NORMAL TENSION GLAUCOMA

Guest author

SHARBEEN 

Ajmal Khan Tibbiya College 

Aligarh, India

INTRODUCTION

Glaucoma is a multifactorial neurodegenerative disorder. The fundamental nature of this disease is a pathology of the optic nerve. The single most important factor determining it's rate and severity is intra-ocular pressure (IOP).

The level of IOP appears to determine whether the etiological factor will lead to development of progressive glaucomatous damage or not.

Around half of all individuals having IOP of 35 mmHg develop glaucomatous cupping and visual field damage. With IOP between 21-30 a smaller percentage of patients develop Glaucoma. Individuals having statistically normal range of IOP less often develop Glaucoma but their numbers are significantly high (around 50%) among all Glaucoma groups.

There is no fundamental difference between Normal tension glaucoma (NTG) and primary open angle Glaucoma (POAG) except that the etiological triggers or pathologic process is accelerated at a lower level of IOP in NTG.

A normal IOP does not necessarily guarantee against developing glaucoma. 

Patients with NTG often have IOP between 15-20 mmHg.

CLINICAL FEATURES

(1) Patients with NTG often have parapapillary atrophy (PPA) of the optic nerve with cupping. There is absence of retinal pigment epithelium in the region of PPA and visual field (VF) loss is most conspicuous in the corresponding region.

(2) Feature of cupping: Some patients have a notch in the optic cup (a highly localized region of thin or absent neuro-retinal rim which is sometimes called “focal ischemic” type of cupping).

It is associated with a highly localized dense arcuate field defect or even a dense upper hemifield defect.

Other discs have diffuse shallow cupping and a pale color of the disc and surrounding tissue. This is called “senile sclerotic” disc. There is apparently some association of focal ischemic type to vascular dysregulation and of senile sclerotic type to systemic atherosclerosis.

(3) Splinter hemorrhages are most frequently seen in NTG.

(4) There can be intermingling of POAG and NTG in the same family.

(5) Patients with NTG often have features of Flammer’s Syndrome.

(6) Some eyes with signs of glaucoma maybe related to an acute ischemic episode (“shock induced neuropathy”) or chronic obstructive arterial disease. Often glaucomatous changes in these patients are non-progressive.

DIAGNOSIS 

NTG is usually discovered due to an abnormal disc appearance. Mild cupping may be overlooked unless VF shows scotomas near or below fixation, prompting a more careful examination of the disc.

Certain features which point towards diagnosis of NTG include:

Family history of glaucoma, prominent crescent or halo of absent RPE adjacent to the disc, splinter hemorrhages, tendency towards cold hands and feet, low blood pressure (BP), wearing socks at night while sleeping and migraine headaches.

DIFFERENTIAL DIAGNOSIS 

(1) Large physiologic cup

(2) Congenital anomaly of disc

(3) Anterior ischemic optic neuropathy

(4) Branch retinal vein occlusion

(5) “Giant” drusen of optic nerve

(6) Orbital or intra-cranial tumor

(7) Inaccurate tonometry

(8) Variable IOP

(9) Previously elevated IOP (related to previous steroid use or resolved uveitis)

(10) POAG, where IOP has been lowered by systemic medications (e.g. systemic beta-blockers for systemic hypertension)

(11) Special form of NTG: Shock-induced neuropathy. It is related to a previous cardiovascular episode or atherosclerosis.

It is hypothesized that NTG could be a primary form of glaucoma unrelated to IOP. These patients may continue to progress despite significant lowering of IOP (upto 8-10 mmHg).