Correlation of Asymmetric Damage With Asymmetric Intraocular Pressure in Normal-Tension Glaucoma (Low-Tension Glaucoma)

1988 ◽  
Vol 106 (7) ◽  
pp. 898-900 ◽  
Author(s):  
M. J. Cartwright ◽  
D. R. Anderson
Ophthalmology ◽  
1989 ◽  
Vol 96 (9) ◽  
pp. 1312-1314 ◽  
Author(s):  
Andrew Crichton ◽  
Stephen M. Drance ◽  
Gordon R. Douglas ◽  
Michael Schulzer

Eye ◽  
1994 ◽  
Vol 8 (5) ◽  
pp. 521-523 ◽  
Author(s):  
Clemencia De Vivero ◽  
Colm O'brien ◽  
Lumina Lanigan ◽  
Roger Hitchings

2005 ◽  
Vol 64 (3) ◽  
Author(s):  
S.D. Mathebula

Glaucoma is a chronic or acute disease in which optic nerve damage occurs in a characteristic way. In  primary  open  angle  glaucoma  (POAG),  the manifestations of the optic nerve damage include visible excavation that develops in the optic nerve head and regions of the retina lose ability to detect all the elements that go into the total sensory prod-uct called vision.1, 2  When these regions worsen and enlarge to coalesce, the result is blindness.The intraocular pressure (IOP) has a causative role in producing the damage. All eyes have an in-ternal pressure to keep them inflated, perhaps 17 mmHg on the average, ± 5 mmHg standard devia-tion. In at least two thirds of the eyes that suffer glaucomatous damage, the intraocular pressure is high, at least a bit above the pressure found in 95% of the non-glaucomatous population. The cut-off is in the region of 20 to 22 mmHg used by most definitions.2 However, a normal or even low intra-ocular pressure can be harmful to some eyes, and when it is, the person has normal or low tension glaucoma. The traditional treatment of glaucoma has logically been to lower the intraocular pres-sure, to prevent further damage to the optic nerve, though previous damage is not undone.


1994 ◽  
Vol 38 ◽  
pp. S177-S182 ◽  
Author(s):  
Luciano Quaranta ◽  
Gianluca Manni ◽  
Francesco Donato ◽  
Massimo G. Bucci

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