Klein and colleagues show a significant correlation between blood
pressure – both systolic and diastolic – and intraocular pressure
(IOP).[1] Law et al. recently showed that blood pressure lowering drugs
prevent a significant proportion of headaches; however, the causal
relation between hypertension and headache – whether migrainous or non-
migrainous -- remains ambiguous.[2] In the absence of a clear...
Klein and colleagues show a significant correlation between blood
pressure – both systolic and diastolic – and intraocular pressure
(IOP).[1] Law et al. recently showed that blood pressure lowering drugs
prevent a significant proportion of headaches; however, the causal
relation between hypertension and headache – whether migrainous or non-
migrainous -- remains ambiguous.[2] In the absence of a clear link between
headache and hypertension, hypertensive headache has also been regarded as
a myth or “socio-psychological” disorder[3] despite a typical circadian
pattern and throbbing character.[2]
A statistically significant inverse relation between blood pressure –
both systolic and diastolic -- and non-migrainous headache in a large
cross-sectional study[4] indicates that there is a third, critical,
idiosyncratic perfusion-related variable between hypertension and
headache. Migraine is not a pan-trigeminal disorder.[5,6] In humans, pain
and temperature fibers from only the ophthalmic area descend to the lower
limit of the first cervical spinal segment; this long held view is
supported by sectional studies at and below the obex for severe trigeminal
neuralgia. Nuchal pain in migraine or hypertensive headache likely
involves ophthalmic nerve fibres.[6] Additionally, photophobia of migraine
is a reflex involving the ophthalmic nerve. Third, ipsilateral migraine
aura or headache has never been reported following enucleation or
evisceration of the eye.[5,6] Dental extraction (upper or lower jaw) is
only rarely associated with migrainous headache.[7] Headache, migrainous
or non-migrainous, primarily involves the ophthalmic division of the
trigeminal nerve.[5,6]
A nexus between migraine, autonomic dysfunction, and IOP has been
recently proposed.[6] Autonomic hypofunction prevails in migraine patients
and can underlie sudden ocular choroidal congestion in diverse stressful
clinical circumstances; mechanical deformation of the corneo-scleral
envelope might generate both the scintillating scotoma as well the
headache of migraine.[5,6] Remarkably, a higher blood pressure is
correlated with a higher IOP.[1] Tamponade function of IOP maintains
ocular integrity; a higher IOP limits ocular choroidal hyperperfusion and
possibly prevents the development of headache at relatively higher levels
of blood pressure. Every physiological function has an upper threshold;
the tamponde effect of rising IOP is probably overwhelmed in severe or
malignant hypertension, hypertensive encephalopathy, and pheochromocytoma-
related surges of blood pressure.[8]
The common action by which migraine prophylactic agents prevent
attacks likely involves a lowering of the IOP; propranolol, atenolol,
metoprolol, nadolol, clonidine, flunarizine, verapamil, diuretics and
angiotensin converting enzyme inhibitors lower IOP.[1,5,6] Intriguingly,
the prophylactic effect of migraine preventing agents is not predictable
or dose-dependent, a feature that might reflect the ceiling effect in
lowering IOP. Also, lowering IOP beyond a certain critical threshold –
that varies for every individual – can aggravate the tendency to develop
ocular choroidal congestion and mechanical deformation of the pressure-sensitive ophthalmic nerve fibers of the iris and the chamber angle.
Vasodilating anti-hypertensive agents like nifedipine, hydralazine, and
enalapril commonly induce headache possibly by a combination of lowering
the IOP and inducing choroidal congestion.
Rather than being a simple function of blood pressure, headache in
hypertension patients appears to be the outcome of a complex interaction
between autonomic function, choroidal perfusion and IOP, the many trait-
and state-dependent factors that determine the mechanical properties of
the corneo-scleral envelope, and the endogenous pain control mechanism.[8] Hypertension-associated headache – migrainous or non-migrainous,
spontaneous or antihypertensive drug-induced -- is not “all in the mind”;
a clear link with variations of the IOP appears to be emerging.
References
1. Klein BEK, Klein R, Knudtson MD. Intraocular pressure and systemic
blood pressure: longitudinal perspective: The Beaver Dam Eye Study. Br J
Ophthalmol 2005;89:284-7.
2. Law M, Morris JK, Jordan R, Wald N. Headaches and the treatment of
blood pressure. Results from a meta-analysis of 94 randomized placebo-
controlled trials with 24 000
participants. Circulation 2005;112:2301-6.
3. Friedman D. Headache and hypertension: refuting the myth. J Neurol
Neurosurg Psychiatry 2002;72:431.
4. Hagen K, Stovner LJ, Vatten L, Holmen J, Zwart J-A, Bovim G. Blood
pressure and risk of headache: a prospective study of 22 685 adults in
Norway. J Neurol Neurosurg Psychiatry. 2002;72:463-466.
5. Gupta VK. Lamotrigine, migraine aura and headache: tightening the
Gordian knot of primary headache? J Neurol Neurosurg Psychiatry. (28
November 2005). Available at:
http://jnnp.bmjjournals.com/cgi/eletters/76/12/1730#764
6. Gupta VK. Migrainous scintillating scotoma and headache is ocular
in origin: a new hypothesis. Med Hypotheses. 2005 (In press). Available
online 13 December 2005.
7. Strauss RA, Eschenroeder TA. Hemiplegic migraine following third
molar extractions under intravenous sedation. J Oral Maxillofac Surg
1989;47:184-6.
8. Gupta VK. Does the mysterious link between hypertension and
headache lie at the level of the eye? Circulation (In press).
In a thought-provoking editorial in BJO entitled “Why is the
amblyopic eye unstable?” C. Hoyt raised two very important issues relating
to the treatment of human amblyopia. First, there is currently no
effective alternative to occlusion therapy for treating amblyopia. Second,
there is considerable “slippage” of visual acuity after cessation of
occlusion therapy. Our sole purpose in responding to this...
In a thought-provoking editorial in BJO entitled “Why is the
amblyopic eye unstable?” C. Hoyt raised two very important issues relating
to the treatment of human amblyopia. First, there is currently no
effective alternative to occlusion therapy for treating amblyopia. Second,
there is considerable “slippage” of visual acuity after cessation of
occlusion therapy. Our sole purpose in responding to this editorial is to
draw attention to some very recent work, showing significant long-term
improvements in visual performance in the adult amblyopic eye that,
potentially, could be adapted for use as an effective alternative to
occlusion therapy.
Visual perceptual learning – improved visual performance on a given
psychophysical task after extensive training – is a well-established
phenomenon in the normal visual system1. This form of learning is often
tightly coupled to stimulus characteristics encoded early in visual
cortex, such as the orientation or spatial frequency (size) of a visual
stimulus. The stimulus specificity of perceptual improvements through
training suggests that some aspect of neural processing -whether it be the
tuning of individual neurons or the weighting of synaptic connections -
remains malleable or ‘plastic’, even in the adult visual system.
Recent studies have shown that this form of neural plasticity is not
restricted to the normal visual system. Indeed, with an appropriate
training regime one can produce a marked improvement in visual performance
of the adult amblyopic eye. Perceptual learning produces a 50-60%
improvement in Vernier acuity (positional acuity) of the adult amblyopic
eye2. Crucially, in some subjects this improvement in Vernier acuity
transfers to other forms of spatial discrimination such as Snellen acuity.
By way of example, one amblyopic observer improved from a pre-training
value of 20/42 (~6/12), attaining 20/20 (6/6) after extensive training on
the Vernier task2. This suggests that the adult amblyopic visual system
retains a great deal more neural plasticity than previously supposed. Such
improvements in visual performance are not limited to acuity tasks. A
longitudinal study found that training on a contrast detection task led to
a 2-fold improvement in the contrast sensitivity of the amblyopic eye,
with minimal “slippage” 12 months after the cessation of training3.
At present, relatively little is known about the benefits of
perceptual learning in childhood amblyopia during the “sensitive period”.
Given the greater degree of neural plasticity in the developing visual
system, one would imagine that the benefits of perceptual learning might
greatly outstrip those observed in the adult population. Having said this,
a recent study on the efficacy of perceptual learning in previously
treated amblyopic children did not support this supposition4. While the
children (aged 7 to 10 – beyond the sensitive period as defined by
Professor Hoyt) showed significant improvements after 7 to 10 sessions,
the results were no better than those of adults. Further work with “fresh”
(untreated) and younger amblyopes is required to corroborate and extend
these initial findings to younger children, and to determine the “dose-
response” function for perceptual learning.
Several large-scale clinical studies in the UK and USA have shown
that standard occlusion therapy is effective in treating human amblyopia.
However, the benefits are far from universal and a significant number of
children (~ one third) gain little or no visual benefit despite protracted
treatment5. This is unfortunate given that occlusion therapy is difficult
to implement, is often associated with some degree of distress to the
child and may have an impact on educational development. As Professor Hoyt
correctly notes in his original editorial, no alternative treatment
strategies currently exist for these individuals. The development of
perceptual learning as a clinical tool may rectify this situation and
provide an alternative method both for the treatment of amblyopia and for
eliminating or reversing “slippage” once treatment has ceased. Moreover,
if the initial perceptual learning studies in children with amblyopia
withstand further experimental scrutiny and deliver encouraging results in
younger and previously untreated children, the 250-year old practice of
‘patching’ the amblyopic eye may be supplanted or at the least
supplemented by a new treatment protocol.
References
1. Fine, I & Jacobs, R.A. (2002) Comparing perceptual learning tasks:
A review. Journal of Vision 2, 190-203.
2. Levi DM (2005) Perceptual learning in adults with amblyopia: A
reevaluation of the critical periods in human vision. Developmental
Psychobiology. 46, 222-232
3. Polat, U., Ma-Naim, T., Belkin, M. & Sagi, D. (2004) Improving
vision in adult amblyopia by perceptual learning. Proceedings of the
National Academy of Sciences of the United States of America 101, 6692-
6697.
4. Li, R.W., Young, K.G., Hoenig, P. & Levi, D.M. (2005)
Perceptual learning improves visual performance in juvenile amblyopia.
Investigative Ophthalmology and Visual Science. 46, 3161-3168.
5. Clarke MP, Wright CM, Hrisos S, Anderson JD, Henderson J,
Richardson SR. (2003). Randomised controlled trial of treatment of
unilateral visual impairment detected at preschool vision screening. BMJ
327, 1251-1256.
Ben S. Webb, Paul V. McGraw Visual Neuroscience Group
School of Psychology
University of Nottingham, UK
Dennis M. Levi School of Optometry
UC Berkeley, USA
I read with great interest your extremely
valuable article. I have been working in the field of PTC and optic nerve sheath decompression for about 12 years now and my clinical experience very much supports the findings in your work. There are variable degrees of papilledema in the same patient with the same level ICP and variable
responses of patients to medical therapies decreasing the ICP, with some p...
I read with great interest your extremely
valuable article. I have been working in the field of PTC and optic nerve sheath decompression for about 12 years now and my clinical experience very much supports the findings in your work. There are variable degrees of papilledema in the same patient with the same level ICP and variable
responses of patients to medical therapies decreasing the ICP, with some patients responding and some patients needing surgery. There are patients who respond to CSF shunting procedures and those who do not,
leading to the indication of optic nerve sheath decompression.
I proposed a new theory called the pressure dissociation
theory, which suggests a pressure dissociation between the ICP and
the subarachnoid pressure of the optic nerve due to the presence of a
valve mechanism related to subarachnoid trabeculations. This may be a
crucial factor in determining the response to decompressing the central
compartment.
I also suggested that PTC may be classified into communicating and
non-communicating according the degree of communication between the
subarachnoid space of the optic nerve and the central compartment.
The clinical variability in this disease suggests a great
variability
in the communication that may be very important in determining who will
respond to therapy.
I suggest that this paper should have another phase
studying cadavers having PTC with and without visual loss and I think
that
this may be different from the normal population.
Your work opens the way for more understanding of
visual loss in papilledema due to PTC .
Sherif AK Amer MD ophthalmology
Cairo University
Consultant neuroophthalmologist
National Eye Center
Egypt
We thank Drs. Tsai et al. for their interest in our article and for
the opportunity to clarify the data of our study. Drs. Tsai et al.
correctly point out that intraocular pressures (IOP), axial lengths (AL),
corneal curvatures, and refractive errors change overtime following
glaucoma surgery. The purpose of our study was not to follow the changes
of ocular dimensions after combined cataract operatio...
We thank Drs. Tsai et al. for their interest in our article and for
the opportunity to clarify the data of our study. Drs. Tsai et al.
correctly point out that intraocular pressures (IOP), axial lengths (AL),
corneal curvatures, and refractive errors change overtime following
glaucoma surgery. The purpose of our study was not to follow the changes
of ocular dimensions after combined cataract operation and trabeculectomy
with mitomycin C using separate incisions (combined operation) overtime,
but to characterize these changes when the ocular dimensions were
relatively stable.
The large majority (75%) of our patients who received
combined operations had the ocular dimension measured and the IOP recorded
for analysis 6 months of more after the combined operation. Eight patients
(33%) had measurements obtained 12 months or more after the operation, 10
patients (42%) obtained between 6 to 11 months, and 6 patients (25%)
obtained between 1 to 2 months. With the possibility that these 6 patients
with a short follow-up may have unstable ocular dimensions and affect the
interpretation of the results, we re-analyze our data of the 18 patients
who had the data collected at 6 months or more after the combined
operation. The significances of the results remain unchanged.
After a combined operation in these 18 patients, the mean axial length is
significantly shortened from 24.13 (1.04) mm to 24.02 (1.06) mm
(p<0.00001). The mean axial length reduction after combined operation
(109 (61) µm) is still larger than the reduction after cataract operation
alone (75 (38) µm), but does not remain statistical significant (p=0.07)
with a smaller sample size. The axial length reduction after combined
operation correlates significantly with the postoperative IOP (p=0.008).
There is a mean with the rule (WTR) surgically induced corneal astigmatism
of 0.42 (0.71) D by vector analysis, and a significant increase of mean
keratometry reading of 0.24 (0.42) D after a combined operation. There is
no significant difference between the expected and observed refractive
errors.
In addition, all patients in this study received a standard regimen
of topical steroid and antibiotic after the combined operation. Topical
steroid was started with 4 times daily and tapered 1 drop per week for 4
weeks. Topical antibiotic was used 4 times daily for 1 week from
postoperative day 1.
Previous studies on changes of axial length after trabeculectomy were
based on ultrasound biometry, which requires physical contact with the eye
by a transducer or a saline immersion bath. The use of a more precise non-
contact method of measurement, avoiding indentation or deformation of a
soft globe after trabeculectomy has clear advantage. Although induction of
a mean WTR corneal astigmatism after trabeculectomy with or without using
mitomycin C had been reported, studies on corneal astigmatism induction
after combined operation with more recent surgical technique were few. It
may not be directly applicable to compare results of ocular dimension
changes in trabeculectomy alone or cataract operation alone to combined
cataract operation and trabeculectomy.
In the study by Claridge et al., polar values as a balance between
with the rule (WTR) and against the rule (ATR) components of any given
astigmatism were calculated.[1] An increase in polar value indicates a
shift towards WTR astigmatism whereas a decrease indicates a move towards
ATR astigmatism. Authors described three patterns of postoperative corneal
topography changes: superior corneal steepening, superior corneal
flattening, and complex regional variations in corneal topography that did
not fit any particular pattern. In the superior corneal steepening, the
polar value of the simulated keratometry increased from preoperative value
of 0.6 D to 1.0 D at 1 month and 3 months postoperatively, which was a 0.4
D WTR change. For the superior flattening group, the polar value increased
from -0.3 D preoperatively to +0.1 D at 1 month and 0.0 D at 3 months
postoperatively. The WTR change was 0.7 to 0.8 D.[1] The overall mean
induced astigmatism reported by Kook and coauthors in patients who had
trabeculectomy with mitomycin C application was larger at 1 month (+1.08 D
x 90 degree) and 3 months (+1.23 D x 90 degree) after operation, and
smaller at 6 months (+0.94 D x 90 degree) and 12 months (+0.65 D x 90
degree) after operation.[2] By re-analyzing our data excluding patients
with less than 6 months of follow-up, we were able to characterize the
changes when the ocular dimension became more stable after the operation.
However, we agree with Drs Tsai at al that the intraoperative use of
mitomycin C may affect wound healing and has long-lasting influences on AL
and corneal curvature than operation without the use of antimetabolite,
and future study with a long-term follow-up is warrant.
Sincerely Yours,
Simon K. Law, MD
Glaucoma Division
Ophthalmology Department
Jules Stein Eye Institute
University of California Los Angeles
References:
1. Claridge KG, Galbraith JK, Karmel V, Bates AK. The effect of
trabeculectomy on refraction, keratometry and corneal topography. Eye.
1995;9 ( Pt 3):292-298.
2. Kook MS, Kim HB, Lee SU. Short-term effect of mitomycin-C
augmented trabeculectomy on axial length and corneal astigmatism. J
Cataract Refract Surg. 2001 Apr;27(4):518-523.
Law and co-authors have contributed valuable data on the effect of
combined cataract surgery and trabeculectomy with mitomycin C (MMC) on
ocular dimensions. [1] While it is unclear from the report whether all
patients' data were collected at the same interval postoperatively and
when the postoperative data were collected. As we know, the change in
intraocular pressure, axial length (AL), and corneal cu...
Law and co-authors have contributed valuable data on the effect of
combined cataract surgery and trabeculectomy with mitomycin C (MMC) on
ocular dimensions. [1] While it is unclear from the report whether all
patients' data were collected at the same interval postoperatively and
when the postoperative data were collected. As we know, the change in
intraocular pressure, axial length (AL), and corneal curvature after
surgery could be different at varied follow-up period.
In a study by Claridge and coauthors, the induced with-the rule
astigmatism after trabeculectomy was 2.63 diopters (D) at 1 month and
decreased to 1.24 D by 3 months. [2] Additionally, intraoperative
application of MMC in trabeculectomy may affect wound healing process by
inhibition of fibroblast proliferation, and therefore has long-lasting
influences on AL and corneal curvature. As reported previously by Kook and
coauthors, [3] the mean AL was significantly less postoperatively and
changed throughout the 12 month follow-up (-0.54mm at 1 week, -1.15mm at 1
month, and -0.9 mm at 12 months). The overall mean induced astigmatism
was maximal at 3-month postoperatively (+1.23 D x 90°) and gradually
decreased to +0.65 D x 90° at 12 months.
On the other hand, the use of topical steroid or non-steroid anti-
inflammatory agents could affect on wound healing, and have been reported
to have significant influences on ocular dimensions after operation. [4]
It would also be necessary to clarify on this issue with the information
of the postoperative medications. Further prospective study with a long-
term follow-up period is warranted to help ascertain the change of ocular
dimensions after combined cataract and glaucoma surgery with MMC is a
temporary or long-term effect.
References
1. Law SK, Mansury AM, Vasudev D, et al. Effects of combined cataract
surgery and trabeculectomy with mitomycin C on ocular dimensions. Br J
Ophthalmol 2005;89:1021-5.
2. Claridge KG, Galbraith JK, Karmel V, et al. The effect of
trabeculectomy on refraction, keratometry and corneal topography. Eye
1995;9:292¡V8.
3. Kook MS, Kim HB, Lee SU. Short-term effect of mitomycin-C
augmented trabeculectomy on axial length and corneal astigmatism. J
Cataract Refract Surg 2001;27:518¡V23.
4. Masket S. Comparison of the effect of topical corticosteroids and
nonsteroidals on postoperative corneal astigmatism. J Cataract Refract
Surg 1990;16:715-8.
We read with great interest the article by Vysniauskiene et al.1
Their efforts in evaluating the intraocular pressure (IOP) changes of the
contralateral eyes after trabeculectomy with mitomycin C (MMC) is
appreciated. They concluded that a month after trabeculectomy, the mean
IOP in contralateral eyes decreased. Of note, among the 24 fellow eyes in
the study, 11 (45.8%) had topical ocular hyp...
We read with great interest the article by Vysniauskiene et al.1
Their efforts in evaluating the intraocular pressure (IOP) changes of the
contralateral eyes after trabeculectomy with mitomycin C (MMC) is
appreciated. They concluded that a month after trabeculectomy, the mean
IOP in contralateral eyes decreased. Of note, among the 24 fellow eyes in
the study, 11 (45.8%) had topical ocular hypotensive therapy. Among the
remaining 13 (54.2%) who had not, 12 of them had undergone trabeculectomy
with MMC. We would be grateful if the authors may like to share with us
their opinions as to whether the presumed “ophthalmotonic consensual
reaction?may be modified in an unknown way by the topical medications or
surgery, thereby affecting the interpretation of their results.
The decision by ophthalmologist to offer trabeculectomy is likely to
be made at a point when the IOP is high on the variation curve. Therefore
the decreased IOP in the fellow eye could be due to the “regression to the
mean effect. The IOP of the fellow eye was measured 1 day before surgery,
as well as 1 day and 1 month after surgery. As the study was conducted
between 1995 and 2000, we would be interested to know the long term IOP
changes after surgery. We suggest that this may help to lessen the effect
of regression to the mean, as well as to see how long will the
“ophthalmotonic consensual reaction? persist beyond 1 month.
As the IOP in glaucoma patients is unlikely to follow a normal
Gaussian distribution, and it appeared that the data set was not yet
tested for normality, the use of non-parametric counterparts such as
Wilcoxon signed rank test is probably more appropriate.
We would like to commend the authors for conducting the study on this
interesting topic. We wish that the issues raised will help broaden the
discussion.
References
1 I Vysniauskiene, T Shaarawy, J Flammer, IO Haefliger. Intraocular
pressure changes in the contralateral eye after trabeculectomy with
mitomycin C.
2 Weekers L. Modification experimentales de l'ophtalmotonous.
Reaction ophtalmotonique consenuelle. Arch Ophthalmol (Paris) 1924;41:641-
58.
I should like to congratulate the authors for the article citing
the original publication on peripheral fading by Troxler (1804).
However, as editor of the website on the work of the Swiss
philosopher Ignaz Paul Vital Troxler (1780-1866) who started as physician
and ophthalmologist before engaging in research on anthropological and
political subjects, I regret that after 201 years, the publication of 18...
I should like to congratulate the authors for the article citing
the original publication on peripheral fading by Troxler (1804).
However, as editor of the website on the work of the Swiss
philosopher Ignaz Paul Vital Troxler (1780-1866) who started as physician
and ophthalmologist before engaging in research on anthropological and
political subjects, I regret that after 201 years, the publication of 1804 is often cited in an incomplete and/or misleading way.
Troxler used to sign his publications in the world's first
ophthalmological journal (i.e. "Ophthalmologische Bibliothek", edited by
K. Himly and J.A.Schmidt) with "D." for "doctor". Therefore,the fact that
the early neurophysiologist and neuropsychologist "D.Troxler" and the
political philosopher I.P.V.Troxler are identical has often been overlooked
in the medical literature, despite the fact that Troxler's concept of
perception has had an important impact on the development of modern
neuropsychological research.
I should like to suggest that, in references to "Über das
Verschwinden gegebener Gegenstände innerhalb unseres Gesichtskreises" (On
the disappearance of given objects from our visual field), the author be
cited as "Troxler D.(I.P.V.)", to facilitate identification.
I kindly invite you to visit the website
http://www.troxlerforum.ch which contains a biographical summary, a bibliography and some references on research related to Troxler's works on visual perception.
Sincerely Yours,
Hans U. Iselin M.D. CH-4310 Rheinfelden
(Switzerland)
We read with interest the article by Gupta and colleagues describing
their findings in an investigation of the utility loss associated with
glaucoma. When considered in light of previous investigations this work
makes an important contribution to our limited understanding of the
influence of culture, socio-economic status, and ethnic background on
health state preference. It is particularly gratifying...
We read with interest the article by Gupta and colleagues describing
their findings in an investigation of the utility loss associated with
glaucoma. When considered in light of previous investigations this work
makes an important contribution to our limited understanding of the
influence of culture, socio-economic status, and ethnic background on
health state preference. It is particularly gratifying to see this done in
glaucoma, a disease where there has been very limited work done towards
utility estimate.
There are some aspects of the results of this study that bear
clarification. First, we ask that they comment on staging glaucoma using
visual acuity rather than visual field loss. Clinical staging of glaucoma
by loss of visual field is the method preferred by glaucoma specialists,[1]
and both utility loss (as measured by the EQ-5D)[2] and cost of care[3] have
been shown to be responsive to this measure. Second, it would be good to
report the number of study participants who refused to trade any time (or
risk blindness or death due to surgery). In previous work, this proportion
has substantial.[4] Finally, we ask that they comment more fully what some
may consider an inconsistency in the findings. They found that on average
people with glaucoma are willing to accept a 14% risk of death to
eliminate their disease, but only a 3% risk of blindness, leading us to
assume that among the people in this sample, being blind is worse than
being dead. This has not been found in previous studies of the utility
associated with blindness.
Just as Dr. Gupta and his colleagues speculate that there might be a
cultural or socio-economic basis for the substantially higher utility loss
associated with glaucoma he found in his sample (when contrasted with the
work of Jampel4), it is possible that these apparently “inconsistent”
findings might be the result of differing views of visual disability in
our industrialized society (with nearly universal access to—although not
necessarily utilization of—health care and rehabilitative services),
versus that found in a developing country. If these findings are indeed
valid and supported by additional research, it would make an important
contribution to our understanding of preference based measures by
providing evidence that preferences for health states (and thus variance
in reported utility) may vary based upon socio-economic factors. While
some have suggested that this is not the case,[5] such a finding would be
consistent with recent reports that reported utility varies by race and
other factors.[6,7]
References:
1. Hodapp E, Parrish RK, Anderson DR. Clinical Decisions in Glaucoma.
St. Louis: Mosby, 1993.
2. Alm A, Kobelt G, Bergstrom A, Chen E, Linden C. Measuring Utility in
Glaucoma. 2005 Annual Meeting Association for Research in Vision and
Ophthalmology Fort Lauderdale, Florida.
3. Lee PP, Walt J, Doyle JJ, Kotak SV, Evans SJ, Budenz DL, et al. A Multi
-center, Retrospective Pilot Study of Resource Utilization and Costs
Associated with Severity of Disease in Glaucoma. Archives of Ophthalmology
2005;Accepted for Publication.
4. Jampel HD, Schwartz A, Pollack I, Abrams D, Weiss H, Miller R. Glaucoma
Patients' Assessment of Their Visual Function and Quality of Life. Journal
of Glaucoma 2002;11(2):154-63.
5. Brown GC, Brown MM, Sharma S, Beauchamp GR, Hollands H. The
reproducibility of ophthalmic utility values. Transactions of the American
Ophthamological Society 2001;99:199-204.
6. Bravata DM, Nelson LM, Garber AM, Goldstein MK. Invariance and
Inconsistency in Utility Ratings. Medical Decision Making 2005;25(2):158-
67.
7. Wittenberg E, Divi N, Halpern E, Araki SS, Prosser L, Weeks JC. The
Effect of Age, Race and Gender on Utility Values for Hypothetical Health
States. 2004 Annual Meeting Society for Medical Decision Making Atlanta
Georgia.
When reading the article we were a bit surprised by the
extremely positive declaration of the clinical results after subthreshold
diode micropulse photocoagulation. The authors stated that
subthreshold diode micropulse laser photocoagulation minimises
chorioretinal damage in the management of CSMO and demonstrates a
beneficial effect on visual acuity and CSMO resolution (in 96% of all
treated eyes, n=...
When reading the article we were a bit surprised by the
extremely positive declaration of the clinical results after subthreshold
diode micropulse photocoagulation. The authors stated that
subthreshold diode micropulse laser photocoagulation minimises
chorioretinal damage in the management of CSMO and demonstrates a
beneficial effect on visual acuity and CSMO resolution (in 96% of all
treated eyes, n=95). However, we have
the strong feeling that the presented results may not support this
conclusion. Moreover, the basic mechanism of the proposed laser
interaction is unclear. It is most likely that
nothing than marginal thermal side effects occurred in the retina
during treatment.
Conventional laser therapy is regarded as effective in treating CSMO.
Unwanted side effects as e.g. induction of CNV or subretinal fibrosis
principally do not appear if laser parameters for threshold exposition are
carefully used. Generally a new laser method must measure against this gold
standard, so that at least comparable results are obtained. This seems not to be the case in the present article.
Conclusions such as "visual acuity was stable or improved in 85% of treated eyes" are questionable if Tab.2 shows stabilization in only 76.8% of eyes (+ < 3 ETDRS lines) and only 8.4% achieved significant better visual acuity (also 14.7% lost more
than 3 lines). Regarding Tab.1 and Tab.3 overall visual acuity
became worse and not better and nearly none of the p-values showed
significance (if p-value was significant visual acuity was worse).
As stated by the authors, the validity of this pilot study is
limited by its small size and retrospective nature. In fact no uniform
postoperative patient follow-up was performed and only the "last available
visual acuity measure" was taken for outcome assessment. This value was
obtained between 3 and 29 (mean 12.2 months), which underlines a high variability. In other words, the results
might only reflect the spontaneous untreated course of CSMO. Also
questionable is the postoperative gradation of CSMO as "worse, better and
resolved". There were no OCT scans taken
either pre- or post-operatively to verify macular thickness. Also,
angiography seems to be performed only in patients who appeared to need
additional treatment. Thus from none of the presented results could it be
objectively concluded that CSMO improved in 96% of eyes.
Finally it is
stated in the results section that in "79% of eyes exhibiting complete
resolution of CSMO postoperatively had significantly better visual
outcomes compared to 17% of eyes with persistent and 4% of eyes with
worsening macular oedema (table 8)". However, Tab.8 clearly demonstrates
that only 8% (n=6) with resolved oedema (n=75) gained 3 or more lines,
which is significantly better, but that 84% (n=63) had only stable visual
acuity within + 3 lines visual acuity change, whereas also additional 8%
had significant vision loss (Tab.8). Thus the proposed positive clinical
result in terms of CSMO resolution and visual acuity improvement could not
been followed.
Independent of clinical results, the mechanism of the
micropulse laser method is unclear. Since there
were no ophthalmoscopically nor angiographically visible laser
damage in the tissue, one has to ask, what happens to the fundus
during treatment? As proven in many experimental
studies conventional laser photocoagulation leads to primary destruction
of the RPE since it absorbs about 60% of the energy from a green laser
beam. The RPE damage is repaired within 7 days by migration and
proliferation of neighbour cells and this seems to lead to an enhanced
pump-function of the new RPE cells leading to resolution of CSMO. Bruch´s
membrane usually stays intact, thus no potential CNV induction is
expected. Because of the long laser exposition times of about 100ms during
irradiation, thermal damage to photoreceptors leads to
irreversible laser scotoma.
In both laser treatments (thermal laser and SRT) the primary RPE
damage can be demonstrated by angiography revealing leakage from the
damaged RPE site, thus the mode of action of the laser treatment can
clearly be proven and is comprehensible. This is not the case in the
article by Luttrull et al. who used repetitive laser pulses of 100µs pulse
duration (which are - at required energies for RPE damage - too long to
spare photoreceptors) within an envelope of 300ms. Temperature
calculations for the laser parameters set in this article reveal an
increase of tissue temperature of 1.8°C per pulse within the laser spot
(taken into account that there is just a 20% energy absorption within the
RPE/choroid complex at 810nm wavelength). The mean temperature increase in
the centre of the laser spot is - due to heat accumulation at the high
repetition rate of 500Hz - about only 11°C after 300ms. Neither thermal
nor thermomechanical based tissue alterations are expected for this low
short time temperature increase. Consequently it might be not remarkable
that - as also stated in the discussion section - the angiographical
visible diabetic leakage after therapy mostly persisted. The discussion of possible mechanisms of this kind of
micropulse laser irradiation as e.g. up- and down- regulation of different
growth factors or heat-shock proteins is speculative.
An aim to provide an optimised keratoprosthesis, with excellent
biointegration, and all other properties meeting ideal requirements, is
one we share with the authors of the recent article entitled “Hydroxyapatite promotes superior keratocyte adhesion and proliferation in comparison with current keratoprosthesis skirt materials”.[1] However, the current paper includes some points that require clarificatio...
An aim to provide an optimised keratoprosthesis, with excellent
biointegration, and all other properties meeting ideal requirements, is
one we share with the authors of the recent article entitled “Hydroxyapatite promotes superior keratocyte adhesion and proliferation in comparison with current keratoprosthesis skirt materials”.[1] However, the current paper includes some points that require clarification.
PHEMA (spelled in full: poly(2-hydroxyethyl methacrylate)is a non-toxic polymer of the toxic monomer HEMA, though cytotoxicity is still possible if non-reacted monomer has not been fully removed. The ' polyhydroxyethyl methacrylate' the authors obtained for their study was not fully described, and may have been contact lens blanks, unlikely to have been processed for 'implantable quality'. Whether the samples had been fully extracted was not stated, nor was the hydration of the samples when used for the study. Contact lens blanks are not designed for cell adhesion and the results of this study, with regard to PHEMA, are entirely predictable and have been previously reported.
The commercially available keratoprosthesis AlphaCor is made from a form of PHEMA, specifically modified for its intended purpose within the cornea. In particular, the AlphaCor OPTIC is made from a relatively low water content, but hydrated, microporous form, similar to the samples evaluated by the authors, specifically because it does not encourage cellular adhesion (epithelial coverage is not desired for this model, nor would adherent posterior cells and membranes be desirable).
In contradistinction, the biointegratable SKIRT region of AlphaCor is
made from a macroporous form of PHEMA with a very high water content; this material, with its interconnecting channels, has been optimised to promote viable biocolonisation, which has been extensively described in the literature. The authors of the present article do concede that cells 'may behave differently in colonising a 3-D porous keratoprosthesis skirt': indeed they do. Further, very subtle modifications of the sponge structure significantly affect all aspects of biointegration.
Both early trial results, such as the preliminary cases cited by the authors, and current results for over 250 AlphaCor devices, have been extensively presented and made available to all device users. Histology now available from AlphaCor devices explanted from human recipients confirms that the biointegration process in humans is similar to that previously shown in the animal model, and maintained in the long term. As expected, specific inflammatory processes can cause localised reversal of biointegration in areas of stromal melting. Certainly, porosity itself does not prevent melting processes, as is also seen in relation to hydroxyapatite keratoprostheses and orbital implants.
There is no argument that keratoprosthesis materials and design
require ongoing revision and improvement. The authors' findings in
relation to hydroxyapatite are interesting, although as they note, this
rigid material has its own limitations. Novel approaches are undergoing early evaluation and may offer benefits. However, at present,
in our view, AlphaCor is a device worthy of consideration for those in whom a donor graft would fail.
Disclosure: Celia Hicks is Medical Director of CooperVision Surgical,
manufacturer of AlphaCor. The Biomaterials and Polymer Research department of the Lions Eye Institute has a financial interest with CooperVision Surgical through support of departmental funding, travel and research.
References
1. J S Mehta, C E Futter, S R Sandeman, R G A F Faragher, K A Hing, K E Tanner, and B D S Allan. Hydroxyapatite promotes superior keratocyte adhesion and proliferation in comparison with current keratoprosthesis skirt materials. Br. J. Ophthalmol. 2005; 89: 1356 – 1362.
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An aim to provide an optimised keratoprosthesis, with excellent biointegration, and all other properties meeting ideal requirements, is one we share with the authors of the recent article entitled “Hydroxyapatite promotes superior keratocyte adhesion and proliferation in comparison with current keratoprosthesis skirt materials”.[1] However, the current paper includes some points that require clarificatio...
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