Can Pulsatile Ocular Blood Flow Be a Predictor of Future Visual Field Loss in Normal-Tension Glaucoma?

2000 ◽  
pp. 153-155
Author(s):  
R. A. Hitchings
Author(s):  
David Kuerten ◽  
Matthias Fuest ◽  
Peter Walter ◽  
Babac Mazinani ◽  
Niklas Plange

Abstract Purpose To investigate the relationship of ocular blood flow (via arteriovenous passage time, AVP) and contrast sensitivity (CS) in healthy as well as normal tension glaucoma (NTG) subjects. Design Mono-center comparative prospective trial Methods Twenty-five NTG patients without medication and 25 healthy test participants were recruited. AVP as a measure of retinal blood flow was recorded via fluorescein angiography after CS measurement using digital image analysis. Association of AVP and CS at 4 spatial frequencies (3, 6, 12, and 18 cycles per degree, cpd) was explored with correlation analysis. Results Significant differences regarding AVP, visual field defect, intraocular pressure, and CS measurement were recorded in-between the control group and NTG patients. In NTG patients, AVP was significantly correlated to CS at all investigated cpd (3 cpd: r =  − 0.432, p< 0.03; 6 cpd: r =  − 0.629, p< 0.0005; 12 cpd: r =  − 0.535, p< 0.005; and 18 cpd: r =  − 0.58, p< 0.001), whereas no significant correlations were found in the control group. Visual acuity was significantly correlated to CS at 6, 12, and 18 cpd in NTG patients (r =  − 0.68, p< 0.002; r =  − 0.54, p< .02, and r =  − 0.88, p< 0.0001 respectively), however not in healthy control patients. Age, visual field defect MD, and PSD were not significantly correlated to CS in in the NTG group. MD and PSD were significantly correlated to CS at 3 cpd in healthy eyes (r = 0.55, p< 0.02; r =  − 0.47, p< 0.03). Conclusion Retinal blood flow alterations show a relationship with contrast sensitivity loss in NTG patients. This might reflect a disease-related link between retinal blood flow and visual function. This association was not recorded in healthy volunteers.


2003 ◽  
Vol 13 (2) ◽  
pp. 162-175 ◽  
Author(s):  
E. Ravinet ◽  
A. Mermoud ◽  
R. Brignoli

Purpose Almost five years have elapsed since the introduction of latanoprost on several markets and considering the large number of publications dealing with it, the authors felt that it was worth re-evaluating the drug. Methods The criterion used to select trials for inclusion in the review was: all articles mentioning the drug in common electronic data-bases; these were then screened and considered, on the basis of methodological quality. Results Experimental data suggest that latanoprost acts by remodeling the extracellular matrix in the ciliary muscle, thus increasing the flow of aqueous humor through the ciliary muscle bundles of the uveoscleral pathway. POAG Latanoprost persistently improves the pulsatile ocular blood flow in primary open angle glaucoma (POAG). Recent trials confirmed the greater IOP-lowering efficacy of latanoprost vs. timolol, dorzolamide, brimonidine and unoprostone. Trials lasting up to 24 months showed that latanoprost is effective in long-term treatment of POAG and ocular hypertension (OH), with no signs of loss of efficacy when compared to timolol or dorzolamide. Latanoprost provides better control of circadian IOP. Non-responders to b-blockers should preferably be switched to latanoprost monotherapy before a combination therapy is started. The possibility of a fixed combination of latanoprost and timolol has been explored, with promising results. NTG Latanoprost is effective in normal tension glaucoma (NTG), lowering IOP, improving pulsatile ocular blood flow and increasing ocular perfusion pressure. Other Glaucomas Latanoprost may provide effective IOP control in angle-closure glaucoma after iridectomy, in pigmentary glaucoma, glaucoma after cataract extraction and steroid-induced glaucoma. However, latanoprost was effective in only a minority of pediatric cases of glaucoma and is contraindicated in all forms of uveitic glaucoma. Safety In the articles reviewed, new or duration-related adverse events were reported.


1998 ◽  
Vol 82 (7) ◽  
pp. 731-736 ◽  
Author(s):  
L. Fontana ◽  
D. Poinoosawmy ◽  
C. V Bunce ◽  
C. O'Brien ◽  
R. A Hitchings

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Jaewan Choi ◽  
Michael S. Kook

Primary open angle glaucoma (POAG) is a multifactorial disease characterized by progressive retinal ganglion cell death and visual field loss. It is known that alterations in intraocular pressure (IOP), blood pressure (BP), and ocular perfusion pressure (OPP) can play a significant role in the pathogenesis of the disease. Impaired autoregulatory capacity of ocular blood vessels may render tissues vulnerable to OPP changes and potentially harmful tissue ischemia-reperfusion damage. Vascular risk factors should be considered more important in a subgroup of patients with POAG, and especially in patients with normal tension glaucoma (NTG) with evidence of unphysiological BP response. For example, reduction of BP during the nighttime has an influence on OPP, and increased circadian OPP fluctuation, which might stand for unstable ocular blood flow, has been found to be the consistent risk factor for NTG development and progression. Central visual field may be affected more severely than peripheral visual field in NTG patients with higher 24-hour fluctuation of OPP. This review will discuss the current understanding of allegedly major systemic and ocular hemodynamic risk factors for glaucoma including systemic hypertension, arterial stiffness, antihypertensive medication, exaggerated nocturnal hypotension, OPP, and autonomic dysregulation.


2011 ◽  
Vol 2 ◽  
pp. 332-336 ◽  
Author(s):  
Michal S. Nowak ◽  
Piotr Jurowski ◽  
Roman Gos ◽  
Marek E. Prost ◽  
Janusz Smigielski

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