• Chief, Glaucoma division, Jules Stein Eye Institute, Los Angeles,
1997 to present
• David May II Professor of Ophthalmology, UCLA School of Medicine,
Los Angeles, 2004 to present
• Recipient of the Jules Francois Prize of the Belgian Ophthalmological Society for research on optic nerve damage in glaucoma, 1989
• Principal Investigator of Clinical Measurements of Optic Nerve Damage in Glaucoma
(R01-EY12738), 2001 to 2006
• Recipient of the AAO's Senior Achievement Award (1999), Secretariat Award (2004), and Certificate of Appreciation for outstanding contributions to quality care (2005)
• Chair, the AAO's Quality of Care Committee Glaucoma Panel, 1991 to 2000
• Member of the ARVO Program Committee, Glaucoma Section, 1997 to 2000
• Chair, AAO's Preferred Practice Committee, 2000 to 2005
1. How did your training under Marvin Sears, MD, and George Spaeth, MD,
affect your career path?
The founder and first chair of the Yale School of Medicine's Department of Ophthalmology and Visual Science, Marvin taught me the foundations of both clinical and investigative science. He was a brilliant physiologist and pharmacologist and an astute observer. Marvin taught me how to make the important observations, and he showed me how to translate them into improved patient care or into new avenues of research and discovery.
The director of the glaucoma service at Wills Eye Hospital in Philadelphia, George Spaeth is a superb clinician and surgeon. He taught me how to take care of patients by first listening to them. My career-long interest in the optic nerve in glaucoma was sparked by my year of fellowship with him and our subsequent interactions.
Both of these mentors set me squarely on an academic career path.
2. Why did you direct your early research to glaucomatous optic nerve damage?
During my years of training, the focus of glaucoma care and investigation shifted away from the anterior segment and IOP toward the optic nerve. This change was both in terms of diagnosis and treatment. It became apparent that glaucoma was a complicated disease, indeed a heterogeneous set of diseases for which the final common pathway is optic nerve damage that we call glaucoma. It is important to begin to understand the mechanisms that cause that damage so we can begin to approach the disease in a more fundamental way—by directly treating the molecular mechanisms of retinal ganglion cells' death.
3. What do you think the future holds for the earlier detection of glaucomatous
damage to tissue?
We have made important improvements over the past 2 decades in terms of recognizing early glaucomatous damage to the optic nerve. Quantifiable measurements of optic nerve damage with contemporary imaging techniques have highlighted this improvement. We now have the ability to recognize small amounts of progressive impairment. The importance of future investigations will not focus on how early we can recognize damage, but rather on which patients will have damage that progresses the fastest and when we should begin treatment.
4. Do you think that subjective psychophysical testing will become passé?
This form of testing will be with us for a long time. The promise of objective testing is attractive, but there are many problems related to it that need to be solved. It is still a very “noisy” test, even more so than subjective testing at present.
5. What three pearls would you impart to today's ophthalmology residents
and glaucoma fellows?
First, never lose your passion for learning. Second, always put the patient first. Third, listen to your patients; only then will you be able to communicate the information and provide the care that they really need.
