, low-voltage fast activity, spike-and-wave activity and periodic spikes, were also found in regions of seizure spread, with periodic spikes only emerging from mesial temporal sclerosis. Each of the seven patterns was accompanied by a significant increase in high-frequency oscillations upon seizure-onset. Overall, our data indicate that: (i) biologically-distinct epileptogenic lesions share intracranial electroencephalographic seizure-onset patterns, suggesting that different pathological substrates can affect similarly networks or mechanisms underlying seizure generation; (ii) certain pathologies are associated with intracranial electroencephalographic signatures at seizure-onset, e.g. periodic spikes which may reflect mechanisms specific to mesial temporal sclerosis; (iii) some seizure-onset patterns, including periodic spikes, can also be found in regions of spread, which cautions against relying on the morphology of the initial discharge to define the epileptogenic zone; and (iv) high-frequency oscillations increase at seizure-onset, independently of the pattern.