Reislev Nina L, Kupers Ron, Siebner Hartwig R, Ptito Maurice, Dyrby Tim B
Danish Research Centre for Magnetic Resonance, Section 714, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital Hvidovre, Kettegaard Allé 30, 2650, Hvidovre, Denmark.
BRAINlab, Department of Neuroscience and Pharmacology, Faculty of Health & Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Brain Struct Funct. 2016 Jul;221(6):2891-903. doi: 10.1007/s00429-015-1078-8. Epub 2015 Jul 2.
Visual deprivation from birth leads to reorganisation of the brain through cross-modal plasticity. Although there is a general agreement that the primary afferent visual pathways are altered in congenitally blind individuals, our knowledge about microstructural changes within the higher-order visual streams, and how this is affected by onset of blindness, remains scant. We used diffusion tensor imaging and tractography to investigate microstructural features in the dorsal (superior longitudinal fasciculus) and ventral (inferior longitudinal and inferior fronto-occipital fasciculi) visual pathways in 12 congenitally blind, 15 late blind and 15 normal sighted controls. We also studied six prematurely born individuals with normal vision to control for the effects of prematurity on brain connectivity. Our data revealed a reduction in fractional anisotropy in the ventral but not the dorsal visual stream for both congenitally and late blind individuals. Prematurely born individuals, with normal vision, did not differ from normal sighted controls, born at term. Our data suggest that although the visual streams are structurally developing without normal visual input from the eyes, blindness selectively affects the microstructure of the ventral visual stream regardless of the time of onset. We suggest that the decreased fractional anisotropy of the ventral stream in the two groups of blind subjects is the combined result of both degenerative and cross-modal compensatory processes, affecting normal white matter development.
出生时的视觉剥夺会通过跨模态可塑性导致大脑重组。尽管人们普遍认为先天性失明个体的初级传入视觉通路会发生改变,但我们对高阶视觉流中的微观结构变化以及失明 onset 如何影响这种变化的了解仍然很少。我们使用扩散张量成像和纤维束成像来研究 12 名先天性失明、15 名迟发性失明和 15 名正常视力对照者的背侧(上纵束)和腹侧(下纵束和下额枕束)视觉通路中的微观结构特征。我们还研究了 6 名视力正常的早产儿,以控制早产对大脑连通性的影响。我们的数据显示,先天性和迟发性失明个体的腹侧视觉流而非背侧视觉流中的各向异性分数降低。视力正常的早产儿与足月出生的正常视力对照者没有差异。我们的数据表明,尽管视觉流在没有来自眼睛的正常视觉输入的情况下在结构上发育,但失明会选择性地影响腹侧视觉流的微观结构,而与 onset 时间无关。我们认为,两组失明受试者腹侧流中各向异性分数的降低是退行性和跨模态补偿过程的综合结果,影响了正常的白质发育。