IMH and iERM are vitreo-macular interface disorders that are related to age and occur in elderly individuals. The pathogenesis of both is closely related to the relationship between the vitreous and the macula. The pathogenesis of IMH is an abnormal vitreous macular adhesion, which leads to anterior and posterior traction of the vitreous to the macula. The pathogenesis of iERM is closely related to posterior vitreous detachment. It can be found from the pathogenesis that the difference between IMH and iERM is whether there is an abnormal adhesion in the vitreous macular region when posterior vitreous detachment occurs. The local pathological changes in the macula may be closely related to the exclusive occurrence of an abnormal adhesion in the macula.
The macula is thin, and 100% of the blood supply comes from the choroid. Therefore, changes in the choroid are likely to be related to local pathological changes in the macula. Previous studies have shown that chorioretinopathy involving the macula associated with choroidal thickening includes central serous chorioretinopathy, polypoid chorioretinopathy and Vogt Koyanagi Harada [33-35], while age-related macular degeneration, diabetic retinopathy, pathological myopia, and retinal dystrophy lead to a decrease in choroidal thickness [36-40].
The choroidal thickness measurement is affected by many factors, such as imaging time, refractive error, age, axial length, and sex. In this study, there was no difference in age or sex composition between the IMH and iERM groups. Axial length in the iERM group was shorter than that in the IMH group, but there was no significant difference. Therefore, the factors affecting choroidal thickness in the two groups were comparable. Most previous studies on idiopathic macular hole and choroidal thickness showed that the choroidal thickness was thinner than that of normal people. Although some studies did not correct the influencing factors of the choroid, such as axis length [23,24], the same conclusion was reached in some studies that corrected axis length [4,25]. The relationship between the iERM and choroidal thickness has not been determined. Some studies have found that the thickness of the iERM with traction is greater than that of the normal control group [29], but many studies have not found a relationship between the iERM and choroidal thickness [27,28,30]. Our results show that choroidal thickness in patients with IMH is lower than that in patients with ERM, with comparable ages and axial lengths, which is consistent with previous results.
Studies have shown that, although the choroidal thickness in the macular area of an IMH is thinner, the central thickness of the macula is still the thickest in the macular area [4,23], and choroidal thickness was measured manually, rather than automatically calculated via the software instrument. Our study found that the choroidal thickness of 1 mm around the macular fovea is almost the thinnest in the macular area. Since our study measured the average thickness of 1 mm under the macular fovea of patients undergoing vitrectomy with an automatic analysis model, such inconsistency may be related to the method of measurement used and the composition of IMH patients.
The choroidal measurement method used in this study is an automatic recognition system based on deep learning choroidal sublayer thickness and CVI, which can measure choroidal thickness in different parts of the macula and choroidal thickness in different vascular layers [32] The results show that the choroidal thickness within 1.5 mm around the fovea in the IMH group is thinner than that in the iERM group, but there is no difference in the choroidal thickness 1.5-2.5 mm away from the fovea between the two groups, The choroidal thickness in the sublayers was analysed and showed that the thinning of the LVCL occurred within 1 mm of the fovea in the centre of the macula in the IMH group, and the thinning of MVCL and SMCL were basically consistent with the thinning of the whole choroid. These results showed that, compared with iERM, choroidal thinning of IMH mainly occurred in the MVCL and SVCL in the centre of the macula.
We also compared the CVI in the macular region between the two groups. The results showed that the CVI in the IMH group was higher than that in the iERM group within 1 mm of the macular fovea. The analysis of other parts and LVCL and MVCL showed that there was no difference in the CVI between the two groups. These results suggest that the increase in the CVI in IMH patients may mainly occur in the SVCL in the centre of the macula, which is roughly consistent with the thinning of choroidal thickness. We analysed the possible reasons why the CVI in the IMH group was higher than that in the iERM group. One is that the thinning of foveal choroidal thickness may mainly occur in the matrix, and the other is the compensatory change in the choroidal microvessels after the thinning of foveal choroidal thickness.
The results of this study show that after excluding influencing factors such as age, sex and axial length, the choroidal thickness of IMH is significantly lower than that of iERM, indicating that the difference in choroidal thickness is an independent influencing factor between these two vitreo-macular interface disorders. Our study and most previous studies are cross-sectional, so a causal relationship could not be determined. It has been found that changes in choroidal blood perfusion occur before the complete formation of macular holes [41]. Some authors also conducted a prospective study on patients with macular thinning and found that 86% (6/7) of patients with macular thinning, pigment epithelial window defects and no PVD developed a macular hole [42]. These results show that the structural changes in the macula are closely related to the occurrence of IMH.
In view of the above results, we found that changes in choroidal thickness play an important role in the pathogenesis of IMH and iERM. First, the normal choroidal thickness in patients with iERM indicates that the blood and oxygen supply of the choroid is basically normal. Its effect on the vitreous body may be due to the ageing of the vitreous body caused by the relatively normal metabolism of the choroidal retina and the occurrence of PVD, which may lead to the formation of the iERM. Second, macular choroidal thickness decreased in patients with IMHs. Although there may be compensatory changes in choroidal vessels, they may still affect the metabolism of the macula. The local metabolic abnormality of the macula may lead to the adhesion of the vitreous macula, resulting in a macular hole. Another disease of macular choroidal thickness reduction and abnormal adhesion of the vitreoretinal region is high myopia. The macular complication of high myopia is also due to the adhesion and traction of the vitreous to the macula, resulting in retinoschisis and a macular hole [43,44].
There are a few limitations in our study. First, this group of cases is a retrospective study of patients who underwent vitrectomy. Most patients are in the later stage of the disease, which may lead to selection bias. Second, there were relatively few cases in this group, which were not compared with the normal control group and need to be supplemented by follow-up research.
In summary, we concluded that the choroidal thickness of an IMH was significantly thinner than that of the ERM, which was mainly manifested in 3 mm in the macular centre and the MVCL and SVCL layers of the choroid after excluding influencing factors such as age, sex, and axial length. The choroidal vascular index of an IMH was higher than that of the iERM. These findings suggest that the choroid may be involved in the pathogenesis of IMH and iERM.