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Volume
2, Number 2 |
March
2007
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OGS
PRESIDENT'S MESSAGE
In
this issue of the OGS e-journal, we describe fascinating work that was
recently published in Investigative Ophthalmology and Vision Science
(IOVS) by Algis Vingrys and colleagues. The work considered whether
dietary modification of polyunsaturated fatty acid intake can affect
intraocular pressure (IOP). While clinicians have hypothesized such
effects for some time, Vingrys’ work, which was performed in a
rat model, provides direct evidence for how this can be achieved. We
all are well aware of the role that diet and vitamin supplements play
in the management of macular degeneration. It is not inconceivable that
we may someday find ourselves encouraging individuals at risk for glaucoma
to consume more fish in order to enhance their Omega 3 fatty acid intake.
Algis is an associate editor of this journal, and, with two of his co-authors
Bui and Nguyen, is based at the Department of Optometry, University
of Melbourne, Australia. This latest work serves to underscore the increasingly
important contributions being made by optometry in the field of glaucoma
research. In the same issue of IOVS, Ron Harwerth and colleagues describe
their work exploring the relationship between the retinal nerve fiber
layer and perimetry. Ron is also a member of this society and performed
his work at the University of Houston, College of Optometry.
As encouraging and stimulating as these works are, we also must remember
that glaucoma research within Optometry frequently has been under recognized
and under funded. This year, the Optometric Glaucoma Society, in partnership
with the American Optometric Foundation has established an Ezell Fellowship
program that will for the first time provide direct support for post-graduate
research in glaucoma. This is a new direction for Optometry and one
that promises to affect future patient care.
One measure of how a profession is developing is its contributions to
the knowledge base underlying its sphere of practice. Optometry has
made many important contributions in binocular vision, contact lenses,
and ocular surface disease, to name a few. It is only in recent years
that vision scientists such as Drs. Vingrys and Harwerth have received
international recognition as contributors to the glaucoma literature,
and these achievements have been realized with a minimum of support
from our profession. This new fellowship will help develop the young
men and women who will sustain and further our knowledge base in glaucoma,
to the benefit of our patients.
In order to endow an Ezell Fellowship, the OGS must raise $200,000.
We hope to achieve this through individual and corporate donations.
We are especially reaching out to members of the optometric profession
for support. Donations should be made payable to the American Optometric
Foundation, specifying that the funds are sent in support of the OGS-Ezell
Fund, and mailed to the American Optometric Foundation, 6110 Executive
Blvd. Suite 506, Rockville, MD 20852. All contributions are tax deductible.
Additional information on the Ezell Fellowship program is available
at http://www.aaopt.org:80/aof/scholarship/ezell/index.asp
as well as on the Optometric Glaucoma Society website.
Please join us in supporting this important new step for the OGS, for
Optometry, and for our patients.
Murray Fingeret, OD
President, Optometric Glaucoma Society
murrayf@optonline.net
EDITORIAL
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Defining
Diagnostic Limitations
When a disease or at-risk state is present, arriving at and recording
a diagnosis is a fundamental part of an eye examination. The diagnosis
is important because it clarifies the eye condition(s) present and provides
information for stakeholders in the patient’s care, which is used
in part to guide subsequent management.
Establishing an accurate diagnosis can be aided by considering a number
of key rules. Firstly, sufficient clinical evidence should be available
to reasonably exclude other differential diagnoses. For example, a diagnosis
of pigmentary glaucoma cannot be made if the associated anterior signs
are not detected.
Secondly, a clear and current definition for the condition is required
to ensure that the clinical evidence fits the diagnosis. For some time,
a frequently-used definition for primary open angle glaucoma (POAG) was,
"a slowly progressive optic atrophy, characterized by midperipheral
visual field loss and excavated appearance of the optic disc" (1).
This definition worked at the time because it conceptualised what were
considered to be the 4 key features of POAG (slowly progressive, optic
nerve disease, characteristic ONH appearance and characteristic loss of
visual function). However, with increasing knowledge, definitions used
for disease can change. A commonly used current definition is "a
multifactorial optic neuropathy in which there is characteristic atrophy
of the optic nerve head" (2).
Thirdly, it is important to understand the limitations of a diagnosis.
At any point in time, there will always be debate about how to define
a condition, including POAG (3,4). A limitation of the older definition
stated above is that evidence exists demonstrating that early POAG is
not only associated with midperipheral loss, but central losses also (5,6,7).
More importantly, we now know that in early glaucoma, pathological changes
can occur at the optic nerve head without associated loss of visual function,
at least as measured by current conventional tests. A limitation of the
common current definition may be that it does not contain the requirement
for the condition to be progressive, on the basis that apparent early
optic nerve head characteristics that remain unchanged cannot represent
disease. Taking this into consideration, a more appropriate definition
for POAG is a multifactorial optic neuropathy in which there is characteristic
and progressive atrophy of the optic nerve head.
Finally, initial diagnoses can be incorrect or may have been complicated
by the fact that more than a single disease was present. Just because
a diagnosis has already been made, this does not mean it cannot be revised
when new or additional evidence becomes available. In clinical situations,
open-minded clinicians question diagnoses at each follow-up examination,
especially when new information becomes available. Of course, this can
also mean that if the definition for a disease changes, so can the diagnosis.
Paul GD Spry, PhD, BSc, MCOptom DipGlauc
Editor-in-Chief
paul.spry@ubht.nhs.uk
References
1. Quigley HA, Vitale S (1997). Models of Open-angle glaucoma prevalence
and incidence in the United States. Investigative Ophthalmology and Visual
Science; 38(1): 83 - 91.
2. Rand Allingham et al. (2005) Shields Textbook of Glaucoma. 5th edition.
Lippincott, Williams and Wilkins, Philadelphia, USA.
3. Bathija R, Gupta N, Zangwill L, Weinreb RN (1998). Changing definition
of glaucoma. J Glaucoma; 7(3):165-9.
4. Kroese M, Burton H (2003). Primary open angle glaucoma. The need for
a consensus case definition.J Epidemiol Community Health. ;57(9):752-4.
5. Piltz JR, Swindale NV, Drance SM. (1993). Vernier thresholds and alignment
bias in control, suspect and glaucomatous eyes. J Glaucoma; 2: 87-95.
6. McKendrick AM, Johnson CA, Anderson AJ, Fortune B (2002). Elevated
vernier acuity thresholds in glaucoma. Invest Ophthalmol Vis Sci; 43(5):1393-9.
7. Kanadani FN et al. (2006). Structural and functional assessment of
the macular region in patients with glaucoma. Br J Ophthalmol; 90 (11):
1393-7.
NEW
IDEAS AND PAPERS
Diets Deficient in
Omega-3 Fatty Acids Result in Higher Intraocular Pressure
The recent study by Nguyen et al. (1) considers the role that
dietary Omega-3 fatty acid modification may have in glaucoma management.
This study is important because it evaluates the impact that a simple
life-style modification i.e. dietary intake of Omega-3 fatty acid rich
foods, can have on intraocular pressure (IOP), which is widely recognized
to be the major modifiable risk factor for glaucoma.
These researchers showed that when rats were raised on diets very deficient
in Omega-3 fatty acid, this resulted in a 13-23% IOP elevation as
animals aged. To put this value in perspective, it is similar in magnitude
to the effect produced by some glaucoma medications. Moreover, this
study showed that the higher IOP in Omega-3 deficient animals probably
resulted from a higher resistance to aqueous outflow. As clinicians,
we may be faced with the alluring possibility that dietary modification
can be used to complement the IOP lowering induced by aqueous suppressants.
This work, taken with Japanese epidemiological data, might suggest that
a life-long diet high in Omega-3 fatty acids may reduce the risk of
developing high IOP later in life.
As is the case with all research there are some caveats to consider.
The main finding in this study was that a difference in IOP and outflow
facility existed between animals that had sufficient versus extremely
deficient dietary Omega-3 fatty acids. It did not compare animals with
sufficient versus supplemented Omega-3 levels. Just how much dietary
Omega-3 is needed to prevent one from being deficient? The authors acknowledge
this by stating, "… future studies will have to determine
the dose response for Omega-3 dietary intake on IOP." It also did
not directly address the effect of dietary Omega-3 fatty acids on glaucoma
per se - these animals did not have experimental glaucoma. Although
one would assume that lower IOPs should mean less risk of glaucoma development,
or glaucomatous progression, this remains to be determined. One final
point is that fish, particularly oily fish, are not the only source
of Omega-3 fatty acids. Interestingly, oily fish become high in Omega-3
by being at the top of a food chain that has algae low on the totem
pole. Leafy green vegetables may also be high in Omega-3 and simultaneously
low in Omega-6. Flax seed, meat from grass fed animals (possibly also
the milk & cheese from such grazers) and eggs from free-range chickens
eating lots of insects and greens may also contain Omega-3s, though
these are of the "shorter-chain" variety (alpha-linolenic
acid).
Shaban Demirel BScOptom, PhD
Brad Fortune OD, PhD
References
1.Nguyen CT, Bui BV, Sinclair AJ, Vingrys AJ (2007). Dietary omega 3
Fatty acids decrease intraocular pressure with age by increasing aqueous
outflow. Invest Ophthalmol Vis Sci; 48(2):756-62.
OPTIC
NERVE REVIEW
Disc
Hemorrhage in Glaucoma
Steven Drance first described a disc hemorrhage as a sign of glaucoma
damage back in the 1970’s. The funduscopic appearance is typically
that of a flame shaped hemorrhage within one disc diameter of the optic
nerve. These hemorrhages are usually located superficially in the superior
temporal or inferior temporal nerve fiber layer, the location where glaucoma
damage is most prevalent. If the hemorrhage is located on the optic nerve
head, the appearance is more blot-like rather than flamed shaped.
Figure 1. Inferior
temporal disc hemorrhage in a glaucoma suspect. The presence
of a disc hemorrhage in a glaucoma suspect indicates glaucoma
damage and the need for treatment.
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Figure 2. Red-free
photo of same patient in figure 1 six weeks later. Note resolution
of disc hemorrhage with the appearance of a wedge defect in
the retinal nerve fiber layer. This patient developed a new
superior visual field defect.
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The etiology of a disc hemorrhage in glaucoma is debatable. The ischemic
theory suggests that the hemorrhage is the result of a microvascular infarct
to the optic nerve. The mechanical theory proposes a shift in the blood
vessel from loss of neural-retinal rim tissue as the cause the hemorrhage.
From a clinical perspective, the appearance of a new disc hemorrhage in
a glaucoma or glaucoma suspect patient is a cause for concern. It provides
strong evidence to initiate treatment in a glaucoma suspect patient and
to intensify treatment in an established glaucoma patient (1).
The incidence of disc hemorrhage in glaucoma patients varies from 2-23%.
They are more common in patients with normal tension glaucoma than high
tension glaucoma. Clearly, disc hemorrhages are transient in nature and
will resolve in 4-8 weeks after their initial occurrence. Therefore many
disc hemorrhages are missed because our follow up intervals exceed the
longevity of the hemorrhage. Because both the presence of disc hemorrhages
and their frequency of occurrence are associated with progressive damage,
it is important to view the optic nerve of all glaucoma patients at their
follow up visits.
Figure 3. The
appearance of a new disc hemorrhage (superior) in a glaucoma
patient suggests progressive damage and the need to intensify
treatment or scrutinize for non-compliance with medications.
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Figure
4. Blot hemorrhage on the optic nerve in a patient with an acute
posterior vitreous detachment. This type of hemorrhage can mimic
a Drance hemorrhage.
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Although cross-sectional population studies have demonstrated the strong
association between disc hemorrhages and prevalent glaucoma, they also
were found in patients without definite glaucoma (2). It is likely that
some of these individuals may be new, incident glaucoma cases or patients
with established but early disease, in which haemorrhages precede other
glaucomatous disc signs or visual field loss. Disc hemorrhages not related
to glaucoma may be seen in patients with diabetes, hypertension and other
vasculopathies. The presence of addition retinal hemorrhages, exudates
or cotton wool spots throughout the posterior pole differentiates them
from a Drance hemorrhage. Anterior ischemic optic neuropathy may also
present with disc hemorrhages, however swelling of the optic nerve in
association with sudden vision loss is also present. Finally, patients
who present with posterior vitreous detachments may also develop a disc
hemorrhage when the vitreous separates from the optic nerve (3). However,
these patients will report a recent onset of floaters.
Anthony B. Litwak, OD, FAAO
Reference
1. Kim SH, Park KH (2006). The relationship between recurrent optic disc
hemorrhage and glaucoma progression. Ophthalmology; 113: 598-602.
2 .Healey PR, Mitchell P, Smith W, Wang JJ (1998). Optic Disc Hemorrhages
in a Population with and without Signs of Glaucoma. Ophthalmology 1998;
105: 216-223.
3. Horton RO, Potter JW, Semes LP (1985). Peripapillary hemorrhages in
acute posterior vitreous detachment. J Am Optom Assoc.; 56: 937-9.
VISUAL
FIELD REVIEW
Perimetric Artifacts
The visual fields in this issue show three classic artifacts that clinicians
may encounter during testing.
The first shows the effect that improper positioning of the trial lens
can have on field results. I call this a "keyhole effect"
because it resembles the field restriction produced when peaking into
a keyhole. This outcome will result when the trial lens is positioned
too far away from the patient OR when either the lens or the patient
is not centrally aligned. In either case the edge of the correcting
lens clips the patient’s field of view and creates an artifactual
field loss at the edge. It can be manifest as a depression affecting
the entire circumference of the visual field or as a loss to one side
or other, as shown in Figure 1. Some of these artifacts can arise during
testing even after the proper placement of the trial lens, if the patient
is allowed to either drop their shoulder (loss of centre line) or retract
their head from the forehead rest by pivoting about their chin. The
result given in Figure 1 needs to be differentiated from the temporal
loss found in glaucoma and shown in an previous
issue of this journal.
Figure 1.
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Figure 2.
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Figure 3.
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The second artifact (Figure 2) demonstrates an inverse ‘clover
leaf’ or ‘cauliflower’ pattern typical of a patient who
has a functional loss or shows a learning effect. The nature of the
loss reflects the interaction of the testing sequence with the learning
or functional process. In terms of learning, patients who are slow in
getting going have depressed sensitivity values at the primary seed
points (9 degrees in each quadrant). Dependent on how fast they pick-up
what is required of them, the secondary neighboring points will also
be depressed and so on. Eventually the patient will reach their normal
dB-level to yield this inverse clover leaf pattern. This pattern is
the opposite of the more conventional clover-leaf whereby patients start
off the test with ‘normal’ sensitivity values at primary seed
points. As they become inattentive (bored) or fatigued, their performance
declines yielding lower sensitivity values at subsequent test locations.
As with the inverse clover-leaf described above, the time point at which
this occurs determines how this will affect the test result. Figure
3 is an example where the patient lost attention soon after testing
of the primary seed points was complete.
In terms of learning effects, the seminal paper on this issue comes
from Wood et al. (1) who reported that patients will fall into four
groups, those who are: (A) instantly reliable, (B) reliable after doing
one eye, (C) reliable after about 4-5 tests, and (D) never reliable,
where reliable means maximal and stable dB values.
Algis Vingrys BScOptom, PhD
Reference
1. Wood JM, Wild JM, Hussey MK, Crews SJ (1987). Serial examination
of the normal visual field using Octopus automated projection perimetry.
Evidence for a learning effect. Acta Ophthalmol; 65(3): 326-33.
IMAGE
REVIEW
These
images are from a 62 year old white male who presented for a comprehensive
examination. With correction, his visual acuity was 20/20 in each eye.
The patient denied any history of ocular disease or trauma. His last
eye examination was 2 years ago and was given a clean bill of health.
At
the onset of this exam, an FDT N30-5 screening field was performed which
was full in each eye. The intraocular pressure was 15 mm Hg OD and 16
mm Hg OS. The cup/disc ratio (CDR) was relatively large, along with
a difference in CDR between the eyes. This led to pachymetry (580 µm
OD, 584 µm OS) and visual fields (24-2 SITA-Standard) being performed.
The visual fields were reliable and full in each eye.
Figure 1.
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Figure 2.
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Figure
1 shows the retina and optic nerve photographs for the right eye. The
optic disc is average in size and the ISNT rule is evaluated as being
borderline due to the superior region appearing thin when compared to
the nasal sector. There is a vessel running through the central portion
of the cup that appears to be suspicious. Still, the retinal nerve fiber
layer (RNFL) is intact and neither peripapillary atrophy (PPA) nor disc
hemorrhages are present. Figure 2 shows the left eye with the both the
CDR and the optic disc appearing to be larger than that in the right
eye. In this eye the ISNT rule appears to be obeyed with the retinal
nerve fiber layer (RNFL) intact, and neither PPA nor disc hemorrhages
are present. Comparing figures 1 and 2 it is apparent that the left
disc is larger than the right, which explains the increased C/D ratio.
Note that the refractive errors were similar between the two eyes.
Figure 3.
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Figure 4.
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Figure 3 is a printout from the HRT 3. The images are of good quality
and the disc area is different between the eyes (OD 1.93mm2,
OS 2.48mm2). The CDR is larger in the
OS with the rim area, rim volume, and RNFL thickness seen as reduced
compared with the disc size. The GDx printout (Figure 4) is also of
acceptable quality with an exaggerated split RNFL bundle seen in the
superior bundle in each eye. While the Nerve Fiber Indicator (NFI) is
below 30 in each eye, the thickness maps, deviation maps and TSNIT plots
raise some suspicions as certain regions are viewed as being questionable.
Figure 5 shows the OCT Stratus RNFL printout. The images are also of
acceptable quality and all areas of the printout are falling within
a normal range. The superior split bundles seen in the GDx printout
are also visible in this printout.
Figure 5.
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In summary, this is an example of an individual with asymmetric optic
disc sizes, right larger than left which has led to asymmetric cupping.
This is not an unusual situation as the Blue Mountains Eye Study showed
this to occur in approximately 5% of the population. Still the optic
discs have been judged as suspicious, with the patient being monitored
as a glaucoma suspect. Imaging done at the first exam indicates that
this patient’s appearance is unusual and requires follow-up. Monitoring
over time with imaging will allow changes to be detected.
Murray Fingeret, OD
OGS
MEMBER RESEARCH PROFILE
Many
OGS members are research-active, performing relevant and highly topical
work that helps improve our understanding of glaucoma and provides an
evidence-base for clinical practice. In this issue we will profile founding
OGS member Dr Chris A. Johnson, presently a Visiting Professor in the
Department of Ophthalmology at the University of Iowa.
Dr Johnson’s research interests have followed a variable path during
his research career, beginning with peripheral motion detection and
oculomotor adjustments, to vision standards for various occupational
requirements and transportation safety, to non-invasive analysis and
diagnosis of ocular and neurologic disorders. This has led to a productive
venture, resulting in more than 300 publications in scientific and clinical
journals. Over the past 20 years, Dr. Johnson’s research has been
primarily directed towards functional (perimetry, electrophysiology,
clinical psychophysics) and structural (stereo photographs, HRT measures,
and other imaging procedures) assessment of glaucoma and other ocular
and neurologic disorders, with perimetry being the predominant topic
of interest. In addition, computer simulation and mathematical modeling
of ocular disease has been another area of interest to Dr. Johnson.
In this view, Dr. Johnson has conducted long-term longitudinal evaluations
of patients with glaucoma or who are at risk of developing glaucoma.
Currently, Dr. Johnson’s primary research interests are concerned
with the development and validation of methods to distinguish between
dysfunctional ("sick") and unresponsive ("dead")
neural elements using noninvasive clinical test procedures, development
and refinement of methods to perform visual field screening, and defining
the relationship between structural and functional losses in glaucoma
and other optic neuropathies. For most of these research topics, Dr.
Johnson has approached them from a variety of perspectives, including
basic visual science studies to determine the underlying physiological
and pathological basis for these phenomena, longitudinal clinical evaluations
of patients with ocular and neurologic disorders, computer simulation
and mathematical modeling of the research topic, statistical and analytic
data assessments, practical application of laboratory findings to clinical
and real world environments, and validation of findings through independent
studies.
MEETING
NEWS
Highlights from the Annual Meetings of the
Optometric Glaucoma Society and the American Academy of Optometry
This year’s OGS meeting program began with a lecture by Dr. Andrew
Hartwick, entitled, "Imaging RGC function and dysfunction in vitro."
Dr. Hartwick demonstrated how retinal ganglion cells (RGCs), studied
in both purified cultures and retinal whole-mounts, display a period
of dysfunction prior to death when challenged with non-lethal doses
of excitatory neurotransmitters such as the endogenous transmitter glutamate.
In particular, Dr. Hartwick presented evidence that dysregulation of
calcium homeostasis occurs prior to cell death when glutamate or NMDA
are applied, although the presence of glutamate uptake inhibitors were
required to observe the effect in retinal whole mounts. Interestingly,
however, there were no apparent differences between RGC calcium responses
from adult rat eyes with experimental glaucoma compared with fellow
control eyes. This leaves open the ongoing issue of whether excitotoxic
death of RGCs plays a role in glaucoma. Dr. Hartwick’s other studies
should continue to shed light on this issue. Meanwhile, it was clear
that Dr. Hartwick’s OGS Travel Award was well-deserved; it also
helped him to share his results with the larger audience attending the
AAO annual meeting scientific poster session(s).
OGS Annual Meeting
delegates
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The OGS program continued with Dr. Ron Harwerth’s lecture on "Visual
fields and RGC losses in patients with glaucoma." Dr. Harwerth
presented recent work comparing histological RGC counts across the retina
with in vivo measures of structure (OCT RNFL thickness measurements)
and function (standard perimetric sensitivity measurements). There were
compelling correlations between measures and evidence that perimetry
measures declined prior to RNFL thickness measurements. The latter suggests
a period of dysfunction precedes cell death and axon loss from the RNFL.
Dr. Harwerth presented some of these findings again during his AAO lecture
as the recipient of Charles F. Prentice Medal Award, one of the highest
honors bestowed by the Academy "to an outstanding scientist who
has contributed significantly to the advancement of knowledge in the
visual sciences."
Dr. Balwantray Chauhan then delivered the first of his paired lectures,
"Choosing endpoints for clinical studies and trials" followed
later in the day by his delivery of the Inaugural President’s Lecture:
"Truths, half truths and lesser truths, a practical guide to the
recent clinical trials in glaucoma." Dr. Chauhan demonstrated to
all OGS attendees the breadth of his interests in glaucoma. His work
in perimetry, optic nerve imaging, and pathophysiology (e.g. he was
one of Dr. Hartwick’s dissertation advisors) always demonstrates
keen clinical insight and a creative, but rigorous approach to scientific
problems. Dr. Chauhan also shared his insights, criticisms and caveats
about glaucoma trials again during Ellerbrock continuing education sessions
at the Academy meeting.
The OGS and the Academy both were also privileged to hear an excellent
series of lectures given by this year’s OGS Honoree, Dr. Harry
Quigley and his colleague from the Wilmer Eye Institute, Dr. David Friedman.
Along with Dr. Steve Hahn, these internationally-renown glaucoma specialists
and clinician-scientists challenged the status quo in several critically
important areas, including "Compliance, persistence and adherence:
glaucoma therapy--the nasty secrets", "Doctor-patient communication",
and "New views of the mechanisms of angle closure glaucoma".
One of the most salient take-home messages was the importance of each
patient’s’ compliance with their treatment plan. In practice,
all the best diagnostic tests, carefully considered interpretations,
availability of highly efficacious drugs and surgical interventions
are all meaningless if a patient does not trust and follow caregiver’s
recommendations, engage in open, honest communication, and repeatedly
return for review appointments.
All three of these superb guests characteristically delivered lectures
that were data-driven in essence, thoughtful, and convincing. This series
documented major barriers to effective compliance and adherence, many
possible solutions, and sobering implications for public health and
policy challenges. Drs Quigley, Friedman and Hahn all humbly shared
stories of patients who lost vision primarily because of non-compliance,
arguably a failure of doctor-patient connection rather than of medicine
or surgery per se. Then they focused on proven strategies for improving
the depth and effectiveness of those connections.
The final OGS meeting session consisted of a lecture by Dr. Bill Hare,
from the Department of Biological Sciences at Allergan Pharmaceuticals,
on the "Rationale for the use of memantine in the treatment of
chronic glaucoma." Dr. Hare highlighted the research and development
trail for the neuroprotective drug memantine. Concluding with the current
ongoing international, multi-centered, prospective, longitudinal clinical
trial, in which thousands of glaucoma patients are enrolled, Dr. Hare
began with some basic neurophysiology and pharmacology, then discussed
results from early laboratory-based animal studies, and more recent
pre-clinical studies. Whatever the outcome of the memantine trial, this
was a fascinating glimpse into the world of pharmaceutical R&D and
a great way to conclude this year’s annual OGS meeting.
Brad Fortune, OD PhD
1st
Annual Optometric Glaucoma Society Residents Glaucoma Course
September 14-16, 2007
Alcon Campus, Ft. Worth, TX
The Optometric Glaucoma Society will be holding its first program dedicated
to glaucoma specifically for Optometric residents on September 14-16,
2007. The course is designed for residents who are beginning their program
in July 2007 and have a strong interest in glaucoma. Alcon will be providing
sponsorship with the program being done under the auspices of the Optometric
Glaucoma Society (OGS). Program Directors are Murray Fingeret, OD and
Ian Ben Gaddie, OD. The course will begin with a reception Friday evening,
followed by a full day of lectures on Saturday. The program will complete
at 12:30pm on Sunday. Lodging, travel, and food will be provided for
each individual taking part in the program.
For the first course, we are only able to accommodate one resident from
a program affiliated with each of the Colleges of Optometry. The resident
does not have to be based at a school or college to participate, but
the program has to be accredited. We will be making selections in early
July, looking for residents who have an interest in glaucoma and would
like to apply this knowledge and interest during their residency year.
Candidates will be selected by a committee based upon input from the
school’s residency director as well as faculty recommendations.
Objectives of the course are to:
1. Enhance the resident’s knowledge of glaucoma
2. Describe new areas related to glaucoma
3. Discuss the role of clinical research within glaucoma and explain
how the resident, with support from their facility, may become involved
in clinical research
Applications and information will be available at the OGS website
www.optometricglaucomasociety.org
Optometric Glaucoma Society Educator Summit
On Tuesday, December 5, the OGS held an Educator Summit prior to the
OGS Annual meeting in Denver in order to share ideas amongst the glaucoma
didactic instructors from the various colleges of optometry. The meeting
was co-chaired by founding OGS members Tom Lewis and Joseph Sowka. Twenty-two
individuals representing 15 colleges of optometry met to discuss curricular
issues and challenges surrounding glaucoma education. One of the most
significant outcomes was the opportunity for all instructors present
to learn what is being taught by colleagues in other colleges and allow
open discussion regarding various syllabi presented. The second half
of the meeting involved the development of a standard curriculum for
glaucoma. There was excellent input from all participants and a rough
draft of a model glaucoma curriculum was generated. This draft is going
to be the start and this initiative will be ongoing. At the conclusion,
we expect to have developed a model curriculum for glaucoma that encompasses
all vital aspects of glaucoma.
The Educator Summit was an excellent opportunity for the didactic glaucoma
instructors from the colleges of optometry to meet. Those attendees
that were not OGS members were invited to attend the OGS Annual Meeting
the following day and were encouraged to consider membership in the
OGS.
CLINICAL
QUESTIONS AND ANSWERS
If you would like us to answer a clinical
question, please send it to paul.spry@ubht.nhs.uk
with "OGS question" as the subject. The questions can concern
anything related to glaucoma, for example, analysis of an optic nerve
image, optic disc, a challenging case or side effect of a medication.
We welcome your questions and we will try to address as many as possible
in each issue.
Question: If thinner corneas are at a higher risk for glaucoma
then are people who undergo LASIK going to have a higher risk of someday
developing glaucoma? Or is that putting the chicken before the egg?
Douglas R. Anderson, MD, answers: Everyone comes with traits,
some of which correlate with other traits. Some with dark skin are quite
muscular and co-ordinated, have thick connective tissue, and a greater
sense of rhythm than others. Some with myopia are studious and like
to read. Some with mathematical skills are musically inclined. Cause-and-effect
versus simple association, or why there should be an association at
all, is sometimes difficult to understand. To give an ocular example,
we do understand that small eyes tend to be hyperopic, and also to have
small anterior chambers that lead to angle closure. We can say that
small eyes result in hyperopia and also result in angle closure, but
not that hyperopia causes angle closure. They are two results from a
common cause.
So it is with corneal thickness. It has been shown that having a thin
cornea increases the likelihood that a non-glaucomatous person with
high tonometer readings will develop manifest glaucoma. The cause-and-effect
relationships are unclear. Certainly a thinner cornea has different
biomechanical properties than a thicker one, and this affects the reading
obtained with the tonometer at a given level of intraocular pressure.
One explanation for the observed risk could therefore be that the tonometer
reading is falsely low, so the higher risk relates to the fact that
the IOP is actually higher than the tonometer indicates. Another possibility
is that a thin cornea may have resulted from some aspect of connective
tissue development that also affected the sclera and lamina cribrosa,
so that these structures have different, and more dangerous, biomechanical
properties than in another person. No one knows which is the explanation,
or whether there is an element of truth in both.
If it has simply to do with the tonometer readings being inaccurate,
then indeed, altering the cornea surgically may change the tonometer
reading with a given IOP. Given the opportunity, it may be wise to obtain
several representative IOP readings before corneal surgery, and then
several after all healing has taken place, with the assumption that
the nature of the surgery did not actually change the dynamics that
affect IOP, so we are simply determining for future reference how much
the surgery changed the relationship of the tonometer's reading and
the true IOP. If, however, there is a relationship between native corneal
thickness and risk from characteristics of the posterior connective
tissue, one would not expect for that component of risk to have changed
after corneal surgery, and the pre-operative corneal thickness still
represents a level of risk, because the properties of the sclera and
lamina cribrosa remain the same.
We must remember that the only firm evidence is that a thin cornea increases
the likelihood of developing glaucoma if you have elevated tonometer
readings without having already developed glaucoma. Evidence is much
weaker that once a person has glaucoma, the corneal thickness increases
the risk for rapid or severe glaucomatous damage and vision loss. Certainly,
if a person has had glaucoma for quite some time, and has been stable
on therapy, the course of events on therapy is a much stronger guide
to continued management than any baseline features the patient may have.
If a person is stable with an IOP of 15 mm Hg, we may not care whether
the initial IOP was 24 mm Hg or 35 mm Hg. Similarly, it does not make
sense to change management of a patient who has been stable for 10 years
simply because his cornea is thinner than another equally stable person
whose cornea is of normal thickness.
To summarize, if LASIK causes the tonometer to give falsely low readings,
the true level of risk, as judged in the future from the IOP reading,
may be masked. For this reason, knowing how different are representative
pre-operative and post-operative readings may be helpful. However, to
the degree that a thin cornea is a reflection of weak connective tissue
in the eye posteriorly, the risk is unchanged by LASIK. Even though
the reason for a relationship between corneal thickness and risk of
developing glaucoma is not known, there is no rationale for a change
in actual risk if the cornea is made thinner by LASIK. However, our
estimate of that risk when making management decisions may be faulty
if we fail to make mental note of how the tonometer reading was affected
by LASIK.
Douglas R. Anderson, M.D. is Professor of Ophthalmology and Douglas
R. Anderson Chair in Ophthalmology at Dept of Ophthalmology, Univ. of
Miami Leonard M. Miller School of Medicine, Bascom Palmer Eye Institute.
POLL
RESULTS FROM VOLUME 2, ISSUE 1
Our most recent poll question was "Do you
perform office hours diurnal intraocular pressure measurement (day phasing)?
Your responses have been tabulated. Twenty-two percent reported performing
this test on a regular basis. Forty-one percent indicated that they
only performed this test on their patients with presumably controlled
intraocular pressure yet progressive glaucoma. Thirty-six percent of
respondents indicated they never perform diurnal intraocular pressure
measurements. This group broke down as 16% citing logistical constraints
as the limiting factor whereas 20% of respondents did not believe the
result of such a test would impact their management. In summary, these
poll results tell us that 80% of respondents think that diurnal IOP
measurement may inform patient care, and that it would be performed
more often if logistical obstacles were removed.
Thank you to everyone who voted in our previous poll. Please
vote in this issue's poll questions! All votes are completely
anonymous.
John McSoley, OD
Editor
in Chief
Paul Spry PhD MCOptom
Associate Editors
Brad Fortune, OD,
PhD
Shaban Demirel, BScOptom,
PhD
Algis Vingrys BScOptom,
PhD
|
Editorial Board
Douglas Anderson MD
Paul Artes PhD MCOptom
Dick Bennett OD
Murray Fingeret, OD
Ron Harwerth, PhD
Chris Johnson, PhD
Tony Litwak, OD
John McSoley, OD
Ron Melton, OD
Bruce Onofrey, OD, RPh
Leo Semes, OD
Randall Thomas, OD
Thom Zimmerman, MD, PhD
Art/Production Director
Joe Morris
Project Coordinator
Janice Miller
|
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