Berkeley Eye Center

PurposeTo determine refractive or biometric variables that might be predictive of increased intermediate vision in patients receiving an Eyhance monofocal intraocular lens (IOL).MethodsThis prospective, single-center, bilateral, non-randomized, open-label, observational study included a total of 110 subjects (220 eyes). Subjects had been previously bilaterally implanted with an Eyhance monofocal IOL (Johnson & Johnson Vision Care, Inc.) and were later divided into 2 groups based on their postoperative visual acuity. Subjects that had binocular distance corrected intermediate visual acuity (DCIVA) of 0.2 logMAR or better were classified into the Enhanced Group, and the remaining subjects were classified into the Non-Enhanced Group. Refractive outcomes and biometric measurements were compared between groups.ResultsThe number of subjects in each group was 61 for the Enhanced Group, and 49 for the Non-Enhanced Group. There were significant differences in pupil size between groups, with pupil sizes in the Enhanced Group significantly smaller than in the Non-Enhanced Group (p < 0.01). Subjects also reported significantly more dysphotopsias in the Non-Enhanced Group compared to the Enhanced Group (p = 0.03). Multiple regression analysis identified pupil size and axial length as significant predictors of increased monocular intermediate vision.ConclusionThe results of this study suggest that pupil size could be a predictor of increased intermediate vision in a patient receiving an Eyhance monofocal IOL.

ABSTRACT Clinical relevance Patients prescribed pilocarpine ophthalmic solution are advised to be cautious when driving at night, but studies evaluating the effects of pilocarpine hydrochloride ophthalmic solution 1.25% (pilo), approved to treat presbyopia, on driving at night are lacking. Background This double-masked, crossover, phase 3b study evaluated night-driving performance with pilo or the placebo once daily. Methods Forty-three adults (40–55 years) with presbyopia impacting daily activities and mesopic, high-contrast, binocular distance-corrected near vision 6/12–6/30 were randomised to bilateral treatment with pilo followed by placebo or placebo followed by pilo (with a ≥7-day washout between interventions). Night-driving performance was evaluated at twilight at a closed-circuit course. Primary efficacy endpoint: overall composite night-driving performance Z score at the end of the 7–14-day intervention period, 1 hour post-instillation. Pilo was considered non-inferior if the lower limit of the 95% confidence interval (CI) for the least squares mean difference (LSMD, pilo minus placebo) was >–0.25. Other efficacy endpoints: individual components of the night-driving performance test (hazard avoidance rate; road sign recognition rate and distance; pedestrians recognition distance; overall driving and lane-keeping times) and night-driving experience questionnaire. Safety included treatment-emergent adverse events (TEAEs). Results The mean overall composite Z scores were −0.121 (pilo) and 0.118 (placebo). The LSMD (pilo minus placebo) was −0.224 (95% CI, −0.346, −0.103), with 3 of the 7 individual tasks being significantly better with the placebo. The questionnaire did not reveal significant differences between pilo and the placebo. There were no serious or severe TEAEs and no TEAE-related discontinuations. The most common ocular TEAEs were headache and visual impairment with pilo (both 27.9%), and dry eye (7.0%) with the placebo. Conclusion The overall performance of night driving was inferior with pilo, compared with placebo. The study findings are consistent with the current class labelling and provide evidence to inform regulators and assist clinicians considering prescribing pilo to adults who seek treatment of presbyopia symptoms and drive at night. ClinicalTrials.gov identifier: NCT04837482.

Herpes zoster ophthalmicus (HZO) arises because of the reactivation of latent varicella-zoster virus (VZV) infection in the trigeminal nerve ganglion and typically presents with ocular manifestations. However, infrequent neurological complications can also be seen. Rarely occurring, orbital apex syndrome presents itself as a severe complication of HZO, characterized by the involvement of multiple cranial nerves and vascular structures within the orbital apex. A 70-year-old male patient being followed for HZO developed orbital apex syndrome after 14 days of treatment, resulting in ophthalmoplegia, vision loss, and significant morbidity. Clinical diagnosis was confirmed by magnetic resonance imaging of the orbit. The treatment involved a combination of systemic steroid and antiviral therapy, resulting in a favorable resolution of ophthalmoplegia within six months. However, optic-neuropathy-induced vision loss was irreparable. Early recognition, antiviral therapy, and multidisciplinary management are crucial in preventing permanent visual impairment and neurological deficits associated with this uncommon complication.

The mechanism by which angiogenic endothelial cells break the physical barrier of the vascular basement membrane and consequently sprout to form new vessels in mature tissues is unclear. Here, we show that the angiogenic endothelium is characterized by the presence of functional podosome rosettes. These extracellular-matrix-degrading and adhesive structures are precursors of de novo branching points and represent a key feature in the formation of new blood vessels. VEGF-A stimulation induces the formation of endothelial podosome rosettes by upregulating integrin α6β1. In contrast, the binding of α6β1 integrin to the laminin of the vascular basement membrane impairs the formation of podosome rosettes by restricting α6β1 integrin to focal adhesions and hampering its translocation to podosomes. Using an ex vivo sprouting angiogenesis assay, transgenic and knockout mouse models and human tumour sample analysis, we provide evidence that endothelial podosome rosettes control blood vessel branching and are critical regulators of pathological angiogenesis.

Lymphatic research has progressed rapidly in recent years. Lymphatic dysfunction has been found in myriad disorders from cancer metastasis to transplant rejection; however, effective treatment for lymphatic disorders is still limited. This study investigates the role of angiopoietin-2 (Ang-2) in corneal inflammatory lymphangiogenesis (LG) in vivo and in lymphatic endothelial cell (LEC) functions in vitro. Standard suture placement model was used to study Ang-2 expression in inflamed cornea, and corneal LG and hemangiogenesis (HG) responses in Ang-2 knockout mice. Moreover, human LEC culture system was used to examine the effect of Ang-2 gene knockdown on LEC functions using small interfering RNAs (siRNAs). The effect of siRNA treatment on corneal LG was also assessed in vivo. Angiopoietin-2 was expressed on lymphatic vessels and macrophages in inflamed cornea. While corneal LG response was abolished in Ang-2 knockout mice, the HG response was also significantly suppressed with disorganized patterning. Moreover, anti-Ang-2 treatment inhibited LEC proliferation and capillary tube formation in vitro and corneal LG in vivo. Angiopoietin-2 is critically involved in lymphatic processes in vivo and in vitro. Further investigation of the Ang-2 pathway may provide novel insights and therapeutic strategies for lymphatic-related disorders, which occur both inside and outside the eye.

Young eyes compensate for the defocus imposed by spectacle lenses by changing their rate of elongation and their choroidal thickness, bringing their refractive status back to the pre-lens condition. We asked whether the initial rate of change either in the ocular components or in refraction is a function of the power of the lenses worn, a result that would be consistent with the existence of a proportional controller mechanism. Two separate studies were conducted; both tracked changes in refractive errors and ocular dimensions. Study A: To study the effects of lens power and sign, young chicks were tracked for 4 days after they were fitted with positive (+5, +10 or +15 D) or negative (-5, -10, -15 D) lenses over one eye. In another experiment, biometric changes to plano, +1, +2 and +3 D lenses were tracked over a 24 h treatment period. Study B: Normal emmetropisation was tracked from hatching to 6 days of age and then a defocusing lens, either +6 D or -7 D, was fitted over one eye and additional biometric data collected after 48 h. In study A, animals treated with positive lenses (+5, +10 or +15 D) showed statistical similar initial choroid responses, with a mean thickening 24 μm h(-1) over the first 5 h. Likewise, with the low power positive lenses, a statistically similar magnitude of choroidal thickening was observed across groups (+1 D: 46.0 ± 7.8 μm h(-1); +2 D: 53.5 ± 9.9 μm h(-1); +3 D 53.3 ± 24.1 μm h(-1)) in the first hour of lens wear compared to that of a plano control group. These similar rates of change in choroidal thickness indicate that the signalling response is binary in nature and not influenced by the magnitude of the myopic defocus. Treatments with -5, -10 and -15 D lenses induced statistically similar amounts of choroidal thinning, averaging -70 ± 15 μm after 5 h and -96 ± 45 μm after 24 h. Similar rates in inner axial length changes were also seen with these lens treatments until compensation was reached, once again indicating that the signalling response is not influenced by the magnitude of hyperopic defocus. In study B, after 48 h of +6 D lens treatment, the average refractive error and choroidal changes were found to be larger in magnitude than expected if perfect compensation had taken place, with a + 2.4 D overshoot in refractive compensation. Taken together, our results with both weak and higher power positive lenses suggest that eye growth is guided more by the sign than by the magnitude of the defocus, and our results for higher power negative lenses support a similar conclusion. These behaviour patterns and the overshoot seen in Study B are more consistent with the behaviour of a bang-bang controller than a proportional controller.