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Chen Y, Hughes G, Chen X, et al. Genetic variants associated with different risks for high tension glaucoma and normal tension glaucoma in a chinese population. Invest Ophthalmol Vis Sci. 2015;56:2595–600. Phelps CD, Corbett JJ. Migraine and low-tension glaucoma: a case-control study. Invest Ophthalmol Vis Sci. 1985;26(8):1105–8. In this study, 38% of diagnosed pathologies did not affect the anterior visual pathway and were not the cause of disc cupping. Most of the participants of the research were patients diagnosed with primary empty sella and patients with pituitary microadenoma. Beattie and Trope [ 19] had previously reported that the coexistence of primary empty sella and glaucomatous optic neuropathy is likely a coincidence. In the case of positive MRI results, it is crucial to assess the influence of the brain pathology on the clinical picture of NTG before the diagnosis of compressive optic neuropathy is established.

The mean age of NTG patients reported in many studies is around 60 [ 16]; in another study by the authors of this article, the patients' mean age was about 70 [ 17], which is similar to the mean age of the participants of the current study. Younger age (under 50) at diagnosis in the current study was never related to clinically significant pathologies detected at neuroimaging. It seems that prevalence of NTG in younger patients, just like unilateral involvement, may be a feature of the typical course of NTG. In the current study, the most common reason for neuroimaging in NTG patients was unilateral involvement. NTG is believed to be dependent on general rather than ocular factors, and that is why it is supposed to be more symmetrical than POAG with high initial IOP. However, in our group, only 6.9% patients with unilateral excavation had clinically significant pathology in the brain. It was the penultimate reason for neuroimaging as far as the frequency of found pathologies is concerned. It may indicate that asymmetry is quite typical at least in some NTG cases: about 25% patients with NTG presented with unilateral field loss at diagnosis [ 11]. Additionally, patients with NTG may present with asymmetric field loss [ 12] related to unequal IOP [ 13, 14] or ocular blood flow [ 15] between the eyes. Although IOP lowering has some beneficial effect on the progression of NTG in some patients while progression continues in others, (different thresholds?) there is, however, no known mechanism that could explain what causes a lower threshold for pressure-induced damage in some patients. This of course should not prevent ophthalmologists from lowering IOP in their patients. Perfusion deficit and vascular dysregulation Cho HK, Kee C. Population-based glaucoma prevalence studies in Asians. Surv Ophthalmol. 2014;59:434–47.Normal tension glaucoma (NTG) is an optic nerve neuropathy that presents with optic disc excavation, visual field loss in spite of intraocular pressure <21 mm Hg. Progressive visual field loss and disc excavation can continue despite of pressure lowering of 30% of IOP. There are however, also a substantial number of patients who do not progress even without treatment. A substantial number of older NTG patients also suffer from Alzheimers disease, a finding that raises the question whether or not NTG is an early manifestation of a more generalized neurodegenerative disease. At the same time, some NTG patients share features of vascular dysregulation, which raises the question whether NTG is an optic nerve disease in a diseased body. In analogy therefore NTG might be a diseased optic nerve in a toxic CSF environment. It has been suggested that disturbances in ocular blood flow are a major risk factor in the pathogenesis of NTG [ 13, 14]. Vascular complication, such as vasospasms, vasosclerosis, small vessel disease, and autoregulatory dysfunction, leading to perfusion deficits of the ON head, the retina, the choroid or the retrobulbar vessels, might influenc Another “mechanical” concept in the pathophysiology of glaucoma is focused on the lamina cribrosa [ 25, 26]. The lamina cribrosa is a crucial structure on the pathway of the intraocular axons to the intraorbital portion of the optic nerve. The nutrition of the axons within the lamina cribrosa is considered to be dependent on oxygen and nutrition from the capillaries within the lamina cribrosa. Damage to axons, capillaries and astrocytes in the biomechanical paradigm is thought to be caused by lamina cribrosa deformation and IOP-related stress and strain onto axons, capillaries and astrocytes within the lamina cribrosa [ 25]. Experiments in animals showed that the optic nerve head rim tissue thinning exceeds peripapillary retinal nerve fiber thinning [ 27]. The appealing part of this concept is that it could explain the pattern of visual field loss in glaucoma. The obvious question however is, if vascular damage is considered in this concept why does the optic nerve head not show cotton wool spots?

Mozaffarieh M, Flammer J: New insights in the pathogenesis and treatment of normal tension glaucoma. Curr Opin Pharmacol. 2013, 13 (1): 43-49. 10.1016/j.coph.2012.10.001. Wostyn P, De Groot V, Van Dam D, Audenaert K, Killer HE, De Deyn PP. Glaucoma considered as an imbalance between production and clearance of neurotoxins. Invest Ophthalmol Vis Sci. 2014;55:5351–2. The study has some potential limitations. First, it was conducted in one centre and the results may be different in different populations. Additionally, presence of relative afferent pupillary defect which may be helpful in indication was not included as inclusion criterion. The authors decided to include patients with clinically unilateral form of the disease. The follow-up of the included patients was not planned. That is why there is the possibility of misdiagnosing the patients with asymmetric NTG at presentation as unilateral disease. All patients from the group of young NTG patients were negative in MRI neuroimaging. However, the group may be too small to conclude and needs to be confirmed in the next studies.All patients meeting the inclusion criteria who agreed to participate in the research had MRI scans performed on the brain and both orbits with a 1.5-Tesla Magnetic Resonance Scanner (Optima 360, GE Healthcare). The scans were carefully evaluated by experienced neuroradiologists (RP, BS). Any pathology found was classified as either possibly interfering with the glaucoma diagnosis or not significant. Cursiefen C, Wisse M, Cursiefen S, Jünemann A, Martus P, Korth M. Migraine and tension headache in high-pressure and normal-pressure glaucoma. Am J Ophthalmol. 2000;129(1):102–4. Galassi F, Giambene B, Varriale R. Systemic vascular dysregulation and retrobulbar hemodynamics in normal-tension glaucoma. Invest Ophthalmol Vis Sci. 2011;52:4467–71.