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Peripheral arterial disease (PAD) is a prevalent vascular abnormality. Claudication represents an early yet common manifestation of PAD. A clinical history and physical examination combined with an ankle-brachial index can help make a diagnosis of claudication. 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. After ruling out other systemic diseases and vascular abnormalities related to normal-tension glaucoma, we found peripheral arterial disease as a probable vascular abnormality related to normal-tension glaucoma in our patient. To our knowledge, this is the first time such a case has been reported. Thus, further research is needed to determine the relevance of these results to the general population. Gasser P, Flammer J, Guthauser U, Mahler F. Do vasospasms provoke ocular diseases? Angiology. 1990;41:213–20. Harris A, Siesky B, Wirostko B: Cerebral blood flow in glaucoma patients. J Glaucoma. 2013, 22 (05): 46-48.

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. Certain authors have argued that there might be a slightly different morphology of the NTG optic nerve head [ 21, 22]. Applying new diagnostic tools, such as Heidelberg retina tomography (HRT) some studies suggest that the discs may be larger and the cups deeper in NTG patients than in patients with high pressure-induced POAG [ 23, 24]. Whether or not this is true in all populations is still a matter of debate. Choi J, Jeong J, Cho HS, Kook MS. Effect of nocturnal blood pressure reduction on circadian fluctuation of mean ocular perfusion pressure: a risk factor for normal tension glaucoma. Invest Ophthalmol Vis Sci. 2006;47(3):831–6. Compressive neuropathy typically presents with pale optic disc and much less frequently with excavated pale disc; both cooccur with the clinical features of optic nerve atrophy. Classical clinical findings of compressive neuropathy are slowly progressive visual loss and optic nerve atrophy. Some clinicians believe it is possible to distinguish between excavation of the optic disc caused by glaucoma and compressive lesion of the anterior visual pathways only on the basis of clinical features. The possibility of glaucoma specialists successfully distinguishing between glaucomatous and nonglaucomatous neuropathy on the basis of colour fundus photography and VF results was evaluated in some studies, and up to 88.1% of glaucoma cases and 75% of optic neuropathy cases were correctly classified [ 18]. Other studies reported an accuracy of 75–80% in diagnosing glaucoma and an accuracy below 50% in diagnosing other optic neuropathies [ 10, 19]. Greenfield et al. [ 20] concluded that compressive lesions of the anterior visual pathway should be evident on clinical examination, including more specific features: optic nerve pallor, vertically aligned visual field defects, and visual acuity less than 20/40. Our study confirmed that vertical VF defect was related to brain pathology in 71.4% of cases, to worsening BCVA in 50% of cases, and to pale disc in 18.1%. NTG suspect patients with these symptoms clearly need neuroimaging. 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).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].

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].

Results

Levene RZ: Low tension glaucoma: a critical review and new material. Surv Ophthalmol. 1980, 24 (6): 621-664. 10.1016/0039-6257(80)90123-X. Beltrame JF, Sasayama S, Maseri A. Racial heterogeneity in coronary artery vasomotor reactivity: differences between Japanese and Caucasian patients. J Am Coll Cardiol. 1999;33(6):1442–52. Delaney Y, Walshe TE, O’Brien C. Vasospasm in glaucoma: clinical and laboratory aspects. Optom Vis Sci. 2006;83(7):406–14. 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. Mi XS, Yuan TF, So KF. The current research status of normal tension glaucoma. Clin Interv Aging. 2014;9:1563–71.

Katai N, Yoshimura N. Apoptotic retinal neuronal death by ischemia-reperfusion is executed by two distinct caspase family proteases. Invest Ophthalmol Vis Sci. 1999;40:2697–705. Grunwald JE, Piltz J, Hariprasad SM, DuPont J. Optic nerve and choroidal circulation in glaucoma. Invest Ophthalmol Vis Sci. 1998;39(12):2329–36.

Neurological evaluation of the NTG patient

Andrews RM, Griffiths PG, Johnson MA, Turnbull DM. Histochemical localisation of mitochondrial enzyme activity in human optic nerve and retina. Br J Ophthalmol. 1999;83:231–5. 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.

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. Sugiyama T, Moriya S, Oku H, Azuma I. Association of endothelin-1 with normal tension glaucoma: clinical and fundamental studies. Surv Ophthalmol. 1995;39(Suppl 1):S49–56. Bonomi L, Marchini G, Marraffa M, et al. Prevalence of glaucoma and intraocular pressure distribution in a defined population. The Egna-Neumarkt Study. Ophthalmology. 1998;105:209–15.NTG is caused by impaired CSF circulation in the subarachnoid space of the optic nerve and this results in a toxic damage to the nerve.