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Jia C.H.,PLA General Hospital of Nanjing Military Command
Zhonghua yi xue za zhi | Year: 2010

To study the neural mechanism of visual cortical deficits between anisometropic and strabismic amblyopia comparatively by BOLD-fMRI retinotopic mapping. Ten anisometropic amblyopes, 10 strabismic amblyopes and 9 normal subjects underwent fMRI with retinotopic mapping and luminous spots stimuli (spatial frequency: 6 cpd, contrast: 0.5). 1.5T MRI system was used to obtain functional images of visual cortex. Responses in primary and secondary visual cortex were compared among the dominant (normal subject group), anisometropic and strabismic amblyopic eyes by one-way ANOVA, successively analyzed by paired-samples t test between amblyopic eyes and fellow fixing eyes (anisometropic and strabismic amblyopia group respectively). Their fMRI deficits of amblyopes were analyzed regressively in two amblyopia groups respectively. The result of one-way ANOVA showed significantly a lower activation (average T value) in V1, V2, V3, Vp and V7 visual areas (P < 0.05, P values 0.018, 0.007, 0.002, 0.000, 0.025 respectively) between anisometropic amblyopia and normal group. This was in accordance with the result of paired-samples t test between amblyopic eyes and fellow fixing eyes in anisometropic amblyopia group (P < 0.05, P values 0.035, 0.007, 0.020, 0.009, 0.023 respectively). Statistical difference was found in V1, V2 and Vp areas between strabismic amblyopia and normal group (P < 0.05, P values 0.010, 0.007 & 0.003 respectively). The paired-samples t test in strabismic amblyopia group showed statistical difference only in V2, Vp areas (P < 0.05, P values 0.026 and 0. 009 respectively. ). So the two results were discordant. Between the two amblyopic groups, there was no statistical difference (P > 0.05) except in V7 area (P < 0.05, P value = 0.048). There was no causal relation between the primary visual cortical deficits and the secondary cortex in amblyopia (P > 0.05). Anisometropic amblyopia and strabismic amblyopia both have functional deficits in the primary and secondary visual cortex. The neural mechanism of secondary visual cortical deficits may be more complex than decreased cortex activation induced by the deficit of primary cortex. In the primary cortex, strabismic amblyopia and anisometropic amblyopia have neuronal deficits and/or abnormal interaction. In addition, strabismic amblyopia may also have suppressive influences of the fixing eyes upon the amblyopic eyes. Anisometropic amblyopia has the neural undersampling at a high spatial frequency in the secondary visual cortex as compared to amblyopic amblyopia. Source


Jia C.-H.,PLA General Hospital of Nanjing Military Command | Lu G.-M.,PLA General Hospital of Nanjing Military Command | Zhang Z.-Q.,PLA General Hospital of Nanjing Military Command
National Medical Journal of China | Year: 2010

Objective: To study the neural mechanism of visual cortical deficits between anisometropic and strabismic amblyopia comparatively by BOLD-fMRI retinotopic mapping. Methods: Ten anisometropic amblyopes, 10 strabismic amblypes and 9 normal subjects underwent fMRI with retinotopic mapping and luminous spots stimuli (spatial frequency: 6 cpd, contrast: 0.5). 1.5T MRI system was used to obtain functional images of visual cortex. Responses in primary and secondary visual cortex were compared among the dominant (normal subject group), anisometropic and strabismic amblyopic eyes by one-way ANOVA, successively analyzed by paired-samples t test between amblyopic eyes and fellow fixing eyes (anisometropic and strabismic amblyopia group respectively). Their fMRI deficits of amblyopes were analyzed regressively in two amblyopia groups respectively. Results: The result of one-way ANOVA showed significantly a lower activation (average T value) in V1, V2, V3, Vp and V7 visual areas (P < 0.05, P values 0.018, 0.007, 0.002, 0.000, 0.025 respectively) between anisometropic amblyopia and normal group. This was in accordance with the result of paired-samples t test between amblyopic eyes and fellow fixing eyes in anisometropic amblyopia group (P < 0.05, P values 0.035, 0.007, 0.020, 0.009, 0.023 respectively). Statistical difference was found in VI, V2 and Vp areas between strabismic amblyopia and normal group (P < 0.05, P values 0.010, 0.007 & 0.003 respectively). The paired-samples t test in strabismic amblyopia group showed statistical difference only in V2, Vp areas (P < 0.05, P values 0.026 and 0.009 respectively.). So the two results were discordant. Between the two amblyopic groups, there was no statistical difference (P > 0.05) except in V7 area (P < 0.05, P value = 0.048). There was no causal relation between the primary visual cortical deficits and the secondary cortex in amblyopia (P > 0.05). Conclusion: Anisometropic amblyopia and strabismic amblyopia both have functional deficits in the primary and secondary visual cortex. The neural mechanism of secondary visual cortical deficits may be more complex than decreased cortex activation induced by the deficit of primary cortex. In the primary cortex, strabismic amblyopia and anisometropic amblyopia have neuronal deficits and/or abnormal interaction. In addition, strabismic amblyopia may also have suppressive influences of the fixing eyes upon the amblyopic eyes. Anisometropic amblyopia has the neural undersampling at a high spatial frequency in the secondary visual cortex as compared to amblyopic amblyopia. Copyright © 2012 by the Chinese Medical Association. Source

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