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Visual electrophysiological evaluation in paclitaxel-treated patients. Pathophysiological mechanisms involved in retinal and optic nerve dysfunctions

机译:紫杉醇治疗患者的视觉电生理学评价。视网膜和视神经功能障碍的病理生理机制

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We studied 30 breast cancer patients to clarify the underlying pathophysiological mechanisms of visual pathway involvement during paclitaxel treatment. Pattern visual-evoked potentials (VEPs) and transient, 30 Hz flicker (FLK) and oscillatory potential (OP) white flash electroretinograms (ERG) were performed before treatment, after the third and sixth cycles, and at the end of treatment. Abnormal pretreatment VEP and OP and FLK changes were observed in respectively about 75% and just under 50% of the patients; transient ERG was normal in over 90%. Serial recordings: VEP unchanged; ERG b-wave latency increased at the end of therapy; OP and FLK mildly attenuated. Various combinations of ERG, OP, FLK and VEP changes occurred in 50%, and poorly correlated with the visual symptoms reported by 12 patients. A few patients had stable and persistent subclinical electrophysiological changes. The high incidence of pretreatment, subclinical electro-physiological abnormalities correlated with the administration of tamoxifen and/or other chemo-therapeutic drugs most of the patients had been taking before starting paclitaxel. On the basis of our findings, we suggest that the more likely mechanism of visual symptoms and electrophysiological changes during paclitaxel administration is vascular dysregulation in the retina or ischemic mechanisms when the optic nerve is involved.
机译:我们研究了30名乳腺癌患者,以阐明紫杉醇治疗期间视觉途径参与的潜在病理生理机制。图形视觉诱发电位(VEPS)和短暂的,30赫兹闪烁(FLK)和振荡电位(OP)白色闪光电图(ERG)处理前进行,第三和第六次循环后,在治疗结束。观察到异常预处理VEP和OP和FLK变化,分别约75%,只在50%以下;瞬态ERG在90%以上正常。系列录音:VEP不变; ERG B波延迟在治疗结束时增加; OP和FLK温和地减弱。 ERG,OP,FLK和VEP变化的各种组合发生在50%,与12名患者报告的视觉症状相比不良。少数患者具有稳定且持续持续的亚临床电生理学变化。预处理的高发期,亚临床电生理异常与他莫昔芬和/或其他化疗治疗药物的患者中大部分人都开始紫杉醇之前一直采取的管理有关。在我们的研究结果的基础上,我们建议在紫杉醇给药期间更可能的视觉症状和电生理变化机制是视网膜或缺血机制时的血管失调。

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