Exploding head syndrome: new observations.

BACKGROUND AND PURPOSE: The etiology of 'exploding head syndrome' (EHS) is currently highly controversial and its management is unknown. The object was to explore these. METHODS: This observational study describes my personal experience of EHS and discusses its implications. RESULTS: I experienced, while suffering from EHS, recurrent episodes of transient cardiac arrests due to sick sinus syndrome. Implantation of a cardiac pacemaker resulted in immediate, dramatic, permanent cessation of both cardiac arrest episodes and EHS. This has not been reported previously. CONCLUSIONS: This striking temporal relationship indicates a possible association between EHS and sick sinus syndrome.

Orbital vascular anatomy.

The anatomy of the orbital vascular bed is highly complex, with tremendous interindividual variations. The main source of blood supply to the orbit is by the ophthalmic artery, the first branch of the internal carotid artery. The origin, course, and branches of the ophthalmic artery, and the genesis of the variations in origin, course, and branching pattern of the ophthalmic artery are discussed. The external carotid artery normally contributes only to a small extent to the orbital blood supply via the infraorbital artery and orbital branch of the middle meningeal artery.The complex, highly variable and confusing orbital venous system can be divided into: (i) main orbital veins (superior and inferior ophthalmic veins), (ii) inconstant orbital veins (middle and medial ophthalmic veins and four collateral veins), (iii) orbital venous networks, and (iv) various venous tributaries. All these are described briefly.

Vitreous and retinal amino acid concentrations in experimental central retinal artery occlusion in the primate.

PURPOSE: Vitreous and retinal amino-acid concentrations were evaluated in a primate model of central retinal artery occlusion (CRAO) to study the role of glutamate excitotoxicity in acute retinal ischaemia. METHODS: Unilateral, acute CRAO was produced by temporary clamping of the central retinal artery for 190 min in four elderly rhesus monkeys. Fundus photography, fluorescein angiography, and electroretinogram were performed before and during CRAO, and after unclamping the artery. Vitreous samples were obtained before and after CRAO in both eyes, and analysed for 13 amino-acid concentrations using high-pressure liquid chromatography. The animals were killed 350 min after retinal reperfusion, and the retinal tissue was submitted for amino-acid analysis. RESULTS: In all four eyes, the macula showed the 'cherry red spot'. The CRAO was confirmed by fluorescein angiography and decreased b-wave on electroretinogram. Retinal histology confirmed ischaemic changes in the inner retina. Changes in all 13 vitreous amino-acid concentrations after CRAO (including glutamate) were not significantly different between study and control eyes (P = 0.09 to 0.82). All retinal amino-acid concentrations (including glutamate) were not significantly different between two eyes (P = 0.07-0.93). CONCLUSIONS: In the primate model of acute inner retinal ischaemia induced by transient CRAO, we were unable to detect significantly elevated concentrations of vitreous and retinal glutamate. Our primate model has the advantage of closely modelling the CRAO in humans. Further basic and clinical studies are needed to elucidate the role of glutamate excitotoxicity in retinal ischaemia.

Posterior ischaemic optic neuropathy: clinical features, pathogenesis, and management.

PURPOSE: To investigate and present a comprehensive account of the clinical features, pathogenesis, and management of posterior ischaemic optic neuropathy (PION). METHODS: This retrospective study is based on 53 consecutive eyes of 42 patients with PION seen in my clinic since 1973, who fulfilled the inclusion criteria. They were systematically evaluated, treated, and followed by me. All patients had initially detailed ophthalmic evaluation of the anterior and posterior segments, including visual field with Goldmann perimeter and fluorescein fundus angiography. All patients aged 50 years and older were also investigated for giant cell arteritis (GCA). Every attempt was made to rule out other causes of visual loss. Follow-up evaluation was similar to the initial evaluation except angiography. Aetiologically, PION can be divided into three types: arteritic due to GCA, nonarteritic not due to GCA, and surgical following a surgical procedure. Steroid therapy was given to only those nonarteritic PION patients who opted to try that, but was given to all arteritic PION patients. RESULTS: PION was nonarteritic in 28 patients (35 eyes), arteritic in 12 (14 eyes), and surgical in three (four eyes). Visual acuity varied between 20/20 and no light perception--it was count fingers or less in 19 of 35 eyes with nonarteritic PION, four of 14 in arteritic, and all four with surgical PION. The most common visual field defect was central visual loss, alone or in combination with other types of visual field defects. Initially, optic disc and fundus showed no abnormality but the disc usually developed pallor in about 6-8 weeks. Aggressive treatment with high-dose systemic steroid during the very early stages of nonarteritic PION produced significant improvement of visual acuity as well as visual fields, but not so in arteritic or surgical PION. However, some spontaneous visual improvement also occurred in some untreated nonarteritic PION cases. CONCLUSIONS: PION is a distinct clinical entity but should be diagnosed only after exclusion of all other causes of visual loss. In all patients older than 50, GCA must be ruled out. There is usually marked visual loss, with central field defect being the most common. The study suggests that high-dose steroid therapy in nonarteritic PION, soon after the onset of visual loss, resulted in significant visual improvement compared to the untreated cases, but not in arteritic and surgical PION.

Role of thrombocytosis in diagnosis of giant cell arteritis and differentiation of arteritic from non-arteritic anterior ischemic optic neuropathy.

PURPOSE: To investigate the role of thrombocytosis in the diagnosis of giant cell arteritis (GCA), and differentiation of arteritic (A-AION) from non-arteritic (NA-AION) anterior ischemic optic neuropathy; and comparison of the sensitivity and specificity of platelet count to that of erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and some other hematologic variables in the diagnosis of GCA. METHODS: This retrospective study is based on 121 temporal artery biopsy confirmed GCA patients and 287 patients with NA-AION seen in our clinic. For inclusion in this study, all GCA patients, at their initial visit, prior to the initiation of corticosteroid therapy, must have had ESR (Westergren), platelet count and complete blood count, and temporal artery biopsy. From 1985 onwards CRP estimation was done. For inclusion in this study, all NA-AION patients at the initial visit must have undergone evaluation similar to that described above for GCA, except for temporal artery biopsy. Wilcoxon rank-sum test and the two-sample t-test were used to compare hematologic variables between GCA patients with and without visual loss, between those with and without systemic symptoms, and also between GCA and NA-AION patients. Pearson correlation coefficient was computed to measure the association of platelet counts and the other hematologic variables with ESR. Receiver operating characteristic (ROC) curves were constructed for ESR, CRP, platelet count, combinations of ESR and platelet count, and CRP and platelet count, hemoglobin, hematocrit, and white blood cell (WBC) count and the area under the curve (AUC) were compared. RESULTS: Comparison of ESR, CRP, and hematologic variables of GCA patients and of A-AION with the NA-AION group, showed significantly (p <0.0001) higher median levels of ESR, CRP, platelet count, and WBC count and lower levels of hemoglobin and hematocrit in the GCA patients and A-AION than in NA-AION. Comparing AUC of the ROC curve between ESR and platelet count, ESR was a better predictor of GCA compared to platelet count (AUC of 0.946 vs. 0.834). There was a slight improvement in prediction of GCA using the combination of ESR and platelet count (AUC=0.953). The other hematologic variables had an AUC that was smaller than platelet count (0.854 for hemoglobin; 0.841 for hematocrit), with WBC being the least predictive of GCA (AUC=0.666). The AUC of the ROC curve for CRP was 0.978. There was no improvement in prediction of GCA using platelet count in combination with CRP (AUC=0.976). CONCLUSIONS: Patients with GCA had significantly (p <0.0001) higher values of platelet count, ESR, CRP and WBC but lower values for hemoglobin and hematocrit compared to the NA-AION group. Predictive ability of an elevated platelet count did not surpass elevated ESR or CRP as a diagnostic marker for GCA. Thrombocytosis may complement ESR. Hemoglobin, hematocrit and WBC were much less predictive of GCA. Elevated CRP had a greater predictive ability for GCA compared to ESR or the other hematologic parameters; thrombocytosis in combination with CRP did not yield an improvement in prediction of GCA.

Ipsilateral recurrence of nonarteritic anterior ischemic optic neuropathy.

PURPOSE: To report the prevalence of recurrence of nonarteritic anterior ischemic optic neuropathy (NA-AION) in the same eye and possible contributing risk factors. DESIGN: Cohort study. SETTING: Institutional. STUDY POPULATION: The study includes 594 consecutive patients (829 eyes) with a diagnosis of NA-AION and follow-up of at least two months after the onset of NA-AION, examined in the Ocular Vascular Clinic since 1973. Simple progression of visual loss during an episode of NA-AION was not considered a fresh episode. INTERVENTION OR OBSERVATION PROCEDURES: Every patient had ophthalmic evaluation, including visual acuity, visual fields with a Goldmann perimeter, intraocular pressure, and slit lamp and ophthalmoscopic evaluation at initial visit and at each follow-up visit. The patients also had systemic evaluation; some patients had echocardiography (166 patients) and 24-hour ambulatory blood pressure (BP) monitoring-the latter was investigated in 80 patients (17 with and 63 without recurrence of NA-AION) who consented to participate in this study which was started in 1989. While optic disk edema was present, the patients were followed every 2 to 3 weeks. Once the optic disk edema resolved, they were followed up after 3 months, 6 months, and then at yearly intervals unless they had some new visual complaint. MAIN OUTCOME MEASURES: Prevalence of a fresh episode of NA-AION in the same eye, and comparison of ocular and systemic risk factors between patients with and without recurrence of NA-AION in the same eye. RESULTS: Of the 594 patients (829 eyes) in the study, recurrence of NA-AION in the same eye occurred in 45 patients (53 eyes) with a median follow-up of 3.1 years (range 2 months to 30.5 years) from the first onset of NA-AION. The Kaplan-Meier survival curve showed cumulative percentage of recurrence of NA-AION from first episode to second episode at three months 1.0%+/-0.4%(SE), at 6 months 2.7%+/-0.7%, at one year 4.1%+/-0.9%, and 2 years 5.8%+/-1.1%. There was no significant association between recurrence of NA-AION and the systemic conditions that were examined, except for nocturnal arterial hypotension. Overall patients with a recurrence of NA-AION had a significantly lower mean nighttime minimum diastolic BP (P =.003) and greater mean percentage drop during sleep in diastolic BP (P =.011) than those with no recurrence of NA-AION; all other measures of nocturnal hypotension were not significantly predictive. CONCLUSIONS: Recurrence of NA-AION in the same eye is uncommon (6.4%). Our study indicates that nocturnal diastolic arterial hypotension may be a risk factor; however, since this is a multifactorial disease, other so far unknown risk factors may also play a role. The role of various risk factors which may contribute to the recurrence of NA-AION is discussed.

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.

Rate of visual field loss and long-term visual outcome in primary open-angle glaucoma.

PURPOSE: To evaluate long-term visual field outcome in primary open-angle glaucoma. METHODS: In this retrospective cohort study, 40 eyes of 40 patients with primary open-angle glaucoma with elevated intraocular pressure and a minimum of 8-year longitudinal series of visual fields were plotted with Goldmann perimeter. Eyes with any other ocular disease except cataract were excluded. Manual grid templates were used to quantify the visual fields. Linear regression was performed to estimate the rate of visual field decline. Pertinent clinical factors were evaluated for statistical association with the rate of decline. Long-term clinical outcome including visual acuity, rate of legal blindness, and rate of medical and surgical interventions was also measured. RESULTS: In the 40 eyes studied, with a mean follow-up of 14 years, the visual field score decreased at the rate of -1.5% per year. Overall, 68% showed significant decrease, and the rate of decrease among these eyes was -2.1% per year. Five eyes became legally blind from glaucoma; the cumulative rate of blindness from glaucoma was 19% at 22 years. Higher intraocular pressure and greater number of antiglaucoma medications on initial presentation were associated with faster and slower deterioration of visual field (compared with the average), respectively. CONCLUSIONS: With standard glaucoma therapy, the rate of visual field loss in primary open-angle glaucoma is slow. Lower intraocular pressure and more antiglaucoma medications are associated with slower visual field decline. Legal blindness from glaucoma is 19% over a follow-up of 22 years.

The blood supply of the optic nerve head and the evaluation of it - myth and reality.

Evidence has gradually emerged that there is vascular insufficiency in the optic nerve head (ONH) in both anterior ischemic optic neuropathy (AION) and glaucomatous optic neuropathy (GON); thus both represent ischemic disorders of the ONH. Together these diseases constitute a major cause of blindness or seriously impaired vision in man. Consequently there has recently been great interest in the ONH circulation in health and disease and in how to evaluate it. Many studies of the subject have been published, with conflicting interpretations and claims. The basis of the inconsistent information seems to be confusion on some fundamental issues concerning the ONH circulation itself. The objective of this paper is to differentiate myths and misconceptions from reality about the ONH blood supply; to elucidate the reasons for disagreement on the blood supply of the ONH; and to evaluate the reliability and validity of various methods currently used to measure ONH blood flow.

Blood flow in the optic nerve head and factors that may influence it.

In the recent past there has been great interest in the blood supply of the optic nerve head (ONH), how to evaluate ONH blood flow, and what factors influence it, in health and disease. This is because evidence has progressively accumulated that there is vascular insufficiency in the ONH in both anterior ischemic optic neuropathy (AION) and glaucomatous optic neuropathy (GON)-two major causes of blindness or of seriously impaired vision in man. For the management and prevention of visual loss in these two disorders, a proper understanding of the factors that influence the blood flow in the ONH is essential. The objective of this paper is, therefore, to review and discuss all these factors. The various factors that influence the vascular resistance, mean blood pressure and intraocular pressure are discussed, to create a better basic understanding of the ONH blood flow, which may help us toward a logical strategy for prevention and management of ischemic disorders of the ONH.

Systemic diseases associated with various types of retinal vein occlusion.

PURPOSE: To investigate systemic diseases associated with various types of retinal vein occlusion. METHODS: We investigated prospectively in 1090 consecutive patients with retinal vein occlusion, almost all Caucasian (consistent with the racial pattern here), the prevalence of associated systemic disorders before or at the onset of various types of retinal vein occlusion. The patients were categorized into six types of retinal vein occlusion based on defined criteria: nonischemic and ischemic central retinal vein occlusion, nonischemic and ischemic hemi-central retinal vein occlusion, and major and macular branch retinal vein occlusion. The patients had a detailed ophthalmic and systemic evaluation according to our protocol. For data analysis, patients were divided into three age groups: young (younger than 45 years), middle-aged (45 to 64 years), and elderly (65 years or older). The observed prevalence rates of major systemic diseases were compared among central retinal vein occlusion, hemi-central retinal vein occlusion, and branch retinal vein occlusion using a polytomous logistic regression analysis adjusting for gender and age. Logistic regression adjusting for age and gender was also used to compare the observed prevalence of systemic disease between nonischemic and ischemic in central retinal vein occlusion and hemi-central retinal vein occlusion and between major and macular branch retinal vein occlusion. These observed prevalence rates were also compared with those expected in a gender-matched and age-matched control population from estimates from the US National Center for Health Statistics. RESULTS: There was a significantly higher prevalence of arterial hypertension in branch retinal vein occlusion compared with central retinal vein occlusion (P < .0001) and hemi-central retinal vein occlusion (P = .028). Branch retinal vein occlusion also had a significantly higher prevalence of peripheral vascular disease (P = .0002), venous disease (P = .011), peptic ulcer (P = .031), and other gastrointestinal disease (P < .0001) compared with central retinal vein occlusion. The proportion of patients with branch retinal vein occlusion with cerebrovascular disease was also significantly (P = .049) greater than that of the combined group of patients with central retinal vein occlusion and patients with hemi-central retinal vein occlusion. There was no significant difference in prevalence of any systemic disease between central retinal vein occlusion and hemi-central retinal vein occlusion. A significantly greater prevalence of arterial hypertension (P = .025) and diabetes mellitus (P = .011) was present in the ischemic central retinal vein occlusion compared with the nonischemic central retinal vein occlusion. Similarly, arterial hypertension (P = .0002) and ischemic heart disease (P = .048) were more prevalent in major branch retinal vein occlusion than in macular branch retinal vein occlusion. Relative to the US white control population, the combined group of patients with central retinal vein occlusion and patients with hemi-central retinal vein occlusion had a higher prevalence of arterial hypertension (P < .0001), peptic ulcer (P < .0001), diabetes mellitus (in ischemic type only, P < .0001), and thyroid disorder (P < .0001). The patients with branch retinal vein occlusion showed a greater prevalence of arterial hypertension (P < or = .005), cerebrovascular disease (P = .007), chronic obstructive pulmonary disease (P = .012), peptic ulcer (P < .0001), diabetes (in young only, P = .0005), and thyroid disorder (P = .003) compared with the US white control population. CONCLUSIONS: The findings of our study revealed that a variety of systemic disorders may be present in association with different types of retinal vein occlusion and in different age groups, and that their relative prevalence differs significantly, so that the common practice of generalizing about these disorders for the entire group of patients with retinal vein occlusion can be misleading. The presence of a particular associated systemic disease does not necessarily imply a cause-and-effect relationship with that type of retinal vein occlusion; the particular disease may or may not be one of the risk factors in a multifactorial scenario predisposing an eye to develop a particular type of retinal vein occlusion. Based on our study, we think that apart from a routine medical evaluation, an extensive and expensive workup for systemic diseases is unwarranted in the vast majority of patients with retinal vein occlusion.

Scientific literature and gospel truth.

We live in an age of science, an age in which science impacts practically every phase of our life. In the field of medicine, our entire understanding of diseases and their management depends on scientific knowledge. To obtain that knowledge, we rely on the published scientific literature. Therefore, the sanctity of science must be fiercely guarded. In medicine, true science leads to valid treatment--and preservation of the life, health and (for ophthalmologists) eyesight of our patients. A corrupted science results in corrupted scientific knowledge which in turn, in medicine, leads to wrong treatment and harm to the patients.

Optic disc vasculitis.

BACKGROUND: Our studies had indicated that optic disc vasculitis (ODV) is a distinct clinical entity. We investigated the presentation and clinical characteristics of ODV and determined the efficacy of systemic corticosteroids in its management. METHODS: From 1973 to 1997, we investigated 32 patients (34 eyes) with ODV. The information was obtained by complete medical and ophthalmic history taking and a detailed ophthalmic examination at the initial and follow-up visits. Non-parametric analysis of demographic characteristics and Cox proportional hazard modeling of treatment outcomes was performed. RESULTS: The most common presenting symptom was blurred vision (in 31/34 eyes--91.2%). Visual acuity was 6/12 or better in 82.4% and 6/30 or better in 94.1% of the eyes. All eyes had an enlarged blind spot, vitreous cells and optic disc edema. Fluorescein angiography demonstrated retinal peripapillary phlebitis in 52.6% of the eyes. Systemic hypertension in young patients (P=0.004) and frequency of smoking (P=0.004 for males, P=0.046 for females) were significantly higher than in the general population. Treatment with systemic corticosteroids improved the rate of resolution of optic disc edema and vitreous cells, reducing median resolution times (P=0.042). There was a tendency towards improved central visual fields with treatment (P=0.09). Final visual acuity was 6/12 or better in 25 (92.6%) and 6/18 or better in all of the 27 eyes followed by us. CONCLUSION: Our study indicates that our cases represent a distinct clinical entity of ODV and not just a potpourri of unilateral optic disc edema of different etiologies. It is a self-limiting disease, usually with good prognosis, and benefits from treatment with systemic corticosteroids. The presence of retinal peripapillary phlebitis on fluorescein angiography suggests mild vasculitis of the optic nerve head as the primary pathological mechanism in this disorder.

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.

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.

Ophthalmoscopic appearance of the normal optic nerve head in rhesus monkeys.

PURPOSE: To evaluate the ophthalmoscopic appearance of the normal optic disc, parapapillary region, and retinal nerve fiber layer in rhesus monkeys. METHODS: Color stereo fundus photographs of 17 normal eyes of 17 rhesus monkeys aged between 13 and 23 years were morphometrically evaluated. RESULTS: The neuroretinal rim was significantly (P: < 0.008) broadest in the inferior disc region followed by the superior disc region, the nasal region, and the temporal region. Retinal nerve fiber layer visibility was significantly highest in the inferior temporal fundus region followed by the superior temporal fundus region, the superior nasal fundus region, and the inferior nasal fundus region. It decreased significantly (P: < 0.001) with increasing age. The retinal arterioles were significantly (P: < 0.01) wider in the inferior temporal and superior temporal fundus regions than in the superior nasal and inferior nasal fundus regions. The alpha zone of parapapillary atrophy (14/17 or 82.4%) occurred significantly (P: < 0.001) more often than the beta zone (2/17 or 11.8%). In 15 eyes (88. 2%), the foveola was located inferior to a horizontal line drawn through the center of the optic disc. Neuroretinal rim shape and area and size of alpha and beta zones of parapapillary atrophy were independent of age. CONCLUSIONS: As in humans, in normal rhesus monkeys the neuroretinal rim has a typical physiologic configuration that spatially correlates with the retinal arteriole diameter, retinal nerve fiber layer visibility, and position of the foveola inferior to the center of the optic disc. Neuroretinal rim shape is independent of age. Retinal nerve fiber layer visibility decreases significantly with increasing age. These findings may be useful for the early detection and differentiation of experimental optic nerve damage in rhesus monkeys.