Retinal sublayer defect is independently associated with the severity of hypertensive white matter hyperintensity
Retinal sublayer defect is independently associated with the severity of hypertensive white matter hyperintensity
复制标题
视网膜下层缺陷与高血压白质高信号的严重程度独立相关
DOI:
10.1002/brb3.1521
复制
发表时间:
2019-12-25
影响因子:
3.1
通讯作者:
Han, Zhao
中科院分区:
文献类型:
--
作者:
Qu, Man;Kwapong, William Robert;Han, Zhao
Purpose To investigate the association of specific retinal sublayer thicknesses on optical coherence tomography (OCT) imaging with brain magnetic resonance imaging (MRI) markers using the Fazekas scale in hypertensive white matter hyperintensity (WMH) subjects. Methods Eighty-eight participants (32 healthy controls and 56 hypertensive white matter hyperintensity subjects) underwent retinal imaging using the OCT and MRI. A custom-built algorithm was used to measure the thicknesses of the retinal nerve fiber layer (RNFL) and ganglion cell layer and inner plexiform layer (GCIP). Focal markers for white matter hyperintensities were assessed on MRI and graded using the Fazekas visual rating. Results Hypertensive WMH showed significantly reduced (p < .05) RNFL and GCIP layers when compared to healthy controls, respectively. A significant correlation was found between the RNFL (rho = -.246, p < .001) and GCIP (rho = -.338, p < .001) of the total participants and the Fazekas score, respectively. Statistical differences were still significant (p < .05) when correlations were adjusted for intereye correlation, age, hypertension, smoking, body mass index, and diabetes. Among the cases of hypertensive WMH, higher Fazekas scores were significantly associated (p < .05) with the thinning of both the RNFL and GCIP layers after adjustment of age and other risk factors. Conclusions Retinal degeneration in the RNFL and GCIP was independently associated with focal lesions in the white matter of the brain and deteriorates with the severity of the lesions. We suggest that imaging and measurement of the retinal sublayers using the OCT may provide evidence on neurodegeneration in WMH.