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首页> 外文期刊>Clinical EEG and neuroscience: official journal of the EEG and Clinical Neuroscience Society (ENCS) >Visual Evoked Potentials in Infants With Diffuse Periventricular Leukomalacia
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Visual Evoked Potentials in Infants With Diffuse Periventricular Leukomalacia

机译:弥漫性脑室周围白质软化婴儿的视觉诱发电位

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Periventricular leukomalacia (PVL) is characterized by necrosis of the cerebral white matter in the dorsolateral portions of the lateral ventricles. PVL causes motor, sensory, and cognitive deficits. The aim of this study was to analyze the conduction characteristics of the visual pathway in infants with diffuse PVL using visual evoked potentials (VEPs). We studied 11 healthy infants (mean age 3.3 ± 1.3 months) and 17 with diffuse PVL (mean age 2.9 ± 0.8 months and mean gestational age 31.9 ± 3.1 weeks). The N75, P100, and N135 wave latencies; the interwave N75-PI00 and P100-N135 latencies; and the N75-P100 and P100-N135 amplitudes were measured in the occipital leads. VEPs were recorded during binocular stimulation at an angle of 120' from the Fz-Oz lead. Healthy children had mean N75, P100, and N135 wave latencies of 84.4 ± 5.8, 143.4 ± 30.6 and 222.9 ± 40.4 ms, respectively. The mean interwave N75-P100 and P100-N135 latencies were 59.0 ± 28.6 and 79.5 ± 13.6 ms, respectively. Compared with the healthy group, infants with PVL had longer N75 and NI35 latencies at 92.3 ± 15.3 (P = .05) and 265.0 ms ± 60.3 (P = .05), respectively. The interwave latency P100-N135 (105.5 ± 29.1 ms; P = .017) was longer in children with PVL than in healthy infants. Infants with diffuse PVL had mild alterations in their N75, P100 and, particularly, their N135 latencies. These increases in P100-N135 interwave latencies could be because of damage to the genicuiocortical pathways and V2-V3 networks.
机译:脑室周围白质软化症(PVL)的特征是侧脑室背外侧部分脑白质坏死。 PVL导致运动,感觉和认知缺陷。这项研究的目的是使用视觉诱发电位(VEP)分析弥散性PVL婴儿的视觉通路的传导特性。我们研究了11例健康婴儿(平均年龄3.3±1.3个月)和17例弥散性PVL(平均年龄2.9±0.8个月,平均胎龄31.9±3.1周)。 N75,P100和N135波潜伏期;波间N75-PI00和P100-N135延迟;在枕骨中测量N75-P100和P100-N135的振幅。在双眼刺激过程中,与Fz-Oz导线成120'角记录了VEP。健康儿童的平均N75,P100和N135波潜伏期分别为84.4±5.8、143.4±30.6和222.9±40.4 ms。 N75-P100和P100-N135的平均波间延迟分别为59.0±28.6和79.5±13.6 ms。与健康组相比,PVL婴儿的N75和NI35潜伏期更长,分别为92.3±15.3(P = .05)和265.0 ms±60.3(P = .05)。 PVL患儿的波间潜伏期P100-N135(105.5±29.1 ms; P = .017)长于健康婴儿。弥散性PVL的婴儿的N75,P100,尤其是其N135潜伏期有轻度改变。 P100-N135波间潜伏期的增加可能是由于对基因微球途径和V2-V3网络的破坏。

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