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Volume
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August
2006
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OGS
PRESIDENT'S MESSAGE
I
would like to welcome everyone to this issue of the OGS e-journal. This
issue completes our first year of publishing and I would like to thank
Richard Andes and Richard Black from Pfizer, Inc. for extending our
unrestricted grant for another year. This issue is being circulated
to a wide audience as we are trying to make as many people as possible
aware of this journal. If you would like to continue receiving this
e-journal, information on how to sign up may be found at the by
clicking on this link.
I would like to thank Paul Spry, our editor-in-chief and associate editors
Shaban Demirel, Brad Fortune and Algis Vingrys as well as the editorial
board for having worked tirelessly to produce each issue. We welcome
your comments, questions and feedback and, please let us know of how
we can make this e-journal better. We have a section addressing questions
posed by readers so feel free to send in the question(s) you always
wanted to ask.
Optometry’s role in glaucoma is expanding. This is best illustrated
by viewing the table of contents from the August issue of Optometry
and Vision Science. This special issue dealt with glaucoma, and many
of the original research papers were done by optometrists. This is not
surprising as many optometrists have been involved in the management
of glaucoma for well over a decade. The sophistication shows in regards
to the instrumentation we purchase, the clinical outcomes we achieve
and slowly but surely, the clinical research we develop.
Hopefully this momentum can continue. One area that we need to develop
is creating opportunities for young optometric researchers interested
in glaucoma. Optometry has not held glaucoma research as a priority,
and rather has developed and performed important work in cornea, contact
lenses and visual science. Hopefully glaucoma’s time has come and
this will be the next area Optometry concentrates on as our students
and profession are ready.
Murray Fingeret, OD
President, Optometric Glaucoma Society
murrayf@optonline.net
EDITORIAL
 |
Progressive
Visual Field Testing
All clinicians managing glaucoma must decide how frequently to examine
patients. Those who have taken part in such discussions know that it is
a not straightforward question to answer, primarily because of the considerable
heterogeneity that exists amongst patients diagnosed with chronic glaucoma:
no two individuals’ conditions, or risk factors for progression,
are alike. In my experience, follow-up intervals are pragmatically categorised
into two groups;(1) short - intervals for those with uncontrolled IOP,
who require regular examinations to establish the effectiveness of new
treatment interventions on IOP; and (2) longer follow-up intervals for
those whose IOP is purportedly controlled. This latter group is generally
larger and requires more lengthy examination and thorough assessment of
the key outcome measures (disc, field) that determine whether current
IOP control is maintaining the ideal outcome of stability. So, how often
should these patients be reviewed? In the last OGS E-journal poll we asked
our readership how often they measured the visual field on stable glaucoma
patients. The answers we received (see below) varied from less than annually
to more than 3 times per year, although 95% of respondents tested
fields either once or twice per year. The justification for less frequent
testing could be that longer inter-test intervals would allow truly progressive
patients to be readily identified just by eyeballing the field plots.
This may be reasonable for the substantial majority of ‘controlled’
glaucoma patients but may miss those individuals who, rarely and unpredictably,
progress rapidly. The argument for frequent testing is that it may rapidly
detect small statistically significant changes.
Studies on the subject of visual field test frequency have demonstrated
that increasing the test frequency from annually to three times per year
take years off the time to detection of statistically significant progression
(1), although conversely can negatively impact ability to correctly identify
stable field series (2) or may invoke the law of diminishing returns such
that testing beyond a certain frequency affords very little information
benefit (3). A further option, proposed in a paper by NM Jansonius at
the recent International Perimetric Society meeting, held in Portland,
Oregon USA from July 11-14th (4) found that performing an annual test
combined with rapid repeat testing if progression was suspected did no
worse than regular testing with either 2 or 4 tests per year in terms
of time to progression detection, and identification of truly worsening
fields. Putting all this into context, these studies tell us that definite
progressive defects, by which I mean statistically significant changes
in threshold sensitivities, can be identified promptly and effectively
and that this information can be obtained by either sufficiently regular
testing with reasonable frequency, or alternatively by retesting rapidly
if doubt exists as to whether the field stable.
As with all good questions though, the answer begs another question, what
degree of visual field change is clinically important? This question is
a very different debate.
Paul GD Spry, PhD, MCOptom, DipGlau,
Editor-in-Chief
paul.spry@ubht.nhs.uk
References
1. Viswanathan AC, Hitchings RA, Fitzke FW (1997). How often do patients
need visual field tests? Graefes Arch Clin Exp
Ophthalmol.;235(9):563-8.
2. Gardiner SK, Crabb DP (2002). Frequency of testing for detecting visual
field progression.Br J Ophthalmol.;86(5):560-4.
3. Wild JM, Hutchings N, Hussey MK, Flanagan JG, Trope GE (1997). Pointwise
univariate linear regression of perimetric sensitivity against follow-up
time in glaucoma. Ophthalmology;104(5):808-15.
4. http://webeye.ophth.uiowa.edu/ips/Meetings/Portland-2006.htm
OGS
DEBATE
This is the first in
a new occasional series where we have asked individuals to make an argument
for or against an area of discussion. In this issue, the motion is,
"Monocular treatment trials are the ideal way to verify the effectiveness
of initial anti-glaucoma medications."
In favor of monocular treatment trials
Initiation of topical medical therapy in one eye as a tool to judge
efficacy of a therapeutic agent is a traditional approach employed by
many clinicians. Increased demands for clinical efficiency have prompted
some practitioners to forego this step. The value of the monocular trial
has recently been called into question (1, 2).
In a retrospective review of 52 patients, it was shown that the reduction
of intraocular pressure in the first eye was not always predictive of
the response for the second eye (1). This comparison was based on a
single pressure reading pre- and post-treatment in each eye. Although
this appears to provide evidence to question the usefulness of the monocular
trial it falls far short of supporting their widespread abandonment.
The main reason for this is that the study used single measurements,
and single measurements do not provide high-validity quantifications
of IOP. Single measures can be impacted by a number of sources of measurement
noise, including systematic and unsystematic errors related to instrumentation,
technique and clinician, not to mention physiological and pathophysiological
variation. Can we be sure that all these factors were controlled in
this retrospective study? Also, are the 52 patients sufficiently representative
of all glaucoma patients to change practice and abandon such trials
for good?
First of all, when assessing IOP there is no substitute for an adequate
baseline. Whenever possible, this baseline includes multiple IOP readings,
optimally at various times of the day because intraocular pressure fluctuates.
Such a baseline can be achieved before starting a monocular treatment
trial. Decisions to initiate or change therapy and judgments of therapeutic
benefit of medications may be best made with the benefit of more than
one IOP reading, ideally both before and after starting a new medication.
Combined with a monocular trial, this approach may provide the best
chance of assessing the true effectiveness of a medication.
Observation of the fellow eye during a monocular trial allows us to
be more confident that the treated eye enjoys a meaningful therapeutic
response because it provides a control for variability common to both
eyes. This may be particularly true with second and third agents where
the additional effect of the medications, although important, may not
achieve the same magnitude as the first agent. Therapeutic benefit may
be less obvious or exaggerated in these cases. Multiple pressure readings
can be helpful here. Again, while imperfect, the control of the fellow
eye in a monocular trial may provide valuable insight, and potentially
prevents us from both ruling out effective medications and continuing
to use those that are ineffective.
We are fortunate to practice at a time when we have many therapeutic
options to offer our patients. It is important to have a sense of what
each component of our therapeutic regimen is contributing to patient
care. The monocular treatment trial provides us with the best chance
of this.
John McSoley, OD
References
1.Realini T, Fechtner RD, Atreides SP, Gollance S. The uniocular drug
trial and second-eye response to glaucoma medications. Ophthalmology
2004:111: 421-426.
2. Sit AJ, Liu JH, Weinreb RN. Asymmetry of right versus left intraocular
pressures over 24 hours in glaucoma patients.
Against monocular treatment trials
The monocular therapeutic drug trial was devised to help clinicians
distinguish between the therapeutic intraocular pressure (IOP) effect
of a newly-initiated medication and the spontaneous variations in IOP
known to occur over time. Treatment is initiated in one eye, and the
therapeutic effect is calculated as the change in the treated eye (composed
of both therapeutic and spontaneous changes) minus the change in the
untreated eye (solely a spontaneous change assuming no crossover effect).
The monocular trial is fundamentally dependent on the validity of several
assumptions. At the heart of the trial is the assumption that spontaneous
IOP variation is symmetric between fellow-eye pairs so that the untreated
eye can serve as a control for the treated eye. There is substantial
data to suggest that this is not true. Our group has demonstrated significant
asymmetric IOP fluctuations between fellow eyes of both normal subjects
and glaucoma patients (1) and others have recently reported dissimilarity
of diurnal curves between eyes of both normals (2) and glaucoma patients
(3).
A second assumption of the monocular trial is that the untreated eye’s
IOP is not affected by treatment of its fellow eye. This is known to
be a false assumption, as the crossover effect has been well established
for beta-blockers (although less completely characterized for newer
drug classes). In the Ocular Hypertension Treatment Study, fellow eyes
of eyes treated with a topical beta-blocker experienced a mean 1.5 mmHg
IOP drop (4).
Following a "successful" monocular trial, the drug is then
applied bilaterally, with the assumption that efficacy will be equal
between fellow eyes. This may also be a false assumption. While our
data suggest good correlation of IOP reduction in fellow eyes treated
with the same drug (5), another group has found poor correlation between
right and left eyes treated simultaneously with the same drug (Young
A et al. Association for Research in Vision and Ophthalmology 2006,
abstract # 437).
Given that the assumptions underlying the monocular trial are of questionable
validity at best, we evaluated the ability of a "successful"
monocular trial to predict the IOP response seen when the drug was then
added to the fellow eye. Perhaps not surprisingly, we found absolutely
no correlation between first-eye and second-eye IOP responses when both
were treated sequentially using the monocular drug trial (6).
Because of the dynamic nature of IOP, we cannot easily or accurately
characterize long-term IOP behavior with only a single measurement.
We routinely advocate getting multiple pre-treatment measurements to
better characterize baseline IOP before beginning treatment. Why, then,
do we so willingly make efficacy judgments based on a single on-treatment
IOP using the seriously flawed monocular trial? False conclusions based
on the monocular trial can lead to continued use of an ineffective medication,
or worse, discontinuation of an effective medication. A more rigorous
method of evaluating drug efficacy is to compare the mean of several
pre-treatment IOP readings to the mean of several on-treatment IOP readings,
and to avoid the knee-jerk tendency to switch treatments if the first
on-treatment IOP is not at target.
Tony Realini, MD
Associate Professor, West Virginia University, Dept of Ophthalmology
References
1. Realini T, Barber L, Burton D. Frequency of asymmetric intraocular
pressure fluctuations among patients with and without glaucoma. Ophthalmology
2002;109:1367-1371.
2. Liu JH, Sit AJ, Weinreb RN. Variation of 24-hour intraocular pressure
in healthy individuals: right eye versus left eye. Ophthalmology
2005;112:1670-1675.
3. Sit AJ, Liu JH, Weinreb RN. Asymmetry of right versus left intraocular
pressures over 24 hours in glaucoma patients. Ophthalmology 2006;113:425-430.
4. Piltz J, Gross R, Shin DH et al. Contralateral effect of topical
beta-adrenergic antagonists in initial one-eyed trials in the ocular
hypertension treatment study. Am J Ophthalmol 2000;130:441-453.
5. Realini T, Vickers WR. Symmetry of fellow-eye intraocular pressure
responses to topical glaucoma medications. Ophthalmology 2005;112:599-602.
6. Realini T, Fechtner RD, Atreides SP, Gollance S. The uniocular drug
trial and second-eye response to glaucoma medications. Ophthalmology
2004;111:421-426.
To vote in this debate, and in this issues polls, click
here.
NEW
IDEAS AND NEW PAPERS
Anatomical
and perceptual evidence for the impact of glaucoma on the visual pathway
beyond the optic nerve
There are several papers in the literature demonstrating abnormalities
of the lateral geniculate nucleus and visual cortex in non-human primate
models of glaucoma. A pair of recent papers by Gupta et al (1, 2) highlight
the fact that abnormalities in these higher structures of the posterior
visual pathway will also occur as a result of human glaucoma, and have
an important influence on our patients’ visual system, performance
and potential quality of life. The first paper (1) presents a clinicopathological
case report of a 79 year old male with recently diagnosed glaucoma. Humphrey
visual field (VF) grayscale plots at the time of diagnosis (1 year prior
to death from acute viral myocarditis) showed severe bilateral superior
hemifield loss, but also suggested that sensitivity was near normal across
most of the inferior fields. Not surprisingly, transverse sections through
the intracranial portion of each optic nerve showed marked atrophy and
axonal loss, particularly inferiorly, as compared with age-matched control
specimens. The inferior bank of the calcarine (primary visual) cortex
was also thinned relative to control samples. The overall volume of the
lateral geniculate nucleus (LGN) was reduced by about 30% compared with
controls, and cells of both magno- and parvocelluluar layers were smaller
than those in control brains (although the difference in cell size was
more robust for the magnocellular layers). The results confirm that neural
degeneration occurs at multiple levels of the central nervous system in
glaucoma. One potentially interesting finding in their paper, which was
not elaborated upon in their discussion, is that the volume of the LGN
was reduced overall, but was not just limited to the posterolateral aspect
that would correspond (generally) to the superior VF. Does this suggest
that LGN abnormalities occur even when VF sensitivity is near normal?
Does this suggest that LGN neurons might be exquisitely sensitive to reduced
input (as a result of either retinal ganglion cell loss or abnormal signaling)?
One of the authors, Dr. Yücel, confirmed (personal communication)
that: "the height of the LGN in the glaucoma case appears to be
decreased in the medial and lateral aspects in the photo" but cautioned,
"however the total volume of the LGN based on serial sections is
also decreased in the glaucoma case, and the shape of the human LGN shows
high interindividual variation compared to monkey LGNs." He indicated
that they are planning follow-up studies so that these findings can "be
examined preferably in a series of cases".
Nonetheless, additional work from this group, also published in the same
issue of the British Journal of Ophthalmology (2) demonstrated stereopsis
deficits in both glaucoma patients and glaucoma suspects with normal standard
VFs, despite good visual acuity in both eyes (>20/30) and less than
one Snellen line difference between eyes. This finding underscores the
potential functional consequences of cortical abnormalities, which they
(and others) have so nicely characterized in previous work. Collectively,
this work reminds us that we should listen to and believe our patients
when they complain of vision troubles, even if their standard visual field
and visual acuity are normal.
Brad Fortune OD PhD
References
1. Gupta N, Ang LC, Noel de Tilly L, Bidaisee L, Yucel YH. Human glaucoma
and neural degeneration in intracranial optic nerve, lateral geniculate
nucleus, and visual cortex. Br J Ophthalmol. 2006;90:674-678.
2. Gupta N, Krishnadev N, Hamstra SJ, Yucel YH. Depth perception deficits
in glaucoma suspects. Br J Ophthalmol. 2006;90:979-981.
Should you test the right eye or left eye first in automated perimetry?
Does order matter?
Most clinicians are aware that results from perimetry reflect more than
meets the eye. Hovering behind this is the word ‘psychophysics’
which examines the intersection of psychology and physics. We can accurately
measure the brightness of a stimulus spot or the contrast of a pattern
and thus pin down the physical part of this interaction. But what about
the psychological part? Estimating a patient’s concentration, fatigue
and response errors are always difficult. Additionally, if these factors
change with testing duration then the eye test order might be important.
This is especially true if normative data were collected with eye test
order kept constant.
A recent paper by Barkana et al (1) brings some data to bear on this question.
In their study, conducted on 47 consecutive patients meeting inclusion
criteria in a glaucoma subspecialty practice, the customary eye test order
(OD then OS) was reversed (OS then OD) and changes in visual field parameters
were sought. The investigators used the relatively rapid SITA standard
24-2 test on the Humphrey visual field analyzer. In short, there was no
difference in visual field outcomes or patient reliability indicators
in right eye first versus left eye first test sequences. The authors conclude
that for SITA standard 24-2 the eye test order can be reversed without
any significant effect. Previous investigators, using longer duration
full threshold 30-2 tests, found that there were differences. Perhaps
this suggests that the short test durations afforded by use of SITA 24-2
allow our patients to be largely untroubled by fatigue.
In contrast to this finding, a recent examination of eye test order in
frequency doubling perimetry (FDT) by Anderson and Johnson (2) suggests
that eye test order does matter for this procedure. Anderson and colleagues
(3) revisited this topic in their presentation at the recent IPS meeting
and suggest that the adaptation profile is not simple for this type of
perimetry. Gardiner et al (3) also reported interesting adaptational effects
for short wavelength automated perimetry (SWAP) during their presentation
at the recent IPS meeting.
In summary, when confronted with the question "does eye test order
matter in automated perimetry," think of quantum physics. The answer
is both yes and no depending on the test.
Shaban Demirel BScOptom, PhD
References
1. Barkana Y, Gerber Y, Mora R, Liebmann JM, Ritch R. Effect of eye testing
order on automated perimetry results using the Swedish Interactive Threshold
Algorithm standard 24-2. Archives of Ophthalmology 2006;124:781-4.
2. Anderson AJ, Johnson CA. Effect of dichoptic adaptation on frequency-doubling
perimetry. Optometry and Vision Science 2002;79:88-92.
3. Abstracts from the recent International Perimetric Society (IPS) meeting
in Portland, Oregon appear in the following pdf file. Clickable link to
the following. http://webeye.ophth.uiowa.edu/ips/Meetings/2006/IPS06_program.pdf
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. We would like to tell you about the work of these
individuals and in this issue we will profile founder OGS member John
Flanagan PhD, MCOptom, FAAO, who is Professor at both the School of
Optometry, University of Waterloo and the Department of Ophthalmology
and Vision Sciences, University of Toronto., Director of the Glaucoma
Research Unit, Toronto Western Research Institute, Senior Scientist
at the Toronto Western Hospital, University Health Network and member
of the Institute of Medical Sciences, Faculty of Medicine, University
of Toronto.
Dr. Flanagan’s research interests are primarily in the area of
glaucoma. A major initiative for the last ten years has been working
with a multidisciplinary team to understand the role of ocular biomechanics,
particularly of the optic nerve and lamina cribrosa, in the pathogenesis
of glaucomatous optic neuropathy. Finite element models have been developed
using both generic and patient specific reconstructions of optic nerve
region, in order to investigate the strains generated within the tissues
following an increase in IOP. Of late the research has focused on the
role of sclera in determining the optic nerves biomechanical response.
The models have also led to the development of primary cell culture
models of glaucoma that are capable of reproducing the biomechanical
environment by controlled stretching of the human optic nerve head cells.
Oxygen and carbon dioxide levels can also be manipulated to induce controlled
levels of hypoxia. Along with investigating basic aspects of the cellular
response to insult, the cell culture models have been used to probe
mechanisms of neuroprotection.
Dr. Flanagan is also interested in the role of ocular hemodynamics in
patients with glaucoma, including the investigation of retinal vascular
reactivity and diurnal variations in ocular perfusion, IOP, blood pressure
and ONH topography. Research continues in the area of clinical psychophysics
and imaging of the optic nerve and nerve fibre layer, and the understanding
of the structure/function relationship. Additional research interests
include investigating the role of sleep physiology in the development
and progression of aspects of glaucoma, and the development of a sterile,
universal, barrier system for contact ophthalmic devices.
Dr. Flanagan collaborates with a retinal research group and has a particular
interest in diabetic macular edema, its natural history and the predictive
risk factors for its development. This program of research has included
the development of techniques to image retinal edema.
VISUAL
FIELD REVIEW
Is
this a case of bilateral glaucoma?
This 66 year old female was referred for your opinion as a glaucoma
suspect. Optic nerve head evaluation revealed vertical cup-to-disc ratios
of Right 0.8 and Left 0.85. The patient had IOPs of R 18 and L 20 mmHg.
Your visual field testing gives the following outcomes. What is your
diagnosis?
Figure A
|
Figure B
|
This
is an interesting case of bilateral field loss. In this patient both
field results are reliable and fail on the criteria detailed in the
last edition (abnormal GHT, PSD or Pattern Deviation defect cluster).
So the case might be one of bilateral glaucoma. However, any field loss
that affects BOTH eyes needs to rule out cortical causes. Glaucoma field
losses point to, or involve, the blindspot and display nasal steps.
Cortical defects point to, or involve, fixation and show vertical (Chamblin)
steps. In our case both eyes involve fixation and show vertical steps.
The vertical step can be easily evaluated by comparing the dB values
across the mid-line. The left eye shows the following, starting just
above fixation and moving downward: -6/-25; -4/-29; -5/-29; -12/-27
and -8/-26. All five are abnormal (> 4-6 dB difference). Likewise
the right eye has abnormality from the second point below fixation downward:
-3/-30; -7/-29 and -9/-17. For diagnostic purposes, the presence of
2 points respecting the vertical in each eye is suspicious and 3 points,
diagnostic of a cortical defect. Edge points should be viewed with caution.
In this case the nature and number of affected points is consistent
with a cortical cause of field loss. The comparison across the vertical
is simple to perform and valid because the respective points lie at
the same eccentricity, so the only difference between them should arise
from short-term fluctuation. In cases where the difference between neighbors
exceeds more than 2x short-term fluctuation (approximately 2 dB centrally
and 3 dB peripherally) a vertical step is suspected. This case demonstrates
how to evaluate a visual field in the presence of binocular defects.
The patient reports a history of stroke 3 years earlier. However, the
left eye also shows a defect that points to, or involves, the
blindspot in the superior arcuate region: this provides support for
the complicated diagnoses of low tension glaucoma and a left cortical
defect. The clinician needs to base their diagnosis on repeat field
tests, IOP, anterior chamber and optic nerve assessment.
Algis Vingrys BScOptom, PhD
IMAGE
REVIEW
This 53 year old African American Male was recently
diagnosed with primary open angle glaucoma. The damage is greater in
the left eye (field loss is present only for the left eye), and the
following are the fundus photographs and imaging printouts from the
HRT 3, GDx VCC and OCT Stratus. Figures A and B show the optic nerves,
which are average in size. The right optic nerve obeys the ISNT rule,
zone beta peripapillary atrophy is present temporally and there are
no signs of retinal nerve fiber layer (RNFL) loss or disc hemorrhages.
The left optic disc does not obey the ISNT rule as the neuroretinal
rim tissue is thinner superiorly. There is zone beta peripapillary atrophy
from 1-5 o’clock. Neither disc hemorrhages nor RNFL defects are
present.
Figure A
|
Figure B
|
The basics of analyzing printouts from imaging instrumentation are similar
to observing disc photos, and the first step is to analyze image quality.
Are the optic nerves centered within the frame, the image evenly illuminated
and in focus, and for each instrument, is the quality indicator within
the expected range? For the HRT 3 image (Figure C), the image quality
is excellent in both eyes. The disc size is average. The cup is larger
in the left eye and the rim area and rim volume smaller in the OS. The
RNFL is also thinner in OS, and the Moorfields Regression Analysis is
within normal limits for the right eye in all sectors but for the left
eye, several sectors are flagged superiorly and nasally as having a
less than 5% chance of falling within the range found in a normal population.
Figure C
|
In evaluating the GDx VCC printout (Figure D), image quality is excellent
and the nerve fiber layer maps are dark blue for each eye, though darker
for OS. The deviation maps show a series of contiguous pixels flagged
for the left eye with RNFL thickness as unlikely to fall within the
normal range. The band of flagged points extends both superiorly and
inferiorly from the optic disc and the TSNIT curves show loss in both
eyes. The right TSNIT curve is still within the normal band (but barely),
while the left eye shows loss superiorly and inferiorly. The figure
comparing the RNFL TSNIT curves show the loss to be greater for the
left eye.
Figure D
|
The OCT Stratus printout (Figure E) is also of very good quality (signal
strength = 8). The RNFL analysis for the right eye is different from
the GDx in that it appears to be healthy and within the normal limits.
Examining the TSNIT curve, the OS shows loss which is greatest superiorly.
The parameters are also flagged only for the left eye.
Figure E
|
In summary, these printouts from three instruments show damage to be
found in the left eye. The HRT and OCT shows the right eye to be healthy
while the GDx shows damage also occurring in the OD. The HRT and OCT
show loss in the left eye to be present only superiorly while the GDx
shows loss in both superior and inferior hemiretinae.
Murray Fingeret, OD
OPTIC
NERVE REVIEW
Imaging of the Retinal Nerve Fiber Layer in
Glaucoma
There is a long learning curve (6-12 months) to be proficient in the
clinical evaluation of the retinal nerve fiber layer (RNFL). Many variables
can affect the visibility of the RNFL such as media clarity, fundus
pigmentation and age of the patient. Patients are also born with different
numbers of ganglion cell axons which creates a physiologic variation
of the normal RNFL. In our last OGS issue, we discussed the clinical
evaluation of the RNFL. New technologies have been developed to exam
the RNFL and compare the information with normal data bases. Clinical
instruments using these technologies include the GDx, OCT and HRT. This
article will briefly describe these instruments and how do interpret
the RNFL data from these devices.
The GDx VCC (Carl Zeiss Meditec) (see Quarterly Image section Figure
D) uses polarized light to measure the retardation of the RNFL, which
is assumed to be directly related to the RNFL thickness. Color coded
retardation maps should mimic the clinical evaluation of the RNFL. These
maps should show greater retardation (reds and yellows) indicating thicker
areas of RNFL in the superior and inferior arcuate bundles and less
retardation (blue) in the papillo-macular and nasal bundles where the
RNFL is physiologically thinner. In glaucoma, the retardation values
in the superior and inferior arcades are decreased. The GDx uses deviation
plots to compare the retardation values of the RNFL to an aged-matched
normative data base. Points outside of 95% of the normal data base are
flagged with a color coded symbol. The TSINT plot measures the RNFL
thickness 360 degrees around the optic nerve and compares it to a zone
of 95% of the normal values. There are also numeric TSNIT parameters,
which can also be compared with the normal data base. The Nerve Fiber
Layer Indicator (NFI) (1-99) is a compilation of values derived by the
GDx to estimate whether the test is within the normal database (usually
less than 30) vs abnormal (greater than 40). Unfortunately, there is
no exact number that separates patients into normal and abnormal findings.
The GDx has a comparison program that allows the doctor to analyze serial
scans over time. The GDx is strictly a RNFL device.
The OCT3 (Carl Zeiss Meditec) (see Quarterly Image section Figure E) is
an optical coherence tomographer that provides cross sectional imaging
of the retina and optic nerve. A circular scan can be used to measure
the RNFL 360 degrees around the optic nerve. TSINT plots are generated
and compared with an age-matched normative data base. Numeric values
are calculated for quadrant and sector ratios. These values are compared
to the normal data base and color coded for statistical probability.
Serial scans can be compared over time. The OCT also measures optic
nerve topography and can assist in the diagnosis and management of retinal
diseases.
The HRT (Heidelberg Engineering) (see Quarterly Image section Figure
C) is a confocal scanning laser ophthalmoscope that performs a series
of coronal slices of the retina and optic nerve similar to CT or MRI.
16-64 scans are reconstructed to form a 3 dimensional image of the optic
nerve and retina. The HRT measures the relative height of the RNFL.
This is accomplished by setting a standard reference plane of 50 microns
beneath the surface of the retina in the papillomacular bundle. The
RNFL thickness is calculated from this reference plane to the surface
of the retina. These values are compared with an age-matched normative
database. The values are plotted in a "retinal profile" which
is similar to the TSNIT plots on the GDx and OCT. There are also numeric
values that are calculated and compared to the normal data base for
the height variation contour and mean RNFL thickness. The HRT also measures
optic nerve topography and performs a Moorfield’s Regression Analysis
for glaucoma diagnosis. Serial HRT scans can be monitored for progression
over time.
All three instruments have the ability to measure and analyze the RNFL.
However, interpretations of the scans should never be performed in isolation.
Imaging data should be correlated with other clinical findings to confirm
or question their significance. Incorporating the evaluation of the
RNFL, whether clinical or with auxiliary testing of the GDx, OCT or
HRT can add useful information in the diagnosis and management of glaucoma
patients.
Anthony B. Litwak, OD, FAAO
ANGLE
REVIEW
Gonioscopy can be one of the most challenging
parts of baseline glaucoma examination. In the poll review of the OGS
E-Journal issue 3 we promised a full gonioscopy review and this is now
available at http://www.optometricglaucomasociety.org/EJSupp/Gonio.html.
This angle review is an excerpt from this review article.
Using indentation gonioscopy to distinguish between appositional
and synechial angle closure
If an angle appears occluded or extremely narrow (see Figure 1) indentation
gonioscopy can help distinguish between the reasons for closure. Indentation
gonioscopy is best accomplished with the smaller diameter, flatter base
curve of the 4-mirror type lenses. Gently applying pressure with the
lens displaces aqueous toward the peripheral part of the angle. This
also increases the diameter of the limbus pulling structures peripherally
and posteriorly. If the angle opens with indentation (see Figure 2),
this demonstrates appositional closure.
Appositional closure involves the peripheral iris being in contact with
the angle, particularly the trabecular meshwork, but not adherent to
it. Indentation gonioscopy can help differentiate between appositional
and synechial closure.
Figure 1
|
Figure 2
|
Peripheral anterior synechiae (PAS) are adhesions of the peripheral
iris to the angle wall. These suggest contact of the iris with the angle
and / or inflammation having occurred. PAS may occur at any level, from
isolated, thin high adhesions to low broad ones (see Figure 3). It is
helpful to distinguish between peripheral anterior synechiae and iris
processes.
John McSoley, OD
QUARTERLY
CASE
A 59 year-old black female was first seen on
September 18, 2001. The reason for her visit was that for the past month
she had been seeing cobwebs. Her medical history included treatment
for hypertension over the past 20 years. Best-corrected visual acuity
(BCVA) was 20/20 in each eye. Family history by report was noncontributory.
IOP was 16 mm Hg in each eye at 10:30 AM. The anterior segment was unremarkable
in each eye and the angles appeared open by Van Herick estimation.
Pupil dilation revealed mild nuclear and cortical lens changes and uncomplicated
posterior vitreous detachment (PVD) in each eye. The optic disc and
macula were within age-expected normal appearances in each eye. Since
the acute PVD had been asymptomatic for over 4 weeks and no predisposing
conditions to retinal detachment were found, we asked the patient to
return for evaluation one year later.
During the follow-up visit September 30, 2002, the patient’s personal
history remained unchanged but she now reported that her father had
glaucoma, and had become blind. BCVA was 20/25 in the right (mild lens
changes) and 20/20 in the left eye. IOP was 23 and 22 mm Hg in the right
and left eyes, respectively. We conducted a more extensive glaucoma
work-up. The optic discs are shown in Figures 1 and 2; the SITA-standard
visual fields (November 4, 2002) are shown in Figures 3 and 4.
Figure 1. Optic
disc (OD) Note vertical elongation of the cup.
|
Figure 2. Optic
disc (OS). Note inferior notch and corresponding darkening of
the RNFL.
|
The right field was unreliable. It is not uncommon
for some patients to take one, or in some cases more, field tests to
learn what is required and to get used to responding appropriately.
The reliable left visual field results show the Glaucoma Hemifield Test
(GHT) outside normal limits. Also, the Mean Deviation (MD) and Pattern
Standard Deviation (PSD) are flagged in each eye as falling within the
lower 0.5% of the normal distribution and there is a large cluster
of test locations with depressed sensitivity. This defect pattern is
consistent with a glaucomatous visual field defect and corresponds with
the inferior neuroretinal rim (NRR) damage in Figure 2. Gonioscopy showed
trabecular meshwork but no ciliary body band, signifying a slightly
narrowed but non-occludable and physiological angle in each quadrant
of each eye. The pachymetry readings were 525 and 516 µm in the
right and left eyes, respectively.
Figure 3. Humphrey
Field Analyzer 24-2 SITA-standard visual field (OD)
|
Figure 4 Humphrey
Field Analyzer 24-2 SITA-standard visual field (OS)
|
The patient was offered a treatment option of
travoprost (Travatan) evening dosing and asked to return in one month.
We established the target IOP range as a reduction of at 25-40% below
the most recent pressure, i.e. a goal of 14-17 mmHg. The diagnosis was
primary open angle glaucoma (POAG).
Initially, the IOP declined but did not reach target range and the patient
was switched between different prostaglandin analogues (PA) although
none achieved the target IOP as a monotherapy.
At follow-up on October 14, 2003, optic disc appearances were unchanged
and visual field testing was repeated. On this occasion, reliable visual
field test results were obtained from both eyes demonstrating advanced
and bilateral deep paracentral sensitivity losses threatening fixation
in the same hemifield of both eyes (see Figures 5 and 6). These results
reinforced the importance of achieving target IOP in this patient.
Figure 5. Humphrey
Field Analyzer 24-2 SITA fast (OD)
|
Figure 6. Humphrey
Field Analyzer 24-2 SITA fast (OS)
|
A second agent brinzolamide (Azopt) with b.i.d.
dosing was prescribed in additional to the current latanoprost (Xalatan).
When the IOP failed to respond sufficiently to reach target, this was
switched from brinzolamide to dorzolamide (Trusopt). This combination
has maintained the IOP in the target range over follow-up through the
end of 2005 when the patient was last seen.
Key points
1. Patients may have many diagnoses. This case presented with PVD and
over the course of a year showed increased IOP, optic disc damage and
visual field depression consistent with the location of disc damage.
2. Prostaglandin analogs are first-line treatment options. This case
demonstrates that if one member of any class of agents does not achieve
target pressure, then use of an additional agent from another medication
class is more likely to be successful than switching between agents
in the same class.
3. Brinzolamide (Azopt) is formulated as a suspension to maintain pH
at 7.2 (near neutral); whereas dorzolamide (Trusopt) is in solution
at a lower (more acidic) pH so patients may complain of stinging on
instillation and may tolerate it less for this reason.
4. Patients who produce unreliable visual field test results are more
likely to produce reliable results as they become familiar with the
test.
Leo Semes, OD
PEARLS
FROM THE EXPERTS
"One should also use a narrow, short beam
of the slit lamp when doing gonioscopy so that light does not go through
the pupil, and also NOT use a fixation light as either results in pupil
constriction and can open an angle that would be closed in the dim light
conditions conducive of angle closure. The whole point of gonioscopy
in such cases is to assess if an angle is susceptible to pupil block
angle closure and in need of an iridotomy"
Paul Palmberg, MD
MEETING
NEWS
17th International Perimetric Society Visual
Field and Imaging Symposium, July 11-14th, Portland, Oregon, USA.
One of the most outstanding highlights of this year’s International
Perimetric Society (IPS) Meeting was Dr. Lars Frisen’s keynote
address, "Reclaiming the Periphery". Dr. Frisen’s lecture
reminded us that there is more to perimetry than the central 30 degrees.
Dr. Frisen demonstrated how peripheral visual field testing can reveal
such diverse disorders as those of the lateral geniculate nucleus and
optic disc hypoplasia. He presented cases of patients whom had lost
between 50% and 100% of visual field function following epilepsy
surgery. He reviewed anatomical mapping studies that showed wide variations
from the traditional teaching regarding the position of Myer’s
loop, for example, and how surgery or traumatic brain injury will impact
the visual field.
From a very practical standpoint, Dr. Frisen described the limiting
aspects of the peripheral visual field. These include anatomic features,
which will vary by individual, but generally be the eyelids vertically,
the nose medially and the pupil temporally. Recognizing these limits,
one can appreciate the functional limitations of perimetry but still
use the technique for realistic exploration of the outermost extent
(and/or potentially abnormal limits) of the visual field.
Dr. Frisen ended by discussing lesser-known methods of perimetry. These
included differential light sensitivity (DLS), ring (which he labeled
as impractical), motion and rarebit perimetry. Software to run and analyze
each of these is downloadable as freeware. Specifically, rarebit uses
small targets of high and fixed contrast in non-overlapping areas of
the visual field and the patient simply responds whether the presentation
was seen or not. Advantages include simplicity, extent of the visual
field tested and good repeatability.
This year’s IPS meeting also included a novel foray into "imaging"
with one full session being dedicated to a symposium organized by Dr.
Claude Burgoyne, entitled, "Imaging to Assess Optic Nerve Head
Susceptibility".
Some of the highlights from that session are summarized here:
1. Dr. C. Burgoyne. Using high-resolution, three-dimensional reconstructions
of the anterior optic nerve from monkeys with unilateral experimentally
elevated IOP, Burgoyne and colleagues showed that Bruch’s Membrane
Opening enlarges as a result of increased IOP. Further studies will
confirm whether this can be measured clinically and if it will become
an index of susceptibility to glaucoma damage or be able to monitor
progression of the disease in diagnosed cases.
2. Dr. JC Downs and Dr. I Sigal. Stress and strain properties of the
ONH have become the subject of intense and detailed scrutiny. Behavior
of the lamina cribrosa in response to IOP changes have been studied
in monkey models. Preliminary indications suggest that the material
properties of the lamina may provide a target for imaging technologies
that would allow predicting, in vivo, an individual’s susceptibility
to glaucomatous damage. Currently no such technique is available.
3. Dr. BC Chauhan. A 4-year monitoring study in patients with ocular
hypertension and very early glaucoma suggests that the type of structural
changes at the optic disc (superpixel change maps of the Heidelberg
Retina Tomograph, HRT) are similar to those seen with progressing patients
who have more advanced disease.
4. Dr. R Zuckerman. This presentation suggested the potential for metabolic
mapping of the retina and optic disc by measurement of fluorescence
anisotropy of flavin adenine dinucleotide (FAD) within mitochondria.
Specifically applied to glaucoma, this form of "objective perimetry"
of retinal metabolic function, combined with structural analyses currently
available (e.g. OCT, HRT) has been used to correlate changes in local
metabolism with demonstable structural changes in the very earliest
stages of POAG (before cell death occurs).
There were also dozens of other exciting presentations focused on the
more traditional topics of the IPS (e.g. novel stimuli, thresholding
algorithms and applications of perimetry) by clinicians and scientists
from all over the globe. It was a pleasure to see that so many of our
own OGS members offered outstanding contributions to the meeting, especially
this year’s hosts: Drs Chris Johnson and Shaban Demirel!
The abstracts of the meeting are accessible from the IPS website: http://webeye.ophth.uiowa.edu/ips/.
PHARMACY
REVIEW
Carbonic Anhydrase Inhibitors
The group of mediations known as carbonic anhydrase inhibitors (CAIs)
were first introduced in 1949 (1) and are unsubstituted aromatic derivatives
of para-aminobenzenesulfonamide. Although the drug is classified as
a sulfonamide, it does not possess any antibacterial activity. The mechanism
of action of CAI is relatively straightforward. Physiologically, aqueous
humor is secreted by the ciliary epithelium. This active process is
dependent, in part, on an adequate local blood supply and the presence
of the enzyme carbonic anhydrase (CA). CA is present in great excess
throughout the body, including the eye. More than 99% must be inhibited
before formation of aqueous is diminished (2). The ability of CAIs to
inhibit this key enzyme has made them a valuable tool to control elevated
intraocular pressures (IOP’s). Fluorophotometric studies indicate
that acetazolamide (a systemic CAI agent) can reduce aqueous production
in humans by 21 to 27% (3).
Systemic Analogues
There are several CAIs available systemically. One, acetazolamide (Diamox)
is available as a 125mg and 250mg tablet or as a 500mg. sustained release
capsule. It is also available in 500mg. vials for IV administration.
Orally administered acetazolamide is absorbed by the intestinal tract
with more than 80% excreted by tubular secretion in the kidney (4).
Acetazolamide produces its maximum effect at 2 hours post dosing and
lasts for up to 6 hours. The sustained release dosage form produces
its maximum effect at 6-18 hours and can last up to 24 hours (5).
The side-effects associated with the use of systemic acetazolamide may
be significant. Acetazolamide is a sulfonamide and has the potential
to produce reactions in people sensitive to sulfonamide compounds. Because
it is a non-selective CA inhibitor, it inhibits CA throughout the body.
This may produce malaise, fatigue, weight loss, and loss of libido (6).
Most importantly it has the potential to produce serious blood dyscrasias
and aplastic anemia (7). Because the majority of cases of aplastic anemia
occur within the first 6 months of therapy, it is recommended that a
complete blood count (CBC) be performed prior to therapy, with repeat
counts at 1, 3, 6 and 12 month, and then yearly thereafter for long-term
use. It is important to monitor for evidence of persistent sore throat,
fever, fatigue, pallor, ecchymosis, epistaxis, purpura or jaundice.
Besides use in the management of elevated IOP, acetazolamide can also
benefit those with chronic macular edema (8). Because of the significant
incidence of systemic side-effects as well as a topical alternative,
oral acetazolamide is rarely used to treat primary open-angle glaucoma
(POAG). Rather, its major use is in the management of acute elevations
of IOP found with acute glaucomas. This would include elevated IOP in
uveitic glaucomas, hyphema, angle-closure and post-operative pressure
spiking.
Another of the systemic CAIs is methazolamide (Neptazane), which is
a popular alternative due to its superior potency and reduced side-effect
profile when compared to acetazolamide (9). Neptazane has greater lipid
solubility and fewer renal side-effects. It also has a longer half-life
(10-14 hours). This results in less frequent dosing. A dose of 25mg
administered every 12 hours may produce significant IOP reduction with
minimal side-effects (10). Dosages greater than 50mg every 8 hours produce
no additional significant IOP reductions and can result in a marked
increase in systemic side-effects. If the patient’s IOP fails to
be controlled on the maximal dose of methazolamide, they should be switched
to acetazolamide. In spite of its lower potency, it does exhibit greater
efficacy than methazolamide. Whilst methazolamide is licensed for use
in the USA, it is not available in all countries.
A third oral CAI, dichlorphenamide (Daranide) acts as both a potent
CA inhibitor and as a thiazide diuretic. It does not exhibit any additional
efficacy or reduced side-effects compared to acetazolamide or methazolamide
and, as a consequence, is rarely prescribed. The usual dose can range
from 25-100mg every 8 hours.
Topical CAI’s
The use of CAIs in the management of POAG has increased dramatically
with the introduction of topical agents. Typically, topical CAIs are
used as complementary agents because the IOP reduction obtained with
monotherapy generally does not achieve target IOP. For reasons that
are not entirely clear, CAIs often lower the IOP by a similar amount
when added to other agents (11).
In 1995, dorzolamide (Trusopt) became the first topical CAI approved
for the treatment of POAG and is available as a 2% solution with
a suggested dosing frequency of TID. In a study by Wilkerson (12) the
drug was administered TID for 4 weeks and like acetazolamide, demonstrated
peak activity 2 hours post administration, with an average IOP reduction
of 18.4%. It also produced an increase in corneal thickness. In
a 1 year study by Strahlman (13) that compared it to timolol and betaxolol
the IOP lowering effect of TID dorzolamide (23%) was similar to
BID timolol (25%) and betaxolol (21%).
According to Merck and co., inc product data, the most commonly reported
adverse effects of dorzolamide include stinging and discomfort (33%)
and bitter taste (26%). Superficial punctuate keratitis (SPK) occurs
in 10% of individuals, with blurred vision, dryness, tearing and
photophobia at an incidence rate of less than 5%. A total of 5%
discontinue the medication for lid edema and conjunctival irritation.
Dorzolamide is buffered at an acidic pH. This allows it to be dispensed
as a 2% solution. Unfortunately, the low pH contributes to the significant
incidence of stinging that occurs during drug administration. The suggested
dosing interval for dorzolamide is TID. Although it has been suggested
that dorzolamide produces increased corneal thickness several studies
discount this phenomenon. In a study by Egan et al. (14) the researchers
induced hypoxic corneal edema in test subjects. The use of dorzolamide
did not increase corneal recovery time when compared to the control
group.
An alternative topical CAI, Brinzolamide (Azopt) Alcon Labs, inc. has
a similar effect on IOP as dorzolamide. Their efficacy is equivalent.
However, brinzolamide differs from dorzolamide in several important
ways. It is buffered at a more neutral pH. This produces less discomfort
on instillation (15) and results in reduced solubility of the drug,
hence it is prepared as a 1% suspension that requires shaking. Similar
to dorzolamide, the dosage written on the package insert is TID though
most clinicians use these agents on a bid dosage since they are typically
used with other agents. Indeed this practice is reflected in licensing
in the United Kingdom, where this agent is licensed for bid use, increasing
to TID "if necessary."
Although the topical CAI’s should not be combined with oral CAI’s,
they are compatible with and provide additive IOP reduction with all
other topical glaucoma drugs. Dorzolamide is available in combination
with timolol maleate 0.5% as a combination topical agent (Cosopt).
Systemic side-effects with topical agents are extremely rare. However
there is a potential for sensitivity in sulfonamide sensitive patients.
The drug should also be avoided in pregnant patients.
Bruce Onofrey, OD, RPh, FAAO
References
1. Grant, WM Acetazolamide in treatment of glaucoma. Arch ophthalmol
1954;51:735-39.
2. McCannel, CA: Acetazolamide lowers IOP in sleep in humans. Graefes
Arch Clin exp Ophthalmol 230:518, 1992.
3. Maren, TH Carbonic anhydrase: Chemistry, physiology and inhibition.
Physiol Rev 47:495, 1967.
4. Maren, TH The rates of movement of Na(+), Cl(-) and HCO3(-) from
plasma to posterior chamber: Effect of aceazolamide and relation to
the treatment of glaucoma. Invest Ophthalmol 15:356, 1976.
5. Berson, FG: Acetazolamide dosage forms in the treatment of glaucoma.
Arch Ophthalmol 98:1051, 1980
6. Epstein, DL: Carbonic anhydrase inhibitor side-effects. Arch
Ophthalmol 95:1378, 1977
7. Turtz CA: Toxicity due to acetazolamide. Arch Ophthalmol 60:130,
1958
8. Cox, SN: Treatment of chronic macular edema. Arch Ophthalmol
106:1190, 1988
9. Maren, TH: The pharmacology of methazolamide in relation to the treatment
of glaucoma. Invest Ophthalmol Vis Sci 16:730, 1977
10. Coop, DH: Neptazane in glaucoma. Br J Ophthalmol 43:602, 1959
11. O'Connor DJ, Martone JF, Mead A. Additive intraocular pressure lowering
effect of various medications with latanoprost. Am J Ophthalmol.
2002 Jun;133(6):836-7.
12. Wilkerson, M: For-week safety and efficacy study of dorzolamide.
Arch Ophthalmol 111:1343, 1993.
13. Strahlman, E:A double-masked randomized 1 year study comparing dorzolamide,
timolol and betaxolol. Arch Ophthalmol 113:1009,1995.
14. Egan, CA, et al: Effect of dorzolamide on corneal endo thelial function
in normal human eyes. Invest Ophthalmol Vis Sci. 1998 1;39: 23-9
15. Silver, LH: Ocular comfort of brinzolamide 1% ophthalmic suspension
compared with dorzolamide 2% ophthalmic solution. Surv Ophthalmol.
2000 Jan;44 Suppl.
POLL
RESULTS FROM OGS E-JOURNAL VOLUME 1, ISSUE 3
A majority of our respondents (64%) perform
visual field tests annually on their stable glaucoma patients. Shorter
testing strategies have gained in popularity over the past several years.
This shift from traditional full threshold test strategy with its longer
test time is evident with only 12% of our poll respondents employing
this type of test. Faster testing algorithms are widely used in clinical
practice and have appeared more frequently in publications and clinical
studies in recent years.The poll results demonstrate that SITA strategies
are now the strategy of choice amongst our respondents with SITA-standard
being the most frequently ordered test. It is interesting to note that
10% of participants rely on other tests in place of standard perimetry.
Twenty-five percent of respondents make use of frequency doubling technology,
either FDT or Matrix, in addition to white-on-white perimetry. Only
4% employ short wavelength automated perimetry (SWAP or blue-on-yellow).
Almost 2/3 of our respondents rely solely on white-on-white perimetry
for visual field testing.
MELTON & THOMAS-
THEIR VIEWS
Perspective on pachymetry
There can be no debate as to the appropriateness of measuring central
corneal thickness in all glaucoma suspects: those with suspicious cupping
(independent of IOP) and those with IOP greater than 21mmHg. There can
be debate regarding the need for more than one measurement in each patient,
unless the patient has had corneal ablative refractive surgery. Our
opinion is that one assessment per patient is adequate in virtually
all other circumstances. It appears well established that corneas thinner
than 555 microns are an independent risk factor in an inversely proportionate
manner; that is, the thinner the cornea below 555 microns, the greater
the risk for glaucoma.
"IOP/CCT conversion tables" seem to be used in a variety of
ways. The question of whether and how to intelligently use these tables
(if at all) appears to have many diverse approaches. We have found that
some doctors seem obsessed with "micromanaging" the theorized
converted values of the IOP suggested by CCT. This is probably an unwise
and minimally productive exercise. Our perspective is that CCT needs
to be sequestered into thirds: thin, neutral, thick. The key point in
all of this is that thin corneas portend greater risk for glaucoma than
do mid-range or thicker corneas. Beginning in the vicinity of 555 microns,
the thinner the CCT, the greater the risk for glaucoma. For example,
a person with a 490 CCT is more likely to develop glaucoma than someone
with a 590 CCT. Simply noting that a cornea is thin, neutral, or thick
is really all that is necessary to blend the CCT measurement into the
overall assessment of glaucoma risk. Note also that a thin cornea not
only imparts greater risk for glaucoma development, it also places eyes
with glaucoma at greater risk for progression.
In summary, IOP/CCT conversion tables are probably clinically accurate
within 50 to 75 microns of 545 microns, but to use these tables in such
a manner is almost always nonproductive. Let’s just keep it simple;
the thinner the cornea (below 555 microns) the greater the risk for
the development of glaucoma, or glaucomatous progression.
Randall K. Thomas, OD, and Ron Melton, OD
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.
Q. "Do you have a suggestion for a reference that would
be clinically helpful regarding the grading and evaluation of the optic
nerve? Also, do you have a reference for basics of visual field result
analysis?"
A. There a number of new or recently revised glaucoma textbooks
providing high-quality information on optic nerve head (ONH) evaluation.
In particular, "Shields’ Textbook of Glaucoma" has a
relatively new 5th edition (2005) provides extensive coverage of every
aspect of glaucoma. In terms of a summary reference from a clinician-scientist
with a research interest in clinical evaluation of the nerve head, a
review article by Jonas et al. although written some time ago, remains
highly recommended (Jonas JB, Budde WM, Panda-Jonas S (1999). Ophthalmoscopic
evaluation of the optic nerve head. Surv Ophthalmol; 43(4): 293-320.)
In terms of visual fields, good reference texts include "Visual
Fields" by David B Henson (Oxford University Press, Oxford, 2nd
edition) and "Automated Static Perimetry" DR Anderson and
VM Patella (2nd Edition, Mosby, St Louis, 1999). For interpretation
of the Humphrey Field Analyzer results, "Essential Perimetry. The
Field Analyzer Primer" by A Heijl and VM Patella is an accessible
and user-friendly guide. Individual copies may be requested from your
local Zeiss representative.
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 B | |
