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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. There is further indirect evidence of altered blood flow in NTG patients: A much higher prevalence of sleep apnoea–hypopnea syndrome in NTG patients [ 56, 57], compromised peripheral endothelial cell function [ 48, 58] and increased plasma levels of endothelin-1 (ET-1) [ 59, 60, 61]. Although upregulated ET-1 levels are considered a risk factor for NTG, there are data in a Japanese study that show no difference of ET-1 levels between NTG, POAG and normal adults under 60 years of age [ 62]. 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.

Mroczkowska S, Ekart A, Sung V, Negi A, Qin L, Patel SR, Jacob S, Atkins C, Benavente-Perez A, Gherghel D: Coexistence of macro- and micro-vascular abnormalities in newly diagnosed normal tension glaucoma patients. Acta Ophthalmol. 2012, 90 (7): 553-559. 10.1111/j.1755-3768.2012.02494.x. Killer HE, Subramanian PS. Compartmentalized cerebrospinal fluid. Int Ophthalmol Clin. 2014;54:95–102.Chiu C, Miller MC, Caralopoulos IN, et al. Temporal course of cerebrospinal fluid dynamics and amyloid accumulation in the aging rat brain from three to thirty months. Fluids Barriers CNS. 2012;9:3.

Polak K, Luksch A, Frank B, Jandrasits K, Polska E, Schmetterer L. Regulation of human retinal blood flow by endothelin-1. Exp Eye Res. 2003;76(5):633–40.Toda N, Nakanishi-Toda M. Nitric oxide: ocular blood flow, glaucoma, and diabetic retinopathy. Prog Retin Eye Res. 2007;26(3):205–38. 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%).

Lai SW, Lin CL, Liao KF. Glaucoma may be a non-memory manifestation of Alzheimer’s disease in older people. Int Psychogeriatr. 2017:1–7. 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. Linden C, Qvarlander S, Johannesson G, et al. Normal-tension glaucoma has normal intracranial pressure: a prospective study of intracranial pressure and intraocular pressure in different body positions. Ophthalmology. 2017;1–8. Ours is the second case in the literature presenting the association of Buerger’s disease, retinal artery occlusion and NTG. Decreased cerebral blood flow has also been associated with glaucomatous damage and visual field deficits. (12) Doppler imaging has demonstrated increased blood flow resistance and decreased blood flow velocities in the OA of patients with NTG, thus suggesting the role that changes in blood supply can play and/or correlate with in optic nerve head pathology [ 21]. Thus, in our case, left carotid artery stenosis associated with thrombosis accompanied by Buerger’s disease is another risk factor causing retinal artery occlusion and NTG in the same eye. While bilateral arteriolar constriction, optic nerve head changes and visual field defects may have been caused by vasospasm and local ocular blood flow disturbance due to Buerger’s disease, advanced glaucomatous damage in the left eye (while the right eye had moderate damage) and BRAO may have been caused by the additive effect of left carotid artery stenosis.

References

The differential diagnosis procedure for distinguishing between NTG and compressive neuropathy of the optic nerve is neuroimaging. However, the indications are not clear. Some ophthalmologists point to the need to give an MRI scan to every NTG patient, while others perform neuroimaging only in the presence of specific additional clinical features (in addition to IOP within the normal range) that are not typical for glaucoma [ 8, 9]. Kaiser HJ, Schoetzau A, Stumpfig D, Flammer J. Blood-flow velocities of the extraocular vessels in patients with high-tension and normal-tension primary open-angle glaucoma. Am J Ophthalmol. 1997;123(3):320–7. Phelps CD, Corbett JJ: Migraine and low-tension glaucoma: a case–control study. Invest Ophthalmol Vis Sci. 1985, 26 (8): 1105-1108. 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.