Yamamoto and coworkers present in their paper the effect of
simultaneous intravitreal injection of a mixture of 4mg triamcinolone
acetonide (TA) and 25?g tissue plasminogen activator (tPA) to treat
macular edema due to central retinal vein occlusion (CRVO) ?1?. The
authors included 20 eyes. Best corrected visual acuity (BCVA) improved
three lines or more in 65%, 55%, 55% and 53% of eyes and the mea...
Yamamoto and coworkers present in their paper the effect of
simultaneous intravitreal injection of a mixture of 4mg triamcinolone
acetonide (TA) and 25?g tissue plasminogen activator (tPA) to treat
macular edema due to central retinal vein occlusion (CRVO) ?1?. The
authors included 20 eyes. Best corrected visual acuity (BCVA) improved
three lines or more in 65%, 55%, 55% and 53% of eyes and the mean macular
thickness decreased from 1072 ?m to 455, 450, 480 and 409 ?m (p<0.001)
at 1, 3, 6 and 12 months, respectively. Fifteen (75%) of the 20 eyes
required at least one additional injection to prevent a recurrence of
macular edema.
We congratulate the authors for their important study and want to add two
aspects from our clinical experience.
In a previous study we investigated the vitreomacular interface in
patients with a history of CRVO or branch retinal vein occlusion (BRVO).
We demonstrated that the posterior vitreous cortex stays attached more
frequently in cases of retinal vein occlusion in comparison to healthy age
-related controls. Hence, there is explicit evidence, that an attached
posterior vitreous might be a co-factor in the development of CRVO or BRVO
[2]. Recently, the vitreomacular interface and the adhesion status of the
posterior vitreous cortex towards the internal limiting membrane (ILM) of
the retina is getting more and more into the focus of interest as the
adhesion status of the posterior vitreous may play an important role in
the pathogenesis of different posterior pole pathologies [3].
Evidence could be demonstrated by Charbonnel and coworkers demonstrating
vitrectomy with arterio-venous (AV) crossing sheathotomy to be of benefit
in the management of BRVO, particularly in eyes with no previous posterior
vitreous detachment (PVD) [4]. The effect of vitrectomy with or without
sheathotomy for macular edema associated with branch retinal vein
occlusion (BRVO) was compared in 36 eyes by Yamamoto and coworkers [5].
Both AV sheathotomy and simple PVD significantly reduced macular edema
associated with BRVO. However, there was no significant difference in the
improvement of macular function following either procedure. As a result,
the posterior vitreous may play an improtant role in the course of macular
edema secondary to retinal vein occlusion.
Tissue plasminogen activator (tPA) is a possible treatment option for
retinal vein occlusion despite the fact that venous thrombi are presumed
to play an important role in the pathogenesis of CRVO. The authors used in
their treatment a combination of intravireal steroids and tPA since
corticosteroids decrease fibrinolytic activity and blood flow may be
compromised. The authors describe that they used tPA in a local
application into the eye to avoid the serious complications associated
with systemic administration.
Tissue plasminogen activator may cause an additional
pathophysiological cascade when applicated in the vitreous cavity.
Depending on the presence of plasminogen, plasmin is generated due to
enzymatic activity by tPA. Due to blood-barrier breakdown secondary to
retinal vein occlusion, plasminogen may be present in higher
concentrations. Clinical studies presented by Murakami and coworkers could
demonstrate for 21 eyes with attached vitreous in CRVO that 16 eyes
developed PVD after intravitreal application of tPA followed by incease of
visual acuity and decrease of retinal thickness [6].
We congratulate Yamamoto and coworkers for their results and
recommend to evaluate additionally the vitreomacular interface in macular
edema secondary to retinal vein occlusion especially when intravitreal tPA
is administered, as PVD may be induced and the course of the desease
consecutively be influenced.
References:
1. Yamamoto T, Kamei M, Sayanagi K, Matsumura N, Nishida K, Sakaguchi H,
Tsujikawa M, Tano Y. Simultaneous intravitreal injection of triamci-nolone
acetonide and tissue plasminogen activator for central retinal vein
occlusion: a pilot study. Br J Ophthalmol. 2011;95:69-73.
2. Bertelmann T, Kicova N, Messerschmidt-Roth A, Irle S, Sekundo W,
Men-nel S. The vitreomacular interface in retinal vein occlusion. Acta
Ophthalmol. 2011 Feb 11. doi: 10.1111/j.1755-3768.2010.02101.x.
3. Mennel S, Meyer CH & Schmidt JC (2010): The Role of the
Vitreous in the Pathogenesis of Age-Related Macular Degeneration. Klin
Monatsbl Augenheilk 227: 1-5
4. Charbonnel J, Glacet-Bernard A, Korobelnik JF, Nyouma-Moune E,
Pour-naras CJ, Colin J, Coscas G & Soubrane G (2004): Management of
branch retinal vein occlusion with vitrectomy and arteriovenous
adventitial sheato-tomy, the possible role of surgical posterior vitreous
detachment. Graefe`s Arch Clin Exp Ophthalmol 242:223-228
5. Yamamoto S, Saito W, Yagi F, Takeuchi S, Sato E, Mizunoya S.
Vitrectomy with or without arteriovenous adventitial sheathotomy for
macular edema associated with branch retinal vein occlusion. Am J
Ophthalmol. 2004;138:907-14
6. Murakami T, Takagi H, Ohashi H, Kita M, Nishiwaki H, Miyamoto K,
Watanabe D, Sakamoto A, Yamaike N & Yoshimura N (2007): Role of Pos-
terior Vitreous Detachment induced by Intravitreal Tissue Plasminogen Ac-
tivator in Macular Edema with Central Retinal Vein Occlusion. Retina
27:1031-1037
Bartlett et al. have reported on the clinical viability of the MPS
9000, a heterochromatic flicker photometry (HFP) device used to estimate
macular pigment optical density (MPOD).[1] Coefficient of repeatability
(CoR) values were used to determine the test-retest repeatability and
reproducibility of the MPS 9000. While the observed CoR of 0.33 is indeed
high, and, superficially at least, raises concern regarding the clin...
Bartlett et al. have reported on the clinical viability of the MPS
9000, a heterochromatic flicker photometry (HFP) device used to estimate
macular pigment optical density (MPOD).[1] Coefficient of repeatability
(CoR) values were used to determine the test-retest repeatability and
reproducibility of the MPS 9000. While the observed CoR of 0.33 is indeed
high, and, superficially at least, raises concern regarding the clinical
application and interpretation of the device, I would suggest that the
author's interpretation of their data, and resultant conclusion in this
paper, that a change in MPOD of less than 0.33 "is very likely to be due
to measurement noise", is both misleading and inaccurate.
The reported CoR (ranging from 0.25 to 0.33) is in fact a measure of
the 95% limits of agreement (LoA), as proposed originally by Bland and
Altman, and is calculated as the mean +/- 1.96SD.[2] By definition, this
value provides an interval, within which 95% of test-retest measurement
differences lie, in this case 0.33.[2-4]
On the basis of this reported coefficient of repeatability, the
authors suggest that any change in repeated measures of MPOD of less than
0.33 on the MPS 9000, should be interpreted as measurement noise, and
could not be assumed to be of clinical importance.[1] In other words, the
authors interpret their coefficient of repeatability values as an
indicator of the amount of change that can occur between readings and
still be classed as measurement noise. Such a conclusion would suggest a
fundamental lack of understanding of this useful statistical tool on the
Author's behalf. Confining the analysis to increases in MPOD (as would be
expected clinically in response to dietary modification or
supplementation), the simple interpretation of a CoR value of 0.33 is
that, in the test-retest data, the observed increase in MPOD was less than
0.33 for 97.5% of subjects, or conversely, that the probability of
detecting a test-retest increase in MPOD greater than 0.33 in the test
population is only 2.5%.
Expanding on this statistical interpretation further, it can be seen
that if the CoR value is halved to 0.17 (mean + 1SD), 84% of subjects
would be expected to exhibit retest increases less than this 0.17 value.
If, for example, during routine clinical practice, a retest increase in
MPOD of 0.17 was noted for a particular patient, on the basis of the
Bartlett et al. results,[1] one could interpret that the probability of
such a change being due to measurement noise is as little as 16%, and for
an increase of 0.33, the probability is as little as 2.5%. In other words,
on the basis of probability, such differences would more than likely
represent a genuine change in MPOD rather than measurement noise as is
suggested by Bartlett et al.[1]
Extracting the data from the Bartlett et al. paper, [1] it can be
observed that the test - retest difference is < 0.1 in close to two-
thirds of their subject data. The data also reveals a significant
influence of two outliers on the magnitude of the observed CoR. For one
subject, the difference in MPOD between visits is an incredible 0.69, and
for another, the difference is greater than 0.4 in the opposite direction.
Simple exclusion of these outliers dramatically improves the CoR to ~0.23.
Similar interpretations have been adopted by the same group in a number of
recent papers, and ultimately, the general validity of the HFP technique,
and its applicability to clinical practice have thereby been called into
question by the group.[5] Given that (a) the results here from just two
subjects are observed to have a significant and adverse effect on the
reported CoR, (b) the test-retest values are quite repeatable for a very
high percentage of subjects, and (c) the authors repeatedly demonstrate a
lack of understanding of the appropriate statistical interpretation of
their data, their broad conclusions would, therefore, seem neither
reasonable nor sustainable.
The suggestion that "any change less than 0.33 units should not be
considered clinically significant as it is very likely to be due to
measurement noise" is simply incorrect. A more appropriate conclusion to
this paper might have been to suggest that, for clinical practice, a
number of measurements of MPOD might be used to provide an average MPOD
value, to thereby ensure that the value obtained is maximally robust, and
that cases of obviously poor performance on the test can be identified.
References
1. Bartlett H, Stainer L, Singh S et al. Clinical evaluation of the
MPS 9000 Macular Pigment Screener. Br J Ophthalmol 2010;94:753-6.
2. Bland J, Altman D. Statistical methods for assessing agreement
between two methods of clinical measurement. Lancet 1986;1:307-10.
3. Bland J, Altman D. Measuring agreement in method comparison
studies. Stat Methods Med Res 1999;8:135-60.
4. Atkinson G, Nevill AM. Statistical methods for assessing
measurement error (reliability) in variables relevant to sports medicine.
Sports Med 1998;26(4):217-38.
5. Bartlett H, Howels O, Eperjesi F. The role of macular pigment in
clinical practice: a review. Clin Exp Optom 2010;93(5):300-8
We read with great interest the article by Good et al. titled
"Sustained elevation of intraocular pressure after intravitreal injections
of anti-VEGF agents." Authors of other case series have reported
sustained intraocular pressure (IOP) elevation following bevacizumab and
ranibizumab injections. Good et al. conducted a retrospective chart
review of 215 eyes receiving anti-VEGF injections to answer the following
ques...
We read with great interest the article by Good et al. titled
"Sustained elevation of intraocular pressure after intravitreal injections
of anti-VEGF agents." Authors of other case series have reported
sustained intraocular pressure (IOP) elevation following bevacizumab and
ranibizumab injections. Good et al. conducted a retrospective chart
review of 215 eyes receiving anti-VEGF injections to answer the following
questions:
1) What is the frequency of sustained IOP elevation after anti-VEGF
injections?
2) What is the frequency of sustained IOP elevation in patients receiving
ranibizumab versus bevacizumab?
3) Is glaucoma a risk factor for sustained IOP elevation in these eyes?
With respect to the first question, the authors report that 13 of 215
(6%) eyes developed sustained IOP elevation after treatment with anti-VEGF
injections. Nine of the eyes with sustained IOP elevation were treated
with bevacizumab originating from a single compounding pharmacy. The
authors hypothesize that the bevacizumab molecule itself may not be the
cause of the IOP elevation, but rather the packaging, transportation, or
storage of the medication. If these 9 cases are excluded, only 4 of 206
(1.9%) developed sustained IOP elevation. The significance of this
number, too, must be interpreted with caution. In the absence of a
control group, it is impossible to determine if this number is different
from similarly matched untreated eyes followed over time. Indeed,
randomized controlled clinical trials have not reported increased rates of
sustained ocular hypertension after ranibizumab injections. ,
With respect to the second question, the authors report that three of
96 (3.1%) eyes treated with ranibizumab developed sustained IOP elevation
compared to 10 of 101 (9.9%) eyes of patients treated with bevacizumab
(p=0.049). When the eyes that received bevacizumab from the particular
pharmacy were excluded, only 2.4% of bevacizumab treated eyes developed
sustained IOP, which is similar to the 3.1% rate in ranibizumab treated
eyes. However, accurate comparison between the two groups requires
consideration of follow-up times, which the authors do not report. Unless
every patient had equivalent lengths of follow-up, these data would be
more appropriately summarized as cumulative incidence (events per eye per
year), or in a Kaplan-Meier curve, either of which would control for
varying follow-up time.
With respect to the third question, the authors report that seven of
21 (33%) eyes with glaucoma treated with anti-VEGF injections developed
sustained IOP elevation, which was higher than the overall rate of
sustained IOP elevation using a Fisher exact test (p<0.001). Again,
variable follow-up times must be considered when comparing these groups.
The Kaplan-Meier curve presented in figure 1 compares all patients to
glaucoma patients as a function of interval between injections, not as a
function of follow-up times. More importantly, in the absence of a
control group of untreated eyes with glaucoma, it is impossible to
determine if the IOP elevation is due to the anti-VEGF injections,
injection of fluid itself into the eye, or simply the natural course of
the disease.
In summary, not accounting for variable follow-up and the absence of
control eyes severely limits the conclusions that can be drawn from this
paper. Based on the results presented, one cannot conclude that anti-VEGF
injections result in increased risk of sustained IOP elevation. In
addition, one cannot conclude that glaucoma patients receiving anti-VEGF
injections are at increased risk of sustained IOP elevation compared to
glaucoma patients not receiving these injections.
In a recently published article by Chandra et al. the authors have
stated that they conducted a "case-controlled" study to examine the
anticoagulant effectiveness of warfarin in vitreoretinal surgery.(1)
However, this study was conducted on a cohort of patients receiving pars
plana vitrectomy (PPV); 60 patients who received warfarin (exposure) on
the day of PPV were selected. These 'exposed' pati...
In a recently published article by Chandra et al. the authors have
stated that they conducted a "case-controlled" study to examine the
anticoagulant effectiveness of warfarin in vitreoretinal surgery.(1)
However, this study was conducted on a cohort of patients receiving pars
plana vitrectomy (PPV); 60 patients who received warfarin (exposure) on
the day of PPV were selected. These 'exposed' patients were matched to
other patients receiving PPV but not taking warfarin (unexposed) on age,
sex, and presenting complaint. These patients were then followed for
perioperative and long term complications. Thus, this is not a case-
control study rather it is a matched cohort study. As a result, the
statistical analysis raises concerns. Matching in a cohort study does not
necessarily eliminate the need for control of matching factors in the
analysis; censoring (competing risks, death, loss to follow-up) can
produce imbalances thereby limiting the extent of matching only to those
among the original counts of persons for whom matching was applied.(2) In
other words, an association of exposure and the matching factors could be
observed for the remaining persons and the observed person-time.2
Furthermore, even if no censoring occurs and one examines risk, control of
matching factors would still be necessary to obtain valid standard
deviation estimates.(3,4) In contrast, case-control studies require
control of matching factors associated with exposure rather than risk.
Moreover, with variable follow-up duration and censoring a matched
survival (time-to-event) analysis producing hazard ratios would have been
a better strategy than reporting the p-values alone; censoring has not
been mentioned in the article.
REFERENCES
1. Chandra A, Jazayeri F, Williamson T. Warfarin in vitreoretinal
surgery: a case controlled series. Br J Ophthal 2010.
http://bjo.bmj.com/content/early/2010/11/11/bjo.2010.187526.full.html.
2010.
2. Rothman K, Greenland S. Modern Epidemiology. 2nd ed. Philadelphia:
Lippincott Williams & Wilkins; 1998.
3. Greenland S, Robins J. Estimation of a common effect parameter
from sparse follow-up data. Biometrics. 1985;41:55-68.
4. Weinberg C. On pooling across strata when frequency matching has
been followed in a cohort study. Biometrics. 1985;41:103-116.
We have a few concerns on the report by Clemson CM et al on the
efficacy of valproic acid (VPA) in 7 patients with retinitis pigmentosa
(RP) [1]. Was the time period of 6 months for using VPA the maximum time
that was allowed by the institutional review boards? The degree to which
the retina was affected by RP was not mentioned in each case (either in
the form of photographic evidence or by electro...
We have a few concerns on the report by Clemson CM et al on the
efficacy of valproic acid (VPA) in 7 patients with retinitis pigmentosa
(RP) [1]. Was the time period of 6 months for using VPA the maximum time
that was allowed by the institutional review boards? The degree to which
the retina was affected by RP was not mentioned in each case (either in
the form of photographic evidence or by electrophysiological studies). Age
-matched appropriate controls need to be incorporated in future studies as
younger retinas or retinas lesser affected by RP usually respond better to
treatment [2]. Conversion of vision from Snellens acuity chart into logMAR
has a risk of wrongly estimating visual acuity given the inherent pitfalls
of the Snellens acuity test [3]. Therefore to extrapolate and show
improvement in the mean of visual field and visual acuity is
inappropriate. The authors did not report the number of visual field
plots that were done pre-treatment (except patient 5), as an improvement
in visual field in patients could be an improvement in the learning curve
and not a real improvement in visual field.
Although this paper calls for a well-designed prospective case-
control study, it does provide proof-of-concept that valproic acid may
have retinal neuroprotective effects as observed in animal models [4, 5].
VPA offers neuroprotection and neuroregeneration in a histone-acetylation-
independent manner, more likely involving the Wnt (wingless-type MMTV
integration site family)/beta-catenin signalling pathway [5]. Sustained
Wnt2b expression helped maintain undifferentiated retinal stem cells in
the ciliary marginal zone, promoted proliferation of retinal stem cells in
vitro, including regeneration of rhodopsin-positive photoreceptor cells in
the RP mouse model. VPA and related HDAC inhibitors could potentially be
valuable drugs for patients with retinal degenerative disorders and should
not be discounted without good evidence to the contrary.
References:
1. Clemson CM, Tzekov R, Krebs M, Checchi JM, Bigelow C, Kaushal S.
Therapeutic potential of valproic acid for retinitis pigmentosa. Br J
Ophthalmol. 2011;95:89-93.
2. Eballe AO, Koki G, Emche CB, Bella LA, Kouam JM, Melong J.
Blindness and visual impairment in retinitis pigmentosa: a Cameroonian
hospital-based study. Clin Ophthalmol. 2010;4:661-5.
3. McGraw P, Winn B, Whitaker D. Reliability of the Snellen chart.
BMJ 1995;310:1481-2.
4. Biermann J, Grieshaber P, Goebel U, Martin G, Thanos S, Di
Giovanni S, Lagr?ze WA. Valproic acid-mediated neuroprotection and
regeneration in injured retinal ganglion cells. Invest Ophthalmol Vis Sci.
2010;51:526-34.
5. Osakada F, Ooto S, Akagi T, Mandai M, Akaike A, Takahashi M. Wnt
signalling promotes regeneration in the retina of adult mammals. J
Neurosci. 2007;27:4210-9.
Dear Editor, we thank West et al. for their interest in our paper.
Firstly, we wish to point out that as stated in our paper's conclusion, we
fully endorse early surgery in all cases of paediatric & adolescent
blowout fracture. We are committed to educating referrers and colleagues
in other specialities to recognize & refer these patients as soon as
possible. Secondly, West et al claim that we did not adequatel...
Dear Editor, we thank West et al. for their interest in our paper.
Firstly, we wish to point out that as stated in our paper's conclusion, we
fully endorse early surgery in all cases of paediatric & adolescent
blowout fracture. We are committed to educating referrers and colleagues
in other specialities to recognize & refer these patients as soon as
possible. Secondly, West et al claim that we did not adequately highlight
patients with white-eyed blowout fractures who they presume have muscle
ischaemia and poorer outcomes. Jordan et al's paper on white-eyed blowout
fractures postulated that perimuscular soft tissue entrapment causes
muscle ischaemia due to a "compartment-type syndrome"1. This remains
unproven. Iliff et al's clinical and experimental animal study could not
confirm the existence of orbital compartment syndromes in blowout
fractures2. They identified direct muscle damage, nerve contusion and
incarceration of the muscular fascial network as more likely causes of
postoperative diplopia. If muscle ischaemia was present, urgent surgery
(within hours) to prevent muscle necrosis would be indicated. Other
causes of muscle damage may not require the same degree of urgency.
Further information on the causes of diplopia and prospective randomized
trials comparing outcomes after various intervals to surgery are required.
Until more is known, our stance on white-eyed blowout fractures is not
dogmatic: each case is considered individually and surgery is performed as
soon as practicable. This approach does not preclude urgent surgery if it
is required.
West et al. also stated that our results may have been better if our
patients with white-eyed blowout fractures had undergone earlier surgery.
They compared our results with three studies 3-5. Unfortunately, each
study presents its results differently. We described diplopia on extreme
gaze as self-reported or elicited on examination. We consider these
children did not have significant diplopia. Ethanadan et al describe a
similar group with diplopia as not "relevant" for day to day activites3.
Gerbino et al describe three motility outcomes: full extraocular muscle
recovery, diplopia in supraduction & vertical diplopia4. They did not
state if postoperative diplopia in their cases was functionally
significant or elicited on examination only. Bansagi et al used a
numerical scale for comparing supraductions before and after surgery
instead of reporting on diplopia5. Comparison of our results and those of
other studies is difficult. We do not accept that our results are
necessarily inferior to other studies' results when consensus on
describing motility outcomes is lacking.
1. Jordan DR, Allen LH, White J et al: Intervention within days for
some orbital floor fractures: The white-eyed blowout. Ophthal Plast
Reconstr Surg 1998;14(6):379-390.
2. Iliff N, Manson PN, Katz J et al. Mechanisms of extraocular muscle
injury in orbital fractures. Plast Reconstr Surg 1999;103:787-99
3. Ethunandan M, Evans BT. Linear trapdoor or "white-eye" blowout
fracture of the orbit: not restricted to children Br J Oral Maxillofac
Surg. 2010 May 12 [Epub ahead of print]
4. Gerbino G et al. Surgical Management of Orbital Trapdoor Fracture
in Pediatric Population. J Oral Maxillofac Surg 2010; 68: 1310-1316.
5. Bansagi ZC, Meyer DR. Internal orbital fractures in the pediatric
age group: characterization and management. Ophthalmology 2000; 107(5):
829-836.
Newsham's recent article on the management of amblyopia is timely but
misdirected.
Illusions concerning occlusion therapy are repeated with tourettic
persistence despite a lack of supporting objective scientific evidence.
(Gregson R. Why are we so bad at treating amblyopia. Eye 2002;16:461-2)
Reports of effective treatment are diminished by the number of
subjects who decide to discontinue treatment. Of tho...
Newsham's recent article on the management of amblyopia is timely but
misdirected.
Illusions concerning occlusion therapy are repeated with tourettic
persistence despite a lack of supporting objective scientific evidence.
(Gregson R. Why are we so bad at treating amblyopia. Eye 2002;16:461-2)
Reports of effective treatment are diminished by the number of
subjects who decide to discontinue treatment. Of those who continue
treatment approximately 20 percent, particularly those with initial acuity
less than 20/125, fail to improve. Of those who do improve by three or
more lines on a Snellen chart, which may still leave them unable to read
or perform other important tasks, (Stifter E, Burggasser G, Hirmann E,
Thaler A,et al. Monocular and binocular reading performance in children
with microstrabismic amblyopia. Br J Ophthalmol. 2005;89:1324-9.) about
half will regress to initial levels after discontinuation of patching.
Assessing the usefulness of this therapy is limited by a lack of untreated
controls, failure to consider the placebo effect, and improvement due to
increasing literacy, age, and familiarity with the tests. A myriad of
treatment protocols including acupuncture, drugs, tinted lenses,
exercises, sewing eyelids, refractive surgery, and many other remedies
have comparable outcomes. "The diversity of treatment protocols
accentuates another dilemma owing to our paucity of knowledge on the dose-
effect relation - a situation one finds hard to imagine for any comparably
established therapy outside ophthalmology. In other words we have no
understanding of the dose-effect relation of occlusion in amblyopia
therapy." (Simonsz HJ, et al. Electronic monitoring of treatment
compliance in patching for amblyopia. Strabismus 1999 ;7:113-23.)
The traditional concepts of the etiology of amblyopia were developed
before the availability of means for axial length measurement, MRI's, or
magnification corrected retinal photography. Recent studies, notably
(Pineles SL, Demer JL. Bilateral abnormalities of optic nerve size and
eye shape in unilateral amblyopia. Am J Ophthalmol 2009;148:551-7 and
Lempert P. Retinal area and optic disc rim area in amblyopic, fellow, and
normal hyperopic eyes: A hypothesis for decreased acuity in amblyopia.
Ophthalmology 2008;115:2259-61) indicate that the presumably amblyopic
eyes have optic nerve hypoplasia as well as additional structural defects.
Other reports demonstrate that both eyes are have impaired function of
different severity and anatomy which indicates that amblyopia really a
binocular disorder.
Redirecting attention to prenatal conditions that are associated with
optic nerve hypoplasia is likely to be more effective than continued
adherence to traditional therapies in preventing vision impairment in
children.
Dear editor:
Yamamoto and coworkers present in their paper the effect of simultaneous intravitreal injection of a mixture of 4mg triamcinolone acetonide (TA) and 25?g tissue plasminogen activator (tPA) to treat macular edema due to central retinal vein occlusion (CRVO) ?1?. The authors included 20 eyes. Best corrected visual acuity (BCVA) improved three lines or more in 65%, 55%, 55% and 53% of eyes and the mea...
Bartlett et al. have reported on the clinical viability of the MPS 9000, a heterochromatic flicker photometry (HFP) device used to estimate macular pigment optical density (MPOD).[1] Coefficient of repeatability (CoR) values were used to determine the test-retest repeatability and reproducibility of the MPS 9000. While the observed CoR of 0.33 is indeed high, and, superficially at least, raises concern regarding the clin...
We read with great interest the article by Good et al. titled "Sustained elevation of intraocular pressure after intravitreal injections of anti-VEGF agents." Authors of other case series have reported sustained intraocular pressure (IOP) elevation following bevacizumab and ranibizumab injections. Good et al. conducted a retrospective chart review of 215 eyes receiving anti-VEGF injections to answer the following ques...
To The Editor,
In a recently published article by Chandra et al. the authors have stated that they conducted a "case-controlled" study to examine the anticoagulant effectiveness of warfarin in vitreoretinal surgery.(1) However, this study was conducted on a cohort of patients receiving pars plana vitrectomy (PPV); 60 patients who received warfarin (exposure) on the day of PPV were selected. These 'exposed' pati...
Dear Editor,
We have a few concerns on the report by Clemson CM et al on the efficacy of valproic acid (VPA) in 7 patients with retinitis pigmentosa (RP) [1]. Was the time period of 6 months for using VPA the maximum time that was allowed by the institutional review boards? The degree to which the retina was affected by RP was not mentioned in each case (either in the form of photographic evidence or by electro...
Dear Editor, we thank West et al. for their interest in our paper. Firstly, we wish to point out that as stated in our paper's conclusion, we fully endorse early surgery in all cases of paediatric & adolescent blowout fracture. We are committed to educating referrers and colleagues in other specialities to recognize & refer these patients as soon as possible. Secondly, West et al claim that we did not adequatel...
Newsham's recent article on the management of amblyopia is timely but misdirected. Illusions concerning occlusion therapy are repeated with tourettic persistence despite a lack of supporting objective scientific evidence. (Gregson R. Why are we so bad at treating amblyopia. Eye 2002;16:461-2)
Reports of effective treatment are diminished by the number of subjects who decide to discontinue treatment. Of tho...
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