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Dr Kerry Hempenstall, Senior Industry Fellow, School of Education, RMIT University, Melbourne, Australia.

First published Nov 15, 2013. Updated 28/10/2017

My blogs can be viewed on-line or downloaded as a Word file or PDF at https://www.dropbox.com/sh/olxpifutwcgvg8j/AABU8YNr4ZxiXPXzvHrrirR8a?dl=0


 

It sounds like a no brainer. You need vision to read. If reading isn’t happening, surely it could be a vision problem? In like vein, you need a hand to write. However, if you can’t write, is it necessarily a hand problem? Well, neither conclusion necessarily follows. Perhaps you’ve simply never been taught to write, or you have some disability, such as a significant intellectual disability. So, a hand is a necessary condition for handwriting, but it is not a sufficient condition. Similarly, vision may be a necessary condition for reading, but it is not a sufficient condition. If there is a problem with reading, it sounds at least plausible that vision may be the source of the problem. Indeed, extreme levels of visual disability can preclude conventional reading. But, what about those struggling with reading whose visual problems are adequately corrected with optometric lenses and those whose corrected vision is considered within the normal range by optometric assessment? Could there be some other vision problem not assessed or detected by conventional optometry?

First, a comment on the history of attempts to find underlying processes to explain and ameliorate reading problems. The history of education is littered with claims of resolving educational problems by improving underlying processes presumed to be important, for example, visual perception, balance, primitive reflexes, auditory processing speed, perceptual motor skill, brain patterns, short term memory,and so on. Generally speaking, these endeavours have not been rewarded (Arter & Jenkins, 1979). In some cases, the interventions didn’t improve the underlying processes; in some, they did improve the underlying processes but had no impact on reading skill. In others, there were difficulties in accurately assessing the processes and/or teaching them effectively. It has been a perennial search for this holy grail - remove the obstacle to learning and attainment will then occur. The normal curve of attainment will be beneficially disrupted. If you could achieve that state, then effective teaching of reading would become less crucial for those who struggle. What a boon for those educators who continue to believe that reading is a natural phenomenon.

However, this underlying process approach has so far represented an educational cul de sac. There were intractable problems in each of: ascertaining precisely what these core fundamental skills were, then accurately assessing them, and then teaching them effectively.

“Process training has always made the phoenix look like a bedraggled sparrow. You cannot kill it. It simply bides its time in exile after being dislodged by one of history's periodic attacks upon it and then returns, wearing disguises or carrying new noms de plum, as it were, but consisting of the same old ideas, doing business much in the same old ways” (Mann, 1979, p. 539).

The perceptual-motor deficit theory was very strong in the 1960’s and 1970’s, and an industry of intervention programs erupted. Though some children became adept at drawing lines accurately within parallel boundaries, there was no reliable impact on reading progress (Arter & Jenkins, 1979). In fact the meta-analysis performed by Kavale and Forness (1985) produced an overall effect size for perceptual-motor training of 0.08, which is considered a small effect (Cohen, 1988). What was not readily apparent at that time was that learning to read was the most effective way to master many of those skills – hence valuable instructional time was better spent on the target task. “If the goal is for children to learn a particular skill (like reading), it is more efficient to teach it directly than to expect it to transfer from other learning” (Singer & Balow, 1981, p. 107). Kavale’s (1990) summary of research into direct instruction concluded that the direct instruction is five to ten times more effective for struggling students than are practices aimed at altering unobservable learning processes such as perception.

More recently, Fuchs, Hale, and Kearns (2011) reviewed the evidence generally for such cognitively focussed aptitude-treatment interactions, asking the question: “Among low-performing students, do cognitively focused interventions promote greater academic growth than business-as-usual instruction?”(p.101). Their conclusions?

“There was no evidence for the notion that when a treatment is matched to a cognitive deficit it produces better effects … Scientific evidence does not justify practitioners’ use of cognitively focused instruction to accelerate the academic progress of low-performing children with or without apparent cognitive deficits and an SLD label. At the same time, research does not support “shutting the door” on the possibility that cognitively focused interventions may eventually prove useful to chronically nonresponsive students in rigorous efficacy trials” (p.101-102).

As Fuchs et al. point out, the history of failure of underlying processing approaches doesn’t mean that the next big thing won’t work. It simply means that an array of strong empirical, independent evidence is necessary - because to back yet another lame horse has serious implications for struggling students. Even if the interventions are non-harmful, there is an opportunity-cost for students (and often a financial cost to parents), and a residue of negative emotion for both parents and child when the approach has no discernible effect.

There are two major areas of interest in judging whether an approach has merit. The first is to consider whether the theoretical constructs behind the approach are consistent with what is known about a given educational issue. Is there face validity? This is not a perfect pass-fail test, as occasionally a new paradigm makes earlier theories redundant. However, that is rare. In the case of the various approaches that implicate vision problems as the cause of reading problems, one would acknowledge that they sound plausible (to a greater or lesser degree). In fact, the early history of reading research emphasised visual over language-based causation.

The second criterion goes beyond the theoretical relevance, and is the issue of whether addressing the reading problem by intervening at the visual level has a positive impact. So, it is then an empirical issue, rather than a purely theoretical one.

The reading process requires some quite tricky eye movements. Rather than the eyes moving smoothly across a line of print, they travel in little staccato-like jerks called saccades (covering about 8 letter spaces usually), followed by brief fixations (250 ms) during which we gain visual information. These figures are not invariant, and may vary markedly with differences in text difficulty. It’s easy to envisage problems occurring for some students in this complex visuo-perceptual coordination task, not to mention the impact of the complexity involved in fluent orthographic processing.

Saccades challenge the visual system by producing abrupt changes in the retinal stimulus as the visual field image moves over the retina. Our brain ignores the retinal motion and compensates for the repositioning of gaze, generating perceptual constancy. Psychophysical studies in humans and electrophysiological data in primates indicate that, although not perceived, visual stimulation during saccades continues to be processed in the visual system, influencing processes at refixation (Ibbotson & Cloherty, 2009). The extent to which retinal motion modulates word processing in reading remains unknown. In addition to such visual effects, central mechanisms mediated by brain regions that control eye movements and attention alter visual processing after saccades. In primates, thalamic recordings typically reveal transsaccadic suppression followed by enhancement (Reppas et al., 2002; Royal et al., 2006). This pattern has been identified in a number of cortical visual areas (Ibbotson and Krekelberg, 2011), although results remain variable at the single-neuron level and controversial (Wurtz, 1969; DiCarlo and Maunsell, 2000; Gawne and Martin, 2002; Ibbotson et al., 2008; MacEvoy et al., 2008). Central suppression, reported from 100 ms before onset to 50 ms after the end of saccades, is thought to decrease the sensation of image motion in active vision (Burr et al., 1994; Ross et al., 2001). Postsaccadic facilitation lasting 200–400 ms presumably amplifies visual sensitivity at fixation (Ibbotson and Cloherty, 2009). In the absence of behavioral measures it is not known, however, if and how these opposite neural effects, individually or together, alter perception. Further, there is as yet no evidence that central postsaccadic mechanisms modulate word processing” (Temereanca et al., 2012, p.4482).

So, it’s quite a challenge to learn to read. Making it tougher is that, as opposed to the relative ease with which oral language develops, evolution hasn’t provided us with a dedicated brain module for reading – “rather (it is) the result of a neuronal recycling from an area of the brain that evolution has dedicated to the recognition of certain forms, notably intersections of straight lines or curves’ (Quercia, Feiss, & Michel, 2013, p., 873).

“Reading is certainly the most complex oculomotor activity that modern humans use daily. The processing involved is classically separated into lower and higher levels. The first corresponds to the different steps involved in the ocular capture of the word’s image, which is the start of cerebral analysis in the occipital cortex. The second represents the different cognitive phenomena that permit the identification of and then represent and make sense of the word just read. The constant interdependence between these phenomena, notably during the oculomotor phase of reading, makes this separation artificial” (Quercia, Feiss, & Michel, 2013, p. 869)

Research has noted that there are numerous visual skills in which a proportion of students diagnosed with dyslexia have been shown to be deficient. For example, Quercia,Feiss, and Michel (2013) list a number of them:

“Numerous scientific studies have also documented the presence of eye movement anomalies and deficits of perception of low contrast, low spatial frequency, and high frequency temporal visual information in dyslexics. Anomalies of visual attention with short visual attention spans have also been demonstrated in a large number of cases. Spatial orientation is also affected in dyslexics who manifest a preference for spatial attention to the right. This asymmetry may be so pronounced that it leads to a veritable neglect of space on the left side. The evaluation of treatments proposed to dyslexics whether speech or oriented towards the visual anomalies remains fragmentary” (Quercia, Feiss, & Michel, 2013, p.869).

Vellutino and Fletcher (2005) also described some low level visual deficits, in particular involving the magnocellular system:

“Difficulties in learning to read have also been attributed to low-level visual deficits, in particular, visual tracking problems caused by oculomotor deficiencies (Getman, 1985); visual masking effects caused by a hypothesized deficit in the “transient visual system” (Badcock & Lovegrove, 1981; Breitmeyer, 1989; Lovegrove, Martin, & Slaghuis, 1986; Stein, 2001); and abnormalities in visual motion perception (Eden et al., 1996). Moreover, transient system and motion perception deficits have both been linked to dysfunction in the magnocellular visual subsystem. The magnocellular subsystem is one of two parallel components of the visual system, the other being the parvocellular system. The magnocellular system consists of large neurons that are sensitive to movement and rapid changes in the visual field. It is often called the “transient system,” insofar as it is presumed to be responsible for suppressing the visual trace that normally persists for a short duration (250 milliseconds) after a visual stimulus has disappeared. The parvocellular system consists of densely packed, small neurons that are sensitive to color and fine spatial details. In reading, the parvocellular system is believed to be operative during eye fixations and the magnocellular (transient) system is believed to be operative during saccadic movements of the eyes” (p.366).

Among other deficits that have been proposed as important are visual attention span (Bosse, Tainturier, & Valdois, 2007), and sluggish attentional shifting (Lallier, Donnadieu, Berger, & Valdois, 2010).

Such a list of apparent deficits sounds compelling; however, just because they co-occur doesn’t demonstrate that one causes the other. So, a demonstrated relationship between two events may not be a causal one, or it may be causal but not in the direction expected. Additionally, it is possible that both the correlated spheres are caused by a third variable. There has been an analogous finding in medicine in relation to back pain. Imaging techniques (MRI, CT, X-ray, etc.) are often recommended by doctors endeavouring to treat back pain, a condition that most people experience to some degree at some time in their life. The images will often show problems with the structure of the back, and doctors may recommend various therapies to treat the apparent site of the back problem. However, the empirical evidence has found that treating the apparent problem is not superior to no treatment at all. So, intrusive operations can be performed with no positive impact on back pain, but often reduced mobility is a consequence. Most (not all) back conditions resolve themselves eventually anyway, whether the patient rests or simply remains active. Why should this be so? When studies were performed in which people with no back pain were provided with imaging, the results were surprising. There were wonky looking backs among the symptom-free population too. This suggests that the structural problems shown in the images were incidental to the back pain, not central or necessarily causal. They appeared to be a likely source of the distress, but weren’t, because resolving the structural issue didn’t fix the problem.

In a similar manner, the presence of a range of visual problems among struggling readers does not of itself mean that they are causes of reading problems. Although significant visual differences have been found between dyslexic and normally developing readers, only about 30% of dyslexics are so affected (Ramus et al., 2003). As with the back pain analogy, one can find visual processing deficits in skilled readers too, which indicates that a visual processing deficit is not a defining characteristic of dyslexia. The identified oculomotor anomalies are considered by the majority of researchers to be secondary to difficulties of cognitive analysis of language (Quercia, Feiss, & Michel, 2013).

"Although it may be accurate that many students with LD have underlying neurological and/or processing disorders, researchers and educators have been singularly unsuccessful at reliably identifying these difficulties and designing specific treatments to remediate them. … However, it is important to note that despite lack of support for process identification and treatment models, they continue to persist." (Vaughn & Linan-Thompson, 2003, p. 141).

Another finding regarding dyslexic readers’ eye movements was that they were subject to a higher rate of regressive eye movements than good readers. That is, their focus frequently shifted back to the left along the line instead of the right. It accompanies, therefore it causes! The product of this faulty logic was that a lot of children wasted potential instructional time with eye exercises. "Reading is visual, isn't it - this child has a visual problem; therefore, we should fix the visual problem in order to resolve the reading problem". The trouble was that regressive eye movements do not cause reading problems - they are a consequence of reading problems. If you fix the reading problem through effectively teaching the alphabetic concept and provide adequate opportunities for practice, lo and behold, the regressive eye problems go away.

On the other hand, even if such processing skills are not a significant cause of reading problems, there could be a role for visual skill assessment as early predictors of reading problems. Assuming that these skills can be assessed in quite young children (prior to the introduction of reading instruction), it may be possible to discover and intervene earlier than occurs at present – after reading failure has occurred (Facoetti et al., 2010). The visual attention task used in one study employed tests that asked children to pick out specific symbols in the presence of visual distractions (Franceschini, Gori, Ruffino, Pedrolli, & Facoetti, 2012).

Stop Press!

A new 2017 study makes new visual claims:

A recent paper (Oct 2017) claims to have found that the true cause of dyslexia is actually visual - not deficits in phonology, vocabulary, syntax, and other components of spoken language. Yes, really. I know – we’ve heard this claim in the past. This new study (Left–right asymmetry of the Maxwell spot centroids in adults without and with dyslexia) has received a deal of breathless media reporting. However, a scathing review in a post entitled Blue Cell Dyslexia by literacy research expert Mark Seidenberg (see at http://languagelog.ldc.upenn.edu/nll/?p=35144&utm_source=dlvr.it&utm_medium=twitter) casts serious doubt about the worth of the study. It documents numerous flaws that he argues should have led to the paper’s exclusion from publication in a serious journal. For example the confusing of a correlation with causation. See for yourself. The paper in question is:

Le Floch, A., & Ropars, G. (2017). Left–right asymmetry of the Maxwell spot centroids in adults without and with dyslexia. Proc. R. Soc. B., 284(20171380). 1-10. Retrieved from http://rspb.royalsocietypublishing.org/content/284/1865/20171380

http://m.kfvs12.com/kfvs12/db_383321/contentdetail.htm?full=true&contentguid=YSQo6EAA&pn&ps#display

Other experts, authors join in

Jack Fletcher, chair of the Department of Psychology at the University of Houston, echoed Siedenberg’s criticisms.

“This study is like most visual theories of dyslexia – it manufactures a theory of reading to accommodate a visual finding,” he said.

The researchers “confuse associations with causality,” he said. "Dyslexia is a dysfunction of the brain, not what the eyes do to the brain," he said. “What they found does not explain the reading problem,” he said. "Further testing would have revealed other differences between dyslexics and non-dyslexics." Most of the research on connections between image reversals and dyslexia is dated, he said. Much of it dates to the 1970s and 1980s. Image reversal is not a cause for dyslexia, Fletcher said - and finding research that contradicted their findings should not have been hard to find for the French scientists.

“Relationships between letter reversals and dyslexia has been overwhelmed by the contradictory articles they don’t cite,” he said. “That’s just bad science.” Joe Elliott of the University of Durham in England is the co-author of “The Dyslexia Debate," which compares past and present research on the subject and compares reading difficulties caused by dyslexia and other learning disabilities. “The reality is that theories of all kinds are always coming through, but there never seems to be an intervention that is known to work,” Elliott said. “I have been persuaded several times by vision specialists in the past (whose area is a mystery to most of us), but promises that this is the big explanation for reading difficulty/dyslexia always turn to dust.”

Copyright 2017 Raycom News Network. All rights reserved.


So, what are researchers reporting about the assertion of the centrality of vision problems in reading difficulty?


“Reading disability research has also established that reading difficulties are not caused by visual deficits of the types most often proposed over the years. Contrary to popular belief, impaired readers do not see letters and words in reverse, nor do they suffer from inherent spatial confusion or other visual anomalies of the types proposed in the early literature. More recent research provides suggestive evidence that some poor readers may suffer from low-level sensory deficits in both the visual and auditory spheres, but the evidence is inconclusive, and in, some instances, equivocal and controversial. Moreover, no causal relationships have been established between such deficits and difficulties in learning to read”.

Vellutino, F.R., Fletcher, J.M., Snowling, M.J., & Scanlon, D.M. (2004). Specific reading disability (dyslexia): What have we learned in the past four decades? Journal of Child Psychology and Psychiatry 45(1), 2–40.


A further problem for the vision research is the variation across studies in the definition of dyslexia, and hence the techniques employed to assess dyslexia and reading:

“The diagnostic criteria widely differ between studies. Whereas lower word reading is one of the most common criteria for defining dyslexia, the usage of a discrepancy criterion (e.g. age, grade or IQ discrepancy) is quite different, additionally the magnitude of discrepancy (e.g. 1, 1, 1.5 or 2 standard deviations below the norm) varies greatly. These differences might lead to the identification of different sub-groups from the large population suffering from dyslexia and to different grades of severity of affectedness” (Schulte-Körne & Bruder, 2010, p.1805).


Not all students with dyslexia have these deficits, some students without dyslexia have these deficits, and addressing these deficits has not been reliably been shown to alleviate the reading problems.

“Orthoptic rehabilitation inspired by “behavioral vision therapy” is sometimes proposed when there are disturbances in saccades or in pursuit (the ability to visually locate and follow an object) in the dyslexic. No scientific study has shown the merits of this therapy” (p.876).

Quercia, P., Feiss, L., & Michel, C. (2013). Developmental dyslexia and vision. Clinical Ophthalmology, 7, 869–881.


“Eye exercises have been purported to improve a wide range of conditions including vergence problems, ocular motility disorders, accommodative dysfunction, amblyopia, learning disabilities, dyslexia, asthenopia, myopia, motion sickness, sports performance, stereopsis, visual field defects, visual acuity, and general well-being. Small controlled trials and a large number of cases support the treatment of convergence insufficiency. Less robust, but believable, evidence indicates visual training may be useful in developing fine stereoscopic skills and improving visual field remnants after brain damage. As yet there is no clear scientific evidence published in the mainstream literature supporting the use of eye exercises in the remainder of the areas reviewed, and their use therefore remains controversial” (p.82).

Rawstron, J.A., Burley, C.D., & Elder, M.J. (2005). A systematic review of the applicability and efficacy of eye exercises. Journal of Pediatrics, Ophthalmology, and Strabismus, 42(2), 82–88.


“Data were available for 5822 children, of whom 172 (3%) met the criteria for SRI. No association was found between SRI and strabismus, motor fusion, sensory fusion at a distance, refractive error, amblyopia, convergence, accommodation, or contrast sensitivity. Abnormalities in sensory fusion at near were mildly higher in children with SRI compared with their peers (1 in 6 vs 1 in 10, P = .08), as were children with stereoacuity worse than 60 seconds/arc (1 in 6 vs 1 in 10, P = .001). … Four of every 5 children with SRI had normal ophthalmic function in each test used. A small minority of children displayed minor anomalies in stereoacuity or fusion of near targets. The slight excess of these children among those with SRI may be a result of their reading impairment or may be unrelated. We found no evidence that vision-based treatments would be useful to help children with SRI.” (p. 1057)

Creavin, A.L., Lingam, R., Steer, & Williams, C. (2015). Ophthalmic abnormalities and reading impairment. Pediatrics, 135(6), 1057-1065.

“Compared with previous studies, the current study was more robust in that children with reading impairment were compared with a general cohort population rather than with controls selected from schools and clinics. Pediatric clinicians should follow the American Academy of Pediatrics policy recommending instruction in phonics, word analysis, and reading fluency and comprehension as effective, evidence-based treatment for dyslexia. Also, unless results of routine vision screening are abnormal, a referral to an eye specialist is not indicated.” (p.1)

Stein, M.T. (2015). Visual training methods are ineffective for dyslexia. New England Journal of Medicine: Journal watch, June 2, 2015. Retrieved from http://www.jwatch.org/na38060/2015/06/02/visual-training-methods-are-ineffective-dyslexia


 

“Because they are difficult for the public to understand and for educators to treat, learning disabilities have spawned a wide variety of scientifically unsupported vision-based diagnostic and treatment procedures. Scientific evidence does not support the claims that visual training, muscle exercises, ocular pursuit-and-tracking exercises, behavioral/perceptual vision therapy, "training" glasses, prisms, and colored lenses and filters are effective direct or indirect treatments for learning disabilities. There is no valid evidence that children who participate in vision therapy are more responsive to educational instruction than children who do not participate (p.818). … Visual problems do not cause dyslexia. Scientific evidence does not support the efficacy of eye exercises, behavioral/perceptual vision therapy, training glasses, or special tinted filters or lenses in improving the long-term educational performance in these complex pediatric neurocognitive conditions. Recommendations for multidisciplinary evaluation and management must be based on evidence of proven effectiveness demonstrated by objective scientific methodology.106,112,239,270,276 It is important that any therapy for learning disabilities be scientifically established to be valid before it can be recommended for treatment.106 Because vision therapy is not evidence based, it cannot be advocated” (p.849).

American Academy of Pediatrics, Handler, S.M., Fierson, W.M. & the Section on Ophthalmology and Council of Association for Pediatric Ophthalmology and Strabismus, and American Association on Children with Disabilities, American Academy of Ophthalmology, American Certified Orthoptists. (2011). Joint Technical Report—Learning disabilities, dyslexia, and vision. Pediatrics,127, 818-856.


“Optometric training (vision training)"

It is important in children with learning difficulties to exclude visual acuity problems … Few professionals would argue against the notion that every child with difficulty should have either an accurate and valid visual acuity screening test performed by a competent professional or, alternatively, should be assessed by an ophthalmologist or an optometrist. Where there are problems with visual acuity, it is appropriate to recommend corrective lenses. In the rare circumstance where other significant visual pathology is detected, then treatment should be directed appropriately.

Optometrists play an important role in detecting and treating visual acuity problems in children and young people. However over recent years an increasing number of optometrists have begun to undertake a more extensive assessment of children with learning disabilities. In addition to visual acuity, they have also tested for problems such as difficulty with convergence and accommodation, claiming that these problems contribute significantly to a childâs reading difficulties beyond their effect on visual acuity. In many instances (perhaps in the majority) they recommend that the child wear spectacles which will assist with the problem and, in a significant number of instances, recommend that the child undergo optometric or vision training.

This therapy usually involves, in addition to the wearing of spectacles, various forms of eye exercises, and additionally may include other activities such as perceptual training, general body movements designed to improve visual perception, and other interventions. Halveston has concluded that, Eye exercises, although they have many proponents, have never been shown in a well conducted study to be of any value for students with learning disabilities (Halveston 1987).

While a number of studies, generally in the optometric literature, argue for the validity of these sorts of visual assessments and for the benefits of vision training in improving learning disabilities, there is little reliable and widely supported evidence to support claims that such intervention is beneficial, and vision training has been strongly criticised by a number of individuals and learned colleges (Beauchamp 1986; American Academy of Pediatrics 1984; Metzer and Warner 1984).

National Health & Medical Research Council of Australia. (2009). Alternative Therapies for ADHD. Retrieved from http://www.mental-health-matters.com/disorders/mood-disorders/bipolar/941-altervative-therapies-for-adhd?tmpl=component&type=raw&showall=1


“What implications may be drawn from all this? Scientific evidence does not justify practitioners’ use of cognitively focused instruction to accelerate the academic progress of low-performing children with or without apparent cognitive deficits and an SLD label. At the same time, research does not support “shutting the door” on the possibility that cognitively focused interventions may eventually prove useful to chronically nonresponsive students in rigorous efficacy trials” (p.101-102).

Fuchs, D., Hale, J.B., & Kearns, D.M. (2011). On the importance of a cognitive processing perspective: An introduction. Journal of Learning Disabilities, 44(2), 99-104.


Behavioural optometry

"The Royal Australian and New Zealand College of Ophthalmologists (RANZCO) has today reacted to the recent Channel 7 News report on behavioural optometry, condemning the coverage for failing to acknowledge the lack of research and evidence to support the practice. “Primary dyslexia and learning disabilities are complex neurocognitive conditions and are not caused by vision problems. There is no evidence to suggest that eye exercises, behavioural vision therapy, or special tinted filters or lenses improve the long-term educational performance of people affected by dyslexia or other learning disabilities,” said RANZCO President A/Prof Mark Daniell.

“It is irresponsible to promote behavioural optometry to treat these conditions without letting people know that it is an unproven practice. Parents of children with dyslexia and other learning disabilities want to do what’s best for their children and it is unfair to give them false hope in expensive treatments and aids for which there is no evidence.”

In an article in RANZCO’s members’ magazine Eye2Eye last year, Prof Frank Martin et al examined the role of ophthalmologists in the management of dyslexia. The article highlighted the need for management of dyslexia and learning disability to be based on science, “not on arbitrary and capricious dogma” and pointed out that there is no credible evidence to support claims for treatment that is not based on appropriate remedial reading intervention. The article concluded that that “As doctors, ophthalmologists have a responsibility to help families make the best use of limited resources. We should steer families away from unproven interventions that consume resources and thus interfere with the implementation of proven methodologies such as educational and language based therapy.”

RANZCO supports and concurs with the joint statement on learning disabilities, dyslexia, and vision by the American Academy of Ophthalmology (AAO), the American Academy of Pediatrics (AAP) and the American Association for Pediatric Ophthalmology and Strabismus (AAPOS) [i].Joint Statement: Learning Disabilities, Dyslexia, and Vision is a comprehensive policy document and states that “It is important that any therapy for learning disabilities be scientifically established to be valid before it can be recommended for treatment.” and goes on to say that “…the evidence does not support the concept that vision therapy or tinted lenses or filters are effective, directly or indirectly, in the treatment of learning disabilities.”

See the Eye2Eye article at https://ranzco.edu/media-and-advocacy/blog/eye2eye-spring-2016-feature-article


Tinted (Irlen) lenses


Helen Irlen was a psychologist working with adults with reading difficulties during the 1980s. She believed that she had detected a visual stress problem in many of them that involved undue sensitivity to certain light frequencies. The frequencies varied among the individuals, and she developed assessment to determine which frequencies were problematic for each client. She named the condition Scotopic Sensitivity Syndrome, and began to prescribe coloured lenses, either as glasses or as overlays, to reduce this visual stress.

She described various visual sensations reported by clients as print that ran down the page like a river, blurriness, and words sliding off the page. See simulations below.

 

 

“Visual perceptual distortions … can include blurred or double vision, and illusions of shape, colour, and motion (i.e., letters appear to move, float, or flicker).”

Chouinard, BD, Zhou, Cl, Hrybousky, S, Kim, ES, Commine, J. (2011). A functional neuroimaging case study of Meares-Irlen syndrome/visual stress (MISViS). Brain Topography, 25(3), 293–307.

The success or otherwise of the prescribed overlay or glasses was determined by the response of the client as to whether it helped. Obviously, this approach to evaluation produces its own problems. It was enthusiastically and uncritically adopted in many places, including Australia, particularly following a "60 Minutes" television show that boosted its profile in 1988. The approach has been and remains controversial, both because it has been argued that there is no such condition and that the treatment has not been demonstrated to be effective in well-designed studies.

Studies from the early days up to the present have failed to demonstrate any beneficial impact of this approach on reading:

The failure to find significantly greater improvement for the experimental groups over the control group for the total period, despite subjects' reports of improved print clarity, may be partly related to the lack of effective letter-sound analysis and synthesis skills and to the use of a word-identification strategy of guessing based on partial visual analysis.

Robinson, G.L., & Foreman, P.J. (1999). Scotopic sensitivity/Irlen syndrome and the use of coloured filters: A long-term placebo controlled study of reading strategies using analysis of miscue. Perceptual and Motor Skills, 89, 35-52.


“Learning disabilities are common conditions in pediatric patients. The etiology {causes} of these difficulties is multifactorial, reflecting genetic influences and abnormalities of brain structure and function. Early recognition and referral to qualified educational professionals is critical for the best possible outcome. Visual problems are rarely responsible for learning difficulties. No scientific evidence exists for the efficacy of eye exercises "vision therapy" or the use of special tinted lenses in the remediation of these complex pediatric neurological conditions.”

National Health and Medical Research Council. (1997). Attention Deficit Hyperactivity Disorder. Retrieved from http://www.health.gov.au/nhmrc/publications/adhd/part23.htm


“There was no evidence that visual overlays had a beneficial, differential effect on reading skills in reading-spelling disabled children” (p.791).

Iovino, I., Fletcher, J.M., Breitmeyer, B.G., Foorman, B.R. (1998). Colored overlays for visual perceptual deficits in children with reading disability and attention deficit hyperactivity disorder: Are they differentially effective? Journal of Clinical and Experimental Neuropsychology, 20, 791-806.


“Although there has been some vigorous debate in the literature, especially in Australia, about the validity of the theory and the benefits of Irlen lenses (Robinson and Conway 1994, Chan and Robinson 1989), it has been suggested that any reported improvements may be motivational or due to placebo effect rather than the effect of the lens themselves (Stanley 1987, 1990). There is still a paucity of conventional, methodologically rigorous research that clearly demonstrates the benefit of these lenses, and at this time no strong evidence exists”.

Australian National Health and Medical Research Council (2001). Retrieved from http://www.health.gov.au/nhmrc/publications/adhd/part23.htm


“Current research does not support the validity or presence of an actual visual perceptual dysfunction termed "scotopic sensitivity syndrome." Therefore the use of this term is meaningless. … There is evidence that the underlying symptoms associated with SSS are related to identifiable vision anomalies, e.g., accommodative and convergence dysfunctions, in the majority of patients”.

American Optometric Association. (2003). Retrieved from http://tireandbible.blogspot.com.au/2004/10/use-of-tinted-lenses-for-treatment-of.html#comments


So, there is a history of dispute about Irlen Lenses and scotopic sensitivity. Given that educational research is improving in quality, what do more recent studies report?

“An interesting observation is that Irlen lenses showed small effect sizes if the experimental group was compared to an untreated control group [41]. If the experimental group was compared to a placebo control group, effect sizes were negligible [33, 41]. This finding confirms earlier systematic reviews that could not prove any positive effect of coloured lenses on literacy achievement, and suggests that results are mainly due to placebo effects” [48,49].

Galuschka, K., Ise, E., Krick, K., & Schulte-Korne, G. (2014). Effectiveness of treatment approaches for children and adolescents with reading disabilities: A meta-analysis of randomized controlled trials. PLoS ONE, 9(2): e89900. doi:10.1371/journal.pone.0089900


“Recommendations for multidisciplinary evaluation and management must be based on evidence of proven effectiveness that is demonstrated by objective scientific methodology.4,45,60 It is important that any therapy for learning disabilities be scientifically established to be valid before it can be recommended for treatment.60 Currently, there is no adequate scientific evidence to support the view that subtle eye or visual problems cause learning disabilities.8,30,31,45,46,48–59 Furthermore, the evidence does not support the concept that vision therapy or tinted lenses or filters are effective, directly or indirectly, in the treatment of learning disabilities.# Thus, the claim that vision therapy improves visual efficiency cannot be substantiated” (p.843).

Handler, S.M., Fierson, W.M. and the Section on Ophthalmology and Council of Association for Pediatric Ophthalmology and Strabismus, and American Association on Children with Disabilities, American Academy of Ophthalmology, American Certified Orthoptists. (2011). Joint Technical Report—Learning disabilities, dyslexia, and vision. Pediatrics, 127, 818-856. Retrieved from http://pediatrics.aappublications.org/content/124/2/837.full.html.


“The Irlen diagnostician diagnosed Irlen syndrome in 77% of our poor readers. We found no evidence for any immediate benefit of Irlen colored overlays as measured by the reading-rate test or the global reading measure. Our data suggest that Irlen colored overlays do not have any demonstrable immediate effect on reading in children with reading difficulties” (p.932).

Ritchie, S.J., Della Sala, S., & McIntosh, R.D. (2011). Irlen colored overlays do not alleviate reading difficulties. Pediatrics, 128(4), 932-938.


“Statistically, children with dyslexia or related learning disabilities have the same ocular health as children without such conditions. No scientific evidence supports claims that the academic abilities of children with learning disabilities can be improved with treatments that are based on colored lenses. (18-20). These more controversial methods of treatment may give parents and teachers a false sense of security that a child's reading difficulties are being addressed, which may delay proper instruction or remediation. The expense of these methods is unwarranted, and they cannot be substituted for appropriate educational measures”.

American Academy of Ophthalmology (2009). Learning Disabilities, Dyslexia, and Vision - A Joint Statement of the American Academy of Pediatrics, American Association for Pediatric Ophthalmology and Strabismus and American Academy of Ophthalmology. Retrieved from http://www.aao.org/about/policy/upload/Learning-Disabilities-Dyslexia-Vision-2009.pdf


“The prescription of tinted lenses to assist children and adults with reading difficulties is based on the theory that poor readers have the problem of excessive sensitivity of the retina to particular frequencies of the light spectrum (Irlen 1983). Affected persons are said to report distortions of print when attempting to read. These include blurriness, problems with focusing for any length of time, and additional difficulties including problems with concentration, headache, and so on. This visual dysfunction, named ‘scotopic sensitivity’, is said to be minimised by the use of tinted, nonoptical lenses (called Irlen lenses) which are claimed to filter out those frequencies of the light spectrum to which a person may be sensitive. Although there has been some vigorous debate in the literature, especially in Australia, about the validity of the theory and the benefits of Irlen lenses (Robinson and Conway 1994, Chan and Robinson 1989), it has been suggested that any reported improvements may be motivational or due to placebo effect rather than the effect of the lens themselves (Stanley 1987, 1990). There is still a paucity of conventional, methodologically rigorous research that clearly demonstrates the benefit of these lenses, and at this time no strong evidence exists suggesting that they should be recommended in children with ADHD who have concomitant learning difficulties (Martin, MacKenzie, Lovegrove et al 1993)”.

National Health & Medical Research Council of Australia. (2009). Alternative Therapies for ADHD. Retrieved from http://www.mental-health-matters.com/disorders/mood-disorders/bipolar/941-altervative-therapies-for-adhd?tmpl=component&type=raw&showall=1


“Irlen syndrome is yet another example of a medical diagnosis and treatment that was promoted prior to adequate scientific evidence to establish that it is real, and treatments based upon the diagnosis are effective. A quarter of a century later evidence is still lacking, and what evidence we do have that is reasonably rigorous is negative. The most parsimonious interpretation is that Irlen syndrome is not real. The label is being applied to a heterogeneous group of patient who have many other conditions. Colored lens therapy does not appear to work”.

Novella, S. (2013). Irlen Syndrome. Science Based Medicine. Retrieved from http://www.sciencebasedmedicine.org/irlen-syndrome/


A systematic evidence review (Albon, et al., 2008) concluded that there is insufficient evidence of the effectiveness of colored lenses for dyslexia.

"Meta-analysis and qualitative assessment of eight included RCTs did not show that the use of coloured filters led to a clear improvement in reading ability in subjects with reading disability. It was not possible to comment on whether coloured filters can improve symptoms of visual stress that may be associated with reading disability due to a lack of available evidence. Based on the evidence obtained from this systematic review there can be no major implications for current practice in the treatment of reading disability”.

Albon, E., Adi, Y., & Hyde, C. (2008). The effectiveness and cost-effectiveness of coloured filters for reading disability: A systematic review. DPHE Report No.67. Birmingham, UK: West Midlands Health Technology Assessment Collaboration (WMHTAC).


“Visual complaints in general are made by many healthy children and Irlen-Meares (so-called) scotopic sensitivity syndrome can also be detected among skilled readers”.

Lopex, R., Yolton, R.L., Kohl, P., Smith, D.L., & Saxerud, M.H. (1994). Comparison of Irlen scotopic sensitivity syndrome test results to academic and visual performance data. Journal of American Optometric Association, 65, 705–14.


As with many treatments touted as the answer to educational problems, uncritical acceptance remains an issue in educational systems:

“More than 70% of teachers in training endorsed Irlen lenses or coloured overlays as effective treatments for dyslexia”.

Bain, S. K., Brown, K.S., & Jordan, K.R. (2009). Teacher candidates' accuracy of beliefs regarding childhood interventions. The Teacher Educator, 44(2), 71-89.


 

"In two studies using a survey on teacher knowledge of basic language constructs (Washburn et al., 2011a, 2011b), we asked preservice and inservice teachers to indicate their understanding of five true and false statements about characteristics and treatment of dyslexia. In both studies we found the majority of preservice and inservice teachers understood that individuals with dyslexia often experience difficulty with language-based activities (decoding, spelling), but an overwhelming majority of teachers indicated that colored overlays and/or tinted lenses would help individuals with dyslexia.” (p.10)

Washburn, E.K., Mulcahy, C.A., Malatesha Joshi, R., & Binks-Cantrell, E. (2016). Teacher knowledge of dyslexia. Perspectives on Language and Literacy, Fall, 2016, 9-13.


A final comment on Irlen Lenses arises from the Promethean Trust, a Norwich-based charity for dyslexic children, which found that the use of a cursor has eliminated the need for colored overlays or lenses. The cursor is simply a piece of card or plastic, approximately the size of a business card, with a notch cut out of one corner. The reader (or the remedial teacher) uses this to track print from left to right, and at the same time the card prevents the eyes from wandering ahead. Although no formal research has been conducted, it is likely that most cases of visual confusion result from the eyes moving in mini-saccades when the reader encounters an unfamiliar word. This occurs as the reader subconsciously tries to scramble letters to achieve a 'fit' with a familiar word. This creates the subjective impression that the letters 'won't stay still'. http://www.k12academics.com/disorders-disabilities/scotopic-sensitivity-syndrome/treatment#.UgLsAW3Cea4


What about for individuals with ADHD?


“UNPROVEN TREATMENTS Food allergen elimination diets are not effective, nor are sugar restriction, dietary supplements, mega-vitamins, or herbal treatments.EEG biofeedback, sensory integration training, auditory integration training, optometric training (i.e., Irlen lenses), chiropractic therapy, metronome therapy, or Dore cerebellar training do not have evidence-based efficacy and only have been shown effective in open studies without a control (p.561)".

Pierce, K. (2011). Treatment of Attention-Defi cit/Hyperactivity Disorder. Pediatric Annals, 40(11), 556-562.


Magnocells:

What has the research to contribute to the debate on the magnocellular theory of dyslexia?


“Visual and auditory perception deficits in dyslexia have been reported since the beginning of dyslexia research (Hinshelwood,1895; Morgan, 1896; Borel-Maisonny, 1951). Since then, it has been repeatedly shown that phonological processing is one of the most relevant factors for learning to read and spell and is impaired in dyslexic children, adults and in compensated adults (for reviews see Rack, 1994; Snowling, 2000; Ramus et al., 2003). Based on observations of aphasic children in the 1970’s (Tallal and Piercy, 1973a) a temporal processing theory was formulated in order to explain perceptual deficits that could account for the phonological processing deficits observed in dyslexia (Tallal, 1980a, 2004). Since then numerous studies were conducted to explore the basic auditory deficits in dyslexia by investigating the ability to discriminate non-speech stimuli (Farmer and Klein, 1995; McArthur and Bishop, 2001). The temporal processing theory was extended to the perception of non-linguistic visual stimuli (Stein, 2001). … Visual sensory impairments in dyslexia have been explained by deficient functioning within the fast processing transient pathway of the visual system, known as the visual magnocellular pathway (Stein, 2001; Ramus, 2004; Sperling et al., 2006; Laycock and Crewther, 2008). The magnocellular pathway is characterized by large cells widely distributed across the retina and projects, via the ventral lateral geniculate nucleus, to the visual cortex and thereafter largely to the posterior parietal cortex. Magnocells specialize in motion and positional relationships, and preferentially mediate fast temporal resolution, low contrast, and low spatial frequencies (Merigan and Maunsell, 1993). Anatomically, magnocellular deficits might be attributed to cortical anomalies in the visual system (Galaburda et al., 1985, 1994), where neurons in the lateral geniculate nucleus were found to be smaller and less structured (Livingstone et al., 1991). Although promising, these findings should be regarded with some degree of caution as they result from the investigation of brains of poorly defined dyslexics and have not yet been replicated in a more accurately defined groups. Furthermore, possible developmental delays, acquired and genetic illnesses may have influenced brain anatomy in these cases. Nonetheless, these findings are important for the validity of the magnocellular theory (Stein, 2001) … the magnocellular pathway contributes to the rapid integration of visual information when reading, via spatial, temporal and attentional processes, including the control, direction and organization of saccadic eye-movements.” (p.1795-6).

Schulte-Körne, G., & Bruder, J. (2010). Clinical neurophysiology of visual and auditory processing in dyslexia: A review. Clinical Neurophysiology, 121(11), 1794–1809.


“As regards magnocellular dysfunction, it has been suggested that dyslexics suffer from a deficit in the inhibitory function of the transient system. This deficit is said to produce a visual trace of abnormal duration that creates masking effects and consequent visual acuity problems when these children are reading connected text. Indirect evidence for this suggestion has been provided by studies demonstrating that poor and normal readers have different contrast sensitivity functions, such that poor readers require greater luminosity than normal readers when processing low spatial frequency grids (Badcock & Lovegrove, 1981; Lovegrove et al., 1986; Martin & Lovegrove, 1984). Observations of abnormal motion perception in individuals with dyslexia are offered as confirmatory evidence of magnocellular dysfunction in this population (Eden & Zeffiro, 1998). Additional support for this possibility is provided by anatomical and electrophysiological studies demonstrating structural and functional anomalies in the magnocellular pathways of a small number of dyslexic individuals (Lehmkuhle, Garzia, Turner, Hash, & Baro, 1993; Livingstone, Rosen, Drislane, & Galaburda, 1991). However, no causal relationship has been established between transient system dysfunction and early reading difficulties. Moreover, there is no evidence that dyslexic readers experience visual acuity and visual masking problems under normal reading conditions … “Finally, intervention studies based on visual deficit hypotheses do not appear to facilitate the word recognition difficulties that reflect the core difficulty in children with dyslexia (Iovino, Fletcher, Breitmeyer, & Foorman, 1999). Thus, we doubt that anomalies in low-level visual processes associated with magnocellular dysfunction are causally related to difficulties in learning to read, though such anomalies may well serve as biological markers signifying deficits in other systems that may be impaired in dyslexia (Eden & Zeffiro, 1998; Fletcher et al., 1999)” (p.367).

Vellutino, F.R., & Fletcher, J.M. (2005). Developmental dyslexia. In Margaret J. Snowling and Charles Hulme (Eds). The science of reading: A handbook. Maldon, MA: Blackwell Publishing, pp. 362-378.


“However, not all studies have demonstrated a connection between visual temporal processing, orthographic processing and dyslexia. Some studies found no significant differences between children with dyslexia and controls (e.g. Farmer & Klein, 1993; Reed, 1989), whereas others found significant differences at both short and long ISIs (e.g., Bretherton & Holmes, 2003; Cestnick & Jerger, 2000) or only at the long ISIs (Share et al., 2002). In addition, some studies reported that only a small number of children with dyslexia had visual temporal processing deficits (e.g., Gibson et al., 2006; Wright & Conlon, 2009), and measures of visual temporal processing were only weakly related to measures of orthographic processing (e.g. Chiappe, Stringer, Siegel, & Stanovich, 2002; Chung et al., 2008; Landerl & Willburger, 2010) (p.112).

Georgiou, G.K., Papadopoulos, T.C., Zarouna, E., & Parrila, R. (2012). Are auditory and visual processing deficits related to developmental dyslexia? Dyslexia, 18(2), 110-29.


“Abstract: In seven experiments, we investigated whether compensated and uncompensated adults with dyslexia show different patterns of deficits in magnocellular visual processing and in language processing tasks. In four visual tasks, we failed to find evidence of magnocellular deficits in either group. However, both groups of adults with dyslexia showed deficits in component language skills, and the degree of reading impairment predicted the nature and extent of these deficits” ( p.389)

Birch, S & Chase, C.H. (2004). Visual and language processing deficits in compensated and impaired dyslexic college students. Journal of Learning Disabilities, 37, 389 412.


“ … the issue of causality is pivotal, as visual magnocellular dysfunction could be an epiphenomenon of the reading disorder rather than its cause. Demonstration of causality has been practiced in studies investigating phonological deficits in dyslexia and is best achieved via a two-step process (Goswami, 2003). First, a reading level-match design is used, whereby dyslexic children are not only contrasted to chronological age-matched controls, but also younger normal readers matched to the dyslexics on reading level. Deficits manifested in the dyslexics compared to both the age-matched and reading level-matched groups would suggest a causal role in dyslexia (because the dyslexics are impaired given both their developmental and reading level). This can then be tested further by assessing the efficacy of an intervention addressing the same deficit. Such studies (behavioral and more recently, brain imaging) have been used to demonstrate not only that there is a causal relationship of phonological awareness on reading (Bradley and Bryant, 1983; Frith and Snowling, 1983; Olson et al., 1989; Snowling, 1980; Hoeft et al., 2006, 2007), but also that there are beneficial effects on reading after phonological training (Alexander and Slinger-Constant, 2004; Eden et al., 2004).

 Here we first confirmed the existence of a relationship between reading ability and brain activity in area V5/MT during 180 Neuron 79, 180–190, July 10, 2013 ª2013 Elsevier Inc. the perception of visual motion, allowing us to establish agreement with prior studies. Specifically, earlier work reported correlations between reading aptitude and behavioral performance on magnocellular visual tasks (Talcott et al., 2000; Wilmer et al., 2004; Witton et al., 1998) and parallel work has examined the relationship between reading proficiency and brain activity collected during magnocellular tasks (Ben-Shachar et al., 2007; Demb et al., 1997). The latter studies (Ben-Shachar et al., 2007; Demb et al., 1997) employed sinusoidal grating stimuli, while the former behavioral studies often employed tasks involving coherent motion random dot kinematogram stimuli. Our first experiment demonstrated consistency with this literature as we found (1) activity in area V5/MT in response to the perception of visual motion in a group of adults and children with normal reading skills and (2) a correlation between the strength of this V5/MT signal and reading proficiency as measured on standardized tests.

 Having verified this relationship for our task, we then used the same task to compare activity in area V5/MT between dyslexic children and their age-matched as well as reading level matched controls. Between-group differences for both types of comparisons would suggest a causal role for the visual magnocellular deficit and pave the way for an intervention study that trains the magnocellular visual system, with the goal of improving reading skills. However, our study, while showing differences between dyslexics and controls matched on age, failed to demonstrate differences for the reading level-match comparison, thereby instead suggesting the possibility that altered visual magnocellular function represents an epiphenomenon of dyslexia. That is, magnocellular dysfunction may be a side effect of dyslexia, emerging along with other deficits that are the primary cause of the reading problem (Eden and Zeffiro, 1998; Ramus, 2004). Alternatively, it is possible that magnocellular dysfunction is not actually related to dyslexia per se but merely reflects magnocellular function in the context of a person’s reading experience. In the case of dyslexia, impoverished visual magnocellular function may simply be the effect of less reading experience.” (p. 181)

Olulade, O. A., Napoliello, E. M., & Eden, G. F. (2013). Abnormal visual motion processing is not a cause of dyslexia. Neuron, 79, 180-190.


“Developmental dyslexia is a reading disorder, yet deficits also manifest in the magnocellular-dominated dorsal visual system. Uncertainty about whether visual deficits are causal or consequential to reading disability encumbers accurate identification and appropriate treatment of this common learning disability. Using fMRI, we demonstrate in typical readers a relationship between reading ability and activity in area V5/MT during visual motion processing and, as expected, also found lower V5/MT activity for dyslexic children compared to age- matched controls. However, when dyslexics were matched to younger controls on reading ability, no differences emerged, suggesting that weakness in V5/MT may not be causal to dyslexia. To further test for causality, dyslexics underwent a phonological-based reading intervention. Surprisingly, V5/MT activity increased along with intervention-driven reading gains, demonstrating that activity here is mobilized through reading. Our results provide strong evidence that visual magnocellular dysfunction is not causal to dyslexia but may instead be consequential to impoverished reading” (p.1).

Having established that the visual magnocellular deficit is likely to be an epiphenomenon of dyslexia, we then provided the dyslexic children with a phonological-based reading intervention, which resulted in better reading ability, and, somewhat surprisingly, also in greater activity in right area V5/MT during visual motion perception. This final result is important in that it reveals information about the mechanism by which phonological and visual deficits may come to coexist in dyslexia. Specifically, they do not support the above-mentioned models (Eden and Zeffiro, 1998; Ramus, 2004) that have argued that dyslexia is best described as a condition that gives rise to sensory deficits in addition to the language-based problem. Instead our results demonstrate that the acquisition of reading has a positive influence on magnocellular visual system function, as demonstrated by the increase in right V5/MT activity after reading gains in the dyslexics. Since dyslexia impedes reading acquisition, it is most likely that the differences in magnocellular function reported here and elsewhere between dyslexics and their typically reading peers may be attributed to their lower reading level and less reading experience. In other words, the magnocellular visual deficit is a consequence and not the cause of impoverished reading.

Several ideas have been put forward to explain the mechanism by which weaknesses in the magnocellular visual system might affect reading (Boden and Giaschi, 2007; Stein, 2001). It has been argued that the magnocellular system is involved in direction of visual attention, visual search, and eye movements and that these problems directly impact a person’s ability to read accurately (Eden et al., 1994). However, since our results do not support a causal relationship, it becomes necessary to look at the other side of the same coin and consider how subdued magnocellular function in dyslexia might be a result of lower reading ability. For example, extensive eye movements associated with reading experience may serve to train processes linked to the dorsal magnocellular system such as oculomotor control, visual attention, and spatial position encoding (Boets et al., 2011). From this viewpoint, one can agree on a relationship between reading and magnocellular function, even if the precise mechanisms are not well understood. However, it is likely that learning to read is followed by changes in the magnocellular system and not vice versa. Further, this theory would hold that reading acquisition exerts an influence on the size of neurons in the magnocellular layers of the LGN, or the amount of activity in area V5/MT, with the degree of influence modulated by the amount of reading experience. This model provides a parsimonious account of the findings reported to date.

It is important to keep in mind that reading is a uniquely human skill that is explicitly taught over several years of formal schooling. During this time, significant functional changes occur as a direct consequence of learning to read, as has been shown with fMRI (Gaillard et al., 2003; Schlaggar et al., 2002; Turkeltaub et al., 2003). However, reading does not have a sufficiently long evolutionary history that would reserve dedicated neural populations specifically to this skill. Therefore, reading makes use of brain areas that were most likely dedicated to other functions, an idea that has been captured in the ‘‘neuronal recycling hypothesis’’ (Dehaene et al., 2010). As such, the process of learning to read most likely results in diminishing of some skills, while at the same time promoting others. The consequential outcomes of reading acquisition have been elegantly revealed in studies contrasting literates with illiterates, demonstrating that the profound anatomical and physiological effects that learning to read has on the brain exist within and well beyond brain regions directly associated with reading (Carreiras et al., 2009). (p.185).

Olulade, O. A., Napoliello, E. M., & Eden, G. F. (2013). Abnormal visual motion processing is not a cause of dyslexia. Neuron, 79, 180-190.


“A subgroup of children with dyslexia (11 of 21) showed some visual temporal processing problems that appear to be associated with orthographic processing deficits. However, given the finding that a significant number of children without a visual processing deficit also showed orthographic processing deficits, we cannot conclude that lower-level deficits in visual processing lead to orthographic processing deficits” (p.123).

Georgiou, G.K., Papadopoulos, T.C., Zarouna, E. & Parrila, R. (2012). Are auditory and visual processing deficits related to developmental dyslexia? Dyslexia, 18(2), 110-129.


“Developmental dyslexia is a reading disorder, yet deficits also manifest in the magnocellular-dominated dorsal visual system. Uncertainty about whether visual deficits are causal or consequential to reading disability encumbers accurate identification and appropriate treatment of this common learning disability. Using fMRI, we demonstrate in typical readers a relationship between reading ability and activity in area V5/MT during visual motion pro- cessing and, as expected, also found lower V5/MT activity for dyslexic children compared to age- matched controls. However, when dyslexics were matched to younger controls on reading ability, no differences emerged, suggesting that weakness in V5/MT may not be causal to dyslexia. To further test for causality, dyslexics underwent a phonological-based reading intervention. Surprisingly, V5/MT activity increased along with intervention-driven reading gains, demonstrating that activity here is mobilized through reading. Our results provide strong evidence that visual magnocellular dysfunction is not causal to dyslexia but may instead be consequential to impoverished reading” (p.1).

Olulade, O. A., Napoliello, E. M., & Eden, G. F. (2013). Abnormal visual motion processing is not a cause of dyslexia. Neuron, 79, 1-11. doi:10.1016/j.neuron.2013.05.002


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