Dorzolamide, visual function and ocular hemodynamics in normal-tension glaucoma.

The purpose of this study was to determine how a topical carbonic anhydrase inhibitor, dorzolamide, alters visual function and ocular blood flow in persons with normal-tension glaucoma. Eighteen normal tension glaucoma patients, after washout of other ocular medications, were treated for four weeks with 2% dorzolamide, three times daily. A control group of eleven other normal-tension glaucoma patients received placebo eye drops. Patients were studied before treatment, and after two and four weeks of treatment. Each study included assessment of central visual function (contrast sensitivity), intraocular pressure (IOP), and several aspects of ocular hemodynamics, including measures of retinal arteriovenous passage time, retinal arterial and venous diameters, and flow velocities in the ophthalmic, central retinal, and posterior ciliary arteries. Dorzolamide significantly reduced IOP at two and four weeks (each p<0.01), and at the same time increased contrast sensitivity at both three and six cycles per degree (each p<0.05). Neither of these variables changed significantly in the control group. Dorzolamide also accelerated retinal arteriovenous passage time of fluorescein dye, at constant retinal arterial and venous diameters (p<0.05), but failed to change flow velocities in any retrobulbar vessel. The ability of dorzolamide to improve contrast sensitivity in persons with normal-tension glaucoma may be related to either IOP reduction or altered ocular perfusion.     

The impact of ocular blood flow in glaucoma

Two principal theories for the pathogenesis of glaucomatous optic neuropathy (GON) have been described--a mechanical and a vascular theory. Both have been defended by various research groups over the past 150 years. According to the mechanical theory, increased intraocular pressure (IOP) causes stretching of the laminar beams and damage to retinal ganglion cell axons. The vascular theory of glaucoma considers GON as a consequence of insufficient blood supply due to either increased IOP or other risk factors reducing ocular blood flow (OBF). A number of conditions such as congenital glaucoma, angle-closure glaucoma or secondary glaucomas clearly show that increased IOP is sufficient to lead to GON. However, a number of observations such as the existence of normal-tension glaucoma cannot be satisfactorily explained by a pressure theory alone. Indeed, the vast majority of published studies dealing with blood flow report a reduced ocular perfusion in glaucoma patients compared with normal subjects. The fact that the reduction of OBF often precedes the damage and blood flow can also be reduced in other parts of the body of glaucoma patients, indicate that the hemodynamic alterations may at least partially be primary. The major cause of this reduction is not atherosclerosis, but rather a vascular dysregulation, leading to both low perfusion pressure and insufficient autoregulation. This in turn may lead to unstable ocular perfusion and thereby to ischemia and reperfusion damage. This review discusses the potential role of OBF in glaucoma and how a disturbance of OBF could increase the optic nerve's sensitivity to IOP.     

Normal-tension glaucoma with reversed ophthalmic artery flow

PURPOSE: To describe a case of normal-tension glaucoma with bilateral complete occlusion of the internal carotid artery. METHODS: A 58-year-old man who had a 2-year history of normal-tension glaucoma in the left eye presented with ocular ischemic syndrome. To evaluate the orbital circulation, cerebral angiography and color Doppler imaging were performed. RESULTS: Cerebral angiography showed bilateral complete occlusion of the internal carotid artery and collateral blood supply through the right and left ophthalmic arteries, in which the flow was reversed. Moreover, color Doppler imaging revealed lower blood flow velocities in the left central retinal and short posterior ciliary arteries, suggesting a steal phenomenon. CONCLUSION: Normal-tension glaucoma in the present case may be caused by chronic reduction of retrobulbar blood flow resulting from a steal phenomenon.     

Ocular hemodynamics in normal tension glaucoma: effect of bimatoprost

BACKGROUND: Altered ocular perfusion plays a role in the pathophysiology of normal tension glaucoma. Prostaglandin-like substances are very effective in lowering intraocular pressure. Less data are available regarding the influence of these compounds on ocular perfusion. In the present study the effects of bimatoprost, which has recently been shown to increase the vascular tone of ciliary arteries in vitro, on the blood flow velocity are investigated. PATIENTS AND METHODS: n = 9 eyes from 9 normal tension glaucoma patients were subjected to color Doppler imaging (CDI) before and during a 3 - 5 week therapy with bimatoprost. RESULTS: Bimatoprost reduces intraocular pressure from 14.0 +/- 0.4 to 11.0 +/- 0.5 mmHg (n = 9; P < 0.001). Systolic as well as diastolic blood flow velocities, resistive index (RI) and pulsatility index (PI), measured by CDI, were unaltered in the presence of bimatoprost. DISCUSSION: Bimatoprost does not influence blood flow velocities in the retrobulbar vessels. The in vitro observation of increased vascular tone in the presence of bimatoprost seems not to be relevant for ocular hemodynamics.     

Simultaneous management of blood flow and IOP in glaucoma.

Factors other than intraocular pressure (IOP) elevation must be involved in initiation and progression of glaucoma. An additional element in disease causation may be ischemia in the retina and optic nerve head. Ischemic damage to neurons in the CNS is similar mechanistically and histopathologically to changes seen in glaucoma. Further, glaucoma patients with normal IOP show clear evidence for cerebral and ocular ischemia. Aging and atherosclerosis reduce the ability of the eye to autoregulate blood flow when ocular perfusion pressure changes: the dependence of blood flow on perfusion pressure links ischemia to IOP. Consequently, neuroprotective treatments for glaucoma should be designed to both reduce IOP and improve ocular nutrient delivery.     

Progress in measurement of ocular blood flow and relevance to our understanding of glaucoma and age-related macular degeneration.

New technologies have facilitated the study of the ocular circulation. These modalities and analysis techniques facilitate very precise and comprehensive study of retinal, choroidal, and retrobulbar circulations. These techniques include: 1. Vessel caliber assessment; 2. Scanning laser ophthalmoscopic fluorescein angiography and indocyanine green angiography to image and evaluate the retinal circulation and choroidal circulation respectively; 3. Laser Doppler flowmetry and confocal scanning laser Doppler flowmetry to measure blood flow in the optic nerve head and retinal capillary beds; 4. Ocular pulse measurement; and 5. color Doppler imaging to measure blood flow velocities in the central retinal artery, the ciliary arteries and the ophthalmic artery. These technique have greatly enhanced the ability to quantify ocular perfusion defects in many disorders, including glaucoma and age-related macular degeneration, two of the most prevalent causes of blindness in the industrialized world. Recently it has become clear, in animal models of glaucoma, that retinal ganglion cells die via apoptosis. The factors that initiate apoptosis in these cells remain obscure, but ischemia may play a central role. Patients with either primary open-angle glaucoma or normal-tension glaucoma experience various ocular blood flow deficits. With regard to age-related macular degeneration, the etiology remains unknown although some theories include primary retinal pigment epithelial senescence, genetic defects such as those found in the ABCR gene which is also defective in Stargardt's disease and ocular perfusion abnormalities. As the choriocapillaris supplies the metabolic needs of the retinal pigment epithelium and the outer retina, perfusion defect in the choriocapillaris could account for some of the physiologic and pathologic changes in AMD. Vascular defects have been identified in both nonexudative and exudative AMD patients using new technologies. This paper is a comprehensive update describing modalities available for the measurement of all new ocular blood flow in human and the clinical use.     

Retrobulbar hemodynamics in normal-tension glaucoma with asymmetric visual field change and asymmetric ocular perfusion pressure

PURPOSE: To investigate retrobulbar hemodynamics by means of color Doppler imaging in normal-tension glaucoma with asymmetric visual field change and asymmetric ocular perfusion pressure. METHODS: Forty-nine consecutive patients who met the enrollment criteria were enrolled in a prospective study. We measured intraocular pressure at 2-hour intervals for 24 hours and performed color Doppler imaging of the orbital arteries, 48-hour ambulatory blood pressure monitoring, and visual field testing. Color Doppler parameters were compared between subjects with higher ocular perfusion pressure in the eye that had a better mean deviation (concordant group) and worse mean deviation (discordant group). RESULTS: In the eyes with the better mean deviation, the end-diastolic velocity of the ophthalmic artery was significantly slower in the discordant group (P=.0145), while in the eyes with the worse mean deviation, the peak systolic and end-diastolic velocities of the ophthalmic artery were significantly slower and the resistance index of the ophthalmic artery was significantly higher in the discordant group (P=.0395, P=.0088, and P=.0324, respectively). In the concordant group, the end-diastolic velocity of the central retinal artery was slower in eyes with a worse mean deviation. CONCLUSION: Retrobulbar hemodynamics are significantly altered in patients with normal-tension glaucoma who have better ocular perfusion pressure in the eye that has a worse mean deviation.     

Effect of bimatoprost on ocular circulation in patients with open-angle glaucoma or ocular hypertension

Purpose To study the effect of bimatoprost 0.03% (Lumigan) on ocular hemodynamics in patients with open-angle glaucoma or ocular hypertension.Methods One randomly selected eye of each of 26 patients with open-angle glaucoma or ocular hypertension was enrolled. Each patient received a drop of bimatoprost 0.03% once daily for 1 month. The effect of bimatoprost on ocular circulation was assessed by color Doppler imaging (CDI), which measured peak systolic, end-diastolic blood flow velocities and resistance indices in the ophthalmic, posterior ciliary and central retinal arteries. Retrobulbar hemodynamics by CDI, intraocular pressure by Goldmann applanation tonometer, blood pressure by cuff, and heart rate by palpation were measured at baseline and at 1 month after bimatoprost treatment.Results Blood flow velocities and resistance indices in all retrobulbar vessels showed no statistically significant differences between baseline and bimatoprost condition (P>0.05). Bimatoprost lowered intraocular pressure significantly (P<0.001), with a mean change of 6.5 mmHg (27%) after 1 month of treatment. The systolic (P=0.38) and diastolic (P=0.74) blood pressures and pulse rate (P=0.94) did not show statistically significant differences during the study period.Conclusions The results of this study suggest that topical bimatoprost 0.03% significantly reduces intraocular pressure in patients with open-angle glaucoma or ocular hypertension. However, it does not have any effect on retrobulbar hemodynamics in open-angle glaucoma and ocular hypertension.The authors have no commercial or proprietary interest in any of the equipment and medication mentioned in this study     

Therapeutic strategies for normal-tension glaucoma

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.     

Role of cerebrospinal fluid pressure in the pathogenesis of glaucoma

The pathogenesis of normal (intraocular) pressure glaucoma has remained unclear so far. As hospital‐based studies showed an association of normal‐pressure glaucoma with low systemic blood pressure, particularly at night, and with vasospastic symptoms, it has been hypothesized that a vascular factor may play a primary role in the pathogenesis of normal‐pressure glaucoma. That assumption may, however, be contradicted by the morphology of the optic nerve head. Eyes with normal‐pressure glaucoma and glaucomatous eyes with high‐intraocular pressure can show a strikingly similar appearance of the optic nerve head, including a loss of neuroretinal rim, a deepening of the optic cup, and an enlargement of parapapillary atrophy. These features, however, are not found in any (other) vascular optic neuropathy, with the exception of an enlargement and deepening of the optic cup in arteritic anterior ischaemic optic neuropathy. One may additionally take into account (i) that it is the trans‐lamina cribrosa pressure difference (and not the trans‐corneal pressure difference, i.e. the so‐called intraocular pressure) which is of importance for the physiology and pathophysiology of the optic nerve head; (ii) that studies have shown that the anatomy of the optic nerve head including the intraocular pressure, the anatomy and biomechanics of the lamina cribrosa and peripapillary sclera, retrobulbar orbital cerebrospinal fluid pressure and the retrobulbar optic nerve tissue pressure may be of importance for the pathogenesis of the highly myopic type of chronic open‐angle glaucoma; (iii) that studies have suggested a physiological association between the pressure in all three fluid filled compartments, i.e. the systemic arterial blood pressure, the cerebrospinal fluid pressure and the intraocular pressure; (iv) that an experimental investigation suggested that a low cerebrospinal fluid pressure may play a role in the pathogenesis of normal (intraocular) pressure glaucoma; and (v) that recent clinical studies reported that patients with normal (intraocular) pressure glaucoma had significantly lower cerebrospinal fluid pressure and a higher trans‐lamina cribrosa pressure difference when compared to normal subjects. One may, therefore, postulate that a low cerebrospinal fluid pressure may be associated with normal (intraocular) pressure glaucoma. A low systemic blood pressure, particularly at night, could physiologically be associated with a low cerebrospinal fluid pressure, which leads to an abnormally high trans‐lamina cribrosa pressure difference and as such to a similar situation as if the cerebrospinal fluid pressure is normal and the intraocular pressure is elevated. This model could explain why patients with normal (intraocular) pressure glaucoma tend to have a low systemic blood pressure, and why eyes with normal (intraocular) pressure glaucoma and eyes with high‐pressure glaucoma, in contrast to eyes with a direct vascular optic neuropathy, show profound similarities in the appearance of the optic nerve head.     

Colour Doppler imaging in normal pressure glaucoma patients

AIM: Ocular hemodynamics is of great interest in glaucoma, especially since vascular disturbances may play a pathogenetic role in disease development. To investigate the hemodynamic differences between normal pressure glaucoma patients and normal volunteers, flow velocities of the retrobulbar vessels were measured by colour Doppler imaging. METHOD: 15 patients with normal pressure glaucoma (NPG) and 15 healthy volunteers underwent colour Doppler imaging (CDI) of the retrobulbar vessels. The patients and the volunteers were especially gender- and age-matched. Peak systolic velocities (PSV), end-diastolic velocities (EDV), and resistive indices (RI) of the ophthalmic artery and central retinal artery were obtained. RESULTS: In NPG patients, PSV and EDV in the central retinal artery were significantly decreased, whereas RI was increased in central retinal artery and the ophthalmic artery. CONCLUSION: Colour Doppler imaging is a non-invasive technique that allows further estimation of the ocular circulatory status. Particularly in the group of patients with disturbed hemodynamics, like NPG patients, it was able to show a reduction of the retrobulbar hemodynamics.     

Blood flow in glaucoma

PURPOSE OF REVIEW: Glaucoma, one of the leading causes of blindness in the world, is characterized by progressive visual field loss and distinctive excavation of the optic nerve head. Although elevated intraocular pressure is the major risk factor, there is increasing evidence that the pathogenesis of glaucoma is also linked to altered ocular blood flow. This review summarizes the recent publications relevant to blood flow in glaucoma. RECENT FINDINGS: Several studies indicate that a perfusion instability, rather than a steady reduction of ocular blood flow, might contribute to glaucomatous optic neuropathy. The main cause of the instability is a disturbed autoregulation in the context of a general vascular dysregulation. The underlying mechanism of such a vascular dysregulation is not known. A dysfunction of both the autonomic nervous system and vascular endothelial cells is discussed. SUMMARY: The mechanical and vascular theories are not mutually exclusive; on the contrary, a vascular dysregulation increases the susceptibility to intraocular pressure. Therapeutically, therefore, both an intraocular pressure reduction and an improvement of the ocular blood flow might be considered.     

Update on prospective glaucoma intervention studies

BACKGROUND: Previously published prospective therapeutic intervention studies in ocular hypertension and glaucoma are summarized. MATERIAL AND METHODS: The concept of intraocular pressure reduction was evaluated in normal tension glaucoma ["Early manifest glaucoma trial (EMGT)"], the "Collaborative normal-tension glaucoma study (CNTGS)" and ocular hypertension ["Ocular hypertensive study (OHTS)" as well as the "European glaucoma prevention study (EGPS)"]. Early open angle glaucoma patients were included in the EMGT trial as well as the "Collaborative initial glaucoma treatment study (CIGTS)", whereas advanced glaucoma patients were examined in the "Advanced glaucoma intervention study (AGIS)". RESULTS: The study design, the results and the conclusions will be highlighted in the text. CONCLUSIONS: The therapeutic concept of intraocular pressure reduction decreases the risk of progression by 50 % in normal tension glaucoma, ocular hypertension and early open angle glaucoma. The mean pressure reduction to 12 mmHg in advanced glaucoma abolished visual field progression. The natural course of the disease documented by the control groups is now known. Sensitive glaucoma progression detection is clinically available by glaucoma change probability maps (Humphrey-full threshold perimetry) used in the EMGT.     

Glaucoma progression is associated with decreased blood flow velocities in the short posterior ciliary artery

BACKGROUND: An altered perfusion of the optic nerve head has been proposed as a pathogenic factor in glaucoma. AIM: To investigate potential differences in the ocular haemodynamics of patients having glaucoma with progressive versus stable disease, as well as healthy volunteers. METHODS: Peak-systolic velocity (PSV), end-diastolic velocity (EDV) and resistivity index in the short posterior ciliary artery (SPCA), central retinal artery (CRA) and ophthalmic artery were recorded in 114 consecutive patients having glaucoma with an intraocular pressure (IOP) < or =21 mm Hg, as well as in 40 healthy volunteers, by colour Doppler imaging (CDI). RESULTS: Of the 114 patients with glaucoma, 12 showed glaucoma progression (follow-up period: mean 295 (standard deviation (SD) (18) days). CDI measurements in these patients showed decreased PSV and EDV in the SPCA (p<0.001 and p<0.05, respectively) and decreased PSV in the CRA compared with patients with stable glaucoma and healthy controls (p<0.05). No differences in flow velocities were found for the ophthalmic artery. IOP and systemic blood pressure was similar in all the three groups. CONCLUSIONS: Progressive glaucoma is associated with decreased blood flow velocities in the small retrobulbar vessels supplying the optic nerve head. The detected difference could represent a risk factor for progression of glaucomatous optic neuropathy.     

Interocular difference in progression of glaucoma correlates with interocular differences in retrobulbar circulation

PURPOSE:To evaluate the correlation between interocular difference in progression of glaucomatous damage and interocular differences in retrobulbar blood flow. METHODS:On the basis of a retrospective analysis of visual fields, progressive damage was identified in 20 patients with primary open-angle glaucoma. As a parameter of interocular difference in progression of visual field damage, the angle (gamma) between the regression lines of the visual field index mean defect over time per eye was calculated for each subject. The relationship between the angle gamma and interocular differences in intraocular pressure and retrobulbar color Doppler imaging parameters was analyzed by a multiple linear regression analysis in a stepwise forward approach. RESULTS:With larger interocular differences in progression of glaucomatous damage, lower mean blood flow velocities in the ophthalmic artery (partial r = -.69; P <. 0016), higher resistivity indices in the central retinal artery (partial r =.48; P <.0456), and higher peak systolic velocities in the ophthalmic artery (partial r =.52; P <.0285) were noted in the eyes with more marked progression of damage (multiple r =.71; P <. 0099). Interocular differences in progression of visual field damage were not related to intraocular pressure or extent of visual field damage. CONCLUSION:Independent of the extent of the interocular difference in glaucomatous damage and intraocular pressure, interocular difference in progression of glaucomatous visual field damage correlates with interocular difference in retrobulbar hemodynamic parameters.     

Vascular risk factors for primary open angle glaucoma: the Egna-Neumarkt Study

OBJECTIVE: To assess the impact of vascular risk factors on the prevalence of primary open angle glaucoma. DESIGN: Population-based cross-sectional study. PARTICIPANTS: Four thousand two hundred ninety-seven patients more than 40 years of age underwent a complete ocular examination in the context of the Egna-Neumarkt Glaucoma Study. INTERVENTION: Ocular examinations were performed by trained, quality-controlled ophthalmologists according to a predefined standardized protocol including medical interview, blood pressure reading, applanation tonometry, computerized perimetry, and optic nerve head examination. MAIN OUTCOME MEASURES: Prevalences of ocular hypertension, primary open-angle glaucoma, normal-tension glaucoma, and other types of glaucoma were determined. Correlation coefficients were calculated for the association between systemic blood pressure and age-adjusted intraocular pressure (IOP) and between age and both intraocular and systemic blood pressures. Odds ratios were computed to assess the risk of primary open-angle glaucoma and normal-tension glaucoma in relation to systemic hypertension or antihypertensive medication, blood pressure levels, diastolic perfusion pressure, and a number of other cardiovascular risk factors. RESULTS: A positive correlation was found between systemic blood pressure and IOP, and an association was found between diagnosis of primary open-angle glaucoma and systemic hypertension. Lower diastolic perfusion pressure is associated with a marked, progressive increase in the frequency of hypertensive glaucoma. No relationship was found between systemic diseases of vascular origin and glaucoma. CONCLUSIONS: Our data are in line with those reported in other recent epidemiologic studies and show that reduced diastolic perfusion pressure is an important risk factor for primary open-angle glaucoma.     

Pattern of visual field defects in normal-tension and high-tension glaucoma

There are probably two major types of causative factors in open-angle glaucoma: pressure-dependent and pressure-independent. If clinical features such as the pattern of visual field defects differ between normal-tension and high-tension glaucoma, the differences may provide an insight for discriminating between the pressure-dependent and the pressure-independent damage in open-angle glaucoma. This article gives a brief review of the most recent studies including reports wherein progression or pattern of visual field defects in normal-tension and high-tension glaucoma or primary open-angle glaucoma are addressed. Further deterioration of the visual field in 5 years is expected in about 50% of eyes with normal-tension glaucoma in which intraocular pressure is one of the contributing factors. This figure may be greater than that seen in eyes with primary open-angle glaucoma where intraocular pressure is controlled with surgery in the middle teens. When eyes with normal-tension glaucoma and high-tension glaucoma or primary open-angle glaucoma were matched for extent of overall visual field loss, many studies noted a difference in the pattern of visual field defects between the two groups. Visual field defects in normal-tension glaucoma are relatively more localized and closer to fixation, especially in the nasal superior quadrant and may be more predominant in the lower hemifield. Results of other psychophysical tests also appear to support the above findings.     

The impact of glaucoma medication on parameters of ocular perfusion

Whereas intraocular pressure is considered a major risk factor in glaucoma, growing evidence now indicates that ocular ischemia plays a major role too. By virtue of this and because many existing medications are able to interact with vasculature, altering ocular blood flow, it is essential that current and future medications for glaucoma be evaluated for their effect on ocular circulation. The authors review published papers examining the effect of topical and some systemic medications on ocular blood flow, focusing mostly on data from the human eye. The authors provide a comprehensive review on the effect of subclasses of medications (eg, carbonic anhydrase inhibitors, beta-blockers, alpha-adrenergic agonists, and prostaglandin analogues on optic nerve head, and on retinal, choroidal, and retrobulbar circulation. The various claims for enhancements or reduction of ocular circulation within each class of medication are reviewed and evaluated.     

A comparative study of betaxolol and dorzolamide effect on ocular circulation in normal-tension glaucoma patients

OBJECTIVE: To determine whether dosages of a selective beta-blocking agent (betaxolol) and a topical carbonic anhydrase inhibitor (dorzolamide), sufficient to significantly lower intraocular pressure (IOP), have similar or disparate impact on the retinal and retrobulbar circulation. DESIGN: Counterbalanced crossover, with open-label use of medications. PARTICIPANTS: Nine persons with normal-tension glaucoma (NTG). INTERVENTION: After a 3-week drug washout, NTG patients were studied after 1 month of treatment with either dorzolamide or betaxolol, with determinations of IOP and retinal and retrobulbar hemodynamics. MAIN OUTCOME MEASURES: At baseline and after treatment with each drug, retinal arteriovenous passage time was determined by scanning laser ophthalmoscopy after fluorescein dye injection, and flow velocities in the central retinal and ophthalmic arteries were measured with color Doppler ultrasonography imaging. RESULTS: Betaxolol and dorzolamide each lowered IOP significantly, with these changes apparent and maximal after 2 weeks (each P < 0.05). In contrast, dorzolamide (but not betaxolol) accelerated arteriovenous passage of fluorescein dye in the inferior temporal quadrant of the retina (P < 0.05). Neither drug affected arteriovenous passage in the superotemporal retina or any aspect of central retinal or ophthalmic artery flow velocity after either 2 or 4 weeks. CONCLUSIONS: Although both dorzolamide and betaxolol are effective ocular hypotensive agents and their topical instillation leaves retrobulbar hemodynamics unaltered, dorzolamide alone accelerates inferotemporal retinal dye transit.     

Nocturnal blood pressure reduction: effect on retrobulbar hemodynamics in glaucoma

BACKGROUND:Several studies suggest that nocturnal reductions in systemic blood pressure (BP) may be associated with onset or progression of glaucomatous optic neuropathy. The present study aimed to find out whether reductions in nocturnal BP are linked to retrobulbar blood flow perturbations in glaucoma patients.METHODS:Fifteen patients with non-progressing glaucoma and 15 controls were studied in the evening ("baseline") and then at a point of significantly reduced arterial BP during the night. Flow velocities were measured with color Doppler imaging (CDI) in the ophthalmic, central retinal, and nasal and temporal short posterior ciliary arteries, and with transcranial Doppler (TCD) in the middle cerebral artery. BP, corrected for posture, was monitored throughout the night.RESULTS:Maximal posture-corrected nocturnal BP reductions were similar in patients and controls. The reductions were about 10% for each group ( P<0.01). At baseline, patients had lower peak systolic and end-diastolic velocity ( P<0.05) in the short posterior ciliary arteries than controls. Flow velocities in these arteries remained constant in glaucoma patients, while controls showed significant declines. Patients and controls demonstrated blood flow velocities unchanged from baseline in the central retinal, ophthalmic, and middle cerebral arteries during nocturnal BP reduction.CONCLUSIONS:In patients with non-progressing glaucoma there was no evidence of cerebral or retrobulbar hemodynamic abnormalities during nocturnal BP dips. Posterior ciliary arterial blood flow velocities were similar in glaucoma patients and controls during nocturnal BP dips.