Central corneal thickness and thickness of the lamina cribrosa in human eyes

PURPOSE: Since central corneal thickness may inversely influence the amount and rate of progression of glaucomatous optic nerve damage and because lamina cribrosa thickness may be of importance in susceptibility to glaucoma, it was the purpose of the present study to evaluate whether central corneal thickness is related to lamina cribrosa thickness. METHODS: The histomorphometric study included 111 enucleated nonglaucomatous eyes of 111 white subjects. On anterior-posterior histologic sections through the pupil and the central optic disc region, the thickness of the cornea, lamina cribrosa, and peripapillary sclera and the shortest distance between the intraocular space and the cerebrospinal fluid space were measured. Axial length ranged between 20 and 32 mm. RESULTS: Mean central corneal thickness (mean +/- SD: 616.6 +/- 108.3 microm) and mean central lamina cribrosa thickness (378.1 +/- 117.8 microm) were statistically independent of each other (P = 0.15; correlation coefficient, r = 0.14). In a similar manner, lamina cribrosa thickness at the optic disc border was statistically independent of central corneal thickness (P = 0.51; r = 0.06) and peripheral corneal thickness (P = 0.34; r = 0.09). In a parallel way, peripapillary scleral thickness (P = 0.84) and the shortest distance between the prelaminar space and cerebrospinal fluid space (P = 0.10) were statistically independent of central corneal thickness. CONCLUSIONS: In nonglaucomatous human globes, central corneal thickness may not correlate significantly with lamina cribrosa thickness, peripapillary scleral thickness, and shortest distance between intraocular space and cerebrospinal fluid space. Histologic artifact and sectioning methods could partially account for the lack of an association. The study results may suggest clinically that an assumed relationship between central corneal thickness and susceptibility to glaucoma cannot be explained by an anatomic correspondence between corneal thickness and histomorphometry of the optic nerve head.     

Quantitative study of collagen and elastin of the optic nerve head and sclera in human and experimental monkey glaucoma.

Quantitative studies of collagen density and fibril size distribution as well as elastin density were carried out in the optic nerve head and sclera of human and experimental monkey glaucoma eyes. The collagen fibrils of the normal lamina cribrosa are smaller and more uniform in size than those of the sclera. This feature may be an adaptation to maximize either elasticity or resistance to mechanical stress. In glaucomatous nerve heads, there is a major disruption of the structure of the lamina cribrosa beam structure, including a decrease in collagen density. The peripapillary sclera undergoes similar collagen density changes to those in the nerve head in human glaucoma eyes. Elastin fiber density is unchanged in the glaucomatous nerve heads that we studied.     

3-D histomorphometry of the normal and early glaucomatous monkey optic nerve head: lamina cribrosa and peripapillary scleral position and thickness

PURPOSE: To delineate three-dimensionally the anterior and posterior surfaces of the lamina cribrosa, scleral flange, and peripapillary sclera, to determine the position and thickness of these structures within digital three-dimensional (3-D) reconstructions of the monkey optic nerve head (ONH). METHODS: The trephinated ONH and peripapillary sclera from both eyes of three monkeys with early glaucoma (EG; one eye normal, one eye given laser-induced EG) were serially sectioned at 3-mum thickness, with the embedded tissue block's face stained and imaged after each cut. Images were aligned and stacked to create 3-D reconstructions, within which Bruch's membrane opening (BMO) and the anterior and posterior surfaces of the lamina cribrosa and peripapillary sclera were delineated in 40 serial radial (4.5 degrees interval) digital sagittal sections. For each eye, a BMO zero reference plane was fit to the 80 BMO points, which served as the reference from which all position measurements were made. Regional laminar, scleral flange, and peripapillary scleral position and thickness were compared between the normal and EG eyes of each monkey and between treatment groups by analysis of variance. RESULTS: Laminar thickness varied substantially within the normal eyes and was profoundly thicker within the three EG eyes. Laminar position was permanently posteriorly deformed in all three EG eyes, with substantial differences in the magnitude and extent of deformation among them. Scleral flange and peripapillary scleral thickness varied regionally within each normal ONH with the scleral flange and peripapillary sclera being thinnest nasally. Overall, the scleral flange and peripapillary sclera immediately surrounding the ONH were posteriorly displaced relative to the more peripheral sclera. CONCLUSIONS: Profound fixed posterior deformation and thickening of the lamina are accompanied by mild posterior deformation and thinning of the scleral flange and peripapillary sclera at the onset of confocal scanning laser tomography (CSLT)-detected ONH surface change in young adult monkey eyes with early experimental glaucoma.     

Three-dimensional reconstruction of normal and early glaucoma monkey optic nerve head connective tissues

PURPOSE: To introduce high-resolution, digital three-dimensional (3-D) reconstruction of the connective tissues of the optic nerve head (ONH). METHODS: Trephinated ONH and peripapillary sclera from both eyes of three monkeys with early glaucoma (EG; one eye normal, one eye given laser-induced EG) were embedded in paraffin and serial sectioned at 3-mum thickness from the vitreous surface through the orbital optic nerve, with the embedded tissue block face stained and imaged after each cut. Each image was aligned, and then the scleral canal wall, sclera, border tissue of Elschnig, Bruch's membrane, lamina cribrosa, optic nerve septa, pial sheath, and vasculature were delineated as unique objects. Delineated images were stacked, color mapped, and volume rendered and then serial sagittal and transverse digital sections of the resultant voxel geometries were viewed and measured. RESULTS: Substantial differences in the 3-D architecture of the peripapillary sclera, scleral canal wall, and lamina cribrosa were present among the three normal eyes. All three EG eyes displayed permanent posterior deformation of the central lamina cribrosa, as well as expansion of the anterior and posterior neural canal openings in comparison with their respective contralateral normal control eyes. Peripherally, whereas laminar deformation was greatest inferiorly or superiorly in all three EG eyes, statistically significant deformation was present in all four quadrants of all three eyes. CONCLUSIONS: High-resolution, digital 3-D reconstructions of the load-bearing connective tissues of the monkey ONH confirm that the ONH connective tissues are profoundly altered at the onset of detectable ONH surface change in experimental glaucoma.     

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.     

Collagen fibrillar network in the optic nerve head of normal monkey eyes and monkey eyes with laser-induced glaucoma--a scanning electron microscopic study

PURPOSE: To examine the three-dimensional organization of collagen fibrils in the lamina cribrosa of normal monkey eyes and monkey eyes with laser-induced glaucoma. METHODS: Intraocular pressure elevation and glaucomatous optic discs were obtained in one eye of three adult monkeys by repeated applications of argon laser to the chamber angle. The monkey eyes were enucleated, and the collagen fibrillar network was investigated by scanning electron microscopy after cell maceration with 10% sodium hydroxide and conductive staining. RESULTS: In normal monkey eyes, round to oval shaped regular laminar pores through which axon bundles exited were observed in the lamina cribrosa. The straight, column-like pores or openings were formed by multilayered laminar plates that aligned vertically in parallel with the optic nerves. The surface of the laminar plates was covered by delicate, loosely arranged collagen fibrils. The inner surface of the pores was smooth, made up of well-packed collagen fibers. In glaucomatous eyes, the laminar pores were clogged by tightened collagen fibrils. The inner surface of the pores was irregular, and the pores were narrowed or distorted. CONCLUSIONS: Alterations in the three-dimensional organization of collagen fibrils were demonstrated in the optic nerve head of glaucomatous monkey eyes. The architectural changes may affect the flexibility and resilience required of the lamina cribrosa in supporting optic nerve fibers.     

Distribution and expression of transforming growth factor-beta and platelet-derived growth factor in the normal and glaucomatous monkey optic nerve heads.

PURPOSE: Remodeling of the extracellular matrix occurs in the lamina cribrosa in progressed glaucomatous optic nerve damage including disc cupping. We examined immunohistochemical changes in the transforming growth factor (TGF)-beta and platelet-derived growth factor (PDGF) in the optic nerve head in an experimentally induced glaucoma model. METHODS: We used 3 cynomolgus and 2 Japanese monkey eyes. Glaucoma was induced by repeated argon laser photocoagulation of the chamber angle. Eyes were enucleated after disc cupping had formed 3 to 5 months after photocoagulation. The optic nerve head was examined for expression of TGF-beta1, -beta2 and -beta3 and PDGF-A and -B in frozen sections and by the biotin ExtraAvidin-alkali phosphatase method. RESULTS: Normal monkey eyes showed TGF-beta1, -beta2 and -beta3, and PDGF-A and -B in the optic nerve head including the nerve fibers, glial cells, and vascular cells. Glaucomatous eyes showed stronger expression of TGF-beta1 and -beta2 in the glial cells around the lamina cribrosa. The staining intensities for TGF-beta3, PDGF-A and -B were the same as in normal eyes. CONCLUSIONS: Eyes with experimental glaucoma showed higher expression of TGF-beta1 and -beta2 around the lamina cribrosa. These findings may show upregulation of extracellular matrix production as related to remodeling of the lamina cribrosa in glaucoma.     

Optic disc histomorphometry in normal eyes and eyes with secondary angle-closure glaucoma

The intrapapillary region of the optic disc shows ophthalmoscopical changes in glaucoma. In search of a histological correlate, this region was examined histomorphometrically in serial sections of 21 human eyes with secondary angle-closure glaucoma and 28 control eyes with malignant choroidal melanoma. The lamina cribosa was significantly (P less than 0.05) thinner, the optic cup deeper and wider, the peripapillary scleral ring finer, and the corpora amylacea count was lower in glaucoma eyes than in control eyes with normal optic nerves. There was no significant difference in optic disc diameter. The decrease in lamina cribrosa thickness may be one of several factors leading to glaucomatous optic nerve fiber loss. Due to a decrease in the relative height the inner limiting membrane should not be taken as the reference level for optic-cup-depth measurement. A high corpora amylacea count may point to a normal optic nerve fiber population.     

Changes in transforming growth factor-beta and platelet-derived growth factor in the optic nerve head in monkey experimental glaucoma

PURPOSE: Remodeling of the extracellular matrix occurs in the lamina cribrosa in progressed glaucomatous optic nerve damage including disc cupping. We examined immunohistochemical changes in the transforming growth factor (TGF)-beta and platelet derived growth factor (PDGF) in the optic nerve heads in experimentally induced glaucoma. METHODS: We used 3 cynomolgus and 2 Japanese monkey eyes. Glaucoma was induced by repeated argon laser photocoagulation of the chamber angle. Eyes were enucleated after disc cupping had formed 3 to 5 months after treatment. The optic nerve head was examined for expression of TGF beta 1, beta 2, and beta 3, and PDGF A and B in frozen sections and by the biotin-ExtrAvidin-Alkali Phosphatase method. FINDINGS: Normal monkey eyes showed TGF beta 1, beta 2, and beta 3, and PDGF A, and B in the optic nerve head including the nerve fibers, glial cells, and vascular cells. Glaucomatous eyes showed stronger expression of TGF beta 1 and beta 2 in the glial cells around the lamina cribrosa. The staining intensities for TGF beta 3, PDGF A, and PDGF B were the same as in normal eyes. CONCLUSION: Eyes with experimental glaucoma showed higher expressions of TGF beta 1 and beta 2 around the lamina cribrosa. This finding may show upregulation of extracellular matrix production as related to remodeling of the lamina cribrosa in glaucoma.     

Histomorphometry of the circular peripapillary arterial ring of Zinn–Haller in normal eyes and eyes with secondary angle‐closure glaucoma

Acta Ophthalmol. 2010: 88: e317–e322

Abstract.

Purpose: To examine the location and size of the peripapillary arterial circle of Zinn–Haller (PACZH) and its associations with other eye measures in normal eyes and eyes with secondary angle‐closure glaucoma. Methods: The study included 29 human globes enucleated because of malignant choroidal melanoma (n = 19) (control group) or because of secondary angle‐closure glaucoma (n = 10). Anterior–posterior histological sections were morphometrically evaluated. Results: The PACZH was present in all eyes. The glaucoma group and the control group did not vary significantly in the distance from the PACZH to Bruch’s membrane (297 ± 67 versus 270 ± 67 μm; p = 0.29), optic disc border (281 ± 103 versus 391 ± 170 μm; p = 0.07), optic disc centre (1059 ± 191 versus 978 ± 205 μm; p = 0.30) and retrobulbar cerebrospinal fluid space (173 ± 58 versus 172 ± 81 μm; p = 0.97) nor in the minimal PACZH diameter (39 ± 18 versus 36 ± 18 μm; p = 0.74) and maximal PACZH diameter (78 ± 37 versus 65 ± 25 μm; p = 0.36). The PACZH location, measured as distance from Bruch’s membrane, disc border, disc centre and cerebrospinal fluid space, was not significantly associated with axial length (p > 0.39), horizontal globe diameter (p > 0.17) and vertical globe diameter (p > 0.22). Both diameters were statistically independent of axial length (p = 0.72 and p = 0.58, respectively), horizontal globe diameter (p = 0.60 and p = 0.41, respectively) and vertical globe diameter (p = 0.64 and p = 0.52, respectively). All parameters were statistically independent of age (p > 0.10) and gender (p > 0.10). Conclusions: The PACZH was present in all human eyes examined and did not vary significantly in location and diameter between eyes with secondary angle‐closure glaucoma and nonglaucomatous eyes, nor between myopic versus hyperopic eyes.     

Anatomic relationship between lamina cribrosa, intraocular space, and cerebrospinal fluid space

PURPOSE: The lamina cribrosa, as the main structural element of the optic nerve head, forms a pressure barrier between the intraocular space and the retrobulbar space. The function as a pressure barrier may have importance for the pathogenesis of ocular diseases related to intraocular pressure and/or cerebrospinal fluid (CSF) pressure, such as the glaucomas. The purpose of the present study was to examine the anatomic relationship between the lamina cribrosa, the intraocular pressure space, and the retrobulbar cerebrospinal pressure space in eyes with glaucoma. METHODS: The study included 53 globes enucleated because of malignant choroidal melanoma (n = 42) without involvement of the optic nerve (control group) or because of painful absolute secondary angle-closure glaucoma (n = 11; glaucoma group). Anterior-posterior histologic sections through the pupil and the optic disc were morphometrically evaluated. RESULTS: In the glaucoma group compared with the control group, the lamina cribrosa was significantly (P < 0.001) thinner, the part of the outer lamina cribrosa surface directly exposed to the pia mater and indirectly exposed to the CSF space was significantly (P = 0.001) wider, and the shortest distance between the intraocular space and the CSF space was significantly (P < 0.001) shorter. The posterior lamina cribrosa surface in direct contact with the pia mater was located close to the optic disc border. CONCLUSIONS: The thickness of the lamina cribrosa and the anatomic relationships between the intraocular space and the CSF space differ significantly between normal and glaucomatous eyes. The findings may be of importance for the pathogenesis of glaucomatous optic neuropathy.     

Morphologic changes in chronic high-pressure experimental glaucoma in rhesus monkeys

PURPOSE: To investigate morphologic changes in the posterior segment of the eye and optic nerve head (ONH) in rhesus monkeys with experimental glaucoma, and to evaluate the effect of age and vascular disease on the glaucomatous damage. METHODS: This study was conducted in 36 eyes of rhesus monkeys 11 to 24 years of age. Experimental glaucoma was produced by laser photocoagulation of the anterior chamber angle in 28 eyes, and the remaining 8 eyes served as the nonglaucomatous group. Of the 28 glaucomatous eyes, 19 belonged to animals with experimental atherosclerosis and chronic arterial hypertension (A-H group); the remaining 9 had no A-H (non-AH group). Among the 8 eyes without glaucoma, 5 belonged to A-H animals and the remaining 3 to animals without A-H. All eyes underwent IOP measurements and fundus photography before laser photocoagulation and serially thereafter for 4 to 60 months (median 22.5 months). After enucleation, eyes were fixed in formalin for light microscopic studies. Morphologic abnormalities were evaluated and graded. Correlation analyses between morphologic parameters and clinical data were performed. RESULTS: The highest IOP ranged from 44 to 80 mmHg, but during the follow-up period median IOP was mostly 28 mmHg (mean 27+/-4.8 mmHg). On histopathologic examination, the eyes showed moderate to severe atrophy of the temporal peripapillary choroid (67%), choriocapillaris (70%), and RPE (12%); axonal atrophy in the retinal nerve fiber layer (85%), prelaminar region (69%), lamina cribrosa (66%), and retrolaminar region (82%); fibrous septal thickening in the lamina cribrosa (77%) and retrolaminar region (86%); bowing backward of the lamina cribrosa (77%); overall tissue atrophy in the prelaminar region (81%); and retinal ganglion cell atrophy (74%). The data showed a positive correlation between the ONH damage and atrophic changes in the temporal peripapillary choroid, and suggested greater damage in animals with A-H than in those without A-H. CONCLUSION: Vascular disease may influence glaucomatous damage in the ONH, as damage in the ONH was greater in animals with A-H than in those without A-H. A similar relationship also may exist between age and glaucomatous damage, but this needs to be investigated further in a larger study. It is postulated that the bowing back of the lamina cribrosa seen in optic disc cupping is produced by retrolaminar septal fibrosis and axonal loss. Although elevated IOP no doubt played an important role, the data suggest that the glaucomatous changes that were observed in this study are not simply mechanical in nature (due to the raised IOP), but may represent a multifactorial phenomenon.     

Blood flow of the optic nerve head and peripapillary retina in exfoliation syndrome with unilateral glaucoma or ocular hypertension

BACKGROUND: The purpose was to study whether any differences exist in the optic nerve head (ONH) and peripapillary retinal blood flow between the two eyes of patients with unilateral exfoliation glaucoma or ocular hypertension (OHT) with exfoliation syndrome. METHODS: This cross-sectional study included 50 patients. All had exfoliation syndrome with glaucoma or OHT in one eye, and these eyes comprised the study group. The fellow eyes, all normotensive, comprised the control group. Blood flow was measured with scanning laser Doppler flowmetry in the lamina cribrosa region, in the rim area, and on the peripapillary retina. Multiple linear regression analyses were used to identify any associations between different factors and differences in flow. RESULTS: Flow in the rim area was significantly higher in the study eyes than in the control eyes, with a mean difference of 172 arbitrary units (P = 0.001). The difference of 40 units in the laminar area was of borderline significance (P = 0.065) and no significant difference was found in the peripapillary retina (P = 0.530). In the study eyes, blood flow of the ONH lamina and rim area decreased with increasing glaucomatous damage, and treatment with topical timolol was associated with reduced blood flow in the lamina cribrosa and rim area. Perfusion pressure was associated only with flow in the peripapillary area (P = 0.021). CONCLUSIONS: Advanced glaucomatous damage was associated with reduced flow both in the lamina cribrosa and the rim area but not in the peripapillary retina. Treatment with topical timolol was associated with decreased flow in the ONH.     

Histological changes of high axial myopia

To describe pathological changes in the anatomy of highly myopic (axially elongated) eyes, enucleated globes were examined by light microscopy and ocular structures were measured histomorphometrically. These studies revealed that highly axially myopic eyes show continuous thinning of the sclera starting at or behind the equator with a maximal thinning at the posterior pole; a profound thinning of the choroid decreasing from ∼250 to <10 μm in extreme axial myopia, secondary macular defects in the Bruch''s membrane associated with a complete loss of retinal pigment epithelium and choriocapillaris, and retinal photoreceptors; a Bruch''s membrane of normal thickness in contrast to the profound thinning of the choroid and the sclera; an up to 10-fold elongation and thinning of the peripapillary scleral flange as anterior roof of the orbital cerebrospinal fluid space, and subsequently a retrobulbar extension of the cerebrospinal fluid space; an increased distance of the peripapillary arterial circle of Zinn–Haller to the optic disc border; an elongation and thinning of the lamina cribrosa with a subsequently decreased distance between the intraocular pressure compartment and the retrobulbar orbital cerebrospinal fluid pressure compartment; an increasing exposure of the peripheral posterior lamina cribrosa surface to the cerebrospinal fluid space, no longer buffered by the solid optic nerve tissue; and the development and enlargement of parapapillary gamma zone, in contrast to a myopia-independent parapapillary beta zone. These anatomical changes may be associated with high axial myopia-related complications such as an increased susceptibility of glaucomatous optic neuropathy and myopic retinopathy.     

Lamina cribrosa thickness and spatial relationships between intraocular space and cerebrospinal fluid space in highly myopic eyes

PURPOSE: To evaluate the spatial relationships of the intraocular space, the cerebrospinal fluid space, and the lamina cribrosa in highly myopic eyes. METHODS: The study included 36 human globes with an axial length of more than 26.5 mm that showed marked glaucomatous optic nerve damage (n = 29; highly myopic glaucomatous group) or in which the optic nerve was affected by neither glaucoma nor any other disease (n = 7; highly myopic normal group). Two non-highly myopic control groups included 53 globes enucleated because of malignant choroidal melanoma (n = 42; non-highly myopic normal group) or because of painful absolute secondary angle-closure glaucoma (n = 11; non-highly myopic glaucomatous group). Anterior-posterior histologic sections through the pupil and the optic disc were morphometrically evaluated. RESULTS: In both highly myopic groups compared with both non-highly myopic groups and in the highly myopic glaucomatous group compared with the highly myopic normal group, the lamina cribrosa was significantly (P < 0.001) thinner. Correspondingly, the distance between the intraocular space and the cerebrospinal fluid space was significantly (P < 0.05) shorter in the highly myopic normal group than in the non-highly myopic normal group and in the highly myopic glaucomatous group than in the highly myopic normal group. CONCLUSIONS: In highly myopic eyes, the lamina cribrosa is significantly thinner than in non-highly myopic eyes, which decreases the distance between the intraocular space and the cerebrospinal fluid space and steepens the translaminar pressure gradient at a given intraocular pressure, which may explain the increased susceptibility to glaucoma in highly myopic eyes. As in non-highly myopic eyes, thinning of the lamina cribrosa gets more pronounced in highly myopic eyes if glaucoma is also present.     

Cerebrospinal fluid pressure in ocular hypertension

Background: To assess the lumbar cerebrospinal fluid pressure (CSF‐P) in ocular hypertensive subjects with elevated intraocular pressure (IOP) but without development of glaucomatous optic nerve damage. Methods: The prospective interventional study included 17 patients with ocular hypertension and 71 subjects of a nonglaucomatous control group. All patients underwent a standardized ophthalmologic and neurological examination including measurement of lumbar CSF‐P. In the ocular hypertensive group, the IOP was corrected for its dependence on central corneal thickness (IOP_corrected). The trans‐lamina cribrosa pressure difference (Trans‐LCPD) was calculated as IOP_corrected ? CSF‐P. Results: CSF‐P was significantly (p < 0.001) higher in the ocular hypertensive group (16.0 ± 2.5 mmHg) than in the control group (12.9 ± 1.9 mmHg). CSF‐P was significantly associated with IOP_corrected (p < 0.001; r = 0.82). In multivariate analysis, CSF‐P was significantly correlated with IOP_corrected (p < 0.001) and marginally significantly with mean blood pressure (p = 0.05). Trans‐LCPD was not associated significantly with blood pressure (p = 0.69). Conclusion: Some ocular hypertensive subjects with increased intraocular pressure measurements (after correction for their dependence on central corneal thickness) had an abnormally high lumbar cerebrospinal fluid pressure. Assuming that lumbar cerebrospinal fluid pressure correlated with orbital cerebrospinal fluid pressure, one may postulate that the elevated retro‐lamina cribrosa pressure compensated for an increased intraocular pressure. The elevated retro‐lamina cribrosa pressure may have led to a normal trans‐laminar pressure difference in the eyes with elevated intraocular pressure, so that glaucomatous optic nerve damage did not develop. Intraocular pressure, cerebrospinal fluid pressure and arterial blood pressure were correlated with each other.     

角膜滞后量在青光眼中的作用

青光眼是全球首位不可逆致盲性眼病,其具体发病机制尚不清楚,但颇受重视的是眼压和房水流出通道等方面。近年,研究人员开始越来越多地关注非压力依赖因素如角膜滞后量(CH)在青光眼中的作用。CH是角膜的生物力学参数,它反映了角膜的黏性阻力,即吸收和分散能量的能力。CH在临床上很容易获得,可作为眼后部组织生物力学特性的替代标志物,如筛板和乳头周围巩膜,这些组织可能与青光眼损伤的易感性有关。有研究提供了CH与青光眼临床相关结果之间的联系的证据。本文综述了CH在青光眼中的作用的最新发现,从CH的测量方法、CH与中央角膜厚度、青光眼性视野进展、视盘损害、视网膜神经纤维层缺失等方面进行了归纳和总结。     

Evaluation of peripapillary choroidal thickness in unilateral normal-tension glaucoma

Purpose

To evaluate the association of normal-tension glaucoma and peripapillary choroidal thickness.

Participants

Sixty-one patients with normal-tension glaucoma in one eye.

Methods

Spectral domain optical coherence tomography (SD-OCT) scans were obtained to estimate peripapillary choroidal thickness in a group of unilateral normal-tension glaucoma patients. The average peripapillary choroidal thicknesses of the glaucomatous eye and the nonglaucomatous eye of each patient were compared, and the choroidal thickness underlying the retinal nerve fiber layer defect in the glaucomatous eye was compared with the choroidal thickness of a compatible position in the contralateral normal eye. The associations of peripapillary choroidal thickness with independent parameters including the presence of glaucoma, age, sex, refractive error, axial length, central corneal thickness, intraocular pressure, visual field mean deviation, visual field pattern standard deviation, and systemic disease were assessed with mixed model univariate and multivariate analyses.

Results

The average peripapillary choroidal thickness was not statistically significantly different in the glaucomatous and nonglaucomatous eyes of the patients (P = 0.52). There was no definite difference between the choroidal thickness underlying the retinal nerve fiber layer defect in the glaucomatous eye and the choroidal thickness of a compatible position in the contralateral normal eye, indicating that there was no correlation of the retinal nerve fiber layer with choroidal thickness. Age (P = 0.004) and axial length (P ≤ 0.0001) were negatively associated with peripapillary choroidal thickness.

Conclusions

In unilateral normal tension glaucoma, there was no significant intereye difference in choroidal thickness measured with SD-OCT. The structural features of the choroid may not be associated with normal-tension glaucoma.     

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.     

Correlation of Peripapillary Choroidal Thickness and Retinal Nerve Fiber Layer Thickness in Normal Subjects and in Patients with Glaucoma

Purpose: This study was designed to compare the normal and glaucomatous eyes regarding retinal nerve fiber layer (RNFL) thickness and peripapillary choroidal thickness (PCT), and to investigate the correlation of RNFL thickness and PCT. Subjects and Methods: Subjects were selected as a convenience sample of those from a tertiary referral practice of glaucoma. Thirty-two glaucomatous eyes were accepted as group 1; 30 normal eyes were accepted as group 2. Groups were compared for RNFL thickness and PCT. Correlations of RNFL thickness and PCT were assessed for each peripapillary location. Results: Mean inferior and superior RNFL thickness in group 1 were significantly lower than the control group; mean thicknesses of temporal and nasal quadrants were not different in the two groups. Mean PCT at 500 µm distance in the inferior, at 1500 µm distance in the superior, at 500, 1000, and 1500 µm distance in the temporal, and at 1000 and 1500 µm distance in nasal quadrants were found to be significantly thinner in the glaucoma group compared with the control group. Retinal nerve fiber thickness was strongly correlated with PCT at all points of inferior quadrants at 500 µm distance in the superior. There was no correlation between RNFL thickness and PCT at any point in the control group. Conclusion: Peripapillary choroidal thickness was thinner in glaucomatous eyes compared with normal eyes. Correlation of PCT and RNFL thickness found in patients with glaucoma did not exist in normal subjects.