Purpose. To investigate the thickness of the retinal nerve fiber layer (RNFL) and choroid in patients who have migraines in comparison to healthy controls. Methods. This study included 76 eyes and patients in the migraine group, 36 with aura (MWA group) and 40 without (MWoA group), and 38 eyes as control subjects. The RNFL and macular thicknesses were analysed with standard OCT protocol while choroidal thickness was analysed with EDI protocol in all subjects. Choroidal thickness was measured at the fovea, 1500 µm nasal and 1500 µm temporal to the fovea in a horizontal section. Results. The mean RNFL thickness for nasal and nasal inferior sectors was significantly thinner (P ≤ 0.018) in the migraineurs' eyes than in those of the controls, as was the mean choroid thickness at the fovea and measured points (P < 0.0001). However, the mean macular thickness was not significantly different between the groups. Conclusions. This study suggests that migraine leads to a reduction in the peripapillary RNFL thickness and to thinning in choroidal structures. These findings can be explained by a chronic ischemic insult related to migraine pathogenic mechanisms and these findings are considered supportive of the relationship between glaucoma and migraine.

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Aim. To assess the effects of mydriatics commonly used in clinical practice on choroidal thickness and anterior chamber change. Methods. This was a prospective, randomized, controlled, double-blinded study including a single eye of the participants. The subjects were assigned into 4 groups to receive tropicamide 1%, phenylephrine 2.5%, cyclopentolate 1%, and artificial tears. At the baseline, anterior chamber parameters were assessed using a Pentacam Scheimpflug camera system, and choroidal thickness (CT) was measured using a spectral-domain OCT with Enhanced Depth Imaging (EDI) modality. All measurements were repeated again after drug administration. Results. Increases in pupil diameter, volume, and depth of anterior chamber were found to be significant (p = 0.000, p = 0.000, and p = 0.000, resp.), while decreases in the choroidal thickness were found to be significant in subjects receiving mydriatics (p < 0.05). Conclusions. The study has shown that while cyclopentolate, tropicamide, and phenylephrine cause a decrease in choroidal thickness, they also lead to an increase in the volume and depth of anterior chamber. However, no correlation was detected between anterior chamber parameters and choroidal changes after drug administration. These findings suggest that the mydriatics may affect the choroidal thickness regardless of anterior chamber parameters. This study was registered with trial registration number 2014/357.

Cataractous lenses have been found to have a distribution of the intracellular ionic environment, the concentrations of potassium and magnesium decreasing and the concentrations of sodium and calcium increasing relative to the cytosol of most cells. This arises as a result of changes to lens membrane characteristics causing an increase in lens membrane permeability. These changes have been found to be initiated as a result of normal ageing of the human lens. In this study, total Ca2+, K+, Na+ and Mg2+ contents have been determined in human normal and cataractous lenses using atomic absorption and flame emission spectroscopy. The normal human lens Ca2+ is between 0.15 and 0.5 miromol g(-1) fresh lens weight; in senile cataracts the value increased up to 9.31 micromol g(-1) ( p < 0.0001). The normal levels of Na+, Mg2+ and K+ are 20, 5.5 and 60 micromol g(-1) respectively; these changed to 136.10, 3.60 and 9.33 micro mol g(-1), respectively in cataractous senile human lenses ( p < 0.002, p < 0.002 and p < 0.01). The remarkable differences in these elements may play some role in cataractogenesis.

This study revealed that choroidal thickness measured using SD-OCT increased in women with preeclampsia and healthy pregnant women but the increase in choroidal thickness in preeclampsia was lower than the healthy pregnant controls. This lower rise in choroidal thickness can be generally attributed to the markedly increased systemic vascular vasospasm secondary to preeclampsia.