Virtual Reality (VR) headsets create immersion by displaying images on screens placed very close to the eyes, which are viewed through high powered lenses. Here we investigate whether this viewing arrangement alters the binocular status of the eyes, and whether it is likely to provide a stimulus for myopia development. We compared binocular status after 40-minute trials in indoor and outdoor environments, in both real and virtual worlds. We also measured the change in thickness of the ocular choroid, to assess the likely presence of signals for ocular growth and myopia development. We found that changes in binocular posture at distance and near, gaze stability, amplitude of accommodation and stereopsis were not different after exposure to each of the 4 environments. Thus, we found no evidence that the VR optical arrangement had an adverse effect on the binocular status of the eyes in the short term. Choroidal thickness did not change after either real world trial, but there was a significant thickening (≈10 microns) after each VR trial (p < 0.001). The choroidal thickening which we observed suggest that a VR headset may not be a myopiagenic stimulus, despite the very close viewing distances involved.

Aim: To evaluate the acceptability, effectivity, and side effects of a monovision spectacle correction designed to reduce accommodation and myopia progression in schoolchildren. Methods: Dominant eyes of 11 year old children with myopia (−1.00 to −3.00 D mean spherical equivalent) were corrected for distance; fellow eyes were uncorrected or corrected to keep the refractive imbalance ⩽2.00 D. Myopia progression was followed with cycloplegic autorefraction and A-scan ultrasonography measures of vitreous chamber depth (VCD) for up to 30 months. Dynamic retinoscopy was used to assess accommodation while reading. Results: All children accommodated to read with the distance corrected (dominant) eye. Thus, the near corrected eye experienced myopic defocus at all levels of accommodation. Myopia progression in the near corrected eyes was significantly slower than in the distance corrected eyes (inter-eye difference = 0.36 D/year (95% CI: 0.54 to 0.19, p = 0.0015, n = 13); difference in VCD elongation = 0.13 mm/year (95% CI: 0.18 to 0.08, p = 0.0003, n = 13)). After refitting with conventional spectacles, the resultant anisometropia returned to baseline levels after 9–18 months. Conclusions: Monovision is not effective in reducing accommodation in juvenile myopia. However, myopia progression was significantly reduced in the near corrected eye, suggesting that sustained myopic defocus slows axial elongation of the human eye.

Purpose. To investigate the effects of atropine on choroidal thinning induced by hyperopic retinal defocus. Methods. Ten young adults with myopia (−1.00 D to −5.00 D) viewed a video at 6 metres for 60 minutes on successive days. On day 1, one eye (control) was distance corrected with a contact lens; the other (experimental) eye wore a contact lens imposing 2.00 D of hyperopic retinal defocus. Sub- and perifoveal choroidal thickness (SFCT, PFCT) were monitored with optical coherence tomography. On day 2, the procedure was repeated but the experimental eye had received one drop of 0.5% atropine 22 hours earlier. Results. On day 1, eyes exposed to hyperopic defocus developed progressively thinner choroids (SFCT (baseline) = 253 ± 32 μm versus SFCT (40 mins) = 244 ± 31 μm, p=0.004), whereas SFCT and PFCT in control eyes did not change (p>0.17). On day 2 (22 hours after instilling atropine), baseline SFCT and PFCT were not different to day 1 (p>0.05) and hyperopic defocus failed to thin the choroid (max change in SFCT = +2 ± 2 μm, p=0.36). Conclusions. Atropine abolished choroidal thinning induced by hyperopic defocus without changing baseline choroidal thickness. The results suggest that atropine inhibits signals associated with hyperopic defocus, for example, from lag of accommodation during near work. This trial is registered with ACTRN12617001519347.

Purpose. To investigate the change in axial eye dimensions resulting from stretching the sclera by acute elevation of intraocular pressure (IOP). methods. IOP was increased to 100 mm Hg for 1 hour through an intravitreal cannula, while ocular component dimensions were monitored every 10 minutes with A-scan ultrasound in anesthetized animals (10 chicks and 10 tree shrews). In addition, immunocytochemical detection of α-smooth muscle actin (α-SMA) using a monoclonal antibody was conducted in the sclera of the tree shrew and the chick. results. In both species, axial eye length immediately and significantly (P < 0.0001) increased on elevation of IOP to 100 mm Hg: chick to 103.9%, tree shrew to 101.2% (mean percentage of original measured at 15 mm Hg). After 1 hour of maintained pressure, chick eyes showed a further significant increase in axial length (to 108.6%), but axial length of tree shrew eyes decreased (to 100.3%) to the point that it was not significantly different from the original value at 15 mm Hg. Immunocytochemical studies of age-matched tissue demonstrated the presence of α-SMA–containing fibroblasts (myofibroblasts) within tree shrew but not chick sclera. conclusions. Elevation of IOP caused axial elongation of chick eyes, but a consistent reduction in axial length of tree shrew eyes. The presence of myofibroblasts, demonstrated in tree shrew but not chick sclera, suggests that the reduction in axial length of tree shrew eyes may have been caused by activation of a contractile mechanism involving scleral myofibroblasts. Such a mechanism may play a role in the regulation of eye size and refractive development.