Corneal biomechanics has evolved from being a topic of scientific curiosity to one of growing interest among ophthalmic researchers based on appreciation that knowledge of the cornea’s biomechanical properties may have relevance in a variety of clinical applications.

Better understanding of corneal elasticity and strain might allow for more predictable outcomes after incisional and photoablative corneal surgery, enable identification of patients at risk for ectasia and lead to the development of methods for more accurate measurement of IOP. However, exploring those opportunities and ultimately bringing them into the hands of practitioners depends on the availability of tools that can precisely and reproducibly measure corneal biome-chanical behavior.

Working at the cutting edge in this field, Cole Eye Institute fellow William J. Dupps, M.D., Ph.D., who will be joining the staff

in July, is developing non-invasive technology for evaluating the biomechanical properties of the cornea. Along with collaborating biomedical engineers Andrew Rollins, Ph.D., and Matthew Ford, B.S., at Case Western Reserve University, he has developed and is testing a system that uses high-speed optical coherence tomography (OCT) and sophis-ticated software to measure and map the magnitude and direction of tissue displace-ments within the layers of the cornea.

The information can be displayed in a two-dimensional, cross-sectional colored map in which the various colors represent levels of strain intensity. In addition, the system is able to generate a vector map that provides a more complete representation of strain by presenting information on direction as well as magnitude. Software is also being developed that will provide a full three-dimensional reconstruction of strain data within corneal tissue.

New Tool for Measuring Corneal Biomechanical Properties Developed at Cole Eye Institute

Cole Eye Institute Spring 2006

Ophthalmology Update

Oncology, p. 4New Data Shed Light on Risk of Choroidal Nevi Malignant Transformation

Retina, p. 5Research Continues to Support Intravitreal Ranibizumab’s Role in AMD

Genetics, p. 7Leber’s Congenital Amaurosis Meeting Coming to Cleveland in July

New Staff, p. 16The Cole Eye Institute Welcomes Andrew P. Schachat, M.D.

Continued on page 2

William J. Dupps, M.D., Ph.D.

So far, the technique has been investigated in a number of ex vivo experiments using porcine and human donor eyes to evaluate strain changes in the corneal layers in response to various experimental stimuli. Reproducibility and validation experiments are also ongoing, and the results overall are encouraging regarding the system’s performance and capabilities.

“Non-invasive OCT-based strain mapping appears to be a very promising and exciting tool for identifying previously undetectable changes inside the cornea and on its surface that will give us much greater understanding of regional differences in corneal biome-chanical properties,” says Dr. Dupps.

One study investigated changes that occurred in response to increases in IOP. The results showed that as IOP was incrementally raised, there were corresponding increases in the amount of strain within various layers of the cornea. The OCT-based technique is also being used to characterize dynamic changes in strain patterns occurring during a continuous IOP change. Consistent with the understanding that biomechanical properties are not uniform throughout the depth of the cornea, that study showed differences in the displacements of the anterior and posterior portions of the cornea.

“A key feature of this technique is that it provides more than a bulk estimate of elasticity for the entire cornea. It allows us to evaluate local differences in biomechanical behavior that may be very important in ectasia, corneal wound healing and astigmatic responses to refractive surgery,” Dr. Dupps said.

In another experiment in which the cornea was cut to about 50% depth, marked het-erogeneity was noted in the strain patterns at different levels of the cornea. There were consistent strain patterns within individual sublayers, but the strain varied in direction between sublayers.

“Preliminary results suggest that sublayers were sliding in opposite directions, and that is an interesting finding considering that one hypothesis for the etiology of keratoconus is that the layers of the cornea are prone to slipping,” Dr. Dupps notes.

Measuring Corneal Biomechanical Properties, (Continued from page 1)

5 mmHg

10 mmHg

15 mmHg

20 mmHg

25

0

Magnitude in μm

Figure 2:

Map of displacement

magnitudes during

IOP change.

Figure 1: Unprocessed OCT

video during IOP decrement.

2

He expects that a technique for mapping corneal strain might find its most important application in the early detection of keratoconus and other corneal ectasias, where it could improve efforts to exclude at-risk patients from keratorefractive surgery and enhance the sensitivity of genetic studies in which early recognition of the disease phenotype is critical.

“More sensitive and specific tools are needed to screen for pre-clinical keratoconus. With current methods based on evaluation of topography and corneal thickness, surgeons are still turning away patients with nonspecific topographic abnormalities who may have benefited from surgery while treating others who only in retrospect should have been excluded. We hope that mapping corneal material properties will enable us to find focal biomechanical abnormalities that are present even before gross changes—such as thinning and topographic irregularity—are detectable,” he says.

Other potential applications of this technology include investi-gating corneal wound integrity in corneal transplantation and monitoring biomechanical responses to refractive surgery that then could be incorporated into the surgical plan to achieve a more predictable result. However, the list of possible uses is long, believes Dr. Dupps, whose own doctoral training in biomedical engineering has always colored his approach to clinical ophthalmology.

“Ultimately, our toolbox for evaluating corneal biomechanical behavior will need to contain a variety of instruments, each providing a different mode of measurement to more fully de-scribe these complex phenomena. In addition, translation of this information into clinical use will occur at a much greater pace in multidisciplinary collaborations like the one we have developed in Cleveland, which takes full advantage of local resources for advancing our basic understanding of the cornea and the diseases that affect it,” concludes Dr. Dupps.

Looking toward the future

Figure 3: 2-D Stromal

Displacement Vector Field.

3

Choroidal nevi are common lesions that are frequently

monitored because they are considered the precursor for

choroidal melanomas and clinical distinction between

those two lesions may initially be difficult. However, reli-

able data regarding the risk of malignant transformation of

choroidal nevi have been lacking.

To address that gap in

knowledge, Arun D. Singh,

M.D., of the Cleveland

Clinic Cole Eye Institute,

undertook a rigorously

designed study based

on nationwide data for

choroidal nevi prevalence

and choroidal melanoma

incidence. The results,

published in Ophthalmol-

ogy [Singh AD, et al. Ophthalmology 2005;112:1784-89],

showed that about 6% of the white, adult population in the

United States has a choroidal nevus, but that only about 1

in 10,000 of those lesions undergoes malignant transfor-

mation each year.

“This is the first study investigating this question using

national, population-based data, and it demonstrates that

while choroidal nevi are frequent, there is no need to panic

when one is diagnosed because those lesions only rarely

become malignant,” says Dr. Singh, who is Director of

the Department of Ophthalmic Oncology at the Cole Eye

Institute.

“A newly diagnosed choroidal nevus should be photo-

graphed and its size recorded. However, further surveil-

lance need only be periodic, perhaps every 6 months for

the first year or two in order to rule out growth, and annu-

ally or biannually thereafter,” he continues.

In Dr. Singh’s study, the data on choroidal nevi prevalence

were derived from three large, well-conducted studies

that were identified through a systematic literature review

and selected for consideration based on strict inclusion

criteria. Using the prevalence rate data from those studies

and statistics from the 2000 U.S. census, the number of

Americans with choroidal nevi was determined. Age- and

race-matched annual incidence rates for primary choroidal

melanoma were derived from the Surveillance, Epidemiol-

ogy, and End Result program database, and those values

were converted to numbers of Americans with choroidal

melanoma using the census information.

The ratio of the number of individuals with choroidal nevi

and the number with choroidal melanoma represented the

annual rate of malignant transformation. The overall average

rate was 1 in 8,845. When the results were stratified by

age into 5-year subgroups, the malignant transformation

rate increased progressively with age with a minimum

value of 1 in 269,565 for the youngest cohort, ages 15

to 19 years old, and a maximum value of 1 in 3,664

among persons 80 to 84 years old.

Despite its methodological strengths, Dr. Singh acknowl-

edges his study has some limitations. First, the analysis

assumes all choroidal melanomas arise from nevi whereas

there are documented cases of a choroidal melanoma

arising de novo.

“The good news is the rate of malignant transformation

calculated in this study provides an estimate of the

maximum risk. We would expect the true rate to be lower

considering the possibility of a melanoma developing in

the absence of a precursor lesion,” he explains.

In addition, the calculated transformation rate applies to

“standard garden variety” choroidal nevi, defined in the

study as lesions measuring 0.75 to 6 mm in diameter and

less than 1 mm in height, and only to the population of

white, American adults.

“The risk for larger, so-called suspicious nevi is expected

to be higher, and there are also no reliable data regarding

the prevalence of nevi in non-white and younger

populations,” Dr. Singh says.

He notes that definitive data regarding the rate of malignant

transformation of choroidal nevi would require a very large

prospective study enrolling thousands of patients and years

of follow-up.

“Obviously, such a study will never be conducted because

it would be cumbersome and costly. From a practical

standpoint, it becomes necessary to rely on mathematically

derived data. Therefore, this study has value for patient

management and is not without clinical significance,”

Dr. Singh concludes.

Institute Researcher Provides Robust Data on Risk of Choroidal Nevi Malignant Transformation

Arun D. Singh, M.D.

�

Newly reported data from a Phase III clinical study evaluating intravitreal treatment with ranibizumab (Lucentis, Genentech) have reinforced opinions that this investigational anti-VEGF therapy represents a significant advance for the treatment of exudative age-related macular degeneration (AMD).

At the Macula 2006 meeting in January, Cole Eye Institute retinal specialist Peter K. Kaiser, M.D., first reported the highly positive 1-year results from the ANti-VEGF Antibody for the Treatment of Predominantly Classic CHORoidal Neovascularization in AMD (ANCHOR) study. Dr. Kaiser is principal investigator for the ANCHOR study at the Cole Eye Institute, which is one of more than 83 investigational sites participating in the international Phase III trial.

ANCHOR randomly assigned 423 patients with predominantly classic, subfoveal choroidal neovascularization (CNV) due to AMD to double-masked therapy with either intravitreal ranibizumab 0.3 mg (140 patients), ranibizumab 0.5 mg (140 patients) or verteporfin (Visudyne) photodynamic therapy (PDT) (143 patients). Patients in the ranibizumab groups received monthly injections for 24 months plus sham PDT every 3 months as needed based on determination of leakage. The patients in the PDT group received sham injections monthly and repeat PDT every 3 months as needed.

The 1-year results showed ranibizumab met its primary efficacy endpoint for maintaining or improving best corrected visual acuity (BCVA) – 94% of patients treated with ranibizumab 0.3 mg and 96% of patients receiving ranibizumab 0.5 mg fulfilled the criterion of losing less than 15 ETDRS letters compared with only 64% of those treated with PDT. Even

more impressive, however, results from secondary efficacy analyses showed ranibizumab exhibited significant benefits for actually improving vision. This is the first study to show average visual improvement in predominantly classic CNV. The study also continued to demonstrate a favorable safety profile with low rates of serious ocular adverse events and no significant systemic toxicity concerns.

Results of secondary efficacy analyses in the ANCHOR trial showed that while PDT-treated patients on average lost 9.5 letters of vision over 12 months, patients in the ranibizumab 0.3 mg and 0.5 mg groups had average gains of 8.5 letters and 11 letters, respectively. In addition, a clinically signifi-cant improvement in vision (gain of 15 letters or more) was achieved by almost 36% of patients treated with ranibizumab 0.3 mg and by 40% of those receiving the higher dose of the anti-VEGF antibody, compared with only about 6% of the controls receiving PDT. Also at 1 year, visual acuity 20/40 or better occurred in 31% of patients in the ranibizumab 0.3 mg group and 39% of those treated with ranibizumab 0.5 mg compared with only 3% of PDT patients. Since this vision is required for driving, this offers a big quality of life improve-ment for patients.

“At entry into the studies, few patients had 20/40 or better acuity, whereas after 1 year of treatment with ranibizumab, more than one-third had vision good enough to drive or perform other visual tasks of daily living. That is a phenomenal result and I cannot underscore enough how important this difference is for patients,” observes Dr. Kaiser.

New treatments for wet

age-related macular degeneration

(seen in this eye) represent

a significant advance.

Latest Results Increase Excitement over Intravitreal Ranibizumab for Wet AMD

Peter K. Kaiser, M.D.

5

Continued on page 6

The 1-year results associated with ranibizumab treatment in the ANCHOR trial mirror those achieved in the Minimally classic/occult trial of the Anti-VEGF antibody Ranibizumab In the treatment of Neovasuclar AMD (MARINA) study. The 1-year MARINA data were reported in July 2005. The MARINA trial was also a multicenter, double-masked Phase III study. It enrolled 716 patients with minimally classic or occult with no classic CNV due to AMD who were randomly assigned to ranibizumab 0.3 mg or 0.5 mg or sham injection. As in ANCHOR, after 1 year in the MARINA study, about 95% of patients treated with ranibizumab had maintained or improved vision and about 30% had a gain of 15 or more letters. Among sham-treated patients, 62% maintained or improved BCVA and only about 5% had a 15 letter or greater gain in visual acuity. Similarly, in the MARINA trial, almost 40% of ranibizumab patients achieved 20/40 or better visual acuity compared with only 11% of sham-treated controls.

“Since its approval, verteporfin PDT has been the gold standard for predominantly classic CNV due to exudative AMD.However, the benefit of PDT is measured by its ability to slow progressive vision loss. Rarely, did patients exhibit visual improvement. Ranibizumab is the first option that is actually able to improve vision in a significant proportion of patients, and that makes it a dramatic improvement over PDT. More importantly, the combined results of the ANCHOR and MARINA studies offer patients vision benefit with ranibizumab regardless of lesion’s angiographic subtype,” Dr. Kaiser says.

Both the ANCHOR and MARINA studies were planned as 2-year trials. Based on the positive results from the interim analysis at 1 year, patients originally assigned to the PDT arm in ANCHOR are being given access to ranibizumab for the duration of the study while the patients in the sham injection

arm of the MARINA study were crossed over to receive month-ly injections of ranibizumab.

Throughout clinical trial experience, intravitreal ranibizumab has been associated with a good safety profile. In ANCHOR, ocular adverse events reported more often in the ranibizumab group than in the PDT arm were conjunctival hemorrhage, increased IOP, eye pain and vitreous floaters. Those events were mild to moderate in severity. Rates of endophthalmitis and uveitis were less than 1%.

“Ocular and systemic safety appear to be excellent for this treatment. The local side effects are those we would expect with an intravitreal injection, and the systemic adverse events are typical of problems that occur in the elderly population enrolled in these trials,” Dr. Kaiser says.

He has been intimately involved in the ranibizumab clinical research program since it was launched, and the Cole Eye Institute is continuing its active role in ongoing trials. It is participating in the HORIZON extension study, an open-label trial allowing treatment with ranibizumab for eligible patients who participated in previous ranibizumab studies, and is one of the study centers in the Phase IIIb 1-year open-label safety study known as SAILOR (Safety Assessment of In-travitreal Lucentis fOR AMD) where patients with exudative AMD can receive ranibizumab for all forms of exudative AMD. In addition, Dr. Kaiser serves as the study chair for Cleveland ROCS (Ranibizumab for Other CauseS of CNV), an open-label study evaluating ranibizumab in patients with CNV related to etiologies other than AMD or pathologic myopia.

Genentech filed a Biologics License Application in December 2005 for ranibizumab with the FDA. Dr. Kaiser says he is hopeful it will be available later in 2006.

Intravitreal Ranibizumab for Wet AMD (Continued from page 5)

Ophthalmic Puzzler, Part I

By W. Michael Stapleton, M.D., and Steven E. Wilson, M.D.

A 21-year-old Arabic male presented to the Refractive

Surgery Department at Cleveland Clinic’s Cole Eye

Institute complaining of poor visual quality with glare and

halos for the previous 2 months. Symptoms began after

bilateral primary laser in situ keratomileusis (LASIK) was

performed in another country. Preoperative examination

included a manifest refraction of -5.00 D sphere in both

eyes, keratometry 39.00 D OD and 39.50 D OS and

pachymetry 581 μm OD and 586 μm OS. Anterior

segment and fundus examinations were unremarkable.

The early postoperative course was normal, and he

was otherwise healthy and taking no medications.

Upon examination, UCVA was found to be 20/30 OD and

20/60 OS. Manifest refraction in the right eye was -0.75

D sphere with BSCVA 20/15. In the left eye, it was -1.25

D sphere with BSCVA 20/15. Cycloplegic refraction was

-0.50 sphere OD and -0.75 sphere OS. Slit-lamp examina-

tion revealed superiorly hinged flaps with a diameter of

approximately 8 mm in both eyes. The remaining anterior

segment examination, fundus examination and IOP mea-

surements were normal. Corneal topography revealed flat

curvatures (37.25 D OD, 36.70 D OS) and well-centered

LASIK ablations on corneal topography (Figure 1).

What is the differential diagnosis and what further

testing should be performed? See page 8. 6

The Cleveland Clinic Cole Eye Institute is helping host the Foundation for Retinal Research’s (FRR) fourth Bi-Annual Leber Congenital Amaurosis Conference (LCA) July 28 to 31.

The meeting will feature scientific presentations about the disease as well as break-out sessions to allow families

affected by LCA to connect and learn from each other. About 75 families are expected to attend.

“The conference will provide the latest information to the families, give them the opportunity to have genetic and other testing done, let them meet with a number of LCA researchers and provide a forum for the exchange of ideas on how they can best help their children at different ages and different stages of development,” explains Elias I. Traboulsi, M.D., Head of the Cole Eye Institute Department of Pediatric Ophthalmology and Director of The Center for Genetic Eye Diseases.

He explains that the FRR’s every-other-year meeting moves to a new location each time. The decision to have it in Cleveland came about through the relationship Dr. Traboulsi has with a Cleveland-area woman who is active in the organization and whose affected son is his patient.

“We have a strong interest in LCA at the Cole Eye Institute and we have evaluated quite a few patients who have it,” he says. “Also, we have the facilities to provide electroretinograms, blood analysis, retinal photography and other testing to families attending the conference.”

The sessions will be held at the new Intercontinental Hotel and Conference Center on Cleveland Clinic’s campus and the examinations, by appointment only, will be at Cole Eye Institute July 27 and 28. The event will also utilize the resources of Cleveland Sight Center, located across the street from Cleveland Clinic’s campus. The center, which provides resources to blind and visually impaired children and adults, will be providing child care during the meeting and letting the families access its self-help/daily living skills training area.

Speakers scheduled to attend the meeting include Irene Maumenee, M.D., Josseline Kaplan, M.D., Ph.D., Edwin Stone, M.D., Ph.D., Stephen P. Daiger, Ph.D., Stephanie A. Hagstrom, Ph.D., Robert Koenekoop, M.D., Ph.D., Constance L. Cepko, Ph.D., Jean Bennett, M.D., Ph.D., Srinivas R. Sadda, M.D., Mark Humayun, M.D., Gerald Chader, Ph.D., M.D., Krzysztof Palczewski, Ph.D., Eugene de Juan, M.D., and Dr. Traboulsi.

For more information or to register, please contact The Foundation for Retinal Research at 630.978.0547 or visit www.tfrr.org.

Leber Congenital Amaurosis Conference Coming to Cleveland

Elias I. Traboulsi, M.D.

Figure 1.

Patient’s corneal topography

after LASIK.

�

Differential Diagnosis

Patients seek LASIK and other refractive techniques to reduce or eliminate their dependency on corrective lenses. However, optimal outcomes do not always occur. Undercorrection is one of the most commonly reported complications. Residual myopia greater than 1.0 D occurs in 11.3% to 59% of LASIK cases, depending on the degree of preoperative myopia and other factors.1

LASIK may also induce changes in visual quality or best spectacle-corrected vision in some patients. This is often an indicator of the presence of irregular astigmatism. Central islands, flap misalignment, flap striae, ablation decentration, epithelial in-growth and diffuse lamellar keratitis (DLK) have been identified as complications that can cause irregular astigmatism and its related symptoms.2

Some LASIK patients may only have an altered quality of vision at night in the form of glare, halos or starbursts. In published studies, 25.4% to 58.4% of refractive patients indicated they experienced glare, starbursts or halos at night at some point in their postoperative course.3-5 Symptoms generally improve over time. Pop and Payette6 showed that 25.6% of patients were symptomatic at 1 month, but that number fell to 4.7% one year after surgery. Night vision symptoms also exist in untreated patients, and it is possible that this 4.7% represents baseline in the general population.7 Explanations offered for the time-dependent reduction in night symptoms include psychological adjustment to new vision, corneal healing3 and central neural adaptation.3,8

Risk factors for developing night vision symptoms reported from a major review of refractive surgery for myopia include: high corrections, large pupil size, small ablation zone diameters, decentered ablations, flap striae, epithelial ingrowth, flap misalignment and dry eye.9 More recently, wavefront technology shows an association between higher-order optical aberrations (HOA) and visual quality, such as glare, halos, starbursts and doubling.10

Ophthalmic Puzzler, Part II (continued from page �)

Figure 3.

Left-eye wavefront analysis

before enhancement.

�

Diagnosis

Manifest and cycloplegic refractions revealed mild undercor-rection in the patient. However, the significant glare and halos he reported were out of line with this level of undercorrection. Examination showed no evidence of DLK, flap striae, epithelial in-growth or flap misalignment. Corneal topography revealed well-centered ablations with no evidence of central islands (Figure 1). BSCVA of 20/15 in both eyes also indicated that irregular astigmatism was an unlikely source for the patient’s complaints.

Preoperative keratometry in the patient was flat and may have contributed to the development of symptoms. Flatter corneal curvatures have been associated with starburst,4 but others have suggested that preoperative keratometry has no associa-tion with night vision complaints.6

Birgit et al.11 indicated that glare and halos following LASIK are caused by a combination of factors: pupil size, corneal swelling and reduction in transparency of optical tissues. If the pupil is greater in diameter than the ablation zone diam-eter, light may not be distinctly focused on the retina. Light from the ablated zone will focus closer to the retina, whereas light from the non-ablated zone, which gains access through the peripheral pupil, would have the same depth of focus as the pre-operative cornea. The resultant duplication of focusing light can cause glare or halos because of the superimposed in-focus and out-of-focus images on the retinal plane.11

This condition may be aggravated at night when the pupil diameter approaches and surpasses the ablation zone diameter. However, the role of pupil size and ablation zone diameters in night symptoms is controversial. Evidence has also shown that pupil size is not correlated with glare and halos follow-ing LASIK.3,6,12,13 In our patient, photopic pupil size was 3.5 mm and scotopic pupils were 5.0 mm. Modern ablation zone diameters typically exceed 6.5 mm. Even if large pupil size contributes to nighttime symptoms, this is an unlikely cause for our patient’s complaints.

Corneal swelling or loss of transparency in optical tissues can cause light to scatter. Both of these conditions can occur after keratorefractive surgery, and the scattering may cause patients

to experience glare or halos. Halo size perceived by LASIK

patients has been found to gradually decrease during the first 6 months of follow-up. However, even after 6 months, halos measure almost twice the pre-operative size.11

Optical aberrations are influenced by refractive surgery. Defocus (sphere) and astigmatism, the so-called lower-order aberrations, are decreased in order to reduce the need for corrective lenses. Wavefront analysis has shown that HOA (third-order and above) increase, especially after traditional ablations that are not driven by wavefront analyses. In the case of spherical aberration, they are increased up to four times pre-operative levels.14

The highest amounts of HOA are third-order (including coma) and fourth-order (including spherical aberration),15 and HOA has been associated with visual quality reduction at night. Chalita and Krueger10 found that spherical aberration was significantly associated with glare and starburst formation, and horizontal coma was associated with double vision under scotopic lighting. Though not significant, these authors also noted a trend with halo symptoms and HOA. Spherical aber-ration is thought to be worse after refractive surgery because of the corneal flattening created by treatments for myopia, while coma tends to increase due to uneven flattening seen in decentered ablations.14

McCormick et al.15 identified refractive surgery patients with persistent glare, halos and starbursts (6 months to 5 years after primary surgery). Wavefront analysis in this symptomatic group showed significantly elevated HOA compared with untreated patients (3.5 fold) and asymptomatic post-LASIK patients (2.3 fold). HOA are also more prominent at night, as values double with each millimeter increase in pupil diameter.15

Wavefront aberrometry was performed in our patient (Figures 2 and 3), revealing high HOA levels: total HOA was 1.35 μm OD and 0.95 μm OS. Spherical aberration was 0.73 μm OD and 0.60 μm OS, and coma was 1.05 μm OD and 0.72 μm OS. In addition, the wavefront refraction (-0.84 +0.44 x 74 and -1.42 =0.21 x 131) correlated poorly with manifest and cycloplegic refractions.

How would you treat this patient?

Figure 2.

Right-eye wavefront analysis

before enhancement.

�

Management

Re-treatment after LASIK is performed in 10% to 50% of pri-mary cases by 1 year after surgery.16 FDA approval has not yet been granted for custom LASIK enhancements. One concern is that more tissue is removed in custom treatments. Studies have shown that custom retreatments may ablate up to two times deeper than standard ablations, so patients with corneas that have already been thinned by prior surgery should be carefully screened.17

Overthinning impairs corneal integrity and can even cause iatrogenic ectasia. Despite the risks, however, several reports have shown wavefront-guided re-treatments to be safe and effective for eliminating night vision symptoms and HOA induced by standard refractive procedures.10,18-20 Others also showed significant HOA reduction, although the effect on symptoms was not reported.16,21,22 Schwartz et al.21 measured the reduction for total HOA from 1.31 μm pre-enhancement to 0.85 μm post-enhancement, and spherical aberration reduced from 1.06 μm to 0.65 μm.

Our patient was offered custom wavefront enhancement to treat his undercorrection and elevated HOA (in association with severe night vision symptoms). He was informed of the off-label nature of this treatment, but chose to proceed in hopes that his symptoms would be reduced.

Enhancement was performed without complication, and the patient noted improvement in his overall vision at postop day 1. By 1 week, there was a dramatic subjective improvement in glare and halos, and wavefront analysis revealed significant reduction in HOA (Figure 4, Figure 5 and Table 1). Total HOA was 0.54 μm OD and 0.43 μm OS, spherical aberration was 0.34 μm OD and 0.30 μm OS and coma was 0.18 μm OD and 0.25 μm OS.

The remaining examination was only notable for mild punctate epithelial staining in the right cornea consistent with LASIK-induced neurotrophic epitheliopathy. The patient was instructed to apply non-preserved artificial tears four to six times a day and followup with his refractive surgeon at home.

Figure 5.

Left-eye wavefront analysis

after enhancement.

Figure �.

Right-eye wavefront analysis

after enhancement.

10

References

1. Perez-Santonja JJ, Ayala MJ, Sakla HF, Ruiz-Moreno JM, Alio JL. Retreatment after Laser In Situ Keratomileusis. Ophthalmology. 1999; 106:21-28.

2. Ambrosio R, Wilson SE. Complications of laser in situ keratomileusis: etiology, prevention, and treatment. J Refract Surg. 2001; 17:350-379.

3. Tahzib NG, Bootsma SJ, Eggink F, Nabar VA, Nuijts R. Functional outcomes and patient satisfaction after laser in situ keratomileusis for correction of myopia. J Cataract Refract Surg. 2005; 31:1943-1951.

4. Bailey MD, Mitchell L, Dhaliwal DK, Wachler B, Zadnik K. Patient Satisfaction and Visual Symptoms after Laser in Situ Keratomileusis. Ophthalmology. 2003; 110:1371-1378.

5. Jabbur NS, Sakatani K, O’Brien TP. Survey of complications and recommendations for management in dissatisfied patients seeking a consultation after refractive surgery. J Cataract Refract Surg. 2004; 30:1867-1874.

6. Pop M, Payette Y. Risk Factors for Night Vision Complaints after LASIK for Myopia. Ophthalmology. 2004; 111:3-10.

7. Klyce SD. Night Vision after LASIK: The Pupil Proclaims Innocence. Ophthalmology. 2004; 111:1-2.

8. Wilson SE. Wave-front analysis: are we missing something? Am J Ophthalmol. 2003; 136:340-342.

9. Fan-Paul NI, Li J, Miller JS, Florakis GJ. Night Vision Disturbances After Corneal Refractive Surgery. Surv Ophthal 2002; 47:533-546.

10. Chalita MR, Krueger RR. Correlation of aberrations with visual acuity and symptoms. Ophthalmol Clin N Am. 2004; 17:135-142.

11. Birgit L, Pieh S, Schmidinger G, Hanselmayer G, Simader C, Reitner A, Skorpik C. Glare and halo phenomena after laser in situ keratomileusis. J Cataract Refract Surg. 2003; 29:444-450.

12. Ambrosio R, Schallhorn SC, Wilson SE. The importance of pupil size (part I). Refractive Surgery Outlook. American Academy of Ophthalmology. Fall, 2002.

13. Ambrosio R, Schallhorn SC, Wilson SE. The importance of pupil size (part II). Refractive Surgery Outlook. American Academy of Ophthalmology. Winter, 2002.

14. Moreno-Barriuso E, Lloves JM, Marcos S, Navarro R, Llorente L, Barbero S. Ocular Aberrations before and after Myopic Corneal Refractive Surgery: LASIK-Induced Changes Measured with Laser Ray Tracing. Invest Ophthalmol Vis Sci. 2001; 42:1396-1403.

15. McCormick GJ, Porter J, Cox IG, MacRae S. Higher-Order Aberrations in Eyes with Irregular Corneas after Laser Refractive Surgery. Ophthalmology. 2005; 112:1699-1709.

16. Hersh PS, Fry KL, Bishop DS. Incidence and Associations of Retreatment After LASIK. Ophthalmology. 2003; 110:748-754.

17. Castanera J, Serra A, Rios C. Wavefront-guided Ablation With Bausch and Lomb Zyoptix for Retreatments After Laser in situ Keratomileusis for Myopia. J Refract Surg. 2004; 20:439-443.

18. Salz JJ. Wavefront-guided Treatment for Previous Laser in situ Keratomileusis and Photorefractive Keratectomy: Case Reports. J Refract Surg. 2003; 19:S696-S702.

19. Durrie DS, Stahl JE, Schwendeman F. Alcon LADARWave CustomCornea Retreatments. J Refract Surg. 2005; 21:S804-807.

20. Gimbel HV, Sofinski SJ, Mahler OS, van Westenbrugge JA, Ferensowicz MI, Triebwasser RW. Wavefront-guided Multipoint (Segmental) Custom Ablation Enhancement Using the NIDEK NAVEX Platform. J Refract Surg. 2003; 19:S209-S216.

21. Schwartz GS, Park DH, Lane SS. CustomCornea wavefront retreatment after conventional laser in situ keratomileusis. J Cataract Refract Surg. 2005; 31:1502-1505.

22. Chalita MR, Krueger RR. Alcon CustomCornea Wavefront-guided Retreatments After Laser in situ Keratomileusis. J Refract Surg. 2004; 20:S654-S660.

Pre- Post- Pre- Post- Enhancement, Enhancement, Enhancement, Enhancement, OD OD OS OS

Total HOA 1.35 0.5� 0.�5 0.�3

Spherical 0.�3 0.3� 0.60 0.30Aberration

Coma 1.05 0.1� 0.�2 0.25

Table 1.

Root mean square wavefront

aberrations.

11

Distinguished Lecture Series

The Cole Eye Institute Distinguished Lecture Series provides a forum for renowned researchers in the visual sciences to present their latest findings. This series of lectures features advances in many areas of ophthalmic research presented by noted basic and clinical scientists from throughout the world. Ample opportunity for questions and answers is provided.

All lectures are held on Thursdays from 7 to 8 a.m. in the James P. Storer Conference Room on the first floor of The Cole Eye Institute, Cleveland Clinic Foundation. Registration is not required. For questions, please call 216.444.5832.

May 1�, 2006

Ocular Surface Cell Dynamics

M. Elizabeth Fini, Ph.D. Professor and Scientific Director Bascom Palmer Eye Institute Walter G. Ross Chair in Ophthalmic Research University of Miami, Miller School of Medicine Miami, FL

June �, 2006

Molecular Basis of Corneal Clarity and Avascularity

Dimitri T. Azar, M.D. Associate Chief of Ophthalmology Director of Cornea, External and Refractive Surgery Harvard Medical School Massachusetts Eye and Ear Infirmary Boston, MA

July 20, 2006

Cellular Remodeling of the Retina in Response to Detachment

Steven K. Fisher, Ph.D. Professor Department of Molecular, Cellular and Developmental Biology Neuroscience Research Institute University of California, Santa Barbara Santa Barbara, CA

September 1�, 2006

Pathogenic Mechanisms in Uveoretinitis

John V. Forrester, M.D. Cockburn Professor and Head Department of Ophthalmology University of Aberdeen Institute of Medical Sciences Foresthill Aberdeen, Scotland

October 1�, 2006

Circadian Clocks and Neuromodulators in the Retina

P. Michael Iuvone, Ph.D. Professor Department of Pharmacology Emory University Atlanta, GA

November 16, 2006

Making Sense of Neuronal Diversity: A Bottom-Up View of the Retina

Richard H. Masland, Ph.D. Charles A. Pappas Professor of Neuroscience Harvard Medical School Investigator, Howard Hughes Medical Institute Boston, MA

Physicians are cordially invited to attend

the following ophthalmic continuing

medical education courses at The Cleve-

land Clinic Cole Eye Institute. All courses

will be held in the James P. Storer Con-

ference Center on the first floor.

For more information, contact Jane Sardelle, program coordinator, at 216.���.2010 or �00.223.22�3, ext. �2010, or sardelj@ccf.org.

Programs In Ophthalmic Education

2005-2006

12

New Developments in Retina: Trials, Drugs and New Techniques

Saturday, May 20, 2006 �:00 a.m. to 5:00 p.m.

Course Directors: Peter K. Kaiser, M.D. Vitreoretinal Department Cole Eye Institute

Jonathan E. Sears, M.D. Vitreoretinal Department Cole Eye Institute

Cole Eye Institute Faculty: Hilel Lewis, M.D. Chairman and Director

Andrew P. Schachat, M.D. Vice Chairman for Clinical Affairs

Rishi P. Singh, M.D. Vitreoretinal Fellow

Rafael L. Ufret-Vincenty, M.D. Vitreoretinal Fellow

Guest Faculty: Allen C. Ho, M.D. Professor of Ophthalmology Thomas Jefferson University Retina Service Wills Eye Hospital Philadelphia, PA

Jason S. Slakter, M.D. Vitreous-Retina-Macula Consultants of New York Clinical Professor of Ophthalmology New York University New York, NY

Description: This meeting is designed for retinal specialists and general ophthalmologists who diagnose and treat retinal disease. The lectures will update participants on the newest clinical trials in retina, especially in age-related macular degeneration and diabetic retinopathy. In addition, faculty members, who are all experts in the field of retina, will offer current treatment options for vitreoretinal conditions normally seen in clinical practice with particular emphasis on the newly released drugs.

Objectives: At the conclusion of this course, participants should be able to:

1. Describe recent clinical trials in age-related macular degeneration and diabetic retinopathy. 2. Distinguish the differences between the new anti-VEGF drugs. 3. Compare various treatment modalities and clinical trial results. 4. Describe the use of steroids in age-related macular degeneration and diabetic retinopathy. 5. Explain how new imaging devices are enhancing retinal diagnosis.

Registration fee: $100. Receive a $25 discount by registering online.

Annual Research, Residents & Alumni Meeting

Thursday, June 15, 2006 (Poster Reception) 5:00 p.m. to �:30 p.m.

Friday, June 16, 2006 (Meeting/Graduation Ceremony) �:00 a.m. to midnight

Course Directors: Hilel Lewis, M.D. Chairman, Division of Ophthalmology Director, Cole Eye Institute

Careen Y. Lowder, M.D., Ph.D. Uveitis Department Cole Eye Institute

Keynote Speaker: Paul R. Lichter, M.D. F. Bruce Fralick Professor of Ophthalmology Chair, Department of Ophthalmology and Visual Sciences Director, University of Michigan Kellogg Eye Center Ann Arbor, MI

Description: This program provides a scientific forum to present clinical and basic science research of the Cole Eye Institute residents, fellows, staff, alumni and invited ophthalmologists.

The goal of this meeting is to pursue and present the highest-quality, original, thought-provoking clini-cal research papers. In addition to the educational aspects of the program and learning about new and ongoing investigations, this event offers an excellent opportunity to meet current residents, fellows, new faculty and invited ophthalmologists and to make and renew friendships.

Objectives: At the conclusion of this course, participants should be able to:

1. Recognize the most up-to-date concepts and treatments in research and clinical ophthalmology. 2. Identify current basic science research in age-related macular degeneration. 3. Explain the rationale and status of the most current treatments for uveitic and diabetic macular edema. 4. Discuss outcomes of complicated glaucoma and cataract surgery. 5. Describe the latest techniques in refractive surgery.

Registration fee: $100. Receive a $25 discount by registering online.

Programs In Ophthalmic Education

2005-2006

13

CLINICAL TRIALSThe following studies are currently enroll-ing. All studies have been approved by the Institutional Review Board. Genetics

Studies of the Molecular Genetics of Eye Diseases

Objective: To map the genes for inherited eye diseases. To screen candidate genes for mutations in a variety of genetic ocular disorders, including ocular malformations, congenital cataracts and retinal dystrophies. Contact: E. Traboulsi, M.D., at 216.444.4363 or S. Crowe, C.O.T., at 216.445.3840 The Genetics of Strabismus

Objective: To discover the genes that cause some strabismus syndromes, including those for accommodative esotropia, con-genital esotropia, congenital ocular fibrosis syndrome, intermittent exotropia, Brown syndrome and Duane syndrome. Contact: E. Traboulsi, M.D., at 216.444.4363 or S. Crowe, C.O.T., at 216.445.3840 Pediatrics

Infant Aphakia Treatment Study

Objective: To determine whether infants with a unilateral congenital cataract are more likely to develop better vision follow-ing cataract extraction surgery if (1) they undergo the primary implantation of an IOL or (2) they are treated primarily with a contact lens. Contact: E. Traboulsi, M.D., at 216.444.4363 or S. Crowe, C.O.T., at 216.445.3840 Retinal Diseases

Protocol B�A-MC-MBDL Reduction in the Occurrence of Center-Threatening Diabetic Macular Edema

Objective: The primary objective of this study is to test the hypothesis that oral administration of 32 mg per day of ruboxistaurin for approximately 36 months will reduce, relative to placebo, the oc-currence of center-threatening diabetic macular edema as assessed by fundus photography in patients with non-clinically significant macular edema and nonprolif-erative diabetic retinopathy at baseline. Contact: P. Kaiser, M.D., at 216.444.6702 or L. Schaaf, R.N., at 216.445.4086

Protocol B�A-MC-MBCU The Effect of Ruboxistaurin on Clinically Significant Macular Edema in Patients with Dia-betes Mellitus, as assessed by Optical Coherence Tomography

Objective: The primary objective of this study is to test the hypothesis that oral administration of 32 mg per day of ruboxistaurin for 18 months will reduce the baseline to endpoint changes in central macular thickness, as measured by OCT in patients with CSME. Contact: P. Kaiser, M.D., at 216.444.6702 or L. Schaaf, R.N., at 216.445.4086 A Six-Month Phase 3, Multicenter, Masked, Randomized, Sham-Con-trolled Trial (with Six-Month Open-Label Extension) to Assess the Safety and Efficacy of 700 μg and 350 μg Dexamethasone Posterior Segment Drug Delivery System

Objective: To evaluate the safety and efficacy of the 700 μg DEX PS DDS Ap-plicator System and 350 μg DEX PS DDS Applicator System compared with a Sham DEX PS DDS Applicator System (needle-less applicator) for six months in patients with macular edema following branch retinal vein occlusion or central retinal vein occlusion. The safety of the 700 μg DEX PS DDS Applicator System will be assessed for an additional 6 months in patients who qualify for treatment in an open-label safety extension. Contact: P. Kaiser, M.D., at 216.444.6702 or L. Schaaf, R.N., at 216.445.4086 A Randomized Trial Comparing Intra-vitreal Triamcinolone Acetonide and Laser Photocoagulation for Diabetic Macular Edema

Objective: To determine whether intravit-real triamcinolone acetonide injections at doses of 1 mg or 4 mg produce greater benefit, with an acceptable safety profile, than macular laser photocoagulation in the treatment of diabetic macular edema.Contact: P. Kaiser, M.D., at 216.444.6702 or L. Holody, C.O.A., at 216.445.3762

A 3-Year, Phase 3, Multicenter, Masked, Randomized, sham-Controlled Trial to Assess the Safety and Efficacy of �00 μg and 350 μg Dexamethasone Posterior Segment Drug Delivery Sys-tem (DEX PS DDS) Applicator System in the Treatment of Patients with Diabetic Macular Edema

Objective: To evaluate the safety and efficacy of the 700 μg DEX PS DDS Ap-plicator System and 350 μg DEX PS DDS Applicator System compared with a Sham DEX PS DDS Applicator System (needle-less applicator) in patients with diabetic macular edema. Contact: P. Kaiser, M.D., at 216.444.6702 or L. Schaaf, R.N., at 216.445.4086 A Phase IIIb, Multicenter Study To Evaluate the Safety and Tolerability of Ranibizumab in Naïve and Previ-ously Treated Subjects with Choroidal Neovascularization Secondary to Age-Related Macular Degeneration

Objective: To estimate the incidence of ocu-lar and non-ocular serious adverse events in subjects treated for 12 months with 0.3 mg or 0.5 mg intravitreal ranibizumab. Contact: P. Kaiser, M.D., at 216.444.6702 or Lynn Bartko, R.N., at 216.444.7137

Glaucoma

Advanced Imaging for Glaucoma

Objective: Advanced Imaging for Glaucoma (AIG) is a multi-center bioengineering partnership sponsored by the National Eye Institute to develop advanced imaging technologies to improve the detection and management of glaucoma. The advanced imaging technologies include optical coherence tomography, scanning laser polarimetry and scanning laser tomography. The technologies will be evaluated in a longitudinal five-year clinical trial composed of glaucoma suspects, glaucoma patients and normal subjects. Contact: S. Smith, M.D., M.P.H., at 216.444.4821 or L. Holody, C.O.A., at 216. 445.3762

1�

Cole Eye InstituteStaffHilel Lewis, M.D. Chairman, Division of Ophthalmology Director, Cole Eye Institute Specialty/Research Interests: Vitreoretinal surgery for complicated retinal detach-ment and trauma, age-related macular degeneration, diabetic retinopathy, retinal photocoagulation, instrument development

Bela Anand-Apte, M.B.B.S., Ph.D. Ophthalmic Research Department Research Interest: Angiogenesis

John W. Crabb, Ph.D. Ophthalmic Research Department Research Interests: Age-related macular degeneration, inherited retinal diseases

Marc A. Feldman, M.D. Ophthalmic Anesthesia Specialty Interests: Ophthalmic surgery anesthesia, preoperative assessment, resident education

Richard E. Gans, M.D., F.A.C.S. Comprehensive Ophthalmology Department Specialty Interests: Cataract, glaucoma, diabetes

Philip N. Goldberg, M.D. Comprehensive Ophthalmology Department Specialty Interests: Cataract, glaucoma

Froncie A. Gutman, M.D. Vitreoretinal Department Specialty Interests: Retinal vascular dis-eases, laser therapy, diabetic retinopathy

Stephanie A. Hagstrom, Ph.D. Ophthalmic Research Department Research Interests: Inherited forms of retinal degeneration, including macular degeneration and retinitis pigmentosa

Joe G. Hollyfield, Ph.D. Ophthalmic Research Department Research Interests: Retinal degeneration, retinal diseases

Bennie H. Jeng, M.D. Cornea and External Disease Department Specialty/Research Interests: Corneal transplantation, ocular surface disease, limbal stem cell transplantation, artificial corneas, eyebanking, cataracts

Peter K. Kaiser, M.D. Vitreoretinal Department Specialty/Research Interests: Vitreoretinal diseases, age-related macular degenera-tion, retinal detachment, diabetic retinopa-thy, endophthalmitis, posterior segment complications of anterior segment surgery

Gregory S. Kosmorsky, D.O. Neuro-Ophthalmology Department Specialty Interests: Neuro-ophthalmology, cataract, refractive surgery

Ronald R. Krueger, M.D., M.S.E. Refractive Surgery Department Specialty/Research Interests: Refractive surgery, lasers, refractive corneal pathology, lamellar corneal transplants, investigational clinical trials

Roger H.S. Langston, M.D. Cornea and External Disease Department Specialty Interests: Cornea and external disease, corneal transplantation

Careen Y. Lowder, M.D., Ph.D. Uveitis Department Specialty/Research Interests: Uveitis, intraocular inflammatory diseases, pathology

Andreas Marcotty, M.D. Pediatric Ophthalmology and Strabismus Department Specialty Interests: Pediatric ophthalmology, adult strabismus

Shari Martyn, M.D. Comprehensive Ophthalmology Department Specialty Interests: Cataract, glaucoma, diabetes

David M. Meisler, M.D. Cornea and External Disease Department Specialty/Research Interests: Corneal and external disease, inflammatory and infectious diseases of the cornea, corneal transplantation, refractive surgery

Michael Millstein, M.D. Comprehensive Ophthalmology Department Specialty Interests: Cataract, glaucoma, refractive surgery

Neal S. Peachey, Ph.D. Ophthalmic Research Department Research Interests: Visual loss associated with hereditary retinal degeneration

Victor L. Perez, M.D. Cornea and External Disease Department Specialty/Research Interests: Cornea and external diseases, uveitis, medical and surgical treatment of autoimmune inflam-matory conditions of the cornea and ocular surface

Julian D. Perry, M.D. Oculoplastic and Orbital Surgery Department Specialty/Research Interests: Aesthetic facial surgery/fat transplantation and repositioning, acellular human dermal graft matrix, new bovine hydroxyapatite orbital implant, thyroid eye disease/rate of strabismus after decompression surgery for dysthyroid orbitopathy

Edward J. Rockwood, M.D. Glaucoma Department Specialty/Research Interests: Glaucoma, glaucoma laser surgery, combined cataract and glaucoma surgery, glaucoma filtering surgery with antimetabolite therapy, glaucomatous optic nerve damage, congenital glaucoma

Allen S. Roth, M.D. Comprehensive Ophthalmology Department Specialty Interests: Corneal transplanta-tion, refractive surgery, cataract and implant surgery

Andrew P. Schachat, M.D. Vitreoretinal Department Vice Chairman for Clinical Affairs Specialty/Research Interests: Age-related macular degeneration, diabetic retinopathy, medical retina

Jonathan E. Sears, M.D. Vitreoretinal Department Specialty/Research Interests: Pediatric and adult vitreoretinal diseases, pediatric retinal detachment, inherited vitreoretinal disorders, retinopathy of prematurity, other acquired proliferative diseases

David B. Sholiton, M.D. Comprehensive Ophthalmology Department Specialty Interests: Cataract and implant surgery, glaucoma, oculoplastics

Arun D. Singh, M.D. Ophthalmic Oncology Department Specialty/Research Interests: Adult and pediatric ocular tumors, uveal mela-noma, genetics of retinoblastoma, retinal capillary hemangioma, von Hippel-Lindau disease

Scott D. Smith, M.D., M.P.H. Glaucoma Department Specialty/Research Interests: Glaucoma, cataract, prevention of eye disease, international ophthalmology, congenital glaucoma

Elias I. Traboulsi, M.D. Pediatric Ophthalmology and Strabismus Department Center for Genetic Eye Diseases Specialty/Research Interests: Ocular diseases of children, genetic eye diseases, strabismus, retinoblastoma, congenital cataracts, childhood/congenital glaucoma

Steven E. Wilson, M.D. Cornea and External Disease and Refractive Surgery Departments Specialty/Research Interests: Refractive surgery, corneal healing

216.���.2020 The Cleveland Clinic Cole Eye Institute

15

Andrew P. Schachat, M.D., Joins Cole Eye Institute Staff

Andrew P. Schachat, M.D., has joined The Cole Eye Institute as vice chairman for clinical affairs.

Dr. Schachat, a specialist in medical retina, has been on the staff of the Wilmer Ophthalmological Institute at Johns Hopkins University in Baltimore since 1984. He is editor-in-chief of Ophthalmology, the journal of the American Academy of Ophthalmology.

“We are thrilled to have recruited such a pre-eminent ophthalmologist to join our staff,” says Hilel Lewis, M.D., chairman of the Cole Eye Institute. “He will provide valuable guidance to help the clinical staff achieve even greater success and will be an excellent addition to our retina service as well.”

Dr. Schachat explains that he was attracted to Cleveland Clinic by Dr. Lewis’ commitment to excellence in all areas.

“As I have watched the Cole Eye Institute, I have been very impressed by the staff as well as the residents and fellows,” he says. “It is clear that this is developing into the leading clinical ophthalmology program in the world.”

“I am eager to work with the team and do whatever is needed to contribute to their overall success. I also look forward to the opportunity to focus more on clinical affairs and help continue the recruitment of world-class faculty,” he adds. “This is a wonderful opportunity.”

Dr. Schachat completed a vitreoretinal and oncology fellowship at Wills Eye Hospital in Philadelphia in 1983, completed his residency at Wilmer in 1982 and graduated from the Johns Hopkins University School of Medicine in 1979.

He has previously served as the American Academy of Ophthalmology’s Secretary for Quality Care (1996-2001) as well as on many other Academy committees, including the EyeNet Editorial Advisory Board, the Bylaws and Rules Committee, the Outcomes Program Committee and the Basic and Clinical Science Course Committee. He was previously associate editor of Archives of Ophthalmology. He received the Academy’s Senior Honor Award in 1998 and has published numerous books and book chapters and more than 240 journal articles.

He is a member of many organizations, including the American Academy of Ophthalmology, Macula Society, Retina Society, American Society of Retina Specialists, Association for Research in Vision and Ophthalmology, Pan American Association of Ophthalmology, American Medical Association, Society of Heed Fellows, Wills Fellows Association and Wilmer Residents Association. He is a past president of the Maryland Society of Eye Physicians and Surgeons.

Andrew P. Schachat, M.D.

Ophthalmology Update, a publication of The Cleveland Clinic Cole Eye Institute, provides information for ophthalmologists about state-of-the-art diagnostic and man-agement techniques and current research.

Please direct any correspondence to:

Steven E. Wilson, M.D. Cole Eye Institute / i32 The Cleveland Clinic Foundation 9500 Euclid Avenue Cleveland, Ohio 44195

Phone 216.444.5887 Fax 216.445.8475

Director and Division Chairman Hilel Lewis, M.D.

Editor-in-Chief Steven E. Wilson, M.D.

Editorial Board Julian D. Perry, M.D. Jonathan E. Sears, M.D.

Managing Editor Beth Thomas Hertz

Art Director Barbara Ludwig Coleman

Photographers Don Gerda Deborah Ross, C.R.A.

The Cleveland Clinic Foundation is an indepen-dent, not-for-profit, multispecialty academic medical center. It is dedicated to providing quality specialized care and includes an outpatient clinic, a hospital with more than 1,000 available beds, an education division and a research Institute.

Ophthalmology Update is written for physicians and should be relied upon for medical education purposes only. It does not provide a complete overview of the topics covered and should not replace the independent judgment of a physician about the appropriateness or risks of a procedure for a given patient.

Physicians who wish to share this information with patients need to make them aware of any risks or potential complications associated with any procedures.

© The Cleveland Clinic Foundation 2006

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