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Nutritional Optic Neuropathy
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
William Sultan, Giulia Amore, Uchenna Francis Nwako, Stacey Aquino Cohitmingao, Samuel Asanad, Alfredo Sadun
Normal tension glaucoma shares similar insidious and bilateral visual acuity loss, although arcuate visual field defects, excavation of the inferior rim and inferior optic nerve thinning may help differentiate it from NON. Multiple studies show an association between OPA1 polymorphisms and normal tension glaucoma.
Medical and Mathematical Background
Published in Arwa Ahmed Gasm Elseid, Alnazier Osman Mohammed Hamza, Computer-Aided Glaucoma Diagnosis System, 2020
Arwa Ahmed Gasm Elseid, Alnazier Osman Mohammed Hamza
Eye doctors usually use several tests to detect glaucoma. These are usually categorized as functional or image-based assessments. Functional assessment includes measurement of IOP (tonometry) and visual field examination. Image-based evaluation relies on optic nerve head imaging devices to determine optic nerve head structural damage or thinning of the retinal nerve fiber layer (RNFL). Examples of such imaging devices are Retinal Fundus Camera, Heidelberg Retinal Tomography (HRT), and Optical Coherence Tomography (OCT). Nonetheless, most of these methods have their own limitations. Measurement of IOP was reported to have a poor sensitivity of around 50% (Sommer et al., 1991). This is partially due to cases of normal tension glaucoma, where patients have a condition in which optic nerve damage and vision loss have developed even with a normal pressure inside the eye. The visual field examination is often time-consuming and found to be unreliable due to factors such as the patient’s fatigue and learning effects. Image-based evaluation using HRT and OCT are highly costly and are usually only available at tertiary hospitals, thus limiting its outreach.
How to master MCQs
Published in Chung Nen Chua, Li Wern Voon, Siddhartha Goel, Ophthalmology Fact Fixer, 2017
By definition, normal tension glaucoma is diagnosed after excluding other causes. Optic nerve meningioma causes compressive optic neuropathy. Brain scan seldom reveals a cause in most cases of normal tension glaucoma. A dense paracentral scotoma encroaching upon fixation is a common finding. Although betaxolol has been shown to be neuroprotective in animal models, there has been no convincing evidence which proves its use in delaying progression in normal tension glaucoma. The Collaborative Normal Tension Glaucoma Study found that reducing IOP by greater than 30% delayed the rate of visual field progression.
Seasonal variation in neurohormones, mood and sleep in patients with primary open angle glaucoma – implications of the ipRGC-system
Published in Chronobiology International, 2021
Helle Østergaard Madsen, Ida Hageman, Miriam Kolko, Henrik Lund-Andersen, Klaus Martiny, Shakoor Ba-Ali
We included 24 outpatients with POAG and 24 age- (± 3 years) and sex-matched control individuals. All participants returned for follow-up, including saliva sampling and questionnaires and 16/24 glaucoma patients and 20/24 controls provided valid pupillometric assessments in both seasons. At follow-up, one POAG participant had undergone local surgery for a malignant melanoma and one control participant had undergone cardiac bypass surgery. One control participant presented with possible glaucomatous optic nerve head changes, normal IOP and a discrete visual field defect (2 dB). The participant was diagnosed with early normal tension glaucoma after referral to the glaucoma clinic. The removal of the data from this participant did not alter the results, and the data were thus maintained in the analysis. The cortisol data from one control participant with abnormally high cortisol levels across the 24-h period were not included. Sensitivity analysis with the removal of the melatonin data from this participant revealed no changes to the results, and they were therefore maintained in the analysis.
Balancing treatments for patients with systemic hypertension and glaucoma
Published in Expert Opinion on Pharmacotherapy, 2020
Aakriti G. Shukla, Reza Razeghinejad, Jonathan S. Myers
The treatment of patients with normal tension glaucoma remains one of the most challenging aspects of glaucoma management. Treatment becomes incrementally more challenging for those with systemic hypertension. After first-line agents (as described above) have been exhausted, second and third-line therapies can be tried. If vasospasm seems to be a prevailing component, with associated migraines, disc hemorrhages, or Raynaud’s phenomenon, consider avoiding beta blockers to prevent potential IOP-independent mechanisms from contributing to glaucoma progression[53]. The concern for reduced nocturnal perfusion is often higher in this group, and this would suggest avoiding oral antihypertensive medications at bedtime. However, the recent Hygia trial suggests that the systemic risks associated with this approach may outweigh the potential ocular benefits[62]. Furthermore, we do not recommend management with non-evidence-based treatments such as salt-loading, which has been advocated to elevate nocturnal blood pressure in settings where overnight ocular perfusion is a concern. Finally, our group does not feel that the evidence for a vascular pathogenesis of glaucoma development and progression is adequate to change blood pressure targets for individuals with systemic hypertension and glaucoma.
Bilaminar Mechanics of the Human Optic Nerve Sheath
Published in Current Eye Research, 2020
Andrew Shin, Joseph Park, Alan Le, Vadims Poukens, Joseph L. Demer
The biomechanical properties of the human ON sheath are important to understanding of the mechanical loads on the ON and its critical juncture with the globe at the elastic fiber ring that borders the lamina cribrosa (LC).42 Finite element models of this mechanical behavior were first developed to clarify the effects of IOP and intracranial pressure on the LC and surrounding ocular tissues,43,44 but have recently been expanded to include effects of eye movements.14,22,45 Since MRI demonstrates that the ON and sheath exhaust their redundancy and tether the globe against the MR muscle in adduction exceeding about 26º1 in a manner that correlates with OCT evidence of peripapillary deformation,22,46,47 ON sheath mechanical behavior has become of particular interest. It has recently been proposed that eye movement, particularly adduction, may produce repetitive strain injury to the ON and thus constitute an IOP-independent mechanism of optic neuropathy in glaucoma.3,22 This has been proposed to be a major contributor to so-called “normal tension glaucoma” that now represents the most prevalent form of primary open angle glaucoma worldwide.3