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Altered white matter connectivity associated with visual hallucinations following occipital stroke

机译:枕中风后与幻觉相关的白质连通性改变

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Introduction Visual hallucinations that arise following vision loss stem from aberrant functional activity in visual cortices and an imbalance of activity across associated cortical and subcortical networks subsequent to visual pathway damage. We sought to determine if structural changes in white matter connectivity play a role in cases of chronic visual hallucinations associated with visual cortical damage. Methods We performed diffusion tensor imaging (DTI) and probabilistic fiber tractography to assess white matter connectivity in a patient suffering from continuous and disruptive phosphene (simple) visual hallucinations for more than 2?years following right occipital stroke. We compared these data to that of healthy age‐matched controls. Results Probabilistic tractography to reconstruct white matter tracts suggests regeneration of terminal fibers of the ipsilesional optic radiations in the patient. However, arrangement of the converse reconstruction of these tracts, which were seeded from the ipsilesional visual cortex to the intrahemispheric lateral geniculate body, remained disrupted. We further observed compromised structural characteristics, and changes in diffusion (measured using diffusion tensor indices) of white matter tracts in the patient connecting the visual cortex with frontal and temporal regions, and also in interhemispheric connectivity between visual cortices. Conclusions Cortical remapping and the disruption of communication between visual cortices and remote regions are consistent with our previous functional magnetic resonance imaging (fMRI) data showing imbalanced functional activity of the same regions in this patient (Rafique et?al, 2016, Neurology, 87, 1493–1500). Long‐term adaptive and disruptive changes in white matter connectivity may account for the rare nature of cases presenting with chronic and continuous visual hallucinations.
机译:简介视力丧失后出现的幻觉是视觉皮层中异常的功能活动以及视觉通路受损后相关皮层和皮层下网络活动的不平衡所致。我们试图确定在与视觉皮层损伤相关的慢性视觉幻觉的情况下,白质连通性的结构变化是否起作用。方法我们进行了弥散张量成像(DTI)和概率纤维束成像,以评估右枕中风后连续2年以上患有连续性和破坏性phosph(简单)视幻觉的患者的白质连通性。我们将这些数据与年龄匹配的健康对照者进行了比较。结果概率束摄影术可重建白质束,提示患者同侧视听辐射的终末纤维再生。然而,从同侧视觉皮层播种到半球内外侧膝状体的这些束的反向重建的排列仍然被打乱。我们进一步观察到受损的结构特征,以及连接视皮层与额叶和颞叶区域的患者白质束的扩散变化(使用扩散张量指数测量),以及视皮层之间的半球连接性。结论皮质再映射以及视觉皮质与远端区域之间的通讯中断与我们先前的功能磁共振成像(fMRI)数据一致,该数据显示该患者同一区域的功能活动不平衡(Rafique et al,2016,Neurology,87, 1493–1500)。白质连通性的长期适应性和破坏性变化可能是慢性和连续性视觉幻觉病例罕见的原因。

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