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Yoichiro Masuda, Satoshi Nakadomari, Hiroshi Horiguchi, Shigeyuki Kan, Satoru Miyauchi, Hiroshi Tsuneoka, Brian A. Wandell; Organization Of Human Cortical Maps In Macular Degeneration. Contrast Between Congenital and Acquired Patients. Invest. Ophthalmol. Vis. Sci. 2012;53(14):4374.
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© ARVO (1962-2015); The Authors (2016-present)
Macular degeneration (MD) patients have a central retinal lesion and a corresponding region in V1 that is deprived of retinal input (lesion projection zone, LPZ). In previous studies with of patients with acquired juvenile MD (JMD), we observed task-dependent responses in the LPZ; such responses are not present in normal controls. We hypothesized that the responses in acquired JMD patients is explained by an imbalance between feed-forward signals and feed-back signals without any reorganization of neural circuit (Masuda et al., 2008). However, patients with congenital MD have abnormal cortical signals at an earlier age, during the critical period. To understand whether the timing of the onset of MD (congenital vs. acquired juvenile) has an influence on V1 circuit organization, we compared V1 LPZ responses in congenital and acquired JMD subjects.
We obtained functional magnetic resonance imaging (fMRI) experiments in adult human subjects with congenital and acquired JMD as well as healthy controls. We measured the fMRI signals in visual cortex elicited by two kinds of stimuli. (1) Drifting contrast patterns: subjects either viewed the stimuli passively or performed a stimulus judgment task. (2) Moving-bar stimuli: we estimated the population receptive field (pRF) size with passive viewing. In healthy subjects we presented stimuli that mimicked the conditions shown to the JMD subjects.
In all JMD patients we observed fMRI responses in the cortical projection zones of their functional retina. In the congenital JMD patient, the V1 responses extended into the region of V1 that would ordinarily be deprived of retinal input. These responses were present in both passive and task-conditions. In an acquired JMD subject, the V1 responses only extended into the LPZ when the subject performed a judgment task. There were no responses in the simulated V1 LPZ of healthy controls under any conditions. The estimated pRF size in the V1 LPZ of the congenital JMD was 14deg, which far exceeds the pRF size measured in this portion of posterior calcarine cortex in control subjects (1 deg).
In the congenital JMD patient, the V1 LPZ responds to visual stimuli in both passive and task conditions. This pattern of results differs from the acquired JMD patient, in which the responses are only present in the task condition. We propose that the V1 LPZ responses in the congenital JMD patient, but not the acquired JMD patient, are due to reorganized feed-forward circuitry.
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