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Advances in
eISSN: 2377-4290

Ophthalmology & Visual System

Opinion Volume 7 Issue 7

Differences between the Characteristics of Normal Tension Glaucoma and High Tension Glaucoma

Burak Turgut,1 Fatoş Altun Turgut2

1Department of Ophthalmology, Yuksek Ihtisas University, Turkey
2Elazig Training and Research Hospital, Turkey

Correspondence: Burak Turgut, Professor of Ophthalmology, YuksekIhtisas University, Faculty of Medicine, Department of Ophthalmology, 06520, Ankara, Turkey, Tel +90 312 2803601

Received: November 22, 2017 | Published: December 11, 2017

Citation: Turgut B, Turgut FA (2017) Differences between the Characteristics of Normal Tension Glaucoma and High Tension Glaucoma. Adv Ophthalmol Vis Syst 7(7): 00250. DOI: 10.15406/aovs.2017.07.00250

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Normal tension glaucoma is a type of primary open angle glaucoma in which the intraocular pressure is in the normal range. Although both normal tension glaucoma and high-tension glaucoma resemble clinically each other, there are some differences between both of them. In this editorial, I aim to summarize the differences between the characteristics of these glaucoma types. If these are well-known, the diagnosis and management of normal tension glaucoma will be easier.

Keywords: normal tension glaucoma, normal pressure glaucoma, normotensive glaucoma, high-pressure glaucoma, high tension glaucoma, differences, characteristics


NTG, normal tension glaucoma; NPG, normal pressure glaucoma; POAG, primary open angle glaucoma; HPG, high pressure glaucoma; HTG, high tension glaucoma; RNFL, retinal nerve fiber layer; OD, optic disc; RGCs, retinal ganglion Cells; IOP, intra-ocular pressure; GON, glaucomatous optic neuropathy; CNTGS, collaborative normal tension glaucoma study; ODH, optic disc hemorrhage; CCT, central cornea thickness; CSFP, cerebro-spinal fluid pressure; ONPP, optic nerve perfusion pressure; PVD, peripheral vascular dysregulation; OBF, ocular blood flow; OSAS, obstructive sleep apnea syndrome


Glaucoma is defined as a multifactorial and progressive optic neuropathy which usually caused by the effects of elevated intraocular pressure (IOP). Glaucomatous optic neuropathy (GON) is characterized by the excavation of the optic nerve head (ONH), thinning of the retinal nerve fiber layer (RNFL) and the axons of by retinal ganglion cells (RGCs) and eventually the specific loss of visual field (VF).1 Primary open-angle glaucoma (POAG) is the most common type of chronic progressive GON with the absence of the association of any ocular disease. POAG includes two types as ''high pressure glaucoma (HPG)/high-tension glaucoma (HTG)'' and normal-pressure glaucoma (NPG)/normal tension glaucoma (NTG).1–5 There are significant overlapping characteristics between both glaucoma types. However, they may be separated by some marked differences in the aspects of risk factors, pathogenesis, OD findings, RNFL thickness and VF defects.6–47 Comparison of the characteristics of both glaucoma types has been given in Table 1.





Normal with wide diurnal fluctuations, nocturnal spikes

High with normal range diurnal fluctuations                                                                                              

Sexual Predisposition                                                



Possible Specific Risk Factor

ODH, ischemic/occlusive vascular disease
(Migraine, Raynaud, diabetes, cardiac arrhythmia, stroke)
addition to elevated IOP

High IOP (primary continuous causative risk factor), Genetic mutation, advanced age, black race, older age, systemical vascular diseases


Older average 10 years than HPG


Usually over 50 years old

OD Sign

Narrow NRR, a larger OD surface area, thinner
inferior/inferotemporal NRR, deep, focal NRR thinning/notching, OD pit

Diffuse NRR thinning, classical GON signs

GON Pathogenesis

Neuro-degeneration, IOP-independent mechanisms
(LC weakness or abnormalities, abnormal easily triggered apoptosis,
low ONBP, low CSFP, local PVD, enhanced sensitivity to physiologic IOP,
hypotension, hematologic abnormalities)

Neurodegenerative and IOP-dependent mechanisms, vascular, genetic, and biochemical mechanisms


More frequently beta-zone PPA

Beta-zone PPA


Frequently lower

Maybe lower


Earlier, inferotemporal


VF Defects

More focal, central, deeper and closer to fixation

Deeper, superior nasal step, inferior and superior paracentral

Suggested VF testing protocol




Maybe thinner than average


Genetic Mutation in which


TIGR, Myocilin

Systemical BP

Increased diastolic BP and larger dips in BP overnight



More common

Less common


Strongly impaired

Maybe impaired


Strongly associated

May be associated


Slower to HPG in the absence of beta-blocker treatment                                                  


Table 1 The comparison of the characteristics of NTG and HTG1,2,4,8,9,11,12,15-20,22–47

It has been considered that NTG might occur due to IOP-independent pathogenic factors such as peripheral vascular dysregulation (PVD), hypotension, mechanical factors such as lamina cribrosa (LC) abnormalities and weakness, and enhanced sensitivity of the optic nerve to physiologic IOP. However, CNTGS showed that a 30% or more reduction of the IOP value in normal range belonging the patient achieved a significant slowdown in the progression of the NTG.6 On the other hand, HTG is often an IOP-dependent glaucoma type. IOP plays a great role in the pathogenesis of this glaucoma typ.1 In conclusion, as seen in Table 1, compared to those with HTG, the common distinctive findings in the patients with NTG are an IOP value in normal range; female predisposition; optineurin gene mutation; thinner CCT; larger OD size; larger/deeper OD cupping; thinner LC; frequent NRR notching; earlier and focal RNFL loss; frequent beta zone peripapillary atrophy; frequent OD hemorrhage; frequent pit; deeper, closer to fixation, steeper slopes, more localized and central VF defects; peripheral vascular dysregulation (low nocturnal optic nerve perfusion pressure, cold extremities, impairments in the nail fold capillary, retinal and choroidal blood flow), ocular perfusion abnormalities and vasospastic/ischemic disorders in pathogenesis; associated hematologic abnormalities, obstructive sleep apnea syndrome and blood loss.2,3,7–47



Conflicts of interest

The authors declare that there is no conflict of interest regarding the publication of this paper.




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