Background: To assess the safety and efficacy of supracapsular implantation with optic capture of the posterior chamber intraocular lens in Chinese children with aphakic after traumatic cataract.

Methods: It was a retrospective case series study. Fifteen cases (15 eyes) Chinese children received supracapsular implantation with optic capture of the posterior chamber intraocular lens. Pre- and post-operative visual acuities were recorded. Intra- and post-operative complications were observed. The follow-up period ranged from 7 to 43 (28.7±7.2) months.

Results: Implantation of optic capture of the posterior chamber intraocular lens was successfully performed in 15 eyes. The best corrected visual acuity (BCVA) ranged from 0.3 to 1.0 (0.61±0.19). No optic axis opaque was found in 15 eyes with optic capture. The major complications of optic capture were iris posterior synechia and intraocular lens (IOL) precipitates. Intraocular dislocation was found in one case three weeks after the operation.

Conclusions: Supracapsular implantation with optic capture of the posterior chamber intraocular lens is safe and effective for the treatment of traumatic cataract in Chinese children.

Abstract: The article discusses the early abandonment of mechanical theories about eye enlargement in degenerative myopia at the turn of the 20th century. At that time, the number of theories about myopia grew unrestricted, but with scant support from the experimental field. The mechanical theories vanished as a new wave of metabolism-based theories appeared, propelled by the huge advances in molecular biology. Modern techniques allow reconsidering those theories and to put them to test with higher confidence.

Background: Patching an eye for a period of 2 hours results in a period of plasticity where inter-ocular balance shifts in favor of the patched eye. Acetylcholine has been shown to improve visual function and augment adult neural plasticity. Here we evaluate whether administering the cholinesterase inhibitor donepezil enhances the magnitude or duration of the patching induced shift in ocular balance.

Methods: We used a double-blind drug treatment design to test the effect of donepezil and patching on the shift in ocular balance. We used a well-known binocular phase combination task to measure ocular balance before and after treatment.

Results: Our results demonstrate that donepezil does not enhance, and may actually reduce the magnitude and duration of the patching-induced shift in ocular balance.

Conclusions: Patching induced adult neural plasticity does not appear to be modulated by the cholinergic system, however, increased dose or longer drug administration periods may yield significant results. Future studies on binocular rivalry are in the pipeline.

Background: Short-term monocular deprivation has been recently shown to temporarily increase the sensitivity of the patched eye. Many studies have patched subjects for an arbitrary period of 2.5 hours, but for no principled reason. Our goal is to show a relationship, if any, between the length of patching duration and the strength of its effect.

Methods: We tested nine subjects with three different patching durations: 1-, 2-, 3-hour. Four of the nine subjects were patched for 5-hour. Monocular deprivation was achieved by the use of a translucent eyepatch. A session included two rounds of baseline testing of interocular eye balance, patching, and post-patching tests. Each post-patching test occurred at 0, 3, 6, 12, 24, 48, 60 and 96 minutes after patching to track the patching effect over time. Every subject performed two sessions per condition.

Results: One-hour patching produced a small shift in ocular dominance. A larger shift occurred from 2-hour patching, but 3-hour patching produced a comparable effect to the one measured after 2-hour patching.

Conclusions: These results show a saturation of the patching effect beyond 2-hour patching. Hence, we believe that 2-hour patching duration is the optimal duration for eye dominance changes induced by monocular deprivation.

Background: Visual deficits, caused by ocular disease or trauma to the visual system, can cause lasting damage with insufficient treatment options available. However, recent research has focused on neural plasticity as a means to regain visual abilities. In order to better understand the involvement of neural plasticity and reorganization in partial vision restoration, we aim to evaluate the partial recovery of a visual deficit over time using three behavioural tests. In our study, a partial optic nerve crush (ONC) serves as an induced visual deficit, allowing for residual vision from surviving cells.

Methods: Three behavioural tests—optokinetic reflex, object recognition, and visual cliff—were conducted in 9 mice prior to a bilateral, partial ONC, then 1, 3, 7, 14, 21, and 28 days after the ONC. The optokinetic reflex test measured the tracking reflex in response to moving sinusoidal gratings. These gratings increase in spatial frequency until a reflex is no longer observed, i.e., a visual acuity threshold is reached. The object recognition test examines the animal’s exploratory behaviour in its capacity to distinguish high versus low contrast objects. The visual cliff test also evaluates exploratory behaviour, by simulating a cliff to observe the animal’s sense of depth perception. All three tests provide an estimate of the rodent’s visual abilities at different levels of the visual pathway.

Results: The partial optic nerve crush resulted in a total loss of visual acuity as measured by the optokinetic reflex. The deficit did not show improvement during the 4 following weeks. Despite the visual cliff test showing a non-significant decrease in deep end preference 1-day post ONC, though this was not the case for subsequent test occasions. The object recognition test showed no significant trends.

Conclusions: In conclusion, the optokinetic reflex test showed a significant loss of function following the visual deficit, but no recovery. However, a complimentary pilot study shows visual recovery using lighter crush intensities. The spatial visual function does not seem to be affected by the ONC, suggesting that the object recognition and visual cliff tests, in their current design, may rely on somatosensory means of exploration.

Background: The complexity of the glaucoma pathophysiology is directly reflected on its experimental modeling for studies about pathological mechanisms and treatment approaches. Currently, a variety of in vivo models are available for the study of glaucoma, although they do not reach an exact reproduction of all aspects characterizing the human glaucoma. Therefore, a comprehensive view of disease onset, progression and treatment efficacy can only be obtained by the integration of outcomes deriving from different experimental models.

Methods: The present article summary experimental procedures and analytical methodologies related with two experimental models of glaucoma belonging to the classes of induced intraocular pressure (IOP)-elevation and genetic models, methyl cellulose (MCE)-induced ocular hypertension and DBA/2J mouse strain. Point-by-point protocols are reported with a particular focus on the critical point for the realization of each model. Moreover, typical strength and drawbacks of each model are described in order to critically handle the outcomes deriving from each model.

Discussion: This paper provides a guideline for the realization, analysis and expected outcomes of two models allowing to study IOP-driven neurodegenerative mechanisms rather than IOP-independent neurodegeneration. The complementary information from these models could enhance the analysis of glaucomatous phenomena from different points of view potentiating the basic and translational study of glaucoma.

Background: The complexity of the glaucoma pathophysiology is directly reflected on its experimental modeling for studies about pathological mechanisms and treatment approaches. Currently, a variety of in vivo models are available for the study of glaucoma, although they do not reach an exact reproduction of all aspects characterizing the human glaucoma. Therefore, a comprehensive view of disease onset, progression and treatment efficacy can only be obtained by the integration of outcomes deriving from different experimental models.

Methods: The present article summary experimental procedures and analytical methodologies related with two experimental models of glaucoma belonging to the classes of induced intraocular pressure (IOP)-elevation and genetic models, methyl cellulose (MCE)-induced ocular hypertension and DBA/2J mouse strain. Point-by-point protocols are reported with a particular focus on the critical point for the realization of each model. Moreover, typical strength and drawbacks of each model are described in order to critically handle the outcomes deriving from each model.

Discussion: This paper provides a guideline for the realization, analysis and expected outcomes of two models allowing to study IOP-driven neurodegenerative mechanisms rather than IOP-independent neurodegeneration. The complementary information from these models could enhance the analysis of glaucomatous phenomena from different points of view potentiating the basic and translational study of glaucoma.