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. 2020 Oct 1;10(1):16239.
doi: 10.1038/s41598-020-73415-3.

Evidence of cortical thickness reduction and disconnection in high myopia

Affiliations

Evidence of cortical thickness reduction and disconnection in high myopia

Ya-Jun Wu et al. Sci Rep. .

Abstract

High myopia (HM) is associated with impaired long-distance vision. accumulating evidences reported that abnormal visual experience leads to dysfunction in brain activity in HM even corrected. However, whether the long-term of abnormal visual experience lead to neuroanatomical changes remain unknown, the aim at this study is to investigate the alternation of cortical surface thickness in HM patients. 82 patients with HM (HM groups), 57 healthy controls (HC groups) were recruited. All participants underwent high-resolution T1 and resting-state functional magnetic resonance imaging (MRI) scans. The cortical thickness analysis was preformed to investigate the neuroanatomical changes in HM patients using computational anatomy toolbox (CAT 12) toolbox. Compare with HCs, HM patients showed decreased the cortical surface thickness in the left middle occipital gyrus (MOG), left inferior parietal lobule (IPL), right inferior temporal gyrus (ITG), right precuneus, right primary visual area 1 (V1), right superior temporal gyrus (STG), right superior parietal lobule (SPL), right occipital pole, and right the primary motor cortex (M1), and increased to the parietal operculum (OP4) (P < 0.01, FWE-corrected), the mean cortical thickness of right orbitofrontal cortex (OFC), right dorsolateral prefrontal cortex (DLPFC) and right subcallosal cortex showed negatively correlation between clinical variables (axis length (ALM), the average macular thickness (AMT), keratometer (KER) 1, KER2, the mean KER, the mean macular fovea thickness (MFK), the refractive diopter) in HM patients. Our result mainly provided an evidence of cortical thickness reduction and disconnection in visual center and visual processing area, and cortical thickness increase in left multimodal integration region in HM patients. This may provide important significance of the study of the neural mechanism of HM.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Figure 1
Figure 1
Cerebral cortical thickness patterns in with HC (A) and HM (B) subjects (LH light hemisphere, RH right hemisphere, HM high myopic control, HC healthy control).
Figure 2
Figure 2
Comparison of local cortical thickness between the HM group and the HC group (P < 0.01, FWE-corrected). Prussian blue indicates a significantly lower cortical thickness value, and crimson indicates a significantly higher cortical thickness value (LH light hemisphere, RH right hemisphere, HM high myopic control, HC healthy control).
Figure 3
Figure 3
Positive connectivity network and group comparison in the region of interest in left hemisphere (seed) with altered regional cortical thickness in HM subjects (LH light hemisphere, RH right hemisphere, HM high myopic control, HC healthy control, MOG middle occipital gyrus, IPL inferior parietal lobule, OP parietal operculum).
Figure 4
Figure 4
Positive connectivity network and group comparison in the region of interest in right hemisphere (seed) with altered regional cortical thickness in HM subjects (LH light hemisphere, RH right hemisphere, HM high myopic control, HC healthy control, ITG inferior temporal gyrus, V1 primary visual area 1, STG right superior temporal gyrus, SPL right superior parietal lobule, M1 right the primary motor cortex, OP parietal operculum, PCUN precuneus).

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