Decline In Acuity Research Articles

Neovascular AMD: Where do we go from here?

In the age of anti-vascular endothelial growth factor (VEGF) therapy, we are fortunate as clinicians to have three great options in the treatment of neovascular age-related macular degeneration (AMD). Yet we still face a dilemma, in that we lack a truly sustainable treatment strategy. For various reasons, as a group we cannot maintain a monthly injection regimen for patients and are giving far less, approximately half of that, be it bevacizumab, ranibizumab, or aflibercept (Holekamp et al, 2014). Unfortunately, this comes at a cost: changing from monthly to as-needed injections has been associated with a decline in visual acuity almost back down to baseline (Singer et al, 2012; Silva et al, 2013).

Occult Macular Dystrophy.

Occult macular dystrophy is an inherited macular dystrophy characterized by a progressive decline of bilateral visual acuity with normal fundus appearance, fluorescein angiogram and full-field electroretinogram. This case report presents a 20-year-old female patient with bilateral progressive decline of visual acuity for six years. Her visual acuity was 3-4/10 in both eyes. Anterior segment and fundus examination, fluorescein angiogram and full-field electroretinogram were normal. She could read all Ishihara pseudoisochromatic plates. Fundus autofluorescence imaging was normal. There was a mild central hyporeflectance on fundus infrared reflectance imaging in both eyes. Reduced foveal thickness and alterations of the photoreceptor inner and outer segment junction were observed by optical coherence tomography in both eyes. Central scotoma was also found by microperimetry and reduced central response was revealed by multifocal electroretinogram in both eyes. These findings are consistent with the clinical characteristics of occult macular dystrophy.

Large cross-sectional study of presbycusis reveals rapid progressive decline in auditory temporal acuity

The auditory system relies on extraordinarily precise timing cues for the accurate perception of speech, music, and object identification. Epidemiological research has documented the age-related progressive decline in hearing sensitivity that is known to be a major health concern for the elderly. Although smaller investigations indicate that auditory temporal processing also declines with age, such measures have not been included in larger studies. Temporal gap detection thresholds (TGDTs; an index of auditory temporal resolution) measured in 1071 listeners (aged 18–98 years) were shown to decline at a minimum rate of 1.05 ms (15%) per decade. Age was a significant predictor of TGDT when controlling for audibility (partial correlation) and when restricting analyses to persons with normal-hearing sensitivity (n = 434). The TGDTs were significantly better for males (3.5 ms; 51%) than females when averaged across the life span. These results highlight the need for indices of temporal processing in diagnostics, as treatment targets, and as factors in models of aging.

Manual aiming in healthy aging: does proprioceptive acuity make the difference?

The present study examines whether non-active older adults are more dependent on visual information when executing aiming movements and whether age-related declines in proprioception play a mediating role herein. Young (N=40) and older adults (N=38) were divided into physically active and non-active subgroups based on self-reported sports participation levels. In experiment 1, participants executed wrist-aiming movements with and without visual feedback. In experiment 2, passive proprioceptive acuity was assessed using wrist motion detection and position matching tests. Results showed similar aiming accuracy across age groups both with and without visual feedback, but older adults exhibited longer movement times, prolonged homing-in phase, and made more corrective submovements. Passive proprioceptive acuity was significantly affected by physical activity level and age, with participants in the active group scoring better than their non-active peers. However, these declines did not predict performance changes on the aiming task. Taken together, our observations suggest that decline in proprioceptive acuity did not predict performance changes on the aiming task and older adults were able to compensate for their decreased motion and position sense when allowed sufficient time. In line with these observations, we proposed that older adults are able to compensate for their decline in proprioception by increasing their reliance on predictive models.

Odor-Specific Loss of Smell Sensitivity with Age as Revealed by the Specific Sensitivity Test.

The perception of odor mixtures plays an important role in human food intake, behavior, and emotions. Decline of smell acuity with normal aging could impact food perception and preferences at various ages. However, since the landmark Smell Survey by National Geographic, little has been elucidated on differences in the onset and extent of loss in olfactory sensitivity toward single odorants. Here, using the Specific Sensitivity test, we show the onset and extent of loss in both identification and detection thresholds of odorants with age are odorant-specific. Subjects of Chinese descent in Singapore (186 women, 95 men), aged 21-80 years, were assessed for olfactory sensitivity of 10 odorants from various odor groups. Notably, subjects in their 70s required 179 times concentration of rose-like odorant (2-phenylethanol) than subjects in the 20s, while thresholds for onion-like 2-methyloxolane-3-thiol only differed by 3 times between the age groups. In addition, identification rate for 2-phenylethanol was negatively correlated with age throughout adult life whereas mushroom-like oct-1-en-3-ol was equally identified by subjects across all ages. Our results demonstrated the girth of differentiated olfactory loss due to normal ageing, which potentially affect overall perception and preferences of odor mixtures with age.

Tau-Driven Neuronal and Neurotrophic Dysfunction in a Mouse Model of Early Tauopathy.

This work highlights the potential molecular mechanisms by which initial tauopathy induces neuronal dysfunction. Combining clinically used electrophysiological techniques (i.e., electroretinography) and molecular analyses, this work shows that in a relevant model of early tauopathy, the retina of the P301S mutant human tau transgenic mouse, mild tau pathology results in functional changes of neuronal activity, likely due to selective impairment of brain-derived neurotrophic factor signaling via its receptor, TrkB. These findings may have important translational implications for early diagnosis in a subset of Alzheimer's disease patients with early visual symptoms and emphasize the need to clarify the pathophysiological changes associated with distinct tauopathy stages to support informed therapeutic decisions and guide drug discovery.

Post-Marketing Survey of Adverse Events Following Ocriplasmin.

To study the post-marketing safety profile of ocriplasmin (Jetrea; ThromboGenics, Iselin, NJ) as experienced by retinal physicians in the United States. Two thousand four hundred sixty-five retinal physicians were surveyed regarding their frequency of use of ocriplasmin and reports of ocular adverse events. There were 270 respondents (11%) who reported treating 1,056 eyes with ocriplasmin. The reports of adverse events (AE) were as follows: acute decline in visual acuity (16.95%), development of submacular fluid or serous retinal detachment (10.23%), dyschromatopsia (9.09%), progression of vitreomacular traction to macular hole (8.71%), development of retinal detachment (2.65%), development of retinal tear (1.99%), development of afferent pupillary defect (1.80%), electroretinography abnormalities (0.57%), crystalline lens instability (0.38%), and vasculitis (0.28%). Although the frequency of some ocular AEs reported in this study are comparable to those reported in the phase 3 registration trials, additional phase 4 safety studies are warranted to better understand the pathophysiology and clinical relevance of ocular AEs of ocriplasmin.

Comparison between the EX-PRESS P-50 implant and trabeculectomy in patients with open-angle glaucoma.

PurposeTo evaluate the EX-PRESS P-50 implant compared to standard trabeculectomy (TBC).MethodsSingle-center prospective randomized study; 20 eyes of 20 patients were treated with the EX-PRESS P-50 implant, and 20 eyes of 20 patients with TBC, over a 19-month period. Records of all patients were reviewed and compared. Success was defined as intraocular pressure (IOP) <21 and >5 mmHg or a decrease of 30% of IOP. Failure was defined as >21 mmHg or decline in visual acuity. Statistical analysis was made with Student’s t-test and χ2 test analyzed with SPSS version 13.0.ResultsThe average follow-up was 8.6 months (±4.9 months) for the EX-PRESS P-50 group and 9.6 months (±5.3 months) for the TBC group. The postoperative visual acuity and IOP were not significantly different. We report more complications in the EX-PRESS P-50 group. At 3, 6, and 12 months follow-up, the control group was found to be free of complications, whereas multiple complications were observed in the EX-PRESS P-50 group at 3 and 6 months follow-up. We found no differences in either group with respect to success.ConclusionBoth procedures are equally effective for the treatment of glaucoma, with 80% success in the EX-PRESS P-50 group and 72.7% in the control group.

Bilateral, Simultaneous, Acute Angle Closure Glaucoma in Pseudophakia Induced by Chlorthalidone.

Purpose. To report two persons with acute, bilateral, and simultaneous angle closure glaucoma in pseudophakia secondary to uveal effusions induced by administration of chlorthalidone. Methods. Case reports. Results. Bilateral shallow anterior chambers and high intraocular pressure with decline in visual acuity were reported in two patients within days of intake of chlorthalidone for systemic hypertension. Gonioscopy confirmed appositional angle closure while choroidal detachment and ciliochoroidal detachment were revealed on ultrasonographic studies. Discontinuing chlorthalidone and institution of aqueous suppressants to reduce IOP and cycloplegics reversed angle closure and glaucoma. Conclusions. Reports of angle closure glaucoma in pseudophakic eyes induced by idiosyncratic reaction to chlorthalidone confirms that osmotic changes in the crystalline lens has no role in the pathogenesis of drug induced glaucoma and reaffirms that glaucoma is secondary to ciliochoroidal detachment and ciliary body rotation and edema.

Dissociations of the Fluocinolone Acetonide Implant: The Multicenter Uveitis Steroid Treatment (MUST) Trial and Follow-up Study

To describe fluocinolone acetonide implant dissociations in the Multicenter Uveitis Steroid Treatment (MUST) Trial. Randomized clinical trial with extended follow-up. Review of data collected on the first implant in the eye(s) of participants. Dissociation was defined as the drug pellet no longer being affixed to the strut and categorized as spontaneous or surgically related. A total of 250 eyes (146 patients) had at least 1 implant placed. Median follow-up time after implant placement was 6 years (range 0.5-9.2 years). Thirty-four dissociations were reported in 30 participants. There were 22 spontaneous events in 22 participants; 6-year cumulative risk of a spontaneous dissociation was 4.8% (95% confidence interval [CI]: 2.4%-9.1%). The earliest event occurred 4.8 years after placement. Nine of 22 eyes with data had a decline in visual acuity ≥5 letters temporally related to the dissociation. Thirty-nine implant removal surgeries were performed, 33 with replacement. Twelve dissociations were noted during implant removal surgeries in 10 participants (26%, 95% CI 15%-48%); 5 of these eyes had a decline in visual acuity ≥5 letters after surgery. The time from implant placement to removal surgery was longer for the surgeries at which dissociated implants were identified than for those without one (5.7 vs 3.7 years, P < .001). Overall, visual acuity declined 15 or more letters from pre-implant values in 22% of affected eyes; declines were frequently associated with complications of uveitis or its treatment. There is an increasing risk of dissociation of Retisert implants during follow-up; the risk is greater with removal/exchange surgeries, but the risk of both spontaneous and surgically related events increases with longevity of the implants. In 22% of affected eyes visual acuity declined by 15 letters. In the context of eyes with moderate to severe uveitis for years, this rate is not unexpected.

Showing their true colours: Possible secular declines and a Jensen effect on colour acuity — More evidence for the weaker variant of Spearman's Other Hypothesis

ABSTRACT Spearman's Other Hypothesis predicts that the common factor amongst sensory discrimination measures corresponds to general intelligence (g). The co-occurrence model predicts that low-complexity physiological information-processing indicators reliably measure g across cohorts, and should therefore decline with time due to genetic changes in the broader population. As strong relations exist between general sensory discrimination and g, such measures should show evidence of secular declines. This is tested using N-weighted temporal regression of square-root Total Error Scores (√ TES), obtained from four Western normative samples published in the 1980s, 90s and 2000s (combined N = 752) evaluated using the Farnsworth–Munsell 100-Hue colour acuity test (disattenuated g loading = .78). A significant temporal β value of .37 was found (controlling for national IQ), suggesting a decline in colour acuity equating to a reduction in g of − 3.15 points per decade. Analysis of the subset of the cohorts aged 20–29 years, in which colour acuity is maximized, reveals a larger secular decline (β = .67, N = 199, − 5.85 points per decade). The small number of studies employed in these analyses makes these findings tentative however. Also consistent with a weaker variant of the Other Hypothesis is the finding that 100-Hue acuity-IQ correlations are associated with the Jensen effect. The aggregate vector correlation across two studies is .63 (N = 932.5, p

Longitudinal Change of Circumpapillary Retinal Nerve Fiber Layer Thickness in Children With Optic Pathway Gliomas.

To evaluate longitudinal changes in circumpapillary retinal nerve fiber layer (RNFL) thickness, as measured by spectral-domain optical coherence tomography (SD OCT), in children with optic pathway gliomas. Longitudinal cohort study. Global and quadrant-specific circumpapillary RNFL thickness measures were acquired using either a hand-held SD OCT during sedation or a table-top SD OCT in children old enough to cooperate. Vision loss was defined as either a 0.2 logMAR decline in visual acuity or progression of visual field. Percent change in circumpapillary RNFL thickness in eyes experiencing vision loss was compared to eyes with stable vision. Fifty-five eyes completed 250 study visits. Ten eyes (18%) from 7 patients experienced a new episode of vision loss during the study and 45 eyes (82%) from 39 patients demonstrated stable vision across study visits. Percent decline of RNFL thickness between the baseline visit and first event of vision loss event was greatest in the superior (-14%) and inferior (-10%) quadrants as well as global average (-13%). Using a threshold of ≥10% decline in RNFL, the positive and negative predictive value for vision loss when 2 or more anatomic sectors were affected was 100% and 94%, respectively. Children experiencing vision loss from their optic pathway gliomas frequently demonstrate a ≥10% decline of RNFL thickness in 1 or more anatomic sectors. Global average and the inferior quadrant demonstrated the best positive and negative predictive values. Circumpapillary RNFL is a surrogate marker of vision and could be helpful in making treatment decisions for children with optic pathway gliomas.

The value of multifocal electroretinography to predict progressive visual acuity loss in early AMD.

To investigate, in a prospective study, the role of multifocal electroretinography (mfERG) for predicting visual acuity decline in early age-related macular degeneration (AMD) with time. Twenty-six early AMD patients (12 males and 14 females, mean age 66.9 ± 9.8; range 46-82 years) were included in the study. A complete ophthalmic examination and mfERG (Retiscan, Roland Germany, ISCEV standard protocol) were performed at the study entry (baseline), after 20 and 24 months. The first-order kernel mfERG responses were analyzed by ring analysis. The amplitude density (AD) of the first positive peak (P1, nV/deg(2)), the P1 amplitude (µV) and P1 implicit time (ms) for Rings 1 (central) to 6 (most peripheral) were evaluated. Data were statistically analyzed by analysis of variance and receiver operating characteristic (ROC) curves. The loss in the mfERG Ring 1 AD from normal control values, recorded at baseline, was correlated with the decrease in ETDRS visual acuity with time (P = 0.004). ROC analysis showed that, after 24 months, the average decline in visual acuity was greater (3 letters vs 0.4 letters, P = 0.0021) in patients whose Ring 1 P1 AD at baseline was equal to or less than 65.9 nV/deg(2), compared to those with higher AD values. Both P1 amplitude and AD of Ring 1 had an area under the curve of 0.702 (95% confidence interval 0.50-0.92) with a sensitivity of 64.3% (35.14-87.24%) and a specificity of 91.7% (61.52-99.79%). The present results indicate that mfERG P1 amplitude and AD of Ring 1 may be highly specific to predict visual acuity decline in early AMD.

Do not turn a blind eye to alkyl nitrite (poppers)!

Recreational users of poppers must be informed about the risk of developing poppers-associated maculopathy and the possible cumulative risk when taking poppers in combination with sildenafil. We suggest that it is an accumulative increase in cGMP which is harmful for the photoreceptor cells and may cause poppers-associated maculopathy (Fig. 1). A possible association between the use of poppers and maculopathy with visual loss was first described in 2004 (Pece et al. 2004). Poppers is the popular name for alkyl nitrite which is a short-acting, volatile drug used by inhalation. To better understand this possible association, we looked into the medical history and drug use of 10 patients with poppers-associated maculopathy. Seven patients (70%) were HIV positive, for which one patient was treated with a proteinase inhibitor at time of onset. Sixty per cent used sildenafil in combination with poppers: three were HIV positive and three were HIV negative. It may be that patients, who use poppers most, are those who get HIV and are more prone to the development of a maculopathy due to a higher cumulative dose of poppers. However, if poppers alone were a sufficient cause of maculopathy, far more women and heterosexual men would be expected among a cohort of users. Among the general population, 4% use poppers. In the homosexual community, about two per cent of the population, 30% take poppers and 6% are HIV positive (Swearingen & Klausner 2005). Hence, an additional factor like the concentration of cGMP may be the key substance damaging the photoreceptor cells in poppers-associated maculopathy. Upon oxidation, alkyl nitrites give rise to nitric oxide (NO). NO stimulates guanylate cyclase which converts guanosine triphosphate (GTP) to cyclic guanosine monophosphate (cGMP). Guanylate cyclase (GC) is found in the cell body of the photoreceptor cell, that is the retinal cones (Ferrendelli & De Vries 1983). cGMP is an important substance in the photo-transduction cascade which allows Ca2+ and Na2+ to enter the cell, causing depolarization of the cell. However, very high levels of calcium will damage the photoreceptor cell (Sharma & Rohrer 2007). When patients are infected with human immunodeficiency virus (HIV), their cytokines IL-1, IL-6, interferon-gamma and TNF-alpha will increase. These cytokines activate inducible nitric oxide synthase 2 (iNOS-2), which has been shown to increase the level of NO and cGMP in the retina. In the present series, one patient was treated with a proteinase inhibitor. Proteinase inhibitors inhibit cytochrome P450 3a4. As sildenafil is broken down by cytochrome P450 3a4, proteinase inhibitors will cause an increased and prolonged concentration of sildenafil in the blood of patients using sildenafil. This indicates that also treatment of HIV patients with proteinase inhibitors might add to the development of a poppers-associated maculopathy. The three patients who were HIV negative used sildenafil besides poppers. One patient used poppers frequently for years, without any visual problems. But when he first used a combination of sildenafil and poppers, he noticed a sudden decline in visual acuity. Sildenafil, a phosphodiesterase inhibitor, prevents the degradation of cGMP. Phosphodiesterase VI is a component of the photo-transduction cascade of the photoreceptor cells. So inhibition of phosphodiesterase VI, as can be seen after the use of sildenafil, causes an increased concentration of cGMP in the photoreceptor cells. Inhibition of phosphodiesterase IV was found to induce an accumulation of cGMP with degeneration of cones in pigs (Martínez-Fernández de la Cámara et al. 2013). So, sildenafil, HIV and/or proteinase inhibitors influence a common pathway through which a rise in cGMP is induced and may thus increase the risk of developing a poppers-associated maculopathy.

Older nursesʼ experiences of providing direct care in hospital nursing units: a qualitative evidence systematic review protocol

Older nursesʼ experiences of providing direct care in hospital nursing units: a qualitative evidence systematic review protocol

Defining response to anti-VEGF therapies in neovascular AMD.

The introduction of anti-vascular endothelial growth factor (anti-VEGF) has made significant impact on the reduction of the visual loss due to neovascular age-related macular degeneration (n-AMD). There are significant inter-individual differences in response to an anti-VEGF agent, made more complex by the availability of multiple anti-VEGF agents with different molecular configurations. The response to anti-VEGF therapy have been found to be dependent on a variety of factors including patient's age, lesion characteristics, lesion duration, baseline visual acuity (VA) and the presence of particular genotype risk alleles. Furthermore, a proportion of eyes with n-AMD show a decline in acuity or morphology, despite therapy or require very frequent re-treatment. There is currently no consensus as to how to classify optimal response, or lack of it, with these therapies. There is, in particular, confusion over terms such as 'responder status' after treatment for n-AMD, 'tachyphylaxis' and 'recalcitrant' n-AMD. This document aims to provide a consensus on definition/categorisation of the response of n-AMD to anti-VEGF therapies and on the time points at which response to treatment should be determined. Primary response is best determined at 1 month following the last initiation dose, while maintained treatment (secondary) response is determined any time after the 4th visit. In a particular eye, secondary responses do not mirror and cannot be predicted from that in the primary phase. Morphological and functional responses to anti-VEGF treatments, do not necessarily correlate, and may be dissociated in an individual eye. Furthermore, there is a ceiling effect that can negate the currently used functional metrics such as >5 letters improvement when the baseline VA is good (ETDRS>70 letters). It is therefore important to use a combination of both the parameters in determining the response.The following are proposed definitions: optimal (good) response is defined as when there is resolution of fluid (intraretinal fluid; IRF, subretinal fluid; SRF and retinal thickening), and/or improvement of >5 letters, subject to the ceiling effect of good starting VA. Poor response is defined as <25% reduction from the baseline in the central retinal thickness (CRT), with persistent or new IRF, SRF or minimal or change in VA (that is, change in VA of 0+4 letters). Non-response is defined as an increase in fluid (IRF, SRF and CRT), or increasing haemorrhage compared with the baseline and/or loss of >5 letters compared with the baseline or best corrected vision subsequently. Poor or non-response to anti-VEGF may be due to clinical factors including suboptimal dosing than that required by a particular patient, increased dosing intervals, treatment initiation when disease is already at an advanced or chronic stage), cellular mechanisms, lesion type, genetic variation and potential tachyphylaxis); non-clinical factors including poor access to clinics or delayed appointments may also result in poor treatment outcomes. In eyes classified as good responders, treatment should be continued with the same agent when disease activity is present or reactivation occurs following temporary dose holding. In eyes that show partial response, treatment may be continued, although re-evaluation with further imaging may be required to exclude confounding factors. Where there is persistent, unchanging accumulated fluid following three consecutive injections at monthly intervals, treatment may be withheld temporarily, but recommenced with the same or alternative anti-VEGF if the fluid subsequently increases (lesion considered active). Poor or non-response to anti-VEGF treatments requires re-evaluation of diagnosis and if necessary switch to alternative therapies including other anti-VEGF agents and/or with photodynamic therapy (PDT). Idiopathic polypoidal choroidopathy may require treatment with PDT monotherapy or combination with anti-VEGF. A committee comprised of retinal specialists with experience of managing patients with n-AMD similar to that which developed the Royal College of Ophthalmologists Guidelines to Ranibizumab was assembled. Individual aspects of the guidelines were proposed by the committee lead (WMA) based on relevant reference to published evidence base following a search of Medline and circulated to all committee members for discussion before approval or modification. Each draft was modified according to feedback from committee members until unanimous approval was obtained in the final draft. A system for categorising the range of responsiveness of n-AMD lesions to anti-VEGF therapy is proposed. The proposal is based primarily on morphological criteria but functional criteria have been included. Recommendations have been made on when to consider discontinuation of therapy either because of success or futility. These guidelines should help clinical decision-making and may prevent over and/or undertreatment with anti-VEGF therapy.

Atypical retinopathy in patients with nephronophthisis type 1: an uncommon ophthalmological finding.

Progressive retinal degeneration without retinal pigmentation has been repeatedly observed in Korean nephronophthisis (NPHP) type 1 patients with a total homozygous deletion of NPHP1. Retrospective case series. Patients with clinical diagnosis of NPHP and genetic diagnosis of total deletion of NPHP1 (n = 5) were included in this study. Patients with clinical diagnosis of NPHP (n = 57) were screened for total deletion of NPHP1 by polymerase chain reaction (PCR) for the 20 exons of NPHP1. The clinical and ophthalmological findings of NPHP type 1 patients were reviewed. Additionally, four exons of MALL, a gene adjacent to NPHP1, were amplified using PCR, and amplification failure was considered a homozygous deletion encompassing the corresponding exons. Ophthalmological findings in NPHP type 1 patients. Five of 57 patients with clinical diagnosis of NPHP were diagnosed as having NPHP type 1 by genetic analysis. Chronic renal failure was diagnosed in these five patients at 7.9-15.4 years of age. All the patients with NPHP type 1 had progressive decline in visual acuity with various ages of onset (2-17 years). Ophthalmological examinations revealed unexpected findings of retinopathy with large or small flecks, which was compatible with Stargardt-like retinopathy or albipunctatus retinopathy in majority of them (four of five). The genetic study revealed an additional deletion of exon 1 of the adjacent gene MALL. We report the unexpectedly common retinal involvement of NPHP type 1 with an additional MALL deletion in a Korean cohort.

Neuromyelitis optica: a demyelinating disease

Neuromyelitis optica (NMO) also known as Devic’s disease is a demyelinating disease. It involves the central nervous system and predominantly affects the spinal cord and optic nerves. It is characterised by episodes of optic neuritis and/or transverse myelitis. It is often confused with multiple sclerosis. NMO can occur rarely in children but cases of pediatric NMO need specific consideration owing to possible poor visual and motor outcome. We report a case of nine year male child admitted with history of fever followed by sudden weakness of body, sudden decline in visual acuity and involuntary passage of urine. The symptoms were reverted after the use of methylprednisolone. Clinical outcome was favourable with disappearance of sphincter troubles, improvement of visual acuity and progressive disappearance of motor troubles.

A phytochemical-rich diet may explain the absence of age-related decline in visual acuity of Amazonian hunter-gatherers in Ecuador

Myopia is absent in undisturbed hunter-gatherers but ubiquitous in modern populations. The link between dietary phytochemicals and eye health is well established, although transition away from a wild diet has reduced phytochemical variety. We hypothesized that when larger quantities and greater variety of wild, seasonal phytochemicals are consumed in a food system, there will be a reduced prevalence of degenerative-based eye disease as measured by visual acuity. We compared food systems and visual acuity across isolated Amazonian Kawymeno Waorani hunter-gatherers and neighboring Kichwa subsistence agrarians, using dietary surveys, dietary pattern observation, and Snellen Illiterate E visual acuity examinations. Hunter-gatherers consumed more food species (130 vs. 63) and more wild plants (80 vs. 4) including 76 wild fruits, thereby obtaining larger variety and quantity of phytochemicals than agrarians. Visual acuity was inversely related to age only in agrarians (r = −.846, P < .001). As hypothesized, when stratified by age (<40 and ≥ 40 years), Mann-Whitney U tests revealed that hunter-gatherers maintained high visual acuity throughout life, whereas agrarian visual acuity declined (P values < .001); visual acuity of younger participants was high across the board, however, did not differ between groups (P > .05). This unusual absence of juvenile-onset vision problems may be related to local, organic, whole food diets of subsistence food systems isolated from modern food production. Our results suggest that intake of a wider variety of plant foods supplying necessary phytochemicals for eye health may help maintain visual acuity and prevent degenerative eye conditions as humans age.

Rate of vision loss in neovascular age-related macular degeneration explored.

To explore decline in visual acuity in patients with neovascular age-related macular degeneration (n-AMD) awaiting intravitreal bevacizumab or ranibizumab treatment following initial diagnosis and after disease reactivation. Retrospective analysis of 74 treatment-naïve patients (84 eyes) in two centers in Córdoba, Argentina. The time between treatment indication and intravitreal injection, and the changes in BCVA produced during this delay were studied in both periods. A linear regression model to search the impact of time on progression visual impairment was conducted. In both periods, a significant reduction in vision occurred awaiting intravitreal injection. The longer the delay, the greater the vision loss (R2 = 0.55 p < 0.01) and the less improvement following treatment (Pearson coefficient -0.26). The result of the model shows that the change in vision as a function of initial delay were best described by a polynomic model with a mean loss of 5 letters in the first 3 weeks, a slowdown in the rate of change of VA, and a dependence of visual acuity at the moment of diagnosis . The loss of visual acuity after reactivation shows the same behavior as at the onset of the disease but independent of visual acuity prior to reactivation. Visual loss awaiting injection intravitreal anti-VEGF is clinically significant and with an asymptotic pattern, with early rapid loss of vision in both the onset of the disease and the reactivation. Initiation of anti-VEGF treatment must be undertaken urgently, as should retreatment of disease activation to reduce visual loss.