Rudrani Banik, MD,2,4 Jeffrey M. Liebmann, MD,3,5 Robert Ritch, MD2,3,4
Objective: To assess the structure of central optic disc pits (ODPs) using enhanced-depth imaging opticalcoherence tomography (EDI OCT) and to ascertain their clinical significance.
Design: Prospective, cross-sectional study.Participants: Patients with an ophthalmoscopically visible central ODP in either eye, irrespective of accompa-
nying ocular disease, were enrolled from the neuro-ophthalmology and glaucoma referral practices. Each subject witha central ODP was matched with 2 healthy subjects with normal-appearing optic disc within 5 years of age.
Methods: Each participant received a complete ophthalmologic examination including standard automatedperimetry, retinal nerve fiber layer (RNFL) thickness measurement by OCT, and serial horizontal and verticalcross-sectional EDI OCT of the optic nerve head.
Main Outcome Measures: Structure of the lamina cribrosa (LC) in relation to the central ODP in EDI OCTimages.
Results: Eighteen eyes (13 subjects) with a central ODP and 52 healthy eyes (26 controls) were included.Four eyes (2 subjects) with a central ODP were otherwise normal with intact macula, neuroretinal rim, RNFL, andvisual field. Fourteen eyes (11 subjects) with a central ODP had glaucoma with glaucomatous neuroretinal rimthinning, RNFL loss, and corresponding visual field defect. No eye had associated maculopathy. On EDI OCT, thecentral ODP corresponded with a full-thickness defect in the LC center with no serous retinal detachment orherniation of neural tissue through the LC defect. Central ODPs were separated from (type 1) or merged with (type2) the LC opening for the central retinal vascular trunk. In control eyes, no LC defect was detected.
Conclusions: Central ODPs are full-thickness LC defects unassociated with maculopathy and different fromglaucomatous acquired pits of the optic nerve, which represent focal laminar defect adjacent to the disc edge.
Financial Disclosure(s): The authors have no proprietary or commercial interest in any of the materials
Optic disc pits (ODPs) manifest as localized, round orovoid, gray-white depressions in the optic disc.1,2 They canbe classified as either acquired or congenital. These 2 typesmay not be morphologically distinguishable on clinical ex-amination,2 but their typical locations in the optic disc aredifferent. An acquired ODP, often called acquired pit of theoptic nerve (APON), is associated with glaucomatous opticneuropathy and occurs peripherally, slightly temporal to theupper or lower poles of the optic disc, but not in the centerof the disc.3,4 Congenital ODPs commonly occur in thetemporal or inferotemporal disc sector, whereas 20% occurcentrally and 10% are located in other regions of the disc.2
Temporally or inferotemporally located congenital ODPsmay be associated with macular complications, either asserous retinal detachment or as cystoid retinal edema.2,5–8
However, centrally located ODPs have frequently beenoverlooked in clinical practice, and their detailed structureand clinical implications have not been investigated.
We hypothesized that central ODPs might be associatedwith structural defects in the lamina cribrosa (LC) butunassociated with maculopathy and different from acquiredpit of the optic nerve in glaucoma. The LC is a sieve-likestructure with sheets of connective tissue through which retinal
ganglion cell axons pass. Because the LC is considered a Y
rimary site of retinal ganglion cell axon injury in glauc-ma,9–12 it is important to determine whether central ODPs aressociated with defects in the LC and/or disturbances of visualunction. A variety of imaging devices including spectral-omain optical coherence tomography (OCT) have recentlyeen used to evaluate the LC in vivo,13–17 and histologicvidence has demonstrated that volumetric spectral-domainCT of the optic nerve head can capture target structures,
specially the anterior laminar surface.18 Enhanced depth im-ging (EDI) OCT improves the image quality of the deeptructures of the posterior segment,19 and has been used tonvestigate the in vivo microanatomy of the outer retina, cho-oid, and sclera.20–22 It has recently been shown to provideetailed cross-sectional images of the LC.23–25
We evaluated a series of eyes with clinically detectedentral ODPs using EDI OCT to assess their detailed struc-ure relative to the LC and association with serous retinaletachment and standard automated perimetry to assessisual function of those eyes.
atients and Methods
his prospective, cross-sectional study was approved by the New
ork Eye and Ear Infirmary Institutional Review Board. Written,
1ISSN 0161-6420/13/$–see front matterhttp://dx.doi.org/10.1016/j.ophtha.2012.12.034
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informed consent was obtained from all subjects and the studyadhered to the tenets of the Declaration of Helsinki.
We recruited patients with a central ODP seen ophthalmoscop-ically in either eye, irrespective of accompanying ocular disease,from the neuro-ophthalmology and glaucoma referral practices atthe New York Eye and Ear Infirmary from July 1, 2011, toDecember 31, 2011. A central ODP was defined as a localized greyor yellowish round or ovoid depression in the center of the opticdisc. Each patient with a central ODP was matched with 2 normalsubjects within 5 years of age. Normal eyes had normal-appearingoptic discs and visual fields, open iridocorneal angles, intraocularpressure �21 mmHg, and no apparent ocular or systemic abnor-mality that could affect optic nerve structure or visual function. Forboth eyes of each participant, serial horizontal and vertical cross-sectional images (interval between images, approximately 30 �m)of the optic nerve head were obtained using EDI OCT (Spectralis;Heidelberg Engineering, GmbH, Dossenheim, Germany). Circum-papillary retinal nerve fiber layer (RNFL) thickness measurementswere also obtained using the same device. All participants had fullophthalmologic examinations including slit-lamp biomicroscopy,applanation tonometry, dilated fundus examination, color discstereophotography (Stereo Camera Model 3-DX; Nidek Inc, PaloAlto, CA) and standard automated perimetry (Humphrey VF An-alyzer, 24-2 SITA-Standard strategy; Carl Zeiss Meditec, Inc,Dublin, CA). We excluded individuals with previous posteriorsegment intraocular surgery, ocular trauma and optic disc photo-graphs or EDI OCT images of poor quality owing to media opacityor poor patient cooperation.
For EDI OCT of the optic nerve head, we used the methoddescribed in a previous report.24 In brief, the OCT device was setto image a 15°�10° rectangle for horizontal scans (and a 10°�15°rectangle for vertical scans) centered on the optic disc. This rect-angle was scanned with 97 sections and each section had 20 OCTframes averaged. The device was pushed closer to the eye to movethe zero reference plane more posteriorly, which enhanced theimage of deeper structures. This created an inverted image with theinner portions of the retina shown facing downward. The optic discphotographs and EDI OCT images were carefully reviewed by aglaucoma specialist (S.C.P.) to assess the structure of the LC inrelation to the central ODP and the presence of serous retinaldetachment. The eyes with a central ODP were classified accord-ing to the spatial relationship between the central ODP and thecentral retinal vascular trunk (CRVT).
To demonstrate the spatial relationship of the central ODP tosurrounding structures, a 3-dimensional (3D) image was recon-structed using serial EDI OCT images for a representative casewith a central ODP. The EDI OCT scans which had been auto-matically aligned by the built-in software of the OCT device wereexported and then uploaded to commercially available 3D recon-struction software (Amira, Version 5.3.3; Visage Imaging, Inc, SanDiego, CA). Anterior laminar surface, anterior scleral canal andchoroid, retinal arteries, and veins were manually outlined usingthe software for creating a 3D image. The OCT images shown inthis publication were inverted after being exported from the OCTdevice and are negative images with Bruch’s membrane appearingblack rather than white and with vascular shadows appearing aswhite vertical streaks.
4™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™Figure 1. Optic disc photographs, enhanced depth imaging optical cohenerve fiber layer thickness measurements of a control eye (A–H) and 2 nvertical (D, L, T) cross-sectional scans identified intact lamina cribrosa (y(B and D; red and aqua dotted lines, respectively) in the control eye and fseparated from the retinal vessels (red dotted lines) in eyes with a centra
with arrows indicate the locations of the scans (A, I, Q).
esults
hirteen subjects (5 women) with a central ODP in 1 or both eyesmean value � standard deviation age, 61�19 years) and 26ormal subjects with no central ODP in either eye (mean value �D age, 60�16 years) were analyzed. Corrected visual acuitiesanged from 20/20 to 20/25 in all participants.
All eyes in the control group had normal optic discs, maculas,NFL thickness profiles, and visual fields (Fig 1A, F–H). In theDI OCT scans (Fig 1–E), the anterior laminar surface in controlyes had smooth, curvilinear contour and showed no focal LCefect as demonstrated in a previous report.25 The CRVT wasompletely encased by the LC, and there was no gap between theascular wall and the LC.
Two subjects seen in the neuro-ophthalmology practice had aentral ODP in both eyes. These 4 eyes had no accompanyingcular disease. Neuroretinal rim was intact, and circumpapillaryNFL thickness measurement and standard automated perimetryere normal (Fig 1I, N–Q, V–X), and dilated fundus examination
evealed no maculopathy. The EDI OCT revealed that the centralDPs corresponded to full-thickness defects in the center of theC and the defects were filled with neural tissue (Fig 1J–M, R–U).inimal dimpling of prelaminar neural tissue was noted above
he LC defects, but there was no serous retinal detachment in theeripapillary area or herniation of neural tissue extending into theubarachnoid space through the LC defect.
Eleven subjects seen in the glaucoma practice had glaucoma10 with primary open-angle glaucoma and 1 with pigmentarylaucoma) in both eyes, with a range of glaucomatous neuroretinalim thinning, RNFL loss and corresponding visual field defectsFigs 2 and 3). A central ODP was detected in both eyes of 3ubjects and in 1 eye of the remaining 8 subjects. Dilated fundusxamination revealed no maculopathy. EDI OCT findings of theentral ODPs were the same as seen in the 4 eyes with noccompanying ocular disease; full-thickness defects in the centerf the LC and minimal dimpling of prelaminar tissue above the LCefect (Figs 2B–E, J–M, and 3B–E, J–M). No serous retinaletachment or herniation of neural tissue through the LC defectas observed. Based on optic disc photography and EDI OCTndings, there was no morphologic difference between the centralDPs seen in 4 normal eyes and those seen in 14 glaucomatous
yes. However, it was unclear whether the visual field defects inlaucomatous eyes with a central ODP were purely owing tolaucoma or whether the central ODP contributed to the visualeld defects by any degree.
The LC defects corresponding with the central ODPs varied inhysical proximity to the LC pore for the CRVT. We classified theentral ODPs into 2 types depending on their proximity to the LCore for the CRVT: A type 1 central ODP clearly separated by LCissue from the LC pore for the CRVT (Figs 1I–X and 2) and a type
central ODP merged with the LC pore for the CRVT, forming aarge LC opening that includes but does not completely encase theRVT (Fig 3). Three eyes with no accompanying ocular disease andeyes with glaucoma were type 1, and the remaining 9 were type 2.3D reconstruction of serial EDI OCT images illustrated the spatial
elationship between central ODP and retinal vessels (Fig 4).
™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™™tomographic scans, Humphrey 24-2 pattern deviation plots, and retinaleyes with a type 1 central optic disc pit (I–X). Horizontal (B, J, R) anddotted lines) that completely encases the central retinal artery and vein
ickness defects (black arrows) of the lamina cribrosa (yellow dotted lines)The same scans without the labels (C, E, K, M, S, U). The dotted lines
™™™renceormalellow
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Discussion
Using EDI OCT, we demonstrated that a central ODP is afull-thickness defect in the center of the LC separate from ormerged with the LC pore for the CRVT. Central ODPs werenot associated with maculopathy or serous retinal detach-ment, and this might be attributed to the central location of
Figure 2. Optic disc photographs, enhanced depth imaging optical cohenerve fiber layer thickness measurements of the eyes with a type 1 central oscans identified full-thickness defects (black arrows) of the lamina cribrosasame scans without the labels (C, E, K, M). The dotted lines with arrow
the pit. The great majority of maculopathies associated with n
4
ongenital ODPs occur in eyes with temporally or infero-emporally located pits.26–28 In a report with histologicections, the LC was defective in the area of a pit thatccurred in the temporal or inferotemporal periphery nearhe disc margin.26 The vitreous cavity and the subarachnoidpace are separated by peripheral LC and peripapillaryclera. When there is a defect in the LC periphery, overlying
tomographic scans, Humphrey 24-2 pattern deviation plots, and retinalisc pit and glaucoma. Horizontal (B, J) and vertical (D, L) cross-sectionalow dotted lines) separated from the retinal vessels (red dotted lines). Thecate the locations of the scans (A, I).
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Qayum et al � Central Optic Disc Pits
cerebrospinal fluid may leak into subretinal space. Be-cause the central ODPs are far from the subarachnoidspace, herniation of neural tissue through the LC defector cerebrospinal fluid leakage into subretinal space areunlikely, as evidenced by our cases. On another note,APONs occur exclusively in the disc periphery,3,4 and theLC defects corresponding to the APONs were detected
Figure 3. Optic disc photographs, enhanced depth imaging optical cohenerve fiber layer thickness measurements of the eyes with a type 2 central oscans identified full-thickness defects (black arrows) of the lamina cribrosscans without the labels (C, E, K, M). The dotted lines with arrows indi
only in the far periphery of the LC, adjacent to the disc c
dge.25 Therefore, central ODPs should be differentiatedrom APONs in glaucoma.
In our study, 14 of 18 eyes with a central ODP had glau-oma. Considering that most (11/13) subjects in the ODProup were recruited from a glaucoma referral practice, weelieve that this resulted from selection bias. A longitudinaltudy with a larger sample size would elucidate whether a
tomographic scans, Humphrey 24-2 pattern deviation plots, and retinalisc pit and glaucoma. Horizontal (B, J) and vertical (D, L) cross-sectionallow dotted lines) next to the retinal vessels (red dotted lines). The samehe locations of the scans (A, I).
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Ophthalmology Volume xx, Number x, Month 2013
The ODPs located in the disc center are likely con-genital and similar developmentally to the LC openingfor the CRVT. The APONs occur exclusively in the farperiphery of the disc.3,4,25 Congenital ODPs are oftenasymptomatic and are diagnosed as incidental findings onfundus examination.2,27 Visual deterioration typically oc-curs only when congenital ODPs are complicated byother ocular diseases, including macular lesions (macularedema, detachment, or pigment changes) and glauc-oma.2,5– 8 Additionally, Healey and Mitchell29 showed ina population-based study of 3654 participants that 2 ofthe 4 eyes with a central ODP manifested no visual fielddefects, and of the remaining 2 eyes with visual fielddefects, 1 had open-angle glaucoma, and the other had ananomalous disc. Based on these previous reports, central,congenital ODPs are likely to produce no visual dysfunc-tion and require no treatment. In our study, 14 eyes witha central ODP had glaucoma with characteristic neu-roretinal rim thinning, RNFL loss, and correspondingvisual field defect, and the remaining 4 eyes with a centralODP had normal neuroretinal rim, RNFL, and visual field. Nocentral ODP was associated with serous retinal detachment ormaculopathy. Because it was unclear whether the central ODPcontributed to the visual field defects to a small degree, how-ever, further investigation is needed to assess the visual fieldchanges over time in the eyes with a central ODP and no otherabnormality.
Healey and Mitchell29 stated that the centrally locatedODPs likely represent a previously poorly described con-genital abnormality of the LC, possibly associated withembryonic vasculature growth and regression. We haveshown that the central ODP is a full-thickness LC defect.Based on this finding, we hypothesize that a central ODPmay be the result of abnormal timing of hyaloid arteryregression and/or LC development, which could lead to an
Figure 4. Three-dimensional images of the optic nerve head viewed fromcross-sectional enhanced depth imaging optical coherence tomographicgreen � lamina cribrosa; grey � sclera and choroid; red � retinal arterie
open LC pore for the hyaloid artery, manifested clinically as t
6
central ODP. During early ocular development, nutrientsnd blood are supplied to the developing eye by the hyaloidrtery, which originates from the ophthalmic artery, runshrough the center of the eye, and terminates at the posteriorurface of the developing lens.30 Its regression is induced byutophagy and apoptosis, and occurs as the retinal vascula-ure matures,31 typically at the beginning of the third tri-ester. Ultrasonographic imaging revealed no instances of
n intact hyaloid artery in healthy subjects with a gestationalge of �32 weeks.30 However, an intact hyaloid arteryould be seen beyond a gestational age of 32 weeks inubjects with pathologic findings (e.g., trisomy 13, 18, and1), and it was speculated that delayed hyaloid artery re-ression may be associated with retarded early third trimes-er cerebral development.30 The LC begins to develop at aestational age of 16 weeks and continues through 32eeks, when it resembles an adult LC.32 If hyaloid artery
egression is completed after LC development, because ofither delayed hyaloid artery regression or accelerated LCevelopment, the LC pore for the hyaloid artery wouldemain patent and manifest as a central ODP. Because nonef our subjects showed evidence of such systemic findingss trisomy 13, 18, or 21, we hypothesize that the centralDPs may be more likely owing to accelerated LC devel-pment rather than delayed hyaloid artery regression.
Cloquet’s canal serves as a perivascular sheath surround-ng the hyaloid artery in the embryonic eye.33 Persistence ofloquet’s canal was found in most healthy eyes usingigh-speed, ultra–high-resolution spectral-domain OCT andt appeared as a reflective structure extending anteriorlyrom the inferonasal optic nerve head in 14 of 15 eyes.34
he presence or structure of Cloquet’s canal was not as-essed in our study. Future investigation is needed to deter-ine the spatial relationship between Cloquet’s canal and
rent perspectives for the case shown in Fig 1Q, reconstructed using serialRetina and prelaminar neural tissue were not shown. Semitransparent
e � retinal veins; N � nasal; T � temporal.
diffescans.
he central ODP with the LC defect to confirm our hypoth-
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esis that the central ODP may be associated with the hyaloidartery.
Regarding the spatial relationship between the centralODP and the CRVT, the location of the hyaloid arterydictates the location of the central ODP, if the central ODPis the result of an open LC pore for the hyaloid artery. Fortype 1 central ODPs, the hyaloid artery may have beensituated close to, but separate from, the CRVT. For type 2central ODPs, the hyaloid artery may have been situatednext to the CRVT, forming a large LC opening that includesbut incompletely encases the CRVT.
Our results are limited by the small sample size andpossible selection bias caused by recruiting subjects fromglaucoma and neuro-ophthalmology practices. Histologicstudy is also needed to confirm our results based on OCTfindings. Morphometric analysis of the optic disc was notperformed in the present study. Characterization of disc sizeor shape in the eyes with central ODP compared to normal,healthy eyes may provide valuable information.
In conclusion, based on the EDI OCT findings, centralODPs correspond to full-thickness defects of the LC andcan be classified into 2 types depending on their spatialrelationships to the CRVT. They are unassociated withmaculopathy or serous retinal detachment and differentfrom APONs in glaucoma. Further investigation is war-ranted to verify the structural and functional stability ofcentral ODPs. Eyes with vision loss and central ODPsshould be investigated for the cause of visual dysfunction.
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Footnotes and Financial Disclosures
cine, New York, New York.
Pm
FTm
SGrGCa
CSas
8
3. Apple DJ, Rabb MF. Ocular Pathology: Clinical Applicationsand Self-Assessment. 3rd ed. St Louis: Mosby; 1985:14–60.
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2006;142:862–4.
Originally received: October 12, 2012.Final revision: December 14, 2012.Accepted: December 17, 2012.Available online: ●●●. Manuscript no. 2012-1551.1 The George Washington University School of Medicine and HealthSciences, Washington, DC.2 Department of Ophthalmology, New York Eye and Ear Infirmary, NewYork, New York.3 Moise and Chella Safra Advanced Ocular Imaging Laboratory, EinhornClinical Research Center, New York Eye and Ear Infirmary, New York,New York.4 Department of Ophthalmology, New York Medical College, Valhalla,New York.5 Department of Ophthalmology, New York University School of Medi-
resented in part at: the Association for Research in Vision and Ophthal-ology Annual Meeting, Fort Lauderdale, Florida, May 9, 2012.
inancial Disclosure(s):he authors have no proprietary or commercial interest in any of theaterials discussed in this article.
upported by the Ralph and Sylvia Ablon Research Fund of the New Yorklaucoma Research Institute, New York, NY. J.M. Liebmann received
esearch support from Carl Zeiss Meditec, Inc, Heidelberg Engineering,mbH, Optovue, Inc, and Topcon Medical Systems. S.C. Park is the Peterrowley Research Scientist and Assistant Professor at the New York Eyend Ear Infirmary, New York, NY.
orrespondence:ung Chul Park, MD, Department of Ophthalmology, The New York Eyend Ear Infirmary, 310 East 14th Street, New York, NY 10003. E-mail:
