Optometry and Vision Science - Science topic

Very interesting topic. Not much work is available that measures isolated convergence parameters alone.

1. 10.3109/02713689309001827 (small study, 16 subjects) : For the experimental group, the accommodative response/accommodative stimulus (Ar/As) slope increased 0.05 D/D after ingestion of caffeine, and the response AC/A ratio decreased 3.05 delta/D. The y-intercept of the convergence response/accommodative response increased by 3.7 delta in the experimental group. These changes were statistically significant.

2. Ajayi O.B. and George O.G. (2007). Acute effect of caffeine on Amplitude of Accommodation and Near Point of Convergence. West African Journal of Pharmacology and Drug Research. 22/23: pp. 27 – 30. Their result showed that ingested caffeine increases mean AmpofA by almost 2.00D within 30 minutes, and the elevation, though variable across patients is sustained for several minutes. The NPC and AmpofA in the decaffeinated coffee was statically insignificant (P>0.05) within the 0-90minutes of ingestion. However, there was a significant increase in the AmpofA of the experimental group (P< 0.05).

3. https://ojs.klobexjournals.com/index.php/nisebj/article/download/130/195: Most interesting results. The study revealed that the ingestion of caffeine has a significant positive effect on NPC and AmpofA. The effect is dose dependent and gender related.

4. Coon, Sarah, et al. "Caution in Clinical Interpretation of Near Point of Convergence: Influence of Time of Day on Oculomotor Function." Athletic Training & Sports Health Care, vol. 13, no. 1, Jan. 2021, pp. 7+. Gale OneFile: Health and Medicine: When designing a new study you may want to account for the impact of time of day on convergence

5. It would also be good to account for the impact on regular vs non regular drinkers while designing a new study

6. finally it is also important to measure other parameters of accomodation as well as coffee/caffeine tends to affect amplitude of accommodation and pupil size as well. In this study, Amplitude of accommodation rose from 12.4 (±2.2 D) at baseline to 15.8(±2.6 D) at 90 min. Similarly, pupil size increased from 3.4 (±0.4 mm) at baseline to 4.5 (±0.72 mm) at 90 min.

Hello,

when precise transmissive measurements are required, a detector and reference standard light source are used to measure transmittance of an object.

The spectral transmittance, τ(λ), of an object is expressed as the ratio of transmitted spectral flux, Φλt, emitted by a light source and an incident flux, Φλi, which can be measured with a detector.

For all translucent objects, some of the light is absorbed, some is reflected, and some is transmitted. The deviation between these three variables is defined by the characteristics of the object.

Based on the conservation of energy, it can be established that the total amount of light emitted by a light source directed towards an object is equal to the sum of absorption α, transmission τ, and reflection ρ of a particular object.

The detector can only measure the object’s transmission.

An object’s features can be measured using a spectrometer and a broadband reference standard. As not all wavelengths are transmitted through an object equally, it is essential to measure these properties, such as when measuring a material’s UV blocking properties. A spectrometer is capable of accurate measurement of transmittance for each wavelength. A different light source may be needed depending on the type of object to be measured.

Alternatively a colorimeter can be used to establish X, Y and Z values for transmittance based on the required test setup. This setup enables exact measurements for filters with high-density factors, when measurements must be performed at low luminance levels. The light source can again be chosen based on the type of object to be measured, but a white LED would be an ideal choice.

Y have some more info for you in added pdf files.

Best regards

Dr. A. Chandrinos

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.

Hi Myriem Otmani Idrissi

We got it from a group working in a hospital in South Korea.

Check these out.

http://tools.thermofisher.com/content/sfs/manuals/HCEC_PPS.pdf

Cheers

Taufiq

Just came across the following publication:

"Rods progressively escape saturation to drive visual responses in daylight conditions". Nature Communications volume 8, Article number: 1813 (2017).

https://www.nature.com/articles/s41467-017-01816-6.pdf

These issues also depend partly on the population you are studying. In particular, clinical populations are very prone to data loss because (1) participants may not be able to foveate in the desired way during calibration, and (2) participants might move around a lot, despite any use of chin or head rest. Also, notably, eye trackers are more likely to work well with men than women (as men are less likely to enter the study session with mascara and eyeliner). There may be some racial disparities in tracking ability as well, in terms of differences in pupil occlusion (from different eye shapes) and the ability of the tracker to work properly with dark skin tones. Whether these things are issues will also depend largely on what method of tracking you are using, and the specifics of your setup.

People with corneal scarring, corneal reshaping (from using hard lenses--even while not wearing them), prism lenses, and other unusual visual attributes can also have difficulties calibrating, if light does not pass through the eye at the angles that the tracker expects.

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!

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.

I also am a person who has experienced CVI after getting scotomas following laser surgeries.  I have personally taken both types of testing and moving targets are very difficult at any time.  But I can see that the comparison of both might lead to different results.  But when the moving target gets to the scotoma area it disappears and the brain develops a latency that creates a wait for the brain to figure out why the target is gone.and then takes lag time to get the interpretation of the new target to find out if it is the some or a different one..  Hope this helps.   

   I have neither seen nor read of any central cause of congenital deafness, ie due to a cortical lesion.  However, it is probable that a congenital cochlear loss will lead to faulty cortical development, even anatomical changes. 

   On line with Previc's work, I think in normals there is slight but significantly better hearing in right ears, sufficient to induce left hemisphere dominance for speech.  All the evidence suggests that the cortical hemispheres are equipotential at birth, or at least before any auditory input is received.  Hence lateralisation must be peripherally driven.

   Most of the studies I have read on the congenitally deaf have been uninterpretable, since the degree of residual hearing and the onset of the deafness is unstated. 

It is important to distinguish between color deficiency, as tested with Ishihara plates, and color blindness, aka achromatopsia, where there is no perception of colors.  In both conditions, I would not expect any difference in testing between monocular and binocular tests.  

 Dear Mr Lopez,

I'm afraid I don't fully understand your question. I am indeed using a headmounted eye-tracker from pupillabs, the ones I'm using are one of the first models they offered. Based on my experience I would not recommend them for the use on children without customization. 

The main problem that I encounter with my subjects (older patients) is that the eye-tracker is shaped like normal glasses. Normal glasses, however, remain balanced on the head due to the heavy weight of the pieces of the glass. Since the eye-tracker lacks this weight I was forced to use tape to secure the glasses to the participants' forehead.

If you can bypass this mechanical limitation (either through customizing a head strap or by contacting Pupillabs for a custom order) the system might work well for your purpose. 

Since my model was an early version it still suffered from some technical difficulties, but I can definitely vouch for Pupil-lab's great customer service regarding any problems.

Let me know if you have any more questions.

Yes we can

I do not mind This topic. I'm sorry

It depends on individual case. Even then some cases with absolutely no reaction respond to NSAID drops initially, some require steroid drops intensively at the end of PO first week. This is due to multi factorial causes.

Thank you Mark.

Arkadily,  This is an Offner mirror system known as aberration free in terms of spherical aberration, coma and distortion.  But there still remains astigmatism as shown in wavefront analysis of Offner mirror in my attachment.  Regards,  Shigeo

Dear Piraya,

Hypothermic storage at 2–8 °C is perhaps the most widely applied method world-wide; for example, all eye banks in North America use hypothermic storage owing to its perceived simplicity and its effectiveness. On the other hand, the majority of European eye banks use organ culture at 28–37 °C for storing corneas because of the extended storage time compared with hypothermic storage. Non-viable corneal tissue can be stored by freezing, by freeze drying, in glycerol, or in ethanol.

For more on this topic, please read the review article contained in the following link:

Hoping this will be helpful,

Rafik

More than evaluating the wearer it is important to find the difference in the geometry of Hoya and Zeiss lenses. Probably aligning with the geometry of the Hoya which wearer got adapted to will be the solution out. 

No doubt the evidence is not available in the literature. I have asked our optician to collect information from various lens companies.

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

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.

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).

Hey Safal,

There was a study by Karl Gegenfurtner's group which examined the best fixation target to minimize microsaccades. The best one is a mixture between bulls eye and cross hair. You could use such a target and add some random rotation (e.g. jitter) around the center to avoid accomodation.

Greetings, David

Kurtenbach et al found that “activity from the inner retina can contribute significantly to first and second order waveforms”.  .Kurtenbach, A., Leo-Kottler, B., & Zrenner, E. (2004). Inner retinal contributions to the multifocal electroretinogram: patients with Leber's hereditary optic neuropathy (LHON). Documenta ophthalmologica, 108(3), 231-240.

Sadun et al found that even carriers of Lebers had “depressed central responses and abnormal interocular asymmetries with mfERG". Sadun, A. A., Salomao, S. R., Berezovsky, A., Sadun, F., DeNegri, A. M., Quiros, P. A., ... & Sutter, E. (2006). Subclinical carriers and conversions in Leber hereditary optic neuropathy: a prospective psychophysical study. Trans Am Ophthalmol Soc, 104, 51-61.

Dear Frederic, are you looking for corneal SA C12?

Amplitude of accommodation is age related.   If the person has their refractive error fully corrected (for myopia or hyperopia), their amplitude of accommodation would be about the same for a myope as a hyperope at any given age.   There are individual variations in amplitude of accommodation for individuals of the same age.   But their full corrected ammetropia does not alter their amplitude of accommodation.  

You are after the Type B values. These are the systematic offsets and device or measurement uncertainties.

The S/N can be estimated by acquiring a spectrum with a signal and its background. Take the RMS fluctuation of the background as a representation of the noise level. A good exercise for the spectrometer is to measure the S/N as a function of integration time. You should find, the S/N goes as the inverse of the square root of integration time. Count for four times long to get twice the S/N.

The signal uncertainty can be estimated in the first step by the level of A/D conversion of your detector.  A 2 bit convert can read from 0 to 2² - 1 = 3, and its relative uncertainty is 1/4 = 25%. An 8 bit converter by comparison can read to 255 with a relative precision of 0.3%. We can argue points of whether to divide the uncertainty by 2 or not as "fine details for further investigation".

Another estimate of signal uncertainty is just the RMS noise level itself during operation. Alternatively, a much lower value is the RMS noise level of the "dark count" of the spectrometer.

The A/D conversion uncertainty is generally well below the RMS noise level on instruments with A/D converters greater than 8 bit. One way to tell whether you need to consider A/D conversion over RMS is to look for "staircase" steps in your noise signal. The "digitization problem" becomes apparent for example on 8 bit converter systems where the RMS noise is ± 1%. A spectrum of a flat background at the full range of noise might show about 3-4 "staircase steps" (1%/0.3% ~ 3 - 4).

The systematic offset uncertainties are determined by a calibration of the instrument response given a well-known input. You may get a linear or non-linear calibration equation. The uncertainties on your fitting coefficients in a plot of measured response versus expected response are the systematic offsets.

This sounds like a great exercise for a focused lab project to define your instrument. I hope I have given some pointers to further searching even without exact references. Good luck and have fun!

I have no access to real retinas, so I am looking for a software that is capable to simulate the retina function and response to various types of stimuli. I think that Occuscience is used for ex vivo testing of real retinas.

I would do both if feasible. If nothing else, it shows the lengths you are prepared to go to find your answer. 

Below is a link to the video for the flat mounting.

Hi Bruno,

in principle, the simulation of horizontal binocular vision with the vertical camera set should be possible by reprojecting the stereoscopic image to 3D and subsequently projecting the 3D points to the horizontal stereo camera pair. This will have, however, two drawbacks: Due to the different perspective of the horizontal sensors there won't be a 1:1 matching of the points in the image plane. Secondly, the occlusions from the point-of-view of the vertical camera pair will be lost in the virtual horizontal cameras as well, even though there is no occlusion from their point-of-view. Both effects will result in "holes" in the stereo image. Of course these holes could be filled by interpolation, but this might lead to unnatural effects. If the virtual horizontal cameras are not too far away from the real vertical sensor pair (compared to the distance of the object) the results should be acceptable, however.

Best regards, Ralf

Some of the change-blindness demonstrations might fit the bill? Like the dalmatian example, most participants struggle to see the change item, but once they've seen it, as long as they remember that pair of images, by and large they identify the change item instantly. And it is possible to use much simpler stimuli than photographs.

Thanks Carl, I believe this would be helpful. 

Thanks Gail, Can you share that survey tool with me at ikhan@sightsavers.org. it is a great support.

Regards

A phase II study of uniocular, topically applied, latanoprost showed significant IOP reduction in the fellow eye.  So contralateral effects may be more common than you may expect from the total dose.  Remember the unexpected findings with the systemic effects from topical beta-blockers...

Dear Nadine as far as I know much of the debate on visual imagery has shifted to the A.I. and robotics research field, albeit many theoretical insights still come from traditional competing theories (i.e. Kosslyn-like vs. Pylyshyn-like). But if you look for some models it may be worthwhile having a look. Here it is a small sample:

1.Aleksander, I., e Morton, H.B. (2007a). Depictive architectures for synthetic phenomenology. In A. Chella, e R. Manzotti (a c. di), Artificial consciousness. Imprint Acaddemic: Exter, pp. 30-45.

2. Aleksander, I., e Morton, H.B. (2007b). Phenomenology and digital neural architectures. Neural Networks, 20, pp. 932-937.

3. Di Nuovo, A., De La Cruz, V.M., e Marocco, D. (2013). Special issue on artificial mental imagery in cognitive systems and robotics. Adaptive Behavior, 21, 4, 217-221.

4. Marques, G.H., e Holland, O. (2009). Architectures for functional imagination. Neurocomputing, 72, pp. 743-759.

From the psychological point of view, there is still a sort of phenomenological third way between picture-like and propositional accounts; the empirical issues are usually in papers written in italian and are not so current as maybe you wish  but you may look at:

5. Cornoldi, Beni, Giusberti, Massironi, Memory and Imagery, A Visual Trace is not a Mental image. In Martin et al., Theories of Memory, Taylor & Francis, 1998.

1) Trolands refer to the HUMAN VISIBLE radiation, that is, take into account the spectrum of an illuminant and human spectral sensitivity. Luminous transmittance also deals with visible light, so, by definition, converts trolands of the incident light to trolands of the transmitted light.

2) The question is, how to get the luminous transmittance of a given filter.

Basically, you need three curves: spectrum of your light source E(V), transmittance spectrum of your filter T(V), and the visibility curve of the human observer S(V). (Notice that E(V) and T(V) must be in the same units, that is, both represented on either quantal or energy basis).

Then you calculate two integrals I1 = I(E(V)*S(V)dV),  and I2 = I(E(V)*S(V)*T(V)dV). Luminous transmittance = I2/I1.

Practically, it can be done in Excel. Make three columns A = E(V), B = S(V) and C = T(V).

Calculate D = A*B and E = A*B*C. Luminous transmittance = SUM(E)/SUM(D).

What about these guys? 

Hi Samuel

You are absolutely correct.

It is mathematically and scientifically unsound to aggregate or combine data sets that are logically mutually exclusive data sets.

The aggregation of positive and negative spheres into one data set for the purpose of summation and calculation of an arithmetic mean or average value results in data suppression.

The errors resulting from this unscientific and statistically invalid methodology are easily demonstrated: all spherical powers ( including spherical equivalents and mean spheres) are modelled by one dimensional vectors displaced along the rational number line with the magnitudes representing the distance from zero. The positive magnitudes are displaced to the right and the negative magnitudes are displace to the left; I.e. into two opposite and mutually exclusive directions.

For example: Positive Spheres 0,+1,+2,+3 ... Average 6/4 = +1.5

Negative Spheres ... -3,-2,-1,0 Average -6/4 = -1.5

If the data are combined into one data set:

....-3,-2,-1,0,+1,+2,+3 ...... Average 0/7 = 0

That is a major degree of data suppression has occurred and the average does not model the data accurately.

If the Absolute Values are used: 3,3, 2,2,1,1, 0 Average 12/7 = 1.5, however this results in loss of knowledge about the relative numbers of myopes or hyperopes 

This method lead to an over and under estimation of the actual mean value calculated by the two data sets if the data sets are of unequal size e.g. -3,-2,-1,0 Average -1.5 and +3 , +1,0 average 1.33 , while the absolute value calculation 3,3,2,1,1,0,0,is +1.42.

This separation of the mean spheres or spherical equivalents into negative , positive and plano values is consistent with the clinical categories of astigmatism:

Myopic Astigmatism e.g. -3.00/+2.00 x 180 SE = -2.00D

Hyperopic Astigmatism e.g. +1.00/+2.00 x 180 SE = +2.00D

Mixed Astigmatism e.g. -1.00/+2.00 x 180 SE = 0.00D

That is there are 3 logically mutually exclusive categories of astigmatism that need to be taken into account for the purpose of any analysis of surgical correction of astigmatism. 

Jacinto is in fact correct when he highlights Thibos et al methodology; all other methods of astigmatism data analysis are in different ways mathematically flawed and illogical.

A similar argument applies for the analysis of the postop angle of error (AE). There two logically mutually exclusive categories of rotation i.e. anticlockwise(positive) and clockwise(negative).

For example: anticlockwise degrees +30,+20,+10,0 Average 60/4 = +15 degrees

clockwise degrees 0,-10,-20,-30.. Average -60/4 = -15 degrees

If the data are combine into one data set +30,+20,+10,0, -10,-20,-30 Average 0/7=0

In other words total or partial data suppression results when two mutual exclusive data sets are combined for analysis.

If the absolute values are combined into one data set: 30,30,20,20,10,10,0,0 the Average 120/8 = 15 , which is an under estimation of the true value of the average or arithmetic mean and doesn't indicate in which direction, anticlockwise or clockwise, the error is located. This is data suppression at its worst and results in the loss valuable information and doesn't accurately model the clinical  data.

The only accurate analysis that models the data accurately is to separate the data into the logically mutually exclusive mathematical categories of anticlockwise and clockwise before calculating the average or arithmetic mean.

A major refractive surgery journal has recently proposed that these methods be adopted which is leading to great confusion to the journals readers, so your observation is very relevant and more letters to editors outlining this situation should be written.

Regards

Dr Lee Lenton

Hi, 

This can help!

 http://archopht.jamanetwork.com/article.aspx?articleid=1106477

Also, below are the files which contain latest developments!!!

Regards

Amrit

Thank you very much, Alain. Your recommendation was very helpful.

it is the neuroretinal rim decreasing

Hi, 

The following works might be of some help !!!

1.             Chew EY, Clemons TE, Agrón E, et al. Long-term effects of vitamins C and E, β-carotene, and zinc on age-related macular degeneration: AREDS report no. 35. Ophthalmology. 2013;120(8):1604-1611.

2.            Age-Related EDS. Lutein+ zeaxanthin and omega-3 fatty acids for age-related macular degeneration: the Age-Related Eye Disease Study 2 (AREDS2) randomized clinical trial. JAMA: the journal of the American Medical Association. 2013;309(19):2005.

3.            Chew EY, Clemons TE, SanGiovanni JP, et al. Secondary analyses of the effects of lutein/zeaxanthin on age-related macular degeneration progression: AREDS2 report No. 3. JAMA ophthalmology. 2014;132(2):142-149.

4.            Ma L, Yan S-F, Huang Y-M, et al. Effect of lutein and zeaxanthin on macular pigment and visual function in patients with early age-related macular degeneration. Ophthalmology. 2012;119(11):2290-2297.

5.            Ma L, Dou H-L, Wu Y-Q, et al. Lutein and zeaxanthin intake and the risk of age-related macular degeneration: a systematic review and meta-analysis. British Journal of Nutrition. 2012;107(03):350-359.

6.            Evans JR, Lawrenson JG. Antioxidant vitamin and mineral supplements for preventing age‐related macular degeneration. The Cochrane Library. 2012.

7.            Meagher KA, Thurnham DI, Beatty S, et al. Serum response to supplemental macular carotenoids in subjects with and without age-related macular degeneration. British Journal of Nutrition. 2013;110(02):289-300.

8.            Arnold C, Winter L, Fröhlich K, et al. Macular xanthophylls and ω-3 long-chain polyunsaturated fatty acids in age-related macular degeneration: a randomized trial. JAMA ophthalmology. 2013;131(5):564-572.

9.            Tian Y, Kijlstra A, Webers CAB, Berendschot TTJM. Lutein and Factor D: Two intriguing players in the field of age-related macular degeneration. Archives of biochemistry and biophysics. 2015.

10.          Liu R, Wang T, Zhang B, et al. Lutein and Zeaxanthin Supplementation and Association With Visual Function in Age-Related Macular Degeneration. Investigative ophthalmology & visual science. 2015;56(1):252-258.

11.          Margrain TH, Boulton M, Marshall J, Sliney DH. Do blue light filters confer protection against age-related macular degeneration? Progress in retinal and eye research. 2004;23(5):523-531.

Try this reference as a starting point...///mrl

LIM JI, FINE SL, KUES HA, JOHNSON MA.  Visual abnormalities associated with high-energy microwave exposure.  Retina.  1993;(3):….

 A 44-year-old man was accidentally exposed to high-energy microwave irradiation.  After resolution of facial erythema and iritis, he noted a foreign body sensation and blurring of vision.  Ophthalmoscopic examination showed bilateral, small hard drusen.  Ancillary tests were consistent with abnormal cone function.  Electroretinogram testing revealed a marked decrease in the flicker electroretinogram.  Results of D15 and Farnsworth Munsel Hue 100 color tests were abnormal.  Two years later, the patient's visual acuity was stable at 20/25 in both eyes; however, results of flicker electroretinogram test remain markedly decreased.

Cautioning you with the understanding that I have not done any work (research or clinical) on fusional demand for a long time.  However, if memory serves me right,,,  base out prism will increase fusional demand, especially if the point of regard is at near(i.e., within 1 meter of the individual).  Base in prism can be an assist to fusion, thus decreasing the requirement for fusional effort or demand.  Essentially, to improve reading comfort and clarity in low hyperopic patients regardless of their age, the prescribing of low plus power lenses (+0.50 D) with a half diopter of base in prism (0.50 BI) over each eye will endear most patients to you for life.  But, I could be wrong.....

The ETDRS (Early treatment of diabetic retinopathy study) severity scale is probably the most common standard for assessing severity of DR. These criteria are based on the interpretation of fundus photographs looking for the presence of features such as microaneurisms and neovascularisation (ETDRS Report 10, Ophthalmology 1991(98)). Clinically significant progression is often defined as a 2 or 3 step progression on this scale (e.g. Chaturvedi N, et al. Lancet. 2008;372(9647):1394-1402. doi:10.1016/S0140-6736(08)61412-9.)

The efficacy of photocoagulation was established by looking at incidence of visual acuity deterioration. The ETDRS visual acuity chart is often used to measure visual acuity although other methods exist. Clinical significance is often defined as a two line change on an ETDRS chart. Patients undergoing photocoagulation to resolve neo-vascularisation are often monitored using  fluorescein angiography, which allows visualisation of fluid leakage from blood vessels. Photocoagulation for macular edema is monitored using optical coherence tomography (OCT).

Studies investigating other treatments such as anti-VEGF drugs and neuroprotective agents have used other outcome measures such as the multifocal electroretinogram. (e.g. EUROCONDOR study https://clinicaltrials.gov/show/NCT01726075).

Im not familiar with such genes

John. You may like to read my article" Pathogenesis of arcuate field defects in glaucoma" and other articles on my website www.glaucomaparadigmshift.com  which may answer your questions.

Hello Vladimir,

One can hypothesize that the relationship exists between neurobehavioural  variables, including those related to memory, and endogenous circadian rhythmicity.  Blind people who are deprived of light perception have desynchronization of their biological rhythm to free running. Therefore, it is feasible that the loss of circadian rhythmicity and/or sleep homeostatic drive can result in disturbance of sleep architecture,  i.e., lack of sleep stages  believed to be necessary for memory consolidation, producing neurobehavioural deficits.

I do not recall studies that support these hypotheses, however.

Kind regards,

Tatyana

You could also use a Matlab implementation of the original method by Engbert & Kliegl (Engbert, R. and R. Kliegl (2003). "Microsaccades uncover the orientation of covert attention." Vision Res 43(9): 1035-45) by downloading it at http://kobi.nat.uni-magdeburg.de/edfImport or using the file I've attached. 

In previous, I have made work in corneal contour lines by estimating them from high resolution thermogarphical camera, It was very interested to deal with the k reading and biomechanics of cornea at the same time. I received a real signs for either future stability or ectopic change (ectesia). This made the close follow up especially for the KC cases more cleared and sensed w.r.t regular protocols.   

Most of the work with dynamic visual functions has been in typically developing young children. Patricia Sonkson assessed motion perception in young visually impaired children. The information may be imbedded in her general articles about visual impairment. Gordon Dutton has reported on selective ability to perceive motion in severely visually impaired (blindsight) see references below.

Philip, Swetha Sara ; Dutton, Gordon N. Identifying and characterising cerebral visual impairment in children: a review. Clinical and Experimental Optometry, 2014, Vol.97(3), pp.196-208

Boyle, Natalie J ; Jones, David H ; Hamilton, Ruth ; Spowart, Katherine M ; Dutton, Gordon N. Blindsight in children: does it exist and can it be used to help the child? Observations on a case series. Developmental Medicine & Child Neurology, 2005, Vol.47(10), pp.699-702

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.

Because thermal camera lenses captures far infrared waves (thermal waves) emitted from an object. Air can only conduct and cannot produce these waves.

@Marcel M. Lambrechts: This is getting more interesting, some of these are predominantly nocturnal other than diurnal; some depend heavily on acuity vision ( the eagle)  while other may require moderate visual acuity; those requiring moderate visual acuity may have other well developed senses to compensate for their visual deficit. If all the natural principles of use, disuse and excessive use apply, it only logic that "exaggerated" use should lead to vision expression of senescence and could vary among wildlife. Research is still need to concertize these assertions (hypothesis).

The ratio of rate of change of angle over angular size could perhaps do the job. Note that this ratio corresponds to the inverse of time-to-contact. Making this connection might lead you to choose another greek-alphabet letter to designate optical size: Since the seminal work of Lee (Perception, 1976), in the perception-action literature tau is generally associated with optical information about time-to-contact and its rate of change over time, tau-dot, with information about the sufficiency of current deceleration to avoid collision.

Be very careful when taking the eyes out. Sometimes just a little too much pressure and the retina will detach and no matter what you do after it is too late.

Thanks Dear

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.

You can use the nomogram found in:

Han DP and Thompson HS (1983) Nomograms for the Assessment of Farnsworth-Munsell 100-Hue Test Scores. Am Journal of Ophthalmology 95: 622–625

to determine if the values you obtained fall outside the normal ranges from their study.

There are a number of other articles that describe unilateral congenital loss:

Cox J. (1961) Unilateral color deficiency, congenital and acquired. J. opt. Soc. Am. 51, 992-999.

Sloan L. L. and Wollach L. (1948) A case of unilateral deuteranopia. J. opt. Soc. Am. 38, 502-509.

Graham C. H. and Hsia Y. (1959) Studies of color blindness: a unilaterally dichromatic subject. Proc. Nat. Acad. Sci. 15. 96-99.

MacLeod D. I. A. and Lennie P. (1974) A unilateral defect resembling deuteranopia. Mod.Prob.Ophthal.13, 130-134.

You might like to look at this latest PAC presentation. It's a bit long but it kind of tracks through OK.

Vision-Space: Self Reference Pt 4, painting phenomenal field, accessing the umwelt? http://youtu.be/g8rOhQhcl0A

Have you seen these articles that vary in the type of assessments used (direct observation to automated)?

Glen T. Prusky , Nazia M. Alam , Steven Beekman and Robert M. Douglas , Rapid Quantification of Adult and Developing Mouse Spatial Vision Using a Virtual Optomotor System Invest. Ophthalmol. Vis. Sci. December 2004 vol. 45 no. 12 4611-4616

Abdeljalil J1, Hamid M, Abdel-Mouttalib O, Stéphane R, Raymond R, Johan A, José S, Pierre C, Serge P. The optomotor response: a robust first-line visual screening method for mice. Vision Res. 2005 May;45(11):1439-46.

Kretschmer F, Kretschmer V, Kunze VP, Kretzberg J (2013) OMR-Arena: Automated Measurement and Stimulation System to Determine Mouse Visual Thresholds Based on Optomotor Responses. PLoS ONE 8(11): e78058.

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.

Those are impressive pictures, however these are the limitations I see with the method when it comes to measuring the ciliary muscle volume

1. Mn lights up the melanin in the ciliary epithelium, so we assume that the ciliary muscle is within the highlighted area.

2. the pictures show a continuity of the iris, ciliary body and choroid, obviously because all are lined by the pigmented layer. In order to measure the ciliary muscle volume, there needs to be a clear demarcation between the above structures, else there will be inconsistencies in temporal measurements.

In fact, UBM shows a similar structure too, the ciliary body is visualized well. However it is difficult to delineate the ciliary muscle, especially the posterior limit. We take the anterior limit as the scleral spur. Any more ideas addressing the above limitations are welcome.

Hi John,

About twelve years ago I threw in the garbages most of my books on visual perception but I kept six books and the second and third most important were the the two books of Arhneim

-Art and Visual Perception: A Psychology of the Creative Eye

-Visual Thinking

The most important : 

A treatise on painting ,Leonardo, da Vinci,

One of my favorite quote from Leonardo is (from memory):

<<The painter has to learn to paint two things: the human body and the human mind. >>

My interpretation is  that the art of painting is basically the art of discovering the way the visual system (the mind) perceive. Learning to paint is thus learning to paint the mind.  It is not an intellectual discovery but painting discovery that can translate in an enhanced capacity to paint sustained by an implicit visual knowledge.  IN the philosophy of science, Michael Polanyi has a theory of discovery based on making explicit implicit personal knowledge.  It has always been my way of learrning although I was not conscious of it.  But the more one become conscious of it and the more bold (some would say crazy) one become.  The more one instead of trying to learn with the intellect just let the body works the way it work and then the intellect cease to be the leader of the process but only what it evolved to be: a medium of communication, not a way to discover.

I agree with Murat, this is a very plausible explanation and reflects a direct reaction and damage on the site of efektor tissue ,instead of the most complicated reflex mechanism.

Isolation of proteoglycans is a multistep complex process. I isolated the PG of palmar fascia. If you want, I will send you the materials and methods section of my dissertation. unfortunately it is Polish.

I'm trying to size particles in the half micron and up range, with additional information about physical properties. 

Sure there is:

Michael Mrochen published something on that, but also Antonio Guirao, or Damien Gatinel and independently myself.

You can read from my publications These:

de Ortueta D, Arba Mosquera S. Mathematical properties of asphericity: a method to calculate with asphericities. J Refract Surg; 2008; 24: 119-121

Arbelaez MC, Vidal C, Arba Mosquera S. Clinical outcomes of corneal wavefront customized ablation strategies with SCHWIND CAM in LASIK treatments. Ophthalmic Physiol Opt;. 2009; 29: 487-496

Arba Mosquera S, de Ortueta D. Analysis of optimized profiles for ‘aberration-free’ refractive surgery. Ophthalmic Physiol Opt;. 2009; 29: 535-548

Arba-Mosquera S, Merayo-Lloves J, de Ortueta D.  Asphericity analysis using corneal wavefront and topographic meridional fits.  Journal of biomedical optics 2010;15(2):028003

Arba Mosquera S, de Ortueta D.  Correlation Among Ocular Spherical Aberration, Corneal Spherical Aberration, and Corneal Asphericity Before and After LASIK for Myopic Astigmatism with the SCHWIND Amaris Platform.  J Refract Surg. 2011 Jun;27(6):434-43

anyway the Equations you are asking for are:

Thanks Nabin, it would be good to collate some guidance from a series or professional body standards etc. Good project for a masters student or undergrad final year project.

I don't know. I am a "psychoacoustician" ( not "psychooptician" ).

Thank You of Your kind reply. My question didn´t tell all the dramatic story. There was earlier a keratitis (and now a corneal scar and thinning just beside the optical axis) and also there is another thinning place, so Avastin has not been used - neither local korticosteroids (contact lens). Vit "C" 5% drops - we don´t have any experience of that. Can it be used with contact lens? How effective for deep nv? How fast can the effect be seen? Any harmful effects possible? How about cross linking in case of a new keratitis??

no but a collegue recently discussed a report linking a daily 800 mg dose of Chromium Picolinate to improved Vitreal Syneresis.  I have been taking it myself for about one month and my subjective impression is that they are improving.

well wrong recognition of anterior or posterior surfaces, specially in pathologic corneas.

hyperreflections leading to overstimated pachymetries...

I can send you tomorrow an email with more details.

Yes, in children is relatively frequent. Recording EOG and routine Video-EEG and passive eye closure by technicians can help to discriminate between artifacts and anomalies.

Kammer, Lehr, & Kirschfeld (1999) found that a stimulus with high luminance contrast leads to increasingly shorter onset latencies and larger peak amplitudes of the N80, P1, and N130 visual ERP components when compared to low luminance contrast stimuli. As stimulus luminance increases, reaction time to the stimulus decreases (Hughes & Kelsey, 1984; Jaśkowski & Sobieralska, 2004; Kammer, Lehr, & Kirschfeld, 1999). The P1 visual ERP is likely generated by the extrastriate visual cortex (Heinze et al., 1994).

Hi Sandra,

This is an interesting case, thanks for sharing with us. From my point of view there are a couple of thing we could consider for the patient.

Cycloplegic Refraction, Lag of Accommodation and the overall systemic status. As you said there was a narrowing of I1e isopter which could signify some reduction in central sensitivity in which case automated VF could be more valuable.

There are few things that come to my mind by looking at your report:

Systemic Toxicity ( Ethambutol or any drug related toxicity) which might not be detected in early stages even with VEP or ERG.

Accommodative lag

Early Glaucoma (not too sure about this one though).

I hope that helps.

Regards,

Nabin