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Objective To evaluate the incidence of visual field and optic disc progression in glaucoma patients with distinct patterns of optic disc damage. Design Prospective, observational case series. Participants One hundred five patients with open-angle glaucoma. Methods Baseline optic disc photographs of 105 study eyes of 105 patients were reviewed by 2 masked observers and classified according to patterns of disc damage into the following categories: focal, myopic, senile sclerotic, and generalized disc damage. Patients were followed up every 6 months with standard automated perimetry (SAP), high-pass resolution perimetry (HRP), and scanning laser tomography (SLT) with the Heidelberg Retina Tomograph. Main outcome measures Visual field (SAP and HRP) and optic disc (SLT) progression were determined according to predefined criteria. Results Twenty-four eyes were classified into the focal, 8 into the myopic, 12 into the senile sclerotic, and 28 into the generalized group. Eyes from 33 patients could not be classified by the observers into any of these groups and were excluded from further analysis. Although intraocular pressure during follow-up was similar among the four groups, some differences in frequency of progression were observed. Patients with senile sclerotic discs had the lowest rates of visual field progression (both with SAP and HRP) and optic disc progression, although the differences were significant only for optic disc progression ( P = 0.05). Conclusions Patients with senile sclerotic discs showed a tendency towards less visual field and optic disc progression when compared with patients with other types of disc damage.

Objective A recently reported randomized study described the role of intraocular pressure (IOP) in normal-tension glaucoma (NTG) pathogenesis and the effect of therapeutic lowering of IOP. This is a report of an analysis of the natural course of NTG during the time eyes were not receiving therapy, either in the time interval awaiting randomization or after being randomly assigned not to receive treatment to lower the IOP. Design Analysis of prospectively collected data on the long-term course of a cohort of untreated subjects with normal-tension glaucoma, a subset of subjects enrolled in a randomized controlled clinical trial. RANDOMIZATION AND SUBJECT SELECTION: If the field defect in the study eye threatened the point of fixation, the subject was randomly assigned to start on treatment immediately or to be observed without treatment until progression was documented. Otherwise, an eye was randomly assigned only when and if, subsequent to enrollment, it showed visual field progression, progression of optic disc cupping, or a new disc hemorrhage. Participants Data were collected for this report on 160 subjects observed without treatment among a total enrollment of 260. They consist of 49 subjects who were randomly assigned on enrollment not to receive therapy, 24 followed without treatment for a time until later being randomly assigned to treatment, 31 similarly followed without treatment and who were later randomly assigned to be followed for an additional time without treatment, and 56 who enrolled but were never randomly assigned. Main outcome measures Visual field data were used in this report only from the interval during which the eye had not been assigned to receive therapy and were analyzed by two measures of progression: the "survival" time to meeting a criterion of confirmed localized progression and the rate of change in the mean deviation (MD) index over time. Results The four subgroups just described were similar at baseline, except that the average MD index was slightly better for the 56 eyes that never progressed during the period of follow-up. By Kaplan-Meier analysis of all untreated subjects combined, approximately one third showed localized progression within 3 years and about half within 5 to 7 years. Of subjects followed for 3 years or more, 62 of 109 did not show a statistically significant negative slope of MD regressed over time, whereas the others showed a statistically significant MD decline, mainly between -0.2 and -2 db per year. Conclusions Some cases of NTG progress more rapidly than others. Although approximately half of cases showed a confirmed localized visual field deterioration by 7 years, the change is typically small and slow, often insufficient to measurably affect the MD index.

Purpose: The purpose of this study was to observe the blood flow velocity in the retrobulbar vessels of patients with glaucoma with different appearances of optic discs. Methods: Patients with four different disc appearances (focal ischemic discs, myopic glaucomatous discs, senile sclerotic discs, and discs with a generalized enlargement of the cup) were selected from a pool of optic discphotographs. No clinical information from the patients was available during the selection. Color Doppler imaging (CDI) was performed in those patients whose discs clearly belonged to one of the disc patterns. The peak systolic and end diastolic velocity were measured and the resistance index calculated from the central retinal artery, short posterior ciliary arteries and ophthalmic artery. Results: Color Doppler imaging was performed in 24 patients with focal ischemic discs, 26 patients with myopic glaucomatous discs, 16 patients with senile sclerotic discs, and 16 patients with generalized enlargements of the cup. The patients with senile sclerotic discs had statistically significantly lower diastolic velocity and a higher resistance index in their ophthalmic, central retinal and the mean of the short posterior ciliary arteries sampled. These statistical differences persisted for the ophthalmic artery even after correcting the values for the age differences between the groups. Conclusions: Patients with senile sclerotic discs seem to have greater circulatory abnormalities in their retrobulbar vessels studied with color Doppler imaging that are compatible with a higher downstream resistance in these vessels. These circulatory abnormalities could be related to the pathogenesis of the glaucoma in these patients.

Purpose: To study the prevalence of risk factors for glaucoma as well as the pattern of visual field defects and their progression in patients with open angle glaucoma with different and distinct optic nerve appearances. Methods: One thousand seven hundred eleven optic disc stereo photographs of patients with glaucoma and ocular hypertension and of those suspected of having glaucoma were reviewed to identify pure examples of discs with four different optic disc appearances: focal ischemic discs, myopic glaucomatous discs, senile sclerotic discs, and generalized enlargement of the optic cup discs. The clinical charts of the selected patients were reviewed, with emphasis on the presence of predetermined ocular and systemic risk factors. Their automated visual fields also were analyzed. Results: Thirty-four patients with focal ischemic discs, 38 with myopic glaucomatous discs, 22 with senile sclerotic discs, and 23 with generalized enlargement of the optic cup discs were selected. Patients with myopic glaucoma and generalized enlargement of the optic cup discs were significantly younger than patients with focal ischemic and senile sclerotic discs. There were more women in the focal ischemic group. Patients with senile sclerotic discs had a significantly higher prevalence of ischemic heart disease; they also had a higher prevalence of systemic hypertension, which did not reach statistical significance. Migraine was 2.5 times more frequent in the focal ischemic group than in the other groups. Intraocular pressure was significantly higher in the generalized enlargement group. The pattern of visual field defect in the four groups also was distinctly different. Conclusions: Patients with different disc appearances, selected only from their disc photographs, showed differences in their demographic characteristics, prevalence of certain systemic risk factors, intraocular pressure levels, and the pattern of their visual field damage. These findings suggest that these various disc appearances probably represent different populations of patients with glaucoma with, possibly, different pathogenic mechanisms.

The authors studied the effect of multiple threshold determinations on local and global (root-mean-square) short-term fluctuation in 30 subjects (10 controls, 10 glaucoma suspects, and 10 glaucoma patients) with a mean age of 56.70 years. Five custom programs were designed on the Octopus perimeter in which the total number of threshold determinations was equal but in which thresholds at 2 principal locations were determined between 2 and 15 times. One randomly selected eye of each subject was first tested with the standard Octopus programs G1 and 31 followed by the custom programs. Local fluctuation initially increased with the number of threshold determinations and then stabilized after five determinations. Global fluctuation was not influenced by the number of determinations and the values obtained by the shorter custom programs were not significantly different from those obtained by the standard programs. Programs that determine thresholds only twice at a given location may underestimate local fluctuation. Furthermore, local fluctuation is de-emphasized by the "watering-down" effect of estimating global fluctuation.

One hundred forty-three patients with intraocular pressures (IOPs) above 22 mmHg and without visual field defects or any obvious evidence of optic nerve damage were randomly assigned to either a timolol treatment group or no treatment in a 6-year prospective clinical trial. Endpoints were defined as reproducible visual field defects on automatic perimetry, disc hemorrhages, or stereophotographically documented optic nerve head changes. Endpoints developed in 42 patients: 28 visual field defects, 8 changes in disc appearance, and 6 disc hemorrhages. Of the 42 patients, 20 were treated and 22 were not. Survival analysis showed no statistically significant differences in failure time to any endpoints between the two groups. In the untreated group, the time to failure of disc change was related to the mean IOP during the study and also to the changes in the IOP from baseline. A significant correlation was found between initial cup-to-disc ratio and survival time to visual field defects in the untreated group.

To evaluate the incidence of visual field and optic disc progression in glaucoma patients with distinct patterns of optic disc damage.Prospective, observational case series.One hundred five patients with open-angle glaucoma.Baseline optic disc photographs of 105 study eyes of 105 patients were reviewed by 2 masked observers and classified according to patterns of disc damage into the following categories: focal, myopic, senile sclerotic, and generalized disc damage. Patients were followed up every 6 months with standard automated perimetry (SAP), high-pass resolution perimetry (HRP), and scanning laser tomography (SLT) with the Heidelberg Retina Tomograph.Visual field (SAP and HRP) and optic disc (SLT) progression were determined according to predefined criteria.Twenty-four eyes were classified into the focal, 8 into the myopic, 12 into the senile sclerotic, and 28 into the generalized group. Eyes from 33 patients could not be classified by the observers into any of these groups and were excluded from further analysis. Although intraocular pressure during follow-up was similar among the four groups, some differences in frequency of progression were observed. Patients with senile sclerotic discs had the lowest rates of visual field progression (both with SAP and HRP) and optic disc progression, although the differences were significant only for optic disc progression (P = 0.05).Patients with senile sclerotic discs showed a tendency towards less visual field and optic disc progression when compared with patients with other types of disc damage.

Purpose: To study in glaucoma patients the threat to fixation on a Humphrey field analyzer program 10-2 when one of the four innermost paracentral points is defective on program 30-2. Methods: Forty-five eyes of 45 patients with chronic open-angle glaucoma in whom at least one of the innermost four defective paracentral points was reproducibly defective on program 30-2 of the Humphrey perimeter, with a size 3 target, on two consecutive tests, were studied with program 10-2. Results: Of the 45 eyes with an abnormal paracentral point of program 30-2, 30 (66%) also showed involvement of a paracentral point on program 10-2, which was considered a threat to fixation. The remaining 15 were considered not to threaten fixation imminently. Conclusions: In about one third of glaucomatous fields considered to threaten fixation on the standard programs 30-2 and 24-2, the threat was not imminent. The extra evaluation is therefore useful before making radical and precipitous changes in management of the disease.

Background: Despite strictly defined criteria for visual field progression in the ongoing Normal-tension Glaucoma Study, the authors noted a surprisingly large number of patients reaching the endpoint. Traditional methods could not be used to check the diagnostic accuracy of their criteria, because no "gold standard" was established for distinguishing true change from physiologic long-term fluctuation. Methods: The authors developed a statistical method based on the results of duplicate tests for progression in their subjects. This method allowed the authors to assess the sensitivity, specificity, and predictive values of their diagnostic criterion. It also estimated the true incidence of progression and provided standard errors for the estimates. Results: The authors found that their original strict criteria for progression, based on duplicate testing, produced false calls of progression 57% of the time. By raising the requirement for deterioration and by repeating the entire sequence of duplicate testing once more, the authors have successfully reduced the rate of false calls to 2%. Conclusion: Accuracy in recognizing progression is improved by not accepting small changes as evidence of progression and by confirming the findings on repeat testing.

Recent studies have suggested that diffuse field loss and localized visual field loss in glaucomatous patients may have different pathophysiologic mechanisms. Testing that hypothesis requires that some patients present with purely localized field loss and other patients with purely diffuse loss. This article describes four highly selected patients with elevated intraocular pressures, bilateral damage to the optic nerve head, one eye with a classic glaucomatous visual field defect and in the other eye, in the absence of opacities in the media, a diffuse loss of the visual field. Although purely localized loss is very common, the report illustrates purely diffuse loss in the absence of other causes.

Increased intraocular pressure is accepted as a primary etiologic factor for the atrophy of the optic nerve head and visual field defects of high-tension glaucoma. Other factors must be present to explain these findings in low-tension glaucoma. One of the current theories is that low-tension glaucoma is the result of decreased optic nerve perfusion on the basis of vascular disease or other factors such as altered blood viscosity. This study compared the non-invasive vascular profiles, coagulation tests, and rheological profiles of 46 consecutive cases of low-tension glaucoma with 69 similarly unselected cases of high-tension glaucoma and 47 age-matched controls. Despite the multifactorial approach and the use of previously validated objective tests, no significant group differences were detected with any of the above investigations. If vascular disease is important in the etiology of low-tension glaucoma, then it must be localized or vasospastic since this study does not support the concept of a generalized vascular etiology, either of an atheromatous or hyperviscous nature, for the genesis of low-tension glaucoma.

Twenty-five eyes of 25 high-tension glaucoma patients and 25 eyes of 25 low-tension glaucoma patients matched for similar visual field defects had their spectral increment threshold measured. Patients with high-tension glaucoma showed significant losses in both chromatic and achromatic sensitivities when compared with low-tension glaucoma patients. The results support the hypothesis that there may be different mechanisms of damage in glaucoma.

Computerized image analysis was used to determine the normal axonal count and axon diameter distribution in 12 normal human eyes. Mean axon count per nerve was 969,279 ± 239,740 and mean axon diameter was 0.72 ± 0.07 μm. Multiple linear regression disclosed 4909 axons lost yearly ( P = 0.08). Statistical analysis did not show a relationship between axon diameter and age or time to fixation. The inferotemporal sector of the nerve had the highest fiber density ( P = 0.02). The superonasal nerve had higher mean diameters ( P = 0.02). This study may provide a baseline for future pathologic studies.

Forty-two patients with severe visual loss from glaucoma were assigned an Esterman visual function score according to their performance on a binocular visual field test using an automated perimeter. (The Esterman score has been adopted by the AMA as a new standard for rating visual field disability.) The visual function score was correlated with patient responses to questions about perceived visual disability. Monocular visual field results from both eyes using automated suprathreshold static and manual kinetic perimetry were also compared to the binocular Esterman test results. The binocular Esterman test rapidly provided information concerning visual field disability which correlated well with combined monocular results, and with an objectivity lacking in patient responses to a disability questionnaire.

The earliest psychophysical disturbances in color vision, foveal sensitivity, spatial and temporal contrast sensitivity precede nerve fiber bundle defects of the visual field in glaucoma. Optic nervehead changes such as enlargement of the physiological cup, as well as retinal nerve fiber layer losses, also precede visual field defects. Which of these is the earliest change has not yet been recognized. Evidence for more than one mechanism of damage in glaucoma is also presented.

Fifty-nine low-tension glaucoma patients were reviewed with respect to asymmetry of intraocular pressure (IOP) and visual field defects. In the presence of unequal IOP the visual field damage is almost always greater on the side with higher mean IOP. However, only 13 of 47 patients with asymmetric visual field defects had a mean IOP difference between the two eyes of greater than or equal to 1 mmHg. Although in the case of IOP asymmetry visual field damage is greater in the eye with higher mean IOP, other factors must also play an important role in the development of visual field defects in low-tension glaucoma.

The previous descriptions of the optic nerve head were reviewed. A study was done using discriminant analysis, in which an 85% separation was obtained by means of the discriminant function in a prospective study. The false positives showed a higher incidence of subsequent visual field defects from the true negatives. The pitfalls of the use of the optic nerve head appearance in the recognition of glaucomatous visual field defects were discussed.