Importance of circulating platelet aggregates and haemodynamic changes in ophthalmic artery and progression of visual field loss at pseudoexfoliation glaucoma

The aim of this work is to examine the role of circulating platelet aggregates (CPA) at pseudoexfoliation glaucoma (PXG), haemodynamic changes in the ophthalmic artery by ultrasonic color Doppler, searching for visual field progression. Vascular component at PXG and its role in VF progression dynamics has not been sufficiently explained, as well as CPA influence to ischaemic events related to optic nerve damage and VF progression. The examination included 80 patients, where of 35 (44%) men average age 68.3 +/- 7.0 and 45 (56%) women average age 65.7 +/- 7.0 (t = 1.66; p = 0.101). Forthy of them suffered from primary open angle glaucoma (POAG) as a control group (healthy), and 40 from pseudoexfoliative glaucoma (PXG) as an experimental group. All the examinees underwent complete ophthalmological examination: visual acuity, ocular fundus, intraocular pressure measured, anterior eye segment biomicroscopy with gonioscopy performed. Also VF examination was performed three times at 6 months intervals. Laboratory testing of CPA proportion values was performed by means of Wu an Hoak method and ultrasonic measurement of blood perfusion in the carotid tree, particularly concerning ophthalmic artery by means of color Doppler. Obtained decreased values of CPA proportion resulted in hypercoagulability of blood in PXG group. At PXG were also found increased blood flow resistivity indexes in ophthalmic artery (RI AO) and internal carotid artery (RI ACI), resulting with ischemia and hypoxia and finally progression of the visual filed damage. In conclusion, our study shows that examining CPA and ultrasonic monitoring of vascular parameters in ophthalmic artery with color Doppler may be the way of better understanding the vascular role in PXG prognosis.     

Selective laser trabeculoplasty in the treatment of pseudoexfoliation glaucoma in patients allergic to all anti-glaucoma drops

Secondary chronic open-angle glaucoma associated with pseudoexfoliation (PEX) syndrome accounts for approximately 25% of all glaucomas and represents the most common identifiable cause of glaucoma overall. Selective laser trabeculoplasty (SLT) is effective in reducing intraocular pressure (IOP) in glaucomatous patients and has the advantage of preserving surrounding structures. We report here SLT treatment of a 82 year old female with a secondary developed open-angle pseudoexfoliation glaucoma allergic to all anti glaucoma eye drops especially those which contain bensalconium chloridum as preservative. Since patient was allergic also to methyl-cellulose, we performed SLT with water as a mediator. Patient had PEX syndrome for 10 years, immature cataracts on both eyes, and best corrected visual acuity (BCVA) 0.7 on the right and 0.2 on the left eye. We have monitored intraocular pressure (IOP), the changes in the visual field and optic nerve. Preoperative IOP was 28 mmHg on the right and 30 mmHg on the left eye. The follow up period was 24 months with time points for measured parameters every 3 months. After 18 months IOP remained in the normal values (average 17 mmHg) on the right eye, but on the left eye it increased up to 28 mmHg. SLT re-treatment was carried out on the left eye and the IOP stabilized again on the values between 16-18mmHg. There were no significant change in the visual field and optic nerve configuration before and after SLT (C/D value for right eye: 0.3-0.4; C/D left eye: 0.5). Based on this case report, SLT seems to be very effective treatment for maintaining regular IOP in patient with PEX who is allergic to all types of medications.     

Pseudoexfoliative syndrome and pseudoexfoliative glaucoma in Primorsko-Goranska County

The aim of this study is to evaluate pseudoexfoliative glaucoma (PEX) in Primorsko-Goranska County, Croatia, and its characteristics comparing to primary open angle glaucoma (POAG). In the study a hundred patients with open angle glaucoma were examined, twenty six of them had a pseudoexfoliative glaucoma diagnosed. We were following intraocular pressure (IOP) values, visual acuities, visual fields and optical nerve head changes retrospectively. Comparing to primary open angle glaucoma pseudoexfoliative glaucoma in Primorsko-Goranska County has less good prognosis because the IOP is usually higher and more difficult to control, we found progressive loss of retinal ganglion cells and visual field loss develop more rapidly. Because of that pseudoexfoliative glaucoma requires special treatment and following.     

马来酸噻吗洛尔联合拉坦前列腺素治疗高眼压型开角型青光眼的效果

目的:探讨马来酸噻吗洛尔联合拉坦前列腺素治疗高眼压型开角型青光眼的临床效果。方法:选取高眼压型开角型青光眼患者210例,随机分为治疗组和对照组,每组各105例。对照组患者给予马来酸噻吗洛尔治疗,治疗组患者给予马来酸噻吗洛尔联合拉坦前列腺素治疗。观察并比较两组患者治疗前后视力改善情况,眼压、视乳头杯盘比值变化情况,眼结膜充血、眼内干涩、角膜点状浸润以及一过性视觉模糊等不良反应的发生情况等。结果:治疗组患者视力改善率为85.7%,对照组为71.4%,治疗组高于对照组,差异具有统计学意义(P0.05);治疗后两组患者眼压、视乳头杯盘比值均明显下降,且治疗组明显低于对照组,差异具有统计学意义(P0.05)。治疗组患者眼结膜充血、眼内干涩、角膜点状浸润以及一过性视觉模糊等不良反应明显低于对照组,差异具有统计学意义(P0.05)。结论:马来酸噻吗洛尔联合拉坦前列腺素治疗高眼压型开角型青光眼能够改善患者视力水平,值得临床推广应用。此外,我们分析其作用可能与降低视乳头杯盘比值有关。     

Blindness and Glaucoma: A Multicenter Data Review from 7 Academic Eye Clinics

PurposeTo evaluate frequency, conversion rate, and risk factors for blindness in glaucoma patients treated in European Universities.MethodsThis multicenter retrospective study included 2402 consecutive patients with glaucoma in at least one eye. Medical charts were inspected and patients were divided into those blind and the remainder (‘controls’). Blindness was defined as visual acuity≤0.05 and/or visual field loss to less than 10°.ResultsUnilateral and bilateral blindness were respectively 11.0% and 1.6% at the beginning, and 15.5% and 3.6% at the end of the observation period (7.5±5.5 years, range:1–25 years); conversion to blindness (at least unilateral) was 1.1%/year. 134 eyes (97 patients) developed blindness by POAG during the study. At the first access to study centre, they had mean deviation (MD) of -17.1±8.3 dB and treated intraocular pressure (IOP) of 17.1±6.6 mmHg. During follow-up the IOP decreased by 14% in these eyes but MD deteriorated by 1.1±3.5 dB/year, which was 5-fold higher than controls (0.2±1.6 dB/year). In a multivariate model, the best predictors for blindness by glaucoma were initial MD (p<0.001), initial IOP (p<0.001), older age at the beginning of follow-up (p<0.001), whereas final IOP was found to be protective (p<0.05).ConclusionsIn this series of patients, blindness occurred in about 20%. Blindness by glaucoma had 2 characteristics: late diagnosis and/or late referral, and progression of the disease despite in most cases IOP was within the range of normality and target IOP was achieved; it could be predicted by high initial MD, high initial IOP, and old age.     

Mutant myocilin nonsecretion in vivo is not sufficient to cause glaucoma

Glaucoma is a leading cause of blindness, affecting over 70 million people worldwide. Vision loss is the result of death of the retinal ganglion cells. The best-known risk factor for glaucoma is an elevated intraocular pressure (IOP); however, factors leading to IOP elevation are poorly understood. Mutations in the MYOC gene are an important cause of open-angle glaucoma. Over 70 MYOC mutations have been identified, and they lead to approximately 5% of all primary open-angle glaucoma cases. Nevertheless, the pathogenic mechanisms by which these mutations elevate IOP are presently unclear. Data suggest that a dominant interfering effect of misfolded mutant MYOC molecules may be pathogenic. To test this hypothesis, we have generated mice carrying a mutant allele of Myoc that is analogous to a human mutation that leads to aggressive glaucoma in patients. We show that mutant MYOC is not secreted into the aqueous humor. Instead of being secreted, mutant MYOC accumulates within the iridocorneal angle of the eye, consistent with the behavior of abnormally folded protein. Surprisingly, the accumulated mutant protein does not activate the unfolded protein response and lead to elevated intraocular pressure or glaucoma in aged mice of different strains. These data suggest that production, apparent misfolding, and nonsecretion of mutant MYOC are not, by themselves, sufficient to cause glaucoma in vivo.     

Aldosterone: a mediator of retinal ganglion cell death and the potential role in the pathogenesis in normal-tension glaucoma

Glaucoma is conventionally defined as a chronic optic neuropathy characterized by progressive loss of retinal ganglion cells (RGCs) and optic nerve fibers. Although glaucoma is often associated with elevated intraocular pressure (IOP), significant IOP reduction does not prevent progression of the disease in some glaucoma patients. Thus, exploring IOP-independent mechanisms of RGC loss is important. We describe chronic systemic administration of aldosterone and evaluate its effect on RGCs in rat. Aldosterone was administered via an osmotic minipump that was implanted subcutaneously into the mid-scapular region. Although systemic administration of aldosterone caused RGC loss associated with thinning of the retinal nerve fiber layer without elevated IOP, the other cell layers appeared to be unaffected. After chronic administration of aldosterone, RGC loss was observed at 2 weeks in the peripheral retina and at 4 weeks in the central retina. However, administration of mineralocorticoid receptor blocker prevented RGC loss. These results demonstrate aldosterone is a critical mediator of RGC loss that is independent of IOP. We believe this rat normal-tension glaucoma (NTG) animal model not only offers a powerful system for investigating the mechanism of neurodegeneration in NTG, but can also be used to develop therapies directed at IOP-independent mechanisms of RGC loss.     

Evaluation of the intraocular pressure-reducing effect of latanoprost as monotherapy in open-angle glaucoma

Objective of this study was to evaluate the intraocular pressure-reducing effect of latanoprost as monotherapy after replacing current dual therapy in glaucoma patients. The 6-months study comprised 189 patients with primary open angle glaucoma who were treated at least 6 months with two different kind of topical medications (beta-blockers, pilocarpine, dorzolamide and brimonidine). Due to local side effects, multiple dosing regime and inadequately controlled intraocular pressure (IOP), they where switched to latanoprost 0.005% monotherapy. After switched to latanoprost, mean (IOP) was measured at baseline, after 15 days, 2 and 6 months of treatment. After six-months 178 patients had completed the study. These analyses enrolled all patients (n = 189), thus, the Intention-To-Treat (ITT) results were shown instead of the results of the reduced population. IOP was clinically importantly reduced from baseline level. Five patients had uncontrolled IOP. The difference between IOP before (21.9 +/- 2.4) and after 15 days (17.4 +/- 1.7), 2 months (16.7 +/- 1.8) and 6 months (16.6 +/- 1.4) was statistically significant (p < 0.001). 90% patients has reached target IOP < or = 18 mm. A conjunctional hyperaemia in 18 (9%), stinging and itching in 7 (4%) patients was reported. Increased iris pigmentation was seen in 3 (2%) patients. The results of this study indicate that dual therapy in open-angle glaucoma can effectively be replaced by latanoprost monotherapy in many patients.     

Genetically increasing Myoc expression supports a necessary pathologic role of abnormal proteins in glaucoma

Despite the importance of MYOC for glaucoma, the protein's normal function(s) and the pathogenic mechanism(s) of MYOC mutations are not clear. Elevated intraocular pressure (IOP) and glaucoma are sometimes induced by corticosteroids, and corticosteroid use can result in substantially increased MYOC expression. It has been suggested, therefore, that steroid-induced MYOC protein levels cause steroid-induced glaucoma and that protein level-increasing mutations in MYOC contribute to glaucoma not associated with steroid use. A causative role of elevated MYOC levels in steroid-induced glaucoma is controversial, however, and it is not clear if elevated MYOC levels can result in IOP elevation. To directly test if increased levels of MYOC can cause IOP elevation and glaucoma, we generated bacterial artificial chromosome transgenic mice that overexpress Myoc at a level similar to that induced by corticosteroid use. These mice do not develop elevated IOP or glaucoma. Our present findings, along with the absence of glaucoma in mice completely lacking MYOC, show that changing the level of MYOC is not pathogenic (from absent to approximately 15 times normal). These findings suggest that noncoding sequence variants are unlikely to influence glaucoma and that disease pathogenesis in primary open-angle glaucoma patients is dependent upon the expression of abnormal mutant proteins. This work does not support a causative role for increased MYOC levels or the MYOC gene in steroid-induced glaucoma.     

Apolipoprotein E-promoter single-nucleotide polymorphisms affect the phenotype of primary open-angle glaucoma and demonstrate interaction with the myocilin gene

Primary open-angle glaucoma (POAG) is an optic neuropathy that has a high worldwide prevalence and that shows strong evidence of complex inheritance. The myocilin (MYOC) gene is the only one that has thus far been shown to have mutations in patients with POAG. Apolipoprotein E (APOE) plays an essential role in lipid metabolism, and the APOE gene has been involved in neuronal degeneration that occurs in Alzheimer disease (AD). Here, we report that two APOE-promoter single-nucleotide polymorphisms (SNPs) previously associated with AD also modify the POAG phenotype. APOE(-219G) is associated with increased optic nerve damage, as reflected by increased cup:disk ratio and visual field alteration. In addition, APOE(-491T), interacting at a highly significant level with an SNP in the MYOC promoter, MYOC(-1000G), is associated with increased intraocular pressure (IOP) and with limited effectiveness of IOP-lowering treatments in patients with POAG. Together, these findings establish APOE as a potent modifier for POAG, which could explain the linkage to chromosome 19q previously observed by use of a genome scan for this condition and an increased frequency of glaucoma in patients with AD. The findings also shed new light on potential mechanisms of optic nerve damage and of IOP regulation in POAG.     

Effect of latanoprost on intraocular pressure,visual acuity and C-reactive protein

ObjectiveTo investigate the effect of latanoprost on intraocular pressure (IOP), visual acuity and C-reactive protein (CRP) in patients with primary open-angle glaucoma (POAG).MethodsA total of 163 POAG patients (266 eyes) admitted to our hospital from February 2015 to July 2017 were selected and divided into observation group (81 cases, 132 eyes, latanoprost eye drops) and control group (82 cases, 134 eyes, timolol maleate eye drops) according to different treatment plans. The clinical efficacy of the two groups after treatment was evaluated. The IOP, visual acuity and CRP level were compared between the two groups before and after treatment. Then the adverse reactions of the two groups were observed and recorded.ResultsAfter treatment, the total effective rate was 92.59% (75 cases) in the observation group and was 80.49% (66 cases) in the control group, with statistic difference between groups (P < 0.05); The IOP, visual acuity and CRP level between the two groups before treatment showed no statistic difference, the mentioned three indexes of the two groups were significantly improved after treatment, and statistic difference was found before and after treatment (P < 0.05); Moreover, the above three indicators had statistically significant differences between groups after treatment (P < 0.05); The difference of intraocular pressure and visual acuity between the two groups before and after treatment were statistically different (P < 0.05); After treatment, the incidence of adverse reactions in the observation group such as allergy, vomiting, breathlessness and tachycardia were not significantly different from those in the control group (P > 0.05).ConclusionLatanoprost can improve IOP, visual acuity, and CRP levels. It improves eye hemodynamics, and has significant efficacy in treating primary open-angle glaucoma. Also, it has good security.     

Clinical experience with Ex-press Mini Glaucoma Shunt implantation

In this prospective study we wanted to report our experience and to evaluate the efficacy and safety of Ex-press Mini-Glaucoma Shunt implantation under a superficial scleral flap, as a newly and improved surgical technology in a treatment of POAG (Primary open-angle glaucoma) and refractory glaucoma. 44 eyes (35 patients) underwent an implantation of Ex-Press Mini Glaucoma Shunt. We had 21 patients with POAG (60%) and 14 patients with PEXG-pseudoexfoliation glaucoma (40%). The follow-up period was 8.62 + 7.48 months (range 2-22 months). Main outcome measures included postoperative IOP control, postoperative medications and early postoperative complications. The IOP was measured in the following postoperative time-points of 1 day, 1 week, 1, 3, 6, 9 and 12 months. The mean IOP values 1 year postoperatively were reduced for 52.8% compared to preoperative values and the use of medications were reduced for 77%. We had complications like postoperative hypotony (3.5%), choroidal ablation (7%), intraocular hemorrhage (3.5%) and postoperative shunt closure (3.5%). The Ex PRESS Mini Glaucoma Shunt implanted under a superficial scleral flap is relatively safe and effective surgical procedure and provides satisfactory IOP control and medication reduction. However, device related complications remain still a problem.     

Glaucoma and optic nerve repair

Glaucoma is a leading cause of irreversible blindness worldwide and causes progressive visual impairment attributable to the dysfunction and death of retinal ganglion cells (RGCs). Progression of visual field damage is slow and typically painless. Thus, glaucoma is often diagnosed after a substantial percentage of RGCs has been damaged. To date, clinical interventions are mainly restricted to the reduction of intraocular pressure (IOP), one of the major risk factors for this disease. However, the lowering of IOP is often insufficient to halt or reverse the progress of visual loss, underlining the need for the development of alternative treatment strategies. Several lines of evidence suggest that axonal damage of RGCs occurs primary at the optic nerve head, where axons appear to be most vulnerable. Axonal injury leads to the functional loss of RGCs and subsequently induces the death of the neurons. However, the detailed molecular mechanism(s) underlying IOP-induced optic nerve injury remain poorly understood. Moreover, whether glaucoma pathophysiology is primarily axonal, glial, or vascular remains unclear. Therefore, protective strategies to prevent further axonal and subsequent soma degeneration are of great importance to limit the progression of sight loss. In addition, strategies that stimulate injured RGCs to regenerate and reconnect axons with their central targets are necessary for functional restoration. The present review provides an overview of the context of glaucoma pathogenesis and surveys recent findings regarding potential strategies for axonal regeneration of RGCs and optic nerve repair, focusing on the role of cytokines and their downstream signaling pathways.     

Mathematical modeling of the biomechanics of the lamina cribrosa under elevated intraocular pressures

Comprehensive understanding of the biomechanical performance of the lamina cribrosa (LC) and the optic nerve head is central to understanding the role of elevated intraocular pressures (IOP) in chronic open angle glaucoma. In this paper, six closed-from mathematical models based on different idealizations of the LC are developed and compared. This approach is used to create further understanding of the biomechanical behavior by identifying the LC features and properties that have a significant effect on its performance under elevated IOP. The models developed are based on thin circular plate and membrane theories, and consider influences such as in-plane pretension caused by scleral expansion and large deflections. Comparing the results of the six models against a full ocular globe finite element model suggests the significance of the in-plane pretension and the importance of assuming that the sclera provides the LC with a clamped edge. The model that provided the most accurate representation of the finite element model was also used to predict the behavior of a number of LC experimental tests presented in the literature. In addition to the deflections under elevated IOP, the model predictions include the distributions of stress and strain, which are shown to be compatible with the progression of visual field loss experienced in glaucoma.     

Changes of intraocular pressure in patients with open-angle glaucoma in relation to the passage of atmospheric fronts and environmental contamination

Effects of atmospheric frontal passages on intraocular pressure (IOP) in patients with open-angle glaucoma are statistically investigated to show the meteorotropism of this disease. Changes in IOP caused by frontal passages are evident; the response is not identical in all the patients near the day of the passage of a warm front, while on the third day following the passage of the front a well pronounced drop in IOP occurs. Anomalous increases of IOP over several months' duration occurred in the years 1986–7. This finding is explained in relation to the hypothesis of environmental contamination in Central Europe by radioactive cesium nuclides due to the Chernobyl accident.     

Structural and functional neuroprotection in glaucoma: role of galantamine-mediated activation of muscarinic acetylcholine receptors

Glaucoma is the leading cause of irreversible blindness worldwide. Loss of vision due to glaucoma is caused by the selective death of retinal ganglion cells (RGCs). Treatments for glaucoma, limited to drugs or surgery to lower intraocular pressure (IOP), are insufficient. Therefore, a pressing medical need exists for more effective therapies to prevent vision loss in glaucoma patients. In this in vivo study, we demonstrate that systemic administration of galantamine, an acetylcholinesterase inhibitor, promotes protection of RGC soma and axons in a rat glaucoma model. Functional deficits caused by high IOP, assessed by recording visual evoked potentials from the superior colliculus, were improved by galantamine. These effects were not related to a reduction in IOP because galantamine did not change the pressure in glaucomatous eyes and it promoted neuronal survival after optic nerve axotomy, a pressure-independent model of RGC death. Importantly, we demonstrate that galantamine-induced ganglion cell survival occurred by activation of types M1 and M4 muscarinic acetylcholine receptors, while nicotinic receptors were not involved. These data provide the first evidence of the clinical potential of galantamine as neuroprotectant for glaucoma and other optic neuropathies, and identify muscarinic receptors as potential therapeutic targets for preventing vision loss in these blinding diseases.     

Autotaxin-lysophosphatidic Acid axis is a novel molecular target for lowering intraocular pressure

Primary open-angle glaucoma is the second leading cause of blindness in the United States and is commonly associated with elevated intraocular pressure (IOP) resulting from diminished aqueous humor (AH) drainage through the trabecular pathway. Developing effective therapies for increased IOP in glaucoma patients requires identification and characterization of molecular mechanisms that regulate IOP and AH outflow. This study describes the identification and role of autotaxin (ATX), a secretory protein and a major source for extracellular lysophosphatidic acid (LPA), in regulation of IOP in a rabbit model. Quantitative proteomics analysis identified ATX as an abundant protein in both human AH derived from non-glaucoma subjects and in AH from different animal species. The lysophospholipase D (LysoPLD) activity of ATX was found to be significantly elevated (by ∼1.8 fold; n = 20) in AH derived from human primary open angle glaucoma patients as compared to AH derived from age-matched cataract control patients. Immunoblotting analysis of conditioned media derived from primary cultures of human trabecular meshwork (HTM) cells has confirmed secretion of ATX and the ability of cyclic mechanical stretch of TM cells to increase the levels of secreted ATX. Topical application of a small molecular chemical inhibitor of ATX (S32826), which inhibited AH LysoPLD activity in vitro (by >90%), led to a dose-dependent and significant decrease of IOP in Dutch-Belted rabbits. Single intracameral injection of S32826 (∼2 µM) led to significant reduction of IOP in rabbits, with the ocular hypotensive response lasting for more than 48 hrs. Suppression of ATX expression in HTM cells using small-interfering RNA (siRNA) caused a decrease in actin stress fibers and myosin light chain phosphorylation. Collectively, these observations indicate that the ATX-LPA axis represents a potential therapeutic target for lowering IOP in glaucoma patients.     

Rescue of Retinal Function by BDNF in a Mouse Model of Glaucoma

Vision loss in glaucoma is caused by progressive dysfunction of retinal ganglion cells (RGCs) and optic nerve atrophy. Here, we investigated the effectiveness of BDNF treatment to preserve vision in a glaucoma experimental model. As an established experimental model, we used the DBA/2J mouse, which develops chronic intraocular pressure (IOP) elevation that mimics primary open-angle glaucoma (POAG). IOP was measured at different ages in DBA/2J mice. Visual function was monitored using the steady-state Pattern Electroretinogram (P-ERG) and visual cortical evoked potentials (VEP). RGC alterations were assessed using Brn3 immunolabeling, and confocal microscope analysis. Human recombinant BDNF was dissolved in physiological solution (0.9% NaCl); the effects of repeated intravitreal injections and topical eye BDNF applications were independently evaluated in DBA/2J mice with ocular hypertension. BDNF level was measured in retinal homogenate by ELISA and western blot. We found a progressive decline of P-ERG and VEP responses in DBA/2J mice between 4 and 7 months of age, in relationship with the development of ocular hypertension and the reduction of Brn3 immunopositive RGCs. Conversely, repeated intravitreal injections (BDNF concentration = 2 µg/µl, volume = 1 µl, for each injection; 1 injection every four days, three injections over two weeks) and topical eye application of BDNF eye-drops (12 µg/µl, 5 µl eye-drop every 48 h for two weeks) were able to rescue visual responses in 7 month DBA/2J mice. In particular, BDNF topical eye treatment recovered P-ERG and VEP impairment increasing the number of Brn3 immunopositive RGCs. We showed that BDNF effects were independent of IOP reduction. Thus, topical eye treatment with BDNF represents a promisingly safe and feasible strategy to preserve visual function and diminish RGC vulnerability to ocular hypertension.     

Intraocular Pressure Rise in Subjects with and without Glaucoma during Four Common Yoga Positions

Purpose

To measure changes in intraocular pressure (IOP) in association with yoga exercises with a head-down position.

Methods

The single Center, prospective, observational study included 10 subjects with primary open-angle glaucoma and 10 normal individuals, who performed the yoga exercises of Adho Mukha Svanasana, Uttanasana, Halasana and Viparita Karani for two minutes each. IOP was measured by pneumatonometry at baseline and during and after the exercises.

Results

All yoga poses were associated with a significant (P<0.01) rise in IOP within one minute after assuming the yoga position. The highest IOP increase (P<0.01) was measured in the Adho Mukha Svanasana position (IOP increase from 17±3.2 mmHg to 28±3.8 mmHg in glaucoma patients; from 17±2.8 mmHg to 29±3.9 mmHg in normal individuals), followed by the Uttanasana position (17±3.9 mmHg to 27±3.4 mmHg (glaucoma patients) and from 18±2.5 mmHg to 26±3.6 mmHg normal individuals)), the Halasana position (18±2.8 mmHg to 24±3.5 mmHg (glaucoma patients); 18±2.7 mmHg to 22±3.4 mmHg (normal individuals)), and finally the Viparita Kirani position (17±4 mmHg to 21±3.6 mmHg (glaucoma patients); 17±2.8 to 21±2.4 mmHg (normal individuals)). IOP dropped back to baseline values within two minutes after returning to a sitting position. Overall, IOP rise was not significantly different between glaucoma and normal subjects (P = 0.813), all though glaucoma eyes tended to have measurements 2 mm Hg higher on average.

Conclusions

Yoga exercises with head-down positions were associated with a rapid rise in IOP in glaucoma and healthy eyes. IOP returned to baseline values within 2 minutes. Future studies are warranted addressing whether yoga exercise associated IOP changes are associated with similar changes in cerebrospinal fluid pressure and whether they increase the risk of glaucoma progression.

Trial Registration

ClinicalTrials.gov #{"type":"clinical-trial","attrs":{"text":"NCT01915680","term_id":"NCT01915680"}}NCT01915680