Clinical implications of peripapillary atrophy in glaucoma

PURPOSE OF REVIEW: To elucidate peripapillary atrophy in glaucomatous optic neuropathy; its ranking in the morphologic diagnosis of the glaucoma, and its value for the differentiation of various types of chronic open-angle glaucoma, for the separation of glaucomatous eyes from nonglaucomatous eyes, and for the detection of progression of glaucoma. RECENT FINDINGS: Recent studies showed an association of peripapillary atrophy with glaucoma and the eventual development of glaucomatous disc hemorrhages independent of a small neuroretinal rim area, and an association between increasing peripapillary atrophy and progressive glaucoma. A ranking of optic disc parameters to detect glaucomatous damage revealed that the alpha and beta zones of peripapillary atrophy, compared with neuroretinal rim parameters, are less useful. Pseudoexfoliation syndrome without glaucoma is not a risk factor for peripapillary atrophy. In arteritic anterior ischemic optic neuropathy, peripapillary atrophy does not enlarge. Peripapillary atrophy does not differ markedly between Europeans and South Indians. In contrast to the position of the central retinal vessel trunk, the presence and position of cilioretinal arteries do not markedly influence the progression of peripapillary atrophy in glaucoma. SUMMARY: Peripapillary chorioretinal atrophy is one among several morphologic variables to detect glaucomatous abnormalities. Ranking optic disc variables for the detection of glaucomatous optic nerve damage, peripapillary atrophy is a variable of second order. It is useful for the differentiation of various types of chronic open-angle glaucomas. In contrast to glaucomatous eyes, eyes with nonglaucomatous optic nerve atrophy, including eyes after arteritic anterior ischemic optic neuropathy, do not show an enlarged peripapillary atrophy.     

Parapapillary atrophy and retinal vessel diameter in nonglaucomatous optic nerve damage

Parapapillary chorioretinal atrophy and decreased retinal vessel diameter occur in glaucomatous eyes. To evaluate the frequency and degree of these signs in nonglaucomatous optic neuropathy, the authors evaluated morphometrically and compared 47 patients with nonglaucomatous optic nerve atrophy from extraocular causes with 292 patients with primary open-angle glaucoma and 179 normal subjects. Eyes with anterior ischemic optic neuropathy were excluded. The parapapillary atrophy was differentiated into a central zone (beta) with sclera and large choroidal vessels visible by ophthalmoscopy and a peripheral zone (alpha) with irregular pigmentation. Both zones did not differ significantly in the eyes with nonglaucomatous optic neuropathy and the normal eyes. In the glaucomatous eyes, they were significantly larger and occurred more frequently. The retinal vessel diameter was significantly smaller in both groups with optic nerve atrophy than in the normal group. It was concluded that decreased retinal vessel diameters unspecifically suggest optic nerve atrophy. Evaluation of parapapillary chorioretinal atrophy can be helpful in differentiating nonglaucomatous from glaucomatous optic neuropathy.     

Parapapillary retinal vessel caliber. II. Caliber reduction in eyes with glaucoma (a papillometric study of 309 eyes with chronic simple glaucoma compared with 264 normal eyes)

The diameter of the temporal superior or inferior artery and vein was measured at the optic disk border and 2 mm from the disk center in 309 nonselected eyes with chronic primary open-angle glaucoma. The values obtained were compared with those of 264 nonselected normal eyes. The calibers of both vessels were significantly larger in the normal eyes than in the glaucomatous ones (p = 0.000 or p less than 0.01; Wilcoxon-Mann-Whitney test). Their diameters diminished significantly (p less than 0.001) with decreasing width and area of the neuroretinal rim as a whole and when divided into different optic disk sectors, and with increasing optic cup area, horizontal and vertical cup/disk ratios, area of the subtotal to total parapapillary choriopigmentepithelioretinal atrophy, perimetric loss, and glaucoma stage. Thus, the caliber of the parapapillary retinal vessels decreases significantly with increasing glaucomatous optic nerve damage.     

Dark adaptation in glaucomatous and nonglaucomatous optic nerve atrophy

Optic nerve damage is associated with impairment of psychophysical functions. We measured dark adaptation in 21 eyes of 14 normal subjects, 35 eyes of 19 patients with primary open-angle glaucoma, and 7 eyes of 4 patients with nonglaucomatous descending optic nerve atrophy. In the normal subjects light thresholds and time of the shoulder in the dark adaptation curve increased significantly with age. In eyes with glaucomatous or nonglaucomatous optic nerve damage light sensitivity was lower than in normal eyes of age-matched control groups. Rod light sensitivity was significantly (P < 0.05) correlated with neuroretinal rim loss, parapapillary chorioretinal atrophy, and relative afferent pupillary defects. We conclude that velocity and degree of dark adaptation decrease with increasing age. Patients with glaucomatous and nonglaucomatous optic nerve atrophy show decreased light sensitivity especially in the rod part of dark adaptation worsening with advancing optic nerve damage.This study was supported by Deutsche Forschungsgemeinschaft DFG, grant no. Jo 155/2-1, and Dr. Helmut and Margarete Meyer-Schwarting-Stiftung     

Optic disc morphology after arteritic anterior ischemic optic neuropathy

OBJECTIVE: To evaluate the appearance of the nerve head in patients after giant cell arteritis-induced arteritic anterior ischemic optic neuropathy (A-AION). DESIGN: Noncomparative clinical case series. PATIENTS: The study comprised 29 patients who presented with unilateral A-AION and temporal artery biopsy-proven giant cell arteritis. Stereoscopic optic disc photographs, taken of both the affected and unaffected eyes at the onset of the disease and after a follow-up period of 20.10 +/- 25.36 months (median, 11 months; range, 2-102 months), were morphometrically evaluated. MAIN OUTCOME MEASURES: Size and shape of the optic disc, neuroretinal rim, optic cup, and alpha and beta zones of parapapillary atrophy. RESULTS: In the eyes after A-AION, at the end of the study, the neuroretinal rim was significantly (P = 0.002) smaller, and the optic disc cup area was significantly (P = 0.001) larger than those of the contralateral unaffected eyes. Alpha zone and beta zone of parapapillary atrophy did not vary significantly (P > 0.50). CONCLUSIONS: A-AION, like glaucomatous optic neuropathy, results in neuroretinal rim loss and optic disc cupping. However, in contrast to glaucoma, A-AION is not associated with an enlargement of parapapillary atrophy. The reasons and mechanisms responsible for these similarities and dissimilarities are discussed. Marked clinical, morphologic, and histopathologic similarities in optic disc cupping and loss of neuroretinal rim between A-AION and glaucomatous optic neuropathy are highly suggestive of a common mechanism for the development of the two diseases (i.e., ischemia of the optic nerve head). The subject is discussed at length.     

Central retinal vessel trunk exit and location of glaucomatous parapapillary atrophy in glaucoma

OBJECTIVE: To evaluate whether the position of the central retinal vessel trunk exit on the lamina cribrosa spatially correlates with the location of parapapillary atrophy in glaucoma. DESIGN: Clinic-based, observational, cross-sectional study. PATIENTS: Color stereo optic disc photographs of 95 patients with primary or secondary open-angle glaucoma and 65 healthy persons were morphometrically evaluated. The intrapapillary and parapapillary region was divided into four quadrants. We determined the position of the central retinal vessel trunk exit on the lamina cribrosa surface and measured the area of parapapillary atrophy and neuroretinal rim in the four quadrants. MAIN OUTCOME MEASURES: The area of neuroretinal rim and parapapillary atrophy and the position of the central retinal vessel trunk exit. RESULTS: Comparing measurements between opposite disc quadrants showed that beta zone of parapapillary atrophy was significantly (P < 0.05) larger and that the neuroretinal rim was significantly smaller when beta zone and neuroretinal rim were measured in the disc quadrant most distant to the central retinal vessel trunk exit, than if the beta zone and neuroretinal rim were measured in the quadrant containing the vessel trunk exit. Comparing measurements in the disc quadrants between eyes with different positions of the central retinal vessel trunk exit revealed that, in the respective disc quadrant, the beta zone was significantly larger and the neuroretinal rim was smaller in eyes with the vessel trunk exiting in the opposite disc quadrant than in eyes with the vessel trunk exit located in the respective disc quadrant where the measurements were obtained. CONCLUSIONS: Position of the central retinal vessel trunk exit on the lamina cribrosa influences the location of parapapillary atrophy in glaucoma. The longer the distance to the central retinal vessel trunk exit, the more enlarged is parapapillary atrophy and the smaller is the neuroretinal rim. This relationship agrees with the spatial relationship between glaucomatous neuroretinal rim loss and enlarged parapapillary atrophy in glaucoma. Diagnostically, it may indicate that, in eyes with an abnormal configuration of parapapillary atrophy or with an abnormal position of the central retinal vessel trunk exit, early glaucomatous rim changes should be looked for in the disc sector that is most distant to the central retinal vessel trunk exit and where parapapillary atrophy may be relatively large.     

Inter-eye differences in chronic open-angle glaucoma patients with unilateral disc hemorrhages

OBJECTIVE: Flame-shaped optic disc hemorrhages are a hallmark of glaucomatous optic neuropathy. The purpose of this study was to evaluate which parameters differ between companion eyes with and without an optic disc hemorrhage in patients with chronic open-angle glaucoma. DESIGN: Comparative (companion eye) observational case series. PATIENTS: The study included 99 white patients with bilateral chronic open-angle glaucoma and unilateral flame-shaped optic disc hemorrhages. METHODS: All patients underwent qualitative and morphometric evaluation of color stereo optic disc photographs. MAIN OUTCOME MEASURES: Size and shape of the optic disc, neuroretinal rim and parapapillary atrophy, diameter of the retinal vessels, intraocular pressure measurements, and both mean value and loss variance value of the visual field examination. RESULTS: In an intraindividual inter-eye comparison, the eyes with disc hemorrhages and the contralateral eyes without disc bleeding did not vary significantly (P > 0.20) in size and shape of the optic disc and neuroretinal rim, optic cup depth, size of alpha and beta zone of parapapillary atrophy, retinal vessel diameter, intraocular pressure measurements, refractive error, and perimetric indices. CONCLUSIONS: In bilateral chronic open-angle glaucoma, the development of unilateral optic disc hemorrhages does not depend on inter-eye differences in size and shape of the optic disc, neuroretinal rim and parapapillary atrophy, diameter of the retinal vessels, intraocular pressure measurements, or visual field loss.     

Small neuroretinal rim and large parapapillary atrophy as predictive factors for progression of glaucomatous optic neuropathy

PURPOSE: To evaluate which morphologic features of the optic disc are predictive factors for progressive neuroretinal rim loss in chronic open-angle glaucoma. DESIGN: Prospective, observational case series. PARTICIPANTS: The study included 394 eyes of 257 white patients with chronic open-angle glaucoma. Mean follow-up time was 31.8 months (median, 39.7 months). Progression of glaucoma was defined as loss of neuroretinal rim as detected by disc photographs. Presence of optic disc hemorrhages was not taken into account. METHODS: All patients underwent repeated qualitative and morphometric evaluation of color stereo optic disc photographs. Statistical analysis included Kaplan-Meier curves, and bivariate and multivariate Cox regression analysis adjusted for patients' ages. Dependency of left and right eyes from the same subject was taken into account. MAIN OUTCOME MEASURES: Qualitative and quantitative morphologic optic nerve head parameters. RESULTS: Progression of glaucomatous optic nerve changes was detected in 42 eyes (11%). At baseline of the study, neuroretinal rim area (total area, P = 0.03) was significantly smaller, and beta zone of parapapillary atrophy (total area, P = 0.04) was significantly larger in the progressive study group compared with the nonprogressive study group. Neither study group varied significantly in size and shape of the optic disc, optic cup depth, alpha zone of parapapillary atrophy, and diameter of the retinal arteries and veins (P > 0.05). Multiple Cox regression analysis revealed that the progression of glaucoma depended significantly on the area of the neuroretinal rim (temporal sector, P = 0.003) and beta zone of parapapillary atrophy (temporal inferior sector, P = 0.02). CONCLUSIONS: Important morphologic predictive factors for progression of the glaucomatous appearance of the optic nerve head in white persons are small size of neuroretinal rim and large area of beta zone of parapapillary atrophy. Progression of glaucomatous optic nerve head changes is independent of size and shape of the optic disc, size of alpha zone of parapapillary atrophy, retinal vessel diameter, and optic cup depth.     

Parapapillary retinal vessel diameter in normal and glaucoma eyes. II. Correlations

The juxtapapillary diameters of the superior temporal and inferior temporal retinal artery and vein have been shown to be significantly smaller in glaucomatous eyes than in normal eyes. They had been measured in 473 eyes of 281 patients with chronic primary open-angle glaucoma and in 275 eyes of 173 normal subjects. In the current study the vessel diameters were correlated with intra- and parapapillary morphometric data and visual field indices. Only one eye per patient and subject was taken for statistical analysis. The retinal vessel calibers were significantly (P less than 0.001) correlated with: (1) the area of the neuroretinal rim as a whole and in four different optic disc sectors; (2) the rim width determined every 30 degrees; (3) the optic cup area and diameters; (4) the horizontal and vertical cup/disc ratios and (5) the quotient of them; (6) the retinal nerve fiber layer score; (7) the area of the parapapillary chorioretinal atrophy; and (8) the visual field indices. In the same eye the vessel caliber was smaller in that sector where the neuroretinal rim loss was highest and the retinal fiber layer score lowest. In intraindividual comparison the vessels were smaller in that eye with less neuroretinal rim tissue and lower nerve fiber layer score. No significant correlations were found with the form of the optic disc, the area of the peripapillary scleral ring, side, sex and refraction. The correlation coefficients were not significantly different when the control group was matched for age. The parapapillary retinal vessel diameter decreases with advancing glaucomatous optic nerve damage. It is correlated with morphometric intra- and parapapillary glaucomatous changes and perimetric defects.     

Appearance of the optic disk and retinal nerve fiber layer in atherosclerosis and arterial hypertension: an experimental study in rhesus monkeys

PURPOSE: To evaluate changes in the appearance of the optic nerve head and retinal nerve fiber layer of rhesus monkeys with chronic arterial hypertension and atherosclerosis. METHODS: Color stereoscopic fundus photographs of 25 eyes of 25 rhesus monkeys (mean age +/- SD of 20.4 +/- 1.87 years) with chronic experimental systemic arterial hypertension and atherosclerosis (for a mean duration of 89.1 +/- 39.1 months and 104.6 +/- 62.2 months, respectively) were morphometrically evaluated. They were compared with color stereoscopic fundus photographs of 17 eyes of 17 normal monkeys (mean age +/- SD of 19.76 +/- 2.19 years) without any detectable systemic or ocular disease. There was no significant difference in age between the two study groups (P =.22). RESULTS: In the atherosclerotic-arterial hypertensive group, visibility of the retinal nerve fiber layer was significantly (35.691 +/- 5.95 units vs 28.72 +/- 9.18 units, P =.009) less and frequency of localized retinal nerve fiber layer defects was significantly (six of 25 or 24% vs zero of 17 or 0%, P =.01) more than in the normal control group. The two groups did not differ significantly in size of the neuroretinal rim (P =.66), shape of the neuroretinal rim (P >.15), size of alpha (P >.44) and beta (P >.65) zones of parapapillary chorioretinal atrophy, or regional distribution of alpha and beta zones (P >.40). CONCLUSIONS: Chronic experimental arterial hypertension and atherosclerosis do not markedly change the size and shape of the neuroretinal rim or parapapillary atrophy; however, they do lead to reduced visibility of the retinal nerve fiber layer, with localized retinal nerve fiber layer defects indicating optic nerve damage. Thus, unlike glaucomatous optic neuropathy, experimental arterial hypertension and atherosclerosis are not associated with a significant change in the parapapillary atrophy or the neuroretinal rim of the optic disk despite the loss of nerve fibers.     

Thickness of the lamina cribrosa and peripapillary sclera in Rhesus monkeys with nonglaucomatous or glaucomatous optic neuropathy

Purpose: To measure the thickness of the lamina cribrosa and peripapillary sclera in monkeys with a nonglaucomatous optic nerve damage and to compare that with those of monkeys with glaucomatous optic neuropathy. Methods: The study included 22 monkey eyes (Macaca mulatta) which had undergone a temporary experimental central retinal artery occlusion (CRAO) and seven monkey eyes in which experimental glaucoma was unilaterally produced. We measured histomorphometrically the thickness of the lamina cribrosa and peripapillary sclera. Results: The lamina cribrosa was significantly thicker in the CRAO group than in the glaucoma group (central region: 212 ± 46 μm versus 167 ± 17 μm; p = 0.009). The thickness of the peripapillary sclera at the optic disc border (253 ± 39 μm versus 192 ± 21 μm; p = 0.001) and outside of the optic nerve meninges (408 ± 70 μm versus 314 ± 64 μm; p = 0.006) was significantly greater in the CRAO group. Conclusions: In monkey eyes with a temporary CRAO as a model for nonglaucomatous optic nerve damage, the lamina cribrosa is significantly thicker than in monkey eyes with experimental glaucomatous optic nerve damage. It may suggest that the loss of optic nerve fibres might not be the reason for the thinning of the lamina cribrosa in eyes with advanced glaucoma. The thinner peripapillary sclera in the glaucomatous eyes may suggest that the monkey sclera is more vulnerable to stretching with increased intraocular pressure than the human eye for which no glaucoma‐related lengthening of the eyeball and thinning of the peripapillary sclera have been observed.     

The retinal nerve fiber layer in normal and glaucomatous eyes. II. Correlations

The retinal nerve fiber layer is different in normal and glaucomatous eyes. We correlated semi-quantitative data of the retinal nerve fiber layer of 398 eyes with chronic primary open-angle glaucoma and of 234 normal eyes with the intra- and parapapillary morphometric signs and with the perimetric indices. The three parameters "sequence of the fundus sectors concerning the best visibility of the retinal nerve fiber bundles", "visibility of the nerve fiber bundles", and "localized defects" were significantly (p less than 0.001) correlated to 1) area of the neuroretinal rim as a whole and in four different optic disc sectors, 2) neuroretinal rim width determined every 30 degrees, 3) optic cup area, diameters and form, 4) horizontal and vertical cup/disc ratios and the quotient of the horizontal to vertical cup/disc ratio, 5) area and width of zone "Alpha", zone "Beta", and the total parapapillary chorio-retinal atrophy, 6) diameter of the retinal vessels, 7) grade of a "tesselated fundus", and 8) the visual field loss. If only the inferior temporal and the superior temporal sectors were considered, the retinal nerve fiber bundles were less visible in that sector with the largest notch in the neuroretinal rim, the smaller neuroretinal rim area and width, the thinner retinal vessels, and the larger zone "Alpha", zone "Beta", and total parapapillary chorio-retinal atrophy. The glaucomatous changes in the retinal nerve fiber layer are correlated in time and location with the intra- and parapapillary and the perimetric alterations. Evaluation of the retinal nerve fiber layer is a useful method to detect a glaucomatous optic nerve damage.(ABSTRACT TRUNCATED AT 250 WORDS)     

Predictive factors of the optic nerve head for development or progression of glaucomatous visual field loss

PURPOSE: To evaluate which morphologic features of the optic disc are predictive factors for the development or progression of visual field loss in chronic open-angle glaucoma. METHODS: The prospective observational clinical study included 763 eyes of 416 white subjects with ocular hypertension and chronic open-angle glaucoma. During the follow-up time (mean, 67.4 months; median, 65.1; range, 6.2-104.5), all patients underwent repeated qualitative and morphometric evaluation of color stereo optic disc photographs and white-on-white visual field examination. Progression of glaucomatous visual field damage was defined by point-wise regression analysis for each of the 59 locations in the visual field. Outcome measures were qualitative and quantitative morphologic optic nerve head parameters. RESULTS: Development or progression of glaucomatous visual field defects was detected in 106 (13.9%) eyes. At baseline of the study, neuroretinal rim area was significantly (P < 0.002) smaller, the beta zone of parapapillary atrophy (P < 0.003, nasal sector) was significantly larger, and age was significantly higher (P < 0.003) in the progressive study group than in the nonprogressive study group. Both study groups did not vary significantly in size of the optic disc and the alpha zone of parapapillary atrophy. Cox proportional hazard regression analysis revealed that the progression of glaucomatous visual field loss depended significantly on the area of the neuroretinal rim (P < 0.001) and age (P < 0.001), but was independent of diameter of the retinal arterioles and veins. CONCLUSIONS: Morphologic predictive factors for development or progression of glaucomatous visual field defects in whites are small neuroretinal rim area and large beta zone of parapapillary atrophy. Age is an additional nonmorphologic parameter. Progression of glaucomatous optic nerve head changes is independent of the size of the optic disc and alpha-zone of parapapillary atrophy and retinal vessel diameter.     

Follow up of focal narrowing of retinal arterioles in glaucoma

AIM: To evaluate whether focal narrowing of retinal arterioles increases with progressive glaucomatous optic neuropathy. METHODS: Focal narrowing of retinal arterioles and area of neuroretinal rim were morphometrically evaluated on colour stereo optic disc photographs of 59 patients with primary open angle glaucoma, 22 patients with normal pressure glaucoma, 11 patients with secondary open angle glaucoma, and 31 patients with ocular hypertension. Minimum follow up was 8 months. Focal arteriolar narrowing was quantified by calculating the ratio of the vessel width in the broadest to the narrowest vessel part. RESULTS: In the subgroup of patients with progressive glaucomatous optic nerve damage (n = 37), focal narrowing of retinal arterioles increased significantly (p < 0.005) with decreasing neuroretinal rim area. In the subgroup of patients with stable appearance of the optic disc (n = 86), focal narrowing of retinal arterioles did not change significantly (p = 0.79). The positive correlation between increasing focal thinning of retinal arterioles and progression of glaucomatous optic neuropathy was present, although not statistically significant, in all the glaucoma subtypes examined. The location of focal thinning of retinal arterioles did not change in the follow up. CONCLUSIONS: Focal narrowing of retinal arterioles increases significantly with progressive glaucomatous optic neuropathy, independent of the type of glaucoma. It is stable in patients with non-progressive glaucoma. The findings agree with previous reports on a higher degree of focal arteriole narrowing in eyes with pronounced optic nerve damage in comparison with those with moderate optic nerve atrophy or normal eyes. In the clinical management of patients with glaucoma, in some eyes, increasing focal arteriole narrowing may suggest progression of disease.     

Ophthalmoscopic evaluation of the optic nerve head

Optic nerve diseases, such as the glaucomas, lead to changes in the intrapapillary and parapapillary region of the optic nerve head. These changes can be described by the following variables: size and shape of the optic disk; size, shape, and pallor of the neuroretinal rim; size of the optic cup in relation to the area of the disk; configuration and depth of the optic cup; ratios of cup-to-disk diameter and cup-to-disk area; position of the exit of the central retinal vessel trunk on the lamina cribrosa surface; presence and location of splinter-shaped hemorrhages; occurrence, size, configuration, and location of parapapillary chorioretinal atrophy; diffuse and/or focal decrease of the diameter of the retinal arterioles; and visibility of the retinal nerve fiber layer (RNFL). These variables can be assessed semiquantitively by ophthalmoscopy without applying sophisticated techniques. For the early detection of glaucomatous optic nerve damage in ocular hypertensive eyes before the development of visual field loss, the most important variables are neuroretinal rim shape, optic cup size in relation to optic disk size, diffusely or segmentally decreased visibility of the RNFL, occurrence of localized RNFL defects, and presence of disk hemorrhages.     

Optic disc morphology in diabetes mellitus

Background: Diabetes mellitus is a systemic disease affecting multiple tissues throughout the body. This study was performed to evaluate intravitally the diabetic changes of the optic disc Methods: Color photographs of 115 eyes with varying severity of diabetic retinopathy and of 29 normal eyes were morphometrically examined Results: We found that the size and shape of the optic disc, the neuroretinal rim and the parapapillary atrophy did not differ significantly between the diabetic eyes and the normal eyes. These variables were independent of the degree of diabetic retinopathy. There was a tendency toward decreased visibility of the retinal nerve fiber layer and increased optic disc pallor in the diabetic eyes Conclusion: The results indicate that the area and form of the optic disc, the neuroretinal rim and parapapillary atrophy are not altered by diabetes mellitus. This is important for the diagnosis of glaucoma in diabetic patients, since glaucoma leads to a decrease of rim area and an enlargement of parapapillary atrophy. The reduced visibility of the retinal nerve fiber layer, the increased optic disc pallor and the unchanged size of the neuroretinal rim and parapapillary atrophy suggest that diabetes mellitus may be associated with nonglaucomatous optic nerve atrophy.     

Influence of cilioretinal arteries on neuroretinal rim and parapapillary atrophy in glaucoma

PURPOSE: The pattern of neuroretinal rim loss and increase in the area of parapapillary atrophy in glaucoma depend on the localization of the central retinal vessel trunk in the lamina cribrosa. The purpose of the present study was to determine whether, in a similar way, the pattern of rim loss and progression of parapapillary atrophy are influenced by the presence and position of cilioretinal arteries. METHODS: Color stereo optic disc photographs (15 degrees) for morphometric evaluation of the optic nerve head were used to compare the appearance of the optic disc in 41 patients exhibiting unilateral or bilateral cilioretinal arteries in the temporal horizontal disc region with the optic disc morphology of 127 patients without cilioretinal arteries. The areas of the neuroretinal rim and alpha and beta zones of parapapillary atrophy were measured in the total disc and in four disc sectors. RESULTS: Eyes with and eyes without cilioretinal arteries did not differ significantly in the areas of neuroretinal rim and alpha and beta zones of parapapillary atrophy, when measured in the whole optic disc and in the four disc sectors separately; in ratios of the temporal horizontal area to total area of rim and parapapillary atrophy; and in the ratio of temporal horizontal rim area-to-nasal rim area, neither in an interindividual comparison nor in an intraindividual intereye comparison. CONCLUSIONS: In contrast to the position of the central retinal vessel trunk, presence and position of cilioretinal arteries do not markedly influence the pattern of neuroretinal rim loss and progression of parapapillary atrophy in glaucoma.     

Influence of experimental chronic high-pressure glaucoma on age-related macular degeneration in rhesus monkeys

PURPOSE: To assess prospectively whether development of age-related macular degeneration is influenced by experimentally induced chronic high-pressure glaucoma, and whether age-related macular degeneration influences the appearance of the optic nerve head in experimental chronic high-pressure glaucoma in older rhesus monkeys. METHODS: The longitudinal study included 102 eyes of 52 rhesus monkeys. The total study group was divided into a group with experimentally induced unilateral chronic high-pressure glaucoma (n = 40 eyes) and a normal control group (n = 62 eyes). Additionally, arterial hypertension and atherosclerosis were experimentally induced in both study groups in a similar percentage of monkeys. Mean monkey age at the end of the study was 19.6 +/- 3.1 years (range, 13-24 years). The macular region, optic disc, and retinal nerve fiber layer were morphometrically evaluated by color wide-angle fundus photographs taken at baseline and at the end of the study. RESULTS: The degree of age-related macular degeneration, measured as number and area of drusen in the foveal and extrafoveal region of the macula, did not differ significantly between the two study groups. In the glaucomatous group, the degree of macular degeneration was statistically independent of the development of parapapillary atrophy, loss of neuroretinal rim, and decrease in the visibility of the retinal nerve fiber layer. CONCLUSIONS: Development of age-related macular degeneration in rhesus monkeys is independent of concomitant chronic high-pressure glaucoma, including the development of glaucomatous parapapillary chorioretinal atrophy. Conversely, age-related macular degeneration does not markedly influence the course of experimental chronic high-pressure glaucoma or the development of parapapillary atrophy in monkeys.     

非青光眼性大视杯临床分析

目的 探讨非青光眼性疾病引起视杯扩大的病因以及鉴别要点,为临床识别非青光眼性大视杯提供依据。设计 回顾性病例系列。研究对象 12例（19眼）非青光眼大视杯患者。方法 分析比较这些患者的病因、视盘形态学特征以及相关影像资料。主要指标 病因、视盘形态特征以及视功能改变。结果 12例患者中,4例为视神经炎,1例视神经脊髓炎,1例Leber遗传性视神经病变,2例垂体瘤,1例基底节脑出血,1例睫状视网膜动脉阻塞合并视网膜中央静脉阻塞,1例视网膜中央动脉阻塞,1例视神经损伤。所有患者视杯呈弥漫性或局限性扩大,盘沿苍白。视野表现为与原发病相应的缺损。结论 各种视神经疾病和视网膜疾病均有可能导致大视杯,它与青光眼性大视杯的鉴别点在于盘沿色泽、有无盘沿局限性缺失以及视功能异常和视盘改变的相关性。（眼科, 2012, 21: 306-309）