Siniatchkin Michael, Moeller Friederike, Shepherd Alex, Siebner Hartwig, Stephani Ulrich
University Hospital of Pediatric Neurology, Christian-Albrechts-University of Kiel, Schwanenweg 20, D-24105 Kiel, Germany.
Eur J Neurosci. 2007 Jul;26(2):529-36. doi: 10.1111/j.1460-9568.2007.05658.x.
Photosensitive individuals respond with epileptiform electroencephalography (EEG) discharges to intermittent photic stimulation. The pathogenetic mechanisms underlying this photoparoxysmal response (PPR) remain to be clarified. We investigated the involvement of magnocellular and parvocellular pathways in the processing of nonprovocative visual stimuli in healthy subjects with different phenotypic expressions of PPR (15 individuals with a local PPR, i.e. occipital discharges only, and 15 with a PPR propagating to anterior brain regions) and in 17 PPR-negative healthy controls using pattern-reversal visual evoked potentials (VEP). Checkerboard stimulation was performed at a low and a high spatial frequency to preferentially activate the magnocellular and parvocellular pathways. VEP habituation was also assessed over 15 blocks (each 100 trials) of recording. PPR-positive individuals with propagating PPR showed an increase in the N75-P100 and P100-N135 VEP components for both spatial frequencies, whereas individuals with a local PPR had normal VEP amplitudes. Individuals with propagating PPR also showed a stronger VEP habituation and reported more aversive sensations during continuous visual stimulation with the high spatial frequency checkerboard. The selective increase in VEP amplitudes in individuals with propagating PPR corroborates the notion that PPR with propagation is pathophysiologically distinct from local PPR. The increase in VEP amplitudes was independent of the spatial frequency of visual stimulation, indicating an increased neuronal excitability in both the parvocellular and magnocellular pathways. The stronger habituation in these individuals may reflect a compensatory mechanism to stabilize excitability in the visual system.
光敏个体对间歇性光刺激会产生癫痫样脑电图（EEG）放电反应。这种光阵发性反应（PPR）背后的发病机制仍有待阐明。我们使用模式反转视觉诱发电位（VEP），研究了大细胞和小细胞通路在具有不同PPR表型表达的健康受试者（15名具有局部PPR的个体，即仅枕叶放电，以及15名PPR传播至前脑区域的个体）和17名PPR阴性健康对照者处理非刺激性视觉刺激过程中的参与情况。以低空间频率和高空间频率进行棋盘格刺激，以优先激活大细胞和小细胞通路。还在15个记录块（每个块100次试验）中评估了VEP习惯化情况。PPR传播的PPR阳性个体在两种空间频率下，N75 - P100和P100 - N135 VEP成分均增加，而具有局部PPR的个体VEP振幅正常。PPR传播的个体在高空间频率棋盘格的连续视觉刺激过程中也表现出更强的VEP习惯化，并报告了更多厌恶感。PPR传播个体中VEP振幅的选择性增加证实了这样一种观点，即具有传播性的PPR在病理生理上与局部PPR不同。VEP振幅的增加与视觉刺激的空间频率无关，表明大细胞和小细胞通路中的神经元兴奋性均增加。这些个体中更强的习惯化可能反映了一种稳定视觉系统兴奋性的补偿机制。
