aao glaucoma 2013_gla_syllabus.pdf

2013New Orleans

Subspecialty Day

Glaucoma 2013: The Future Is Now! #Glaucoma2013

Glaucoma 2013: The Future Is Now! #Glaucoma2013

Neuro-Ophthalmology 2013: What to Make of This? Recognizing the Distinctive Neuro-Ophthalmic Symptom, Sign, or Test

Oculofacial Plastic Surgery 2013: Blues, Blephs, and Blowouts Pediatric Ophthalmology 2013: Preparing for the Next Generation

2013 Ameri can Academy of Oph thal mology. All rights reserved. No por tion may be repro duced with out express writ ten con sent of the Ameri can Academy of Oph thal mology.

Glaucoma 2013The Future Is Now! #Glaucoma2013 Under Pressure

Program DirectorsThomas W Samuelson MD andDavid S Friedman MD MPH PhD

In conjunction with the American Glaucoma Society

Ernest N Morial Convention CenterNew Orleans, LouisianaSaturday, Nov. 16, 2013

Presented by:The American Academy of Ophthalmology

Commercial Support for the Glaucoma Syllabus provided by

Glaucoma 2013 Planning GroupThomas W Samuelson MDProgram Director

David S Friedman MD MPH PhDProgram Director

Teresa C Chen MDRobert M Feldman MDDavid S Greenfield MDFelipe A Medeiros MD Eydie G Miller-Ellis MDJonathan S Myers MDKouros Nouri-Mahdavi MD Pradeep Y Ramulu MD PhD Kuldev Singh MD MPH

Former Program Directors2012 Wallace L M Alward MD Thomas W Samuelson MD2011 Leon W Herndon MD Wallace LM Alward MD2010 Rohit Varma MD MPH Leon W Herndon MD2009 Donald L Budenz MD MPH Rohit Varma MD MPH

2008 Henry D Jampel MD MHS Donald L Budenz MD MPH2007 Anne Louise Coleman MD PhD Henry D Jampel MD MHS2006 Christopher A Girkin MD Anne Louise Coleman MD PhD2005 Claude F Burgoyne MD Christopher A Girkin MD2004 David S Greenfield MD Claude F Burgoyne MD2003 Kuldev Singh MD MPH David S Greenfield MD2002 Theodore Krupin MD Kuldev Singh MD MPH2001 Robert D Fechtner MD Theodore Krupin MD2000 Jeffrey M Liebmann MD Robert D Fechtner MD1999 Robert N Weinreb MD Jeffrey M Liebmann MD1998 George A Cioffi MD Robert N Weinreb MD1997 Richard A Lewis MD George A Cioffi MD1996 M Bruce Shields MD E Michael Van Buskirk MD

1995 Reay H Brown MD Mary Gerard Lynch MD1994 Richard A Lewis MD

Subspecialty Day Advisory CommitteeWilliam F Mieler MDAssociate Secretary

Donald L Budenz MD MPHDaniel S Durrie MDRobert S Feder MD R Michael Siatkowski MDNicolas J Volpe MD

Jonathan B Rubenstein MD Secretary for Annual Meeting

StaffMelanie R Rafaty CMP, Director, Scientific

Meetings Ann LEstrange, Scientific Meetings SpecialistBrandi Garrigus, Presenter CoordinatorDebra Rosencrance CMP CAE, Vice

President, Meetings & ExhibitsPatricia Heinicke Jr, EditorMark Ong, DesignerGina Comaduran, Cover Design

ii 2013 Subspecialty Day | Glaucoma

Dear Colleague:

On behalf of the American Academy of Ophthalmology and the American Glaucoma Society (AGS), it is our pleasure to welcome you to New Orleans and The Future Is Now! #Glaucoma2013.

As cochairs of the Glaucoma Subspecialty Day Program, we have been honored to work with a superb planning group in organizing this years meeting. The goal for this years Glaucoma Sub-specialty Day is to deliver clinically relevant information for clinicians. We want both general ophthalmologists and specialists to walk away with new concepts to help fine-tune their glaucoma management skills. We worked very hard to involve highly qualified, expert speakers and modera-tors from all over the world to engage the audience throughout the day. We anticipate that this will be an extraordinary educational event, and we are grateful that you have chosen to spend your day at Glaucoma Subspecialty Day.

We have built in ample time for audience response and feedback. The program is structured to be dynamic and interactive. Many of the sessions have been organized in a case presentation platform. Most sessions will include lively, engaging panels that will challenge many of our long-held beliefs concerning glaucoma management. This year we are emphasizing the role of the native lens in glau-coma management, both in terms of combining cataract and glaucoma surgery and regarding the role of the lens in the pathogenesis of narrow and some open-angle glaucomas. The afternoon will feature a session on microinvasive glaucoma surgery and its role in surgical glaucoma management, as well as an in-depth discussion on angle-closure glaucoma. Advances in imaging, diagnosis, and drug therapy will also be featured, including a debate on branded products vs. generics.

We are excited to have Joseph Caprioli MD FACS as the American Glaucoma Society Subspecialty Day Lecturer. His talk is entitled Regional Rates of Field Loss in Glaucoma: Differential Effects of Trabeculectomy. Dr. Caprioli has long been recognized as a leading expert in structural and func-tional correlation and glaucoma progression, and we are grateful to him for sharing his work as our keynote speaker.

In an effort further improve future Subspecialty Day meetings, we request that you assist us by com-pleting the evaluation form. We carefully review all comments to better understand your needs, so please indicate the strengths and shortcomings of todays program.

Again, we welcome you to The Future Is Now! #Glaucoma2013. We hope you find it educational and enjoyable.

Sincerely,

Thomas W Samuelson MD David S Friedman MD MPH PhD Program Director Program Director

2013 Subspecialty Day | Glaucoma iii

Glaucoma 2013 Contents

Program Directors Welcome Letter ii

CME iv

Faculty Listing vi

Program Schedule xiii

Section I: Diagnostic Tests in Glaucoma 1

Section II: Meds, Laser Trabeculoplasty, and Clinical Management Pearls 22

Section III: Challenging GlaucomasOld and New 32

The American Glaucoma Society (AGS) Subspecialty Day Lecture: Regional Rates of Field Loss in GlaucomaDifferential Effects of Trabeculectomy 43

Section IV: The Lens and Glaucoma ManagementCataract Surgery and Combined Procedures 44

Section V: Individualizing Glaucoma Surgery 58

Advocating for Patients 58

Section VI: The Lens and Glaucoma ManagementNarrow Angle, Angle Closure 63

Faculty Financial Disclosure 73

Presenter Index 78

Electronic version of syllabi available at www.aao.org / 2013syllabi

iv 2013 Subspecialty Day | Glaucoma

CME Credit

Academys CME Mission Statement

The purpose of the American Academy of Ophthalmologys Continuing Medical Education (CME) program is to pres-ent ophthalmologists with the highest quality lifelong learning opportunities that promote improvement and change in physi-cian practices, performance or competence, thus enabling such physicians to maintain or improve the competence and profes-sional performance needed to provide the best possible eye care for their patients.

2013 Glaucoma Subspecialty Day Meeting Learning Objectives

Upon completion of this activity, participants should be able to:

Describeinnovationsinthediagnosisandmanagementofglaucoma within their historical context

Comparenewideasregardingthepathophysiologyofglaucomatous vision loss

Evaluatethecurrentstatusofopticdiscandretinalnervefiber layer imaging and its role in diagnosing and manag-ing glaucoma

Demonstratefamiliaritywithcurrentissuesinmedicalandsurgical therapy for glaucoma

Identifyandmanageglaucomasurgicalcomplications

2013 Glaucoma Subspecialty Day Meeting Target Audience

This activity has been designed to meet the educational needs of general ophthalmologists, glaucoma specialists and other oph-thalmologic subspecialists, and allied health personnel who are involved in the management of glaucoma patients.

2013 Glaucoma Subspecialty Day CME Credit

The American Academy of Ophthalmology is accredited by the Accreditation Council for Continuing Medical Education to pro-vide continuing medical education for physicians.

The American Academy of Ophthalmology designates this live activity for a maximum of 7 AMA PRA Category 1 Cred-its. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Self-Assessment Credit

This activity meets theSelf-Assessment CME requirements defined by the American Board of Ophthalmology (ABO). Please be advised that the ABO is not an accrediting body for purposes of any CME program. ABO does not sponsor this or any outside activity, and ABO does not endorse any particular CME activ-ity. Complete information regarding the ABO Self-Assessment CME Maintenance of Certification requirements are available at: http://abop.org/maintain-certification/part-2-lifelong-learning -self-assessment/cme/.

NOTE: Credit designated as self-assessment isAMA PRA Category 1 Creditand is also pre-approved by the ABO for the Maintenance of Certification (MOC) Part II CME requirements.

Teaching at a Live Activity

Teaching instruction courses or delivering a scientific paper or poster is not anAMA PRA Category 1 Creditactivity and should not be included when calculating your totalAMA PRA Category 1 Credits. Presenters may claimAMA PRA Cat-egory 1 Creditsthrough the American Medical Association. Please contact the AMA to obtain an application form at www.ama-assn.org.

Scientific Integrity and Disclosure of Financial Interest

The American Academy of Ophthalmology is committed to ensuring that all continuing medical education (CME) informa-tion is based on the application of research findings and the implementation of evidence-based medicine. It seeks to promote balance, objectivity and absence of commercial bias in its con-tent. All persons in a position to control the content of this activ-ity must disclose any and all financial interests. The Academy has mechanisms in place to resolve all conflicts of interest prior to an educational activity being delivered to the learners.

Attendance Verification for CME Reporting

Before processing your requests for CME credit, the Academy must verify your attendance at Subspecialty Day and/or the 2013 Annual Meeting. In order to be verified for CME or auditing purposes, you must either:

Registerinadvance,receivematerialsinthemailandturnin the Final Program and/or Subspecialty Day Meeting Guide exchange voucher(s) onsite;

Registerinadvanceandpickupyourbadgeonsiteifmate-rials did not arrive before you traveled to the meeting;

Registeronsite;or Scanyourbarcodeatthemeeting.

CME Credit Reporting

Lobby B2 and Lobby G; Academy Resource Center, Hall G - Booth 3239Attendees whose attendance has been verified (see above) at the 2013 Annual Meeting can claim their CME credit online during the meeting. Registrants will receive an email during the meeting with the link and instructions on how to claim credit.

Onsite, you may report credits earned during Subspecialty Day and/or the Annual Meeting at the CME Credit Reporting booth.

Academy Members: The CME credit reporting receipt is not a CME transcript. CME transcripts that include 2013 Annual Meeting credits entered onsite will be available to Academy members on the Academys website beginning Dec. 10, 2013.

NOTE: CME credits must be reported by Jan. 5, 2014. After the 2013 Annual Meeting, credits can be claimed at www.aao.org.

2013 Subspecialty Day | Glaucoma CME Credit v

The Academy transcript cannot list individual course atten-dance. It will list only the overall credits spent in educational activities at Subspecialty Day and/or the Annual Meeting.

Nonmembers: The Academy will provide nonmembers with verification of credits earned and reported for a single Academy-sponsored CME activity, but it does not provide CME credit transcripts. To obtain a printed record of your credits, you must report your CME credits onsite at the CME Credit Reporting booths.

Proof of Attendance

The following types of attendance verification will be available during the 2013 Annual Meeting and Subspecialty Day for those who need it for reimbursement or hospital privileges, or for non-members who need it to report CME credit:

CMEcreditreporting/proof-of-attendanceletters OnsiteRegistrationForm InstructionCourseVerificationForm

Visit the Academys website for detailed CME reporting infor-mation.

vi 2013 Subspecialty Day | Glaucoma

Faculty

Iqbal K Ahmed MDMississauga, ON, CanadaAssistant ProfessorUniversity of TorontoClinical Assistant ProfessorUniversity of Utah

Wallace L M Alward MDIowa City, IA Professor of OphthalmologyUniversity of Iowa

No photo available

Husam Ansari MD PhDNeedham, MA Glaucoma ServiceOphthalmic Consultants of Boston

Tin Aung FRCS PhDSingapore, SingaporeSenior Consultant and Head of

GlaucomaSingapore National Eye CentreProfessor of OphthalmologyNational University of Singapore

Augusto Azuara-Blanco MDBelfast, United KingdomProfessor of Clinical OphthalmologyQueens University Belfast

John P Berdahl MDSioux Falls, SD Assistant Clinical ProfessorUniversity of South Dakota Vance Thompson Vision

Michael V Boland MD PhDBaltimore, MD Assistant Professor and Director of

Information TechnologyWilmer Eye InstituteJohns Hopkins UniversityAssistant ProfessorDivision of Health Sciences InformaticsJohns Hopkins University

James D Brandt MDSacramento, CA Professor of Ophthalmology and

Director, Glaucoma ServiceUniversity of California, Davis

Reay H Brown MDAtlanta, GA Founder, Atlanta Ophthalmology

Associates

2013 Subspecialty Day | Glaucoma Faculty Listing vii

Donald L Budenz MD MPHChapel Hill, NC Kittner Family Distinguished Professor

and Chair of OphthalmologyUniversity of North Carolina at Chapel

Hill

Joseph Caprioli MD FACSLos Angeles, CA Professor of OphthalmologyDavid Geffen School of MedicineUniversity of California, Los AngelesChief, Glaucoma DivisionJules Stein Eye Institute

Wiley Andrew Chambers MDMc Lean, VA Clinical Professor of OphthalmologyThe George Washington University

Teresa C Chen MDBoston, MA Associate Professor of OphthalmologyHarvard Medical SchoolGlaucoma ServiceMassachusetts Eye and Ear Infirmary

Anne Louise Coleman MD PhDLos Angeles, CA Professor of OphthalmologyDavid Geffen School of MedicineUniversity of California, Los AngelesProfessor of EpidemiologyKarin and Jonathan Fielding School of

Public HealthUniversity of California, Los Angeles

Garry P Condon MDPittsburgh, PA Associate Professor of OphthalmologyDrexel University College of MedicineClinical Assistant Professor of

OphthalmologyUniversity of Pittsburgh

E Randy Craven MDBaltimore, MD Chief of GlaucomaKing Khaled Eye Specialist Hospital,

Saudi ArabiaAssociate ProfessorWilmer Eye InstituteJohns Hopkins University

Karim F Damji MDEdmonton, AB, CanadaProfessor of OphthalmologyUniversity of AlbertaResidency Program DirectorUniversity of Alberta

Robert D Fechtner MD FACSNewark, NJ Professor of OphthalmologyNew Jersey Medical SchoolUniversity of Medicine and Dentistry,

New Jersey

viii Faculty Listing 2013 Subspecialty Day | Glaucoma

Robert M Feldman MDHouston, TX Professor of OphthalmologyChairman, Department of

Ophthalmology and Visual ScienceThe University of Texas Health Science

Center at Houston

Ronald Leigh Fellman MD OCSDallas, TX Clinical Associate Professor EmeritusUniversity of Texas Southwestern

Medical Center, DallasPresident, Glaucoma Associates of

Texas, Dallas

Brian A Francis MDLos Angeles, CA Associate Professor of OphthalmologyDoheny Eye InstituteUniversity of Southern California

David S Friedman MD MPH PhDBaltimore, MD Alfred Sommer Professor of

OphthalmologyDana Center for Preventive

OphthalmologyWilmer Eye InstituteJohns Hopkins UniversityProfessor of Epidemiology and

International HealthJohns Hopkins Bloomberg School of

Public Health

Steven J Gedde MDMiami, FL Professor of OphthalmologyBascom Palmer Eye Institute

Christopher A Girkin MDBirmingham, AL Chairman and ProfessorDepartment of OphthalmologyUniversity of Alabama at Birmingham

School of MedicineChief Medical OfficerCallahan Eye Hospital

Thomas A Graul MDLincoln, NE Adjunct Associate Professor of

OphthalmologyUniversity of Nebraska Medical Center

David S Greenfield MDPalm Beach Gardens, FL Professor of OphthalmologyBascom Palmer Eye InstituteUniversity of Miami Miller School of

Medicine

Davinder S Grover MDDallas, TX Associate PhysicianGlaucoma Associates of Texas

2013 Subspecialty Day | Glaucoma Faculty Listing ix

Paul J Harasymowycz MDWestmount, QC, CanadaChief Glaucoma ServiceUniversity of MontrealMedical DirectorMontreal Glaucoma Institute

Mingguang He MD PhDGuangzhou, ChinaProfessor and Associate DirectorZhongshan Ophthalmic Center

Leon W Herndon MDDurham, NC Associate Professor of OphthalmologyDuke University Eye Center

Dale K Heuer MDMilwaukee, WI Professor and Chairman of

OphthalmologyMedical College of WisconsinDirector, Froedtert & the Medical

College of Wisconsin Eye Institute

Henry D Jampel MD MHSBaltimore, MD Professor of OphthalmologyJohns Hopkins University School of

Medicine

No photo available

Leslie S Jones MDWashington, DC Associate Professor of OphthalmologyHoward University

Malik Y Kahook MDDenver, CO Professor of OphthalmologyUniversity of Colorado School of

Medicine

L Jay Katz MDPhiladelphia, PA Professor of OphthalmologyJefferson Medical CollegeDirector of Glaucoma ServiceWills Eye Hospital

Richard A Lewis MDSacramento, CA Past PresidentAmerican Glaucoma SocietyConsultant in GlaucomaSurgical Eye Specialists

x Faculty Listing 2013 Subspecialty Day | Glaucoma

Jeffrey M Liebmann MDNew York, NY Clinical Professor of OphthalmologyNew York University School of

MedicineDirector, Glaucoma ServiceManhattan Eye, Ear and Throat

Hospital

Shan C Lin MDSan Francisco, CA Professor of Clinical OphthalmologyUniversity of California, San FranciscoDirector, Glaucoma ServiceSan Francisco General Hospital

Felipe A Medeiros MDSan Diego, CA Professor of OphthalmologyUniversity of California, San Diego

Sayoko E Moroi MD PhDAnn Arbor, MI Professor of OphthalmologyUniversity of Michigan

No photo available

Sameh Mosaed MDLaguna Hills, CA Assistant Professor of OphthalmologyUniversity of California, Irvine

Jonathan S Myers MDPhiladelphia, PA Associate Attending SurgeonWills Eye InstituteAssistant Professor of OphthalmologyJefferson Medical College

Peter Andreas Netland MD PhDCharlottesville, VA Professor and ChairUniversity of Virginia School of

Medicine

Robert J Noecker MDFairfield, CT Director of GlaucomaOphthalmic Consultants of Connecticut

No photo available

Winifred P Nolan MDLondon, United KingdomConsultant OphthalmologistMoorfields Eye Hospital, London

2013 Subspecialty Day | Glaucoma Faculty Listing xi

Kouros Nouri-Mahdavi MDLos Angeles, CA Assistant Professor of OphthalmologyJules Stein Eye InstituteUniversity of California, Los Angeles

Ki Ho Park MD PhDSeoul, KoreaProfessor of OphthalmologySeoul National University College of

MedicineProfessor of OphthalmologySeoul National University Hospital

Richard K Parrish II MDMiami, FL Professor, University of Miami Miller

School of MedicineAssociate Dean for Graduate Medical

EducationUniversity of Miami Miller School of

Medicine

Thomas D Patrianakos DOChicago, IL Chair, Division of OphthalmologyCook County Health and Hospital

Systems

Nathan M Radcliffe MDNew York, NY

Pradeep Y Ramulu MD PhDClarksville, MD Assistant Professor of OphthalmologyJohns Hopkins University

Douglas J Rhee MDBoston, MA Associate Professor of OphthalmologyMassachusetts Eye & Ear InfirmaryHarvard Medical School

Lisa Fran Rosenberg MDChicago, IL Clinical Associate Professor of

OphthalmologyFeinberg School of MedicineNorthwestern University

Thomas W Samuelson MDMinneapolis, MN Adjunct Associate Professor of

OphthalmologyUniversity of MinnesotaAttending SurgeonMinnesota Eye Consultants, P.A.

xii Faculty Listing 2013 Subspecialty Day | Glaucoma

Joel S Schuman MDPittsburgh, PA Eye and Ear Foundation Professor and

Chairman of OphthalmologyUniversity of Pittsburgh School of

MedicineDirector, UPMC Eye Center

Kuldev Singh MD MPHPalo Alto, CA Professor of OphthalmologyStanford UniversityDirector, Glaucoma ServiceStanford University

Gregory L Skuta MDOklahoma City, OK President and Chief Executive OfficerEdward L Gaylord Professor and ChairDean McGee Eye InstituteUniversity of Oklahoma College of

Medicine

George L Spaeth MD FACSPhiladelphia, PA Esposito Research Professor of

OphthalmologyWills Eye InstituteJefferson Medical College

Angelo P Tanna MDChicago, IL Director, Glaucoma ServiceVice Chair and Associate Professor of

OphthalmologyNorthwestern University Feinberg School

of Medicine

Angela V Turalba MDBoston, MA Instructor in OphthalmologyHarvard Medical School

Steven D Vold MDFayetteville, AR Cataract and Glaucoma Surgery

ConsultantVold Vision, PLLC

Janey Lee Wiggs MD PhDBoston, MA Associate Professor of OphthalmologyHarvard Medical SchoolAssociate Professor of OphthalmologyMassachusetts Eye and Ear Infirmary

Martha M Wright MDMinneapolis, MN Professor of OphthalmologyUniversity of Minnesota

2013 Subspecialty Day | Glaucoma xiii

The Future Is Now! #Glaucoma2013 In conjunction with the American Glaucoma Society

SATURDAY, NOV. 16, 2013

7:00 AM CONTINENTAL BREAKFAST

8:00 AM Welcome and Introductions Thomas W Samuelson MD*

8:02 AM American Glaucoma Society Introduction Kuldev Singh MD MPH*

8:04 AM Announcements and Pre-test David S Friedman MD MPH PhD*

Section I: Diagnostic Tests in Glaucoma

Moderator: Felipe A Medeiros MD*

8:06 AM Case I: The Case of a Glaucoma SuspectTesting and Risk Factor Estimation and Integration Felipe A Medeiros MD* 1

8:08 AM Genetic Testing in Glaucoma: Is It Ready for Prime Time? Janey Lee Wiggs MD PhD* 2

8:15 AM Integrating Risk Factors Into Clinical Decision Making Robert D Fechtner MD FACS* 5

8:22 AM Case II: Glaucoma ProgressionShould We Make Decisions Based on Imaging Alone? Felipe A Medeiros MD* 1

8:24 AM Detecting Structural Progression With Imaging: Where Do We Stand? David S Greenfield MD* 7

8:31 AM New Horizons in Optic Nerve Head Imaging in Glaucoma Joel S Schuman MD* 11

8:38 AM Case III: The Case of a Highly Myopic Patient Felipe A Medeiros MD* 1

8:40 AM Monitoring Highly Myopic Patients Ki Ho Park MD PhD* 12

8:47 AM Corneal Biomechanics: Does It Provide Any Additional Information for Management? Nathan M Radcliffe MD* 15

8:54 AM Case IV: The Case of a Patient With Advanced Glaucoma Progressing With Low IOPs Felipe A Medeiros MD* 1

8:56 AM How to Monitor Visual Field Progression in Advanced Glaucoma Kouros Nouri-Mahdavi MD* 17

9:03 AM What Not to Miss Jeffrey M Liebmann MD* 21

Section II: Meds, Laser Trabeculoplasty, and Clinical Management Pearls

Moderator: Henry D Jampel MD MHS*

9:10 AM Point: The Case for Generic Drugs Wiley Andrew Chambers MD 22

9:16 AM Counterpoint: The Case for Branded Medications Malik Y Kahook MD* 24

9:22 AM Rebuttal Wiley Andrew Chambers MD

9:24 AM Rebuttal Malik Y Kahook MD*

9:26 AM Patient on Prostaglandin: Whats Next? Topical Carbonic Anhydrase Inhibitor Angelo P Tanna MD* 25

9:30 AM Patient on Prostaglandin: Whats Next? Topical Alpha-2 Agonist Lisa Fran Rosenberg MD 26

9:34 AM Patient on Prostaglandin: Whats Next? Beta-Blocker Leslie S Jones MD* 27

9:38 AM Patient on Prostaglandin: Whats Next? Combination Meds Thomas D Patrianakos DO 29

*Indicates that the presenter has financial interest.No asterisk indicates that the presenter has no financial interest.

xiv Program Schedule 2013 Subspecialty Day | Glaucoma

* Indicates that the presenter has financial interest.No asterisk indicates that the presenter has no financial interest.

9:42 AM Laser Trabeculoplasty: Whats Next? Is It First Line? Is It Additive to Prostaglandin? Karim F Damji MD 30

9:46 AM Whats Next Panel Discussion

9:52 AM AGS Foundation: Unmet Needs in Glaucoma George L Spaeth MD FACS* 31

10:00 AM REFRESHMENT BREAK and ANNUAL MEETING EXHIBITS

Section III: Challenging GlaucomasOld and New

Moderators: Teresa C Chen MD, Pradeep Y Ramulu MD PhD* Panelists: Donald L Budenz MD MPH*, Anne Louise Coleman MD PhD*, Dale K Heuer MD*, Sayoko E Moroi MD PhD*, Gregory L Skuta MD*

10:45 AM Case Presentation of Malignant Glaucoma Teresa C Chen MD 32

10:48 AM Malignant Glaucoma Jonathan S Myers MD* 33

10:53 AM Panel Discussion and Summary

10:56 AM Case Presentation of Pregnancy and Glaucoma Pradeep Y Ramulu MD PhD* 36

10:58 AM Pregnancy and Glaucoma Martha M Wright MD 37


11:07 AM Case Presentation of Trauma and Glaucoma Teresa C Chen MD 32

11:09 AM Trauma and Glaucoma Christopher A Girkin MD* 39


11:18 AM Case Presentation of LASIK and Glaucoma Pradeep Y Ramulu MD PhD* 36

11:20 AM LASIK and Glaucoma John P Berdahl MD* 40


11:29 AM Case Presentation of Retisert and Glaucoma Teresa C Chen MD 32

11:31 AM Retisert and Glaucoma Husam Ansari MD PhD* 41


11:39 AM Case Presentation of Keratoprosthesis-Related Glaucoma Pradeep Y Ramulu MD PhD* 36

11:41 AM Keratoprosthesis-Related Glaucoma Angela V Turalba MD 42


The American Glaucoma Society Subspecialty Day Lecture

Moderator: Kuldev Singh MD MPH*

11:49 AM Introduction of the Lecturer Kuldev Singh MD MPH*

11:51 AM Regional Rates of Field Loss in Glaucoma: Differential Effects of Trabeculectomy Joseph Caprioli MD FACS* 43

12:21 PM Presentation of the Award Kuldev Singh MD MPH*

12:23 PM LUNCH and ANNUAL MEETING EXHIBITS

Section IV: The Lens and Glaucoma ManagementCataract Surgery and Combined Procedures

Moderator: Reay H Brown MD* Panelists: Robert M Feldman MD*, Davinder S Grover MD*, Leon W Herndon MD*, Richard A Lewis MD*, Steven D Vold MD*

1:40 PM Why Does Cataract Surgery Lower IOP in Some Patients? Douglas J Rhee MD* 44

2013 Subspecialty Day | Glaucoma Program Schedule xv

* Indicates that the presenter has financial interest.No asterisk indicates that the presenter has no financial interest.

1:48 PM Does a Glaucoma Diagnosis Change the Indication for Cataract Surgery? James D Brandt MD* 45

1:56 PM Combined Phacoemulsification and Angle Surgery: Why I Prefer Canal StentTop 3 Surgical Pearls Iqbal K Ahmed MD* 48

2:01 PM Combined Phaco and Angle Surgery: Why I Prefer Ab Interno TrabeculotomyTop 3 Surgical Pearls Sameh Mosaed MD 49

2:06 PM Combined Phacoemulsification and Angle Surgery: Common Intraoperative and Postoperative Complications Paul J Harasymowycz MD* 51

2:14 PM Combined Phacoemulsification and Filtration Surgery: Does It Still Have Ronald Leigh Fellman MD a Role? Top 3 Surgical Pearls OCS* 52

2:22 PM Combined Phacoemulsification and Endoscopic Cyclophotocoagulation: A Good IdeaTop 3 Surgical Pearls Robert J Noecker MD* 54

2:26 PM Combined Phacoemulsification and Endoscopic Cyclophotocoagulation: Other Options Are Better Steven J Gedde MD* 56

2:30 PM Panel and Audience Response

Section V: Individualizing Glaucoma Surgery

Moderator: Brian A Francis MD* Panelists: Garry P Condon MD, E Randy Craven MD*, L Jay Katz MD*, Peter Andreas Netland MD PhD*, Richard K Parrish II MD*

2:40 PM Advocating for Patients Thomas A Graul MD 58

2:45 PM Matching Surgical Risk to Disease Risk E Randy Craven MD* 60

2:53 PM Case Presentations: Surgical Management of Glaucoma, Phakic Eye Early to Advanced Disease Brian A Francis MD* 62

2:56 PM Panel Discussion of Cases: Which Procedure? Why?

3:08 PM Case Presentations: Surgical Management of Glaucoma, Pseudophakic Eye Early to Advanced Disease Brian A Francis MD* 62

3:11 PM Panel Discussion of Cases: Which Procedure? Why?

3:23 PM REFRESHMENT BREAK and ANNUAL MEETING EXHIBITS

Section VI: The Lens and Glaucoma ManagementNarrow Angle, Angle Closure

Moderator: Augusto Azuara-Blanco MD

4:00 PM The Magnitude of Angle Closure and Failures of Management Wallace L M Alward MD 63

4:08 PM What Is the Evidence That Iridotomy Is Effective at Preventing Angle Closure and Should It Be Done Routinely? If Not, When Is It Mandated? Mingguang He MD PhD 65

4:16 PM Does the Lens Cause Angle Closure? Recent Studies Showing the Benefit From Lens Extraction Tin Aung FRCS PhD* 66

4:24 PM Case I: Acute Angle-Closure Attack, Initial Management Choices Should Cataract Be Done? If So, When? Winifred P Nolan MD 68

4:32 PM Case II: Small Eye, Healthy Young Person, Recurrent Acute IOP Spike Despite Patent Laser Peripheral Iridotomy Michael V Boland MD PhD 69

4:40 PM Case III: Primary Angle-Closure Glaucoma, IOP in 20s, Also Has CataractWhat Should You Do? Shan C Lin MD* 71

4:48 PM Panel Discussion and Summary

4:56 PM Closing Remarks and Post-test Thomas W Samuelson MD*

5:00 PM ADJOURN

2013 Subspecialty Day | Glaucoma Section I: Diagnostic Tests in Glaucoma 1

Case Presentations: Diagnostic Tests in GlaucomaFelipe A Medeiros MD

Case I: The Case of a Glaucoma SuspectTesting and Risk Factor Estimation and Integration

Case II: Glaucoma ProgressionShould We Make Decisions Based on Imaging Alone?

Case III: The Case of a Highly Myopic Patient

Case IV: The Case of a Patient With Advanced Glaucoma Progressing With Low IOPs

2 Section I: Diagnostic Tests in Glaucoma 2013 Subspecialty Day | Glaucoma

Genetic Testing in Glaucoma: Is It Ready for Prime Time? Janey L Wiggs MD PhD

I. Potential Benefits of Gene-Based Testing for Glaucoma

A. Screening: Identify individuals at risk for glaucoma before irreversible damage occurs

B. Diagnosis

1. Establish a molecular diagnosis (ie, a specific mutation in a specific gene)

2. A molecular diagnosis is required for gene-based therapies.

C. Prognosis: Specific gene mutations may be associ-ated with defined phenotypes and outcomes.

II. Current Genetic Testing for Glaucoma

A. Testing for mutations in genes causing early-onset and familial types of glaucoma

1. Disease-causing mutations are known for con-genital glaucoma, anterior segment dysgenesis, juvenile glaucoma and familial forms of normal tension glaucoma (see Table 1).

2. Genetic testing can provide valuable diagnostic and in some cases prognostic information.

3. High specificity but low sensitivity: Mutation testing using the current set of disease-causing genes will identify mutations in approximately 20% of patients.

B. Testing for risk variants in genes associated with common forms of glaucoma with complex inheri-tance

1. Disease-associated risk variants: Risk variants can increase or decrease disease susceptibility.

2. Genetic variants are associated with primary open-angle glaucoma, normal-tension glaucoma,

exfoliation glaucoma, and angle-closure glau-coma (see Table 2).

3. Low specificity, moderate to high sensitivity; risk variant panels may improve specificity.

C. Current recommendations for genetic testing in glaucoma (see Table 3)

1. Patients and/or family members with early-onset disease

a. Congenital glaucoma (CYP1B1, LTBP2)

b. Anterior segment dysgenesis syndromes (PITX2, FOXC1, PAX6)

2. Primary open-angle glaucoma

a. Diagnosis before age 35 (MYOC)

b. Diagnosis after age 35 but with multiple fam-ily members affected (MYOC)

3. Familial normal-tension glaucoma

a. Diagnosis before age 35 (OPTN, TBK1, OPA1)

b. More than 1 family member affected (OPTN, TBK1, OPA1)

D. Genetic testing procedures

1. Obtain DNA sample from patient and/or family members; blood or saliva

2. Whole exon capture test for all disease-causing genes

3. Confirm mutations using traditional sequencing methods.

Table 1. Genes Causing Early-Onset or Familial Glaucoma

Gene Protein Disease References

CYP1B1 Cytochrome p450 Congenital glaucoma Stoilov, 1997

LTBP2 Latent transforming growth factor beta binding protein 2

Congenital glaucoma Ali, 2009

PITX2 Paired-like homeodomain 2 Axenfeld-Riegers Semina, 1996

FOXC1 Forkhead box C1 Anterior segment dysgenesis Nishimura, 1998

PAX6 Paired box 6 Aniridia Jordan, 1992

MYOC Myocilin Primary open-angle glaucoma (juvenile and familial)

Stone, 1997

OPTN Optineurin Familial normal-tension glaucoma Rezaie, 2002

TBK1 TANK-binding kinase 1 Familial normal-tension glaucoma Fingert, 2011


4. Testing carried out in Clinical Laboratory Improvement Amendments (CLIA)-certified laboratory

5. CLIA lab sends a genetic testing report to the referring physician. Genetic counseling is recom-mended.

III. Genetic Testing for Glaucoma in the Future

A. Discovery of additional glaucoma genes will improve genetic testing.

1. More disease-causing genes will improve the sen-sitivity of testing for early-onset glaucoma.

2. More disease-associated genes, and the develop-ment of variant risk panels, will improve the specificity of testing for common complex types of glaucoma.

B. Challenges

1. Correlate gene defects with specific phenotypes and clinical outcomes, making clinically useful diagnostic and prognostic information available

2. Define risk profiles with appropriate specificity and sensitivity

3. Develop gene-based therapies

IV. Is genetic testing ready for prime time?

A. Early-onset and familial glaucoma: Yes.

For the 20% of affected individuals expected to have identifiable mutations (ie, positive tests) the test results are clinically useful.

B. Common age-related glaucoma: Not yet.

Testing results could help establish disease risk esti-mates; however, the clinical utility is limited by the low specificity.

References

1. Ali M, McKibbin M, Booth A, et al. Null mutations in LTBP2 cause primary congenital glaucoma. Am J Hum Genet. 2009; 84(5):664-671.

2. Burdon KP, Macgregor S, Hewitt AW, et al. Genome-wide associa-tion study identifies susceptibility loci for open angle glaucoma at TMCO1 and CDKN2B-AS1. Nat Genet. 2011; 43(6):574-578.

3. Fan BJ, Wiggs JL. Glaucoma: genes, phenotypes, and new direc-tions for therapy. J Clin Invest. 2010; 120(9):3064-3072.

Table 2. Genes Associated With Common Forms of Glaucoma With Complex Inheritance

Gene Protein Disease References

CDKN2BAS None (antisense regulatory RNA) Primary open-angle glaucoma, normal-tension glaucoma

Burdon, 2011; Wiggs, 2012

TMCO1 Transmembrane and coiled-coil domains 1

Primary open-angle glaucoma Burdon, 2011

SIX1/SIX6 SIX homeobox 1 and 6 Primary open-angle glaucoma Wiggs, 2012

CAV1/CAV2 Caveolins 1 and 2 Primary open-angle glaucoma Thorleifsson, 2010

LOXL1 Lysyl oxidase-like 1 Exfoliation syndrome Thorleifsson, 2007

PLEKHA7 Pleckstrin homology domain containing, family A member 7

Angle closure Vithana, 2012

COL11A1 Collagen, type XI, alpha 1 Angle closure Vithana, 2012

Table 3. Recommendations for Glaucoma Gene Testing

Disease Additional Features Gene Tests Comments

Congenital glaucoma None CYP1B1, LTBP2 Include testing for deletions/insertions

Anterior segment dysgenesis (including Axenfeld-Rieger)

None FOXC1, PITX2, PAX6 Include testing for deletions/insertions

Primary open-angle glaucoma Disease onset before age 35 MYOC

Primary open-angle glaucoma Onset after age 35 but more than 1 affected family member

MYOC

Normal-tension glaucoma Onset before age 35 OPTN, TBK1, OPA1 OPA1 causes primary optic atrophy, which can phenotypically overlap with normal-tension glaucoma

Normal-tension glaucoma More than 1 family member affected

OPTN, TBK1, OPA1


4. Fingert JH, Robin AL, Stone JL, et al. Copy number variations on chromosome 12q14 in patients with normal tension glaucoma. Hum Mol Genet. 2011; 20(12):2482-2494.

5. Fingert JH. Primary open-angle glaucoma genes. Eye (Lond). 2011; 25(5):587-595.

6. Jordan T, Hanson I, Zaletayev D, et al. The human PAX6 gene is mutated in two patients with aniridia. Nat Genet. 1992; 1(5):328-332.

7. Nishimura DY, Swiderski RE, Alward WL, et al. The forkhead transcription factor gene FKHL7 is responsible for glaucoma phe-notypes which map to 6p25. Nat Genet. 1998; 19(2):140-147.

8. Rezaie T, Child A, Hitchings R, et al. Adult-onset primary open-angle glaucoma caused by mutations in optineurin. Science 2002; 295(5557):1077-1079.

9. Semina EV, Reiter R, Leysens NJ, et al. Cloning and characteriza-tion of a novel bicoid-related homeobox transcription factor gene, RIEG, involved in Rieger syndrome. Nat Genet. 1996; 14(4):392-399.

10. Stoilov I, Akarsu AN, Sarfarazi M. Identification of three different truncating mutations in cytochrome P4501B1 (CYP1B1) as the principal cause of primary congenital glaucoma (Buphthalmos) in families linked to the GLC3A locus on chromosome 2p21. Hum Mol Genet. 1997; 6(4):641-647.

11. Stone EM, Fingert JH, Alward WL, et al. Identification of a gene that causes primary open angle glaucoma. Science 1997; 275(5300):668-670.

12. Thorleifsson G, Magnusson KP, Sulem P, et al. Common sequence variants in the LOXL1 gene confer susceptibility to exfoliation glaucoma. Science 2007; 317(5843):1397-1400.

13. Thorleifsson G, Walters GB, Hewitt AW, et al. Common variants near CAV1 and CAV2 are associated with primary open-angle glaucoma. Nat Genet. 2010; 42(10):906-909.

14. Vithana EN, Khor CC, Qiao C, et al. Genome-wide association analyses identify three new susceptibility loci for primary angle clo-sure glaucoma. Nat Genet. 2012; 44(10):1142-1146.

15. Wiggs JL, Pierce EA. Genetic testing: who benefits? JAMA Oph-thalmology. Epub ahead of print 2013 Aug 15.

16. Wiggs JL, Yaspan BL, Hauser MA, et al. Common variants at 9p21 and 8q22 are associated with increased susceptibility to optic nerve degeneration in glaucoma. PLoS Genet. 2012; 8(4):e1002654.

17. Wiggs JL. The cell and molecular biology of complex forms of glaucoma: updates on genetic, environmental, and epigenetic risk factors. Invest Ophthalmol Vis Sci. 2012; 53(5):2467-2469.


Integrating Risk Factors Into Clinical Decision MakingRobert D Fechtner MD

Risk Assessment for Glaucoma

Risk assessment is a relatively new concept for glaucoma care, but cardiology has been modeling risk for 50 years. One differ-ence between the 2 fields is that cardiovascular risk predicts an event (such as heart attack or death), while in glaucoma the end-point of progression is less clear-cut or dramatic. Nevertheless, studies have allowed the development of risk calculators to aid in our treatment recommendations. With this emerging evidence in glaucoma, we are beginning to be able to calculate the likelihood of progressive visual loss from glaucoma. Risk factors have long been discussed and now have been quantified in study popula-tions. Validated risk calculators have been published and tools are available online. By understanding and applying the concepts of risk assessment, we can better identify those patients at greater risk who may benefit most from earlier or more aggressive inter-vention. These tools can also help educate patients about the treatment recommendation for an asymptomatic chronic disease.

Major clinical trials have identified risk factors for progression.

Patients at risk progress to develop manifest glaucoma. Those with glaucoma often have progressive and measurable damage. Prospective clinical trials have quantified some of these risk fac-tors. Examples include:

Ocular Hypertension Treatment Study and European Glaucoma Prevention StudyRisk factors for progressing from ocular hypertension to con-firmed glaucoma

Early Manifest Glaucoma Study Risk factors at baseline and at follow-up for progression in newly diagnosed glaucoma patients

Collaborative Normal Tension Glaucoma Trial Risk factors for progression in normal-tension glaucoma

Using Risk Factors to Assess Risk for Progression

Risk factors help us identify which individuals are at greatest risk of progressive glaucomatous damage:

Importantforthequestionable,earlycases Usefulfordifficulttodiagnosecasessuchasatypicaloptic

nerves or unreliable visual fields Mayhelpindeterminationofintensityoftreatmentortar-

get IOP

I. Race (Baltimore Eye Survey, Barbados Eye Study)

A. Blacks at greater risk

1. Onset earlier

2. More severe at time of diagnosis

B. Up to 10% of blacks 70 years old have glaucoma.

II. Family History (maternal side)

III. Intraocular Pressure higher the IOP, greater the risk

IV. Refractive Error myopia (Blue Mountains Eye Study)

V. Systemic Health Suggested as Risk vascular conditions such as diabetes, hypertension

VI. Corneal Thickness

A. Independent risk factor for OHT after taking into account impact upon IOP (OHTS)

B. Independent risk factor in glaucoma with higher baseline IOP (EMGT)

For glaucoma suspect or ocular hypertensive, consider treatment if enough risk factors are present.

For patients with glaucoma, consider increasing inten-sity of surveillance and/or treatment if greater risk of progression

Risk calculators can help inform treatment recommendations and educate patients.

Examples of available risk calculators:

http://ohts.wustl.edu/risk/calculator.html http://www.glaucoma.net/calculator/ https://www.deverseye.org/grc/

Selected Readings

1. Boland MV, Quigley HA, Lehmann HP. The impact of risk calcula-tion on treatment recommendations made by glaucoma specialists in cases of ocular hypertension. J Glaucoma. 2008; 17:631-638.

2. Drance S, Anderson DR, Schulzer M; Collaborative Normal-Ten-sion Glaucoma Study Group. Risk factors for progression of visual field abnormalities in normal-tension glaucoma. Am J Ophthalmol. 2001; 131:699-708.

3. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002; 120:714-720.

4. Leske MC, Heijl A, Hyman L, et al. Predictors of long-term pro-gression in the early manifest glaucoma trial. Ophthalmology 2007; 114:1965-1972.

5. Medeiros FA, Weinreb RN, Sample PA, et al. Validation of a pre-dictive model to estimate the risk of conversion from ocular hyper-tension to glaucoma. Arch Ophthalmol. 2005; 123:1351-1360.

6. Miglior S, Torri V, Zeyen T, et al. Intercurrent factors associated with the development of open-angle glaucoma in the European glaucoma prevention study. Am J Ophthalmol. 2007; 144:266-275.

7. Mitchell P, Lee AJ, Rochtchina E, Wang JJ. Open-angle glaucoma and systemic hypertension: the Blue Mountains Eye study. J Glau-coma. 2004; 13(4):319-326.

8. Ocular Hypertension Treatment Study Group, European Glaucoma Prevention Study Group, Gordon MO, et al. Validated prediction


model for the development of primary open-angle glaucoma in indi-viduals with ocular hypertension. Ophthalmology 2007; 114:10-19.

9. Weinreb RN, Friedman DS, Fechtner RD, et al. Risk assessment in the management of patients with ocular hypertension. Am J Oph-thalmol. 2004; 138:458-467.


Detecting Structural Progression With Imaging: Where Do We Stand?David S Greenfield MD

I. Overview

A. Almost two decades have elapsed since the introduc-tion of computerized imaging technology for assess-ment of the optic nerve and peripapillary retinal nerve fiber layer (RNFL).

B. Imaging technologies such as confocal scanning laser ophthalmoscopy (Heidelberg Retina Tomo-graph [HRT], Heidelberg Engineering; Germany), scanning laser polarimetry (GDxPRO, Carl Zeiss Meditec; Dublin, CA), and optical coherence tomography (OCT) provide objective and quantita-tive measurements that are highly reproducible and show very good agreement with clinical estimates of optic nerve head structure and visual function.1,2

C. Glaucoma is a slowly progressing optic neuropathy characterized by the loss of retinal ganglion cells (RGCs) and their axons. Therefore, the detection of glaucomatous progression is a critical aspect of glaucoma management.

D. This review will provide an update on the use of imaging for detection of progressive glaucomatous optic neuropathy.

II. Basic Assumptions

A. Short and long-term variability / multifactorial mechanisms (instrument, operator, ocular)

B. Statistically significant change

1. Biological change is assumed to have occurred when the magnitude of change statistically exceeds the test-retest variability.

2. Confirmation with repeated testing is required for robust identification of endpoints.

C. Clinically significant change

1. Statistically significant change that is directly or indirectly associated with visual function or qual-ity of life

2. Influenced by life expectancy, disease stage, velocity of change, location of defect, and threat to central acuity

III. Does Imaging Enhance Detection of Progression?

A. Detecting optic disc progression in clinical prac-tice using stereoscopic photography is adversely impacted by disease stage and is challenging in eyes with moderate to advanced glaucoma. In longitudi-nal clinical trials, 40%-61% of endpoints in ocular hypertensive eyes were optic disc endpoints3,4 com-pared with 1%-11% in glaucomatous eyes.5,6

B. Studies with HRT, GDx, and Stratus OCT have shown that on average the decrease in rim area

or RNFL thickness occurs at a faster rate in eyes progressing over time compared to nonprogressing eyes, with the assessment of progression based on stereophotography or visual fields.7,12

C. Recently, the Confocal Scanning Laser Ophthalmos-copy Ancillary Study to the Ocular Hypertension Treatment Study has demonstrated that the rate of rim area loss is approximately 5 times faster in ocular hypertensive (OHT) eyes in which primary open-angle glaucoma (POAG) developed compared with OHT eyes in which it did not.13

D. Spectral domain OCT (SD-OCT) offers higher scan-ning rates (up to 50,000 axial scans per second) and improved resolution (axial resolution 3 to 6 m, transverse resolution 20 m) compared with time domain OCT (TD-OCT). Analysis of serial RNFL thickness maps generated by the SD-OCT facilitates the detection of RNFL progression in glaucoma.14

E. The agreement of progression detection among RNFL, neuroretinal rim, and visual field measure-ments has been shown to be poor, and the rates of progression vary considerably within and between subjects. Given this variability, interpretation of RNFL, neuroretinal rim, and visual field index progression always should be evaluated on an indi-vidual basis.15

IV. Detecting Glaucomatous Structural Progression

A. Optic nerve head (ONH) Photography

Structural features indicative of glaucomatous optic disc progression include progressive increased exca-vation of the optic cup, focal or diffuse narrowing of the neuroretinal rim width, focal or diffuse RNFL atrophy, increase in beta-zone parapapillary atro-phy, and optic disc hemorrhage.16

B. Confocal scanning laser ophthalmoscopy (CSLO)

1. Topographic change analysis (TCA) is a statisti-cally based progression algorithm that accurately detects structural change over time by comparing point-by-point variability between examinations and providing a statistical indicator of change. Agreement for detection of longitudinal changes between TCA, stereophotography, and SAP is poor.17,18

2. Measurement of progression rates using trend analysis of stereometric parameters19 is a use-ful method for detection of progression.20 The rate of neuroretinal rim area loss is considerably faster in glaucoma suspects and OHT patients who progress to POAG, particularly in the inferotemporal sector.13


C. Scanning laser polarimetry (SLP)

1. SLP is able to identify longitudinal RNFL loss in eyes with progressive glaucomatous dam-age.8,21 Strategies to enhance the signal-to-noise ratio, such as enhanced corneal compensation, have been shown to enhance progression detec-tion.22,23

2. Guided Progression Analysis (GPA) is a statisti-cally based progression algorithm that measures regional areas of RNFL loss and rates of RNFL atrophy as compared to either a reference popu-lation or individual variability.24

3. In experimental glaucoma, SLP-measured bire-fringence changes, consistent with axonal cyto-skeletal abnormalities, were found to precede thinning of peripapillary RNFL.25

D. Optical coherence tomography (OCT)

1. RNFL

a. Serial assessment of RNFL thickness using OCT can detect progressive structural dam-age in glaucoma.10,12,26,27

b. Using TD-OCT and SD-OCT,28 RNFL thick-ness parameters have been shown to perform better than macular and ONH parameters for detecting serial glaucomatous change over time.

c. Guided Progression Analysis (GPA) is a statis-tically based progression algorithm that mea-sures regional areas of RNFL loss and rates of RNFL atrophy as compared to baseline images.9,14

2. Macula

a. Longitudinal assessment of total macular thickness can detect progression of glaucoma-tous atrophy.10,29

b. Segmentation of macular layers can provide estimates of RGC thickness with high repro-ducibility30,31 and can detect progressive RGC loss,32 but may be less optimal than circum-papillary RNFL thickness.33

c. Although unproven, macular RGC thickness measurements may be beneficial for progres-sion detection in eyes with advanced glau-coma based upon sparing of the papillomacu-lar bundle until advanced stage glaucomatous damage.

3. ONH

a. Enhanced depth imaging OCT (EDI-OCT) facilitates imaging of deep ONH structures including the lamina cribrosa and has demon-strated focal laminar defects (laminar holes or disinsertions) that are associated with neuro-retinal rim loss and acquired ONH pits.34

b. Longitudinal SD-OCT imaging can detect deep ONH changes in experimental glaucoma

eyes, the earliest of which are present at the onset of CSLO-detected ONH surface height depression.35

c. Serial measurements of ONH rim area and vertical CDR can detect progressive glau-coma.32

d. New automated techniques to identify the optic disc margin using the Bruch membrane opening compared with clinical ONH land-marks may improve the detection of ONH progression.36

V. How Should Imaging Be Integrated in Clinical Practice?

A. Imaging is not a replacement for periodic stereo-scopic optic disc photography, which allows optic disc features to be permanently recorded for future reference.

B. Digital imaging is recommended to facilitate assess-ment of the optic nerve and RNFL as based upon a Consensus Initiative of the World Glaucoma Association,37 and a comprehensive review by the Ophthalmic Technology Assessment Committee Glaucoma Panel of the American Academy of Oph-thalmology.38

C. Serial imaging of the optic nerve and RNFL is rec-ommended as an adjunct to standard perimetry and periodic optic disc photography for assessment of glaucoma progression.

VI. Pitfalls With Imaging

A. Technology undergoes constant evolution.

1. The last decade has produced expansion of data-sets that enable one to differentiate normal from abnormal, provide improved precision, increased resolution and image registration, and constant software upgrades.

2. A sacrifice for such change has been the costs associated with replacing technologies that become outdated or are no longer backwards-compatible with previously collected data.

3. This has certainly negatively impacted longitudi-nal studies seeking to validate the use of imaging for detection of glaucoma progression.

B. Image quality is dependent upon operator skill, patient-related factors such as pupil diameter and media clarity, and instrument-dependent variables. Imaging artifacts exist, such as poorly compensated corneal birefringence using the GDx,1,39-42 or the low signal strength using the OCT.43,44

C. Imaging may produce false identification of glau-coma and its progression,23 or it may fail to detect a glaucomatous optic disc or RNFL. Clinicians should not make clinical decisions based solely on the results of one single test or technology.

VII. The Future

A. The paradigm has shifted from macroscopic to microscopic measurements.


1. Current technologies enable measurement of the optic nerve and RNFL. Higher-resolution SD-OCT devices (27,000 A-scans per second) have been developed with shorter acquisition times and 3-dimensional imaging of posterior segment structures that enable measurement of the RGC thickness.

2. Higher-speed OCT technology such as swept-source OCT (100,000 A-scans per second) may provide an opportunity for imaging deeper struc-tures including the choroid, sclera, and lamina cribrosa.

B. Technologies to measure RGC dysfunction and imaging of cellular and sub-cellular structures may soon follow.

C. Improvements in image registration, eye tracking algorithms, and refinement in software algorithms that differentiate test-retest variability from true bio-logical changes will enhance progression detection.

D. Novel endpoints to estimate the rate of RGC loss based upon a combined structure function index may provide more robust change detection com-pared to isolated structural or functional mea-sures.45,46

VIII. Conclusions

A. Structural and functional endpoints often do not coincide; both are necessary.

B. Imaging does not replace optic disc photography.

C. Imaging of the ONH, RNFL, and macula are useful adjunctive methods for change detection.

D. Trend analyses to quantify rates are important to judge velocity of progression.

References

1. Greenfield DS, Knighton RW, Feuer WJ, Schiffman JC, Zangwill L, Weinreb RN. Correction for corneal polarization axis improves the discriminating power of scanning laser polarimetry. Am J Ophthal-mol. 2002; 134:27-33.

2. Medeiros FA, Zangwill LM, Bowd C, Weinreb RN. Comparison of the GDx VCC scanning laser polarimeter, HRT II confocal scan-ning laser ophthalmoscope, and stratus OCT optical coherence tomograph for the detection of glaucoma. Arch Ophthalmol. 2004; 122:827-837.

3. Kass MA, Heuer DK, Higginbotham EJ, et al. The ocular hyperten-sion treatment study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of pri-mary open-angle glaucoma. Arch Ophthalmol. 2002; 120:701-713.

4. Miglior S, Zeven T, Pfeiffer N, et al. Results of the European Glau-coma Prevention Study. Ophthalmology 2005; 112:366-375.

5. Heijl A, Leske MC, Bengtsson B, Hyman L, Bengtsson B, Hussein M. Reduction of intraocular pressure and glaucoma progression: results from the Early Manifest Glaucoma Trial. Arch Ophthalmol. 2002; 120:1268-1279.

6. Collaborative Normal Tension Study Group. Comparison of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intra-ocular pressure. Am J Ophthalmol. 1998; 126:487-497.

7. Strouthidis NG, Scott A, Peter NM, Garway-Heath DF. Optic disc and visual field progression in ocular hypertensive subjects: detec-tion rates, specificity, and agreement. Invest Ophthalmol Vis Sci. 2006; 47:2904-2910.

8. Medeiros FA, Alencar LM, Zangwill LM, et al. Detection of pro-gressive retinal nerve fiber layer loss in glaucoma using scanning laser polarimetry with variable corneal compensation. Invest Oph-thalmol Vis Sci. 2009; 50:1675-1681.

9. Leung CK, Cheung CY, Weinreb RN, et al. Evaluation of retinal nerve fiber layer progression in glaucoma: a study on optical coher-ence tomography guided progression analysis. Invest Ophthalmol Vis Sci. 2010; 51:217-222.

10. Medeiros FA, Zangwill LM, Alencar LM, et al. Detection of glau-coma progression with stratus OCT retinal nerve fiber layer, optic nerve head, and macular thickness measurements. Invest Ophthal-mol Vis Sci. 2009; 50:5741-5748.

11. Grewal DS, Sehi M, Greenfield DS. Detecting glaucomatous pro-gression using GDx with variable and enhanced corneal compensa-tion using Guided Progression Analysis. Br J Ophthalmol. 2011; 95:502-508.

12. Grewal DS, Sehi M, Paauw JD, Greenfield DS. Detection of pro-gressive retinal nerve fiber layer thickness loss with optical coher-ence tomography using 4 criteria for functional progression. J Glau-coma. 2012; 21:214-220.

13. Zangwill LM, Jain S, Dirkes K, et al. The rate of structural change: the confocal scanning laser ophthalmoscopy ancillary study to the ocular hypertension treatment study. Am J Ophthalmol. 2013; 155:971-982.

14. Leung CK, Yu M, Weinreb RN, Lai G, Xu G, Lam DS. Retinal nerve fiber layer imaging with spectral-domain optical coherence tomography: patterns of retinal nerve fiber layer progression. Oph-thalmology 2012; 119:1858-1866.

15. Leung CK, Liu S, Weinreb RN, et al. Evaluation of retinal nerve fiber layer progression in glaucoma a prospective analysis with neu-roretinal rim and visual field progression. Ophthalmology 2011; 118:1551-1557.

16. Greenfield DS, Parrish RK. Detection of optic disc progression. Comp Ophthalmol Update. 2000; 1:87-96.

17. Vizzeri G, Bowd C, Weinreb RN, et al. Determinants of agreement between the confocal scanning laser tomograph and standardized assessment of glaucomatous progression. Ophthalmology 2010; 117:1953-1959.

18. Bowd C, Balasubramanian M, Weinreb RN, et al. Performance of confocal scanning laser tomograph topographic change analysis (TCA) for assessing glaucomatous progression. Invest Ophthalmol Vis Sci. 2009; 50:691-701.

19. Kamal DS, Garway-Heath DF, Hitchings RA, Fizke FW. Use of sequential Heidelberg retina tomograph images to identify changes at the optic disc in ocular hypertensive patients at risk of developing glaucoma. Br J Ophthalmol. 2000; 84:993-998.

20. Vizzeri G, Weinreb RN, Martinez de la Casa JM, et al. Clinicians agreement in establishing glaucomatous progression using the Hei-delberg retina tomograph. Ophthalmology 2009; 116:14-24.

21. Grewal DS, Sehi M, Greenfield DS. Comparing rates of retinal nerve fibre layer loss with GDxECC using different methods of visual-field progression. Br J Ophthalmol. 2011; 95:1122-1127.

22. Medeiros FA, Zangwill LM, Alencar LM, Sample PA, Weinreb RN. Rates of progressive retinal nerve fiber layer loss in glaucoma measured by scanning laser polarimetry. Am J Ophthalmol. 2010; 149:908-915.


23. Grewal DS, Sehi M, Cook RJ, Greenfield DS. The impact of retar-dance pattern variability on nerve fiber layer measurements over time using GDx with variable and enhanced corneal compensation. Invest Ophthalmol Vis Sci. 2011; 52:4516-4524.

24. Alencar LM, Zangwill LM, Weinreb RN, et al. Agreement for detecting glaucoma progression with the GDx guided progression analysis, automated perimetry, and optic disc photography. Oph-thalmology 2010; 117:462-470.

25. Fortune B, Burgoyne CF, Cull GA, Reynaud J, Wang L. Structural and functional abnormalities of retinal ganglion cells measured in vivo at the onset of optic nerve head surface change in experimental glaucoma. Invest Ophthalmol Vis Sci. 2012; 53:3939-3950.

26. Wollstein G, Schuman JS, Price LL, et al. Optical coherence tomog-raphy longitudinal evaluation of retinal nerve fiber layer thickness in glaucoma. Arch Ophthalmol. 2005; 123:464-470.

27. Sehi M, Zhang X, Greenfield DS, et al. Retinal nerve fiber layer atrophy is associated with visual field loss over time in glaucoma suspect and glaucomatous eyes. Am J Ophthalmol. 2013; 155:73-82 e1.

28. Na JH, Sung KR, Baek S, Sun JH, Lee Y. Macular and retinal nerve fiber layer thickness: which is more helpful in the diagnosis of glau-coma? Invest Ophthalmol Vis Sci. 2011; 52:8094-101.

29. Niles PI, Greenfield DS, Sehi M, Bhardwaj N, Iverson SM, Chung YS. Detection of progressive macular thickness loss using optical coherence tomography in glaucoma suspect and glaucomatous eyes. Eye 2012; 26:983-991.

30. Tan O, Chopra V, Lu AT, et al. Detection of macular ganglion cell loss in glaucoma by Fourier-domain optical coherence tomography. Ophthalmology 2009; 116:2305-14 e1-2.

31. Mwanza JC, Oakley JD, Budenz DL, Chang RT, Knight OJ, Feuer WJ. Macular ganglion cell-inner plexiform layer: automated detec-tion and thickness reproducibility with spectral domain-optical coherence tomography in glaucoma. Invest Ophthalmol Vis Sci. 2011; 52:8323-8329.

32. Na JH, Sung KR, Lee JR, et al. Detection of glaucomatous progres-sion by spectral-domain optical coherence tomography. Ophthal-mology. Epub ahead of print 2013 March 6.

33. Na JH, Sung KR, Baek S, et al. Detection of glaucoma progression by assessment of segmented macular thickness data obtained using spectral domain optical coherence tomography. Invest Ophthalmol Vis Sci. 2012; 53:3817-3826.

34. You JY, Park SC, Su D, Teng CC, Liebmann JM, Ritch R. Focal lamina cribrosa defects associated with glaucomatous rim thinning and acquired pits. JAMA Ophthalmol. 2013; 131:314-320.

35. Strouthidis NG, Fortune B, Yang H, Sigal IA, Burgoyne CF. Lon-gitudinal change detected by spectral domain optical coherence tomography in the optic nerve head and peripapillary retina in experimental glaucoma. Invest Ophthalmol Vis Sci. 2011; 52:1206-1219.

36. Chauhan BC, OLeary N, Almobarak FA, et al. Enhanced detec-tion of open-angle glaucoma with an anatomically accurate optical coherence tomography-derived neuroretinal rim parameter. Oph-thalmology 2013; 120(3):535-543.

37. Weinreb RN, Greve EL. Glaucoma Diagnosis. Amsterdam, The Netherlands: Kugler Publications; 2004.

38. Lin SC, Singh K, Jampel HD, et al. Optic nerve head and retinal nerve fiber analysis: a report by the American Academy of Ophthal-mology. Ophthalmology 2007; 114:1937-1949.

39. Greenfield DS, Huang X-R, Knighton RW. Effect of corneal polar-ization axis on assessment of retinal nerve fiber layer thickness by scanning laser polarimetry. Am J Ophthalmol. 2000; 129:715-722.

40. Bowd C, Medeiros FA, Weinreb RN, Zangwill LM. The effect of atypical birefringence patterns on glaucoma detection using scan-ning laser polarimetry with variable corneal compensation. Invest Ophthalmol Vis Sci. 2007; 48:223-227.

41. Zhou Q, Weinreb RN. Individualized compensation of anterior segment birefringence during scanning laser polarimetry. Invest Ophthalmol Vis Sci. 2002; 43:2221-2228.

42. Bagga H, Greenfield DS, Feuer W. Quantitative assessment of atypical birefringence images using scanning laser polarimetry with variable corneal compensation. Am J Ophthalmol. 2005; 139:437-446.

43. Wu Z, Vazeen M, Varma R, et al. Factors associated with variabil-ity in retinal nerve fiber layer thickness measurements obtained by optical coherence tomography. Ophthalmology 2007; 114:1505-1512.

44. Ray R, Stinnett SS, Jaffe GJ. Evaluation of image artifact produced by optical coherence tomography of retinal pathology. Am J Oph-thalmol. 2005; 139:18-29.

45. Medeiros FA, Zangwill LM, Anderson DR, et al. Estimating the rate of retinal ganglion cell loss in glaucoma. Am J Ophthalmol. 2012; 154:814-24 e1.

46. Meira-Freitas D, Lisboa R, Tatham A, et al. Predicting progression in glaucoma suspects with longitudinal estimates of retinal ganglion cell counts. Invest Ophthalmol Vis Sci. Epub ahead of print 2013 May 9.


New Horizons in Optic Nerve Head Imaging in GlaucomaJoel S Schuman MD

Glaucoma is an optic neuropathy that is the second leading cause of blindness worldwide.1 It is an irreversible disease that affects nearly 15% of the general population over the age of 85.2 One of the areas thought to be of major importance in the development of glaucoma is the optic nerve head (ONH). The ONH contains the lamina cribrosa (LC), a matrix of porous connective tissue beam around which run all the nerves of the retina. Although the pathogenesis of glaucoma is incompletely understood, the prevailing mechanical theory of glaucoma suggests that elevated IOP compresses the ONH and LC, leading to disruption of neuronal axoplasmic transport and subsequent necrosis of the neurons.3

While IOP is the primary modifiable risk factor in glaucoma, patients may experience glaucomatous damage even within a range of pressures that is considered normal.4 Such findings point to a possibility that some LC may be more prone to glauco-matous damage due to a mechanical or architectural susceptibil-ity.3 However, up until recently, noninvasive imaging of the deep ONH structures such as the LC has been impossible.

OCT is a rapidly evolving technology in ophthalmology that can perform noncontact, noninvasive, real-time cross-sectional imaging of posterior eye.5 Recent advances in OCT technology permit the imaging of 3-D volumes of the human ONH and LC microarchitecture in vivo.6

Understanding the microarchitecture of the LC can improve the present knowledge of the pathogenesis of glaucoma. More-over, an increased understanding of mechanical susceptibility to glaucomatous damage may potentially provide an avenue for assessing glaucoma progression based on ONH microarchitec-ture in future studies.

There has been considerable interest in glaucoma research to look directly at the LC, the hypothesized site of glaucoma dam-age. Early ex vivo histological studies identified changes in the LC structure in glaucoma eyes.3 However, histology is prone to fixation artifacts and represents little potential for diagnostic use in patients. In addition, although early in vivo funduscopic examination of the ONH reveals changes on surface features such as cup-to-disc ratio and neuroretinal rim thickness, such structural changes are a late manifestation of the disease pro-cesses, when glaucomatous damage has already occurred.

The LC has become a topic of increasing interest to those in the field of glaucoma. Recent advances in OCT imaging

have finally permitted in vivo imaging of the deep tissues of the ONH.6 It has been readily adopted in the field of ophthalmology and is rapidly becoming the standard of care. However, many of the current in vivo studies are limited to analyzing the LC on a macroscopic level, such as the total thickness,7 or anterior sur-face features such as localized defects8 on 2-D sagittal scans.

The 3-D microarchitecture of the LC, such as the beams through which all axons pass, have not yet been explored in vivo. We believe that the microarchitecture changes in the load-bear-ing structures are equally as important to analyze as the macro-architecture changes. Recent advances in the OCT technology allow us the first look at the LC microarchitecture in vivo.

References

1. Quigley HA, Broman AT. The number of people with glaucoma worldwide in 2010 and 2020. Br J Ophthalmol. 2006; 90(3):262-267.

2. Rudnicka AR, Mt-Isa S, Owen CG, Cook DG, Ashby D. Variations in primary open-angle glaucoma prevalence by age, gender, and race: a Bayesian meta-analysis. Invest Ophthalmol Vis Sci. 2006; 47(10):4254-4261.

3. Burgoyne CF. A biomechanical paradigm for axonal insult within the optic nerve head in aging and glaucoma. Exp Eye Res. 2011; 93(2):120-132.

4. Anderson DR, Drance SM, Schulzer M, et al. Natural history of normal-tension glaucoma. Ophthalmology 2001; 108(2):247.

5. Huang D, Swanson EA, Lin CP, Schuman JS, et al. Optical coher-ence tomography. Science 1991; 254(5035):1178.

6. Nuyen B, Mansouri K, Weinreb RN. Imaging of the lamina cribrosa using swept-source optical coherence tomography. J Curr Glaucoma Pr. 2012; 6(3):113-119.

7. Lee EJ, Kim T-W, Weinreb RN, et al. Three-dimensional evalua-tion of the lamina cribrosa using spectral-domain optical coher-ence tomography in glaucoma. Invest Ophthalmol Vis Sci. 2012; 53(1):198-204.

8. Park H-Y L, Jeon SH, Park CK. Enhanced depth imaging detects lamina cribrosa thickness differences in normal tension glau-coma and primary open-angle glaucoma. Ophthalmology 2012; 119(1):10-20.


Monitoring Highly Myopic PatientsKi Ho Park MD PhD

Multiple large-population-based studies have shown that both low myopia and high myopia present an increased risk of open-angle glaucoma.1 Glaucoma diagnosis in highly myopic patients is challenging because structural and functional glaucomatous changes sometimes coincide with myopic changes of the optic nerve head and eyeball.

Ophthalmoscopy and Photography

In highly myopic patients there are large variations of optic nerve head shape and size, as well as significant peripapillary changes. Highly myopic discs are large and elongated and manifest shal-low cupping, large parapapillary atrophy, and a low frequency of localized retinal nerve fiber layer (RNFL) defect.2-4 When clas-sifying the type of disc hemorrhage according to proximal loca-tion, the lamina cribrosa-type hemorrhage has been found to be more frequent in myopic glaucomatous eyes than in nonmyopic glaucomatous eyes.5

Glaucomatous changes of the optic nerve head, due to their high variability, cannot easily be detected by ophthalmoscopy or disc photography in highly myopic eyes. However, in cases where the RNFL defect is localized, RNFL photography can be effective, and especially so for Asian eyes.6 In a recent study, Kimura et al showed by RNFL photography that highly myopic eyes with early glaucoma are more susceptible than non-highly myopic eyes to papillomacular bundle damage.7

Optical Coherence Tomography

One of the major advancements in the structural assessment of glaucoma is the development of spectral-domain OCT (SD-OCT). When examining highly myopic eyes with OCT however, special attention should be paid to the detection of glaucomatous change. In the interpretation of circumpapillary (cp)-RNFL thickness measurements, for example, the temporal deviations of superior and inferior peaks should be considered. In highly myo-pic eyes, the superotemporal and inferotemporal RNFL thickness humps usually are deviated to the temporal side due to temporal convergence of the superotemporal and inferotemporal RNFL bundles.8-11 The possible underlying causes of this convergence are (1) dragging of nerve fibers to the temporal side during eye-ball elongation or (2) image artifacts consequent upon increased vertical curvature of the retina. Regardless of the cause, temporal convergence in highly myopic eyes can induce pseudo-abnormal RNFL defects both superiorly and inferiorly.10

Recently, attempts have been made to measure with SD-OCT the macular area wherein, in the case of highly myopic eyes, there is less anatomic variability than in the optic nerve head or cp-RNFL. Shoji et al12 and Kim et al13 showed that ganglion cell complex (GCC; NFL+GCL+IPL) thickness is comparable to or a better parameter than cp-RNFL thickness for detection of glau-coma in highly myopic eyes. Choi et al reported the glaucoma-detection ability of macular ganglion cell-inner plexiform layer (GCIPL; GCL+IPL) thickness to be both high and comparable to that of cp-RNFL thickness in highly myopic eyes.14

Employing swept-source OCT, Ohno-Matsui et al found that 16.2% of highly myopic eyes have a pit-like cleft in the area of the optic disc (optic disc pits) or in regions of parapapillary atrophy (conus pits), both of which signs are barely visible oph-thalmoscopically.15 The depths of these pits vary from shallow to deep.

Perimetry

Whereas a nonprogressive glaucomatous subgroup within a young Chinese population has been reported,16 glaucomatous progression in highly myopic eyes, along with the associated risk factors, has been documented as well.17,18 Lee et al found progression of visual field (VF) loss in 57 eyes (21.8%) during a 5-year follow-up period; among this study population, progres-sion of VF loss was most marked in primary open-angle glau-coma patients with myopia greater than -6 D.18

Ohno-Matsui et al, upon a review of the medical records for 492 highly myopic eyes (myopic refractive error > 8 D or axial length 26.5 mm) over a mean follow-up period of 11.6 5.5 years, reported that 13.2% showed newly developed and signifi-cant VF defects.19 The incidence was significantly higher in eyes with an oval optic disc than in eyes with a round optic disc. Con-sidering these results, the authors suggested that high myopia is a high risk factor for VF defect and that highly myopic eyes should be examined at least once yearly. However, it remains unclear whether VF defect is due to glaucoma or to myopia itself.

Case

A 38-year-old highly myopic gentleman was referred to the Glau-coma Clinic of Seoul National University Hospital for diagnosis. In his left eye, the refractive error was -6.0Dsph-0.25Dcylx145 and the IOP was 16 mmHg at baseline examination.

In a February 2005 examination, it was found that the optic nerve head was temporally tilted and showed peripapillary atrophy. The superior and inferior neuroretinal rim manifested thinning, though it was not clear whether this was due to glau-coma or the disc tilt (see Figure 1A). At the 5 oclock border of the disc, a disc hemorrhage was observed, and further, RNFL photography uncovered superior and inferior RNFL defects (see Figure 1B). In correspondence with this photographic evidence, time-domain OCT showed superior and inferior RNFL thinning (see Figure 1C). Finally, the Humphrey C30-2 VF showed supe-rior hemifield defect involving the fixation point, as well as an inferior arcuate defect (see Figure 1D).

In the April 2013 examination, the optic nerve head revealed cup excavation in the 4 oclock region, along with a pit-like lesion at the 5 oclock disc border, where the disc hemorrhage had been detected (see Figure 2A). RNFL photography com-pared with the 2005 image (see Figure 1B) showed widening of the inferior defect toward the fovea (see Figure 2B). In corrobo-ration of this photographic evidence, SD-OCT showed superior and inferior RNFL thinning (see Figure 2C). GCIPL analysis showed both large inferior defects and small superior defects


(see Figure 2D). Swept-source OCT revealed a deep defect of the lamina cribrosa at the 5 oclock position (see Figure 2E), where disc hemorrhage and the pit-like lesion had been observed photo-

graphically. However, the VF did not clearly indicate glaucoma-tous progression (see Figure 2F). Therefore, a time gap between structural and functional change was suspected in this case.

Figure 1. Structural and functional examinations in 2005. A. Disc photograph. B. RNFL photograph. C. Time domain OCT. D. Humphrey visual field.

Figure 2. Structural and functional examinations in 2013. A. Disc photograph. B. RNFL photograph showed progression com-pared with 2005 image. C. Spectral domain OCT. D. GCIPL Analysis. E. Spectral domain OCT (the arrow indicates a deep defect of lamina cribrosa at the 5 oclock position) F. Humphrey visual field.


Conclusions

Diagnosis of glaucoma in highly myopic patients is challenging. Progression can be slow if IOP is within a normal range; in fact, for some individuals, glaucoma does not progress at all over long periods of time or even through most of their lives. None-theless, some suffer vision loss. Considering the characteristics of high myopia, especially the fact that myopic changes of the optic nerve head and eyeball usually coincide with structural and functional glaucomatous changes, it is recommended that both structural and functional tools be utilized in monitoring highly myopic patients.

References

1. Marcus MW, de Vries MM, Junoy Montolio FG, Jansonius NM. Myopia as a risk factor for open-angle glaucoma: a systematic review and meta-analysis. Ophthalmology 2011; 118(10):1989-1994.

2. Jonas JB, Dichtl A. Optic disc morphology in myopic primary open-angle glaucoma. Graefes Arch Clin Exp Ophthalmol. 1997; 235(10):627-633.

3. Dichtl A, Jonas JB, Naumann GO. Histomorphometry of the optic disc in highly myopic eyes with absolute secondary angle closure glaucoma. Br J Ophthalmol. 1998; 82(3):286-289.

4. Hsu SY, Chang MS, Ko ML, Harnod T. Retinal nerve fibre layer thickness and optic nerve head size measured in high myopes by optical coherence tomography. Clin Exp Optom. Epub ahead of print 2013 Apr 8.

5. Kim HS, Park KH, Jeoung JW, Park J. Comparison of myopic and nonmyopic disc hemorrhage in primary open-angle glaucoma. Jpn J Ophthalmol. 2013; 57(2):166-171.

6. Cho BJ, Park KH. Topographic correlation between -zone para-papillary atrophy and retinal nerve fiber layer defect. Ophthalmol-ogy 2013; 120(3):528-534.

7. Kimura Y, Hangai M, Morooka S, et al. Retinal nerve fiber layer defects in highly myopic eyes with early glaucoma. Invest Ophthal-mol Vis Sci. 2012; 53(10):6472-6478.

8. Kang SH, Hong SW, Im SK, Lee SH, Ahn MD. Effect of myopia on the thickness of the retinal nerve fiber layer measured by Cirrus HD optical coherence tomography. Invest Ophthalmol Vis Sci. 2010; 51(8):4075-4083.

9. Chung JK, Yoo YC. Correct calculation circle location of optical coherence tomography in measuring retinal nerve fiber layer thick-ness in eyes with myopic tilted discs. Invest Ophthalmol Vis Sci. 2011; 52(11):7894-7900.

10. Leung CK, Yu M, Weinreb RN, et al. Retinal nerve fiber layer imaging with spectral-domain optical coherence tomography: inter-preting the RNFL maps in healthy myopic eyes. Invest Ophthalmol Vis Sci. 2012; 53(11):7194-7200.

11. Hwang YH, Yoo C, Kim YY. Characteristics of peripapillary reti-nal nerve fiber layer thickness in eyes with myopic optic disc tilt and rotation. J Glaucoma. 2012; 21(6):394-400.

12. Shoji T, Sato H, Ishida M, Takeuchi M, Chihara E. Assessment of glaucomatous changes in subjects with high myopia using spectral domain optical coherence tomography. Invest Ophthalmol Vis Sci. 2011; 52(2):1098-1102.

13. Kim NR, Lee ES, Seong GJ, et al. Comparing the ganglion cell com-plex and retinal nerve fibre layer measurements by Fourier domain OCT to detect glaucoma in high myopia. Br J Ophthalmol. 2011; 95(8):1115-1121.

14. Choi YJ, Jeoung JW, Park KH, Kim DM. Glaucoma detection ability of ganglion cell-inner plexiform layer thickness by spectral-domain optical coherence tomography in high myopia. Invest Oph-thalmol Vis Sci. 2013; 54(3):2296-2304.

15. Ohno-Matsui K, Akiba M, Moriyama M, et al. Acquired optic nerve and peripapillary pits in pathologic myopia. Ophthalmology 2012; 119(8):1685-1692.

16. Doshi A, Kreidl KO, Lombardi L, Sakamoto DK, Singh K. Non-progressive glaucomatous cupping and visual field abnormalities in young Chinese males. Ophthalmology 2007; 114(3):472-479.

17. Perdicchi A, Iester M, Scuderi G, Amodeo S, Medori EM, Recupero SM. Visual field damage and progression in glaucomatous myopic eyes. Eur J Ophthalmol. 2007; 17(4):534-537.

18. Lee YA, Shih YF, Lin LL, Huang JY, Wang TH. Association between high myopia and progression of visual field loss in primary open-angle glaucoma. J Formos Med Assoc. 2008; 107(12):952-957.

19. Ohno-Matsui K, Shimada N, Yasuzumi K, et al. Long-term devel-opment of significant visual field defects in highly myopic eyes. Am J Ophthalmol. 2011; 152(2):256-265.


Corneal Biomechanics: Does It Provide Any Additional Information for Management?Nathan Radcliffe MD

The appreciation that corneal thickness is an important factor for both the assessment of IOP and for the understanding of glaucoma risk has led to investigations regarding the relationship between the cornea and glaucoma. While central corneal thick-ness informs us on the anatomy of the central cornea, the field of corneal biomechanics seeks to understand how the cornea behaves in various situations (eg, during applanation tonometry).

Corneal hysteresis is measured by the Ocular Response Analyzer (Reichert, Corp.; New York, USA), is defined as the difference between the air-jet pressures at inward and outward corneal applanation using noncontact tonometry, and is believed to be a reflection of corneal viscous damping. The Corvis ST (Oculus; Wetzlar, Germany) is an alternative instrument that provides visualization and measurement of the corneal deforma-tion response to an air pulse with an ultrahigh-speed Scheimpflug camera at over 4000 frames/ second. Both systems attempt to determine the influence of biomechanical properties on conven-tional IOP measurements.

While the exact nature of corneal hysteresis is often debated, for the purposes of this discussion we will consider corneal hys-teresis to be a measure of a single corneal biomechanical prop-erty: viscous dampening. This review, however, will focus on clinical data that inform us of the relevance of corneal hysteresis. Therefore we will evaluate the utility of corneal hysteresis as a clinical variable for the care of patients with glaucoma.

Recently, corneal hysteresis has been shown to have a poten-tial role as both an IOP correction factor and as a surrogate marker of an individuals susceptibility to glaucomatous optic neuropathy. IOP measurements that are adjusted for corneal hys-teresis are independent of corneal thickness.1 Clinical data have shown that corneal hysteresis is lower in patients with glaucoma-tous optic neuropathy.2Two retrospective cohort studies have demonstrated that corneal hysteresis is also lower in patients with visual field progression. Congdon and colleagues reported that corneal hysteresis was associated with visual field progres-sion and that corneal thickness was not.3 Corneal thickness was, however, associated with the structural state of glaucoma dam-age (cup-to-disc ratio). De Moares et al recently evaluated factors associated with visual field progression in 153 patients who had taken more than 5 visual field tests (mean: 8.5) over an average of 5 years of follow-up.4 They found that progressing eyes (about 16% of the population) had lower corneal thickness (525.0 34.2 vs. 542.3 38.5 m, P = .04) and lower hysteresis (7.5 1.4 vs. 9.0 1.8 mmHg, P < .01) compared to nonprogressing eyes. In a multivariable analysis, peak IOP, age, and corneal hys-teresis (but not corneal thickness) were significantly associated with progression. A recent study from Chee et al evaluated 103 patients under surveillance for glaucoma and found that corneal hysteresis (more so than corneal thickness) was lower in patients with optic nerve progression by serial fundus photography and was associated with the development or worsening of retinal nerve fiber layer defects.5 However, in the multivariable analysis, only age (not corneal hysteresis) was significantly associated with progression. These studies provided a strong rationale for the investigation of corneal hysteresis in a prospective study of glau-coma progression.

Recently, Medeiros and colleagues sought to evaluate the role of cornealhysteresis as a risk factor for the rate of visual field progression in prospective study of glaucoma patients.6 Eyes with high IOP and low corneal hysteresis had the fastest rates of disease progression, and corneal hysteresis explained a larger amount of the variation in slopes of visual field change than corneal thickness. Patients with a lower baseline corneal hysteresis were at a higher risk for future visual field progres-sion. Unlike corneal thickness, corneal hysteresis can change significantly in nonpathologic situations and in fact increases after IOP reduction with medical therapy.7In a retrospective study of newly diagnosed glaucoma patients who were initiated on IOP-lowering therapy with a prostaglandin analogue, patients with a lower corneal hysteresis at baseline demonstrated greater IOP reduction. Together, these findings paint a complex picture of corneal hysteresis where patients with low hysteresis may have significant pressure lowering but should still be monitored closely given their higher risk of future progression. Limitations to the application of corneal hysteresis include visit-to-visit vari-ability in some patients and influence from other corneal diseases such as keratoconus, which is associated with lower hysteresis. Additionally, the exact meaning of corneal hysteresis as a biome-chanical property is not fully understood. In summary, corneal hysteresis and other biomechanical corneal assessments provide valuable information, particularly regarding the risk of glaucoma progression. In at least four studies to compare the two, corneal hysteresis was more closely correlated to glaucoma progression than corneal thickness. While the existing literature is substan-tive and growing, there is currently sufficient data to support the clinical adoption of hysteresis measurements in patients at risk for glaucoma progression.

References

1. Kotecha A, Elsheikh A, Roberts CR, Zhu H, Garway-Heath DF. Corneal thickness- and age-related biomechanical properties of the cornea measured with the ocular response analyzer. Invest Oph-thalmol Vis Sci. 2006; 47(12):5337-5347.

2. Vu DM, Silva FQ, Haseltine SJ, Ehrlich JR, Radcliffe NM. Rela-tionship between corneal hysteresis and optic nerve parameters measured with spectral domain optical coherence tomography. Graefes Arch Clin Exp Ophthalmol. Epub ahead of print 2013 Mar 22.

3. Congdon NG, Broman AT, Bandeen-Roche K, Grover D, Quigley HA. Central corneal thickness and corneal hysteresis associated with glaucoma damage. Am J Ophthalmol. 2006; 141(5):868-875.

4. De Moraes CV, Hill V, Tello C, Liebmann JM, Ritch R. Lower cor-neal hysteresis is associated with more rapid glaucomatous visual field progression. J Glaucoma. 2012; 21(4):209-213.

5. Medeiros FA, Meira-Freitas D, Lisboa R, Kuang TM, Zangwill LM, Weinreb RN. Corneal hysteresis as a risk factor for glaucoma progression: a prospective longitudinal study. Ophthalmology. Epub ahead of print 2013 May 1.

6. Chee RI, Silva FQ, Ehrlich JR, Radcliffe NM. Agreement of flicker chronoscopy for structural glaucomatous progression detection


and factors associated with progression. Am J Ophthalmol. 2013; 155(6):983-990.

7. Agarwal DR, Ehrlich JR, Shimmyo M, Radcliffe NM. The relation-ship between corneal hysteresis and the magnitude of intraocular pressure redu

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