Thank you for your comments. Two cases with the exfoliation syndrome
and one with pigmentary glaucoma were included in our study. As you
mentioned, dilatation of the pupil often causes a rise of intraocular
pressure in such cases. However, none of the three individuals in our
study had a significant rise of intraocular pressure or progression of
glaucoma.
Sincerely,
George Sp...
Thank you for your comments. Two cases with the exfoliation syndrome
and one with pigmentary glaucoma were included in our study. As you
mentioned, dilatation of the pupil often causes a rise of intraocular
pressure in such cases. However, none of the three individuals in our
study had a significant rise of intraocular pressure or progression of
glaucoma.
Sincerely,
George Spaeth M.D.
We thank Dr Kesarwani for the interest in our article.
In response to the points raised:
1. Inclusion criteria
We attempted to recruit children with X(T) measuring more than 20 prism
dioptres when fixing a 6 metre target, as angles under this amount are
usually felt not to require treatment. However, Dr Kesarwani is correct to
point out that, at the baseline assessme...
We thank Dr Kesarwani for the interest in our article.
In response to the points raised:
1. Inclusion criteria
We attempted to recruit children with X(T) measuring more than 20 prism
dioptres when fixing a 6 metre target, as angles under this amount are
usually felt not to require treatment. However, Dr Kesarwani is correct to
point out that, at the baseline assessment following recruitment to the
study, some children had angles of strabismus measuring < 20 pd. We
were interested to see how the score performed in children with small
angle X(T) and so decided not to exclude them.
2. Stereoacuity values
The reason the distance stereoacuity mean is lower than the near is
probably due to the range of stereoacuities each test provides. For
values of less than 200" for distance
the score will be negative as this is the largest disparity possible (if
tested at 3m) however, one can test up to (down to) a disparity of 600" on
the FNS.
3. Median distance stereoacuity values included values calculated
with adjustment for interpupillary distance.
Once again, we thank Dr Kesarwani for attentive reading of our paper
We read with great interest the recently published article by Bottoni
and associates. However, we would like to express our concerns regarding
their article entitled “Diagnosis of macular pseudoholes and lamellar
macular holes: is optical coherence tomography the gold standard?” Br. J.
Ophthalmol. published online 1 Feb 2008; doi:10.1136/bjo.2007.127597. [1]
In this article, the authors investigate...
We read with great interest the recently published article by Bottoni
and associates. However, we would like to express our concerns regarding
their article entitled “Diagnosis of macular pseudoholes and lamellar
macular holes: is optical coherence tomography the gold standard?” Br. J.
Ophthalmol. published online 1 Feb 2008; doi:10.1136/bjo.2007.127597. [1]
In this article, the authors investigate whether fundus autofluorescence
imaging (FAF) differentiates between macular pseudo hole (MPH) and
lamellar macular hole (LMH).
(First of all, figure 1 has not been presented. I guess it could be a
technical error owing to the PDF rendering process).
Second, although corrected value of the foveal AF intensity was not
found to be significantly different between the two groups (ie,
pseudoholes and lamellar holes), authors concluded that AF imaging may add
useful information as to the differential diagnosis of MPH from LMH.
Moreover, they stated that the presence of foveal AF is consistent with a
loss of foveal tissue and therefore a diagnosis of LMH. We believe there
is an inconsistency between results and
conclusion.
Third, several factors should be considered for evaluating FAF
intensities in different examination and patient. Detector gain, pupillary
alignment, refraction of the eye, lens status and number of the averaged
image could be interfere pixel intensity of the FAF signal and those
should be standardized before quantitative analyses of FAF images. [2] In
the aforementioned article, standardization of the FAF images has not been
clearly stated.
Ratio between the region of interest and background intensity appears
reliable for single mean image quantification. However, bleaching of the
photopigments due to the continuous visible light excitation may influence
results and leads miscalculation. Bleaching with blue light is minimal at
the fovea and is maximum approximately 12 degrees away from the fovea in
the horizontal and vertical meridians. [3] Increment of the pixel
intensity of the FAF image is depending on excitation time and amplitude
of the fotobleaching is related amount of the photopigment and varies
individually. According to our results (article in process), nearly 40%
increment (range 18.8 % to 75.9 %) in FAF luminosity occurs during first
thirty seconds of the excitation. For this reason, obtaining standard FAF
images with accurate luminosity requires at least 30 second fundus
illumination to bleach the photoreceptor pigments.
Considering these biasing factors (acquiring standardized FAF images,
using accurate raw image processing algorithm) may provide more reliable
results. Different analyse technics (i.e. circularity, eccentricity or
transition pattern analyse) may grant the difference.
We thank Bottoni and his associates for their interesting article.
References
1. Bottoni F, Carmassi L, Cigada M, Moschini S, Bergamini F.
Diagnosis of macular pseudoholes and lamellar macular holes: is optical
coherence tomography the gold standard? Br J Ophthalmol. 2008 Feb 1; [Epub
ahead of print] doi:10.1136/bjo.2007.127597
2. Schmitz-Valckenberg S, Holz FG, Fitzke FW. Perspectives in Imaging
Technologies. In: Atlas of Fundus Autofluorescence Imaging, Holz FG,
Spaide RF, Bird AC (editors). Springer – Verlag, Berlin 2007:325-34
I appreciate the letter by Dr. Lempert regarding Dr. Nilsson's
Editorial to our study of the extension of the period of bilateral visual
impairment (BVI) in persons with untreated amblyopia, and the response by
Dr. Nilsson. A slight misunderstanding may arise, however, from the first
sentence of Dr. Lempert's letter: "It is not surprising that amblyopes are
at higher risk of bilateral visual impairm...
I appreciate the letter by Dr. Lempert regarding Dr. Nilsson's
Editorial to our study of the extension of the period of bilateral visual
impairment (BVI) in persons with untreated amblyopia, and the response by
Dr. Nilsson. A slight misunderstanding may arise, however, from the first
sentence of Dr. Lempert's letter: "It is not surprising that amblyopes are
at higher risk of bilateral visual impairment since impaired visual
functions of the fellow eye have been previously demonstrated."
This may seem to imply that we reported extension of the period of
BVI caused by impaired function of the fellow eye. Instead, we reported
that for untreated amblyopes the lifetime risk of BVI was 18% while they
lived on average 7.2 years with BVI, while for non-amblyopes, these
figures were 10% and 6.7 years, respectively. Hence, untreated amblyopia
extended the average expected period living with BVI from 0.7 to 1.3
years. This extension was only or primarily caused by the fact that they
already had decreased function of their amblyopic eye.
We agree with the authors’ recommendation on the need for a sleep
history in the eye clinic and probably having a lower threshold for
referral to sleep physicians for further sleep studies.[1] However, we would
like to bring to their attention other epidemiological studies where
screening tools/sleep history have shown a high prevalence of sleep
disorders in patients with ocular disorders other than...
We agree with the authors’ recommendation on the need for a sleep
history in the eye clinic and probably having a lower threshold for
referral to sleep physicians for further sleep studies.[1] However, we would
like to bring to their attention other epidemiological studies where
screening tools/sleep history have shown a high prevalence of sleep
disorders in patients with ocular disorders other than non- arteritic
anterior ischaemic optic neuropathy (NAION). These include primary open
angle glaucoma (POAG), normal tension glaucoma (NTG), floppy eye lid
syndrome (FES) and more recently central serous chorio-retinopathy
(CSCR).[2-5] The evidence from these studies is summarized in table 1.
The
literature shows a higher prevalence of sleep disorder than that reported
in the general population in the United Kingdom by Ohayon et al (1.9% of
population sample, n=4972) based on the minimal criteria of the
International Classification of Sleep Disorders.[6]
We note the authors have adjusted the statistical analysis for
glaucoma among other factors, but the proportion of patients diagnosed
with glaucoma in the study and control groups is not mentioned. They also
do not mention the ocular diagnosis of the randomly selected control group
from the ophthalmology clinics and if any exclusion criteria, other than
NAION was used. This may be the reason for their study having a lower
proportion of patients with symptoms consistent with SAS than previously
reported. The other reason can be the different screening methods used in
these studies.
Also, the authors do not mention if the patients scoring positive on
the Sleep Apnoea scale of the Sleep Disorders Questionnaire (SA-SDQ) were
referred for sleep studies. Offering polysomnography or even limited sleep
study to the study sample and comparing the outcomes with the SA-SDQ
scores could provide the required evidence or validation, as mentioned by
the authors, on the need for lower cut-off points for this patient sub-group.
We recently conducted a similar study in the general eye clinic
population, which is under consideration for publication at the present
time. Following a review of the various components of the screening
questionnaire; patients with glaucoma were more likely to report episodes
of apnoea, morning headaches, short term memory loss and poor
concentration. We therefore suggest the authors also do a further analysis
of the responses obtained to the 8 questions addressing the specific
symptoms of SAS in the SA-SDQ, as they might be able to provide an
additional weighted score for screening in their patient subgroup.
References
1. Li J, McGwin G, Vaphiades MS, Owsley C. Non-arteritic anterior
ischaemic optic neuropathy and presumed sleep apnoea syndrome screened by
the Sleep Apnoea scale of the Sleep disorders Questionnaire (SA-SDQ). Br J
Ophthalmol 2007; 91:1524-1527.
2. Hakki Onen S, Mouriaux F, Berramdane L, Dascotte JC, Kulik JF,
Rouland JF. High prevalence of sleep disordered breathing in patients with
primary open angle glaucoma. Acta Ophthalmol Scand 2000; 78: 638-641.
3. Marcus DM, Costarides AP, Gokhale P, Papastergiou G, Miller JJ,
Johnson MH, Choudhary BA. Sleep Disorders: A risk factor for normal
tension glaucoma. J Glaucoma 2001; 10: 177-183.
4. McNab AA, The eye and sleep. Clinical Experimental Ophthalmology
2005; 33: 117-25.
5. Leveque TK, Yu L, Musch DC, Chervin RD, Zacks DN. Central serous
chorioretinopathy and risk for obstructive sleep apnoea. Sleep Breath
2007; 11: 253-257.
6. Ohayon MM, Guilleminault C, Priest RG, Caulet M (1997) Snoring and
breathing pauses during sleep: telephone interview survey of a United
Kingdom population sample. BMJ, 314, 860–863.
We want to thank Drs. Martinez and Sanchez for the response to our recent editorial. We are in agreement with them that evidence does exist that blood flow is altered in glaucoma and is suggestive of a
pathogenetic role[1]. We also agree that a variety of methods are being used to evaluate blood flow and these techniques certainly have improved over the last decade and a half.
We want to thank Drs. Martinez and Sanchez for the response to our recent editorial. We are in agreement with them that evidence does exist that blood flow is altered in glaucoma and is suggestive of a
pathogenetic role[1]. We also agree that a variety of methods are being used to evaluate blood flow and these techniques certainly have improved over the last decade and a half.
I would also like to thank Drs. Martinez and Sanchez for calling attention to their article in Acta Ophthalmologica[2] detailing their prospective analysis of blood flow in glaucoma. They are to be congratulated on their work. Unfortunately, in an editorial, space is limited and not all research could be highlighted
to the extent that we would have desired.
The article mentioned by Dr. Martinez and Sanchez is an elegant early step in attempting to prospectively determine blood flow-based risk factors for progression over the mid-term in patients with untreated primary open angle glaucoma. In the 49 patients evaluated by
the authors(23 progressed and 26 non-progressed over three years) differences in
resistivity index as measured with color Doppler, but not baseline
intraocular pressure as in the Early Manifest Glaucoma Trial, predicted
approximately 80-90% of patients who ultimately progressed or remained
stable[2,3].
This work highlights ocular hemodynamics as a possible risk factor
for glaucomatous progression. Their response letter confirms the need
for a more definitive evaluation of blood flow in glaucoma to determine
any relationship to its pathogenesis and if improving this parameter
improves long-term visual outcomes. By doing so we hope that, in the
future, our patients may be more specifically and adequately treated.
References 1. Stewart WC, Feldman R, Mychaskiw MA. Ocular blood flow in
glaucoma: the need for further clinical evidence and patient outcomes
research. Br J Ophthalmol. 2007; 91: 1263-1264.
2. Martinez A, Sanchez M. Predictive Value of Color Doppler Imaging
in a Prospective Study of Visual Field Progression in Primary Open-Angle
Glaucoma. Acta Ophthalmol Scand 2005; 83: 716-723.
Dr Buck et al must be commended for this wonderful article[1] which
takes us one step closer to deciding intervention based on Newcastle
scoring system previously described.[2] However, we seek a few
clarifications.
1.Inclusion criteria: The authors have described the inclusion
criteria for the study to be intermittent exotropia X(T)) of more than or
equal to 20 prism dioptres (pd), for...
Dr Buck et al must be commended for this wonderful article[1] which
takes us one step closer to deciding intervention based on Newcastle
scoring system previously described.[2] However, we seek a few
clarifications.
1.Inclusion criteria: The authors have described the inclusion
criteria for the study to be intermittent exotropia X(T)) of more than or
equal to 20 prism dioptres (pd), for distance fixation and X(T) of less
than or equal to 20 pd at near. A closer look of the results reveals that
the range of values is 0 to 40 pd and 6 pd.to 50 pd for near and distance
respectively (table 2).Has the inclusion criteria been adhered to?
2.As per the table cited, the median and mean stereoacuity values are
more for near than for distance which is contrary to what is expected in a
case of intermittent exotropia. We would request the authors to elucidate
more on this aspect.
3.Median values are 110 sec of arc and 75 sec of arc at baseline and
follow up respectively for near stereoacuity by Frisby test. Similarly
median values are 34 sec of arc and 23 sec of arc for distance
stereoacuity at baseline and follow up by FD2TM distance stereoacuity. We
would like the authors to clarify their testing protocols because these
values are not included in the testing protocols usually followed for
administering these tests.
References
1.Buck D, Hatt SR, Haggerty H, Hrisos S, Strong NP, Steen NI, Clarke MP.
The use of the Newcastle Control Score in the management of intermittent
exotropia. Br J Ophthalmol 2007;91:215-218
2.Haggerty H, Richardson S, Hrisos S, et al. The Newcastle Control
Score: a new
method of grading the severity of intermittent exotropia. Br J Ophthalmol
2004;88:233¨C5.
In a reply to my editorial in the November issue, Dr Lempert raises several valid concerns regarding vision screening for amblyopia. I would like to thank Dr Lempert for his reply and this possibility for a discussion on a difficult and important topic!
I was, however, slightly surprised to find that the reply is written as a rebuttal of my arguments, while I am of the same opinion as Dr Lempert, and have...
In a reply to my editorial in the November issue, Dr Lempert raises several valid concerns regarding vision screening for amblyopia. I would like to thank Dr Lempert for his reply and this possibility for a discussion on a difficult and important topic!
I was, however, slightly surprised to find that the reply is written as a rebuttal of my arguments, while I am of the same opinion as Dr Lempert, and have tried to express this in the editorial!
In the first paragraph Dr Lempert cautions against assuming that treatment for amblyopia normalizes visual function. I absolutely agree, and in my editorial I explicitly state:
“There is a clear need for objective studies on the possible relationship between unilateral amblyopia and functional disabilities. In such studies, comparisons should be made between three groups: (1) normal controls, (2) non-treated amblyopes, and (3) amblyopes after successful treatment.”
Dr Lempert claims that my editorial “implies that lack of screening and treatment of amblyopia cause a lifelong handicap.”
I have never intended to say this, and even find it slightly amusing, since I have countless times been accused of being “anti-screening” when pointing out that we currently do not have evidence to be able say that untreated unilateral amblyopia is disabling! I write “In discussing the rationale for preschool vision screening programmes, more results on possible associations between amblyopia and increased lifetime risk of visual impairment, as well as quality of life/utility measures for unilateral amblyopia, are required.”
Dr Lempert also claims my editorial implies that “treatment offers a significant cost / benefit gain.” I do report on results from previously published papers 1, 2, however, results showing that treatment for spontaneously presenting amblyopia (which these two papers deal with) is cost-efficient must not be confused with evidence for vision screening being cost-efficient!
In the final paragraph Dr Lempert points to the need for effective allocation of medical resources. I, again, agree, and have written in my editorial: “In a world with limited economic resources and ever-growing expenses for medical services, we will most likely see an increasing demand for evaluation, evidence of benefit and proof of cost-effectiveness for government-financed screening programmes.”
I still do believe that van Leeuwen’s paper3 is a very important contribution, and as I conclude my editorial: “As of today, we do not have all of the information required, but van Leewen et al’s work has provided us with very valuable data, moving us closer to determining whether preschool vision screening can be justified.”
References
1. Membreno JH, Brown MM, Brown GC, Sharma S, Beauchamp GR. A cost-utility analysis of therapy for amblyopia. Ophthalmology 2002;109:2265-71.
2. König HH, Barry JC. Cost effectiveness of treatment for amblyopia: an analysis based on a probabilistic Markov model. Br J Ophthalmol 2004;88:606-12.
3. van Leewen R, Eijkemans M, Vingerling JR, Hofman A, de Jong P, Simonsz HJ. Risk of bilateral visual impairment in persons with amblyopia: The Rotterdam Study. Br J Ophthalmol 2007;91:1450-1.
We read with interest the editorial by Miller which comments on the
paper, ‘Epidemiology of giant-cell arteritis in an Arab population: a 22-year study’[1]. The author of the editorial comments on geographical
variation in the incidence of giant cell arteritis and cites evidence
supporting both genetic and environmental aetiologies.
We re-examined the data from our 5 year study[2] looking at...
We read with interest the editorial by Miller which comments on the
paper, ‘Epidemiology of giant-cell arteritis in an Arab population: a 22-year study’[1]. The author of the editorial comments on geographical
variation in the incidence of giant cell arteritis and cites evidence
supporting both genetic and environmental aetiologies.
We re-examined the data from our 5 year study[2] looking at biopsy
proven giant cell arteritis at Leicester Royal Infirmary and identified
the ethnicity of the patients. This unit is the only tertiary ophthalmic
referral centre for the county of Leicestershire, United Kingdom. Census
data from 2001 indicates that ethnic Asians in Leicestershire make up 30%
of the population. Out of a total of 42 biopsies, only 3 cases (7.1%) were
from patients of Asian ethnicity. Whilst our study was not a prospective
population based study, the data lends weight to the idea that GCA is
relatively rare in ethnic Asians.
Interestingly our findings differ from those of Lam et al[3] who found
the prevalence of GCA to be similar in Hispanic and non-Hispanic patients.
Inferences can be made about the aetiology of a disease by examining the
incidence of a disease in migrant populations when the direction of
migration is from an area of low incidence to an area of high incidence.
For example, the incidence of multiple sclerosis in Indian and Pakistani
migrants to the UK has been studied[4] and it has been found that migration
prior to the age of 15 years confers an increased risk of developing
multiple sclerosis, a finding which implicates environmental agents.
Similar prospective studies looking at the relationship between age at
migration and risk of developing GCA may yield more information about the
interplay between genetic and environmental factors.
References
1. Miller NR. Epidemiology of giant cell arteritis in an Arab
population: a 22-year study. Br J Ophthalmol. 2007 Jun;91(6):705-6.
2. Jain S, Shah A, Deane J. Giant cell arteritis. (letter).
Ophthalmology. 2007 Jun;114(6):1235
3. Lam BL, Wirthlin RS, Gonzalez A, Dubovy SR, Feuer WJ. Giant cell
arteritis among Hispanic Americans. Am J Ophthalmol. 2007 Jan;143(1):161-3
4. Dean G, Elian M. Age at immigration to England of Asian and
Caribbean immigrants and the risk of developing multiple sclerosis. J
Neurol. Neurosurg. Psychiatry 1997;63:565-568
We read with great interest the recent commentary by Stewart et al [1] describing the evidence of the blood flow disturbances in the pathogenesis of the glaucomatous damage.
Although I agree with some of the findings of this excellent review, there are some important points that should be addressed:
1.After reading this article, one may think that there is not evidence that ocular bl...
We read with great interest the recent commentary by Stewart et al [1] describing the evidence of the blood flow disturbances in the pathogenesis of the glaucomatous damage.
Although I agree with some of the findings of this excellent review, there are some important points that should be addressed:
1.After reading this article, one may think that there is not evidence that ocular blood flow abnormalities are involved in the pathogenesis of the glaucomatous damage. Different studies, using different devices, point in the same general direction indicating that on average blood flow is decreased in some glaucoma patients, especially in primary open-angle glaucoma (POAG) patients and in patients that progress despite normalized intraocular pressure (IOP) [2]. Furthermore this decrease in blood flow is not confined to the eye alone [3].
2. Many different methods are being used to measure directly or calculate
indirectly in vivo ocular blood flow. Although there is not still a single method that can provide all the relevant information in one reading, the development of newer techniques and their corrected use provides the potential for assessing blood flow in humans.
3. On the other hand, the Authors reveal the lack of evidence of a pathogenic link between glaucoma and impaired ocular blood flow. They asked for a long-term prospective study, that includes carefully selected patient groups, with similar baseline demographic and clinical characteristics, but with dissimilar baseline ocular hemodynamics. We published a paper that prospectively investigated the value of color Doppler imaging of the ophthalmic artery and short posterior ciliary arteries in the prognosis of disease progression in patients with POAG.
[4] When baseline demographic and clinical characteristics were stratified according to whether the eyes progressed during the 3-year follow-up period, the only parameters to show significant differences were the resistivity index of the ophthalmic artery and the resistivity index of the short posterior ciliary arteries.
Our study concluded that poor blood flow in the retrobulbar vessels is closely linked to visual field deterioration in POAG patients.
In conclusion, we think that the understanding of the role of ocular blood flow disturbances in the pathogenesis of glaucoma has improved greatly. We have evidence that ocular blood flow is altered independently from IOP or level of damage in patients with progressive glaucoma, which could represent a primary risk factor for disease progression. In looking forward, we need long-term prospective multicenter studies to evaluate both the impact of ocular blood flow in glaucoma and the benefit of improving ocular blood flow.
References
1. Stewart WC, Feldman R, Mychaskiw MA. Ocular blood flow in
glaucoma: the need for further clinical evidence and patient outcomes research. Br J Ophthalmol. 2007; 91: 1263-1264.
2. Flammer J., Orgül S., Costa VP., et al. The impact of ocular blood flow in glaucoma. Prog Retin Eye Res 2002; 21: 359-393.
3. Gasser P, Flammer J. Blood-cell velocity in the nailfold capillaries of patients with normal-tension and high-tension glaucoma. Am J Ophthalmol. 1991; 111: 585-588.
4. Martinez A, Sanchez M. Predictive Value of Color Doppler Imaging in a Prospective Study of Visual Field Progression in Primary Open-Angle Glaucoma. Acta Ophthalmol Scand 2005; 83: 716-723.
Dear Dr Radcliffe and colleagues,
Thank you for your comments. Two cases with the exfoliation syndrome and one with pigmentary glaucoma were included in our study. As you mentioned, dilatation of the pupil often causes a rise of intraocular pressure in such cases. However, none of the three individuals in our study had a significant rise of intraocular pressure or progression of glaucoma. Sincerely, George Sp...
Dear Editor
We thank Dr Kesarwani for the interest in our article.
In response to the points raised:
1. Inclusion criteria
We attempted to recruit children with X(T) measuring more than 20 prism dioptres when fixing a 6 metre target, as angles under this amount are usually felt not to require treatment. However, Dr Kesarwani is correct to point out that, at the baseline assessme...
Dear Editor,
We read with great interest the recently published article by Bottoni and associates. However, we would like to express our concerns regarding their article entitled “Diagnosis of macular pseudoholes and lamellar macular holes: is optical coherence tomography the gold standard?” Br. J. Ophthalmol. published online 1 Feb 2008; doi:10.1136/bjo.2007.127597. [1] In this article, the authors investigate...
Dear Editor,
I appreciate the letter by Dr. Lempert regarding Dr. Nilsson's Editorial to our study of the extension of the period of bilateral visual impairment (BVI) in persons with untreated amblyopia, and the response by Dr. Nilsson. A slight misunderstanding may arise, however, from the first sentence of Dr. Lempert's letter: "It is not surprising that amblyopes are at higher risk of bilateral visual impairm...
Dear Editor,
We agree with the authors’ recommendation on the need for a sleep history in the eye clinic and probably having a lower threshold for referral to sleep physicians for further sleep studies.[1] However, we would like to bring to their attention other epidemiological studies where screening tools/sleep history have shown a high prevalence of sleep disorders in patients with ocular disorders other than...
Dear editor,
We want to thank Drs. Martinez and Sanchez for the response to our recent editorial. We are in agreement with them that evidence does exist that blood flow is altered in glaucoma and is suggestive of a pathogenetic role[1]. We also agree that a variety of methods are being used to evaluate blood flow and these techniques certainly have improved over the last decade and a half.
I would also lik...
Dear Editor,
Dr Buck et al must be commended for this wonderful article[1] which takes us one step closer to deciding intervention based on Newcastle scoring system previously described.[2] However, we seek a few clarifications.
1.Inclusion criteria: The authors have described the inclusion criteria for the study to be intermittent exotropia X(T)) of more than or equal to 20 prism dioptres (pd), for...
In a reply to my editorial in the November issue, Dr Lempert raises several valid concerns regarding vision screening for amblyopia. I would like to thank Dr Lempert for his reply and this possibility for a discussion on a difficult and important topic!
I was, however, slightly surprised to find that the reply is written as a rebuttal of my arguments, while I am of the same opinion as Dr Lempert, and have...
Dear Editor
We read with interest the editorial by Miller which comments on the paper, ‘Epidemiology of giant-cell arteritis in an Arab population: a 22-year study’[1]. The author of the editorial comments on geographical variation in the incidence of giant cell arteritis and cites evidence supporting both genetic and environmental aetiologies.
We re-examined the data from our 5 year study[2] looking at...
Dear Editor:
We read with great interest the recent commentary by Stewart et al [1] describing the evidence of the blood flow disturbances in the pathogenesis of the glaucomatous damage. Although I agree with some of the findings of this excellent review, there are some important points that should be addressed:
1.After reading this article, one may think that there is not evidence that ocular bl...
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