What is Normal Tension Glaucoma ??
Normal tension glaucoma is a common form of the disease that may be easily missed as intra ocular pressure (IOP) is at or below the commonly accepted normal limit of 21mmhg. As such careful examination of the optic nerve is imperative in recognizing the condition. The main treatment for the disease is lowering IOP by 30% through either therapeutic or surgical means. Despite controlled IOP more than 1 in 10 patients with normal tension glaucoma still have progressive field loss. Factors other than IOP, although not well understood are believed to be the cause. Recent studies have found neuroprotective drugs such as brimonidine further reduce the risk of glaucoma progression.
Normal tension glaucoma is an optic neuropathy which results in a progressive visual field loss due to damage of the retinal ganglion cells. This form of glaucoma accounts for approximately 38.9% of people with primary open angle glaucoma (1). Primary open angle glaucoma effects 1.1% to 3% of the population and the incidence increases with age (1)(2).
The clinical presentation of normal tension glaucoma is similar to other glaucoma’s, including enlarged cup to disc ratio, optic disc hemorrhages (drance), optic disc rim notching, peripapillary atrophy, visual field loss (arcuate scotoma, nasal step), low central corneal thickness, open angles, and retinal nerve fibre layer thinning (3).
In normal tension glaucoma intra ocular pressure does not exceed 21mmhg (4). Currently the main treatment for normal tension glaucoma is the reduction of IOP. A 30% reduction from baseline significantly reduces the risk of progressive field loss, however 12% of people still have worsening glaucoma despite lowering IOP (5). As such it is widely accepted that there are factors other than IOP which contribute to the loss of retinal ganglion cells in normal tension glaucoma (6).
Low blood pressure and a nocturnal drop in blood pressure is associated with visual field loss in normal tension glaucoma (7)(8). Ocular perfusion pressure decreases with low blood pressure, subsequently ocular blood flow decreases resulting in a higher risk of visual field loss. Other factor such as oxidative stress and glutamate excitotoxicity contribute to the progression of normal tension glaucoma (9)(10). Neuroprotective drugs such as brimonidine reduce the risk of normal tension glaucoma progressing (11). Other drugs such as calcium channel blockers, glutamate antagonists, statins and supplements such as ginkgo biloba have been investigated for treating glaucoma through neuroprotection, however further study is required (6).
Currently the mainstay of controlling normal tension glaucoma is the reduction of IOP, whether from therapeutic drugs or surgical techniques such as selective laser trabeculoplasty, trabeculectomy or phacoemulsification with trabecular micro-bypass stent insertion (12).
Before the diagnosis of normal tension glaucoma can be made, other causes of the signs must be ruled out. These include complications of sarcoidosis, optic neuritis, anterior ischemic optic neuropathy, retinal artery occlusion, compressive optic neuropathy, drug induced glaucoma, past cardiovascular events, other types of glaucoma (13). These should also be reconsidered if treated normal tension glaucoma is progressing.
References
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Mitchell P, Smith W, Attebo K, Healey PR. Prevalence of open-angle glaucoma in Australia. The Blue Mountains Eye Study. Ophthalmology. 1996 October; 103(10):1661-9.
Seibold L. Normal Tension Glaucoma. 2014 November; Available at http://www.eyewiki.aao.org. Accessed October 10, 2015.
Shields MB. Normal tension glaucoma: Is it different from primary open angle glaucoma? Curr Opin Ophthalmol.2008 March; 19(2):85-8. [Pubmed]
Collaborative Normal-Tension Glaucoma Study Group. Comparison of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intraocular pressures. 1998 October; 126(4):487-97.
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Charlson ME et al. Nocturnal systemic hypotension increases the risk of glaucoma progression. Ophthalmology. 2014 October; 121(10):2004-12.
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Yanagisawa M, Aida T, Namekata K, Harada T, Shinagawa R, Tanaka K. Arundic acid attenuates retinal ganglion cell death by increasing glutamate/aspartate transporter expression in a model of normal tension glaucoma. Cell Death and Disease. 2015 March; 6(3):e1693. [Pubmed]
Krupin T, Liebmann JM, Greenfield DS, Ritch R, Gardiner S. A randomized trial of brimonidine versus timolol in preserving visual function: results from the Low-Pressure Glaucoma Treatment Study. Am J Ophthal. 2011 April; 151(4).
Saheb H, Ahmed I. Micro-invasive glaucoma surgery: current perspectives and future directions. Curr Opin Ophthalmol. 2012 March; 23(2):96-104.
Freudenthal J, Hampton R. Low Tension Glaucoma. 2014 October; Available at http://www.emedicine.medscape.com. Accessed October 10, 2015.
Wu Z, Huang J, Sadda S. Selective laser trabeculoplasty complicated by cystoid macular edema: report of two cases. Eye Sci. 2012 December; 27(4): 193-7.
Pfizer Australia. Product Information: Xalatan. 2014 January. Available at http://www.pfizerpro.com. Accessed October 10, 2015.
Allergan. Product Information: Alphagan P. 2013. Available at http://www.alphaganp.com. Accessed October 10, 2015.
What is Normal Tension Glaucoma?
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