Pulsatile ocular blood flow in primary open-angle glaucoma and ocular hypertension

Kerr, Jan; Nelson, Patricia; O’Brien, Colm

doi:10.1016/s0002-9394(03)00717-7

Cited by 38 publications

(29 citation statements)

References 22 publications

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“…Several reports had suggested a beneficial effect of latanoprost on pulsatile ocular blood flow in glaucoma patients [66,67,68], but after adjustment of the measured outcome for the effect of the treatment on IOP [69] it could be shown that the former result was simply related to the reduction of the IOP and no improvement of vascular functions seems to occur with this substance. This is congruent with the observation that pulsatile ocular blood flow measurements with the Langham system are closely related to the actual level of IOP [70, 71]. Comparing the effect of latanoprost and brimonidine in patients with normal-tension glaucoma, a slight, but statistically not significant reduction in sphygmomanometric brachial blood pressure measurements was observed with brimonidine [50].…”

Section: Therapeutic Modalitiessupporting

confidence: 80%

Therapeutic Strategies for Normal-Tension Glaucoma

Orgül¹,

Zawinka²,

Gugleta³

2005

Ophthalmologica

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Treatment of normal-tension glaucoma has been a subject of debate for several years. Glaucomatous damage cannot be influenced directly, and current treatment modalities in normal-tension glaucoma are aimed at the control of risk factors. Intraocular pressure is a widely accepted risk factor and its reduction can improve the prognosis in normal-tension glaucoma patients. The repeated demonstration of the importance of hemodynamic factors in normal-tension glaucoma has, however, not been paralleled by a comparable progress in the development of therapeutic modalities capable of influencing favorably ocular blood flow. Today, calcium channel blockers seem to be the most promising adjunctive treatment to be considered in patients with glaucomatous optic neuropathy without increased intraocular pressure.

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Section: Therapeutic Modalitiessupporting

confidence: 80%

Therapeutic Strategies for Normal-Tension Glaucoma

Orgül¹,

Zawinka²,

Gugleta³

2005

Ophthalmologica

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“…11,12 POBF primarily reflects the choroidal circulation and provides diagnostic value especially in detecting ischemic response in ocular tissue, although it is suggested to be more useful for studying intraindividual blood flow changes (ie before and after therapy comparison) rather than interindividual comparison. 13 It has been clinically found to be reduced in a variety of ocular diseases including glaucoma, 14 age-related macular degeneration, 15,16 and diabetic retinopathy. 17 Our previous study has shown that GO patients had significantly reduced POBF as compared to those with Graves' disease only or healthy subjects.…”

Section: Discussionmentioning

confidence: 99%

Pulsatile ocular blood flow change after treatment with systemic steroid in patients with Graves' ophthalmopathy

Tsai

Kau²,

Tsai

et al. 2005

Eye

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Purpose Our previous study has demonstrated an impairment of pulsatile ocular blood flow (POBF) in patients with Graves'ophthalmopathy (GO). Here we further evaluate the haemodynamic change in GO patients after systemic steroid. Methods In a prospective, interventional, consecutive clinical case series, all patients with active and moderately severe GO who underwent systemic steroid treatment were evaluated. The change of POBF and the clinical activity and severity of the disease were assessed. Results In total, 11 patients underwent intravenous methylprednisolone pulse therapy followed by 2-month oral prednisolone therapy. POBF improved from a mean value of 476.5 to 614.7 ll/min (Po0.001) after treatment. Likewise, the mean clinical activity score reduced from 4.8 to 1.6. However, systemic steroid had less effect on the severity of GO. It also revealed that there is a greater improvement of POBF in those with more clinical activity score (44) at the onset. Conclusions Following treatment with systemic steroid we have demonstrated a significant improvement in POBF in patients with GO.

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“…As such, vascular insufficiency and the associated ischemic insult to retinal ganglion cells are implicated in the pathogenesis of glaucoma. It has been shown that primary open-angle glaucoma (POAG) patients have an impaired blood flow in the central retinal artery [21][22][23] , inner retinal vasculature [24] , optic nerve head [25,26] , ophthalmic artery [27,28] and choroid [29,30] . Collectively, these findings support a role for vascular insufficiency in glaucoma although caution must be taken in interpreting the results due to heterogeneous patient groups, small group sizes, differing measurement techniques, the unknown effect of antiglaucoma medications and the varying comparison of POAG patients with either healthy or ocular hypertensive patients.…”

Section: Vascular Insufficiencymentioning

confidence: 99%

Mechanisms of Retinal Ganglion Cell Injury in Aging and Glaucoma

2010

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Aging is the greatest risk factor for glaucoma, implying that intrinsic age-related changes to retinal ganglion cells, their supporting tissue or both make retinal ganglion cells susceptible to injury. Changes to the ocular vasculature, connective tissue of the optic nerve head and mitochondria, which have been documented with advancing age and shown to be exacerbated in glaucoma, may predispose to glaucomatous injury. When considering such age-related changes, it is difficult to separate pathological change from physiological change, and cause from consequence. The insults that predispose aged retinal ganglion cells to injury are likely to be varied and multiple; therefore, it may be more relevant to identify and treat common mechanisms that predispose to retinal ganglion cell failure and/or death. We suggest that mitochondrial dysfunction, as either a cause or consequence of injury, renders retinal ganglion cells sensitive to degeneration. Therapeutic approaches that target mitochondria and promote energy production may provide a general means of protecting aged retinal ganglion cells from degeneration, regardless of the etiology.

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Pulsatile ocular blood flow in primary open-angle glaucoma and ocular hypertension

Cited by 38 publications

References 22 publications

Therapeutic Strategies for Normal-Tension Glaucoma

Therapeutic Strategies for Normal-Tension Glaucoma

Pulsatile ocular blood flow change after treatment with systemic steroid in patients with Graves' ophthalmopathy

Mechanisms of Retinal Ganglion Cell Injury in Aging and Glaucoma

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