Nocturnal sleep stereo-electroencephalography and polygraphy in epileptics.

J Faber, V Vladyka
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Abstract

Focal epileptic activity (FEA) in amygdalohippocampal complexes (AHC) is mostly highly intensive (except in patient BUK where it is nearly missing). Unilateral FEA is hardly ever propagated to the superficial EEG electrodes, bilateral FEA only very rarely (patients BRY and DUS), in some patients solely in deep synchronous sleep (patient LOB). FEA intensity rises in relaxed vigilance and in superficial sleep while tending to decrease in deep synchronous sleep. FEA intensity tends to drop or even disappear in active vigilance during mental activity or paradoxical sleep. Epileptic activity generalized in all the superficial and deep-implanted leads is mostly accompanied by clinical manifestations (absences, twitching, motor automatisms), or to put it the other way round: if a clinical paroxysms is in progress, there is evidence of generalized epileptic activity in all the leads. The time parameter is of no consequence, the inconspicuous motion of the hand is due to a second-lasting discharge of polyspike and wave (patient BRY in sleep). If prolonged discharges remain localized there is subclinical paroxysm (patient IRL). Similar findings were reported by Lieb et al. (1976). All we can add is that the start of an attack depends not only on the amplitude and frequency of the spikes but also on the regularity of spike intervals. Superficial "neocortical" EEG and deep "paleocortical" SEEG exhibit equal sleep stages equally, i.e. either there is synchronization in all the leads (like in synchronous sleep), or there is desynchronization (such as in active vigilance or in paradoxical sleep); those two cortical structures are not antithetical such as in, e.g., rats or cats. The sleep stages show quantitative as well as qualitative changes. There is increasingly more wakefulness and superficial sleep at the expense of spindle and paradoxical sleep. EEG graphoelements often show little differentiation, e.g. the sleep spindles are short and irregular in shape, delta activity is low in amplitude and also irregular in shape, and paradoxical sleep shows insufficient desynchronization in EEG and preserved tonic muscular activity. Epileptic activity variability is often found helpful for the reliable identification of the sleep stage concerned.(ABSTRACT TRUNCATED AT 400 WORDS)

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癫痫患者夜间睡眠立体脑电图和测谎仪。
杏仁海马体复合体(AHC)的局灶性癫痫活动(FEA)大多是高度密集的(除了在BUK患者中几乎没有)。单侧FEA几乎从未传播到浅表EEG电极,双侧FEA仅很少传播(患者BRY和DUS),在一些患者仅处于深度同步睡眠(患者LOB)。FEA强度在放松警觉性和浅睡眠时升高,而在深度同步睡眠时趋于降低。在精神活动或矛盾睡眠的主动警觉性中,FEA强度趋于下降甚至消失。在所有浅表和深层植入的导联中普遍存在的癫痫活动大多伴随着临床表现(缺席、抽搐、运动自动性),或者反过来说:如果临床发作正在进行中,则在所有导联中都有普遍存在的癫痫活动的证据。时间参数无关紧要,手部的不明显运动是由于多峰和波的二次持续放电(患者睡眠中的BRY)。如果长时间的放电仍然局限于局部,则存在亚临床发作(患者IRL)。Lieb等人(1976)也报道了类似的发现。我们所能补充的是,攻击的开始不仅取决于峰值的幅度和频率,还取决于峰值间隔的规律性。浅层“新皮层”脑电图和深层“古皮层”脑电图同样表现出相同的睡眠阶段,即要么所有导联同步(如同步睡眠),要么不同步(如主动警觉性或矛盾睡眠);这两种皮层结构并不像老鼠或猫那样是对立的。睡眠阶段既表现出量变,也表现出质变。越来越多的觉醒和浅睡以牺牲纺锤形睡眠和矛盾睡眠为代价。脑电图图元往往分化不大,如睡眠纺锤波短且形状不规则,三角洲活动振幅低且形状不规则,而矛盾睡眠表现为脑电图不完全去同步和保留强直性肌肉活动。癫痫活动的变异性经常被发现有助于可靠地识别有关的睡眠阶段。(摘要删节为400字)
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