Ocular Blood Flow and Normal Tension Glaucoma

Normal tension glaucoma (NTG) is known as a multifactorial optic neuropathy characterized by progressive retinal ganglion cell death and glaucomatous visual field loss, even though the intraocular pressure (IOP) does not exceed the normal range. The pathophysiology of NTG remains largely undetermine...

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Bibliographic Details
Published in:BioMed research international 2015-01, Vol.2015 (2015), p.1-7
Main Authors: Liu, Xuyang, Tang, Li, Wang, Pei, Fan, Ning
Format: Article
Language:English
Subjects:
Alzheimer's disease
Atherosclerosis
Blood flow
Blood pressure
Endothelium
Eye - blood supply
Glaucoma
Humans
Lasers
Low Tension Glaucoma
Optic nerve
Oxidative stress
Pathogenesis
Physiological aspects
Regional Blood Flow - physiology
Review
Veins & arteries
Velocity
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Summary:Normal tension glaucoma (NTG) is known as a multifactorial optic neuropathy characterized by progressive retinal ganglion cell death and glaucomatous visual field loss, even though the intraocular pressure (IOP) does not exceed the normal range. The pathophysiology of NTG remains largely undetermined. It is hypothesized that the abnormal ocular blood flow is involved in the pathogenesis of this disease. A number of evidences suggested that the vascular factors played a significant role in the development of NTG. In recent years, the new imaging techniques, fluorescein angiography, color Doppler imaging (CDI), magnetic resonance imaging (MRI), and laser speckle flowgraphy (LSFG), have been used to evaluate the ocular blood flow and blood vessels, and the impaired vascular autoregulation was found in patients with NTG. Previous studies showed that NTG was associated with a variety of systemic diseases, including migraine, Alzheimer’s disease, primary vascular dysregulation, and Flammer syndrome. The vascular factors were involved in these diseases. The mechanisms underlying the abnormal ocular blood flow in NTG are still not clear, but the risk factors for glaucomatous optic neuropathy likely included oxidative stress, vasospasm, and endothelial dysfunction.
ISSN:2314-6133
2314-6141
DOI:10.1155/2015/308505