Glaucomatous Optic Cupping and Normal-tension Glaucoma

By: Florence Low

Pathophysiology of glaucomatous optic neuropathy
Glaucoma is characterized by a progressive optic neuropathy associated with visual field loss
during the progression due to intraocular pressure (IOP). These characteristic become the
triad of this disease.
1
There are several mechanisms which lead to neurodegeneration due to
IOP. Increase pressure can block the axonal protein transport leading to retinal ganglion cell
death. Neuropathy may also occur due to excessive physiological response from the stress
condition.
2

Clinical finding in association with optic nerve damage can be shown from the optic
disk examination. In normal condition, optic cups size depends on the number of bulk of
fibres which form the optic nerve that pass through. In glaucomatous condition, optic atrophy
is characterized by enlargement of optic cup due to loss in the disk substance and disk pallor
on cupping area. This differentiated glaucomatous optic atrophy with other form of optic
atrophy; in which there is a widespread pallor with no optic cup increase (OCD is not
increased).
3
There is also a thinning of the neuroretinal rim (NRR) resulting in diffuse
enlargement of the cup. Localized field defects has been associated with focal ischemic of the
optic disk; the damage usually starts at the superotemporal or inferotemporal region because
these are the weakest portion of lamina cribosa.
4


Figure 1 focal ischemia (left) and enlarge disk (right)

Normal tension glaucoma
NTG is a variant of primary open-angle glaucoma (POAG). The difference between
NTG and POAG is IOP which is 21mmHg. However, NPG still has the characteristic of
glaucomatous optic nerve damage, visual field lost consistent with damage progression.
Examination of anterior chamber by gonioscopy shows an open angle.
5

NTG is more prevalent in Japan, Korea and China population, around 80%. Around
15-25% POAG patient has a normal IOP however NTG still increase the risk of developing
POAG.
6

Pathogenesis of NTG is still unclear. It was proposed that glaucomatous optic
neuropathy was due to underlying vascular insufficiency. A study proposed that in NTG, the
development of optic neuropathy is because the normative pressure in the eye is lower than
IOP.
5
In some patient, central corneal thickness (CCT) assessment showed a very low CCT
and overall, NTG patients have lower CCT than POAG patient.
6

In NTG, the treatment is still aimed at reduction of the IOP by at least 30%.
6
Drug of
choices used in the treatment is betaxolol, with the effect of increasing optic nerve blood flow
aside from its IOP-lowering properties.
5




1
Kanski JJ, Bowling B.Glaucoma: evaluation of the optic nerve head.. In: Clinical ophthalmology: a systemic
approach. 7th ed. 2011. Elsevier Saunders.
2
Wax M, Clark A, Civan MM. Mechanism of glaucoma. In: Yanoff M, Duker JS, editors. Ophthalmoloty. 3rd
ed. 2009. Elsevier Saunders.
3
Riordan-Eva P, Whitcher JP. Glaucoma. In: Vaughan and Asburys general ophthalmology. 17th ed. McGraw-
Hill.
4
Yamamoto T, Kitazawa Y. Vascular pathogenesis of normal-tension glaucoma: a possible pathogenetic factor,
other than intraocular pressure, of glaucomatous optic neuropathy. Prog Retin Eye Res. 1998 Jan;17(1):127-
43.
5
Kanski JJ, Bowling B. Glaucoma: normal-tension glaucoma. In: Clinical ophthalmology: a systemic approach.
7th ed. 2011. Elsevier Saunders.
6
Low tension glaucoma. [Online]. Available from: URL: http://emedicine.medscape.com/article/1205508-
overview