全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

Altered White Matter Integrity in the Congenital and Late Blind People

DOI: 10.1155/2013/128236

Full-Text   Cite this paper   Add to My Lib

Abstract:

The blind subjects have experienced a series of brain structural and functional alterations due to the visual deprivation. It remains unclear as to whether white matter changes differ between blind subjects with visual deprivation before and after a critical developmental period. The present study offered a direct comparison in changes of white matter fractional anisotropy (FA) between congenital blind (CB) and late blind (LB) individuals. Twenty CB, 21 LB (blindness onset after 18 years old), and 40 sight control (SC) subjects were recruited. Both the tract-based spatial statistics (TBSS) and voxel-based analysis (VBA) showed lower FA in the bilateral optic radiations in both blind groups, suggesting that the loss of white matter integrity was the prominent hallmark in the blind people. The LB group showed more extensive white matter impairment than the CB group, indicating the mechanisms of white matter FA changes are different between the CB and LB groups. Using a loose threshold, a trend of an increased FA was found in the bilateral corticospinal tracts in the LB but with a smaller spatial extent relative to the CB. These results suggest that white matter FA changes in the blind subjects are the reflection of multiple mechanisms, including the axonal degeneration, deafferentation, and plasticity. 1. Introduction The blind subjects, irrespective of the age of onset, have experienced a series of structural and functional alterations, and they have to make major adjustments to interact effectively with the environment. Numerous functional magnetic resonance imaging (fMRI) studies have revealed that the occipital cortex of the blind subjects shifts its function to process tactile [1] and auditory information [2] and to engage in many higher-level cognitive functions, such as language [3–8], memory [3], and mental imagery [9–11]. Structural MRI studies have shown the decreased gray/white matter volume [12–14] but increased cortical thickness in the occipital cortex [15, 16]. During the past two decades, diffusion tensor imaging (DTI), as a noninvasive means, makes the in vivo evaluation of white matter integrity possible using the fractional anisotropy (FA) [17–19]. The decreased FA may represent the impairment in white matter integrity, in contrast, the increased FA may indicate the increase in white matter integrity [17–19]. Different DTI analytic methods have shown that congenitally blind (CB) or early blind (EB) subjects had atrophy [20] or decreased white matter integrity [21] in the optic radiation (OR), reduced efficiency of the brain anatomical

References

[1]  H. Burton, D. G. McLaren, and R. J. Sinclair, “Reading embossed capital letters: an fMRI study in blind and sighted individuals,” Human Brain Mapping, vol. 27, no. 4, pp. 325–339, 2006.
[2]  C. Poirier, O. Collignon, C. Scheiber et al., “Auditory motion perception activates visual motion areas in early blind subjects,” NeuroImage, vol. 31, no. 1, pp. 279–285, 2006.
[3]  A. Amedi, N. Raz, P. Pianka, R. Malach, and E. Zohary, “Early “visual” cortex activation correlates with superior verbal memory performance in the blind,” Nature Neuroscience, vol. 6, no. 7, pp. 758–766, 2003.
[4]  C. Büchel, C. Price, R. S. J. Frackowiak, and K. Friston, “Different activation patterns in the visual cortex of late and congenitally blind subjects,” Brain, vol. 121, part 3, pp. 409–419, 1998.
[5]  H. Burton, J. B. Diamond, and K. B. McDermott, “Dissociating cortical regions activated by semantic and phonological tasks: a fMRI study in blind and sighted people,” Journal of Neurophysiology, vol. 90, no. 3, pp. 1965–1982, 2003.
[6]  H. Burton, A. Z. Snyder, T. E. Conturo, E. Akbudak, J. M. Ollinger, and M. E. Raichle, “Adaptive changes in early and late blind: a fMRI study of Braille reading,” Journal of Neurophysiology, vol. 87, no. 1, pp. 589–607, 2002.
[7]  H. Burton, A. Z. Snyder, J. B. Diamond, and M. E. Raichle, “Adaptive changes in early and late blind: a fMRI study of verb generation to heard nouns,” Journal of Neurophysiology, vol. 88, no. 6, pp. 3359–3371, 2002.
[8]  P. Melzer, V. L. Morgan, D. R. Pickens, R. R. Price, R. S. Wall, and F. F. Ebner, “Cortical activation during Braille reading is influenced by early visual experience in subjects with severe visual disability: a correlational fMRI study,” Human Brain Mapping, vol. 14, no. 3, pp. 186–195, 2001.
[9]  A. Aleman, L. van Lee, M. H. M. Mantione, I. G. Verkoijen, and E. H. F. de Haan, “Visual imagery without visual experience: evidence from congenitally totally blind people,” NeuroReport, vol. 12, no. 11, pp. 2601–2604, 2001.
[10]  S. Lambert, E. Sampaio, Y. Mauss, and C. Scheiber, “Blindness and brain plasticity: contribution of mental imagery? An fMRI study,” Cognitive Brain Research, vol. 20, no. 1, pp. 1–11, 2004.
[11]  A. Vanlierde, A. G. de Volder, M. C. Wanet-Defalque, and C. Veraart, “Occipito-parietal cortex activation during visuo-spatial imagery in early blind humans,” NeuroImage, vol. 19, no. 3, pp. 698–709, 2003.
[12]  H. Bridge, A. Cowey, N. Ragge, and K. Watkins, “Imaging studies in congenital anophthalmia reveal preservation of brain architecture in “visual” cortex,” Brain, vol. 132, no. 12, pp. 3467–3480, 2009.
[13]  N. Leporé, P. Voss, F. Lepore et al., “Brain structure changes visualized in early- and late-onset blind subjects,” NeuroImage, vol. 49, no. 1, pp. 134–140, 2010.
[14]  M. Ptito, F. C. G. Schneider, O. B. Paulson, and R. Kupers, “Alterations of the visual pathways in congenital blindness,” Experimental Brain Research, vol. 187, no. 1, pp. 41–49, 2008.
[15]  J. Jiang, W. Zhu, F. Shi et al., “Thick visual cortex in the early blind,” Journal of Neuroscience, vol. 29, no. 7, pp. 2205–2211, 2009.
[16]  H. J. Park, J. D. Lee, E. Y. Kim et al., “Morphological alterations in the congenital blind based on the analysis of cortical thickness and surface area,” NeuroImage, vol. 47, no. 1, pp. 98–106, 2009.
[17]  T. Krings, V. A. Coenen, H. Axer et al., “In vivo 3D visualization of normal pyramidal tracts in human subjects using diffusion weighted magnetic resonance imaging and a neuronavigation system,” Neuroscience Letters, vol. 307, no. 3, pp. 192–196, 2001.
[18]  C. P. Lin, W. Y. I. Tseng, H. C. Cheng, and J. H. Chen, “Validation of diffusion tensor magnetic resonance axonal fiber imaging with registered manganese-enhanced optic tracts,” NeuroImage, vol. 14, no. 5, pp. 1035–1047, 2001.
[19]  C. Pierpaoli, P. Jezzard, P. J. Basser, A. Barnett, and G. Di Chiro, “Diffusion tensor MR imaging of the human brain,” Radiology, vol. 201, no. 3, pp. 637–648, 1996.
[20]  J. S. Shimony, H. Burton, A. A. Epstein, D. G. McLaren, S. W. Sun, and A. Z. Snyder, “Diffusion tensor imaging reveals white matter reorganization in early blind humans,” Cerebral Cortex, vol. 16, no. 11, pp. 1653–1661, 2006.
[21]  N. Shu, J. Li, K. Li, C. Yu, and T. Jiang, “Abnormal diffusion of cerebral white matter in early blindness,” Human Brain Mapping, vol. 30, no. 1, pp. 220–227, 2009.
[22]  N. Shu, Y. Liu, J. Li, Y. Li, C. Yu, and T. Jiang, “Altered anatomical network in early blindness revealed by diffusion tensor tractography,” PLoS ONE, vol. 4, no. 9, Article ID e7228, 2009.
[23]  C. Yu, N. Shu, J. Li, W. Qin, T. Jiang, and K. Li, “Plasticity of the corticospinal tract in early blindness revealed by quantitative analysis of fractional anisotropy based on diffusion tensor tractography,” NeuroImage, vol. 36, no. 2, pp. 411–417, 2007.
[24]  F. Schoth, U. Burgel, R. Dorsch, M. H. T. Reinges, and T. Krings, “Diffusion tensor imaging in acquired blind humans,” Neuroscience Letters, vol. 398, no. 3, pp. 178–182, 2006.
[25]  Y. Zhang, S. Wan, J. Ge, and X. Zhang, “Diffusion tensor imaging reveals normal geniculocalcarine-tract integrity in acquired blindness,” Brain Research, vol. 1458, pp. 34–39, 2012.
[26]  S. M. Smith, M. Jenkinson, M. W. Woolrich et al., “Advances in functional and structural MR image analysis and implementation as FSL,” NeuroImage, vol. 23, supplement 1, pp. S208–S219, 2004.
[27]  S. M. Smith, M. Jenkinson, H. Johansen-Berg et al., “Tract-based spatial statistics: voxelwise analysis of multi-subject diffusion data,” NeuroImage, vol. 31, no. 4, pp. 1487–1505, 2006.
[28]  D. Rueckert, L. I. Sonoda, C. Hayes, D. L. Hill, M. O. Leach, and D. J. Hawkes, “Nonrigid registration using free-form deformations: application to breast mr images,” IEEE Transactions on Medical Imaging, vol. 18, no. 8, pp. 712–721, 1999.
[29]  J. Ashburner and K. J. Friston, “Voxel-based morphometry—the methods,” NeuroImage, vol. 11, no. 6, part 1, pp. 805–821, 2000.
[30]  D. K. Jones, M. R. Symms, M. Cercignani, and R. J. Howard, “The effect of filter size on VBM analyses of DT-MRI data,” NeuroImage, vol. 26, no. 2, pp. 546–554, 2005.
[31]  J. Foong, M. R. Symms, G. J. Barker, M. Maier, D. H. Miller, and M. A. Ron, “Investigating regional white matter in schizophrenia using diffusion tensor imaging,” NeuroReport, vol. 13, no. 3, pp. 333–336, 2002.
[32]  T. R. Vangberg, J. Skranes, A. M. Dale, M. Martinussen, A. M. Brubakk, and O. Haraldseth, “Changes in white matter diffusion anisotropy in adolescents born prematurely,” NeuroImage, vol. 32, no. 4, pp. 1538–1548, 2006.
[33]  O. Ciccarelli, A. T. Toosy, S. J. Hickman et al., “Optic radiation changes after optic neuritis detected by tractography-based group mapping,” Human Brain Mapping, vol. 25, no. 3, pp. 308–316, 2005.
[34]  M. Li, J. Li, H. He et al., “Directional diffusivity changes in the optic nerve and optic radiation in optic neuritis,” The British Journal of Radiology, vol. 84, no. 1000, pp. 304–314, 2011.
[35]  F. C. R. Lopes, T. Doring, C. Martins et al., “The role of demyelination in neuromyelitis optica damage: diffusion-tensor MR imaging study,” Radiology, vol. 263, no. 1, pp. 235–242, 2012.
[36]  Y. Liu, Y. Duan, Y. He et al., “A tract-based diffusion study of cerebral white matter in neuromyelitis optica reveals widespread pathological alterations,” Multiple Sclerosis, vol. 18, no. 7, pp. 1013–1021, 2012.
[37]  C. Yu, F. Lin, K. Li et al., “Pathogenesis of normal-appearing white matter damage in neuromyelitis optica: diffusion-tensor MR imaging,” Radiology, vol. 246, no. 1, pp. 222–228, 2008.
[38]  E. L. Simoes, I. Bramati, E. Rodrigues et al., “Functional expansion of sensorimotor representation and structural reorganization of callosal connections in lower limb amputees,” Journal of Neuroscience, vol. 32, no. 9, pp. 3211–3220, 2012.
[39]  B. Draganski, T. Moser, N. Lummel et al., “Decrease of thalamic gray matter following limb amputation,” NeuroImage, vol. 31, no. 3, pp. 951–957, 2006.
[40]  E. C. Jones and T. P. Pons, “Thalamic and brainstem contributions to large-scale plasticity of primate somatosensory cortex,” Science, vol. 282, no. 5391, pp. 1121–1125, 1998.
[41]  A. S. Bock, C. D. Kroenke, E. N. Taber, and J. F. Olavarria, “Retinal input influences the size and corticocortical connectivity of visual cortex during postnatal development in the ferret,” Journal of Comparative Neurology, vol. 520, no. 5, pp. 914–932, 2012.
[42]  Q. Li, Q. Jiang, M. Guo, C. Cai, and X. Yin, “Grey and white matter changes in children with monocular amblyopia: voxel-based morphometry and diffusion tensor imaging study,” The British Journal of Ophthalmology, vol. 97, no. 4, pp. 524–529, 2013.
[43]  H. Murai, Y. Suzuki, M. Kiyosawa, A. M. Tokumaru, K. Ishii, and M. Mochizuki, “Positive correlation between the degree of visual field defect and optic radiation damage in glaucoma patients,” Japanese Journal of Ophthalmology, 2013.
[44]  U. Noppeney, K. J. Friston, J. Ashburner, R. Frackowiak, and C. J. Price, “Early visual deprivation induces structural plasticity in gray and white matter,” Current Biology, vol. 15, no. 13, pp. R488–R490, 2005.
[45]  C. Pierpaoli, A. Barnett, S. Pajevic et al., “Water diffusion changes in wallerian degeneration and their dependence on white matter architecture,” NeuroImage, vol. 13, no. 6, pp. 1174–1185, 2001.
[46]  P. S. Hüppi, S. E. Maier, S. Peled et al., “Microstructural development of human newborn cerebral white matter assessed in vivo by diffusion tensor magnetic resonance imaging,” Pediatric Research, vol. 44, no. 4, pp. 584–590, 1998.
[47]  P. S. Hüppi, S. Warfield, R. Kikinis et al., “Quantitative magnetic resonance imaging of brain development in premature and mature newborns,” Annals of Neurology, vol. 43, no. 2, pp. 224–235, 1998.
[48]  P. Mukherjee, J. H. Miller, J. S. Shimony et al., “Diffusion-tensor MR imaging of gray and white matter development during normal human brain maturation,” American Journal of Neuroradiology, vol. 23, no. 9, pp. 1445–1456, 2002.
[49]  P. Voss, M. Lassonde, F. Gougoux, M. Fortin, J. P. Guillemot, and F. Lepore, “Early- and late-onset blind individuals show supra-normal auditory abilities in far-space,” Current Biology, vol. 14, no. 19, pp. 1734–1738, 2004.
[50]  G. F. Wittenberg, K. J. Werhahn, E. M. Wassermann, P. Herscovitch, and L. G. Cohen, “Functional connectivity between somatosensory and visual cortex in early blind humans,” European Journal of Neuroscience, vol. 20, no. 7, pp. 1923–1927, 2004.
[51]  W. J. Pan, G. Wu, C. X. Li, F. Lin, J. Sun, and H. Lei, “Progressive atrophy in the optic pathway and visual cortex of early blind Chinese adults: a voxel-based morphometry magnetic resonance imaging study,” NeuroImage, vol. 37, no. 1, pp. 212–220, 2007.
[52]  A. Pfefferbaum, E. V. Sullivan, M. Hedehus, K. O. Lim, E. Adalsteinsson, and M. Moseley, “Age-related decline in brain white matter anisotropy measured with spatially corrected echo-planar diffusion tensor imaging,” Magnetic Resonance in Medicine, vol. 44, no. 2, pp. 259–268, 2000.
[53]  P. Kochunov, D. E. Williamson, J. Lancaster et al., “Fractional anisotropy of water diffusion in cerebral white matter across the lifespan,” Neurobiology of Aging, vol. 33, no. 1, pp. 9–20, 2012.

Full-Text

comments powered by Disqus

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133

WeChat 1538708413