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首页> 外文期刊>Brain: A journal of neurology >Spreading convulsions, spreading depolarization and epileptogenesis in human cerebral cortex
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Spreading convulsions, spreading depolarization and epileptogenesis in human cerebral cortex

机译：惊厥，人脑皮层传播去极化和癫痫发生

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Spreading depolarization of cells in cerebral grey matter is characterized by massive ion translocation, neuronal swelling and large changes in direct current-coupled voltage recording. The near-complete sustained depolarization above the inactivation threshold for action potential generating channels initiates spreading depression of brain activity. In contrast, epileptic seizures show modest ion translocation and sustained depolarization below the inactivation threshold for action potential generating channels. Such modest sustained depolarization allows synchronous, highly frequent neuronal firing; ictal epileptic field potentials being its electrocorticographic and epileptic seizure its clinical correlate. Nevertheless, Le?o in 1944 and Van Harreveld and Stamm in 1953 described in animals that silencing of brain activity induced by spreading depolarization changed during minimal electrical stimulations. Eventually, epileptic field potentials were recorded during the period that had originally seen spreading depression of activity. Such spreading convulsions are characterized by epileptic field potentials on the final shoulder of the large slow potential change of spreading depolarization. We here report on such spreading convulsions in monopolar subdural recordings in 2 of 25 consecutive aneurismal subarachnoid haemorrhage patients in vivo and neocortical slices from 12 patients with intractable temporal lobe epilepsy in vitro. The in vitro results suggest that γ-aminobutyric acid-mediated inhibition protects from spreading convulsions. Moreover, we describe arterial pulse artefacts mimicking epileptic field potentials in three patients with subarachnoid haemorrhage that ride on the slow potential peak. Twenty-one of the 25 subarachnoid haemorrhage patients (84) had 656 spreading depolarizations in contrast to only three patients (12) with 55 ictal epileptic events isolated from spreading depolarizations. Spreading depolarization frequency and depression periods per 24h recording episodes showed an early and a delayed peak on Day 7. Patients surviving subarachnoid haemorrhage with poor outcome at 6 months showed significantly higher total and peak numbers of spreading depolarizations and significantly longer total and peak depression periods during the electrocorticographic monitoring than patients with good outcome. In a semi-structured telephone interview 3 years after the initial haemorrhage, 44 of the subarachnoid haemorrhage survivors had developed late post-haemorrhagic seizures requiring anti-convulsant medication. In those patients, peak spreading depolarization number had been significantly higher [15.1 (11.4-30.8) versus 7.0 (0.8-11.2) events per day, P=0.045]. In summary, monopolar recordings here provided unequivocal evidence of spreading convulsions in patients. Hence, practically all major pathological cortical network events in animals have now been observed in people. Early spreading depolarizations may indicate a risk for late post-haemorrhagic seizures.
机译：脑灰质中细胞扩散性去极化的特征是大量离子易位，神经元肿胀和直流耦合电压记录的巨大变化。在动作电位产生通道的失活阈值以上接近完全持续的去极化作用会引发脑部活动的广泛抑制。相反，癫痫发作表现出适度的离子易位和持续的去极化作用，低于动作电位产生通道的失活阈值。这种适度的持续去极化可以同步，频繁地触发神经元。发作性癫痫的电势与其皮层电图和癫痫发作的临床相关。然而，1944年的Le？o和1953年的Van Harreveld和Stamm在动物中描述了在最小的电刺激过程中，由分散的去极化引起的大脑活动的沉默改变。最终，在最初看到的活动压抑扩散期间，记录了癫痫病的潜能。这种散发性惊厥的特征在于散发性去极化的大的缓慢的电位变化的最后肩上的癫痫场电位。我们在此报告了25例体内连续25例连续性动脉瘤性蛛网膜下腔出血患者和2例12例难治性颞叶癫痫患者的新皮质切片在单极硬脑膜下记录的惊厥传播情况。体外结果表明，γ-氨基丁酸介导的抑制作用可防止惊厥扩散。此外，我们描述了模拟慢搏电位峰值的三位蛛网膜下腔出血患者的癫痫场电位的动脉搏动伪影。 25名蛛网膜下腔出血患者中有21名（84）发生了656次扩张性去极化，而仅有3名患者（12名）出现了55次从扩张性去极化分离出的发作性癫痫事件。每24h记录发作的去极化频率和抑郁期的扩散情况显示，在第7天出现了早期峰值和延迟峰值。幸存的蛛网膜下腔出血患者在6个月时结果较差，在此期间，扩散去极化的总数和峰值数量显着较高，而在此期间，总的去极化时期和峰值抑郁期明显更长皮质脑电图监测比患者预后好。在初次出血后3年进行的半结构式电话采访中，蛛网膜下腔出血幸存者中有44人在出血后癫痫发作后期发展，需要抗惊厥药物治疗。在这些患者中，峰扩散去极化数显着更高[15.1（11.4-30.8）每天7.0（0.8-11.2）个事件，P = 0.045]。总而言之，这里的单极录音提供了明确的证据表明患者会出现惊厥。因此，实际上已经在人中观察到动物中所有主要的病理性皮质网络事件。早期散布的去极化可能表示出血后癫痫发作的后期风险。

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