INTRACEREBRAL PROPAGATION OF INTERICTAL ACTIVITY IN PARTIAL EPILEPSY - IMPLICATIONS FOR SOURCE LOCALIZATION

INTRACEREBRAL PROPAGATION OF INTERICTAL ACTIVITY IN PARTIAL EPILEPSY - IMPLICATIONS FOR SOURCE LOCALIZATION
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DOI:
10.1136/jnnp.57.4.435
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发表时间:
1994-04-01
影响因子:
11
通讯作者:
POLKEY, CE
POLKEY, CE
中科院分区:
医学1区
文献类型:
--
作者:
ALARCON, G;GUY, CN;POLKEY, CE

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MEG发作间期癫痫样活动可以由单个偶极子或有限数量的偶极子建模的假设进行了检查。同时记录的发作间期活动的时间过程和空间分布的表面电极和电极旁边的近中颞叶结构在12例癫痫手术进行了评估,以估计在发作间期发作的神经活动存在的限制程度,以及在何种程度上,体积传导和神经传播参与发作间期活动的扩散。此外,发作区和深发作间期活动的患者内地形相关性进行了研究。深度和表面记录的振幅之间的相关性,连同以前的报告所产生的头皮信号的振幅;人工植入偶极子表明,在发作间期癫痫样活动在头皮上记录的深度表面活动的比例约为1:2000。这意味着头皮上记录的大多数此类活动并不是来自深层结构的体积传导,而是在底层新皮层中产生的。此外,在不同记录部位记录的发作间期发作之间的时间延迟高达220 ms,表明发作间期癫痫样活动可以在皮质内神经元传播。大面积的原始皮层和新皮层可以通过三种可能的机制同时或依次活跃:(1)直接通过快速关联纤维,(2)通过快速关联纤维触发沿着新皮层的急剧/缓慢上升。大的新皮层区域的同时激活的低比率可以产生假的等效偶极子定位在更深的结构。频繁的发作间期峰电位活动也可以独立地发生在发作起始区以外的区域,并且其向表面的发作间期传播与其触发癫痫发作的能力无关。结论是:(1)头皮上深部源电磁场的深部-表面比极低;(2)单个偶极子或有限数量的偶极子不是用于外科评估的发作间期活动的适当模型;(3)发作间期活动发作的正确定位不一定意味着癫痫发作在该区域或同一半球。有人建议,直到体积传导和神经生理学传播可以区分,半经验之间的相关性,手术结果,并结合脑磁图,脑电图和MRI的新皮层投影模式的详细术前建模可能比源定位与不切实际的源模型更富有成效。
The hypothesis MEG interictal epileptiform activity can be modelled by single dipoles or by a limited number of dipoles was examined. The time course and spatial distribution of interictal activity recorded simultaneously by surface electrodes and by electrodes next to mesial temporal structures in 12 patients being assessed for epilepsy surgery have been studied to estimate the degree of confinement of neural activity present during interictal paroxysms, and the degree to which volume conduction and neural propagation take part in the diffusion of interictal activity. Also, intrapatient topographical correlations of ictal onset zone and deep interictal activity have been studied. Correlations between the amplitudes of deep and surface recordings, together with previous reports on the amplitude of scalp signals produced by;artificially implanted dipoles suggest that the ratio of deep to surface activity recorded during interictal epileptiform activity on the scalp is around 1:2000. This implies that most such activity recorded on the scalp does not arise from volume conduction from deep structures but is generated in the underlying neocortex. Also, time delays of up to 220 ms recorded between interictal paroxysms at different recording sites show that interictal epileptiform activity can propagate neuronally within cortex. Large areas of archicortex and neocortex can then be simultaneously or sequentially active via three possible mechanisms: (1) by fast association fibres directly, (2) by fast association fibres that trigger rise to sharp/slow along the neocortex. The low ratio of the simultaneous activation of large neocortical areas can yield spurious equivalent dipoles localised in deeper structures. Frequent interictal spike activities can also take place independently in areas other than the ictal onset zone and their interictal propagation to the surface is independent of their capacity to trigger seizures. It is concluded that: (1) the deep-to-surface ratios of electromagnetic fields from deep sources are extremely low on the scalp; (2) single dipoles or a limited number of dipoles are not adequate models for interictal activity for surgical assessment; (3) the correct localisation of the onset of interictal activity does not necessarily imply the onset of seizures in the region or in the same hemisphere. It is suggested that, until volume conduction and neurophysiological propagation can be distinguished, semiempirical correlations between symptomatology, surgical outcome, and detailed presurgical modelling of the neocortical projection patterns by combined MEG, EEG, and MRI could be more fruitful than source localisation with unrealistic source models.