OCT is an imaging technique similar to ultrasound. Unlike ultrasound, which measures acoustic reflectance, OCT measures optical reflectance. OCT has changed the process of diagnosing ophthalmological disorders and has made it possible to visualize he morphology of the retinal cell layer at a high-resolution. Thus, OCT plays an important role in the diagnosis and treatment of ophthalmological disorders.
The results of numerous studies have confirmed that OCT can be used for the early diagnosis of ophthalmic diseases, disease progression monitoring and prognostic evaluation [13, 14]. Studies have shown that optic disc changes or RNFL loss in glaucoma patients can occur earlier than visual field changes are detected by standard automated perimetry, and these characteristics indicate the diagnosis of preperimetric glaucoma [15]. In addition, previous studies have shown that the thickness of the RNFL around the optic disc can be used to predict progression of GO patients [10, 16]. Here, we confirmed that the RNFL of newly diagnosed GO patients was thinner than that of the normal controls. In addition, at the 7-month follow-up, a significant difference in the RNFL thickness around the optic disc and the average RNFL thickness at the initial test was observed in the nasa areas. Sharon Blum Meirovitch et al. found that GO patients had significant thickening in the superior, inferior and nasal RNFL [10]. This result is part of consistent with ours. However, other researchers found that, compared with that in healthy subjects, GO patients with acute dysthyroid optic neuropathy showed thickening of the RNFL [17]. There are several possible explanations for the significant differences in RNFL thickness found in different studies. First, compressive optic neuropathy [18, 19] and orbital and optic nerve tumors lead to thinning of the RNFL, and GO patients also have increased orbital pressure, which may contribute to a decrease in RNFL thickness. Another possible cause of the different observations is inflammation. Thyroid diseases coexist with inflammation and edema in the orbit. Studies have revealed that [20] many GO patients with optic neuropathy have optic disc edema, which is consistent with peripheral RNFL thickening. In addition, compression mechanisms and inflammatory mechanisms may coexist. In this case, patients with inactive GO may have optic disc atrophy and reduced RNFL thickness. Therefore, measuring RNFL thickness for the early diagnosis of GO or for monitoring the progression of the disease may be complicated by influencing factors.
Therefore, we investigated whether macular thickness could be a more stable disease-monitoring. Our study revealed significant reductions in the thickness of the macula in multiple regions between the GO group at baseline and the GO group at follow-up. This indicates that perifoveal thickness may also be a more sensitive indicator of disease progression than RNFL thickness. Macular thinning may occur secondary to the mechanical compression of the orbital contents onto the retina. Similar macular thinning is observed in glaucoma patients, along with RNFL loss [21]. Another possible mechanism of macular thinning may be reduced blood flow to the retina of patients with GO [22]. However, no abnormalities in blood flow were found in our study (negative result, data not shown). Another possible cause may be autoimmune retinopathy resulting from anti-retinal antibody-induced damage [23].
To the best of our knowledge, as GO progresses, the visual function of patients will be damaged, which will be reflected in the visual field and visual acuity, and some patients will obtain a certain degree of recovery after optic nerve decompression. Therefore, we studied the relationship between perifoveal thickness and visual acuity, visual field and intraocular pressure. In our study, there was no correlation between intraocular pressure/visual acuity less than 0.3 and perifoveal thickness, but visual field damage caused the thinning of some perifoveal areas. This indicates that the perifoveal area of GO patients gradually becomes thinner as the disease and visual impairment progresses.
Our study has several limitations. The main limitation is that the number of patients was relatively small, although our results reached a significant level. Conducting our study on a larger scale may reveal subtle differences and correlations. In addition, our GO patients were not divided into the active phase and inactive phase. Dividing patients accordingly may provide more insight into the relationship between retinal thickness and the active phase of the disease.
In summary, our study revealed that the perifoveal thickness of GO patients is different from that of normal individuals, and this thickness further decreases significantly as the disease progresses. The perifoveal thickness of GO patients is related to the impairment of visual function. Therefore, perifoveal thickness may be used as an indicator for the diagnosis of GO disease and the prediction of visual function loss.