The dyslexic Elephant is coming into focus. Summary of today’s presentations at Oxford.

The dyslexic Elephant is coming into focus. Summary of today’s presentations at Oxford.

Yesterday concentrated on recent research into Auditory/phonological processing aspects of dyslexia and identification, prediction and prevention of dyslexia.

 Today, Friday concentrated on issues of Visual attention and neuroimaging beyond Phonology.

There were compelling research reports on the mechanisms and role of visual attention span in reading and dyslexia.

A continuing theme across the day looked at the directionality of the relationship between changes in Neural imaging information and reading experience.

The danger is consistently assuming that a correlation informs us about causality.

There has also been an emerging awareness of the role of the ventral visual stream in the reading process and the relationship between the dorsal visual stream and the ventral visual stream.

Visual attention issues were developed  at the levels of Crowding, eye movements and the visual effects of coloured filters in terms of the increasing or decreasing of blue light into the eye using the Oxford (DRT) yellow and blue glasses.  I now understand more about the dynamics in the use of these.  I had hoped that would happen!

The plasticity of the way the brain deals with sensory data is clear.  Interventions that change the relationship between ‘brain cortex’ areas were a continuing theme.

There is strong evidence that there are pre-existing relationships which can be ‘triggered’ into use or suppressed which to me strongly supports the response of dyslexic student’s visual systems to computer screen optimisation and our longitudinal tracking of the changes.

The group of us with a strong optometric/orthoptic component to our thinking were very aware that up to now this perspective on reading has not really been considered in the neurobiological studies and is probably limiting the understanding of the ‘ecology the mechanism.  There seemed to be a widely accepted view that this will change with collaboration between people at the symposium.

I will attempt more précis of the separate presentations after tomorrow.

Recent advances in dyslexia genetics; Animal models of dyslexia;

 Recent advances in dyslexia genetics; Animal models of dyslexia;

Day 1of the Oxford –Kobe symposium on the neurobiological basis of Dyslexia in Alphabetic, Syllabic and Logographic Scripts.

I said that I would try and prepare précis of what was presented at the symposium. That will be a hard task and will be my version of an abstract. I hope people will comment or suggest different perspectives if they do not seem to be correct or they have a different perspective

I will also give a summary of my thoughts at the conclusion of my ‘abstracts’

The presentations   11^th April. Today Thursday

( Only managed two of the eleven today, so far!)

Silvia Paracchini….Recent advances in dyslexia genetics.

There are major difficulties in investigating this area

Summarised as....

No precise biological markers. 

Cross linguistic heterogeneity

Huge time demands on collecting the data.

The very small predicted effect sizes and hence high sample sizes needed.

The complexity of the phenotype.

The heterogeneity of the ‘phenotypes’ creates a major problem for sample set size even if you start with a ‘large population.’

So the ongoing task is to recruit information from as large a population as possible.

They do actually identify a large population of genes that look a bit ‘guilty’ but each gene seems to be responsible/associated with a wide range of disorders.

One such study is extracting data from the Alspac project. http://www.bristol.ac.uk/alspac/. A study of children born in the 90’s. There is a problem though with the definition of dyslexia and the (?) link with IQ.  So an arbitrary decision is only to consider those who ‘are dyslexic with an IQ greater than 85.  The issue of what IQ is and whether it is dependent on whatever Dyslexia is a point that ought to be discussed.

Another area is the consideration of; Handedness and its genetic origin; especially since it seems to have entered the ‘orthodoxy’ of causation/association in dyslexia. But there appears still to be NO evidence of a genetic link or a co morbid link.

The reference is http://hmg.oxfordjournals.org/content/early/2010/11/03/hmg.ddq475  LH is more common in non-dyslexic people.

I actually think that it is more likely that a LH person in a RH world, will simply be more clumsy, and suffer some negative self-image problems at best that will affect academic a performance and behaviour le3ading to more likely being put forward for ‘labelling’!.

Oh dear what about cross dominance!

There appears to be co-morbidity between levels of ‘IQ’ and dyslexia in terms of associated genes. So should we really consider IQ in defining dyslexia?

……………………………………………………………….

Glenn Rosen….Animal Models of developmental dyslexia, anatomy behaviour and genetics.

This was really about the patterns of migration of neurones into the cortical regions of the brain of dyslexic people

There appears to be issues of auditory discrimination in ‘dyslexic people’ when they have ectopic neurone migrations.

There appears to be genetic evidence which supports this have a real biological basis.

Questions to answer…

Could you mimic this in a mouse?

Were there comparable effects on response or learning behaviour in dyslexic adults and ‘modified mice’?

They used specific strains of mice and create ‘ectopias on either the left or right side.

The next stage was to look at reward based learning in response to rapid tone exposure of different patterns. (Associated with magnocellular processing?).

The non-modified mice noticed/ responded to rapid tonal change.  The modified mice did not.

The cell migrations were induced in prenatal mice foetuses.

You could not do this ethically with humans!

Two techniques used.

One introduced phosphorescent plasmids to stem cells in the developing brain to ‘add a genetic component to ‘light up cell migrations’…  This appears to be supportive of the concept.

Another approach was to introduce genes as plasmids into mouse stem cells to knock out a particular gene.   The NMDA receptors   http://www.ncbi.nlm.nih.gov/books/NBK5287/ were used.   Suppression of synaptic activity.

This was a look at the possible use of therapeutic interventions.

This did not affect cell migration but simply slowed sown the learning process.

It was thought it would disrupt the development of left right cranial asymmetry but this does not appear to be moderated by a single gene... (We need to look at gene ecology I think)

It did disrupt microtubule formation and hence cilium development. This might be significant somewhere... As a wicked thought I started at this point to think about the cilial structure of a cone cell!)

Sorry end of evening!! More tomorrow!

What I want to understand from the Oxford-Kobe symposium

What I want to understand from the Oxford-Kobe symposium.

I want to understand my work in the context of recent research.

There is an  almost universality of the acceptance use of colour background by so many of the organisations working with and for dyslexic people including the two leading ones in the UK; The British Dyslexia Association (http://www.bdadyslexia.org.uk/about-dyslexia/further-information/eyes-and-dyslexia.html )and Dyslexia Action (http://dyslexiaaction.org.uk/news/now-available-dyslexia-action-shop-%E2%80%93-a4-coloured-overlays).In Canada  http://www.dyslexiaassociation.ca/francais/files/ladyslexieetlemilieudetravail.pdf)  in Germany (http://www.legasthenie-info.de/farblese.html)

My own work, and my colleagues has been developed by the use of measurement of reading performance, in terms of s reading speed , saccade length and fixation patterns, monocularly and binocularly as we change the colour background of text on a computer.

The graphs obtained are rather profound, and the benefits to individuals are considerable. I know that many of the people attending the Oxford-Kobe Symposium this week have themselves been through the protocols we developed.  I am also certain that very many of them will use a personalised, font size and font type, adjust the background colour and brightness of their computer screens.  I am also confident that many those who are present have been diagnosed as dyslexic or and Dyspraxic. I confidently hypothesise that a large proportion of them will adjust their computer screens to reduce their difficulty.

BUT….although one presentation is concerned with colour there is little research into the biology/mechanics behind this ‘phenomenon’/choice.

Friday 12:30

Joe Taylor (University of Oxford, UK) The physiological effects of coloured filters on attention

I sometimes think that this is because most research looks at the ‘developing’ of developmental dyslexia. It is very child-centred. With adults (grown –up children!)  the response to changing the appearance of the text seems very important. From my own experience before the age of 10 years there is not a strong effect.  Thus would appear to agree with what is found in terms of phonics interventions, really useful before the age of 10 but then decreasingly so.

A strange change in my thinking has been developed recently. I no longer think of my work as concerned with 'colour'; certainly not anything to do with the use of the word in art ,physics or perception.

When optimising the background for people, we measure the response to 

1. Screen brightness..Luminance.
2. Reduced red pixel brightness...Luminance
3. Reduced green pixel brightness... Luminance
4. Blue Pixel brightness...Luminance

We are looking at the gross effects of changing relative cone stimulation. This is biochemistry and then biophysics.

I can see connections with the ideas of Facoetti et al and Valdois, I think.  What controls the visual attention span and the speed of parallel processing of letters. So perhaps more research will concentrate on this area in the future, after all there are about seven times as many dyslexic people over the age of 10 than less than 10 years old!

Spoonerisms in Chinese and Japanese. Evidence of the role of visual processing?

Spoonerisms in Chinese and Japanese. Evidence of the role of visual processing?

The use of spoonerisms as an example of phonological processing independent of visual processing fascinates me.

Whenever I am asked to ‘do a spoonerism’ in English, I believe that I

1. Envisage the spelling
2. Swap the letters around
3. Say the spoonerism.

I visualise the letter/sound sequence.  This then depends on visual processing.

I would love to know what happens with a Chinese/mandarin reader/speaker or a Japanese does when asked to ‘do a spoonerism’.

http://www.italki.com/question/74335   

This is a URL to a discussion on the topic. Have a look.

It is really important in the question of the role of visual processing in dyslexia.

If it is not possible to do a spoonerism in an ideographic language, we should stop using it as evidence of a phonological processing indicator independent of visual processing.

Is there anyone who could tell me before the Oxford-Kobe conference?

What proportion of adults who are dyslexic would respond to visual intervention?

What proportion of adults who are dyslexic would respond to visual intervention?

Data from Bradford University UK

We are about to hear from the Oxford-Kobe symposium which will include reports on the visual processing aspects of dyslexia as well as phonological processing.

In the last few years there have been few accepted studies in the area of visual interventions.

One report that came out was the outcomes by a study by Jim Gilchrist and others at Bradford University School of Optometry and Vision Science in the UK...

Gilchrist and his colleagues have looked at visual stress problems experienced by Dyslexic undergraduates at Bradford University.

There were 52 dyslexic students referred to the clinic at Bradford Department of Optometry and vision Science. They were taken through specific protocols.

The idea was to identify any visual dysfunctions/ stress that could be an issue for the students and contribute to their problems with text.

As Vision Scientists, they wished to distinguish between reading related visual stress

Originating in Occulomotor / optometric / ophthalmic issues.

Visual stress originating in visual processing problems associated with the pattern or the spatial characteristics of the task, From now on referred to as PRVS.

Occulomotor / optometric / ophthalmic .dysfunction

Did they experience visual stress associated with an optometric dysfunction?

59% of the students had no evidence of any accommodation or vergence problems.

Vergence problems are problems which can be measured as possible faults in the way the muscles maintain stable binocular vision. Usually the intervention is by the use of prisms or exercises optometric or orthoptic Vision therapy.

This component was looking at general uncorrected optometric dysfunction. The vergence dysfunction would have, I assume have been considered at near.

As you can see around 60% showed no evidence of problems with any evidence from this study as possibly having any origin in this area.

 Did they exhibit indicators of Pattern Related Visual stress?  (The PRVS study did not I believe include a reading speed/RAN measure which I would argue is a key indicator.)

Two thirds showed evidence of Pattern related Visual stress...  Colour mediated.

The next question is whether those experiencing PRVS might also benefit from optometric intervention.

Of those who experienced PRVS, 31% also experienced visual stress originating in accommodation (uncorrected focussing problems) and vergence problems. That is 20% of the students.

69% of the students experiencing PRVS had no issues at all which would benefit from optometric intervention.  That is 45% of all the referred students.

A further 20% of the students showed no signs of any issues associated with optometric intervention.

15 % of the referred students showed any evidence of any dysfunction, either PRVS or optometric in origin.  This suggests that their phonological difficulties were totally phonological in origin with no visual component.

The statistics above suggest a moderate relationship between accommodation and vergence dysfunction. This would be expected in terms of the tendency to suppress an eye which is giving a weaker set of visual data from poor focussing.

Importantly it suggests that the PRVS dysfunction is NOT an ophthalmic originating issue but is separate and by implication should be subject to separate intervention. There is a post on the blog which covers two case studies which attempt to quantify the benefits from two separate but parallel interventions .

This would be in agreement with a link to the spatial characteristics of the retina and visual system.

. 

Foveal diameter.

Crowding effects associated with the centre –surround system for edge detection. The diameter of these units being associated with the ratio of red to green sensitive cells which varies from person to person.

Crowding effects associated with the variation in cone cell diameter between people. Some would suggest an inverse relationship between the central foveal cone cells and the diameter of the fovea itself.

Bigger fovea…

 Probably big visual attention span more characters parallel processed at a time

Reduced foveal crowding

Increased perceptual span... more characters per fixation.

Longer saccades

Possible weaknesses in the study

This study can be looked at critically in terms of what definitions and protocols were applied

 For example…

Were the students seen by the department representative of the whole body of dyslexic students at Bradford?

What was the actual definition of PRVS?

It can be argued that the symptoms of PRVS are not necessarily perceived by the ‘person’ it could simply put extra demand on the central executive reducing phonological output in terms of speed and ‘quality’ (prosody/intonation)

What I do know is that the academics, that ran this study, are of the highest calibre and as such the data should not be ignored.

What was reported in a lecture by Jim Gilchrist, was also that many of those who did not get identified as having PRVS, by the selection criteria, nevertheless did respond positively to the use of colour chosen using the Intuitive overlay forced choice selection process. Although this process itself is from a very limited palette.  But no one could understand why.

The idea that several of those not identified as having (the symptoms) of visual stress benefitted from the use of colour can be used to question whether the symptoms of PRVS should be the criteria which limit access to interventions.

If we look instead at the work of Valdois and Facoetti on visual span and crowding and hypothesise that any restriction on visual attention span will decrease the phonological output.

Whether that restriction be from

Crowding.

Focussing problems

Edge detection processing speed

Vergence difficulties... binocular problems

Reducing working pigment density in the cone cells.

Increasing the number of letters processed between saccades

Restriction in visual attention span and reduced edge detection processing will give rise to the following changes which will further limit both visual and phonological performance probably the basis of the reading stamina difficulties virtually universal amongst dyslexic adults.

decrease the lengths of the saccades

Increase the occulomotor muscle tone, decreasing ocular motility.

increase the demand on working memory ( central executive)

increase the difficulties of blending phonemes

slow down the development of automaticity

Reduce the cumulative total reading experience.

Binocular dysfunction

A way of looking at the effects of binocular dysfunction on visual processing speed would be to compare rapid automatic naming speeds under the following three conditions.

Binocular

Monocular right eye … left eye occluded

Monocular right eye occluded.

When I have done this with dyslexic individuals, it is very rare that binocular reading gives rise to greater reading speeds than both monocular.

Usually either the right eye or the left eye gives the greatest reading speed.

Binocularly the reading speed is more often the same as the left or right monocular speed. Sometimes but not often it is slower than either.

When the computer screen has been optimised, then usually this is faster than either eye monocularly.

This suggests that the eyes are then acting synergistically.

Binocularity and visual processing speed.

The binocular instability hypothesis that seems central to the magnocellular deficit hypothesis, suggests that by occluding one eye the reading should be faster, more effective.

But very few dyslexic undergraduates get rid of their ‘visual stresses by occlusion.  Those who can get rid of the visual stress by occlusion, have nearly always been using this already as a strategy to extend their reading stamina and decrease the discomfort.

The dyslexic undergraduates (adults) who report instability of the text usually report it still when viewing text monocularly. The instability has to be then associated with spatial and temporal visual data being collected by the viewing eye. This implies then that the dynamics of image movement on the retina during fixation is important in the edge detection process. When I was participating in a pilot study of crowding, where the image was projected for 50ms time periods I was very aware of ‘seeing’ several images during the exposure as my eye moved extensively within the 50ms period. During a fixation visual data is being collected for up to 200 mS.

When you look at the binocular eyetraces for these people there is usually clear evidence that the visual system is already, subliminally suppressing the data from one eye anyway.

You can see this in some of the other posts for example. http://tinyurl.com/cceec6h

You can calculate the optimal screen settings for a person, monocularly and then apply the settings binocularly. This implies that what is being measured is associated with the biology of a single eye, rather than binocular aspects of the system.

The way the eye movements of both eyes are affected and the synergistic reading performance benefit when reading binocularly could be the basis of further conjecture about the system that is operating.

As a final point; when I have looked at reading performance of fluent readers, the binocular reading performance exceeds monocular performance. In addition when reading English (left to right) the left eye appears to be landing in front of the right eye. I have only ever looked at a fluent bilingual person once. That person was bilingual in Urdu (right to left) and English.  Whichever text was being read the left eye was always in front. This concurs with Gadi Geiger’s work at MIT on visual attention from a ‘pre-computer age. I had a great discussion in Boston, Mas. on this issue ‘earlier this century’.

Fixation disparity

Work with Arnold Wilkins et al, looking at the reading performance of year 7 (6 in the USA) and measuring accommodation, orthoptic and PRVS’ showed only one correlate with default reading performance across the group, fixation disparity.

The fixation disparity, it would seem needs to exist to be a fluent reader!  If there is no disparity, then the reading performance is lower, if it is too high the reading performance is lower. There wo0uld appear to be an optimal fixation disparity for a person.

This would make sense in terms of the way many dyslexic people, but not all are gifted graphically. There seems to be an excess of dyslexic students studying architecture.

It may also be one of the reasons behind why converting text into graphics, by such means as Mind mapping, is reported as being a particularly useful study aid for dyslexic students.

What the use of a binocular eyetracker tells us though is that the amount of binocular disparity employed by a person’s visual system is to some extent task responsive.  Again this would concur with Geiger’s research. The disparity in fluent readers is directional depending on the brains identification of the reading direction needed by the language.

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Cogan’s Occulomotor Apraxia, dyspraxia, dyslexia, binocular instability... a case study

Cogan’s Occulomotor Apraxia, dyspraxia, dyslexia, binocular instability... a case study

Abstract

A study of visual intervention, to improve reading performance (phonological  processing) of a young man originally identified having congenital occulomotor apraxia (COA).COA interferes with visual search mechanisms by restricting the formation of saccadic eye movement, He was then identified as being Dyspraxic and later as he entered Higher education he was assessed for dyslexia and was identified as dyslexic.

This intervention took about 1 hour and application of the findings appears to give rise to a measurable increase in phonological processing speed of 21%...

The testing included recording and measurement of his eye movements, which are subliminal at different stages.

The control of saccades and fixations are managed by the cerebellum in response to visual processing data and in turn feedback to the edge detection data which is a product of the controlled saccades and fixations. This can be considered in the context of the work on the relationship between cerebellum functioning and dyslexia as centred in the UK at the University of Sheffield led by Nicholson and Fawcett. It can also be considered in the context of the ideas on magnocellular deficit and dyslexia developed in UK by John Stein et al at Oxford with its ideas on binocular instability which is considered to be dependent on cerebellar function.

This week I had the privilege of working with a young man (‘A’ )who was diagnosed in his first year of life as having ‘Cogan’s occulomotor apraxia’ ( Google it for more information).

This is a condition which is congenital and is linked with the initiation of saccades; the rapid eye movements which redirect the eyes to new objects of attention. In the graphs on eye movement in previous blogs these are the vertical lines on the graph as the eyes move from one word to the next...Or the end of one line to the beginning of the next line.

It is not that the eyes cannot do these movements; it is that there appears to be a fault in the mechanism which means that they sometimes do and sometimes do not occur.

When using a binocular eyetracker with many dyslexic adults, it is quite common for one of the eyes not to saccade when reading in a default computer screen environment.

When A was young he was diagnosed as being Dyspraxic, which is defined below.

Developmental dyspraxia is an impairment or immaturity of the organisation of movement. It is an immaturity in the way that the brain processes information, which results in messages not being properly or fully transmitted. The term dyspraxia comes from the word praxis, which means 'doing, acting'. Dyspraxia affects the planning of what to do and how to do it. It is associated with problems of perception, language and thought.

A typically broad definition, but it was the origin, in a way, of a great deal of research into Dyslexia at Sheffield University.  Rod Nicholson and Angela Fawcett’s work showed a statistical relationship between muscle tone management and the reading difficulties associated with Dyslexia. This led to intervention work concerned with attempts to train the Cerebellum, which is the brain’s centre for muscle tone management and coordination.  At one extreme it led to the throwing bean bags in the air, wobble boards, to try and remediate ‘the problem’. It also led to the overlap in the protocols for the identification of people with dyslexia and dyspraxia and much confusion.

Children with COA need a proactive interaction to mitigate the effects, such as speech therapy and hand eye coordination excercises. There are strategies which the person develops to initiate saccades, such as head thrust. Brief sideways jerking of the head) As such with appropriate support the effects of the apraxia become less and less disabling as the person goes through their second and third decade.

In the case of A, a remaining issue is his dyslexic characteristic. My task was to investigate what was really happening visually and to find out if his reading performance (phonological processing output!) could be improved by adjusting the visual processing input.

Stage 1

Is there any history of ophthalmic problems?

Visits to opticians suggest that there are no focussing problems that can be dealt with by ophthalmic intervention. .. Vision is normal.  A relatively quick check by myself confirmed this to be the case.

His job is that of a graphic artist. Precise vision is needed for this.  An example of his work is given below. (Google Jakgibberish for more examples)

Stage 2.

Find out about his eye movement management in non reading activities.

The graph below shows A’s eye movements during normal visual activity; looking around the room we were sitting in...

Normally you would expect the two eye traces to be matched with distinct, synchronised saccades and fixations.  The left eye (the red line) does show a few saccades, I can pick out six by the right eye (blue line). There are no clear fixations by the right eye and the right eye goes into a nystagmus occasionally which interrupts the work of the left eye, pulling it sideways.  

Head movements would show up as a sloping graph, but if both eyes were ‘linked together normally the angle of the slope would be the same for both eyes. This is not happening here.

Stage 3... Finding out what happens in default reading conditions, the default is a default (12) font with a white background.

A’s left eye, is moving in a rational way typical of many readers with clear saccades and fixations, but with many regressions . His right eye meanwhile, has been turned in towards his nose (to the left) and is no longer looking towards the text. For his right eye there are no clear saccades except at the ends of lines.

The rest of the time, the movements of his ‘reading left eye’ are not influencing/ controlling his right eye. Although in the third and fourth line, the gradual upward movement during each line suggests that there is some linkage.  You can see three bursts of nystagmus type activity as well.

We can conclude here that there is no initiation of saccades, no ‘visual search’, no attention originating, fixations associated with the right eye, which is a functioning eye.  A decision has been made by his visual system to suppress it! In biological terms this implies that he is getting better visual data, by using visual data from only one eye; his left onewhatever the visual activity.

Stage 4. Get a measurement of reading performance.

Using the same Oral reading fluency test that has been used with over 12,000 adults, A read off a computer screen with a font 12 and ‘white background’

Default Oral reading fluency…….105 wpm

The reading style was stocatal; individual words were being read in syllables; limited blending.

The mean reading speed for this text by dyslexic undergraduates is 138 wpm. For non dyslexic undergraduates it is 184 wpm.  I can quote Standard deviations but not here.

At the conclusion we will measure Oral reading fluency (a measure of phonological processing) with an equivalent text, using whatever optimal settings we identify.

Stage 5..Find out if font size influences reading performance.

 This was undertaken binocularly. The data was unclear. There was a hint that a larger font than default 12 might be useful and it was decided to use

font 16 point for the next stage.

For many dyslexic people there is a clear mathematical relationship between font size and reading performance. See the other posts on this blog.

At this point it became clear that testing A binocularly was going to be too stressful. The screen optimisation continued monocularly using only his ‘good’ left eye. His right eye was covered. This meant that it would still move dependent only on visual data collected by his left eye,

Stage 6... Find out if screen brightness influenced reading performance.

There was a linear relationship between screen brightness and reading performance. Reduction of overall brightness gives rise to a slower reading output. 

For the majority of dyslexic undergraduates the screen brightness needs to be reduced.

Stage 5. Finding out if reading performance was affected by red or green pixel brightness.

A did respond to changing the green pixel brightness but it was a far smaller effect.

Stage 6...Response of reading performance to Blue pixel brightness

There was no response to changing the blue pixel brightness... The magnocellular difference model of developmental dyslexia implies that a response would be expected. But there was none.

Actually very few dyslexic undergraduate respond significantly to changes in blue pixel brightness.

Stage 7...Checking Oral reading performance with the identified screen settings.

This was using a font 16 and the following background screen settings.

Oral reading performance…..127 wpm.

In addition the reading ‘style’ was more fluent, whole word enunciation now being with a clearly prosodic component.

This is a   21% measurable increase in performance. 

I have not yet found a way to quantify Prosodic performance, but I am following the development of The PRAAT methodology in this area. (Please google this if you are interested.)

Stage 8... Finding out how A’s eyes were behaving in the new conditions.

This was not quite what I expected.  But in retrospect his right eye had been covered virtually continuously for about 30 minutes! By the end of reading the text both eyes were starting to work together, this can be seen especially in the third and fourth line.   But there are still the quite distinctive nystagmus zones when the trigger mechanism is breaking down.

A series of readings were then done reading monocularly. From previous experience A was asked to read for a while using only his  right eye and the optimal conditions. This is an attempt to get the ‘brain’used to a new capability.

Left eye covered, using only his right (Poor?) eye.

The interesting thing here is that with the optimal background and with no data coming into his left eye, the data being collected by the right eye was able to enable the control of the movement of his left eye .

Right eye covered, using only his left eye.

With his right eye covered, the data being collected by the left eye, His right eye moved in time with the controlling left eye, although it did not show the crispest saccades and fixations But the fixation disparity (distance between the attention points) of the two eyes was more erratic than when it was the right controlling the left.

Finally an eyetrace was undertaken binocularly with a small font (10 point) such that more data was landing in the foveal area of the retina...

The two eyes are now yoked together, but the font probably too small for the highest quality of fixation.

The graph below shows detail over a 2 second period, which is typical of the entire graph above. Both eyes show clear yoked saccades and fixations, but the right eye shows slight fixation instability. But this is typical of many good readers.

The slight right eye fixation instability most likely would be solved with a slightly larger font.

We will now wait for a while for A to make use of his settings in reading/inputting computer activity during which time it is likely (I think) that there will be a change in the innervations (how many motor end plates are used in the muscle fibres) and control of the core muscle fibres In the occulomotor muscles of his right eye, which are responsible for managing the actual fixations. (This is a new experience for his eye muscles!)

If you are interested in histology and muscle fibre design I commend you to look at them literature ion this area.  Occulomotor muscles are I believe their own class. They are not cardiac, smooth or skeletal in design. They have a fascinating histology and physiology of their own; befitting their role in precise strategic visual data collection.

Wait for the next thrilling instalment in the control of phonological output by the visual processing system!

I look forward to comments and questions.