To test the hypothesis that normal-tension glaucoma (NTG) is caused by an increased pressure difference across the lamina cribrosa (LC) related to a low intracranial pressure (ICP).
Prospective ...case-control study.
Thirteen NTG patients (9 women; median 71 range: 56-83 years) were recruited for investigation with the same protocol as 11 healthy volunteers (8 women; 47 30-59 years). A larger control group (n = 51; 30 women; 68 30-81 years) was used only for ICP comparison in supine position.
ICP and intraocular pressure (IOP) were simultaneously measured in supine, sitting, and 9° head-down tilt (HDT) positions. Trans-lamina cribrosa pressure difference (TLCPD) was calculated using ICP and IOP together with geometric distances estimated from magnetic resonance imaging to adjust for hydrostatic effects.
ICP, IOP, and TLCPD in different body positions.
Between NTG patients and healthy volunteers, there were no differences in ICP, IOP, or TLCPD in supine, sitting, or HDT (P ≥ 0.11), except for IOP in HDT (P = 0.04). There was no correlation between visual field defect and TLCPD, IOP, or ICP and in any body position (P ≥ 0.39). Mean ICP in supine was 10.3 mmHg (SD = 2.7) in the NTG group (n = 13) and 11.3 (2.2) mmHg in the larger control group (n = 51) (P = 0.24).
There was no evidence of reduced ICP in NTG patients as compared with healthy controls, either in supine or in upright position. Consequently, the hypothesis that NTG is caused by an elevated TLCPD from low ICP was not supported.
The purpose of this study was to examine the differences of optic nerve subarachnoid space (ONSAS) volume in patients with normal tension glaucoma (NTG) and healthy controls in different body ...positions.
Eight patients with NTG and seven healthy controls underwent magnetic resonance imaging (MRI) examinations in head up tilt (HUT) +11 degrees and head down tilt (HDT) -5 degrees positions according to a randomized protocol determining the starting position. The ONSAS volume in both body positions was measured and compared between the two groups. The results were analyzed using a generalized linear model.
Between HDT and HUT, the postural ONSAS volume change was dependent on starting position (P < 0.001) and group (P = 0.003, NTG versus healthy). A subgroup analysis of those that were randomized to HUT examination first, coming directly from an upright position, showed that the patients with NTG had significantly larger positional ONSAS volume changes compared to the healthy controls; 121 ± 22 µL vs. 65 ± 37 µL (P = 0.049). Analysis of the ONSAS volume distribution showed different profiles for patients with NTG and healthy controls.
There was a significant difference in ONSAS volume change between patients with NTG and healthy subjects when subjected to posture changes, specifically when going from upright to head-down posture. This indicates that patients with NTG had been exposed to a lower ONSAS pressure when they came from the upright posture, which suggests an increased translaminar pressure difference in upright position. This may support the theory that NTG has a dysfunction in an occlusion mechanism of the optic nerve sheath that could cause abnormally negative ONSAS pressures in upright posture.
Purpose of Review
A pressure difference between the intraocular and intracranial compartments at the site of the lamina cribrosa has been hypothesized to have a pathophysiological role in several ...optic nerve head diseases. This paper reviews the current literature on the translamina cribrosa pressure difference (TLCPD), the associated pressure gradient, and its potential pathophysiological role, as well as the methodology to assess TLCPD.
Recent Findings
For normal-tension glaucoma (NTG), initial studies indicated low intracranial pressure (ICP) while recent findings indicate that a reduced ICP is not mandatory.
Summary
Data from studies on the elevated TLCPD as a pathophysiological factor of NTG are equivocal. From the identification of potential postural effects on the cerebrospinal fluid (CSF) communication between the intracranial and retrolaminar space, we hypothesize that the missing link could be a dysfunction of an occlusion mechanism of the optic nerve sheath around the optic nerve. In upright posture, this could cause an elevated TLCPD even with normal ICP and we suggest that this should be investigated as a pathophysiological component in NTG patients.
Purpose
To evaluate the safety and efficacy of 1.5% dexamethasone nanoparticle (DexNP) drops in eyes with non‐infectious uveitic macular oedema and vitritis.
Methods
In a prospective pilot study, ...DexNP drops were administered four times a day for 4 weeks followed by drops tapering over a period of another 4 weeks. Follow‐up time was 12 weeks.
Results
Five eyes with macular oedema and three eyes with vitritis were included in the study. Best corrected visual acuity (BCVA) significantly improved from a median of 0.2 logMAR to a median of 0.15 logMAR at 4 weeks' time (p < 0.05). Median BCVA was 0.175 logMAR and 0.2 logMAR, at week 8 and 12, respectively (p > 0.05). Macular oedema significantly improved at all time‐points as compared to baseline (p < 0.05) and resolved in all eyes during follow‐up. One eye had macular oedema relapse at week 12. Vitritis improved in all eyes and resolved completely in two eyes. One eye had intraocular pressure (IOP) elevation which was well controlled with topical antihypertensive treatment, and one eye had cataract progression.
Conclusion
This short pilot study demonstrates favourable effect of 1.5% DexNP eye drops on eyes with non‐infectious uveitic macular oedema and vitritis. Further comparative long‐term studies are warranted to assess this effect.
Nicotinamide adenine dinucleotide (NAD) is a REDOX cofactor and metabolite essential for neuronal survival. Glaucoma is a common neurodegenerative disease in which neuronal levels of NAD decline. We ...assess the effects of nicotinamide (a precursor to NAD) on retinal ganglion cells (the affected neuron in glaucoma) in normal physiological conditions and across a range of glaucoma relevant insults including mitochondrial stress and axon degenerative insults. We demonstrate retinal ganglion cell somal, axonal, and dendritic neuroprotection by nicotinamide in rodent models which represent isolated ocular hypertensive, axon degenerative, and mitochondrial degenerative insults. We performed metabolomics enriched for small molecular weight metabolites for the retina, optic nerve, and superior colliculus which demonstrates that ocular hypertension induces widespread metabolic disruption, including consistent changes to α-ketoglutaric acid, creatine/creatinine, homocysteine, and glycerophosphocholine. This metabolic disruption is prevented by nicotinamide. Nicotinamide provides further neuroprotective effects by increasing oxidative phosphorylation, buffering and preventing metabolic stress, and increasing mitochondrial size and motility whilst simultaneously dampening action potential firing frequency. These data support continued determination of the utility of long-term nicotinamide treatment as a neuroprotective therapy for human glaucoma.
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•Nicotinamide is neuroprotective in cell and animal models that recapitulate isolated features of glaucoma.•Systemic nicotinamide administration has limited molecular side-effects on visual system tissue under basal conditions.•Nicotinamide provides a robust reversal in the disease metabolic profile of glaucomatous animals.•Nicotinamide increases oxidative phosphorylation, buffers and prevents metabolic stress, and increases mitochondrial size.
Purpose
To retrospectively evaluate the efficacy and safety of all transscleral cyclophotocoagulation (TCP) treatments performed during a 5‐year period.
Methods
Medical records of all patients, who ...had undergone TCP treatment between 2010 and 2014 at Umeå University Hospital, Sweden, were evaluated. Clinical data including intraocular pressure (IOP), visual acuity (VA), number of topical glaucoma medications, use of oral acetazolamide, retreatments and complications during a 2‐year follow‐up were registered. Global success was defined as IOP 6–18 mmHg with or without glaucoma medication.
Results
Three hundred patients underwent TCP during the time period. Mean IOP at baseline was 29.3 ± 11.0 (mean ± standard deviation) mmHg (n = 297) with a mean reduction of 11.5 (±12.0) mmHg at 1 year (n = 258; p < 0.001) and 12.6 (±12.0) mmHg at 2‐year follow‐up (n = 245; p < 0.001). Global success at 2 years was 64%, achieved by a mean of 1.2 treatments (n = 257). The number of topical glaucoma medications at baseline was 3.1 (±1.0; n = 296) and was reduced by 0.9 (±1.0) medications at 2 years (n = 244; p < 0.001). Use of oral acetazolamide decreased from 30% (n = 90) at baseline to 5.3% (n = 13) at 2 years. In eyes with Snellen VA ≥ 0.1, the mean VA at baseline was 0.55 (±0.3) logarithm of the minimum angle of resolution (logMAR; n = 132) and 1.1 (±0.9) logMAR (n = 76) at 2 years (p < 0.001). No cases of phthisis bulbi were found.
Conclusion
This study displays a substantial and long‐term reduction of IOP following TCP with a decrease in topical and oral glaucoma medications. The treatment appears to be safe but the decrease in VA during follow‐up is a concern that needs further evaluation.
iStent Inject implantation (iStent) or Kahook Dual Blade goniotomy (KDB) in combination with phacoemulsification have a similar IOP-lowering effect in all stages of glaucoma, and medications are ...significantly reduced, especially after KDB.
To compare the 2-year efficacy and safety of iStent or KDB in combination with phacoemulsification in eyes with mild to advanced open angle glaucoma.
A retrospective chart review of 153 patients that received iStent or KDB in combination with phacoemulsification at a single center between March 2019 and August 2020. The main outcome parameters at 2 years were: (1) intraocular pressure (IOP)-reduction ≥20%, with a postoperative IOP ≤18 mm Hg, and (2) a reduction of ≥1 medication. Results were stratified by glaucoma grade.
After 2 years, mean IOP was reduced from 20.3±6.1 to 14.2±4.1 mm Hg in the phaco-iStent group (P<0.001) and from 20.1±6.1 to 14.7±3.6 mm Hg in the phaco-KDB group (P<0.001). The mean number of medications was reduced from 3.0±0.9 to 2.6±1.1 in the Phaco-iStent group (P=0.001) and from 2.3±1.0 to 1.5±1.3 in the Phaco-KDB group (P<0.001). Success regarding IOP-reduction ≥20% with a postoperative IOP ≤18 mm Hg was met by 46% in the phaco-iStent group and by 51% in the phaco-KDB group. A reduction of ≥1 medication was met by 32% in the phaco-iStent group and by 53% in the phaco-KDB group (P=0.013). Eyes with mild to moderate and advanced glaucoma responded equally well to the success criteria.
iStent and KDB, in combination with phacoemulsification, both lowered IOP effectively in all stages of glaucoma. More medications were reduced after KDB, suggesting that it may be a more effective procedure compared with iStent.
To investigate if decrease of IOP affects the volumetric blood flow rate in the ophthalmic artery (OA) in patients with previously untreated ocular hypertension.
Subjects with untreated ocular ...hypertension (n = 30; mean age 67 ± 8 years; 14 females) underwent ophthalmologic examination and a 3-Tesla magnetic resonance imaging investigation. The magnetic resonance imaging included three-dimensional high-resolution phase-contrast magnetic resonance imaging to measure the OA blood flow rate. The subjects received latanoprost once daily in the eye with higher pressure, the untreated eye served as control. The same measurements were repeated approximately 1 week later.
The mean OA blood flow rate before and after treatment was 12.4 ± 4.4 and 12.4 ± 4.6 mL/min in the treated eye (mean ± SD; P = 0.92) and 13.5 ± 5.2 and 13.4 ± 4.1 mL/min in the control eye (P = 0.92). There was no significant difference between the treated and control eye regarding blood flow rate before (P = 0.13) or after treatment (P = 0.18), or change in blood flow rate after treatment (0.1 ± 3.1 vs. -0.1 ± 4.0 mL/min, P = 0.84). Latanoprost decreased the IOP by 7.2 ± 3.1 mm Hg in the treated eye (P < 0.01).
The results indicate that a significant lowering of IOP does not affect the blood flow rate of the OA in ocular hypertension subjects. The ability to maintain blood supply to the eye independent of the IOP could be a protective mechanism in preserving vision in subjects with ocular hypertension.
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