In this study, we observed no significant differences in SFCT and CVI between chronic migraine patients during an attack-free period when compared with the control group. Zengin et al. found that the mean CT was thinner in newly diagnosed (at least 3 months) migraine patients than in the control group (p=0.001). In the same study, they determined that CT decreased significantly in 5 patients during a migraine attack. Reggio et al. also reported that CT was thinner in chronic migraine patients with and without aura compared to the control group (p<0.0001 for both eyes). Likewise, Karaca et al. found that SFCT was thinner in the attack-free period in migraine patients with and without aura compared to the control group (p<0.05). However, CT was similar at all measured points between the migraine subgroups with and without aura (p>0.05). Contrary to these studies, Gunes et al. found that CT was thicker in chronic migraine patients compared to the control group (p<0.001 for both eyes). In their literature review, Ascado et al. summarized the different CT results obtained in migraine patients. Therefore, a different parameter is needed due to the variable nature of CT. In our study, we determined that there was no statistically significant difference in CT and CVI between migraine patients and the normal healthy group. To the best of our knowledge, this is the first study evaluating the CVI in patients with chronic migraine.
Temel et al. investigated CVI in newly diagnosed migraine patients and reported that CVI was significantly decreased in patients with migraine. However, limitations of their study are that it included a relatively small sample size and they only excluded patients who used ergot alkaloids and triptans within 24 hours before examination. Ergot alkaloids and triptans induce arterial and venous vasoconstriction,[26, 27] and the long-term effects of these drugs on CT are unknown. Therefore, the decrease in CVI may be related to the use of these drugs.
Many studies have shown that CT is affected by various factors, especially certain drugs such as sildenafil and antihistamines, smoking, age, and the axial length of the eye.[28–31] While choroidal thinning is seen in choroidal dystrophies and AMD, thickening occurs in diseases such as Vogt-Koyanagi-Harada, central serous retinopathy, and polypoidal choroidal vasculopathy.[32–34] In addition, CT measurements may differ due to examiner bias and interobserver variation.[19, 35] On the other hand, CVI gives more reliable information than CT because LA (vascular), SA (interstitial), and TCA are determined from EDI-OCT images by special software using the binarization method.[18, 19] The rich vascular structure and changes in the connective tissue can be examined in more detail, providing more reliable data about the choroidal structure. For this reason, CVI is increasingly used instead of assessing choroidal structure only by its thickness.
EDI-OCT is a non-invasive method that enables detailed visualization of the choroid. Although ICGA is still considered the gold standard imaging modality in choroidal pathologies such as PCV, its clinical use is declining because of its invasiveness. With EDI-OCT, however, the effects of intraocular pressure and perfusion changes on the choroid can be assessed instantly and non-invasively. OCTA imaging has also seen more widespread clinical use in recent years because it allows non-invasive visualization of retinal and choroidal blood flow. This method uses special software to detect the movement of red blood cells in the vasculature and display vascular flow. Guler et al. used OCTA to examine differences in retinal, peripapillary, and choriocapillaris blood flow between 26 patients with migraine without aura and a healthy control group. They observed no significant difference between the two groups in terms of blood flow in the superficial or deep retina, choriocapillaris, or choroid (choroidal flow area was 9.64 ± 0.44 and 9.65 ± 0.21 mm2 in the migraine and control groups, respectively, p=0.495). Ozcift et al. examined optic disc perfusion, central macular perfusion, and central CT in 38 chronic migraine patients and reported no significant difference in perfusions or CT, although CT was negatively correlated with the duration of migraine disease (r=−0.46, p=0.004).
OCT is excellent for visualizing the retinal and choroidal anatomy but provides no information about the vasculature or circulation. The fact that we detected no statistically significant difference in CVI values between the two groups in our study is consistent with previous studies indicating no change in choroidal flow on OCTA. The inconsistency between OCTA and CT studies may also be due to the relative subjectivity of CT measurement. According to Guler et al., there was no significant difference in retinal and choroidal blood flow in migraine patients, and retinal blood flow was determined by the dynamics of the vascular microenvironment. Rather than CT, more OCTA and CVI data are needed to explain pathophysiological mechanisms, especially in a disease of unclear pathophysiology such as migraine.
Finally, we determined that mean VAS score (8.17 ± 0.33) and monthly attack frequency in the migraine group were not significantly correlated with CT or CVI. This is consistent with the results reported by Zengin et al., who observed no significant relationship between mean VAS score (5.55 ± 2.93) and CT. However, Karaca et al. investigated the relationship between CT and VAS score, Migraine Disability Assessment Score, and Wong-Baker faces pain rating scale score and determined that CT moderately correlated with VAS score and Wong-Baker scores in patients with migraine without aura but not in patients with migraines with aura. In this regard, it is clear that more studies are needed to understand the correlation between CT and different pain scores and migraine frequency.
The present study has some limitations. One important limitation of our study is that changes in CVI were not evaluated during migraine attacks. Different results may be obtained during a migraine attack due to the activation of different pathophysiological mechanisms. Another limitation is the small number of patients included in the study. In addition, as in all CT studies, the manual determination of CT in our study is a limitation because manual segmentation remains a potential source of bias. Software-based automatic determination of CT is needed to eliminate this problem.
In conclusion, the results of this study suggest that CT and CVI do not differ significantly in chronic migraine patients during an attack-free period compared to healthy controls. However, considering the complex pathophysiology of migraine disease, more studies are needed to understand the relationship between migraine and CT.