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I am transplanting a polymer (Parylene-C) coated structure in the anterior chamber of the eye and expect it to reside on the iris, however, almost all of them get adhered to the cornea and not the iris. Is there any eye-physiology-related explanation to that?
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Very interesting video Vladimir Siplivy , thanks!
That is right, the iris movement seems predominant. However, we do see tissues being transplanted to the ACE and they all got vascularized. Now, we are aiming to position our device at the angle of the eye where iris movements are minimal.
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I've just read research which was done in Pakistan where the researcher had achieved very good result (97%) by full time patching in patients between 13 and 35 years old. Let me know your experience or share any research in this regard. 
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Amblyopia treatment has been successful in patients of any age group. Clinical evidence and researches regarding this query suggest that it is possible to improve visual functions in cases of adult amblyopia as well. We have some cases of adult amblyopia with final improvement in visual functions after appropriate refractive correction and combined occlusion and vision therapy. Presence of plasticity in visual system/visual cortex counter the limitation of adult amblyopia treatment. Strabismics have shown some difficulty.
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How should we adjust under COVID-19? Avoid non-urgent surgery?
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Any body suffering from any infectious disease must not go for surgery including eye.
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Why not central corneal cells are involved?
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Great question. I suppose it has to do with vascularity and permeability. Peripheral cornea is near the limbal vessels and intravascular copper is easily deposited at the periphery. Moving inwards the cornea is avascular and therefore no way for intravascular copper to reach. thanks
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Minimum rim width has been adapted by recent OCT devices since it takes more into account variability of the entry of the RNFL axons into the optic nerve canal
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The BMO MRW concept was first shown to have the best diagnostic performance to differentiate glaucomatous from non glaucomatous eyes on the Spectalis platform by Reis ASC, O’Leary N, Yang H, et al. Influence of Clinically Invisible, but Optical Coherence Tomography Detected, Optic Disc Margin Anatomy on Neuroretinal Rim Evaluation. Investigative Ophthalmology & Visual Science. 2012;53(4):1852-1860. doi:10.1167/iovs.11-9309 and in Chauhan BC,, O'Leary N,, Almobarak FA,, et al. Enhanced detection of open-angle glaucoma with an anatomically accurate optical coherence tomography-derived neuroretinal rim parameter. Ophthalmology. 2013; 120: 535-543
For the Cirrus OCT, the MRW is estimated over a continuum as data points are pulled from the data cube. The Cirrus OCT fits a plane to the BMO surface and uses that plane to characterize and correct for how the optic nerve is tilted relative to the retinal surface. Also, the Cirrus corrects for disc size when comparing ONH measurements to normative limits.
It is available from Cirrus OCT model 400 and 4000 (software version 5.0 onwards)
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In Jack Holladay's publication http://www.hicsoap.com/publications/ProperMethodforCalculating.pdf wrote, that proper method for calculating average visual acuity is arithmetic mean of it in LogMAR scale. Usually this value is not much different from the average in the decimal or Snellen scale. However, this is not the case for the standard deviation, especially if variation of visual acuity in the group is small. For example, if all persons in a group have equal VA, SD of VA is 0 in LogMAR scale. But 0 in decimal scale is 1.0 (or 20/20) that seems too high estimate for the zero variability.
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Dear Russel!
When carrying out Ttest for comparison mean visual acuity of several groups LASIK patients, I faced with strange problem. Calculations in the decimal scale were more powerful then in LogMAR scale. In decimal scale I received significant differences more often than in LogMAR scale. But nowdays it is recommended to use only a logarithmic scale for statistical calculations!
Trying to understand this problem, I tried to find an extreme group giving the strangest result in the transition from one scale to another. It seemed to me that the most strange thing was the transformation of the standard deviation in a monotonous group. This caused me some doubts about the applicability of standard statistical formulas in the LogMAR scale. Of course all answers was immediately pointed to my error.
More over Pete Jones in the answer to my other question (www.researchgate.net/post/Is_LogMAR_is_only_proper_way_to_convey_visual_acuity) pointed to a fact that I had not noticed before. Logarithmic correction for positive-skew data can normalize it, but not for negative-skew.
I guess the solution to this problem is as follows.
Visual acuity in the decimal scale has two limits lower =0 and upper, about 2.5-3.0 (due to diffraction on the circular pupil). If the average visual acuity in the group is not very high, the lower limit has a greater impact, and a positive -skew appears in the distribution. In this case, the use of a logarithmic scale should lead to a decrease this skew and an increase the power of parametric statistical methods.
If the average visual acuity in the group is large, the influence of the upper limit is strengthened. A negative skew appears. This effect I observed not only on my data, but also in some other publications. In this case, the transition to a logarithmic scale only enhances this skew and decrease the power of parametric statistical methods, for example Ttest problem I faced in the beginning. Probably it is necessary to refuse the statistical calculations in the LogMAR scale for groups with high visual acuity, despite the prevailing point of view.
I will be gracious to you for any indication of an errors in my reasoning.
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Visual acuity can be expressed using a decimal scale, the minimum angle of resolution in minutes of the arc (MAR), a natural Snellen fraction (like 20/x) and the decimal logarithm of MAR (logMAR). Khoshnood et al. (www.ncbi.nlm.nih.gov/pubmed/21205268) reveal that proper transformation of statistical values from one scale to another is untrivial task, because of the non-linearity of the transformation of VA between scales (for example y=log(x) is non-linear function, y=1/x too etc.). So all statistical calculations are best to carried out within the same scale.
At the moment, the prevailing view is that LogMAR is only proper way of expressing (and statistical processing) of visual acuity data (for example Holladay 2004 www.jcrsjournal.org/article/S0886-3350(04)00125-7/fulltext). But I can not find a detailed justification for this choice. The reference to Fechner's law looks weak, since it works mainly to describe the relationship between objective stimulus strength and it subjective sensation, for example for brightness, but I do not know how it can be applied in the case of spatial resolution.
On the other hand, the visual acuity values in the MAR scale are linearly proportional to the instrumentally measurable size of the minimum readable letter. And in the decimal scale - the maximum distance of distinguishing a letter. Thus, all statistical parameters in these scales can be linearly converted into real measurable values. Example for decimal scale: if first person has VA = 1.0 and can recognize the letter from 6 meters, second person has VA = 0.5 and can recognize same letter from 3 meters, then a person with an average visual acuity (1 + 0.5) / 2 = 0.75 will be able to recognize this symbol from average (6 + 3) / 2 = 4.5 meters. The same (but for letter's size at certain distance) is for MAR scale. In the case of LogMAR it is not so. Since this scale is logarithmic, there is no instrumentally measurable value proportional to the visual acuity in LogMAR (exept letters count in ETDRS chart, but it can hardly be considered as a physical quantity).
With this approach, despite the prevailing viewpoint, LogMAR seems to be the weakest choice among others for presentation and processing of visual acuity data.
Especial thanks to Hans Strasburger for conception of LogMAR as a strange beast and other ideas in answer of my previous question.
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An excellent question, I find! Forgive me thus if my answer is somewhat lengthy.
Yes, everybody is ready to agree that specification and statistical analysis should be done on logMAR. Yet I agree with you that there should be a rationale for the logarithmic scaling on first principles: And there is none as far as I am aware of!!
As to the Fechner scale, Fechner (in his book 1860) made a distinction between *extensive* and *intensive* qualities. If I remember correctly he says he will concern himself mostly with the intensive qualities (like brightness or loudness). For these, the log scale works well (even though Stevens thought that his scale is much better). In contrast, the sensation of length, i.e. of an extensive quality, appears to be approximately linear, and thus not logarithmic. MAR is a prototypical example of an *extensive* (visual) scale. (Length is the standard example in chapters on the Stevens scale in biopsychology text books; how the scale for perceptual length is derived I don’t know, but I assume that it does not work for distance away from the observer; see below).
The argument in Holladay (2004) and by many others is circular: Because steps on the acuity charts are spaced logarithmically, calculations should be done on a logarithmic scale. However, there is no logical reason why one implies the other (except that it is practical). The real question is why steps were chosen logarithmically in the first place.
The reason, I believe, is that the VA scale is intuitively non-linear: The perceptual decrease from 0.2 to 0.1 is obviously bigger in effect than one from 1.0 to 0.9. But I believe that has nothing to do with a log scale and the intuition is based on the fact that VA is the *inverse* of MAR. I.e. the relation between the two is nonlinear and ratios are preserved in the transformation. Intuitively, ratios are thus relevant. A typical example is that 0.2/0.1 is a factor of 2, whereas 1.0/0.9 is a factor of 1.1, even though the distance on the linear scale is the same. Going to the log realm means that ratios are converted to differences, which are then preserved. That does not imply, however, that ratios are the proper distance measure in the first place! In psychological / psychometric language the question is: which scale is on an interval-scale level?
Your argument that VA is linearly related to viewing distance is intriguing because it relies on first principles. It comes down to saying that seeing something from twice the distance can be considered twice as good in some sense. That makes sense. However, distance is not coded directly in the visual system, and the retinal measure is, of course, visual angle. The latter’s lower limit is given by cone spacing, which in turn is closely linked to MAR.
The discipline concerned with scaling (e.g. such that intervals are equal, thus creating an interval scale) is ‘psychometrics’ or ‘psychometric scaling’. It provides sophisticated methods of scaling (e. g. Thurstone scaling). Yet I am not aware of any psychometric-scaling attempts for acuity. So I believe there is as yet no answer what constitutes equal intervals on an acuity scale!
The only perceptual rule I am aware of is that MAR varies linearly with eccentricity in the visual field. This is very well established (Weymouth, 1958; he was the one who advocated MAR in the first place, but people have forgotten that). And this is why I personally prefer MAR over logMAR. For details see my paper in JOV:
When doing statistical analyses based on MAR, I see no necessity of going to a log scale, btw. If somebody shows me distributions of MAR that are heavily skewed (thus preventing standard least-squares statistics) that would convince me otherwise. I think people use logMAR mostly because everybody else does (and because it is equivalent to logVA, and doing statistics with VA is not a good idea).
Michael Bach btw. advocates logVA (that is, minus logMAR), because logMAR goes the wrong way: High logVA means high acuity.
Best,
Hans
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Thyroid exophthalmos
Proptosis ( Unilateral vs Bilateral)
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Yes Dr. Manpreet, you are right, we need to have collaborative demographic study for our race with credible assessment as presently the gap between the observations is too much.
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It's a known believe that elderly people prefer multi dose vials as eye-drops. Could you discuss about avantages vs disavantages? Anybody knows about peer reviewed studies?
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One more point should be noted, psychological perception of mind at subconscious level that's lesser use of eyes drops means little bit problem have, that cause more healing captivity of the cells by neurotransmitters.
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Better understanding a clinical case of consistent IOP reduction 3 months after undergoing EYLEA injection 
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Thanks a lot Victor for your answer.
Best
Carlo
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For the hypertensive retinopathy stadiation there are two main classifications:
1) The Keith-Wagener-Barker classification
2) The Mitchell-Wong classification.
There are few differences between these grading systems.
I would know which one is preferable for a clinical research.
Thank you.
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The arteriosclerotic and hypertensive retinopathy changes in early stages grade I and II are similar in KWB while different in grade III and IV
if you want KWB, do consider age as cofounding factor or exclude elderly
AS retinopathy
grade I - altered AV ratio
grade II - AV crossing changes
grade III - copper wire
grade IV - silver wire
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Wilson's disease is a genetic disorder caused by excess of copper in the body, the treatment includes chelating agents such as trientine and d-penicillamine and zinc acetate (Brand name: Galzin) , I can not understand what is the role of zinc acetate in the treatment?
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" Zinc's mechanism of action involves induction of intestinal cell metallothionein (Mt), which blocks copper absorption from the intestinal track. "
Brewer GJ. Expert Opin Pharmacother. 2001; 2(9): 1473-7.
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A 6 year old girl is complaining of visual blurring for 3 days. She says that her vision is foggy all the time.
Anamnesis is negative for any possibly related disease. Seated at 3 meter distance and for near she doesn't recognize any symbol. How could you proceed with the examination and why?
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I had a similar case. A 5 year old girl with a very low vision in the left eye with no signs of compromise. After performing visual evoked potentials and electroretinogram (with simple skin electrodes and steady-state strategy, 10 minutes) I was sure that there was no diseases. So I said in front of her family that I found a magical lens ... + 0.12 of course. Electrophysiology of vision is my secret weapon!
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I want to use it in order to explore dry eye symptom (Foreign body sensation,Itchy eye,Burning sensation,Teary eye,Photophobia,Red eye) reporting patterns and to better understand symptomatic heterogeneity in the study population.
how many group should I do and according to what the subjects can be put in groups ?
Note : each dry eye symptom was grade as 0 (none of the times ) , 1 ( some of the times) , 2 ( half of the times ) , 3 ( most of the times ) , 4 ( all of the times )
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The important point in dry  eye symptoms is the fact that we have different ocular surface problems that gives the same symptoms .I suggest to have a clinical diagnosis of the type of the ocular surface problem and analyze according  to a clinically documentable signs and symptoms
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The new IOL master 700 has smaller in vivo repeatability SD for most metrics than the Lenstar, eg. 8µ instead of 35µ for AXL, 11µ instead of 40µ for ACD and 12µ instead of 80µ for lensthickness.
However, are these smaller standard deviations of clinical importance, i.e. to what extend would they contribute to a different choice of IOL power in in 'old' formulas like e.g. SRK-T and Holladay 1, and in new formulas, like e.g. Olsen or Barrett ?
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Greetings. Our experience with the IOL master 700 is favorable, although we believe that there are no significant differences with respect to the previously used formulas. For this we take a study at the moment to determine if it is actually more efficient. I also believe that regardless of the formulas that are very important to determine the power of the intraocular lens, the effective position of the lens and the incisions of surgery are determinant in the result.
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How to get good grades in the examination of RNFL peripapillary in OCT, because in most cases the note is yellow and it decreases the confidence in the result.
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Thank you for all remarks about my question!
Best Regards
Romar
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The article Association of Glaucoma-Susceptible Genes to Regional Circumpapillary Retinal Nerve Fiber Layer Thickness and Visual Field Defects Article in Investigative ophthalmology & visual science 58(5):2510 · May 2017 DOI: 10.1167/iovs.16-20797 · License: CC BY-NC-ND 4.0 by Robert Rich is not the full text as described
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The most common glaucoma related genetic factor is the non-functional gulonolactone (L-) oxidase, pseudogene in humans that produces ascorbic acid. IMHO all Primary Open Angle Glaucoma is directly caused by chronic suboptimal plasma ascorbate, and with the universal reduction of retinal atheroma, my practice changed from having the world´s record incidence of diagnosed POAG (the first to introduce non-contact tonometry for all over 16yrs)  to having it virtually eliminated without a single further case in over ten years amongst a contact lens wearing population taking extra vitamin C. This was suppressed by two optometry journals, presumably pharmacy dependent. See Virno et al (1966) and - later confirming -  Bietti (1966) Rome University Eye Clinic.
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we have 30 year old male patient who was given botox for blepharospasm ..last injection 5 months back
now he is having fatiguable asymetric ptosis, what are the possibilites
 RNE and ice pack test normal. NO diplopia.
can botox cause this? 
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Yes, Botox can cause ptosis but you would expect improvement 5 months later. Any pupillary abnormalities?
Botox could have unmasked myasthenia gravis, and would check acetylcholine receptor antibodies. Was the onset acute? Sometimes patients do not realize they had some degree of ptosis all along. Progressive external ophthalmoplegia would be another consideration if the course was more chronic.
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Ophthalmologists often order FFA in uveitis cases. When should it be done and how does it help in management ?
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Good discussion. I agree with Dr Marianne regarding indication for OCT, but FFA is useful in various uveitic conditions and at various stages as described in books if not all. 
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It is used in ophthalmology surgeries 
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@ Selim- You can buy it from us at Next Biosciences: fikile.mnisi@nextbio.co.za. and yes it is used in Ophthalmology. or contact us at +27 11 697 2900 and ask for Fikile.
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On the one hand, Thomas et al reported a wide series of patients with foveal hypoplasia, and they found good correlation between the grade of foveal hypoplasia and the range of visual acuity that those subjects could achieve. On the other hand, some single reports have been published of patients with high grade of foveal hypoplasia and good visual acuity, calling into the question the importance of a foveal pit in achieving good visual acuity. 
What do you think about this matter?
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First of all the groups taken into account are different genetically : 
Sixty-nine patients with foveal hypoplasia (albinism, n = 34; PAX6 mutations, n = 10; isolated cases, n = 14; achromatopsia, n = 11) and 65 control subjects were examined.
This induces a first bias in the evaluation of different types of hypoplasia: in all the aforementioned pathologies the genetic and thus the biomolecular pathway targeted by the specific alteration is different and the evaluation by OCT doesn't allow a morfofunctional differentiation of the subgroups at all. If you consider achromatopsia for example which involves a complete or incomplete development of the cones you will observe a worse visual acuity due to the anatomic absence of the photoreceptors or a part of them.
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As found in the literature The OSDI is a valid and reliable instrument for measuring dry eye disease it is assessed on a scale of 0 to 100, with higher scores representing greater disability. The overall OSDI score defined the ocular surface as normal (0-12points) or as having mild (13-22 points), moderate (23-32 points), or severe (33-100 points) disease.
I think the cutoff should be > 12 , is it correct ?
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The original OSDI questionnaire includes 12 questions. the score for each question ranges from 0 to 4. The formula used to calculate the final OSDI score includes both the number of questions answered and Sum of Scores for All Questions Answered. OSDI score ranges between 0-100 but because some questions may not be applicable to some responders, we can not determine a clear cut off, and cut off level varies based on number of questions answered and sum of scores for all questions answered. the final nomogram looks like a color spectrum ranging from white to orange, light red and finally dark red. The bottom line is when you calculate your patient's score you should look at the nomogram to judge where her/his score falls in the nomogram and judge about severity of dry eye.
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Does your hospital has any guideline for preoperative PHARMACOLOGY management of cataract or glaucoma surgery?
I am trying to collect as many opinions from all over the world
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Local:  Topical Paracaine/lignocaine or peribulbar block . Povidone Iodine paint .
Topical broad spectrum antibiotics starting a day before surgery , dilating agent(Tropicamide phenylephrine) on day of surgery with or without flurbiprofen. Antiglaucoma drugs for glaucoma cases ( Stop prostaglandins and pilocarpine atleast 7 days before surgery)
Oral: Minimal dosage of wide spectrum antibiotics in susceptible cases, analgesics as per need, oral acetazolamide as per surgeon and the case
Regards - Dr Lipi Chakrabarty, Director LIPIKA NETRADHAM, Bhilai-Durg, Chhattisgarh, India
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Cataract surgery in low incoming countries represents a huge economic burden. Which are the best strategies in terms of kind of surgery and which kind of phacomachine will you suggest to use.
Thank you
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oertli phaco machine is the best for this job, I've friend in yemen who perform 700 case on one cassete, and 1500 case without changing the phaco tip. personaly I've tried this machine it was not convenient for me as I am using infinity from Alcon
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someone has the material to recommend about it? thank you all
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Some great references From Drs Jean-Paul & Kaushik. I'm afraid the descriptions are however a bit sketchy. If choroid were the ONLY source of red reflex, we'd see the ribbon pattern of choroidal vessels. The other key element is retinal pigment epithelium (RPE)  which is dark, but not opaque. So it acts as a diffuser screen, fusing the red ribbons of choroid into a homogenous red glow. When RPE is deficient due to myopia, old age or more severe degenerative conditions like choroideremia, the ribbons stand out as "tigroid" or "tessellated" fundus. This also explains the darker red glow in Africans and lighter, more tessellated fundus in Caucasians. We Asians are in the mid-spectrum.
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What could cause autologous serum eye drops to precipitate? A patient has been using the drops for years due to dry eye symtpoms. Recently, three of four production series tended to precipitate when being thawed. Cold agglutinines, cryoglobulines, bacterial contamination was ruled out by lab examinations. FVIII (as one of the factors in cryoprecipitate) was only slightly elevated to 180% (upper norm limit is 150% at our lab). Electrophoresis of serum proteins was normal...any suggestions?
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trehalose, mannitol, sorbitol are among cryoprotectants  you could safely use for that particular application. 
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Globally, the magnitude of occurrences of Pterygium is over 200 million people and the prevalence varies between 0.3 % and 37%.[i]  The fact remains that ocular disorders are caused by the reflected solar radiation from the surface of the earth especially the white and shining surfaces such as snow and water. [ii]
My question is what percentage of Out Patient cases in hospital undergo surgeries?
[i] Lu P, Chen XM., Prevalence and risk factors of pterygium. Int J Ophthalmol 2009;2(1):82-85
[ii] Bergmanson JP, Soderberg PG. The Significance for Ultraviolet Radiation for Eye Diseases. A review with comments on the efficacy of UV Blocking Contact Lenses. Ophtahlmic Physiol.Opt. 1995; 15: 83-91.
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In my own experience most of the females patient opt for surgical treatment. Males being bit reluctant; overall it would be approximately 65% undertaking surgery.
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I m working on detection of Diabetic retinopathy disesase in fundus images. 
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Br J Ophthalmol doi:10.1136/bjophthalmol-2015-307341 Clinical science
Individualised risk assessment for diabetic retinopathy and optimisation of screening intervals: a scientific approach to reducing healthcare costs
S H Lund1,
T Aspelund1,2,
P Kirby3,
G Russell3,
S Einarsson2,
O Palsson2,
E Stefánsson1,2
+ Author Affiliations
1Faculty of Medicine, University of Iceland, Reykjavik, Iceland
2Risk ehf, Reykjavik, Iceland
3Health Intelligence plc, Cambridge, UK
Correspondence to Professor Einar Stefánsson, Department of Ophthalmology, University of Iceland, National University Hospital, 101 Reykjavík 101, Iceland; einarste@landspitali.is
Received 26 June 2015
Revised 10 August 2015
Accepted 19 August 2015
Published Online First 16 September 2015
Abstract
Objective To validate a mathematical algorithm that calculates risk of diabetic retinopathy progression in a diabetic population with UK staging (R0–3; M1) of diabetic retinopathy. To establish the utility of the algorithm to reduce screening frequency in this cohort, while maintaining safety standards.
Research design and methods The cohort of 9690 diabetic individuals in England, followed for 2 years. The algorithms calculated individual risk for development of preproliferative retinopathy (R2), active proliferative retinopathy (R3A) and diabetic maculopathy (M1) based on clinical data. Screening intervals were determined such that the increase in risk of developing certain stages of retinopathy between screenings was the same for all patients and identical to mean risk in fixed annual screening. Receiver operating characteristic curves were drawn and area under the curve calculated to estimate the prediction capability.
Results The algorithm predicts the occurrence of the given diabetic retinopathy stages with area under the curve =80% for patients with type II diabetes (CI 0.78 to 0.81). Of the cohort 64% is at less than 5% risk of progression to R2, R3A or M1 within 2 years. By applying a 2 year ceiling to the screening interval, patients with type II diabetes are screened on average every 20 months, which is a 40% reduction in frequency compared with annual screening.
Conclusions The algorithm reliably identifies patients at high risk of developing advanced stages of diabetic retinopathy, including preproliferative R2, active proliferative R3A and maculopathy M1. Majority of patients have less than 5% risk of progression between stages within a year and a small high-risk group is identified. Screening visit frequency and presumably costs in a diabetic retinopathy screening system can be reduced by 40% by using a 2 year ceiling. Individualised risk assessment with 2 year ceiling on screening intervals may be a pragmatic next step in diabetic retinopathy screening in UK, in that safety is maximised and cost reduced by about 40%.
Epidemiology
Retina
Clinical Trial
Diagnostic tests/Investigation
Public health
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i need a proof if there is a core for exudates in specific area in retinopathy eye or not 
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I suppose that enclosed latest information will be useful
Br J Ophthalmol doi:10.1136/bjophthalmol-2015-307341 Clinical science
Individualised risk assessment for diabetic retinopathy and optimisation of screening intervals: a scientific approach to reducing healthcare costs
S H Lund1,
T Aspelund1,2,
P Kirby3,
G Russell3,
S Einarsson2,
O Palsson2,
E Stefánsson1,2
+ Author Affiliations
1Faculty of Medicine, University of Iceland, Reykjavik, Iceland
2Risk ehf, Reykjavik, Iceland
3Health Intelligence plc, Cambridge, UK
Correspondence to Professor Einar Stefánsson, Department of Ophthalmology, University of Iceland, National University Hospital, 101 Reykjavík 101, Iceland; einarste@landspitali.is
Received 26 June 2015
Revised 10 August 2015
Accepted 19 August 2015
Published Online First 16 September 2015
Abstract
Objective To validate a mathematical algorithm that calculates risk of diabetic retinopathy progression in a diabetic population with UK staging (R0–3; M1) of diabetic retinopathy. To establish the utility of the algorithm to reduce screening frequency in this cohort, while maintaining safety standards.
Research design and methods The cohort of 9690 diabetic individuals in England, followed for 2 years. The algorithms calculated individual risk for development of preproliferative retinopathy (R2), active proliferative retinopathy (R3A) and diabetic maculopathy (M1) based on clinical data. Screening intervals were determined such that the increase in risk of developing certain stages of retinopathy between screenings was the same for all patients and identical to mean risk in fixed annual screening. Receiver operating characteristic curves were drawn and area under the curve calculated to estimate the prediction capability.
Results The algorithm predicts the occurrence of the given diabetic retinopathy stages with area under the curve =80% for patients with type II diabetes (CI 0.78 to 0.81). Of the cohort 64% is at less than 5% risk of progression to R2, R3A or M1 within 2 years. By applying a 2 year ceiling to the screening interval, patients with type II diabetes are screened on average every 20 months, which is a 40% reduction in frequency compared with annual screening.
Conclusions The algorithm reliably identifies patients at high risk of developing advanced stages of diabetic retinopathy, including preproliferative R2, active proliferative R3A and maculopathy M1. Majority of patients have less than 5% risk of progression between stages within a year and a small high-risk group is identified. Screening visit frequency and presumably costs in a diabetic retinopathy screening system can be reduced by 40% by using a 2 year ceiling. Individualised risk assessment with 2 year ceiling on screening intervals may be a pragmatic next step in diabetic retinopathy screening in UK, in that safety is maximised and cost reduced by about 40%.
Epidemiology
Retina
Clinical Trial
Diagnostic tests/Investigation
Public health
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I am working on Insitu ophthalmic gel containing two drugs with molecular weight about 500 and 350.  I need to decide the type of cellophane membrane.
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for ophthalmic gel to perform in-vitro diffusion study  cellophane membrane having pore size 0.22-0.45 micron should be used; having membrane Molecular weight cut-off (MWCO)  10000-18000.
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Hope you will able to help me with this question. I have conducted a research regarding refractive errors. According to my results I have a total number of 150 children with different refractive errors. Among these 150, I have 50 children with myopia, 40 with astygmastismus and 20 with hypermetropia. The rest are anisometropians. Anisometropia is not a type of refractive error. So this is like a trick question...
Would it be better if I wrote instead of 150 children (300 eyes) and then count different refractive errors in each eye separately. This way I wont have anisometropias.
Hope you can help
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Anisometropia, where the refractive error differs in the two eyes, is an important condition (that can lead to amblyopia in children for example) and should be discussed. As Paul mentioned previously, be careful about using data from both eyes of one subject as they are not independent data.  I suggest you read the following paper, which is very good and has free access: 
Armstrong RA Statistical guidelines for the analysis of data obtained from one or both eyes. Ophthalmic Physiol Opt 2013, 33: 7–14.
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Any details about retinal causes of amblyopia or results suggest a relation between retina and amblyopia would be of great help.
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Amblyopia can be organic, meaning that it can occur secondary to a structural abnormality, including retinal disorders. However, reduced visual acuity in organic amblyopia cannot be solely attributed to the primary defect, but rather to a combination of both the structural defect and an added functional factor. That is, the loss of vision is more profound than would be expected from the structural defect alone. 
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Iopidine (apraclonidine) was once used before as a prophylactic drug to prevent IOP spikes before and after glaucoma laser procedures but it seems now to be not in the market anymore
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ALPHAGAN-P ®  (brimonidine 0.15% + purite ophthalmic solution)  also works well for prevention of  IOP spikes post ant. segment laser surgeries. 
Reference: 
Yeom et al. Brimonidine 0.2% versus brimonidine Purite 0.15%: prophylactic effect on iop elevation after Nd:YAG laser posterior capsulotomy. J Ocul Pharmacol Ther. 2006 Jun;22(3):176-81.
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Green technology is becoming more relevant across the board during these economic slowdowns. What is being done to improve its usage in medical sciences ?
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Dr Syed
I took my PhD in nanomedcine drug synthesised by green nanotechnology and i think is a good & new field of research and if you need any help in it i can offer it.
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The mainstay of treatment for an acute attack of angle closure are oral and systemic glaucoma medications. Aside from pilocarpine what is the best glaucoma topical drop to give as an adjunct?
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The first consideration in choosing topical medications in AACG is the IOP, if the IOP is 40mmHg or above, then absorption of topical medications will be hampered. After lowering IOP with systemic medication and/or AC paracentesis then we choose which topical medication would work best based the the ACG mechanism that we think is present. If lenticular then Pilocarpine is not ideal cause this would induce more pupillary block and if the iris is still ischemic and prevents proper absorption, then the Pilocarpine will not have mitotic effect but may even cause forward rotation of the ciliary muscle causing more angle closure. Topical CAI are not as potent to break pupillary block and if ALPI/LI is contemplated, the use of CAI may cause slower resolution of corneal edema which compromises the delivery of laser energy. Alpha2 agonist i.e. Brimonidine BID/TID would be my choice as it is fast acting, duration of of action is about 12hrs and IOP reduction achieved is from 20-30% by several mechanism: decrease aqueous production, some effect of episcleral venous pressure and uveoscleral outflow. Some literatures have also shown Brimonidine to cause some degree of miosis which can address ITC as well. Combination timolol and brimonidine BID is also an option.
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white eyed fracture is many times misleading because of symptoms of nausea vomiting and bradycardia and as such mimics head injury. white eyed fracture needs immediate treatment and this confusion with head injury diagnosis. currently CT scan is best to check for trap door fracture of orbit. 
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I agree that " currently CT scan is best to check for trap door fracture of orbit". 
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Do colleagues note the development or accelerated progression of cataracts after lasik?
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The incidence of cataract may be more in high myopes as such. Therefore, there may be a false bias towards LASIK causing cataract.  The modern lasik procedure has a very short course of post operative steroids  which should not cause cataract.  These patients may tend to get earlier cataract because of  the myopia related ocular anatomy rather than lasik itself.
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I wonder whether infectious agents including oncogenic viruses, bacteria and possibly parasites play any role in the genesis or might acts as a factor or co-factor in the development and prognosis of the ocular tumors
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Dear Manderwad,
Undoubtedly, as already mentioned above, different infectious agents can lead to tumor lesions in eyes. However, some of these agents, especially viruses, may be the genesis of some kinds of cancer and "not merely tumors". The differentiation between these concepts is necessary. On ocular neoplasias induced by viruses, I suggest you the reading, for example, of the reviews:
Carreira et al. HIV and HPV infections and ocular surface squamous neoplasia: systematic review and meta-analysis. Br J Cancer. 2013 Oct 1;109(7):1981-8. doi: 10.1038/bjc.2013.539.
Gichuhi et al. Epidemiology of ocular surface squamous neoplasia in Africa. Trop Med Int Health. 2013 Dec;18(12):1424-43. doi: 10.1111/tmi.12203.
Best regards,
Vitor
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Ocular anexa and eye pathology is rarely seen at our institution and we have no manuals for this item. Any recommendations?
Thanks
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Dear Dr.Waggoner,
Thank you very much for your respected opinion on the matter.
With best wishes,
Marianne
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17 years old Usher patient, po azetatsolamid (growing dose, now 500 mg x2) used since 12/2013. CME is getting worse, but BCVA is still about 0.5-0.6 oa. I read that intravitreal corticosteroid gives only limited and transient response - so maybe not so good idea? Anti- VEGF?? Something else?
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In my opinion you can swith your patient to NSAID drops as you have mentioned- the best for posterior pole is Diclofenac 0.1% 4 times a day and Dexamethasone 0.1% 2 or 4 times a day for 3 months. Good luck !
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There are many accounts showing a superior result from using a femtosecond laser in regards to epithelial ingrowth, flap thickness etc. However, the research is usually performed using older versions of microkeratomes and research showing a clear-cut clinical improvement (visual acuity etc.) seems to be totally lacking. In my clinic, my Amadeus II microkeratome produces excellent results, with a clinical outcome matching the outcome reported from using the femtosecond lasers. Also, complications are minimal compared with an older version of Amadeus I used earlier.
Any thoughts?
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From a vitreoretinal stand point, there is no stress induced at the vitreous base by femtosecond laser in creating the LASIK flaps, whereas any mechanical microkeratome has the potential of inducing vitreoretinal stress.  Although, there is no unequivocal proof in linking LASIK with vitreoretinal complications (e.g. breaks and RD), there are multiple anecdotal case series in the literature showing such complications following LASIK (acute vitreoretinal stress at the vitreous base induced by the mechanical microkeratome is a potential mechanism for such complications).. 
See my following published references:
Chan CK, Arévalo JF, Akbatur HH, Sengün A, Yoon YH, Lee GJ, Tarasewicz DG, Lin SG.  Characteristics of sixty myopic eyes with pre-laser in situ keratomileusis retinal examination and post-laser in situ keratomileusis retinal lesions.  Retina 2004; 24:706-713.
Chan CK, Tarasewicz DG, Lin SG. Relation of pre-LASIK and post-LASIK retinal lesions and retinal examination for LASIK eyes. Br J Ophthalmol 2005; 89: 299-301.
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Dear researchers,
I have a question about accidental leishmaniasis !
The Last day I was working on my recent experiment on a new vaccine against cutaneous leishmaniasis and unfortunately I do all of my research steps lonely ,thus , when I was injecting live stationary pathogenic leishmania major to foot pad of BALB/c mice suddenly some drops of parasites suspension Sprinkled from the syringe to my eye!
I washed my eye immediately, but I want to know that I can take ocular leishmaniasis!!
It seems impossible because the eye environment condition is not suitable for this parasite, but, I want to know your opinion.
I found many article about ocular leishmaniasis as a result of visceral leishmaniasis or cutaneous leishmaniasis like as follow:
*Ocular leishmaniasis
M ModarresZadeh, K Manshai, M Shaddel…-Iranian Journal of Ophthalmology , 2007
*Simultaneous occurrence of ocular, disseminated mucocutaneous, and multivisceral involvement of leishmaniasis.
Philips CA, Kalal CR, Kumar KN, Bihari C, Sarin SK.
Case Rep Infect Dis. 2014;2014:837625. doi: 10.1155/2014/837625. Epub 2014 Feb 18.
*Leishmaniasis of the eyelid mimicking an infundibular cyst and review of the literature on ocular leishmaniasis.
Veraldi S, Bottini S, Currò N, Gianotti R.
Int J Infect Dis. 2010 Sep;14 Suppl 3:e230-2. doi: 10.1016/j.ijid.2009.07.024. Epub 2009 Dec 6. Review.
*[Ocular leishmaniasis in a cat: case report].
Verneuil M.
J Fr Ophtalmol. 2013 Apr;36(4):e67-72. doi: 10.1016/j.jfo.2012.09.006. Epub 2013 Mar 1. French.
and  many other.
Thanks for your comments.
Best
Vahid
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Dear Dr. Chaoqun Yao
Thanks for your kinds and very helpful guides.
It was an interesting article.
I had many dangerous experiments like this with other parasites like Toxoplasma and Leishmania infantum  and I think  that I can say ironman to myself!!
Thanks again.
Vahid
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 Apart of that her IOT was 21,9 mmHg right eye and 23,0 mmHg left eye.
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Would completely agree with Drs. Aquavella and Robaei
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In our practice we often see gas bubbles after emulsified silicone removal. It is known that these bubbles can play vital role in changing (increasing/decreasing) IOP (intra-ocular pressure). So, what do you use for full removal of emulsified silicone from vitreous cavity?
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I agree. These are emulsified small oil bubbles and are difficult to get rid off. Multiple Air fluid exchange at the time of oil removal helps. In addition, rapid movements of the eye in different directions to expose the bubbles helps. These maneuvers need to be performed several times to be successful.
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In patients who underwent glaucoma surgery especially trab surgery , is it safe to do strabismus surgery and which is better the limbal approach or the fornix approach?
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First and most obviously, make sure the patient is fully aware of and consented for the possible complications of operating around trabs/tubes.
Whether the patient has a bleb or a valve, make sure you know the extent of the fibrotic capsule prior to making the conjunctival incision and/or dissection. I combine gentle conj manipulation and very gentle subconjunctival fluid dissection to determine the size and extent of the fibrotic 'no fly zone'. In trabs/ExPress, the capsule is generally small enough to allow access to the rectus insertions, although a small marginal myectomy/tenectomy is sometimes required to avoid cutting the capsule. In the case of valves, especially B350's, the anterior rectus muscles are almost always encapsulated. In this case, I strongly prefer to operate on the other eye if possible. If there is no other choice (if the fibrotic restriction is severe or the other eye has been operated on as well), then you will have to approach the muscle via a deep fornix incision on the side away from the footplate and perform a mid-muscle recession with non-absorbable sutures or a modified marginal myotomy. Check forced ductions often.  Gentle dissection and intensive post-operative steroids is important in all cases.
It is also a good idea to have a cohesive viscoelastic (like Healon GV) and a side port blade handy in case you accidentally violate the capsule and the chamber flattens. In the case of valves, I also keep a ligature suture nearby ready to tie off the tube just in case. It also never hurts to have a glaucoma surgeon on standby!
--Banks
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I working on automatic detection of glaucoma using 3D oct images. I need a dataset of 3D retinal SS-OCT or 3D retinal SD-OCt images. I'm looking for 20-25 images contain glaucomatous eyes, glaucoma suspect and healthy eyes.
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Hello Murat.
I think so, but first of all show me One Glaucomatous eye sd-oct image of the ONH (Optic nerve Head) so that i can check whether your images will work for us or not. if it is fine then your name will be included in paper.  
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Everyday more than 1000 cataract surgeries are done through different eye hospitals, surgical mobile camps and private clinics in Nepal. Patients fall in line and their cataracts are removed. Those who are lucky see good, those who are not are told that they had existing problem at the back of their eyes. Are we treating them ?
I invite likeminded researchers to collect resources for a most needed study- Clinical audit for cataract surgery in Nepal.
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Absolutely, I would also think that a comprehensive evaluation prior to surgery will be of benefit. We have primary eye care clinics in South Africa that deal with many indigent patients requiring cataract surgery but strict treatment protocols are in place to prevent unnecessary surgery and complications.
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Very aggressive OMMP, treatment at this moment Mycophenolate mofetil 1 g x2 and Prednisolon 30 mg/day. Of course it ( increasing pulmonar fibrous or atelectases) might be because of MMP, but I think it´s quite rare side effect.
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There is no precedent for lower airway involvement in mucous membrane pemphigoid. However the larynx may be involved and patients have required a tracheotomy in the past although endoscopic laser surgery for this very rare complication is improving outcomes of laryngeal involvement.
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What are your experiences with Harms screen, Amsler Grid...? Any other ideas?
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a small word on Amsler grid as you asked about it repeatedly: in my experience amsler grid CAN show a defect that is located in or reaching the (para)central area, and in these cases can be used to confirm the extent of the central scotoma. However many (or even most) patients with advanced or end-stage VF defects and proven central scotoma on a 10° VF test will report their amsler as being 'normal', even when explicitely drawn attention to the area of a proven scotoma. This presumably due to cortical processing (see: Bull Soc Belge Ophtalmol. 2003;(287):65-71.
New insights into the subjective perception of visual field defects.
Hoste AM1.)
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Please I need some help with possible differential diagnoses and/or management plan. Fundus photo of an active 47year old male African, Right eye. VA=CF,  exotropia approx. 30o. Lens, cornea, vitreous are all normal. Good pupillary reaction with mild RAPD, IOP 14mmHg. History of decreased vision since childhood. No history of trauma, diabetes, HIV, or hypertension. The left eye is normal. 
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You have presented an interesting case of an adult male with a history of poor vision OD since childhood, a sensory exotropia, healthy nerves and vessels, and a unilateral pigmentary retinopathy. Most likely this is due to old infection, but other possibilities include an old foreign body with siderosis, inflammatory causes such as Harada's disease or AZOOR, old retinal vascular occlusive events or perhaps an atypical presentation of a bilateral process such as retinitis pigmentosa or vitamin A deficiency. Likely infectious causes are onchocerciasis, diffuse unilateral subacute neuroretinitis, syphilis, ophthalmomyiasis, toxoplasmosis, or rubella. As he is from Africa, there are probably several more infectious diseases that may cause a pigmentary retinopathy that I am unfamiliar with. Perhaps someone with expertise in tropical medicine could add to my list. I recommend a careful history, consider a plain-film x-ray if there is a chance of a retained foreign body, then a laboratory work-up for the most likely infectious diseases. If that does not lead to a diagnosis then I would consider electrophysiology studies to rule out unilateral retinitis pigmentosa, but this is unlikely. There are many good papers on the differential diagnosis of unilateral pigmentary retinopathy. Here is one:
Silveira C, Belfort R Jr, Nussenblatt R, Farah M, Takahashi W, Imamura P, Burnier M Jr. Unilateral pigmentary retinopathy associated with ocular toxoplasmosis. Am J Ophthalmol. 1989 Jun 15;107(6):682-4.
Thank you again for presenting an interesting case. Please let us know what you find.
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Is topical preparation of Chlorpheniramine maleate (CPM) only (not in combination) approved by USFDA, EMA or any other regulatory body for allergic conjunctivitis?
If yes, then how CPM is marketed, OTC or scheduled drug.
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One more, again from US FDA ......
According to Drugs@FDA there are no chlorpheniramine maleate products which are FDA approved in a topical or eye drop form for ocular allergy. Drugs@FDA can be accessed at: http://www.accessdata.fda.gov/scripts/cder/drugsatfda/index.cfm
Best Regards,
HT
Drug Information Specialist
Division of Drug Information | Center for Drug Evaluation and Research
Food and Drug Administration
For up-to-date drug information, follow the FDA's Division of Drug Information on Twitter at http://twitter.com/fda_drug_info
This communication is consistent with 21 CFR 10.85(k) and constitutes an informal communication that represents my best judgment at this time but does not constitute an advisory opinion, does not necessarily represent the formal position of FDA, and does not bind or otherwise obligate or commit the agency to the views expressed.
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Eyelid marking before Blepharoplasty !!
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Dr. Rana and Dr. Thabit,
Thanks for the valuable feedback. Actually, brow ptosis examination and detection is vital before any blepharoplasty. So, it was very well considered. 
We are planning a modification in marking of incision than the Rees' Scalpel shaped and Bellinvia et al's technique.
We shall tackle the ROOF on table if required. The furthur elaboration will be discussed after completing our study.
Please comment if anything,
Regards 
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Computer vision syndrome (CVS) is a temporary condition resulting from focusing the eyes on a computer display for protracted, uninterrupted periods of time. Some symptoms of CVS include headaches, blurred vision, neck pain, redness in the eyes, fatigue, eye strain, dry eyes, irritated eyes, double vision, vertigo/dizziness, polyopia, and difficulty refocusing the eyes. These symptoms can be further aggravated by improper lighting conditions (i.e. glare  or bright overhead lighting) or air moving past the eyes (e.g. overhead vents, direct air from a fan). [Source: Wikipedia]
With the increasing access to digital devices, Computer Vision Syndrome is becoming a common ailment
Nowadays ours eyes do not get adequate rest as most of the time we are either on our computer, laptop, i-pad, mobile or watching television. Eye strain caused by excessive use of computer is called Computer Vision Syndrome or digital vision syndrome. It manifests as tiredness, inability to work for long hours, blurring of vision, double vision, watering, redness, itching and pain in eyes. These symptoms will be present in 95 per cent of people who use the computer for more than three hours a day.[Source: The Hindu]
Some Excerpts from the second article:
What To Do
Posture and Exercises
Good posture and regular exercises of back and cervical muscles are a must if you use the computer for more than three to four hours a day.
Lighting
The room should be well illuminated with the light source positioned in a way that light does not fall directly on your eyes or on the screen The light source should be behind the screen or on the ceiling and partially covered. anti-glare screens and spectacles can also help.
Dryness
Normally we blink 10 to 12 times a minute. When we watch TV our blink rate is 5 to 6 a minute and while working on the computer it further goes down to 3 to 4 times a minute. Reduced blinking causes evaporation of tears thereby increasing the osmolarity (concentration) of the tears. The hyperosmolar tears induce inflammation and tear film instability which in turn cause increase reflex lacrimation. In other words, the dry eye caused by Computer Vision Syndrome may present not only as dry eye but may present as watering and inflamed eye.
To overcome this, it is better to have the computer screen 20 to 40 degrees below the eye level. This causes partial closure of the eyes by the lids thereby decreasing the evaporative surface.
Your comments and views are welcome. Muchas Gracias !!
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According to the National Institute of Occupational Safety and Health, CVS affects approximately 90% of the people who spent three hours or more at day looking at a computer. The lighting, air quality, and the time spent focusing on a screen are the main factors that could bring about CVS. Taking breaks by closing your eyes or focusing on objects far away could help give the overused muscles a necessary time out. If giving your eyes a little breather is hard to remember you could set a reminder or timer. Some other variables to consider that could contribute to eyestrain is the environment.  If the room is really bright you could consider tinted glasses or maybe a certain pair of glasses just for computer use. If there is a lot of airflow that is drying out your eyes, some lubricating eye drops might help. Also make sure your settings are so that the font and screen lighting can be read with ease.
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My aim is a survey on what seems to be a very scarcely studied subject and points to evaluate the possibility to outline the state of the art about such matter.
This is a preliminary study related to a possible methodological research about semi-neglected subjects in medicine and biology.
Thank you
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~40 % of my surgeries for RRD-thanks
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I am trying to assess validity of data as regards to effect of strabismus surgery on blood supply to anterior segment of eye.
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Naeem,
I am not an expert, but I believe adult cynomolgus monkeys have been used in the Ophthalmology literature as a valid model for anterior segment ischemia after strabismus surgery.  I've attached two abstracts from PubMed.
Best wishes,
R. Gary Lane
1. Ophthalmology. 1990 Apr;97(4):456-61.
A primate model of anterior segment ischemia after strabismus surgery. The role
of the conjunctival circulation.
Fishman PH(1), Repka MX, Green WR, D'Anna SA, Guyton DL.
Author information:
(1)Wilmer Ophthalmological Institute, Johns Hopkins University School of Medicine,
Baltimore, MD.
Fornix conjunctival incisions in strabismus surgery may provide partial
protection against anterior segment ischemia by preserving the perilimbal
conjunctival-Tenon's circulation, which is disrupted with limbal conjunctival
incisions. Six adult cynomolgus monkeys underwent tenotomies of three or four
rectus muscles by making limbal conjunctival incisions in one eye and fornix
incisions in the other. Iris fluorescein angiography and slit-lamp biomicroscopy
were used to monitor changes. The eyes that had limbal incisions exhibited more
severe anterior segment ischemic changes than the eyes that had fornix incisions
in every instance of four rectus muscle surgery.
PMID: 2326023 [PubMed - indexed for MEDLINE]
2. Ophthalmology. 1987 Oct;94(10):1258-71.
Anterior segment ischemia after recession of various recti. An experimental
study.
Virdi PS(1), Hayreh SS.
Author information:
(1)Department of Ophthalmology, University of Iowa, Iowa City.
In 40 normal adult cynomolgus monkey eyes, recession of various recti in
different combinations was done to evaluate their effects on the anterior
segment. These procedures were done as primary, secondary, tertiary, and fourth
procedures (each separated by several weeks or months), ultimately involving all
four recti in the eyes. In 11 eyes, posterior ciliary arteries (PCAs) were
occluded to determine its effects on the anterior segment. All eyes were examined
by slit lamp, color photography, and fluorescein angiography of the anterior
segment, and tonometry, before surgery and serially thereafter during the
follow-up period. These studies showed that recession of two or three recti
simultaneously in different combinations produced no serious permanent anterior
segment changes, although initially in some of the eyes there was transient
mild-to-moderate anterior segment ischemia. Recession of four recti
simultaneously as a primary procedure produced serious permanent ocular and
anterior segment changes; however, when this was done as a secondary or tertiary
procedure after previous recessions of three or four recti, anterior segment
changes were much fewer and milder than when it was a primary procedure.
Occlusion of all the posterior ciliary arteries in itself produced no important
changes in the anterior segment, but when combined with simultaneous recession of
both the horizontal recti, it produced serious anterior segment changes. In the
light of these findings, the pattern of arterial blood supply of the anterior
segment is discussed.
PMID: 2446229 [PubMed - indexed for MEDLINE]
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A single vial of Avastin(4ml) can be used for up to say 60 patients, how does one ensure sterility of an opened vial and for how long can it be kept without compromising efficacy.
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we keep the avastin for up to 2 weeks
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A 10 year old boy has proptosis of the right eye.. Biopsy results reveal orbital lymphoblastic lymphoma. No brain or bone marrow involvement.
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You have to treat your patient as acute lymphoblastic leukemia with extranodal involvement.
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This topic was covered in this month's JAMA Ophthalmology (https://archopht.jamanetwork.com/article.aspx?articleid=1838342) and reported by Medscape.
Blindness secondary to fillers used in the face is a recognized complication; it has been debated for a few years - certainly, I raised it at a meeting in London in 2012. The paper in JAMA Ophthal refers to (off-label) use in the glabellar area, and, correctly in my opinion, attributes the complication to the anastomoses between branches of the E.C.A. and I.C.A..
Unfortunately, most doctors are oblivious to this risk, and nurses even more so. In fact, I have met, even recently, 'nurse injectors' representing manufacturing companies that had no idea about this potential problem.
My advice to colleagues/ my team is as follows (which I have cut-and-pasted from my comments on Medscape):
1) Certain areas have a higher risk: malar area (medial infraorbital zone) and inferior glabellar area;
2) There can be aberrant vessels and high pressure injecting can increase the risk;
3) Cannulae are 'probably' safer in these danger zones;
4) Hyaluronidase has no established role in addressing this problem, as once the small vessels supplying the retina are occluded then the outcome is rapidly poor. Plus, from a logistical point of view, the hyaluronidase would need to be injected into the common carotid or internal carotid given that the aim is to get the enzyme to the retinal arteries a.s.a.p., and this has it's own risks;
5) Safety should trump aesthetics: I do not inject in the aforementioned danger zones. Many do, and to be honest, the risk of this adverse outcome is minute - but should it happen, it is 100% critical.
If a filler is required in the medial nasojugal area, my feeling is that it should be injected as close to the surface as possible, i.e. very superficially. Of course, the risk of the Tyndall effect is higher that way, but this could be mitigated against by the use of a monophasic filler (at least partly, and at least in theory!).
F.w.i.w., I have met a doctor and the business partner of another doctor who've caused this complication - and who have had the integrity/ strength to talk about their experiences/ learnings - and both have categorically now stopped injected anywhere within a large circumference around each eye.
I'd appreciate the thoughts of clinicians who are experienced in this field.
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Hello Luciann and thank you for your input. Pulling back on the syringe (as opposed to withdrawing the syringe) is of limited value in this case, due to the size of the needle (i.e. affecting easy flow-of-blood), size of arteries (i.e. small, and hence blood not flowing at high velocity), and product in the syringe (i.e. viscous and likely not accommodating of any blood entering into the syringe).
The key thing, as you have said, is knowledge of facial anatomy - and also, in my opinion, awareness of this possible complication. This is why I disagree with nurse-injectors, esp. with regard to fillers. The fact is that they do not have the same degree of training or anatomical knowledge, and, importantly, I know many, many 'nurse injector trainers' that work for Allergan and Galderma and NONE had a clue about this kind of problem (and some even disagreed with this possibility) when I raised it at various events. 
Sadly, money talks, and pharmaceutical companies are more interested in high-volume sales instead of high-quality approaches, so it is better from their points-of-view to have as many injectors as possible, regardless of how low-end they are. 
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I am searching the data about the eyeball volume or size of young Dutch Rabbit (10~20 weeks age) for the research of ophthalmic drug.
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Greetings Hideyuki Mukai,
     Sarnat BG's publication on PubMed titled, "Eye and orbital size in the young and adult. Some postnatal experimental and clinical relationships." Contains experimental data which indicates that the orbital volume in Dutch rabbits ranged from 3.6 ml at 98 days to 5.8 ml at 540 days of age. By 180 days of age the orbital volume had reached about its maximum of 5 ml and was 25% larger than at 100 days of age. The mean orbital volume was less at 540 than at 450 days of age. At 15 days of age the eye volume was about 20% of adult size, at 100 days of age about two thirds, at 180 days of age about 85% of adult size which was reached at about 300 days of age. 
     For your convenience, I have attached the link to where I found the publication on PubMed. I hope that you find this information useful and applicable in your continued ophthalmic research. I wish you the best of luck in your future endeavors, I look forward to hearing from you.
Regards,
Lars Lafferty
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A 42 y/o lady who candidates for PRK for myopia has history of CSCR which treated with laser photocoagulation 5 years ago. BCVA of both eyes are 9/10 and 10/10 with mild metamorphopsia.
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As stated above, surgical trauma doesn't cause CSCR: it is not an inflammatory process. Secondly, it is less common in women, though this gender bias is no longer strong with more women having type A personality. Thirdly, myopia protects against CSCR due to thinner choroid. So the only way this lady can have CSC after refractive procedure is due to anxiety about surgery. Finally, it is worth checking the OCT (old pictures and fresh) to check if she doesn't have any myopic foveoschisis.
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Firm eye padding is frequently recommended as the initial management for moderate hypotony and shallow anterior chamber in the first few days post trabeculectomy. This might result from excessive filtration or a small leak.
Just wondering if there is any evidence out there in support of this, especially the bio mechanics of it. Putting pressure on a hypotonous eye might lead to some increase in the IOP, thereby forcing aqueous out and aggravating the shallow AC.
Would very much appreciate other views on this.
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We used to do firm eye padding for shallow AC following trabeculectomy and got AC formed after some days. It is possible firm eye padding encourages sealing and healing of areas of leakage leading AC formation. I think  this is worthy of (further) research to understand the dynamics.
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The standard textbooks define wet AMD as a neovascular disease. The poor response of wet AMD towards macugen therapy (anti-VEGF against VEGF A 165, a selective antivascular form of VEGF) arises the question whether wet AMD is predominantely a neovascular disease or more than that an exsudative disease. What do you think?
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Wet AMD is both neovascular and exudative. Once these neo-vessels break through the Bruchs membrane and the RPE is interrupted , the barrier is affected and leak is there.
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Meridional (or astigmatic) accommodation is defined as a non-spherical change in accommodation. Although prior evidenced-based findings supported the presence of meridional accommodation in human subjects, the underlying mechanism is still unclear.
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I hope that enclosed paper reflecting cutting-edge research on the topic will be useful.
Good luck !
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Recently Ahn et al. (Cornea 2013; 32:971-975) published promising results on the photocoagulation (514 nm) of pinguecula. Has anybody else experience with this method?
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I never hear about that and having in mind the "pathology" of pinguecula (an alteracion of elstic fibers related with UV radiation exposure) I cannot imagine the rol of laser (photocoagulation)
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A procedure carried out normally during posterior eye examination.
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I recommend using "dilated funduscopic examination".
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Wide use of IV anti-VEGF and more experience shed a light on potential hazards related with local blockage of VEGF
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These are 2014 publications:
To find the answers to this question you may need a proper search.
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At present it is an explosion of intravitreal injections of different antiVEGF in age-related macular degeneration, retinal vein occlusions, diabetic macular edema.
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An explosion of intravitreal injections of different antiVEGF in WET age-related macular degeneration raises new concerns...
For your friend with dry macular
degeneration , at present is useful ICaps R ( ALCON) or LUTAXAMDPLUS ( Santen) supplements, but research is ongoing for new noninvasive treatment.
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The medical treatment of glaucoma has undergone significant development in recent years. Research in this field is focused on improving pre-existing drugs and on the development of new molecules.There is also intense research activity in the search for new therapeutic groups for glaucoma treatment
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I also published on effect of systemic calcium blockade on intraocular pressure some time ago
Kelly SP, Walley TJ. Effect of the calcium antagonist nifedipine on intraocular pressure in normal subjects. Br J Ophthalmol 1988; 72: 216–8.
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Atraumatic extraction was done of right first maxillary molar with buccal infiltration and greater palatine nerve block (lignocaine 2%with adrenaline 1:80,000). The patient complains of blurred vision and pain in the lacrimal gland area of their right side. Pupil reflexes are normal, as is the healing of the socket.
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First of all, was the patient referred to the ophthalmologist to check what was the reason for blurred vision. When the patient complains on blurred vision and pain ? immediately or latter. In my opinion the reason for meantioned abnormalities was local anesthesia into second branch of trigeminal nerve spreaded into first - ophthalmic branch , causing pain in lacrimal gland area due to lacrimal nerve - V1
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Current approach is intravitreal anti-VEGF injectiones.
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Currently most common and most effective treatment approach for diabetic macular edema (DME) is intravitreal injection of anti-VEGF molecules, but this treatment modality exposes the patient to the risks of intra-ocular injections. At present intensive research works are going on to find out the non-invasive alternatives for the management of DME, and some of them are as follows:
Selective Protein Kinase C beta inhibitors [Ruboxistaurin]: As beta isoform of the enzyme PKC mediates many of the detrimental changes of the diabetes in the eyes, so Ruboxistaurin, a selective inhibitor of PKC beta has been developed, which has been shown to prevent many of the diabetes-induced changes in eye both in cell culture and in animal models. Phase 3 clinical trial of ORAL administration of Ruboxistaurin have demonstrated that it reduced the rate of sustained moderate vision loss (loss of 15 or more letters for at least two consecutive study visits) in eyes with definite diabetic macular edema at baseline (10% 32 mg/day study drug versus 25% placebo, P = 0.017). A separate study evaluated the ruboxistaurin specifically in regard to the reduction of progression of retinal thickening from more than 300 µ to within 100 µ of the center as measured in stereoscopic fundus photographs. The 32 mg/day dose reduced progression of DME compared to placebo (hazard ratio = 0.66 (95% CI 0.47-0.93 P = 0.016) (PKC-DMES Study Group, manuscript submitted). This product is currently under regulatory review for the treatment of early diabetic macular edema.
Topical Dexamethasone-Cyclodextrin Microparticle eye drops: M tanito et al conducted a short pilot study and found that topical Dexamethasone-Cyclodextrin eye drops decrease central macular thickness and increase visual acuity in DME patients.
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Neuroprotection is a contemporary approach used in the treatment of glaucoma, retinitis pigmentosa, diabetic retinopathy.
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Dear Marianne, we have been studying retinal diseases for a few decades and in the last decade, have developed the use of save, non-invasive therapies with no side effects reported. These are dietary saffron and near-infrared light therapy. See my publications for example. I'm under Prof Jonathan Stone's group at Sydney Uni and he is the brains behind these studies using saffron and infrared light therapy for AMD, retinitis pigmentosa, Parkinson's disease and Alzheimer's disease. These therapies are said to be protective by reducing oxidative damage and switching on mitochondrial protective pathways.
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I have one big problem with my research. I have one categorical binary dependent variable and three independent (scales) variables and I want to know which of them has the most powerful interaction that DV. I have performed the UNIANOVA on SPSS v.21, but there is something I don't see right or I don't know the right interpretation of the analysis. I know that the question is not complete but, if anyone can help me with some text about the interpretation on the UNIANOVA Analysis?
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Both logistic regression and discriminant analysis involve a categorical response variable; in both cases you may have two or more categories. In the case of logistic regression you model the log-odds as a linear model. The explanatory variables may be categorical or numerical. The output of the logistic regression is a set of probabilities that a case will fall in each of the categories. If p(j) is the probability that a case will be in category j then the odds of category j is Odds(j)=p(j)/{1-p(j)} and the log odds is LN{Odds(j)}. The probability p(j) must be between 0 and 1 and therefore cannot be modelled as a straight line; the Odds must be positive and can also not be modelled as a straight line; however the log-odds can vary between -infinity and +infinity and can be modelled as a straight line. Thus the model is LN(Odds)=b0 +b1X1 + b2X2+ .... and the probability is then p(j)=EXP(b0+b1X1+..)/{1+EXP(b0+b1X1+..)}. This is an s-shaped function called the logistic function.
On the other hand, discriminant analysis is based on an assumption of multivariate normality. To understand the theory of discriminant analysis you must understand the multivariate normal distribution. The explanatory variables must be continuous variables and have a (joint) normal distribution. Among the properties of a multivariate normal distribution are that all linear combinations of the variables have normal distributions and relationships between any of the variables are linear relationships. If you plot a scatter plot of the cases then you always obtain an elliptic cloud of points. The procedure calculates a centre of gravity for each group (in multivariate space) and a distance of each case from each centre of gravity (the distance being the Mahalanobis distance which takes into account the correlation structure among the explanatory variables). These distances are then transformed into probabilities with respect to each category. A case is classified (by the model) into the category with centre of gravity closest to that case.
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Glaucoma is a disease marked by the progressive death of RGCs and often accompanied by increases in IOP and abnormalities involving the ciliary system. But what is the anatomical connection between the two bodies?
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There is no connection between ciliary circulation and RGC’s. In fact the RGC’s are nourished by the central retinal artery and not by ciliary circulation. It is true that RGC’s are dying in glaucoma but not primarily due to apoptosis caused by raised raised IOP. Apoptosis can’t explain early peripheral field loss and selective destruction of the arcuate fibers and an orderly destruction of the nerve fibers, the peripheral first and central vision at the end.
I hypothesize that optic disc is sinking and as result the nerve fibers along with its vasculature are being stretched and broken (severed). RGC’s are dying as a result of retrograde degeneration of proximal end whereas distally the neurons of the LGN due to wallerian degeneration as a result of severance of the nerve fibers.
In nutshell the nerve fibers along with its vasculature are being severed, not atrophied in glaucoma. Analogy: the leg is atrophied, not amputated. Glaucoma may not be an optic disc neuropathy but an optic disc axotomy. I would welcome any feedback.
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The glabellar tap test is used to detect soft neurological (extra pyramidal ) signs in Parkinson's disease
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Thanks Murali. I agree with you and the only other possible use could be to evaluate the afferent reflex of the trigeminal and efferent facial nerve.
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Why is the maximum period 14 weeks?
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Hi Daisy:
I agree with the points that Michael has provided. I have been actively involved in allergy drug development for a number of years. Both of these products are approved for temporary use to relieve symptoms of allergic conjunctivitis. While these products are generally safe to use for longer periods of time, they are used primarily used to treat short-term, seasonal conditions that generally are less than 3-4 months in duration (tree, grass, mountain red cedar, ragweed pollens, and fall moulds) or pink eye. With longer term usage, you may encounter class side effects associated with antihistamines in general (i.e. rebound, and very rarely keratitis). I would also be concerned with using the same bottle for a long period of time. The tip and the solution may become contaminated with bacteria and mould, which when introduced into the eye, will cause an infection. Both products are also classified as a Category C medications which restricts usage in pregnant or beast feeding mothers. Also, please note Michael's response with using these products with contact lenses. These products should not be used with contact lenses, especially the newer silicon based long-term lenses as the preservatives used may be absorbed by a soft contact lens and effect wearability. I do not know what the drug-drug interactions are with using these products with other ocular products used to treat conditions such as glaucoma or with using with a NSAID eye drop after cataract surgery, but wonder if this may be part of the max usage time. This may be something to consider.