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Multispectral retinal image analysis (MRIA) for the assessment of subretinal fibrosis in neovascular age‐related macular degeneration (nAMD)

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AbstractPurpose To investigate the use of MRIA for quantitative characterisation of subretinal fibrosis secondary to nAMD.Methods MRIA images of the posterior pole were acquired over 4 months from 20 eyes including those with inactive subretinal fibrosis and those being treated with ranibizumab for nAMD. Changes in morphology of the macula affected by nAMD were modelled and reflectance spectra at the MRIA acquisition wavelengths (507, 525, 552, 585, 596, 611 and 650nm) were computed using Monte Carlo simulation. Quantitative indicators of fibrosis were derived by matching image spectra to the model spectra of known morphological properties.Results The model spectra were comparable to the image spectra, both normal and pathological. The key morphological changes that the model associated with nAMD were gliosis of the IS‐OS junction, decrease in retinal blood and decrease in RPE melanin. However, these changes were not specific to fibrosis and none of the quantitative indicators showed a unique association with the degree of fibrosis. Moderate correlations were found with the clinical assessment, but not with the treatment program.Conclusion MRIA can distinguish subretinal fibrosis from healthy tissue. The methods used show high sensitivity but low specificity, being unable to distinguish scarring from other abnormalities like atrophy. Quantification of scarring was not achieved with the wavelengths used due to the complex structural changes to retinal tissues in the process of nAMD. Further studies, incorporating other wavelengths, will establish whether MRIA has a role in the assessment of subretinal fibrosis in the context of retinal and choroidal pathology.
Title: Multispectral retinal image analysis (MRIA) for the assessment of subretinal fibrosis in neovascular age‐related macular degeneration (nAMD)
Description:
AbstractPurpose To investigate the use of MRIA for quantitative characterisation of subretinal fibrosis secondary to nAMD.
Methods MRIA images of the posterior pole were acquired over 4 months from 20 eyes including those with inactive subretinal fibrosis and those being treated with ranibizumab for nAMD.
Changes in morphology of the macula affected by nAMD were modelled and reflectance spectra at the MRIA acquisition wavelengths (507, 525, 552, 585, 596, 611 and 650nm) were computed using Monte Carlo simulation.
Quantitative indicators of fibrosis were derived by matching image spectra to the model spectra of known morphological properties.
Results The model spectra were comparable to the image spectra, both normal and pathological.
The key morphological changes that the model associated with nAMD were gliosis of the IS‐OS junction, decrease in retinal blood and decrease in RPE melanin.
However, these changes were not specific to fibrosis and none of the quantitative indicators showed a unique association with the degree of fibrosis.
Moderate correlations were found with the clinical assessment, but not with the treatment program.
Conclusion MRIA can distinguish subretinal fibrosis from healthy tissue.
The methods used show high sensitivity but low specificity, being unable to distinguish scarring from other abnormalities like atrophy.
Quantification of scarring was not achieved with the wavelengths used due to the complex structural changes to retinal tissues in the process of nAMD.
Further studies, incorporating other wavelengths, will establish whether MRIA has a role in the assessment of subretinal fibrosis in the context of retinal and choroidal pathology.

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