Enhancing trabecular outflow by disrupting the actin cytoskeleton, increasing uveoscleral outflow with prostaglandins, and understanding the pathophysiology of presbyopia interrogating Mother Nature: asking why, asking how, recognizing the signs, following the trail.
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Several major areas of work by the author and his international collaborators are reviewed. (1) The ciliary muscle in the non-human primate eye was disinserted at the scleral spur. Pilocarpine was then ineffective in increasing outflow facility, indicating that ciliary muscle contraction mediated the IOP-lowering effect of muscarinic cholinergics. (2) Compounds such as cytochalasins, H-7 and latrunculin A/B, which alter the actin cytoskeleton, cellular contractility and cellular adhesions in cultured trabecular meshwork cells, relaxed trabecular pathway cells and consequently the meshwork itself so as to decrease IOP and enhance trabecular outflow facility in non-human primates. Gene transfer approaches utilizing C3 and caldesmon over-expression by viral vectors to target specific steps in the cellular contractility/cytoskeleton/cell adhesion cascades characteristically altered trabecular meshwork cell morphology and increased outflow facility in organ-cultured anterior segments. (3) Prostaglandin F(2alpha) analogues enhanced matrix metalloproteinase production by ciliary muscle cells and scleral fibroblasts, leading to remodeling of the extracellular matrix of the ciliary muscle and sclera and consequently to increased uveoscleral outflow and decreased IOP in primates. (4) The rhesus monkey was an excellent model for human presbyopia, losing the accommodative response to cholinergic stimulation in the same timeframe relative to lifespan. No changes were found in ciliary muscle enzymes involved in acetylcholine biosynthesis or degradation or in muscarinic receptor numbers or affinity. Contractility of isolated ciliary muscle did not diminish with age, but posterior ciliary muscle attachments stiffened, suggesting a possible role in restricting muscle and consequently lens movement during accommodation. A model to reproducibly stimulate accommodation through central stimulation of the Edinger-Westphal nucleus was developed. Goniovideography and ultrasound biomicroscopic techniques allowed real-time recording and analysis of the accommodation-relevant structures. Surgical ablation of the intraocular structures involved in the accommodation response has led to further understanding of their roles and changes with age related to presbyopia. (5) Global collaborations such as those involved in these studies will be essential in the future, as science becomes "bigger". (+info)
Change in the accommodative force on the lens of the human eye with age.
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The aim of the study was to determine the age-dependence of the accommodative force on the lens in order to make it clear whether the causes of presbyopia are due to lenticular or extralenticular changes. A finite element model of the lens of an 11-, 29- and 45-year-old human eye was constructed to represent the fully accommodated state. Subsequently, the force that was needed to mould the lens into its unaccommodated state was calculated. The force on the lens appeared to be preserved with age, with only a slight increase to a value of approximately 0.06N. In conclusion, the preservation of the net force delivered by the extralenticular ciliary body indicates that the causes of presbyopia must be ascribed to lenticular changes. (+info)
Biomechanical analysis of the accommodative apparatus in primates.
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Computer-based primary visual cortex training for treatment of low myopia and early presbyopia.
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PURPOSE: The NeuroVision technology is a noninvasive, patient-specific, perceptual learning program based on visual stimulation and facilitation of neural connections at the cortical level, involving a computerized visual training regimen using Gabor patches, to improve contrast sensitivity and visual acuity. The efficacy of NeuroVision in enhancing uncorrected visual acuity (UCVA) and unaided contrast sensitivity function (CSF) in patients with low myopia or early presbyopia was evaluated. METHODS: Seventeen patients with low myopia (up to -1.75 D) and 21 patients with early presbyopia (up to +2.50 D add) were recruited in 2 clinical sites. Eleven myopic and 18 presbyopic patients underwent the NeuroVision program (treatment group), and 9 patients performed visual examinations only, serving as a control group. RESULTS: The low myopia treatment group achieved a mean improvement of 2.2 logMAR lines in unaided VA, from 0.42 to 0.20 logMAR. Unaided CSF improved at all spatial frequencies (1.5, 3, 6, 12, 18 cpd). The early presbyopia treatment group achieved a mean improvement of 2.2 logMAR lines in near UCVA, from 0.47 to 0.25 logMAR. Near unaided CSF also improved at all spatial frequencies. The control patients in both arms of the study have not shown any significant change in vision. Additionally, the mean refractive error in all groups remained unchanged after treatment. CONCLUSIONS: Results to date suggest that the NeuroVision technology is effective in improving UCVA and unaided CSF in low myopia and early presbyopia. (+info)
Objective accommodation measurements in prepresbyopic eyes using an autorefractor and an aberrometer.
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