Science topic

Eye Diseases - Science topic

Diseases affecting the eye.
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Dear experts,
Is there any study showing that computer work causes increased eye pressure, a symptom representative of Glaucoma?
I have personally talked with several eye doctors, but they told me that it had not been proven so far. So, I am seeking such new researchers in this regard.
Best regards,
Bahman
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In literature and most population based survey, no correlation between intraocular pressure and computer use has been reported neither has it been established that there is increased risk of intraocular pressure elevation with use of computer. However, more study is needed to prove or dispute this claim.
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I need these images preferable with labelling done for different parts of the eye. Also some animations, graphics, videos would be helpful. I need these to create eLearning Modules for basic training about Eye, Anatomy and Physiology, Eye Disease conditions for Medical Sales Representatives.
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Thanks a lot Nick for sharing these resources. Those were really helpful.
Could you share with me some sites where I can get images, preferably labelled images to make learners understand about Eye Anatomy and physiology.
For example, image or video explaining about sclera etc.
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Several months ago we observed some strange changes around eyes of several individual Siberian hamsters (Phodopus sungorus) in our colony (outbred). I attach pictures. It looks like an irritation-induced change, but we think that it is rather a symptom of disease. In some hamsters, which were kept in sibling pairs the change appeared in one individual, but not in the other. Being advised by our veterinarian we were treating hamsters with antibiotics (enfloxacin - in water, gentamycin - topically), but the treatment was not effective. The change appears only around eyes. BTW, except for this irritation-like change hamsters are in good shape. No body mass loss, fur in good shape.
I would like to ask if anyone has an idea what it can be you ever seen anything like that in your hamsters? Do you have any clue what it could be, and if so how to treat it?
We will be grateful for your help, Michal et al.
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Thanks
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  • Eye disease
  • Blindness
  • Climate change
  • Ozone hole
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The reduced ozone layer has let in high power radiation into our eyes, a phenomenon that has not happened before since the ozone layer was created some 400 million years ago. Now our eyes are vulnerable to damage.
The climate change has only changed the composition of the air, but none of the gases in the air can do damage to our eyes.
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I am working on a Diagnostic tool to help ophthalmologists diagnose Eye Diseases (like Keratitis) . The idea is to upload a picture of the eye and let the python program isolate the features / Lesions from the uploaded picture and present it as output for the Opthalmologist to consider.
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Dear Amit:
Nice to see the researchers started to pay more attentions about the ophthalmic imaging. I have number of research in such field regrading the keratoconus and some other ophthalmic problems. My advice to you that the ophthalmic diseases such as Keratitis are more clear to be diagnosed by the ophthalmologist as it is surface and clear changes and mostly the time periods for it is not so critical (unless it is severe). All the way I suggest to you the open source program called orange, you can find it on the following website:
Regards
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Many people use lenses in order to experience different eye color & also instead of glasses and etc.
It is important to bring lenses out of the eye ,daily otherwise side effects happen like dry eye disease.
So these lenses can be useful.
Is it possible?
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For therapeutic purpose, why not?
Same principle as biodegradable materials.
Site and desgin: as that of the ICL (different material and different purpose)
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In clinics, we often observe different measures of IOP in myosis vs midriasis. What do you think about this procedure and why?
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I think the causes are both mechanic ( pupillary block ) and / or vascular ( ciliary body iperactivity in sustained accomodation ). The last observed cases were young boys coming at my observation after mobile phones using in the waiting room. Beside accomodative myopia they had an abnormal IOP. I'm going to check further this findings. Several papers have been written about the possible link of peaks of the IOP with myopia progression even if they didn't find a clear association. I hope to design a study to disclose this question also.
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IT is a picture of the fundus. I am not sure about what is this indicative of and what landmarks should I take into consideration. I have acquired a lot of such images but I am not able to interpret them.
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Indeed - it is the holangiotic fundus of an albino rat or mouse. The nerve head and retinal vessels look normal - what are the clinical findings of the animal - is there any change in vision or behaviour?
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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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As I said I am working on eye disorders and I found a mutation in a gene which does minor alteration that is a change from leucine to isoleucine, which does not affect the function of protein. Instead I am suspecting at the alteration in regulatory elements. Suggest some Insilico tools to analyse the same. I would like to know computation tools, to analyse change in the regulatory elements due to point mutations. I hope you got my point. I have found a point mutation, which is a causative for an eye disease, the change at aminoacid level does not affect the protein function. Hence wish to know whether it alters the transcription by affecting the regulatory elements and also in post transcription, and whether it affects the stability or it activates any long non coding RNA. Could anyone suggest some online tool to analyze these? And also to pick up cell specific gene expression.
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An eye disorder very frequent  and unknowed of the great majority of physician s is binocular dysfonction from Ehlers-Danlos disease (EDS). The symptoms are visual fatigue and diplopy. The mechanism is propioception disorder from hereditary change of biomechanical characteristics of connective tissue. See my site claude.hamonet.free.fr
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I conducted my research on Corneal Neovascularization (eye disease). we used biofunctional compounds of plants and these compounds showed remarkable inhibition of CNV  with out any side effects, i used rabbit as an animal model. 
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Get your patent protection and talk to Novartis / Alcon. 
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VA is Hand movements
IOP is 14 mmHg
B-scan shows flat retina, no tumor and  a separate compartment in staphyloma connected to the main eyeball.
Video of this patient is attached to show site of staphyloma which is involving inferior half of cornea and sclera.
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I would do an extracapsular cataract surgery with a superior sectoral iridectomy. Of course any surgery in such an eye is high risk surgery, but one may be able to provide ambulatory vision by removing the cataract..
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My friend's nephew in India had ROP stage 5 and has lost his vision. He is age 13 now. We are trying to find a way where he can get his vision.We are seeing different publications online, but not sure how to proceed
2) I saw this video https://vimeo.com/2962835 where they said they got the treatment. We are not sure if it is marketing or genuine. 
3) We are only following the research happening in https://clinicaltrials.gov/
We will be happy to send medical reports to anyone who can help us? We appreciate all your help.
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Mainly animal models you mention there. I think we should have a look at the results of the clinical trial when they are out. Good luck and do not give up.
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Those who treat patients with glaucoma, know that many patients that are on glaucoma treatment, really don`t have glaucoma. As in many other chronic diseases, overdiagnosis and overtreatment are big problems in glaucoma. Nevertheless very few publications have addressed this issue.
Which strategies should be implemented to reduce the problem of overdiagnosis in glaucoma?
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Dear All,
Greetings ! 
Happy New Year !
Overdiagnosis in glaucoma is quite prevalent among the clinical community
Only definitive evidence of glaucoma diagnosis is characteristic optic neuropathy
on dilated 90D or 78D biomicroscopic examination 
The early clinical diagnosis depends much to the experience of clinician on optic nerve head evaluation and is subjective still 
IOP is not sensitive enough for the diagnosis of glaucoma unless is significantly high at multiple point in times 
The more objective OCT may underdiagnose or overdiagnose GON and may give non correlating findings many a times due to poor quality and centration of picture acquisition and due to biologically variable Optic disc morphology
Like to conclude saying that it is better to observe and not treat somebody who doesn't have glaucoma rather than overdiagnosing and treating them giving the burden of long terms medications with its attendant local and systemic side effects, monitory loss and above all psychological trauma of a blinding disease
Discussion with the "glaucoma suspects" and close observation is the key to prevent overdiagnosis and overtreatment, considering the risk factors of glaucoma in a particular suspect
A mutually correlating documented progression in clinical or test wise evaluation is the key to diagnosis and the starting point of treatment
As Doctors we should at least not harm somebody if not treating them 
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do you maintain corticosteroids for a long period?
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Therapy is as for any case of optic neuritis.Steroids are the mainstay but statins,interferon,erythropiotein have also been suggested..
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We need a young and updated researcher in the field of eye research. We need his/her clinical knowledge to complete our discussion section in a manuscript pertinent to eye and ophthalmology. Please contact me for further information.
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I would be interested in  your research.  I am a clinical scientist, having  research experience in corneal physiology. I worked as a Post Doc at Oxford University and  obtained a PhD From UMISTt having worked under Professor Nathan Efron.  I am an active clinician and I am  currently involved in ocular therapeutics.   You could contact me on bay811@ yahoo.com
Kind Regards
Dr  S. Amirbayat
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I understand this to be an ocular irritation related protective mechanism resulting in a reduced upper eyelid position. However, I have had difficulty finding any publications that describe corneal irritation with resulting blepharoptosis. Does anyone have a reference for this condition?
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In chronically inflamed eye associated with blepharospasm ptosis can occur, particularly if tarsal plate is affected due to trachoma, which could be thickening of plate, or thinning affecting LPS insertion on its surface or edge resulting in ptosis. I had recently operated a case by frontalis sling, where severe ptosis occurred due to peripheral keratopathy as result of blepharospasm for 10-12 years. Keratopathy has healed but ptosis was bothering patient, she improved.
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Is anyone aware of any reliable and precise methods for estimates of choroidal thickness using SS-OCT given that both currently used manual (point measurements) as well as automatic algorithms(built in) have their own inherent errors in measurements?
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Generally the technology behind SS-OCT should yield a more accurate choroidal thickness measurement.
Both high definition SD-OCT (manual segmentation of a single scan) and SS-OCT (automated segmentation) are comparable with a minor negligible difference (the SD-OCT is being thicker by 10 - 15 microns) and interchangeable. The difference being more significant the thicker the choroid (and also decreasing accuracy of SD-OCT).
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if let's say the patient is having an cylindrical axis of 90 and they have been corrected at 90 as well. Does the other meridians of the eye was being corrected at the same time as well? I can't find any journal or link about this. please help... thank you so much!
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My answer is Yes, the both meridians are treated simultaneously, which means turning into Emmetropia -normal eye without any refractive error
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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 am currently writing a literature review about sucrose as an intervention during ROP examination. I believe in some NICU’s RetCam is used, in others it is not. There is somewhat conflicting comments in relation to how long these examinations last (1 session). I would appreciate a comment.
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On an average, both indirect ophthalmoscopy and retcam imaging can be performed bilaterally in a child within 10-15 minutes. 
Laser procedures, however, take more time according to the severity of the disease.
The duration may also depend on various factors including the expertise of the examiner, pupillary dilation, co-operation of the child. Bigger babies may not co-operate well both during examination and laser.
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Up to 40% fundal coloboma cases may develop retinal detachment. What is your experience regarding the prophylactic laser of such cases?
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I have experience with retinal laser, but have not used laser for detachment prophylaxis in cases of coloboma. However, unless there is already subretinal fluid, I think that laser in this circumstance is generally contraindicated and only considered on a case-by-case basis. Perhaps a rental specialist could provide a better answer. Hope this helps.
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Man of 58 years-old with trauma (D12 vertebral fracture, fractured left shoulder blade, multiple rib fractures on the left). The scapular fracture treated with immobilization for 30 days (orthopedic). The patient has undergone neurosurgery of reduction / stabilization of the fracture with screws transpedicular D12 D11-D12 L1e kyphoplasty (duration surgery - 1 hour and 25 minutes, anesthesia duration - 2 hours and 15 minutes). The patient was placed in the prone position with the head resting on blankets and turned to the left. Immediately after the operation, during arousal, the patient experienced pain in the left eye, edema and amaurosis. He underwent angiography which showed signs of retinopathy in both eyes and a central retinal artery occlusion in the left eye (CRAO).The patient is diabetic with insulin pump therapy, hyperlipidemic (rosuvastatina), hypertension, occasional smoker or former smoker, hyperhomocysteinemia, assumes Cardioaspirin. The doppler has revealed a thickening of the left carotid artery with a fibro-calcific plaque without significant impairment of flow. In addition, both the CT that the brain MRI showed multiple small areas of gliosis of the white matter, as from vascular cerebral disease. According to your experience, could the prone position to have been the only cause of ocular damage? 
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Bone fracture, post op immobilisation , DM , hyperlipidaemia, carotid plaque etc has the potentiality to develop thrombus and or embolus which can cause blockage of arteriole on their  circulating path way. We ophthalmologist often keep our patient in prone position following VR surgery. There is hardly any report  of CRAO following such procedure. I also agree w other responder that positioning of the patient has not caused CRAO. 
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Do you have any bioplex beads for bradykinin and eotaxin for measurement in allergic eye disease?
Thank you!
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Sorry. We have no such beads.
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A 24 year old healthy male presents with a staph cellulitis, no purulence. 2 days after he presents with a furuncle on other knee. 2 days later he presents with a sty looking lesion on L eyelid. Eyelid lesion develops as a staph abcess related to a hair follicle and suppurating abundantly every morning, affecting soft tissue of orbital socket.
Interested in the mecanism of eyelid infection.
Interested in how common could and eyelid furunclle of this type be.
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The eye lid lesion may be a part of the multiple infectious skin lesions that the patient is manifesting.  most likely the patient has bacteremia .stye is external hordeolum, ie a suppuration of the hair follicle unit of the eyelas, so  equivalent to fur uncle elsewhere. The lid lesions tend to look more dramatic than their counterparts in the body since there is loose skin ,enabling more fluid/ pus to accumulate, the skin is extremely thin (0.5 mm thickness) and There is abundant blood supply so the progress of cellulitis to suppuration may be quicker.
ruling out a systemic cause of immunosuppression may be important . Systemic antibiotics and NSAIDs are recommended . Systems Steroids can be started ,may be 24/48 hrs later,based on severity . If topical Steroid cream is unavoidable on the eye lid, it would be a good idea to check for steroid induced glaucoma after 2-3 weeks of application.
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I'm doing a study on an eye disease and am collecting tears for cytokine analysis. I would like to collect reflex tears from patient participants, but it has been very difficult to do so. I tried generating the sneeze reflex by tickling the nose with a sterile cotton bud, but it didn't work. Then I tried onion vapours, but that didn't work either. Does anyone have ANY suggestions on how I could do this? If onion vapours/cotton-bud worked for you, would it be possible for you to let me know what protocol/procedure you followed?
Any advice would be much appreciated. Thanks.
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Thank you so  much Marianne!
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I'm a PhD student and I'm doing a work to develop  a business model. I also want to know if anyone can tell me where I can find the costs of pre-clinical an clinical trails for eye disorders. 
Thank you
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thank you all
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I want to use a contact lens for rabbit for transplantation of stem cells to the corneal surface with substrate. i want to put a contact lens which can also able to diffuse gas (oxygen and CO2). I want to use this lens just to avoid the problems due to blinking. Please suggest me from where I can get this. Please also suggest me, what other methods would be possible. As I am also not able to suture the cell-substrate sheet. I also would like to get information about other ways to put the cell-substrate patch over the cornea other than chemically defined bioadhesive. Please do help in this. Thanks!!!
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For an adult rabbit, 5 kg or greater, you want a silicone hydrogel lens, such as O2 OPTIX from Alcon.  Most likely need 8.4 - 8.6 mm diameter.  A thicker lens such as a -3.0 OD lens should stay in the eye better.  The nictitating membrane should not be a problem.  Years ago we used to excise the nictitating membrane but risk developing an infection.  Also, the lens should be fairly flat.
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What is the effect of using Viscoat on post op corneal clarity in hard cataracts? Is it evidence based?
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Viscoat is also slightly hyperosmolar which helps draw fluid out of the cornea, facilitating the endothelial function and keeping the cornea clear.   So it not just protection, Viscoat also has a direct beneficial effect on corneal clarity, even should the endothelial cells be slightly compromised.
The hyperosmolarity can be taken advantage of during e.g. intraocular surgery if the view is already compromised due to mild to moderate corneal edema, the cornea will clear after filling the AC with Viscoat, in about 20 minutes.
McCannel CA.  Improved intraoperative fundus visualization in corneal edema: the Viscoat trick.  Retina. 2012 Jan;32(1):189-90. doi: 10.1097/IAE.0B013E318232AE26.
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Is there a difference between automated refraction and manual refraction after cycloplegia in children?
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if eyes are deviated no difference in automated and manual refraction; if eyes are straight there is difference and manual is preferred , for many people it will appear upside down but this is right 
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I am working on calcium signaling in retinal microglial cell and its physiological function. I want to know how the calcium signaling travels in retinal microglial cell and how the calcium signal play role in diabetic retinopathy?
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I hope that my written  papers " Glaucomatous optic neuropathy: role of neuroprotection "  and others find in Research gate wil be helpful. Good luck !
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the latest anti-VEGF drug for retinal vein occlusion, age-related macular degeneration, macular edema is Aflibercept. It is important to examine drug-related systemic side effects (stroke, tromboembolic events,etc.) in therapy by Aflibercept (EYELEA)
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Currently I am being treated for age-related wet macular degeneration with ailea. Having received four inoculations so far with that drug, I can attest to the fact that I have had no side effects while the ailea is much improving the quality of my vision.
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I am looking for a company which is interested in developing and producing special eye glasses that help patients with strabismus. Of course we are talking about companies interested in research at this moment.
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If by managing strbismus you mean facilitating fusion, the only such glasses are ones with ground in or Fresnel prism.  What would you expect to accomplish otherwise?
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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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A resident of Ophthalmology complains from both eyes floater, left eye floater is visible every time and right eye only when looks to white board for more than 3 years, flashing is observable in left eye only once or twice a week. He has just known about this problem when he studied about and states that his left eye had this problem since childhood.  Please give your idea about the risk of RRD  and that he will be an ophthalmologist in the future he is worrying about his profession. 
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Since peripheral retinal degenerations may be asymptomatic, dilated retinal examination is a must for all. In this case since the patient is young and has the floater since childhood, IF a peripheral retinal examination is OK; he may not be at risk for the present time. But if there is trauma or floaters increase, he must have an immediate retinal examination. Otherwise 6 months intervals are ideal. If there is a degeneration of lattice or white with/wo pressure , these are also prone to RRD. and preventive laser photocoagulation may be applied, surrounding the lesion. Good luck for the future ophthalmologist.
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What is your experience with amphotericin b injections in anterior chamber, how often do you inject and how long? What you do if doesn`t help?
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Already have, but no positive dynamic
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Since vitrectomy is already done is there a role for re-vitrectomy?
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I agree with the comments already made, however these are immediate post vitrectomy cases.  In today's world the patient may have had a complete vitrectomy years prior and develop an endophthalmitis from an injection for various conditions.  In these cases tap and inject vs. vitrectomy would be based on the the severity and circumstances, but you can alway tap and inject and still go to the OR.
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See above
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For disturbing  floater  - vitrectomy
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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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In ocular infections, especially in infectious keratitis, microbiological analysis is difficult due to the small amount of material / probe.
What is the best method: directly inoculate the swab or use a transport medium as in eSwab an let the lab do the inoculation?
How to store the swab / the agar plate? What plates to use? Are there any time or temperature limits or implications? What swab system can you recommend?
Can you recommend any references on the topic? 
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Greetings Mathias, the laboratory sample depends on the etiologic agent you're looking for. You should always take two samples, one for gram stain and another for culture. About sample for keratitis diagnosis, corneal scraping is the gold standard.
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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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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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It is mentioned that larger Vertical CDR a risk factor for glaucoma. It is puzzling: why would a larger vertical CDR be a risk factor and not the larger horizontal CDR?
Can it be possible that enlarged vertical CDR represents cases in which glaucoma has already been initiated and the cup has enlarged vertically after the development of notches in the superior and inferior poles of disc?
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Dear Drs. Wegner and Elbendary, I agree with you that no one listens to anyone. I think since glaucoma is a misunderstood disease and there is no consensus therefore everyone is managing glaucoma in his/her own way, which is very unfortunate. I think if something is so basically wrong then it is moral and professional obligation of everyone to liberate glaucoma from ‘cupping’. Concept of cupping given 160 years ago is creating havoc in glaucoma. Cup/disc ratio’s used in glaucoma diagnosis are grossly misleading and unfair to our patients.
Every day I see the subjects born with larger cups and normal IOP being treated as NTGs including children, whereas those with small cup and high IOP being ignored treatment as OHTs. We have to stand up and ask those who are controlling the dissemination of glaucoma knowledge to either prove us the phenomenon of ‘cupping’ or discard it altogether. We would be doing disservice to our profession if we don’t decide on this critical issue: YES or NO. We have heard enough of ‘cupping’ but now it is time to please show us the histological proof of physiological and pathological cupping.
The so called ‘cups’ are nothing more than vestigial fibrous tissue of Bergmeister’s papilla. Moreover, there is no such thing as cupped area being an empty hole. There is no histology to support this doughnut shaped misconception. The reason we don’t see the nerve fibers underneath is because they are covered by this remnant fibrous plate and not because of being empty hole, devoid of nerve fibers.
I propose the that the cups are not enlarging but breaking up due to creation of excavation (empty space) resulting from the severance of nerve fibers. The nerve fibers at the poles (arcuate fibers) have no special affinity for preferential loss. All the of nerve fibers are equally prone to damage since they are always being destroyed in an orderly fashion from peripheral to paracentral and ending with central fibers and never randomly.
I hypothesize that all the 360 degrees of nerve fibers are being severed simultaneously. However, the arcuate fibers being fewer in number compared to the rest would be depleted earlier giving rise to arcuate field defects. It is just the number game and not due to any different pore size of LC or undue sensitivity.
I ignore the cups and examines the glaucomatous discs in context of sinking disc/severance of nerve fibers and its vasculature. The amount of excavation, pallor, sloping, kinking of blood vessels provides enormous amount of information about the every stage of glaucoma. Notching is first sign of excavation in glaucoma. I find this simple method very exciting and correct and we may not need anything else.
My only regret: I wish I had known this in the beginning of my career 50 years ago. The essence is that the nerve fibers are being severed (not atrophied) in glaucoma. Histological proof of severance of nerve fibers lies in the histology of the end-stage glaucomatous disc- totally devoid of nerve fibers and no evidence of posteriorly bowed or cupped LC.
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What normogram do you use for IOP correction?
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Anterior and Posterior Segment OCT: Current Technology and Future Applications
Ashok Garg
9789350909782 - 1/e - 314 pps - 6.75" X 9.5" - Hardback
Includes Interactive DVD-ROM
2014
The book features valuable information on OCT put together by various international experts in this field based on their clinical experience and covers all current and futuristic applications of OCT in ophthalmology. This book has been organized into 31 chapters and covers both anterior and posterior segments indication of OCT including cataract and refractive surgery, phakic lens, glaucoma, oculoplasty, corneal conditions, keratoplasty, neuro-ophthalmology, vitreomacular interface diseases and macular hole, diabetic retinopathy and various other retinal disorders.
The add-on feature of this book is the accompanying interactive video DVD showing the intraoperative use of OCT with various clinical conditions which is hardly accessible elsewhere. This comprehensive book will serve as a beckon light not only to the anterior and posterior segment surgeons, but also to cataract surgeons, retinal specialists and ophthalmologists to stimulate and as well as to enhance therapeutic decision making and monitor the outcome of treatment.
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Left eye: cataract operation done, vhigher IOP, vall medicaments used, diode laser done, no benefit.
AGV implanted, followed by band & bullous keratopathy. Now there is vision, but feeling only light, null.
We were advised that nothing was to be done.
Right eye: cataract began, IOP elevated.
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In a case of aniridia+ Cataract+ Glaucoma- in this case at present right eye need treatment. Most important is to treat glaucoma using anti-glaucoma depending on intraocular pressure. Second important thing is to do cataract surgery- it should be phacoemulsification with capsular bag implantation of IOL. Operating surgeon should prevent complication such as posterior capsular tear as such occurrence will complicate glaucoma. A close follow up of such patient is equally important.
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I read studies that have reported changes in visual outcome just 3 months post-KC surgery. I am looking for any explanation as to why these studies did not wait at least a year before reporting their findings.
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Great Contributions. This is an awesome alternative especially for early stages of KC
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What explains the visual field defects in myopic eyes with posterior staphylomas?
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Dear John Mark Sim De Leon,
Posterior staphyloma, as the diagnosis itslef explains, involves the posterior segment of the eye, typically diagnosed at the region of the macula. Relative pathology provokes deformation of the eye in a way that the eye-length is extended with associated myopia.. It is diagnosed by ophthalmoscopy, which shows an area of retinal excavation in the region of the staphyloma. Concerning visual field defects, you can find some good references in:
Kyoko Ohno-Matsui, Noriaki Shimada, Kenjiro Yasuzumi, Kengo Hayashi, Takeshi Yoshida, Ariko Kojima, Muka Moriyama, Takashi Tokoro Long-term Development of Significant Visual Field Defects in Highly Myopic Eyes American Journal of Ophthalmology,Volume 152, Issue 2, August 2011, Pages 256–265.e1
Young Hoon Hwang, Chungkwon Yoo, Yong Yeon Kim Long-term Development of Significant Visual Field Defects in Highly Myopic Eyes American Journal of Ophthalmology, Volume 152, Issue 5, November 2011, Pages 878-879
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Myopia is common among the students or persons particularly females who have a height less than 5 feet. Mostly its incidence is directly proportional with the shortness of height. We observed that it is less common among the taller students particularity in males who are generally taller than the females.
In most of these patients myopia gradually increase from --1 to --3, and even more within few years after starting to use concave lens.
Causes of this myopia and its deterioration may be due to at least two factors:
1. Students commonly use reading desk with same standard height in the school and at home. Students with short stature have to focus their eyes at a closer distance than taller students. To compensate this closer vision, optical power of the eyes begins to increase during early teenage period and these students become myopic.
2. During correction of myopia ophthalmologists prescribe negative lens usually for constant use. Although these concave lens are not needed for near vision, but due to constant use of the lens according to the physician’s advice, the optical power of the eyes increase gradually to compensate the concave lens and the student increasingly become more myopic. This is a vicious cycle. In this way myopia continues to increase at least during their studentship period. So use of reading desk at school and home with appropriate height of the students should prevent myopia and avoidance of concave lens used for distant vision or use of appropriate lens during closer vision will prevent further deterioration of the affected students or people.
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Interesting model Tom, but where are the studies to support your assertion?
Undercorrection seems to accelerate progression.
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A patient sees 6/9 in each eye and complains of seeing haloes and dry-eye-type symptoms. He has a minor degree of lens opacity and the microcystic corneal dystrophy. How would colleagues manage this patient? Would they proceed to cataract surgery in the first instance?
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You first need to assess the severity of the dry eye since this can get worse after cataract surgery and should therfore be assessed preopertively to secure proper Treatment and prevent decompensation after surgery. If this has been done with lubrication and/or punctum plugs you can proceed to surgery. Be sure that what you have diagnosed is not Fuchs corneal dystrophy since then a triple procedure might be consiedered.
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Although KC is defined as a non-inflammatory condition it has long been my view that inflammation must play a role in the condition. KC progression is associated with allergy, vigorous eye rubbing, and even contact lens wear. We know that all of these situations can cause inflammation so my question is why has the role of this inflammatory process not been further investigated in the pathogenesis of KC? In our practice we aggressively treat the allergy (and rubbing) associated with KC in an attempt to prevent further progression. So far our results have been good with documented changes in corneal topography and Pentacam scans (although not reported in the literature). Your views on this issue will be appreciated.
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I learnt two bases for KC. The first, biomechanical and the second, biochemical. If I am to mention something on the biochemical basis, then I have to state that there occurs some change in collagen type VI expression. An increased level of proteolytic activity alongside the changes in the composition of proteoglycan composition may possibly be associated with KC. Reports of increased cathepsin B and G activity and gelatinase A have been published. Immunolocalized antiproteases have been found to be decreased in KC corneas. Some studies also put forward the view that KC might occur due to the structural change in the epithelium. And eye rubbing excessively might be one of the many reasons for the change brought about to the epithelium. And IL-1 mechanism leading to the tissue loss is not unknown, and this helps with apoptotic cell death.
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I am looking for examples for acquired visual dysfunctions with regards to accidents and/or diseases. Are these dysfunctions stable, declining, or improving? Do they include blindness or what kind of visual capacity?
Thanks in advance!
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Retinal vein occlusion is an examble of acquired visual dysfunctions with regards to diseases.
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Patient aged 71, compensated diabetes, worked and got infected in Iraq after a severe pneumonia. Bacteriology revealed Klebsiella, E. coli and S. aureus.
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I agree with Andrea Leonardi ,when fungal infection is suspected and smear and culture are negative for fungus repeat scraping or even biopsy is necessary to identify fungal material .I am not agree for aqueous humor culture because usually hypopyon is steril.
for treatment i use Natamycin 5% or Amphotericin B and Voriconazol when it doesn't respond to traditional treatment .
You must think to necrotizing Herpetic interstitial keratitis too.
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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.