Multimodal MR-imaging reveals large-scale structural and functional connectivity changes in profound early blindness.
In the setting of profound ocular blindness, numerous lines of evidence demonstrate the existence of dramatic anatomical and functional changes within the brain. However, previous studies based on a variety of distinct measures have often provided inconsistent findings. To help reconcile this issue, we used a multimodal magnetic resonance (MR)-based imaging approach to provide complementary structural and functional information regarding this neuroplastic reorganization. This included gray matter structural morphometry, high angular resolution diffusion imaging (HARDI) of white matter connectivity and integrity, and resting state functional connectivity MRI (rsfcMRI) analysis. When comparing the brains of early blind individuals to sighted controls, we found evidence of co-occurring decreases in cortical volume and cortical thickness within visual processing areas of the occipital and temporal cortices respectively. Increases in cortical volume in the early blind were evident within regions of parietal cortex. Investigating white matter connections using HARDI revealed patterns of increased and decreased connectivity when comparing both groups. In the blind, increased white matter connectivity (indexed by increased fiber number) was predominantly left-lateralized, including between frontal and temporal areas implicated with language processing. Decreases in structural connectivity were evident involving frontal and somatosensory regions as well as between occipital and cingulate cortices. Differences in white matter integrity (as indexed by quantitative anisotropy, or QA) were also in general agreement with observed pattern changes in the number of white matter fibers. Analysis of resting state sequences showed evidence of both increased and decreased functional connectivity in the blind compared to sighted controls. Specifically, increased connectivity was evident between temporal and inferior frontal areas. Decreases in functional connectivity were observed between occipital and frontal and somatosensory-motor areas and between temporal (mainly fusiform and parahippocampus) and parietal, frontal, and other temporal areas. Correlations in white matter connectivity and functional connectivity observed between early blind and sighted controls showed an overall high degree of association. However, comparing the relative changes in white matter and functional connectivity between early blind and sighted controls did not show a significant correlation. In summary, these findings provide complimentary evidence, as well as highlight potential contradictions, regarding the nature of regional and large scale neuroplastic reorganization resulting from early onset blindness.
Laboratory for Visual Neuroplasticity. Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America.
Corinna M
CM
Bauer
Laboratory for Visual Neuroplasticity. Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America.
Gabriella V
GV
Hirsch
Center for Biomedical Imaging. Boston University School of Medicine, Boston, MA, United States of America.
Lauren
L
Zajac
Center for Biomedical Imaging. Boston University School of Medicine, Boston, MA, United States of America.
Bang-Bon
BB
Koo
Crossmodal Perception and Plasticity Laboratory. University of Trento, Trento, Italy.
Olivier
O
Collignon
Laboratory for Visual Neuroplasticity. Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America.
Lotfi B
http://orcid.org/0000-0002-8094-9536
LB
Merabet
D000328:Adult; D016880:Anisotropy; D001766:Blindness / Q000175:diagnosis* / Q000473:pathology*; D001931:Brain Mapping / Q000379:methods; D056324:Diffusion Tensor Imaging / Q000379:methods; D005260:Female; D066128:Gray Matter / Q000473:pathology; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D064847:Multimodal Imaging / Q000379:methods; D009473:Neuronal Plasticity / Q000502:physiology; D010296:Parietal Lobe / Q000473:pathology; D013702:Temporal Lobe / Q000473:pathology; D066127:White Matter / Q000473:pathology