The histologic basis of optic disk pallor in experimental optic atrophy.

We studied the clinical and microscopic appearances of the optic nerve head in squirrel monkeys with optic nerve degeneration produced by optic nerve transection at the orbital apex. The ophthalmoscopic development of optic disk pallor coincided with the loss of nerve fiber bundles and the rearrangement of the remaining disk astrocytes into dense parallel layers across the nerve head. No astrocytic mitoses were observed and the estimated volume of astrocytes increased only slightly from normal. Among the astrocytes in atrophic disks, many capillaries had patent lumens and ultrastructurally normal endothelial cells. Pallor of the optic disk seems to result from a decrease in the transmission of light into the cytoarchitecture of the atrophic nerve head, not from the absence of capillaries or from extensive astrocytic proliferation.     

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     

Nonglaucomatous optic disk atrophy and excavation in the elderly

The causes of nonglaucomatous optic disk atrophy and excavation are enumerated in people 65 years or older: congenital anomalies, myopia, ischemic disorders, transsynaptic degeneration, traumatic, compressive, hereditary, toxic and infectious optic neuropathy.     

The modern methods of monitoring the optic nerve disk and specificity of glaucomatous optic neuropathy in normal-pressure glaucoma

The purpose of the case study was to determine an optimal method for monitoring the condition of the optic nerve disk (OND) and for precising the OND peculiarities in patients with normal pressure glaucoma (NPG). A comparison of the OND calculated parameters obtained for 16 patients (31 eyes), both by the "Rodenstock" scanning laser ophthalmoscope (SLO) and by HRT-II, revealed that the OND parameters calculation preformed by HRT-II was more informative, diversified and automated, which essentially cuts the procedure time. We examined, by HRT-II, a group of 31 patients (61 eyes), comprising patients with high pressure glaucoma (HPG), with suspected NPG and with moderate-pressure glaucoma (MPG) and a group of controls with moderate arterial hypertension. A comparison of OND areas' distributions of three groups (NPG group, MPG group and HPG group) showed that the majority of disks had an area ranging from 2.0 to 2.6 mm2 in the NPG, the same index ranged from 1.8 to 2.2 mm2 in the MPG group, and in the HPG group the disks were evenly distributed by area virtually in all ranks. The OND area was on the average less (2.13 mm2) in an impaired autoregulation versus the group without any symptoms of peripheral vasospasm (2.49 mm2). According to our findings, a higher OND size contributes to aggravating glaucoma at a lower intraocular pressure (IOP). It is noteworthy, that more pronounced changes are observed on the side with a bigger OND area in absence of any other risk factors, e.g. neuro-ophthalmic pathology or stenosis of the main cerebral arteries.     

Central corneal thickness and development of glaucomatous optic disk hemorrhages

PURPOSE: To evaluate whether central corneal thickness influences the development of optic disk hemorrhages in chronic open-angle glaucoma. DESIGN: Prospective observational clinical study. METHODS: The study included 390 eyes of 223 white subjects with chronic open-angle glaucoma observed during a mean follow-up time of 61.3 +/- 36.4 months. Central corneal thickness was measured by corneal pachymetry. RESULTS: The event of optic disk hemorrhages during follow-up was detected in 63 eyes (16.2%). Development of optic disk hemorrhages was, univariately (P = .73) as well as in a multiple Cox regression analysis, controlling for age, sex, normal tension glaucoma, intraocular pressure, neuroretinal rim area, and size of beta zone of peripapillary atrophy, statistically independent (P = .56) of central corneal thickness. CONCLUSIONS: Development of optic disk hemorrhages may not be markedly influenced by central corneal thickness.     

Early detection of glaucomatous damage. II. Changes in the appearance of the optic disk

Once we understand that an increase in the size of the optic disk cup is due to loss of optic nerve fibers combined with some physical tissue rearrangements, it is quite clear that cupping begins as soon as nerve loss begins. Methods to detect cupping are more sensitive to the earliest glaucoma damage than are present field testing methods. This conclusion is supported by large clinical studies and histological demonstration of nerve fiber loss prior to field loss in eyes with abnormal cups, asymmetric cupping, or nerve fiber layer abnormalities. While automated perimetry is likely to increase the sensitivity of detection, better test methodologies are needed to combine with the objectivity of computer-assisted machines. Disk hemorrhages, nerve fiber layer defects, and color vision abnormalities are early signs of damage, supporting the conclusion that damage is present before field loss. A number of other methods await further testing to determine their effectiveness. The idea that the disease glaucoma is defined by a certain visual field finding on the Goldmann perimeter is not valid if we define glaucoma as an eye with a history of elevated IOP and optic nerve damage. While such field loss is a convenient means of defining a particular stage of damage in glaucoma, there are clearly earlier stages of damage, whether we can always detect them or not. No patient should be told that he or she does not have glaucoma, but rather has ocular hypertension, based on a particular visual field finding. As testing and examination methods improve, so, hopefully, will our ability to determine whether damage is present. As this occurs, we will be better enabled to select most rationally those patients who will benefit from therapy. The idea that field testing is relatively insensitive to the earliest glaucoma damage might lead the skeptic to conclude that perimetry is not worth the trouble. This review has indicated that none of our present methods, ophthalmoscopic, psychophysical or otherwise, is perfect. But to omit using any of them (especially field testing) does a great disservice to the glaucoma patient. The greatest usefulness of the new automated instruments is that adequate field testing is now available in a cost-effective form to every ophthalmic office. We need to strive for better detection and follow-up of glaucoma damage to prevent needless blindness.     

视盘血管主干位置在青光眼视神经损害诊断中的作用

目的观察视盘血管主干位置对上、下方盘沿宽度的影响，探讨视盘血管主干位置在青光眼视神经损害诊断中的作用。方法评价眼底照片清晰、视盘血管主干位置明确的视盘459例，其中大视盘131例，中视盘145例，横椭圆形视盘75例，小视盘108例。应用两组独立样本t检验，比较各类视盘的血管偏上组、血管偏下组的上、下方盘沿宽度的差异；比较上方盘沿窄组和下方盘沿窄组的血管位置的差异。结果总体及大视盘、小视盘的血管偏上组的盘沿比（0.467±0.051，0.445±0.040，0.508±0.056）较血管偏下组的盘沿比（0.500±0.066，0.474±0.062，0.546±0.048）小，差异有统计学意义（P=0.000，P=0.045，P=0.018，P值均<0.05）；总体及大视盘、小视盘的上方盘沿窄组的血管比（0.510±0.051，0.508±0.055，0.512±0.036）较下方盘沿窄组的血管比（0.528±0.045，0.533±0.048，0.534±0.045）小，差异有统计学意义（P=0.000，P=0.046，P=0.022，P值均<0.05）。结论视盘血管主干位置偏向侧的盘沿较窄，视盘血管主干位置远离侧的盘沿较宽。大视盘、中视盘、横视盘出现盘沿下方窄、上方宽，血管主干位置偏上，小视盘盘沿上方窄、下方宽，血管主干位置偏下，提示青光眼视神经改变。（中华眼底病杂志，2007，23：118-121）     

Initial glaucomatous optic disk and retinal nerve fiber layer abnormalities and their progression

We attempted to identify the initial glaucomatous changes of the optic disk and retinal nerve fiber layer and to analyze how these changes subsequently progressed. Of 61 eyes of 61 patients with ocular hypertension, 23 (38%) developed glaucoma during ten years of follow-up (range, five to 15 years). The initial sign of glaucomatous damage was diffuse enlargement of the optic disk cup in ten of 23 eyes or generalized thinning of the nerve fiber layer without localized changes in 12 of 23 eyes. We found localized optic disk damage in ten of 23 patients and localized retinal nerve fiber layer damage in 11 of 23 patients alone or in combination with diffuse damage. In 13 of 23 eyes, the cupping ended up in diffuse enlargement with even more profound thinning of the neural rim in the upper and lower temporal disk margins. There seems to be great variability in the appearance and progression of the initial glaucomatous optic disk and nerve fiber layer abnormalities in patients with increased intraocular pressure.     

Beta-zone parapapillary atrophy and multifocal visual evoked potentials in eyes with glaucomatous optic neuropathy

We investigated changes in multifocal visual evoked potential (mfVEP) responses due to beta-zone parapapillary atrophy (ßPPA). Patients with glaucomatous optic neuropathy (GON) with or without standard achromatic perimetry (SAP) abnormalities were referred for mfVEP testing during a 2-year period. Eyes with good quality optic disc stereophotographs and reliable SAP results were included. The mfVEP monocular mean latency delays (ms) and amplitudes (SNR) were analyzed. Age, SAP mean deviation (MD), pattern standard deviation (PSD), and spherical equivalent (SE) were analyzed in the multivariate model. Generalized estimated equations were used for comparisons between groups after adjusting for inter-eye associations. Of 394 eyes of 200 patients, 223 (57%) had ßPPA. The ßPPA eyes were older (59.6 ± 13.7 vs. 56.5 ± 13.7 year, P = 0.02), more myopic (?4.0 ± 3.5 vs. ?1.3 ± 3.5 D, P < 0.01), and had poorer SAP scores (MD: ?4.9 ± 5.2 vs. ?2.6 ± 5.2 dB, P < 0.01; PSD: 4.3 ± 2.9 vs. 2.5 ± 3.0 dB, P < 0.01). By univariate analysis, mean latencies were longer in ßPPA eyes (6.1 ± 5.3 vs. 4.0 ± 5.5 ms, P < 0.01). After adjusting for differences in SE, age, and SAP MD, there was no significant difference between the two groups (P = 0.09). ßPPA eyes had lower amplitude log SNR (0.49 ± 0.16 vs. 0.56 ± 0.15, P < 0.01), which lost significance (P = 0.51) after adjusting for MD and PSD. Although eyes with ßPPA had significantly lower amplitudes and prolonged latencies than eyes without ßPPA, these differences were attributable to differences in SAP severity, age, and refractive error. Thus, ßPPA does not appear to be an independent factor affecting mfVEP responses in eyes with GON.     

Electrophysiological diagnosis in partial optic nerve atrophy syndrome

Vision conduction routes were examined in 75 patients with the syndrome of optic nerve partial atrophy by recording the visual evoked potentials, threshold of electric sensitivity emergence, critical frequency of phosphene disappearance, electroretino- and electroneurograms. The findings of these examinations correlated best of all with the clinical picture when visual evoked potentials (latency increase, decrease of the amplitude with atrophy augmentation, interhemispheric asymmetry in chiasmal and retro-chiasmal involvement) or the critical frequency of phosphene disappearance (reliably reduced if a disease was developing) were recorded. Introduction of electrodes with therapeutic and diagnostic purpose permitted assessment of optic nerve function from the electroneurogram amplitude and time parameters.     

Fluorescein leakage of the optic disc in glaucomatous optic neuropathy

Purpose To identify and quantify the role of capillary leakage of the optic nerve head in digital fluorescein angiography in normal subjects and patients with open-angle glaucoma.Methods We conducted a prospective cross-sectional study in the Department of Ophthalmology of the Technical University of Aachen. Thirty patients with primary open-angle glaucoma (POAG) and 30 healthy age-matched subjects were included. Fluorescein angiograms were performed using the scanning laser ophthalmoscope. The fluorescence of the optic nerve head and the surrounding retina (ratio of leakage) was measured using digital imaging analysis in the late phases of the angiogram (9–10 min).Results The ratio of optic nerve head fluorescence to retinal reference loci was significantly increased (p=0.01) in patients with glaucoma (POAG, 1.38±0.34) compared with normal subjects (1.20±0.19). Intraocular pressure (p=0.0001), visual field indices (mean deviation, p<0.0001; pattern standard deviation, p<0.0001; corrected pattern standard deviation, p<0.0001), and cup to disc ratios (p=0.02) differed significantly between the groups. Age and systolic and diastolic blood pressure showed no significant differences between groups.Conclusion Fluorescein angiography revealed significantly increased vascular leakage of glaucomatous optic nerve heads. An endothelial disruption and fluorescein leakage might be the result of mechanical stress at the level of the lamina cribrosa and/or a sign of ischemic damage. This measurement approach might enable us to judge the severity of optic nerve head leakage, and it is a potential way to evaluate therapeutic regimens.