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would like to thank everyone for the warm response we received in regards
to the introduction of the OGS Electronic Journal. Please tell your
colleagues about this new endeavor. Back issues as well as the ability
to sign up to receive the e-journal are available at www.optometricglaucomasociety.org.
The editorial team consisting of our editor in chief, Paul Spry; our
associate editors Brad Fortune, Shaban Demirel, and Algis Vingrys; and
the editorial board look forward to crafting a journal that meets the
needs of optometrists engaged in the management of glaucoma. Please
continue to provide us with feedback and questions.
One new and important topic related to glaucoma is the issue of patient
adherence with a treatment regimen. Put another way, there is a profound
lack of persistency on the part of many patients in maintaining therapy.
We hope to explore this topic in future issues.
Why is it that recently published studies show many patients do not
continue their therapy? In a recent discussion I had with a friend,
who is a nephrologist by training and actively involved in patient-doctor
communication education, he remarked that no matter how simple you create
the treatment regimen or how great the drug is, these factors will only
improve compliance so far. His belief is that the unforgotten and much
harder component to enhance adherence is doctor-patient communication.
This skill (and I refer to it as a skill similar to performing other
procedures) is often overlooked and underappreciated. Good communication
is difficult, in part because many of us are not used to listening to
our patients. Still as I thought about this, I realized that when I
came away from a doctors visit impressed with the clinician, it
was often because of his/her interpersonal skills.
When I was in optometry school, an instructor who taught the ophthalmic
optics course had a saying that you could do the best refraction but
if the patient could not wear the glasses, what have you really accomplished?
Well, maybe the modern day version is that you can make the best diagnosis,
but if the patient is not using your prescribed therapy, again what
has been accomplished?
Murray Fingeret, OD
President, Optometric Glaucoma Society
down but not out.
Knowledge regarding glaucoma continues to grow at an immense rate: it
doesnt seem like long ago that many texts reported elevated intraocular
pressure (IOP) and open-angle glaucoma were synonymous. Of course, now
we are all very well aware that elevated IOP is neither necessary nor
sufficient to cause glaucoma. Like many other chronic diseases, glaucoma
is best explained as a multi-causal paradigm: IOP simply complements and
interacts with the susceptibility of individuals. The days of elevated
IOP as an essential element of glaucomas diagnostic triad, alongside
optic nerve appearance and loss of visual function, are therefore over.
However, unless it is put into context, this apparent downgrading
of raised IOP from diagnostic to risk factor status, alongside the confounding
effects of corneal thickness on tonometric validity, may give the misleading
impression that IOP measurement is a less important part of routine clinical
examination than it used to be.
Fortunately, there are many studies to dispel such a misconception. The
highest body of evidence to support IOPs current status in glaucoma
care comes from randomised controlled trials. Key trials are summarised
in this issues Clinical Trial Review. Whilst each trial differs
in objectives and methodology, the consensus is that reducing IOP improves
glaucoma group outcomes. Although IOP is only a risk factor, at present
it is also the only currently proven modifiable risk factor that we can
use to help our glaucoma patients.
Paul GD Spry, PhD MCOptom, Editor-in-Chief
CALCULATORS: EVIDENCE-BASED CARE OF OCULAR HYPERTENSION PATIENTS
Your first patient is 50
years old and has ocular hypertension. His risk factors for developing
glaucoma include: no diabetes, a corneal thickness of 590 microns, cup
to disc ratio (C/D) of 0.7, pattern standard deviation of 2.1, and an
intraocular pressure of 26 mm Hg in both eyes. Do you treat with ocular
hypotensive medications? Or do you watch?
Trying to decide whether to treat the above patient is complex without
a tool to simplify the estimate of risk. For example, the Ocular Hypertension
Treatment Study (OHTS)(1,2) suggests that this patient has a lower risk
of developing glaucoma based on age (50 years vs. the average age of
the OHTS patients of 56 years), corneal thickness (590 microns vs. 572.5
within OHTS), and diabetes (history of diabetes was protective); but
a higher risk based on C/D (0.7 vs. 0.39 in the OHTS study), pattern
standard deviation (2.1 vs. 1.9 average in the OHTS study), and intraocular
pressure (26 mm Hg vs. 24.9 mm Hg in the OHTS). Even if one divides
the continuous variables of age, corneal thickness, IOP, and PSD into
thirds and uses 9 different combinations for C/D (0.0-0.8), 1458 (3x3x3x3x2x9)
different combinations of variables exist for ocular hypertension patients.
This creates a large number of different combinations of variables for
any one ocular hypertension patient. Only by using a risk calculator
or a prediction model can one simplify these complex results.
Using our risk calculator(3), the above ocular hypertension patient
has a risk of 21.9% of developing glaucoma over 5 years (Figure).
Clinicians and patients can use this information- in conjunction with
other characteristics such as life expectancy and likelihood to be compliant
with medications- to decide whether to treat. Risk calculators will
allow clinicians to identify and treat only those patients most likely
to develop glaucoma, resulting in decreased costs to society and decreased
side effects to patients.
However, clinicians should only use a risk calculator based on OHTS
for those patients who meet the inclusion and exclusion criteria of
OHTS. For example, clinicians should not assume that eyes with secondary
causes of ocular hypertension, such as pseudoexfoliation or pigmentary
dispersion syndrome, would have similar risk factors to the OHTS study
Recently, other investigators have created risk calculators for ocular
hypertension patients using similar methods(4). Other calculators using
larger sample sizes and new technologies are likely to improve the precision
of the risk estimate in the future. For example, the OHTS group will
be releasing a risk calculator based on the five year results of the
OHTS(1,2) and European Prevention Study(5). Other calculators may improve
the predictive ability by using selective functional testing such as
short-wavelength automated perimetry, or objective structural testing
such as confocal scanning laser ophthalmoscopy(6). In summary, eye care
providers should use one of the currently available risk calculators,
but other risk calculators will be available in the future.
Risk calculators provide an objective method of determining the risk
of developing glaucoma from ocular hypertension. Their results are easy
to understand and easy to apply. Patients, providers, and society will
benefit from their use.
Devers Eye Institute/Discoveries in Sight, 1040 NW 22nd Avenue, Suite
200, Portland, OR 97210. Telephone 503-413-6453; Telefax 503-413-6937
Steven L. Mansberger, MD, MPH
1. Kass MA, Heuer DK, Higginbotham EJ, et al. The
Ocular Hypertension Treatment Study: a randomized trial determines that
topical ocular hypotensive medication delays or prevents the onset of
primary open-angle glaucoma. Arch Ophthalmol 2002;120:701-13; discussion
2. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment
Study: baseline factors that predict the onset of primary open-angle
glaucoma. Arch Ophthalmol 2002;120:714-20; discussion 829-30.
3. Mansberger SL. A risk calculator to determine the probability of
glaucoma. J Glaucoma 2004;13:345-7.
4. Medeiros FA, Weinreb RN, Sample PA, et al. Validation of a predictive
model to estimate the risk of conversion from ocular hypertension to
glaucoma. Arch Ophthalmol 2005;123:1351-60.
5. Miglior S, Zeyen T, Pfeiffer N, Cunha-Vaz J, Torri V, Adamsons I.
Results of the European Glaucoma Prevention Study. Ophthalmology 2005;112:366-75.
6. Zangwill LM, Weinreb RN, Beiser JA, et al. Baseline topographic optic
disc measurements are associated with the development of primary open-angle
glaucoma: the Confocal Scanning Laser Ophthalmoscopy Ancillary Study
to the Ocular Hypertension Treatment Study. Arch Ophthalmol 2005;123:1188-97.
7. Devers OHTN to Glaucoma Risk Calculator: Devers Eye Institute, Legacy
Health System, 2003. PC, MAC, Palm, and C++ versions are available free
IDEAS & NEW PAPERS
Corneal Thickness: Confounder or Risk Factor?
Decades ago Dr Hans Goldmann made it abundantly clear that estimates of
IOP from applanation tonometry depended on assumptions about the cornea.
Assumed properties of an average cornea were incorporated into the devices
design and calibration. It seems this wisdom was somewhat overlooked for
a while but received renewed interest after the Ocular Hypertension Treatment
Study (OHTS) findings suggested that central corneal thickness (CCT) was
one of the most potent predictors of whom would progress from Ocular Hypertension
to Primary Open Angle Glaucoma (POAG)(1).
Since then, case reports invariably quote pachymetry and it is quite common
to hear the question, "What were the pachs?" in any discussion
of a glaucoma patient. It is safe to say that pachymetry has become part
of the standard of care in glaucoma practice, and rightly so. Assessing
CCT prompts us to be mindful that part of the measured IOP is the force
required to bend the cornea. But is there more to it than that? Is CCT
more than just an IOP correction factor?
Two recent papers presented in sequence by Jonas et al and Jonas &
Holbach provide us with useful information(2,3).
In the first paper, longitudinal data were used to seek a correlation
between CCT and both glaucomatous damage and the rate of visual field
progression. They report that CCT was significantly correlated with the
area of the neuroretinal rim (NRR) and patients with thinner corneas had
less rim tissue. They also reported that patients with thinner corneas
had significantly more visual field damage. However, when they sought
a correlation between visual field progression over an average of 5 years
and CCT they found none. The authors concluded that even though CCT was
significantly correlated with the amount of nerve damage at referral,
CCT "...may not play a role in the pathogenesis of progressive glaucomatous
optic nerve damage." They also suggest that the correlation between
amount of damage at presentation and CCT may simply be a selection bias.
Patients with thin corneas are less likely to present with elevated IOPs
and are therefore less likely to be aggressively worked up.
In the second paper, nonglaucomatous human post mortem eyes were used
to seek a correlation between the CCT and the thickness of the lamina
cribrosa. The authors found no significant correlation between corneal
thickness and lamina cribrosa thickness. However, there was obvious histological
distortion during tissue preparation with average corneal thickness after
processing being 617 microns. There is also debate about the relationship
between living and post mortem measures of lamina thickness and these
factors undoubtedly affected the correlations. However the authors make
the following conclusion. "If the results of the present study are
confirmed by other studies, they suggest that an assumed relationship
between central corneal thickness and susceptibility to glaucoma may not
be explained by a correspondence between central corneal thickness and
the thickness of the lamina cribrosa and peripapillary sclera." Until
such confirmation is forthcoming the results of this study must be interpreted
cautiously but taken together these papers suggest that CCT is important
because of its effect on our estimate of the true IOP.
Shaban Demirel, BScOptom, PhD
1. Gordon MO et al. The Ocular Hypertension Treatment
Study: baseline factors that
predict the onset of primary open-angle glaucoma. Arch Ophthalmol. 2004
2. Jonas JB et al. Central corneal thickness correlated with glaucoma
damage and rate of progression.
Invest Ophthalmol Vis Sci. 2005 Apr;46(4):1269-74.
3. Jonas JB, Holbach L. Central corneal thickness and thickness of the
lamina cribrosa in human eyes.
Invest Ophthalmol Vis Sci. 2005 Apr;46(4):1275-9.
OCT scans of the macula for glaucoma diagnosis?
In a recent study from the Bascom Palmer Eye Institute(1),
Bagga and co-authors developed a method of "macular symmetry testing
(MST)" for glaucoma detection. The investigators used optical coherence
tomography (OCT) to measure macular thickness along two radial spokes
extending 2.5 mm temporally from the fovea, 15 degrees above and below
the horizontal raphe. By comparing total retinal thickness across the
horizontal midline (i.e. superotemporal to inferotemporal locations),
they performed a structural analysis analogous to the better-known Glaucoma
Hemifield Test (GHT) of the Humphrey Visual Field Analyzer. Based on
the same rationale, namely that glaucomatous damage is often asymmetric
across the horizontal midline, these investigators sought to evaluate
whether macular thickness measurements would also reflect this asymmetry
and thus be useful for glaucoma detection. As an initial test of this
hypothesis, only patients with reliably asymmetric visual field damage
were studied; the extent of this focal damage varied from mild to moderate,
with a range of mean deviation (MD) values from -0.9 to -15.4 dB (average
= -7.2 dB). The authors found that the macular thickness in the perimetrically
abnormal hemi-zone was significantly less than the corresponding segments
in the perimetrically normal hemi-zone of glaucomatous eyes. There was
no such macular thickness asymmetry in the healthy control population.
Using this control sample to establish normative ranges, 80-85%
of the glaucomatous eyes had abnormal MST results. The receiver operating
characteristic (ROC) analysis revealed a diagnostic accuracy (area under
the ROC curve) of 85%. The authors concluded that "localized
macular thickness changes exist in glaucomatous eyes with regional visual
field loss" and that "the MST may represent a novel strategy
for glaucoma diagnosis."
Some important caveats for the GHT are also applicable to the MST, for
example, diffuse or otherwise symmetric damage to both upper and lower
hemi-zones might escape detection. Co-morbidity such as diabetic, age-related
or other maculopathies might confound the MST. Another general caution
is generalizability of this study: all glaucomatous eyes were required
to have asymmetric visual field loss. The performance of the MST might
not perform as well in an unselected population. Nonetheless, one very
interesting point is that the locations tested by the MST (to 8.5 degrees
eccentricity) correspond to only the most central points measured by
standard automated perimetry (4, or 5 if the foveal test point is included).
Interestingly, these are the very points that are commonly ignored during
analysis of early-to-moderate glaucomatous field loss. One final point
worth mentioning is the recent finding by Leung and colleagues(2) that
OCT scans of the peripapillary retinal nerve fiber layer (RNFL) outperformed
both total macular and macular RNFL thickness measurements (also made
using OCT) in terms of both glaucoma detection and correlation with
visual field parameters. Regarding these three OCT strategies, these
authors concluded that "peripapillary NFL thickness... is still
the best surrogate marker in glaucoma assessment." Perhaps an asymmetry
analysis of peripapillary RNFL thickness (again, in an analogous fashion
to the GHT) would provide an even more powerful diagnostic test. We
anticipate further research comparing OCT scan locations, with and without
asymmetry analyses, in a broader range of glaucomatous eyes to learn
just how powerful this technology can be for glaucoma diagnosis.
Brad Fortune OD, PhD
1. Bagga H, Greenfield DS, Knighton RW. Macular symmetry
testing for glaucoma detection. J Glaucoma. 2005;14:358-63.
2. Leung CK, Chan WM, Yung WH, Ng AC, Woo J, Tsang MK, Tse RK. Comparison
of macular and peripapillary measurements
for the detection of glaucoma: an optical coherence tomography study.
Ophthalmology. 2005 Mar;112(3):391-400.
Peripapillary atrophy in a glaucoma
patient with thinning of the superior temporal rim and inferior
visual field loss. Note inner zone beta from 11 to 4 oclock
characterized by complete atrophy of the RPE and visibility
of the sclera. Note outer zone alpha from 1 to 3 oclock
characterized by irregular hypertrophy of the RPE.
Peripapillary Atrophy and Glaucoma
Glaucoma is the most common optic neuropathy. The mainstay of glaucoma
diagnosis is thorough examination of the optic nerve. There are hallmark
signs of glaucoma damage such as progressive rim tissue loss (increase
in cupping), disc hemorrhage, and retinal nerve fiber layer (RNFL) loss.
These signs can be correlated with visual field testing to corroborate
the diagnosis of glaucoma. There are other less specific optic nerve
signs associated with glaucoma damage. One of these signs and the focus
of this article is peripapillary atrophy (PPA).
Jost Jonas has published numerous articles on PPA and glaucoma. He describes
zones alpha and beta. (See attached Figure and Table) Zone beta is referred
to as the central zone of atrophy adjacent to the optic disc. It is characterized
by complete loss of the retinal pigment epithelium and choriocapillaris
with visibility of the larger choroidal blood vessels and the white sclera.
Zone alpha represents the outer or peripheral zone of PPA (further from
the disc and adjacent to zone beta). Ophthalmoscopically, zone alpha shows
an increase in pigmentary irregularities of the RPE.
zone - outer side adjacent to retina, inner side in touch with
Inner or central
zone - peripheral side adjacent to zone alpha, inner side adjacent
to optic disc
of the RPE and the choriocapillaris; visible large choroidal vessel
irregularities in RPE
of RPE cells & a marked loss of photoreceptors
in normal eyes
seen in glaucoma, but can be seen in 15-20% of normal eyes
Alpha & Beta zone
> Inferior temporal=superior temporal >> nasal
Zone Beta occurs
more often; larger zones; zone sizes correlate with severity of
glaucomatous optic nerve damage. Zone increases with glaucoma
PPA more common
in NTG than OAG
atrophy is closely associated with a disc hemorrhage.
anterior ischemic optic neuropathy and arteritic anterior ischemic
optic neuropathy do not enlarge peripapillary atrophy.
change, Myopic scleral crescent; Tilted optic disc; Sympathetic
ophthalmia; Autosomal dominant optic atrophy.
Zone beta is more specific to glaucoma damage of the optic nerve. There
is an association of adjacent thinning of the neuro-retinal rim tissue
and decrease in RNFL with an increase in size of zone beta. Zone alpha
has less specificity for glaucoma damage and is frequently seen in normal
eyes. On visual field testing, zone beta will correlate to an absolute
scotoma (enlarged blind spot) and zone alpha to a relative scotoma.
An increase in PPA has also been shown to correlate with progressive
In summary, PPA is a less specific sign of glaucoma damage and should
be considered as a secondary level of importance in glaucoma management.
It is still prudent to scrutinize for PPA which may uncover subtle thinning
of the neuro-retinal rim tissue. Comparison of PPA in longitudinal optic
nerve photographs can assist in determining glaucoma progression.
Anthony B. Litwak, OD, FAAO
Len V. Hua
1. Jonas, JB. Clinical implications of peripapillary
atrophy in glaucoma. Curr Opin Ophthalmol 2005; 16:84-88.
2. Curicio, CA, Saunders PL, Younger PW, et al. Peripapillary Chorioretinal
Atrophy. Bruch's membrane changes and photoreceptor loss. Ophthalmology
3. Uchida H, Ugurlu S, Caprioli J. Increasing peripapillary atrophy is
associated with progressive glaucoma. Ophthalmology 1998;105:1541-1545.
Does the 24-2 pattern detect all early glaucoma?
Does this sound like a common debate that you have in the bar with your
colleagues? It really stems from the era of kinetic perimetry (Goldmann
bowl). In those days glaucoma was considered a peripheral disease which,
by default, needed a peripheral field test for detection. This concept
was supported by the many clinical trials in the 70s and 80s
that found some 1-15% of patients with glaucoma have defects that
lie outside of the central 30° region. Does his mean that we need
peripheral tests to detect glaucoma or is the 24-2 adequate?
It is my opinion that we do not need a peripheral test and that the
24-2 may not detect all early losses.
Over the years, the need for peripheral testing has been eroded with
the recognition that the capacity to find central losses is dependent
on the nature and quality of the visual field test. Threshold tests
are now recognised as providing the best method of defect exposure,
and if we add to this the development of tests that reduce stimulus
redundancy, such as FDT, then it is likely that central defects will
always be present in early glaucoma making central testing the method
of choice. This does not mean to imply that a peripheral test should
not be used to give fuller or better definition of the affected area.
But for the purpose of detection, it is useful to review the regions
affected by the disease. The seminal work from Tübingen, based
on a cross sectional study of 2,000 patients with definite or suspect
glaucoma, found the following patterns of field loss:
temporal loss beyond the blindspot (see Figure)
to fixation (encroach within 10°)
Of note is the fact that a mean or average reduction in sensitivity
was not part of this classification but has been recognized by later
The most significant recent research on this issue has been performed
by the Ocular Hypertension Treatment Study (OHTS) Group and its members(1).
This study is particularly informative for clinicians because it has
followed a group of high-risk patients for many years and noted the
development of glaucoma in a subset of people. These investigators find
that field loss in early glaucoma can involve any area of visual space,
with most lying in the arcuate region (59%). The fact that these
people were detected with central testing implies that central field
patterns can adequately expose this disease, although this prospect
was not formally tested. Moreover, the interesting findings are, that:
to fixation can be found in 1% of cases with early glaucoma
depressions (mean defects) are found in 8% of cases, and
temporal wedges are observed relatively often (3.3%)
10-14% of initial field loss occurred in points beyond the 24-2
All of these findings indicate the need for a pattern of points that
will be able to characterise losses across the field including the central
30° and temporal regions (see Figure).
Does this mean that the 24-2 does not have a place in clinical practice--of
course not. In patients who have established loss within 25° it
might be best to use the 24-2 because testing is faster and that pattern
can just as well be used to monitor the loss. The Figure is a field
from a glaucoma suspect showing many of the attributes just described,
have a look at the clinical profile and figure out whether you feel
it is glaucoma or not--the answer will be given at the end
of this issue.
Algis Vingrys BScOptom., PhD
1. Keltner JL, Johnson CA, Cello KE, Edwards MA, Bandermann
SE, Kass MA, Gordon MO and the Ocular Hypertension Treatment Study Group.
Classification of visual field abnormalities in the ocular hypertension
treatment study. Arch Ophthalmol.
This 54 year-old African American male was diagnosed
with primary open angle glaucoma. The optic disc is average in size
and the ISNT rule is not obeyed in either eye. Retinal nerve fiber layer
(RNFL) dropout is noted in each eye, OD between 7-9 oclock (Figure
1) and OS at 5 oclock (Figure 2). Peripapillary atrophy is present
in each eye temporally but far more obvious in the OS. There are no
signs of disc hemorrhage in either eye.
The HRT printout (Figure 3) is broken out into several parts: Cup, Rim,
and RNFL. The image quality is very good for the OD and excellent for
the OS. The printout shows the cup/disc ratio to be 0.78 OD and 0.79
OS and the cup/shape measure is abnormal in both eyes. The rim area
and volume are also reduced significantly and the RNFL measurements
are abnormal in the OS. The Moorfields Regression Analysis (MRA) is
abnormal in each eye (noted by the different symbols on the rim segment).
The combined RNFL profiles show the OS to be thinner. The Glaucoma Probability
Score (GPS) printout (Figure 4) used a relevance vector machine analysis
and is done independent on the contour line. Similar to the Moorfields
Analysis, both global and sector scores are provided. In this case,
the OD is seen as borderline while OS is evaluated as being outside
The GDx images (Figure 5) are of high quality as seen by the Q scores
of 9 for each eye. The optic nerve is in focus, evenly illuminated and
centered. The GDx printout also has several sections: the fundus image,
RNFL map, deviation map, and TSNIT curves. The large RNFL defect in
the OS is clearly visible in the left fundus image. The thickness maps
are color-coded with brighter images corresponding to thicker areas.
From these diagrams, it is apparent that the OS thickness is significantly
reduced. Viewing the deviation maps, both eyes have points flagged at
a significant level and the TSNIT curves show the OD to be barely within
the "normal range" while the OS reduced.
The OCT images are of an acceptable quality: signal strength of 7 OD
and 8 OS. The images are centered, evenly illuminated and no clipping
present. The left side of the printout shows the TSNIT curves, with
the OD barely in the "normal green range" and the OS reduced
(in the red area), especially inferiorly. In the middle of the page
are the sector and quadrants tables, color coded based upon significance.
The OD appears to be adequate in thickness (all areas are green) but
several sectors and quadrants for the OS are flagged (seen by the yellow
or red colors over the score), especially inferiorly. This indicates
that these thickness values are rarely seen in a normal population.
Several of the parameters are also flagged for the OS.
All the imaging printouts for this patient show similar results, done
in slightly different manner. The OS has greater damage, larger cupping
and a thinner RNFL with greater loss inferiorly.
Murray Fingeret, OD
To treat or not to treat ocular hypertension
This 64 year-old patient was sent by a local practitioner for evaluation.
His impression was that she may be a candidate for glaucoma therapy
but had unconvincing evidence on which to base a treatment recommendation.
Looking at her clinical findings, the best corrected visual acuity is
20/25 in each eye due to cataract. She has been treated for hypertension
for the past 10 years with a diuretic. She reports no family history
of glaucoma. She is not a migraineur or diabetic.
Where does one start? We have clinical data on IOP, central corneal
thickness (CCT), optic disc observations and visual fields. (see Figures
1 and 2). The Goldmann applanation reading is 24 mmHg in each eye and
the CCT is 585u and 589u in the right and left eyes, respectively. The
CCT values would suggest that the IOP may be lower than measured but
this is only the first reading for this patient.
Looking closely at the optic discs, the first thing to strike me is
the asymmetry (Figure 1) in cup-to-disc ratio (CDR) as well as optic
disc size. This is a clinical observation that each of us would recognize
and increase our suspicion. As the IOP is identical in each eye, I would
evaluate the visual fields to see if there is any asymmetry that corresponds
with that observed in the discs. The right visual field shows some asymmetry
across the horizontal midline making the glaucoma hemifield test (GHT)
outside normal limits. But this is due to a trial lens artifact in the
right eye. This field needs to be repeated, paying careful attention
to the position of the patient and trial lens. In the OHTS, nearly 90%
of initial visual field defects were not confirmed on retest which indicates
that repeatability cannot be overemphasized. The left visual field result
shows numerous fixation losses which make it appear to be unreliable.
This is due to the blind spot being incorrectly plotted. Note that the
triangle marking the position where the perimeter believes the blind
spot is (and where it places the targets) is just nasal to the location
marked with a zero. The zero marks the actual blind spot position, and
the high number of fixation losses is due to our not correctly plotting
the blind spot and not indicative of poor performance. The technician
performing the fields is alerted to a high number of fixation losses
early in the testing process and should have paused the test and replotted
the blind spot. The other reliability finding of note is the borderline
number of false negative responses (10%) in the left eye, which
is often seen the first time a patient takes the test. It usually disappears
with experience. It has a great deal to do with the patient searching
for their own criterion of when to depress the patient response button.
Lets go back to the optic disc evaluation. We are handicapped
by the two-dimensional representation here. Although the cup looks larger
in the left eye there are few other features of glaucomatous optic neuropathy
present. The rim tissue may appear by color to be healthier in the right
eye. Applying either the ISNT rule(1) or the 5 Rs(2), there appears
to be little evidence for significant damage to either the right or
left optic disc. The disc margins are distinct in both eyes with no
PPA. The CDR appears to be larger in the left eye but the optic disc
is larger as well. The rim tissue in each eye appears to be robust and
no nerve fiber layer defects are obvious. There are no nerve fiber layer
hemorrhages present in either eye. These observations support an impression
of physiological disc status and the absence of pathological changes.
Clinically, we can apply one of the recently reported glaucoma risk
calculators to this patient. Using Mansbergers glaucoma risk calculator(3),
there is a 33.9% and 12.7% risk of developing glaucoma in the
next five years for the right and left eyes, respectively, without treatment
(Figure 3), although these data are dependent on reliable visual field
results. This disagrees with the structural optic disc data, which suggests
that the left eye might be at higher risk (larger cup). Most importantly,
the right eye data is based upon a visual field PSD that is elevated
due to a lens rim artifact and not indicative of the actual visual field
status. If we do the calculations again using a PSD of 1.80 for the
OD (normal PSD and similar to the OS), the calculated risk reduces to
10.3% without therapy and 6% with therapy. This is a HUGE change
and indicative that you need to be careful if using data that may be
suspect. In addition, theoretically risk should be calculated for both
eyes by averaging the results. With this in mind, the risk for both
eyes is 13.2% without therapy and 7.9% with therapy. This would
indicate that the patient is at a borderline risk and observation would
be the appropriate course for now. If data changes, we would need to
We can also look to digital imaging for another opinion. The GDx data
show relatively normal values for NFI (23, 32) with some superior temporal
thinning in the left eye (see Figure 4).
A recent publication from the ancillary study to the OHTS, which looked
at a subset of patients HRT data, suggested several parameters
that would be predictive of future glaucomatous damage: the Moorfields
Regression Analysis (MRA) overall HRT classification has a 14% positive
predictive value and the MRA temporal sector analysis has a PPV of 40%
for values outside the 95% normal range(4). These data suggest that
the patient is at low risk for conversion (see figures 5a and b). Note
that in the GRC, the C/D values used are from HRT data.
In this case, our decision was to observe this patient as an ocular
hypertensive without treatment with a six-month follow-up visit. With
this volume of baseline data and the availability of risk calculators(3,5),
we now have a source of information on which to base future treatment
decisions. Note that the risk calculators should not be generalized
to all OHT cases: they can only be applied to individual scenarios typical
of those used in their design otherwise spurious and inappropriate results
will be obtained. The management recommendation was proposed to and
accepted by the patient. At follow up, we would look for more reliable
visual field data and whether data in support of the diagnosis of glaucoma
Each of us faces dilemmas such as represented by this case. Careful
follow up will guide us to the correct decision. The availability of
risk calculators allows another data point. Treatment decisions should
not be undertaken lightly, but with an abundance of corroborative information,
they can be made with greater confidence.
Leo Semes, OD
1. Jonas JB, Budde WM, Panda-Jonas S. Ophthalmoscopic evaluation of
the optic nerve head. Surv Ophthalmol. 1999; 43: 293-320.
2. Fingeret M, Medeiros FA, Susanna R Jr, Weinreb RN. Five rules to
evaluate the optic disc and retinal nerve fiber layer for glaucoma.
Optometry. 2005; 76 :661-8.
3. Mansberger SL. A risk calculator to determine the probability of
glaucoma. J Glaucoma. 2004;13: 345-7. (http://www.discoveriesinsight.org)
4. Zangwill LM, Weinreb RN, Berry CC, et al. The confocal scanning laser
ophthalmoscopy ancillary study to the ocular hypertension treatment
study: study design and baseline factors. Am J Ophthalmol. 2004;137:
5. Medeiros FA, Weinreb RN, Sample PA, et al. Validation of a predictive
model to estimate the risk of conversion from ocular hypertension to
glaucoma. Arch Ophthalmol. 2005; 123: 1351-60.
FROM THE EXPERTS
In this issue, our pearls are responses from
our experts to questions posed by readers.
Visual Field Variability
"I understand that variability increases as glaucoma defects get
worse BUT I am also under the impression that in early glaucoma, scotomas
may be present on one field and disappear on the next. Am I confusing
variability with stability?"
Chris A. Johnson, Ph.D. answers, "First of all, you are
not alone when it comes to confusion about visual field variability
and stability in glaucoma. A number of investigators are initiating
new test strategies designed to reduce variability from one examination
to the next, developing mathematical models to better understand variability,
and designing innovative statistical methods to evaluate longitudinal
visual field data that is robust to variability. Progress has been made
in all three of these areas, although additional work is needed. Ocular
pathology (e.g., glaucoma) is one of many sources that increases variability
from one test to another, but there are many other factors that increase
variability as well. The multicenter trials in glaucoma are in agreement
that it is currently necessary to confirm visual field changes by repeated
testing in order to maintain high sensitivity and specificity. In particular,
the Ocular Hypertension Treatment Study (OHTS) reported that more than
85% of initial visual field abnormalities are not confirmed on the next
visual field test. A good rule of thumb is that it is best to repeat
the visual field test if a change is suspected. Because poor sleep,
illness and many other factors besides pathology can increase variability,
it is best to repeat the testing on a separate day to minimize the influence
of these factors. Also, the analysis tools that are currently available
on automated perimeters should be employed to assist in clinical determination
of stability, progression or improvement of the visual field status.
This is currently our best solution to the problem, but we hope that
additional research will provide simpler, easier and more cost-effective
solutions in the future."
Ron Harwerth OD, PhD answers, "There are several sources
of variability that affect the accuracy and precision of visual field
measurements, some are physiological and others are subject-related
factors. The variability of sensitivity that increases as glaucoma defects
get worse and is generally assessed by the slope of the psychometric
(frequency-of-seeing) function probably has a physiological basis. A
couple of examples that support the physiological basis of variability
are: 1) Henson, et al. (IOVS, 38:426-435, 1997) showed that variability
increases with the depth of defect and, therefore, must be related to
the amount of ganglion cell loss, and 2) Wall, et al. (IOVS, 41:417-421,
2000) demonstrated that variability is greater with the Size III stimulus
than a Size V stimulus, suggesting that the loss of ganglion cells results
in a reduced sampling of the test target. An increased variability associated
with ganglion cell loss is present for all patients, whether or not
they are experienced in visual field measurements. Another source of
increased variability, subject-related factors, would be expected to
affect new patients more than patients with a lot of perimetry experience
and includes shifts in attention, response criterion, fixation, fatigue,
etc. Subject-related variability will affect the accuracy of visual
field measurements and could result in an apparent localized scotoma
that is present in one exam and absent in the next, which is why most
clinicians consider clusters of abnormal locations more important than
Both variability and stability are reflections of the precision of subjective
measurements of visual sensitivity, but as I understand the usage, clinicians
use "variability" to describe normal pointwise measurement
fluctuations that determine whether the sensitivity at a given location
is statistically normal, within a certain confidence range. In contrast,
"stability" is a clinical description of reproducibility over
time and whether the fluctuations of a patients data are within
statistical probability of being unchanged across measurements. Therefore,
I think that the visual defect that disappears on subsequent measurement
would be described as instability, but it is a consequence of measurement
Contraindications to Treatment
"We have all been told that Prostaglandins should be used with
caution in patients with active anterior uveitis. I have one patient
who presented with anterior uveitis while on travatan. I discontinued
the travatan and treated her but left her on it in the other eye. 3
days later she came in with iritis in the eye still on the travatan
and the one off the travatan was better. I took her off it in both eyes
and waited 3 weeks and tried her back on Xalatan. Within 3 days she
was back with active anterior uveitis. She had no prior history of uveitis.
I have since sent her for surgery and she is scheduled for Trabeculectomy
next month because she has advanced glaucoma and we have run out of
treatment options. My question is, in your experience , when is this
most likely to happen and why. What has the experience been elsewhere
and what types of uveitis are we to be concerned with when using prostaglandins?
For example can we use them safely with post-op cataract patients?"
Douglas R. Anderson, M.D. answers, "The prostaglandin analogues
infrequently cause a true inflammation, even if they cause vessel dilation
of the conjunctiva (hyperemia) and some stinging. However, uveitis specialists
do believe that they aggravate an underlying uveitis or tendency toward
uveitis in some individuals (not all). In some ways it is not surprising
that a prostaglandin analogue would incite inflammation, and it was
a big concern when these drugs were first being developed, because physiologically
some prostaglandins are local mediators of an inflammatory response.
(Other prostaglandins perform other functions). The scientists developing
these drugs for glaucoma studied the slight chemical differences in
various prostaglandins to determine which parts of the molecule were
responsible for particular responses, and the happy surprise was that
they were able to find one with minimal inflammatory tendency that had
a big effect on IOP. However, given genetic differences between people,
some may have receptors that produce inflammation when stimulated by
a prostaglandin that in most people would not produce inflammation.
In the big picture, it is therefore not surprising that some people
respond differently than others to a drug--for example, some are more
responsive than others to the beneficial effect of lowering IOP, and
some are more responsive than others to the adverse effects as well."
The OGS annual meeting was held on December 7th,
2005 in La Jolla, California (see photo above). The meeting was filled
with cutting edge material from some outstanding researchers. The majority
of presentations were from the faculty of the Hamilton Glaucoma Center,
UC San Diego. Some of the presentations included: 1) The use of functional
magnetic resonance imaging (fMRI) and other novel imaging techniques
to map out areas of the brain that no longer receive input in patients
with glaucoma 2) Machine learning classifiers (sophisticated mathematical
processes that can separate groups based on features that may not be
obvious) that are able to detect subtle damage in the visual field of
glaucoma suspects before they would be classified as abnormal using
conventional visual field analysis techniques 3) A discussion of glaucoma
risk calculation based on the findings of the OHTS study and incorporated
into a user-friendly slide rule 4) A study to examine nocturnal
IOP curves in several hundred patients which has led to a reevaluation
of when the IOP is highest 5) A presentation by our honoree, Dr Stephen
Drance, about lessons learned from the Normal Tension Glaucoma Study.
This presentation was peppered with insightful comments, anecdotes and
a healthy back and forward between Drs Drance and a past
honoree, Dr. Douglas Anderson. A supplement of the meeting will be delivered
with the March issue of Review of Optometry. A PDF version will be available
in March online at www.optometricglaucomasociety.org.
The International Perimetric Society will hold its XVIIth meeting in
Portland, Oregon, July 11th - 14th, 2006. Approximately 90 papers and
posters will feature all aspects of automated perimetry, the development
and/or evaluation of new perimetric and psychophysical tests, use of
statistical methods for identifying glaucomatous abnormality and progression,
and related research in glaucoma detection and monitoring. There will
also be a special session on optic nerve head and nerve fiber layer
imaging with emphasis on new techniques for assessing structure and
detecting change. The social program includes an opening reception,
a concert by New York diva Ann Hampton Callaway, an excursion to the
Columbia River Gorge, and the IPS Banquet, which includes a tradition
of delegates singing in national groups. More information can be obtained
from the IPS.
The abstract submission deadline is fast approaching.
The Role of New Zealand Optometrists in Glaucoma
Optometrists in New Zealand have always played some role in the detection
and referral of patients with glaucoma. More recently, and particularly
with the recent introduction of Optometric therapeutic laws, the role
of NZ Optometrists in glaucoma management is becoming better defined.
The Health Practitioners Competence Assurance Act 2003 (HPCAA) came
into effect in 2004, bringing with it the right for suitably trained
Optometrists to prescribe a range of topical medications, but excluding
those for glaucoma. Therefore, Optometrists in NZ do not currently have
the right to prescribe or change glaucoma medications. This said, Optometrists
are increasingly working closely with Ophthalmology in the early detection
of glaucoma and ensuring already diagnosed patients receive timely monitoring,
including IOPs, visual fields and drug compliance. In some instances,
patients with stable glaucoma will see their optometrist at intervals
between their ophthalmology visits, with the optometrist reporting findings
back to the ophthalmologist.
As already mentioned, the major change recently in the practice of Optometry
in NZ has been the introduction of prescribing rights to a wide range
of topical therapeutic agents.
The classes of drugs currently available to Optometrists include: a
select list of antibiotics, anti-virals, anti-allergy medications and
anti-inflammatories as well as combination drugs from these classes.
Prescribing Optometrists need to have undergone an accredited TPA course,
the majority of whom have undergone, or are in the process of undergoing,
the University of Aucklands therapeutic course. The University
of Aucklands Optometry course (BOptom) has progressively undergone
modifications over the past few years so that the present (2006) final
year optometry students will be the first to graduate with full therapeutic
Geraint Phillips is Clinic Director, Department of Optometry and
The University of Auckland, Auckland, New Zealand.
Geraint Phillips BSc, MCOptom, DCLP, OD, Algis Vingrys BScOptom,
Multi-center clinical trials for glaucoma and
related ocular disorders have been quite limited except for the past
15-20 years. These recent investigations have provided valuable insights
into some fundamental questions concerning the management of glaucoma,
spanning a range of clinical concerns. This paper will provide a brief
review of five clinical trials: the Advanced Glaucoma Intervention Study
(AGIS), the Collaborative Initial Glaucoma Treatment Study (CIGTS),
the Collaborative Normal Tension Glaucoma Study (CNTGS), the Early Manifest
Glaucoma Trial (EMGT) and the Ocular Hypertension Treatment Study (OHTS).
AGIS was a multi-center study (11 clinical centers) that began in 1988
and ended in 2001. Medically uncontrolled open-angle glaucoma patients
(591 patients, 789 eyes) were randomized to a treatment sequence of
(1) argon laser trabeculoplasty, trabeculectomy and trabeculectomy (ATT),
or (2) trabeculectomy argon laser trabeculoplasty and trabeculectomy
(TAT). The main findings include a race-treatment interaction for trabeculoplasty
and trabulectomy (African Americans respond better to argon laser trabeculoplasty
first, while Whites do better with trabeculectomy first after 7 years
of follow-up), a decrease in visual field progression with lower intraocular
pressure, an increased risk of cataract formation following trabeculectomy,
and identification of risk factors for failure of the two treatments.
CIGTS enrolled 607 patients and followed them between 1993 and 1997
to determine whether medical therapy or surgical treatment (trabeculectomy)
was more effective in managing newly diagnosed glaucoma patients at
14 clinical centers. The study revealed no difference in visual field
loss between the two groups. Trabeculectomy patients had lower intraocular
pressures, a greater risk of visual acuity loss and cataract development
and local eye symptoms. The findings do not support any alteration of
current practices for managing newly diagnosed glaucoma patients.
CNTGS was a multi-center (24 clinical centers) trial of normal tension
glaucoma patients (20 mm or less intraocular pressure) that enrolled
one eye of 230 patients. Two hypotheses were evaluated: (1) that glaucoma
is intraocular pressure independent, and (2) that intraocular pressure
participates in producing glaucomatous damage in normal tension glaucoma.
One group was carefully observed without treatment, while the other
group had medical and/or surgical treatment to produce a 30% or
more reduction in intraocular pressure. The main findings were that
intraocular pressure reduction was beneficial to normal tension glaucoma
patients by diminishing the rate of progression, and that treatment
should be individualized according to the stage of glaucoma and rate
EMGT is a clinical trial designed to evaluate the effectiveness of reducing
intraocular pressure in early, previously untreated patients with open-angle
glaucoma by comparing one group undergoing trabeculoplasty and medical
therapy to another group undergoing careful observation. In the treated
group, progression of glaucomatous damage was significantly reduced
by approximately 50%. Older age, higher intraocular pressure, exfoliation
and worse Mean Deviation were found to be important risk factors for
OHTS evaluated more than 1,600 patients (25% of which are African
American) at risk of developing glaucoma, but who had reliable visual
fields and optic nerve heads that were within normal limits at baseline.
Half of the patients were randomly assigned to treatment and half underwent
careful observation. Topical medical treatment for five years (20%
or more intraocular pressure reduction) significantly reduced the incidence
of glaucoma by more than 50%, with slightly more than half of the
glaucoma endpoints being optic disc changes and only about 10% of
the endpoints being both optic disc and visual field endpoints. Risk
factors for development of glaucoma included older age, larger horizontal
or vertical cup-to-disc ratio, higher intraocular pressure, greater
pattern standard deviation and thinner central corneal measurements.
A quick literature search can provide references to the full reports
from these studies for those readers wishing to become familiarized
with more detailed information. The results of these trials generally
indicate that treatment significantly reduces the onset and progression
of glaucomatous damage, throughout the entire spectrum of the disease
process. It should also be noted that there are many other clinical
trials underway or completed to evaluate the safety and efficacy of
various treatment regimens, most of which are sponsored by the pharmaceutical
industry. Through these combined efforts, we have gained a better understanding
of the diagnosis and treatment of glaucoma and have identified a number
of additional clinical research questions that need to be evaluated.
Chris A. Johnson, PhD
Not since the introduction of pilocarpine topical therapy in the late
1800s has the management of glaucoma been so affected by the introduction
of a new chemotherapeutic class of agents. The prostaglandins brought
high efficacy, safety and convenience to the treatment of this potentially
devastating condition. The effect of these compounds on the management
of glaucoma is best illustrated by the results of a retrospective review
of the number of glaucoma surgeries performed between 1994 and 1999
(Strutton and Walt 2004). Following the introduction of Latanoprost
in 1996 the number of inpatient glaucoma surgeries dropped by 72%
and the number of outpatient procedures dropped by 42%. The profound
efficacy of this group of medications also provided clinicians with
the ability to have a greater degree of success in medically managing
their patients. This has reduced the number of these patients referred
for glaucoma consultation. Furthermore, since their introduction, the
use of other classes of ocular hypotensive drugs has fallen sharply.
Because of their high efficacy, the number of patients requiring combination
therapy has also fallen. When taken as a whole, the reduction in referrals,
drugs, and surgical procedures has made the management of glaucoma less
costly and more efficient.
The first clinical study of the use of prostaglandins to reduce IOP
was performed by Camras using the compound prostaglandin PGF-2alpha.
It produced a limited reduction in IOP with significant side-effects
that included conjunctival hyperemia, foreign body sensation and headache.
Other prostaglandin analogues which included PGD-2, PGF-2, PGF-2 alpha
isopropyl ester and PGF-2 alpha metabolite isopropyl unoprostone were
all evaluated with limited success. In general, side-effects were significant
and efficacy was low.
A breakthrough came with the development of the prostaglandin analogue
PhXA34. This compound was produced by modification of the PGF-2 alpha
molecule. A phenyl group was added at position 17 and the double bond
at C 13-14 reduced. These changes affected potency as well as reducing
side-effects. This molecule went on to become latanoprost (Xalatan).
Since the release of Xalatan, two additional analogues have been approved:
bimatoprost (Lumigan) and travoprost (Travatan).
Efficacy and Side-effects
Efficacy and side-effects of the PGF-2 alpha analogues appear to be
tied to their affinity for two major receptors: FP and EP1. Efficacy
is directly related to affinity for the FP receptor with all three available
medications showing high affinity for this receptor (MR Hellberg, et
al. 2001, J. Ocular Pharmacol. Therapeu.). This leads to relatively
equivalent efficacy among the three compounds (Parrish, XLT study 2003).
The average IOP drop from baseline ranges from 27-34% (various studies)
with once daily use in the evening.
Several common side effects appear to be associated with affinity for
the EP1, IP and PGD 2 receptors. (Woodward, et al 1996) This may be
the reason for the differing degrees of itching and hyperemia found
in the three competing drugs. Hyperemia is greatest with bimatoprost
and least with latanoprost.
One potential side-effect associated with prostaglandins is the permanent
darkening of the iris. This generally occurs after several months of
therapy and is most common and cosmetically important in those with
green-brown and blue brown irides. The incidence is in the range of
3-8%. The drugs also have the potential to increase the growth of
lashes and periocular pigmentation (Grierson et al, 2004). Lash position
may also be affected. The drug generally produces no adverse pulmonary
or cardiovascular side-effects and has not been shown to affect ocular
hemodynamics. The use of the prostaglandin compounds should be avoided
in eyes with active inflammation or inflammatory glaucoma. Inflammation
can be exacerbated by this class of agent. Caution should be exercised
in pseudophakia and aphakia. Reversible CME has been reported in these
groups. The drug is classified as a category C drug for pregnant patients.
Most important in the management of any disease is patient compliance.
In 2002 Spooner reported that 25-40% of patients discontinued their
topical glaucoma therapy within three months of initiation of therapy.
Still, compliance was best with the prostaglandin analogues. The once
daily dosing regimen for prostaglandins, ease of use, lack of systemic
side-effects and high efficacy are factors that contribute to improved
There is great debate surrounding the efficacy of the different PGs.
This is chiefly a result of conflicting results in two major studies
of relative prostaglandin efficacy (Parrish 2003 and Noecker 2003).
Currently there is a general consensus that the drugs are equivalent.
However, several studies suggest that patients that show lack of efficacy
with one agent may benefit from a trial with another (Kaback et al 2004,
Emerick 2005) although this may be explained by renewed compliance associated
with medication changes.
The DOC (Drug of choice)
The results of the EMGT study suggested that for every millimeter reduction
in IOP there was a corresponding decrease in risk of progression of
glaucoma. Therefore, until another method of risk reduction for glaucoma
is found, the lowering of IOP will remain the method of choice and the
prostaglandin analogues the medical treatment of choice.
We hope to see the current prostaglandin analogues combined with other
anti-hypertensive drugs so that fixed-combination agents become available.
This may improve patient compliance, however is unlikely to produce
a dramatic gain in efficacy compared with the separate use of these
medications. Still several of these medications are available in other
parts of the world but due to the stringent requirements put forth by
the Food and Drug Administration, none have been approved in the U.S.
at this time.
Bruce Onofrey, OD, RPh, FAAO
1. Akarsu C, et al, Short-term effect of latanoprost
on Ocular circulation in ocular hypertension, Cl and Exp. Ophth 2004;32:373-7
2. Bearden W, Anderson R. Trichiasis associated with prostaglandin analog
use, Ophth Plastic and Reconstructive Surg 2004; 20: 320-2
3. De Santis M, et al, Latanoprost exposure in pregnancy, Am J of Ophth.
2004; 138: 305-6
4. Arranaz-Marquez E, Analysis of irises with a latanoprost-induced
change in iris color, Am J of Ophth. 2004; 138: 625-30
5. Przydryga J, et al, Ocular hypotensive efficacy of travoprost in
patients unsuccessfully treated with latanoprost, Current Med. Res and
Opinion 2004; 20: 1341-5
6. Kurtz S, Shemesh G, The efficacy and safety of once-daily versus
once-weekly latanoprost treatment for increased intraocular pressure,
J of Oc Pharm and Ther 2004; 20: 321-7
7. Emerick G, Prostaglandin non-respondersGlaucoma Today 2005; 3:
8. Parrish RK, et al A comparison of latanoprost, bimatoprost, and travoprost
in patients with elevated intraocular pressure: a 12-week, randomized,
masked-evaluator multicenter study. Am J Ophth. 2003; 5: 688-703
9. Spooner JJ et al., Rates of discontinuation and change of glaucoma
therapy in a managed care setting.Am J Manag Care. 2002 Aug;8:S262-70.
PRIMARY CARE OR SUBSPECIALTY
A thought-provoking article
in the November, 2005 Review of Ophthalmology prompted this brief
There are a few things in life that if they were never improved, would
still be fine. Some examples are ice cream, HDTV, airplanes, bicycles,
cataract surgery, contact lenses, shoes, wristwatches. This is not to
say they are perfect, but they are amply sufficient. Glaucoma diagnosis
on the other hand leaves something to be desired. Lets face it,
people pass through eye doctors offices everyday with glaucoma
and the clinician seems blinded (pardon the pun) to its existence. If
glaucoma therapy never improved beyond where it is in March, 2006, virtually
every person with glaucoma would be well cared for. The weak link with
glaucoma is in its detection. The eye care professions, if they really
cared about preventing vision loss from glaucoma, would discipline themselves
to come together and develop creative initiatives to get people to seek
eye care, or at least be meaningfully screened.
One area we have identified is in finding a mechanism to educate primary
care physicians to: (1) become competent at direct ophthalmoscopy, and
(2) be trained to grossly quantify enlargement of optic nerve head cupping.
In this manner, the population screening net would be enlarged. Wouldnt
it be neat if the AGS and the OGS formed teams to go to hundreds of
primary care conferences over the next 3 years and conduct focused workshops
which would result in thousands of eyes joining us in the search for
patients with glaucoma?
Of course, then, would these patients ultimately be seen by a glaucoma-competent
eye doctor? Just this month a patient presented who had been on 4%
pilocarpine for the past 20 years. She faithfully takes her drops QID,
and not one millimeter of the retina could be viewed at the initial
visit. She has carried a diagnosis of diabetes for the past 12 years,
and has never even heard the term "hemoglobin A1C." That same
week, a patient presented with 0.8 cups who had been seen annually for
many years and had never been told he might have glaucoma, and, of course,
had not been worked up. Obviously, there are enormous obstacles hindering
detection, diagnosis, disease quantification, and therapeutic intervention.
Sophomoric bickering on who does what should pale in the face of permanent
In the Review article, a question is asked regarding a hypothetical
shortage of fellowship trained glaucoma subspecialists: "How a
shortage is resolved will depend partly on what the role of optometrists
becomes: will they be primary-care providers, or will that be the province
of ophthalmology?" Glaucoma is not a "province"; it is
a shared responsibility we all should embrace as a united team goal
for a common good. Dr. Spaeth says: "Studies have shown that many
optometrists are good at judging the condition of an optic disc, and
some ophthalmologists are not so good at it. The most important thing
is whether a person is knowledgeable, competent, and well-trained."
Randall Thomas, OD and Ron Melton, OD
This section contains questions from readers
of the journal with answers and comments from editorial board members.
"I would like to purchase an optic imaging instrument to help to
diagnose glaucoma. Which of the instruments - OCT, GDX, HRT - has the
most validity in diagnosing who has glaucoma vs. glc suspects? Do GDX
and OCT give the same results, or is one significantly more valid? Can
I "hang my hat" and rely on the results of any one of them?"
Murray Fingeret OD answers, "Imaging instrumentation is
rapidly becoming part of the glaucoma workup, and its role is to supplement
the examination findings (optic nerve, visual field), not drive the
diagnosis. For example, someone with an apparent healthy optic nerve
and elevated IOP, imaging may reveal subtle changes to the retinal nerve
fiber layer or rim tissue. Several studies have shown that in 25-40%
of conversions, the initial glaucomatous findings are in the visual
field. Does this mean that the optic nerve is entirely healthy? Probably
not, but more likely for different reasons (i.e. small optic nerve),
the changes are difficult to detect. In regards to which instrument
may be "more valid" in diagnostic capabilities, there are
few head to head studies using present day instruments. Older studies
are misleading because they use instruments or software no longer being
made. From the few studies available, the instruments appear to perform
remarkably similar in regards to their diagnostic capabilities. Still
for an individual patient, the OCT may reveal loss that the GDx may
underestimate or vice versa. The same may occur when comparing the HRT
and the RNFL instruments. In regards to "can I hang my hat and
rely on the results", no imaging instrument offers 100% sensitivity
and specificity. Thus the user needs to recognize when the device may
be over or under calling a situation and use the data appropriately.
The imaging instruments represent a large advance in how we can evaluate
the RNFL/Optic Nerve BUT they are far from perfect and it is the "astute"
clinician who understands how to integrate the analysis into the clinical
Optic Nerve Assessment
"It has been my experience, as an optometrist in the Indian Health
Service for more than 16 years, that the ISNT rule does not apply to
normal optic nerves in most cases. Usually, the inferior rim is thicker
than the superior in the normal nerve, but the nasal rim is thicker
than both the superior and the temporal rims. The more appropriate expression
of normality with respect to rim thickness would be IS, then NT."
Douglas R. Anderson, M.D. answers, "The observation that
the nasal side can seem larger than either the inferior or superior
rim is correct, but it depends on whether you include the major vessels
that line the cup as part of the neuro-retinal rim, I think. If you
include only the tissue that is outside the vascular trunk, the remaining
nasal tissue, which is after all the neural tissue, is generally thinner
than the superior or inferior rim. The trick is to think of the neuro-retinal
tissue proper and count the vessels as being part of the cavity. In
my experience the ISNT rule does apply to just about any disc, although
some disagree about the validity of the rule in large discs. And it
is possible you have stumbled on a particular exception among native
Americans. Perhaps you could send photographic examples for us all to
"Now, in rare cases with a temporal wedge field defect, there is
localized loss of tissue in the nasal neuro-retinal rim as the earliest
sign of glaucoma, and this is recognized when there is excavation nasal
to the trunk of vessels. Of course, because anatomy of the disc in the
absence of disease is highly variable, there remain times when any rule
is mimicked by an anomaly, and sometimes it is impossible to say with
certainty that a disc is glaucomatous or not glaucomatous on a single
occasion, but it takes observation over time to see change in anatomy
as a sign of glaucoma."
"I have a patient that is level 5 mentally retarded. It requires
restraint to examine him in any way and would require general anesthetic
to get IOPs or retinoscopy or autorefractor (I've tried the Welch Allyn
hand held). He is taking Topamax. Should I be concerned? Should I have
him put under to determine his status?"
Thom Zimmerman M.D., Ph.D., answers, "With a patient that
is level 5 MR I would put him under general anesthetic in order to get
baseline information on everything. Then, I would follow him the best
that I could until I suspected a change in condition. Then I would put
him back under to verify changes from the established baseline."
Douglas R. Anderson, M.D. answers, "On the mentally retarded
patient, it is simply a difficult patient to examine, and therefore
difficult to be certain of his state. Topomax can cause problems, but
obviously doesn't in everyone. Because he is on Topomax, you might look
at his iris with a flashlight inconspicuously to the side while playing
with him, you may get an idea of the convexity of the iris, feeling
relieved if there is none and considering an examination under anesthesia
if the iris plane seems bulged forward. You might also be helped by
observing his behavior while not being disturbed by your attempt to
touch and examine him. Are his eyes red, does he seem to have pain and
rub his eyes, can he see small things like sugar sprinkles, etc. If
you have no reason to suspect an ocular problem, you may not need to
go looking for one. Why even do a refraction if he sees sufficiently
for whatever daily activities he has. I don't think anyone can really
help you decide what to do without seeing the patient."
If you would like us to answer a clinical question, please send it to
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.
RESULTS FROM OGS E-JOURNAL VOLUME 1, NUMBER 1
The forthcoming World Glaucoma Congress (WGC-2007) will be held
in Singapore, July 18-21, 2007.The Global Glaucoma Society Assembly
will be held on the first day of the WGC: July 21, 2007, in the
- VISUAL FIELD REVIEW
The visual field shown came from a patient with a diagnosis of
POAG with left glaucomatous optic neuropathy. CDR was 0.85 with
clinical observation of nasal disc excavation. Moorfields regression
analysis from HRT II revealed that all three nasal sectors of
the optic disk had rim areas that fell below the lowest 99.9%
of the normal dataset distribution.
Paul Spry PhD MCOptom
Brad Fortune, OD,
Shaban Demirel, BScOptom,
Algis Vingrys BScOptom,
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
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