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Fowkes FG, Aboyans V, Fowkes FJ, McDermott MM, Sampson UK, Criqui MH. Peripheral artery disease: epidemiology and global perspectives. Nat Rev Cardiol. 2017;14(03):156–70.

The mean progression rate in NTG is 0.75 dB per year [ 16], and VF is believed to be stable in NTG in the majority of cases [ 21]. Rapid progression, more than 1.5 dB per year, may indicate underlying compressive neuropathy, which was the case in 40% of patients scanned for this reason. Therefore, a detailed analysis of pattern defect and progression rate seems to be crucial in deciding who should be MRI scanned. This observation raises some intriguing questions. If glaucoma is considered to be a disease of the optic nerve caused by elevated IOP leading to damage of retinal axons, ganglion cells and optic disc excavation, then how is it possible that disc cupping and visual field loss also develop without statistically elevated IOP, presenting with the same morphological appearance of the optic disc as seen in high pressure-induced glaucoma?Grunwald JE, Piltz J, Hariprasad SM, DuPont J. Optic nerve and choroidal circulation in glaucoma. Invest Ophthalmol Vis Sci. 1998;39(12):2329–36. To report a case of a 48-year-old man with Buerger’s disease who presented with bilateral normal-tension glaucoma (NTG). Case presentation Luo XG, Chiu K, Lau FH, Lee VW, Yung KK, So KF. The selective vulnerability of retinal ganglion cells in rat chronic ocular hypertension model at early phase. Cell Mol Neurobiol. 2009;29:1143–51. Tarasoff-Conway JM, Carare RO, Osorio RS, et al. Clearance systems in the brain-implications for Alzheimer disease. Nat Rev Neurol. 2015;11:457–70. Kochkorov A, Gugleta K, Zawinka C, Katamay R, Flammer J, Orgul S. Short-term retinal vessel diameter variability in relation to the history of cold extremities. Invest Ophthalmol Vis Sci. 2006;47(9):4026–33.

Moore D, Harris A, Wudunn D, Kheradiya N, Siesky B. Dysfunctional regulation of ocular blood flow: a risk factor for glaucoma? Clin Ophthalmol. 2008;2(4):849–61. The aim of the study was to determine the frequency of pathologies which can mimic normal-tension glaucoma, observed in the neuroimaging of NTG patients, and to evaluate the frequency of pathologies in each of the additional indications for neuroimaging. 2. Material and Methods

Neurological evaluation of the NTG patient

Vascular dysregulation is suggested to be a main factor in the vascular pathophysiology of glaucomatous optic neuropathy, particularly in NTG [ 41]. Vascular dysregulation is defined as the inability of a tissue to maintain a constant blood supply despite changes in perfusion pressure. Vascular abnormalities and abnormal vascular reaction to local vasospastic and vasodilating agents were discussed. This includes vascular and endothelial diseases [ 48], vasospasm syndrome [ 49, 50] and migraine. All of these were reported as risk factors for optic nerve damage as seen in glaucoma without elevated IOP [ 51, 52, 53]. The collaborative NTG study group [ 51] and other studies [ 54] identified that a history of migraine and the appearance of optic disc hemorrhages were associated with a faster progression of visual field loss. This points towards a vascular component in NTG. The fact that disc hemorrhages can persist for a longer time may indicate that the bleeding may not be a one time effect, but has a more continuous character (private communication with Josef Flammer). It is suggested that vascular dysregulation leads due to an unstable ocular blood flow, resulting in ischemia and to optic nerve damage [ 55]. Yang Z, Klionsky DJ. Mammalian autophagy: core molecular machinery and signaling regulation. Curr Opin Cell Biol. 2010;22:124–31.

The ophthalmic artery (OA) is the main blood supply to the orbit and gives rise to ciliary arteries that supply the choroid and optic nerve head, and to the central retinal artery that supplies the retina [ 12]. Early sclerotic changes and arteriosclerosis of the retinal arteries were previously reported in Buerger’s disease, suggesting that changes in blood flow by vasospasm and thrombotic occlusions ocur within the ocular arteries [ 9, 13]. However, except for our case, there is only one case in the literature that describes Buerger’s disease with dysfunctional regulation of ocular blood flow within the optic nerve head and retinal arteriole having caused NTG [ 13]. Lee JW, Wong RL, Chan JC, Wong IY, Lai JS. Differences in corneal parameters between normal tension glaucoma and primary open-angle glaucoma. Int Ophthalmol. 2015;35:67–72. Among the pathological results, the most frequent brain pathologies were intracranial meningiomas observed in 4 patients (3.1%), followed by optic nerve sheath meningiomas diagnosed in 3 cases (2.4%) and brain glioma in 1 patient (0.8%). Phelps CD, Corbett JJ: Migraine and low-tension glaucoma: a case–control study. Invest Ophthalmol Vis Sci. 1985, 26 (8): 1105-1108. The most common cause of excavation of the optic disc is glaucoma. However, up to 20% cases may result from other pathologies, with the compressive neuropathy as clinically most relevant; in this case, early diagnosis is vision- and even life-saving [ 10]. As previously shown, the risk of another pathology underlying excavation is minimal in high-tension glaucoma [ 11]. The patients with an excavated disc in the absence of elevated IOP as the main causative factor of glaucoma are the most at risk of being misdiagnosed. There is a debate among glaucoma practitioners about the indications for neuroimaging in NTG patients [ 8, 9]. Some claim that such examination is obligatory in differential diagnosis because of the risk of overlooking life-threatening pathologies. However, this time- and money-consuming strategy is not always rational or even possible in busy hospitals. We decided to scan patients fulfilling at least one additional inclusion criterion which makes NTG, an atypical form of primary open-angle glaucoma, even more peculiar. The inclusion criteria in this study were established after reviewing the literature.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. Quigley HA, Broman AT. The number of people with glaucoma worldwide in 2010 and 2020. Br J Ophthalmol. 2006;90:262–7. Eid TE, Spaeth GL, Moster MR, Augsburger JJ. Quantitative differences between the optic nerve head and peripapillary retina in low-tension and high-tension primary open-angle glaucoma. Am J Ophthalmol. 1997;124:805–13. Cellini M, Possati GL, Profazio V, Sbrocca M, Caramazza N, Caramazza R. Color doppler imaging and plasma levels of endothelin-1 in low-tension glaucoma. Acta Ophthalmol Scand Suppl. 1997;224:11–3.

Unilateral normal-tension glaucoma (2) The damage in the visual field inconsistent with optic disc appearance (3) Fast visual field progression (1.5 dB per year or more) assessed according to at least 3 reliable visual field results (4) Worsening of visual acuity of at least 2 lines in the Snellen chart connected neither with lens nor retinal pathology (5) Optic disc excavation accompanied by pallor (6) Patients diagnosed under the age of 50 (7) Scotoma restricted by a vertical line (hemianopia, quadrantanopia, and bitemporal defect).

Killer HE, Jaggi GP, Flammer J, Miller NR, Huber AR. The optic nerve: a new window into cerebrospinal fluid composition? Brain: a J Neurol. 2006;129:1027–30. Tsolaki F, Gogaki E, Tiganita S, et al. Alzheimer’s disease and primary open-angle glaucoma: is there a connection? Clin Ophthalmol. 2011;5:887–90. Orgul S, Cioffi GA, Bacon DR, Van Buskirk EM. An endothelin-1 induced model of chronic optic nerve ischemia in rhesus monkeys. J Glaucoma. 1996;5(2):135–8. Choi J, Lee JR, Lee Y, et al. Relationship between 24-hour mean ocular perfusion pressure fluctuation and rate of paracentral visual field progression in normal-tension glaucoma. Invest Ophthalmol Vis Sci. 2013;54(9):6150–7. Grieshaber MC, Terhorst T, Flammer J. The pathogenesis of optic disc splinter haemorrhages: a new hypothesis. Acta Ophthalmol Scand. 2006;84(1):62–8.