Association of retinal vessel caliber and visual field defects in glaucoma.

PURPOSE: This study evaluates the asymmetry of peripapillary retinal vessel caliber between inferior and superior hemispheres in eyes with visual field defects predominantly in one hemifield. DESIGN: Observational case series. METHODS: In a retrospective study, 64 eyes of 64 patients with primary open-angle glaucoma who had a marked difference in visual field defects between hemifields and who had no history of diabetes, trauma, or vascular occlusive disease were studied. The diameters of the superior and inferotemporal vessels were measured at the optic disk border with calipers on an enlarged image. RESULTS: In 64 eyes, the average ratio of the superior temporal artery diameter to inferotemporal artery diameter was significantly greater in the eyes with predominantly superior visual field defects as compared with those with inferior defects (1.10 +/- 0.22 vs. 0.92 +/- 0.19, respectively, P =.002, two-tailed t test). This indicates that the arteriole corresponding to the hemifield with the greater visual field defect was narrower than the arteriole in the other hemifield. This relationship was confirmed using chi(2) analysis (P =.002) comparing the proportions of eyes with ratios greater or less than normal vessel caliber ratios (normal ratio = 0.95 from data reported by Jonas and associates to the location of the dominant field defect. No statistically significant relationship was detected between retinal vein diameter and localized visual field defects, as determined by both the unpaired t test and chi(2) analysis. CONCLUSION: In eyes with primary open-angle glaucoma, this study demonstrates a strong association between decreased peripapillary arteriole diameter and visual field defects in the corresponding hemifield. This reflects either an ischemic basis for glaucomatous damage or vascular constriction when there are fewer axons to nourish.

Optic nerve blood flow is diminished in eyes of primary open-angle glaucoma suspects.

PURPOSE: The purpose of this study was to evaluate optic nerve blood flow in primary open-angle glaucoma suspect eyes with normal automated visual fields, in an attempt to elucidate how early in the glaucomatous disease process changes in optic nerve blood flow become apparent. METHODS: Twenty-one eyes (21 patients) suspected of having primary open-angle glaucoma were studied prospectively and compared with a previously reported cohort of 22 eyes (22 patients) with primary open-angle glaucoma and 15 eyes (15 subjects) of age-matched controls. Primary open-angle glaucoma suspect eyes had untreated intraocular pressure greater than 21 mm Hg and normal visual fields using Humphrey program 24-2 or 30-2 with a full threshold strategy. Laser Doppler flowmetry was used to measure optic nerve head blood velocity, volume, and flow at four quadrants in the optic nerve, in the cup, and in the foveola of one eye of each patient. The mean flow from the superotemporal rim, inferotemporal rim, and cup was calculated (Flow(3)) and identified as the main outcome measure. Measurements from primary open-angle glaucoma suspect eyes were compared with corresponding measurements from controls and eyes with primary open-angle glaucoma; a Student t test was employed with a Bonferroni corrected P value of.025 to account for comparisons of primary open-angle glaucoma suspects both to controls and to eyes with primary open-angle glaucoma. RESULTS: Compared with controls, Flow(3) was 24% lower in primary open-angle glaucoma suspect eyes (P <.0003). In primary open-angle glaucoma suspect eyes, flow was 16% lower in the superotemporal rim (P <.007), 35% lower in the cup (P <.007), and 22% lower in the inferotemporal neuroretinal rim (P <.029) compared with controls. No significant difference between primary open-angle glaucoma suspect and control eyes was seen in the inferonasal rim, superonasal rim, or foveola. No significant difference was detected at any location between primary open-angle glaucoma suspect eyes and eyes with primary open-angle glaucoma. CONCLUSIONS: Laser Doppler flowmetry detected circulatory abnormalities in primary open-angle glaucoma suspects who did not have any manifest visual field defect. Decreases in flow in glaucoma suspects were similar in magnitude to those of subjects with primary open-angle glaucoma. These data suggest that impaired optic nerve blood flow develops early in the glaucomatous process and does not develop solely as a result of glaucoma damage.

Venous collateral remodeling in a patient with posttraumatic glaucoma.

PURPOSE: To photographically document venous collateral development, remodeling, and regression in a patient with traumatic glaucoma. METHODS: Consecutive fundus photographs were evaluated, labeled, and correlated with the clinical history of a patient with unilateral posttraumatic glaucoma. RESULTS: This report photographically documents the appearance, remodeling, and subsequent disappearance of collateral vessels from venous occlusion on the surface of the optic disk in an eye with increased intraocular pressure and progressive glaucomatous cupping. CONCLUSIONS: Asymptomatic chronic obstruction of a branch retinal vein on the optic disk may cause venous collaterals to develop in the absence of retinal hemorrhages or other signs of venous occlusive disease. Increased intraocular pressure, arteriolarsclerosis, and glaucomatous cupping are risk factors for these occlusions.

Laser Doppler flowmetry of the optic nerve head in glaucoma.

The introduction of ocular laser Doppler flowmetry during the last decade has greatly improved our ability to noninvasively assess the hemodynamics of the optic nerve in patients with glaucoma. Studies with laser Doppler flowmetry have determined that blood flow in the optic nerve is diminished in eyes with primary open-angle glaucoma and that this decrease occurs in patterns consistent with glaucomatous damage. Lower systemic blood pressure is associated with lower blood flow, supporting numerous studies linking systemic hypotension to glaucomatous damage. This direct relationship between systemic blood pressure and optic nerve blood flow has significant implications in terms of the etiology of glaucomatous damage and the treatment of ocular and systemic diseases in the glaucoma patient. Further research is needed to determine whether the circulatory abnormalities of the optic nerve head are a cause or a result of glaucomatous damage.

Effect of intravenous fenoldopam on intraocular pressure in ocular hypertension.

Intravenous fenoldopam, a selective dopamine-1 receptor agonist, was compared with placebo in this randomized, double-blind, two-period crossover study to evaluate its effects on intraocular pressure, aqueous dynamics, and macular blood flow in patients with elevated intraocular pressure or primary open-angle glaucoma. Doses of fenoldopam were titrated up to a maximum of 0.5 microgram/kg/min. Intraocular pressure, measured by pneumotonometry, was the primary outcome variable. Other outcomes included macular blood flow assessed by blue field examination, visual field examined by automated perimetry, aqueous outflow facility measured by tonography, and aqueous humor production determined by fluorophotometry. During infusions of fenoldopam, intraocular pressure increased from a mean baseline level of 29.2 mmHg to a mean maximum level of 35.7 mmHg. During the placebo infusions, pressure increased from a mean baseline of 28.4 mmHg to a mean of 29.0 mmHg at the time point that corresponded to the mean maximum intraocular pressure on the day intravenous fenoldopam was administered, to yield a mean difference in pressure between study days of 6.7 mmHg (P < 0.05). There were no apparent changes in macular blood flow, visual fields, or production or outflow of aqueous humor associated with fenoldopam infusion. The increase in intraocular pressure seen in this population of patients with ocular hypertension during infusions of fenoldopam is consistent with fenoldopam-associated increases in intraocular pressure reported in previous studies of healthy volunteers and of patients with accelerated systemic hypertension. These results further suggest that dopamine-1 receptors play a role in the regulation of intraocular pressure.