Evaluation of the laminar and prelaminar thickness in glaucomatous eyes using Enhanced Depth Imaging-optical coherence tomography technique
Shahin Yazdani, Mohammad Pakravan, Afsaneh Naderi Beni
Objective: To investigate the features of the lamina cribrosa (LC) in in the eyes of patients with primary open angle glaucoma (POAG ), primary angle closure glaucoma (PACG) and pseudoexfoliation glaucoma (PXG) using enhanced depth imaging (EDI) optical coherence tomography OCT.
Design: Prospective, observational study.
Participants: Patients with POAG (n=30 eyes) ,PACG (n=29 eyes ) and PXG (n=29 eyes)
Methods: Complete ophthalmic examination including standard automatic perimetry was performed in all patients. All subjects underwent optic nerve head OCT scanning using the Heidelberg Spectralis OCT EDI mode. Lamina cribrosa thickness (LCT) prelaminar thickness and anterior lamina cribrosa depth (ALD) were determined at 3 areas (mid superior, center, and mid inferior) by 2 examiners.
Main Outcome Measures: The prelaminar and laminar thickness , and lamina cribrosa depth.
Results: Average LCT differed significantly in the groups (POAG: 117.8 ± 14.1 μm, PACG: 129.8 ± 26 μm, PXG: 97.9 ± 18.8 μm). The mean PLT was significantly thinner in eyes with PXG than in those with POAG or PACG.
Among glaucomatous eyes , the POAG group had the greatest (P < 0.05) and the PACG group had the smallest (P< 0.05) mean LC depths. In all subjects ALD was greater than PT.
Only Mean deviation and average NFL were associated with LCT and PLT by multivariate analysis.
Conclusions: Eyes with PXG demonstrate a thinner LC and PLT compared with POAG and PACG eyes and ALD is greater in POAG eyes compared with either PXG and PACG group
Glaucoma is a group of progressive optic neuropathies characterized by degeneration of retinal ganglion cells that results in a corresponding pattern of visual field loss. (1)
Previous studies reports that glaucomatous axonal degeneration is strongly associated with morphological changes within lamina cribrosa (LC), a mesh-like structure in the scleral canal of the optic nerve cup which is composed of a number of porous collagenous plates. (2-5)
pore banding of the lamina cribrosa results axonal degeneration , blocks axoplasmic flow and leads to apoptotic death of retinal ganglion cells (RGCs).(6) Therefore, the lamina cribrosa is assumed to be the principal site of injury associated with glaucomatous axonal damage .
Enhanced depth imaging (EDI) technology was developed to improve image quality of the deeper eye structures, such as the choroid and the LC. (7-9)
Our clinical impression has been that eyes with PXG have a different pattern of ONH appearance with glaucomatous optic neuropathy, i.e. shallow cupping, saucerized rims and pallor.
The current study evaluates the features of lamina cribrosa and relative position of laminar and prelaminar tissues in the optic nerve head in glaucomatous patients using EDI SD-OCT.
All study participants were examined between March 2013 and June 2012 at the glaucoma clinic of Labbafinejad Medical center, Tehran, Iran. The subjects were allocated to three groups: group 1 consisted of patients with Primary Open Angle Glaucoma ; group 2 consisted of patients with Primary Angle Closure glaucoma and group 3 consisted of pseudoexfoliation Glaucoma .
The study protocol was reviewed and approved by the Ethics Committee of Shahid Beheshti University of Medical sciences and adhered to the Declaration of Helsinki.
All participants underwent a complete ophthalmic examination and assessment , including a review of their medical histories, best-corrected visual acuity measurement (to confirm that visual acuity was adequate for automated perimetry), slit-lamp biomicroscopy, Goldmann applanation tonometry, gonioscopy, dilated funduscopic examination , color disc photography, measurement of the central corneal thickness (Tomey Corporation, Nagoya, Japan), a visual field (VF) test (Humphrey Field Analyzer [HFA] using Swedish interactive threshold algorithm 24-2; Carl Zeiss Meditec, Dublin, CA), and SD OCT imaging (Heidelberg Engineering, Dossenheim, Germany) and EDI-OCT (Spectralis; Heidelberg Engineering, Heidelberg, Germany). Experienced ophthalmologists performed the OCT to acquire EDI images.
All participants had multiple previous experiences with HFA testing. To minimize learning effects, the last HFA test was used in the analysis of the current study.
For inclusion, all participants had to meet the following criteria: best-corrected visual acuity of 20/40 or better with a spherical equivalent within within ±6 diopters, cylinder correction within ±3 diopters and axial length of 22 to 25 mm; presence of a normal anterior chamber on slit-lamp and gonioscopic examinations; and reliable HFA results with a false-positive error rate of less than 15%, a false-negative error rate of less than 15%, and fixation loss of less than 20%. Those with any other ophthalmic disease that could cause in HFA defects and patients with a history of diabetes mellitus were excluded.
All groups included patients with glaucomatous VF defects that were confirmed at least by 2 reliable VF examinations and by the appearance of a glaucomatous optic disc. Eyes with glaucomatous VF defects were defined as those demonstrating 2 or more of the following criteria: (1) a cluster of 3 points with a probability of less than 5% on a pattern deviation map in 1 or more hemifield, including 1 point or more with a probability of less than 1% or a cluster of 2 points with a probability of less than 1%; (2) glaucoma hemifield test results outside the normal limits; and (3) pattern standard deviation of less than 5%.
The diagnostic criteria for POAG used in this study included the presence of a normal anterior chamber and open angle on slit-lamp and gonioscopic examinations, a glaucomatous optic disc (diffuse or focal thinning of the neuroretinal rim) with corresponding visual field defects that were confirmed by at least two reliable visual field examinations.
PACG group included patients with narrow angles (eyes in which the posterior trabecular meshwork was not seen for at least 180° on indentation gonioscopy in the primary position), with peripheral anterior synechiae, a glaucomatous optic disc (diffuse or focal thinning of the neuroretinal rim) with a reproducible visual field loss .
Patients with PXG were defined as the presence of typical pseudoexfoliative material on the anterior lens capsule, pupillary margin in mydriasis on slit-lamp biomicroscopy, or both in combination with a raised intraocular pressure of >21 mmHg and a reproducible visual field loss with optic disc cupping and neuroretinal rim thinning, with no evidence of other secondary causes of glaucoma.
Scanning of the Lamina Cribrosa with Heidelberg Spectralis OCT (Spectralis software v. 184.108.40.206, Eye Explorer Software 220.127.116.11; Heidelberg Engineering) ) in the EDI mode was performed after papillary dilation . The standard protocol for obtaining EDI-OCT images was reported previously (9).
The entire ONH was scanned using a 6-mm length line (512 A-scans) with an interval of 50 µm. and an average of 35 horizontal B-scans was produced in the EDI mode. From these B scans, 3 frames (center, mid superior, and mid inferior) that passed through the ONH were selected.
Anterior lamina cribrosa depth (ALD), which was defined as the distance from the Bruch's membrane opening plane to the level of the anterior LC surface which measured at three points (vertical center of reference line, temporally and nasally 100 μm from the center of reference line). The average of the three values was defined as the anterior LC depth of the B-scan.
LC thickness was defined as the distance between the anterior and posterior borders of the LC, with these borders defined by the highly reflective structure below the optic cup.
To measure the prelaminar thickness, a perpendicular line was drawn at the center and at 100μm nasally and temporally from a reference line connecting both ends of Bruch’s membrane opening. The prelaminar thickness was measured along this vertical line from the anterior border of the reflective region (anterior border of the prelaminar tissue) to the anterior border of the highly reflective region (anterior border of the LC) .the mean of 3 values was defined as the prelaminar thickness of the B-scan in each patient and the average of prelaminar thickness of each B-scan was used as the mean prelaminar thickenss. (Figure 1)
LT , ALD and prelaminar thickness were estimated at the presumed vertical center of each of the 3 B-scans . All measurements were obtained with Adobe Photoshop version 12.0 (Adobe Systems, Inc, San Jose, CA) and then converted to real lengths. (Fig 2) All of the measurements were carried out by 2 examiners that were blind to the clinical parameters when assessing them independently determined parameters twice. The mean of those 4 values was used in the main analysis.
To evaluate, interexaminer and intraexaminer reproducibility, 16 randomly selected scans were remeasured by the examiners, and the intraclass correlation was calculated.
Statistical analyses were performed using SPSS software (ver. 17.0; SPSS, Chicago, IL, USA). Differences between the two groups were assessed using Student's t-test for continuous parameters and the χ2 test for categoric parameters. The correlation between parameters was evaluated using the Pearson correlation coefficients and partial correlation coefficients. Regression analysis was used to determine the factors associated with the LC and prelaminar thickness and anterior LC depth in glaucoma patients. A value of P less than 0.05 was deemed to indicate statistical significance.
Fifty -one glaucoma patients (102 eyes) were examined, and 14 eyes were excluded from analysis because of poor-quality EDI OCT images associated with media opacity or poor patient cooperation.
A total 88 eyes were included for analysis; 18 (35.29%) were women. The mean age+/-standard deviation was 60.47 +/-7.45 years (range, 46–74 years). All subjects had been treated with a variety of glaucoma agents, and mean intraocular pressure was 17.1+/-3.5 mmHg. Mean spherical equivalent refraction and visual field mean deviation were 0.36 +/-1.9 diopters (D; range, -5 to 5 D) and -10.9+/-7.5 dB (range, _29.10 to _3.05 dB), respectively. 30 eyes with primary open angle glaucoma, 29 with exfoliative glaucoma, 29 with primary angle closure glaucoma. The demographic and ocular variables are shown in Table 1. There was no statistically significant difference between groups.
Significant differences in the mean lamina cribroa thickness were found between groups 1 and 2 (P=0.04), groups 1 and 3 (P= 0.0001), groups 2 and 3 (P=.0001), . Moreover, as shown in Table 2, lamina cribrosa thicknesses of groups 3 were always thinner than those of groups 1 and 2 in all eyes .
The mean (SD) prelaminar thickness was significantly different among the groups (P =0.00001 ), with lower values in the PXG group compared with either POAG and PACG group (P=0.04)
The mean anterior lamina depth was significantly different among the 3 groups (Table 2; P =0.01), with significantly more anterior lamina depth in the POAG group compared with either PXG and PACG group (P=0.01). In all subjects ALD was greater than PT .
In multivariate regression analyses, LD,prelaminar thickness and anterior laminar thickness was related to average RNF thickness in OCT and the mean deviation of the visual field in perimetry. (P ≤ 0.05; Table 3).
Intraexaminer intraclass correlation coefficient values for LT, prelaminar thickness and ALD were 0.91 ,0.93 and 0.92, respectively. Interexaminer intraclass correlation coefficient values for LT ,prelaminar thickness and ALD were 0.891 ,0.94 and 0.999, respectively.
In the current study we demonstrated significant differences in the lamina and prelaminar thicknesses between the three groups . The PXG group had smaller and PACG group had greater LCT an PLT .
The morphologic changes of the LC in glaucoma eyes has been investigated in previous studies. peripapillary scleral bowing, (10) scleral canal and neural canal expansion (11,12) posterior deformation, (3,5,6,13-14) initial thickening,(14) subsequent thinning,(3,13) and outward migration (15) of the lamina cribrosa have been described in glaucoma.
factors associated with the status and the magnitude of the LC deformation including : disease stage and aging . greater LC displacement is observed in the more advanced glaucomatous eyes and LC deformation was pronounced in younger eyes than older eyes for the same level of functional loss.
Park et al( 16) reported thinner LC in normal-tension glaucoma eyes compared with high-pressure POAG eyes and suggested that a thinner LC in normal-tension glaucoma would make the ONH vulnerable to glaucomatous damage at relatively low eye pressure levels than in high-tension glaucoma eyes.(11,16)
Kim et al (17) reported that eyes with PXG have a thinner LC compared with POAG eyes at similar levels of glaucoma severity and this may explain the worse clinical course of PXG eyes over POAG eyes.
Previous studies using EDI-OCT have reported The prelaminar tissue was significantly thinner in the POAG group than in the NTG group.(18)
relationship between the IOP and prelaminar tissue thickness after glaucoma surgery in patients with POAG was reported and increase in blood volume or a shift of axoplasmic fluid from the peripapillary retinal nerve fibers or lamina may contribute to the increase in prelaminar thickness .(19-20) However, these studies reported changes in prelaminar tissue thickness after an acute IOP change. Our study demonstrated the chronic effect of IOP on prelaminar tissue thickness and identified other factors that influence the thickness.
In patient with chronically elevated IOP the prelaminar tissue subjects to consistent stress leading to tissue remodeling in the extracellular matrix (21-23). In patients with advanced glaucoma due to decreased RGC axons and increased stiffness from tissue remodeling ,compliance is decreased.(24)
in addition to lamina cribrosa, the prelamina tissue , may influence glaucomatous optic nerve damage.
The prelaminar region consists of bundles of optic nerve fibers, astrocytes, capillaries, and extracellular material (25-26), which may become thinned by ischemia (27). ocular blood flow plays an important role in the pathogenesis of glaucomatous optic neuropathy.
A number of studies demonstrated that blood flow velocities were decreased in the choroidal vessel (28) and carotid artyery (29) in PEX-affected eye compared with the fellow eye.
PEX has been shown to affect smaller vessels rather than the major ones.(30) .Moreover, as a result of accumulation of the PEX material in the vessel walls, vascular alterations like increased permeability, obstruction, and loss of small vessels have been described in the PEX syndrome.(31-32)
It seems that variations in optic nerve head blood supply and in ocular blood flow regulation which may explain the reason for lamia and prelamina tissue thinning of the optic nerve head of these patients . (33)
our results consistently demonstrated that the LC depth was greater in POAG eyes than in PXG eyes, and there were significant depth variations among these groups. Our results indicate that PACG patients have thicker LC than POAG patients.
In the current study, we measured AL depth relative to the the BMO. our results demonstrated significant depth variations among the three glaucoma groups.
Past studies reported (34-35) that The averaged mean LC depth and averaged maximum LC depth in the glaucoma group was significantly greater than that in the normal group.
The patients of the PXG group were had shallower LC depths than those in the other groups in the current study.
Our results demonstrated lamina cribrosa displacing posteriorly in most glaucoma eyes and compatible with both studies (34-35).
In contrast to our result of no significant change in anteroposterior LC position between PXG and PACG glaucomas eyes.
Progressive posterior LC displacement occurs in experimental glaucoma in monkey eyes and ex vivo human eyes by histologic examination .(11,14,15,36-38)
The LC forms a barrier between the anterior-posterior force of IOP and the posterior-anterior force of the orbital cerebrospinal fluid pressure. The position of the LC may be determined by the material properties (e.g., compliance, stiffness, or structural rigidity) and geometry (e.g., thickness, shape, or curvature) of the LC and the peripapillary connective tissues and translaminar pressure difference (TLPD).(39)
An interesting finding is that both LCT and prelaminar thickness were significantly thinner and Lamina cribrosa displacement is smaller in PXG group.
Recent study revealed that the marked decrease in stiffness of lamina cribrosa and peripapillary sclera tissues in PEX eyes imply an increased deformability of the ONH and may reflect an inherent tissue weakness rendering these eyes more vulnerable to IOP-induced glaucomatous optic nerve damage.
Therefore, studying and knowing the biological and biomechanical properties of the lamina cribrosa are of prime importance in the pathophysiology of glaucoma.
To the best of our knowledge, this is the first study to compare the difference in prelaminar tissue thickness between patients with POAG ,PXG and PACG .
.According to our multivariate analysis, only RNF and MD were associated with LC and prelaminar thickness.
Lee et al suggested that thinner LC and a larger LC displacement had a significant influence on the rate of progressive RNFL thinning.(40)
There are several limitations in this study. One limitation is obviously the small sample size. Although EDI OCT improved image quality of the lamina cribrosa ,it is still difficult to confidently identify the posterior border of the LC LC in some
Images and these eyes were excluded from the analysis .
However, because intraobserver and interobserver agreements of the measurements were excellent, we believe the reliability of our data is acceptable for the analysis. Finally, all of the subjects were Iranian ; therefore, our results may not be applicable to non-Asian subjects. Further studies with large sample size are needed in other ethnic groups to see the compatibility of the results.
To our knowledge, however, this is the first study to compare the laminar thickness, prelaminar thickness and anterior laminar depth in POAG,PACG and PXG patients.
In conclusion we show that PXG eyes demonstrate thinner LC and prelaminar tissue with smaller lamina cribrosa depth compared with POAG and PACG eyes .These changes may result from a reduction in blood volume or axoplasmic material. Our observations may represent a different condition of eyes with PXG that makes the optic nerves more susceptible or a faster deterioration of the LC as PXG proceeds to affect both retinal ganglion cell axons and the support tissues.
1. Weinreb RN, Khaw PT. Primary open-angle glaucoma. Lancet. 2004; 363: 1711–1720.
2. Anderson DR. Ultrastructure of human and monkey lamina cribrosa and optic nerve head. Arch Ophthalmol. 1969; 82: 800–814.
3. Emery JM, Landis D, Paton D, Boniuk M, Craig JM. The lamina cribrosa in normal and glaucomatous human eyes. Trans Am Acad Ophthalmol Otolaryngol. 1974; 78: OP290-297.
4. Quigley HA, Addicks EM. Regional differences in the structure of the lamina cribrosa and their relation to glaucomatous optic nerve damage. Arch Ophthalmol. 1981; 99: 137–143.
5. Jonas JB, Berenshtein E, Holbach L. Anatomic relationship between lamina cribrosa, intraocular space, and cerebrospinal fluid space. Invest Ophthalmol Vis Sci. 2003; 44: 5189–5195.
6. Quigley HA, Hohman RM, Addicks EM, Massof RW, Green WR. Morphologic changes in the lamina cribrosa correlated with neural loss in open-angle glaucoma. Am J Ophthalmol. 1983; 95: 673–691.
7. Yeoh J, Rahman W, Chen F, Hooper C, Patel P, Tufail A et al. Choroidal imaging in inherited retinal disease using the technique of enhanced depth imaging optical coherence tomography. Graefes Arch Clin Exp Ophthalmol 2010; 248: 1719–1728.
8. Dell’Omo R, Costagliola C, Di Salvatore F, Cifariello F, Dell’Omo E. Enhanced depth imaging spectral-domain optical coherence tomography. Retina 2010; 30: 378–379.
9. Lee EJ, Kim TW, Weinreb RN, Park KH, Kim SH, Kim DM. Visualization of the lamina cribrosa using enhanced depth imaging spectral-domain optical coherence tomography. Am J Ophthalmol 2011; 152: 87–95 e81
10. Yang H, Downs JC, Girkin C, et al. 3-D Histomorphometry of the normal and early glaucomatous monkey optic nerve head: lamina cribrosa and peripapillary scleral position and thickness. Invest Ophthalmol Vis Sci. 2007;48:4597–4607.
11. Bellezza AJ, Rintalan CJ, Thompson HW, Downs JC, Hart RT, Burgoyne CF. Deformation of the lamina cribrosa and anterior scleral canal wall in early experimental glaucoma. Invest Ophthalmol Vis Sci. 2003;44:623–637.
12. Downs JC, Yang H, Girkin C, et al. 3-D Histomorphometry of the normal and early glaucomatous monkey optic nerve head: neural canal and subarachnoid space architecture. Invest Ophthalmol Vis Sci. 2007;48:3195–3208.
13. Quigley HA, Addicks EM, Green WR, Maumenee AE. Optic nerve damage in human glaucoma. II. The site of injury and susceptibility to damage. Arch Ophthalmol. 1981;99:635–649.
14. Yang H, Thompson H, Roberts MD, Sigal IA, Downs JC, Burgoyne CF. Deformation of the early glaucomatous monkey optic nerve head connective tissue after acute IOP elevation in 3-D histomorphometric reconstructions. Invest Ophthalmol Vis Sci. 2011;52:345–363.
15. Yang H, Williams G, Downs JC, et al. Posterior (outward) migration of the lamina cribrosa and early cupping in monkey experimental glaucoma. Invest Ophthalmol Vis Sci. 2011;52: 7109–7121.
16. Park HY, Jeon SH, Park CK. Enhanced depth imaging detects lamina cribrosa thickness differences in normal tension glaucoma and primary open-angle glaucoma. Ophthalmology
17. Kim S, Sung KR, Lee JR, Lee K. Evaluation of lamina cribrosa in pseudoexfoliation syndrome using spectral-domain optical coherence tomography enhanced depth imaging.
Ophthalmology. 2013 Sep;120(9):1798-803
18.Youn Hea Jung, Hae-Young L. Park, Kyoung In Jung, and Chan Kee ParkComparison of Prelaminar Thickness between Primary Open Angle Glaucoma and Normal Tension Glaucoma Patients. PLoS One. 2015; 10(3): e0120634.
19. Reis AS, O'Leary N, Stanfield MJ, Shuba LM, Nicolela MT, Chauhan BC. Laminar displacement and prelaminar tissue thickness change after glaucoma surgery imaged with optical coherence tomography. Invest Ophthalmol Vis Sci. 2012; 53:5819–5826.
20. Lee EJ, Kim TW, Weinreb RN. Reversal of lamina cribrosa displacement and thickness after trabeculectomy in glaucoma. Ophthalmology. 2012; 119:1359–1366.
21. Hernandez MR. Ultrastructural immunocytochemical analysis of elastin in the human lamina cribrosa. Changes in elastic fibers in primary open-angle glaucoma. Invest Ophthalmol Vis Sci. 1992; 33:2891– 2903. PMID: 1526740
22. Hernandez MR, Andrzejewska WM, Neufeld AH. Changes in the extracellular matrix of the human optic nerve head in primary open-angle glaucoma. Am J Ophthalmol. 1990; 109:180–188. PMID: 2405683
23. Hernandez MR, Ye H. Glaucoma: changes in extracellular matrix in the optic nerve head. Ann Med. 1993; 25:309–315. PM
24. Agoumi Y, Sharpe GP, Hutchison DM, Nicolela MT, Artes PH, Chauhan BC. Laminar and prelaminar tissue displacement during intraocular pressure elevation in glaucoma patients and healthy controls. Ophthalmology. 2011; 118:52–59.
25. Hernandez MR, Igoe F, Neufeld AH. Extracellular matrix of the human optic nerve head. Am J Ophthalmol. 1986; 102:139–148. PMID: 2426947
26. Anderson DR, Hoyt WF. Ultrastructure of intraorbital portion of human and monkey optic nerve. Arch Ophthalmol. 1969; 82:506–530. PMID:
27. Hayreh SS, Jonas JB. Optic disc morphology after arteritic anterior ischemic optic neuropathy. Ophthalmology.
2001; 108:1586–1594. PMID
28. Sibour G, Finazzo C, Boles Carenini A. Monolateral pseudoexfoliatio capsulae: a study of choroidal blood flow. Acta Ophthalmol Scand Suppl 1997; 224: 13–14.
29. Scullica L, Buceti R, Castagna I, Ferreri G, Trombetta JJ. Functional aspects of pseudoexfoliation: Physiopathological features. New Trends Ophthalmol 1993; 8: 163–168.
30. Meyer E, Haim T, Zonis S, Gidoni O, Gitay H, Levanon D et al. Pseudoexfoliation: epidemiology, clinical and scanning electron microscopic study. Ophthalmologica 1984; 188(3): 141–147.
31. Repo LP, Teräsvirta ME, Koivisto KJ. Generalized transluminance of the iris and the frequency of the pseudoexfoliation syndrome in the eyes of transient ischemic attack patients. Ophthalmology 1993; 100(3): 352–355.
32. Helbig H, Schlötzer-Schrehardt U, Noske W, Kellner U, Foerster MH, Naumann GO. Anterior-chamber hypoxia and iris vasculopathy in pseudoexfoliation syndrome. Ger J Ophthalmol 1994; 3(3): 148–153.
33. Galassi F, Giambene B, Menchini U. Ocular perfusion pressure and retrobulbar haemodynamics in pseudoexfoliative glaucoma. Graefes Arch Clin Exp Ophthalmol 2007;246(3):411-6.
34. Furlanetto RL, Park SC, Damle UJ, et al. Posterior displacement of the lamina cribrosa in glaucoma: in vivo interindividual and intereye comparisons. Invest Ophthalmol Vis Sci. 2013;54: 4836–4842.
35. Seo JH, Kim TW, Weinreb RN. Lamina cribrosa depth in healthy eyes. Invest Ophthalmol Vis Sci. 2014;55:1241–1250.
36. Radius RL, Pederson JE. Laser-induced primate glaucoma. II. Histopathology. Arch Ophthalmol. 1984;102:1693–1698.
37. Yang H, Downs JC, Sigal IA, Roberts MD, Thompson H, Burgoyne CF. Deformation of the normal monkey optic nerve head connective tissue after acute IOP elevation within 3-D histomorphometric reconstructions. Invest Ophthalmol Vis Sci. 2009;50:5785–5799.
38. Yan DB, Coloma FM, Metheetrairut A, Trope GE, Heathcote JG, Ethier CR. Deformation of the lamina cribrosa by elevated intraocular pressure. Br J Ophthalmol. 1994;78:643–648.
39. Lee DS, Lee EJ, Kim TW, Park YH, Kim J, Lee JW, Kim S.Influence of translaminar pressure dynamics on the position of the anterior lamina cribrosa surface. Invest Ophthalmol Vis Sci. 2015 May;56(5):2833-41.
40. Lee EJ, Kim TW, Kim M, Kim H. Influence of lamina cribrosa thickness and depth on the rate of progressive retinal nerve fiber layer thinning. Ophthalmology. 2015 Apr;122(4):721-9
Table 1. Summary Statistics of Variables in the 3 Subject Groups
Table 2. Summary Statistics of Laminar and Prelaminar Tissue Variables
Table 3. Results of Multivariate Regression Analyses of Laminar and Prelaminar thickness and anterior laminar depth
Fig 1. Measurement of the prelaminar thickness. A perpendicular line from a reference line connecting both ends of Bruch’s membrane opening was drawn at the center and at 100μm nasally and temporally in each B-scan. Mean of 3 prelaminar thickness measurements was defined as the prelaminar thickness .
Fig 2. B-scan image with lines showing the lamina cribrosa (LC) thickness , prelaminar thickness and anterior lamina depth.
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