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NTG Designed for iPhone 11 Case, Heavy-Duty Tough Rugged Lightweight Slim Shockproof Protective Case for iPhone 11 6.1 Inch, Black

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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. 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. The most prominent and common disturbances described in our group of NTG patients were ischemic foci located in different regions of the brain. As the group was not age-matched, we cannot distinguish between a pathology related to NTG and the symptoms of normal aging. However, there are data reporting that ischemic changes in the brain are more common in NTG patients than in control subjects, with the frequency up to 40% [ 25– 28], which suggests that vascular insufficiency in the central nervous system has some relation to the pathogenesis of NTG. Harris et al. [ 29] reported reduced cerebrovascular blood flow velocity and vasoreactivity in open-angle glaucoma patients compared to age-matched control subjects. Additionally, according to some authors, brain ischemic lesions may be associated to some extent with the pattern of visual field damage [ 28] and progression [ 30] in NTG patients. 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 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.

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.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].

Phelps CD, Corbett JJ: Migraine and low-tension glaucoma: a case–control study. Invest Ophthalmol Vis Sci. 1985, 26 (8): 1105-1108. Leighton DA, Phillips CI. Systemic blood pressure in open-angle glaucoma, low tension glaucoma, and the normal eye. Br J Ophthalmol. 1972;56:447–53. Phelps CD, Corbett JJ. Migraine and low-tension glaucoma: a case-control study. Invest Ophthalmol Vis Sci. 1985;26(8):1105–8. Jeganathan VS, Wong TY, Foster PJ, et al. Peripheral artery disease and glaucoma: the Singapore Malay Eye Study. Arch Ophthalmol. 2009;127(7):888–93.Hayreh SS. The role of age and cardiovascular disease in glaucomatous optic neuropathy. Surv Ophthalmol. 1999;43:S27–42.

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. 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. Pressure is a scalar force and therefore unlike a vector, it is not directed. Visual field damage caused by a scalar force would therefore be expected to be rather homogenous over the whole visual field, as the shape of the eye is spherical and the scalar force is the same at every point in the sphere. Visual field loss in glaucoma, however, does not present as a generalized homogenous defect but it rather starts at focal points from where it enlarges [ 5, 6, 7]. Caprioli and Späth [ 8] found visual field defects in NTG to be significantly deeper and closer to fixation than in other types of glaucoma. To explain such focal defects, some authors argue that certain populations of ganglion cells and axons react more sensitively to pressure than others [ 9]. But even if this is the case, such “more sensitive regions” seem to vary between patients. Further, if the IOP is indeed the sole cause for glaucomatous damage in NTG, progression of damage would be expected to stop when the pressure is maximally lowered. This, however, is not the case. Given that there are no data on what the lowest pressure should look like and how it could be achieved, remains an unsolved problem. Further controlled studies may however answer this question about the ideal target pressure in the future.Fingert JH, Robin AL, Stone JL, et al. Copy number variations on chromosome 12q14 in patients with normal tension glaucoma. Hum Mol Genet. 2011;20:2482–94. Yamazaki Y, Drance SM. The relationship between progression of visual field defects and retrobulbar circulation in patients with glaucoma. Am J Ophthalmol. 1997;124:287–95. Cesareo M, Martucci A, Ciuffoletti E, et al. Association between alzheimer’s disease and glaucoma: a study based on Heidelberg retinal tomography and frequency doubling technology perimetry. Front Neurosci. 2015;9:479.

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