Purpose Retinitis Pigmentosa (RP) is a rare retinal disease with progressive degeneration of photoreceptors leading to early peripheral and later central visual loss. It provides a model to analyze visual cortex plasticity since onset age ranges from infancy to adulthood. Prior studies have mostly covered structural or functional alterations in the same cohort; hence we aimed to determine the impact of RP on brain function and structure using magnetic resonance imaging. Methods Brain images of 5 RP subjects (age 37‐66 years, RP duration 6‐42 years) and 10 matched healthy controls were acquired. Retinotopy was used to delineate visual cortical areas. Participants also performed a 1‐back visual task. Results Retinal thickness, visual field, and visual acuity were decreased in RP (p<0.01). Central visual cortex responses were shifted anteriorly into regions usually representing more peripheral locations (p<0.03). Also, V1 and V3 dorsal had higher activation during the task execution (p<0.02). Moreover, cortical thickness was increased in Brodmann areas 7 and 8, and decreased in pericalcarine (p<0.04). Surface area was enlarged in isthmus cingulated, pars orbitalis, and transverse temporal (p<0.02). Caudate volume was also augmented (p=0.01). Conclusion Results suggest brain functional and structural reorganization in RP which is supported by the absence of a silent cortical visual zone, due to unmasking of peripheral responses to central stimuli. Data also suggest top down modulation of attentional higher level regions, and enhanced recruitment of visuospatial orientation mechanisms due to peripheral vision loss. Results are relevant to the development of rehabilitation methods for RP.
Purpose Retinitis Pigmentosa (RP) is a retinal disease characterized by photoreceptor degeneration. Usually, symptoms are early onset night blindness followed by progressive peripheral vision loss, with central vision being later affected. Some patients become blind after several years of disease. We studied the consequences of this progressive loss of visual input in the human brain using Magnetic Resonance Imaging. Methods 13 RP patients (8M, 5F; mean age 47±13yrs; range:23‐66yrs) and 24 age‐matched controls (10M, 14F; mean age 44±13yrs; range 22‐69yrs) were scanned in a 3T Siemens scanner. Cortical thickness (CT), surface area (SA) and subcortical volumes were obtained with Freesurfer. Results Patients’ visual field ranged from 22deg to almost blindness. Self‐reported symptoms’ onset ranged from birth to 45 years of age (mean symptoms’ duration: 30yrs; range 6‐51). Patients showed decreased CT in pericalcarine(p=0.002); cuneus(p<0.001); lingual(p=0.02) and lateral occipital(p=0.007) regions and increased CT in supramarginal(p=0.02), superior frontal(p=0.02) and the parahippocampal(p=<0.02) gyri. Also, cortical SA was decreased only in superior parietal cortex(p<0.009,) and increased in inferior temporal gyrus(p=0.03), isthmus cingulate(p=0.02), banks of superior temporal sulcus(p=0.007), pars orbitalis(p=0.02) and transverse temporal sulcus(p=0.002). Also, the caudate nucleus was increased in RP(p=0.003). Conclusion We conclude that visual input deprivation in RP leads to a large scale subcortical and cortical reorganization of brain resources, with loss in visual processing areas and changes in multimodal integration areas that may compensate for this sensory input loss.
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