Babb T L, Wilson C L, Isokawa-Akesson M
Electroencephalogr Clin Neurophysiol. 1987 Jun;66(6):467-82. doi: 10.1016/0013-4694(87)90093-9.
Comparisons of the patterns of neuronal firing and stereoencephalography (SEEG) recorded from the same microelectrodes chronically implanted in the human limbic system were made in order to study neuronal electrogenesis at onset and during propagation of focal partial complex seizures. Alert or sleeping patients were monitored during spontaneous subclinical seizures (no alterations in consciousness detectable), during auras reported by the patients as typical, and during clinical seizures with loss of consciousness, movements and post-ictal confusion. During subclinical SEEG seizures (ipsilateral, normal consciousness), few neurons increased firing (estimated at only 7%) either at the focus or at propagated sites. During auras, with altered consciousness, there were relatively few neurons that increased firing, with the estimate about 14% or twice as many as during a subclinical seizure. During the onset of a clinical seizure that involved loss of consciousness, movements and post-ictal confusion, many neurons were recruited into increased firing, with an estimate of approximately 36%. During this increased electrogenesis, neurons fired briefly in association with high-frequency local SEEG; however, the bursts were shorter than the SEEG seizure pattern. Apparently, other local neurons were recruited to fire in bursts to sustain sufficient axonal driving for widespread propagation of the seizure. When the focal SEEG slowed, the units stopped firing, which suggested that the 'focal' seizure need not be sustained for more than several seconds because propagated seizure activity was self-sustaining at distant structures. The data lead to the conclusion that SEEG seizures can be generated focally by synchronous firing of fewer than 10% of neurons in the 'epileptic pool.' However, when greater percentages of neurons are recruited in the 'epileptic focus' there is greater propagation to widespread sites, especially contralaterally, which will produce clinical partial complex seizures.
为了研究局灶性部分性复杂性癫痫发作起始期和传播期的神经元电发生,对长期植入人类边缘系统的同一微电极记录的神经元放电模式与立体脑电图(SEEG)进行了比较。在清醒或睡眠的患者中,监测其在自发亚临床发作(未检测到意识改变)、患者报告为典型的先兆发作以及伴有意识丧失、运动和发作后意识模糊的临床发作期间的情况。在亚临床SEEG发作期间(同侧,意识正常),无论是在发作起始部位还是传播部位,只有少数神经元放电增加(估计仅7%)。在伴有意识改变的先兆发作期间,放电增加的神经元相对较少,估计约为14%,是亚临床发作时的两倍。在涉及意识丧失、运动和发作后意识模糊的临床发作起始期,许多神经元被募集而放电增加,估计约为36%。在这种电发生增加期间,神经元与高频局部SEEG相关联短暂放电;然而,这些爆发比SEEG发作模式短。显然,其他局部神经元被募集以爆发式放电,以维持足够的轴突驱动,使癫痫广泛传播。当局部SEEG减慢时,这些神经元停止放电,这表明“局灶性”癫痫发作无需持续超过几秒,因为传播的癫痫活动在远处结构是自我维持的。数据得出结论,SEEG发作可由“癫痫池”中不到10%的神经元同步放电局灶性产生。然而,当“癫痫灶”中有更大比例的神经元被募集时,会有更多的传播至广泛部位,尤其是对侧,这将产生临床部分性复杂性癫痫发作。