On Dyslexia, VSA, and VSP


On Dyslexia, VSA (Visual Signal Acquisition), and VSP (Visual Signal Processing)

Dyslexia (SRD) is an example of a disorder that is symptomatic of a more fundamental and profound neurological problem. It involves elements of dysfunctional visual signal acquisition and processing, in addition to phonological processing trouble. There is no indication that dyslexics are less intelligent than any other people. VSA and VSP dysfunction in dyslexia are extremely common and are both caused in part by the disorder on the one hand, and contribute to reading trouble on the other. There are other forms of learning disability, like problems with attention or mathematics (dyscalculia).

Vision Therapy: Vision therapy alone will not cure or significantly impact upon the severity of true dyslexia (nor other pervasive developmental disorders). VT is still recommended for patients who are able to complete the exercises as this process enables reading therapy. It makes little sense to order a course of reading therapy while the child is having trouble with signal acquisition and processing. VT can run concurrent to reading therapy.

Learning Therapy: drboulet.com therapeutic regimen extends beyond training visual skills and reading capacity. It provides guidance on physical and mental preparation for optimal performance in therapy and in class, including visual dysfunction, lower and higher-cognitive functions, and ‘Retained Primitive Reflexes‘. We also offer comprehensive software-based solutions for building low-level and high-level reading skills from Grade 1 equivalent up.

What follows is a more technical summary of some possible neurological constructs relating to dyslexia in particular, and learning disabilities in general.

Sally Shaywitz offers that dyslexia is an unexpected delay in phonological awareness. Dyslexia is described by Tunmer and Greaney (2010) as comprising four components:

(a) persistent literacy learning difficulties

(b) in otherwise typically developing children

(c) despite exposure to high quality, evidence-based literacy instruction and intervention,

(d) due to an impairment in the phonological processing skills required to learn to read and write.

Defining dyslexia in this manner does not imply that children diagnosed as having dyslexia cannot make progress in learning to read, but rather that they will require more intensive instruction and of longer duration. Furthermore, it is a simple truism that if there is any dysfunction in visual signal acquisition or visual signal processing, reading remediation will be of a longer duration, of decreased efficacy, and potentially of no use at all.

Stein (Stein 1988) asserts that dyslexia has many causes and that as many as 2/3 of ‘dyslexics’ have impaired binocular control and a poor visual sense of direction. ‘…good binocular control is an essential prerequisite for learning to read normally – a not unexpected conclusion when you consider that seeing letters stably and clearly must be as important in reading as matching them with the separate sounds of the spoken word.’ His work also shows that impaired binocular control predicts subsequent failure in reading. I contend that not only binocularity, but several other key aspects of vision (motor and perceptual) all must be accurate and reliable to ensure advancement in reading, and indeed learning. As Dr. Stein states ‘In conclusion, we believe that there is currently good evidence that impaired binocular control may contribute to many of the reading problems of children with dyslexia. An important part of the management of such children is therefore to identify those who suffer from this disability and to attempt to rectify it. Successful treatment can often greatly alleviate their problems, although it by no means removes their need for linguistic training and good remedial teaching.’ It’s a trivial thing to detect and quantify reading trouble via detailed analysis of reading eye movements.

There is support for a magnocellular pathway correlate to dyslexia (Stein 2001) and to signal acquisition dysfunction via motor control problems. Given magnocellular pathways are critical in acquiring peripheral cues and calculating saccadic sequencing, it stands to reason. The thalamus plays a critical role in intra- and inter-sensory integration; the magno and parvo cell pathways interact within the thalamus to create ‘whole’ vision in ‘intra-sensory’ integration, and the thalamus also provides a mechanism for sensory information integration BETWEEN the senses (inter-sensory), as in between hearing and vision.

Stein elaborates on the role of magnocellular/peripheral visual functions. In his view, the development of the visual magnocellular system is impaired in dyslexia (2001). Development of the magnocellular layers of the dyslexic lateral geniculate nucleus (LGN) is abnormal and motion sensitivity is reduced. Furthermore, many dyslexics show unsteady binocular fixation, hence poor visual localization, with left neglect (particularly important in calculating return saccades when reading). Because of this, dyslexics’ binocular instability and visual perceptual instability cause havoc in the acquisition of the visual signal. A reasonable demonstration of this dysfunction would be to read this text while moving the page it is printed upon side to side, and up and down – the letters appear to move around and cross over each other. Since fusion of two images is much more difficult when the images are moving independently, saccadic calculations are next to impossible to make for lack of stable spatial references in the magnocellular, or peripheral, portions of the visual field. So, blanking one eye (monocular occlusion) can improve reading by eliminating the visual confusion (horror fusionis) which occurs in the hunt for word groupings across the page, and thereby closing the loop for saccadic jump calculations. Good magnocellular function, then, is essential for high motion sensitivity and stable binocular fixation, and so also likely impacts upon proper development of orthographic skills. Many dyslexics also have auditory/phonological problems, pointing to medial geniculate involvement. Interestingly, these geniculate nuclei, with vestibular and somatosensory afferents, all contribute to spatial awareness. The role of ‘body awareness’ and physical conditioning vis-a-vis reading and learning dysfunction should not then be ignored, nor should therapy based in developing these two underestimated. This is where physical therapists and trainers, even massage therapists, have a critical role to play. I will also recommend physical exercise, including yoga, and meditation for additional help with learning impediments; I believe that awareness of self will assist in focusing efforts and attention.

Stein, Riddell et al. (1988) also show a link to parvocellular processing trouble in dyslexia. Vergence movements with smaller targets, it was shown, were much more difficult with dyslexia as compared to larger targets, or with no dyslexia. Furthermore, ‘recording vergence eye movement responses to small moving fusion stimuli may be useful in the investigation and treatment of children with reading difficulties’; Visagraph measurements beginning at a first grade reading capacity is effective in eliciting current, or future reading trouble in some cases. The test will not determine whether the problem is in signal acquisition as a primary concern, or in errors of signal processing encroaching upon it, but it does serve to identify early trouble in a great many cases.

Vision for reading appears to engage both parvocellular and magnocellular mechanisms. Reading, then, is an exchange of feedback between awareness of the position of the words on the page and the words themselves – while the parvo pathways acquire word groups on a page (the signal) and sends them forward for semantic analysis (processing), magnocellular pathways calculate positioning of the next saccade and with the frontal eye fields, brainstem and cerebellum, execute as soon as control is released from the parvocellular path to get the next signal into position on the macula. As soon as it can, the parvo mechanism grabs hold of the newly presented signal while the next movement is calculated, then again releases control to VSA mechanisms, and so on. This can happen even hundreds of times per minute It’s likely that there are common elements at play between signal acquisition dysfunction (binocular dysfunction) and specific reading disability. Dysfunction in either signal processing or signal acquisition may impact negatively upon the other, but the one is not likely to be the other’s cause in most cases. That is to say, if both exist, there is likely an organic reading and learning disability present.

It is nonetheless contentious as to whether motor coordination difficulties are a causal factor in dyslexia (specific reading disability (SRD)), or come as a result. I feel this is more an issue of semantics and focus, and is perhaps more of a distraction than it’s worth. Dyslexia relates to phonemic processing after the visual signal has been acquired. With respect to possible links between the organic neural processing disorder known as SRD and signal acquisition acquisition dysfunction, it is my opinion that:

1. They exist apart from one another and are distinct concerns in and of themselves.

2. Some reading dysfunction may appear to be dyslexia but is in fact visual dysfunction.

3. They require their own specific management plan.

4. Dysfunctional signal acquisition will add to trouble associated with dyslexia.

5. It is possible that dyslexia impacts negatively upon reading through both magnocellular and parvocellular mechanisms. That is, in calculation and execution of reading saccades on the one hand, and in fixating on particular grapheme gestalts with sufficient duration and stability to pass the signal to semantic processing, on the other. These assertions are supported in neurology and in behavioural observations. It appears as though dyslexia (or the organic condition(s) which lead to what we call dyslexia) also lead to visual dysfunction.

6. I personally don’t feel there is a subtype of dyslexia caused by signal acquisition dysfunction (‘binocular dysfunction’), yet the link between binocular motor precision and dyslexia are easy to demonstrate and has been studied in some depth in recent years (Bucci, Bremond-Gignac et al. 2008). Reading disability, or impediment, on the other hand can be caused entirely or in part by signal acquisition dysfunction.

7. People with VSAD/VSPD and those with dyslexia generally benefit from remedial reading programs in addition to some forms of vision therapy, such as saccadic and peripheral awareness training.

8. Visual training improves reading whether dyslexia is present or not, but profound dyslexia may well see minimal benefits from even extensive training.

9. Dyslexia requires therapy focused on phonological awareness and sequencing. See (Fawcett and Nicolson 1994).

10. Learning and reading dysfunction is multifactorial and requires that underlying neurophysiological functions be assessed BEFORE treatment is initiated.


Bibliography – For convenience sake, some abstracts have been included here.

Bishop, D. V. (1989). “Unfixed reference, monocular occlusion, and developmental dyslexia–a critique.” Br J Ophthalmol 73(3): 209-215.

Stein and Fowler have proposed that poor binocular control of vergence eye movements is responsible for reading problems in a subset of dyslexic children, and that this subgroup is characterised by unstable performance on Dunlop’s reference eye test. Four predictions from this hypothesis are evaluated in the light of published evidence. First, it is shown that a substantial minority of good readers have unfixed reference. Second, the evidence for a raised prevalence of unfixed reference in dyslexics is reviewed and contradictory findings are discussed. Third, it is argued that there is little support for the view that dyslexics with unfixed reference make different types of reading errors from those with fixed reference: indeed many dyslexics with unfixed reference have non-visual, phonological difficulties. Finally, it is argued that studies which claim that monocular occlusion is a successful treatment for ‘visual dyslexia’ are methodologically flawed and do not provide convincing evidence for this view.

Bucci, M. P., D. Bremond-Gignac, et al. (2008). “Poor binocular coordination of saccades in dyslexic children.” Graefes Arch Clin Exp Ophthalmol 246(3): 417-428.

AIM: To examine the quality of binocular coordination of saccades in dyslexic children in single word reading and in a task requiring fixation of single LED. METHODS: Eighteen children with dyslexia (11.4 +/- 2 years old) and 13 non-dyslexic children of matched age were studied. Horizontal saccades from both eyes were recorded with a photoelectric system (Oculomotor-Bouis). RESULTS: Binocular coordination during and after the saccade in dyslexics is worse than that of non-dyslexic children; the disconjugacy does not depend on the condition. Moreover, dyslexics do not show the stereotyped pattern of disconjugacy (divergence during the saccade and convergence after the saccade). The conjugate post-saccadic drift is larger in dyslexics for both conditions. CONCLUSION: Poor quality of binocular coordination of saccades and drift of the eyes after the saccade, regardless of the task, indicates an intrinsic ocular motor deficiency. Such a deficiency could be related to immaturity of the normal ocular motor learning mechanisms via which ocular motor coordination and stable fixation are achieved. Learning could be based on the interaction between the saccade and vergence subsystems. The cerebellum, but also cortical areas of the magnocellular stream such as the parietal cortex, could be the sites of ocular motor learning.

Fawcett, A. J. and R. I. Nicolson (1994). “Naming speed in children with dyslexia.” J Learn Disabil 27(10): 641-646. A series of tests of naming speed in discrete reaction time format were undertaken by seven groups of children: three groups with dyslexia with mean ages 8, 13, and 17 years; three groups of normally achieving children matched for age and IQ with the dyslexic groups; and a group of 10-year-old children with mild learning difficulties (slow learners) matched for reading age with the est dyslexic group. The children with dyslexia were significantly slower than even their chronological age-matched controls, and equivalent to their reading age-matched controls, on naming colors, digits, and letters, and significantly slower than even their reading age-matched controls on naming pictures of common objects. Overall, performance of the 17-year-old children with dyslexia was closest to that of the 8-year-old controls. Performance of the slow learners was equivalent to that of the youngest children with dyslexia. The results show that children with dyslexia have persistent-and unexpectedly severe-problems in naming speed for all stimuli, regardless of whether or not the stimulus requires grapheme-phoneme decoding.

Gole, G. A., S. N. Dibden, et al. (1989). “Tinted lenses and dyslexics–a controlled study. SPELD (S.A.) Tinted Lenses Study Group.” Aust N Z J Ophthalmol 17(2): 137-141.

We have carried out a randomised prospective controlled trial of the effect of tinted lenses on the reading ability of 24 non-asthmatic dyslexic children aged between nine and twelve years. Reading ability was assessed using the Neale Analysis of Reading. After one school term, there was no significant difference in the change in reading age between treatment and control groups. After two school terms (approximately six months), only 11 children (44%) were still wearing the glasses. Of 381 suitable subjects for entry into the study, 208 were excluded because of a diagnosis of asthma (to avoid effects of medication on cerebral function). As a result, we may have excluded subjects who would have responded favourably to tinted lenses.

Jones, D., Stilley, J., Bither, M., Rounds, R. (2005). “Elementary School Teachers’ Perspectives on Factors Associated With Reading Disability.” Journal of Behavioural Optometry 16(1): 11-16. This paper reports the results of a survey that was designed to investigate the understanding that teachers in several Kansas and Oklahoma schools have about vision and its impact on classroom performance. The respondents were teachers in several Kansas and Oklahoma elementary schools. The results provide evidence that the majority of these teachers were unaware of the potential consequences of visual dysfunctions on reading and learning. Recommendations are made for optometry to proactively educate the elementary school teaching profession regarding these consequences.

Kaufman, P. L. and A. Alm (2003). Adler’s Physiology of the Eye: Clinical Application. St. Louis, Missouri, Mosby. ! Keating, M. P. (2002). Geometric, Physical, and Visual Optics. Woburn, MA, Butterworth-Heinemann.

“Learning disabilities: the role of the developmental optometrist.” J Am Optom Assoc 50(11): 1259-1266. The role of the optometrist in treating children experiencing learning disabilities embraces numerous areas beyond the customary optometric services. Etiological, diagnostic and therapeutic factors are discussed stressing visual functional disorders, perceptual-motor and developmental lags and cognitive style. Their effects on the learning disabled child are analyzed; and the rationale of optometric procedures frequently used in treating LD children is reviewed. The optometrist may also be helpful in counseling patients who have learning readiness problems, reading disorders, psychological difficulties and nutritional deficits.

Stein, J. (1988). “Dyslexia.” BMJ 297(6652): 854. ! Stein, J. (2001). “The magnocellular theory of developmental dyslexia.” Dyslexia 7(1): 12-36.

Low literacy is termed ‘developmental dyslexia’ when reading is significantly behind that expected from the intelligence quotient (IQ) in the presence of other symptoms–incoordination, left-right confusions, poor sequencing–that characterize it as a neurological syndrome. 5-10% of children, particularly boys, are found to be dyslexic. Reading requires the acquisition of good orthographic skills for recognising the visual form of words which allows one to access their meaning directly. It also requires the development of good phonological skills for sounding out unfamiliar words using knowledge of letter sound conversion rules. In the dyslexic brain, temporoparietal language areas on the two sides are symmetrical without the normal left-sided advantage. Also brain ‘warts’ (ectopias) are found, particularly clustered round the left temporoparietal language areas. The visual magnocellular system is responsible for timing visual events when reading. It therefore signals any visual motion that occurs if unintended movements lead to images moving off the fovea (‘retinal slip’). These signals are then used to bring the eyes back on target. Thus, sensitivity to visual motion seems to help determine how well orthographic skill can develop in both good and bad readers. In dyslexics, the development of the visual magnocellular system is impaired: development of the magnocellular layers of the dyslexic lateral geniculate nucleus (LGN) is abnormal; their motion sensitivity is reduced; many dyslexics show unsteady binocular fixation; hence poor visual localization, particularly on the left side (left neglect). Dyslexics’ binocular instability and visual perceptual instability, therefore, can cause the letters they are trying to read to appear to move around and cross over each other. Hence, blanking one eye (monocular occlusion) can improve reading. Thus, good magnocellular function is essential for high motion sensitivity and stable binocular fixation, hence proper development of orthographic skills. Many dyslexics also have auditory/phonological problems. Distinguishing letter sounds depends on picking up the changes in sound frequency and amplitude that characterize them. Thus, high frequency (FM) and amplitude modulation (AM) sensitivity helps the development of good phonological skill, and low sensitivity impedes the acquisition of these skills. Thus dyslexics’ sensitivity to FM and AM is significantly lower than that of good readers and this explains their problems with phonology. The cerebellum is the head ganglion of magnocellular systems; it contributes to binocular fixation and to inner speech for sounding out words, and it is clearly defective in dyslexics. Thus, there is evidence that most reading problems have a fundamental sensorimotor cause. But why do magnocellular systems fail to develop properly? There is a clear genetic basis for impaired development of magnocells throughout the brain. The best understood linkage is to the region of the Major Histocompatibility Complex (MHC) Class 1 on the short arm of chromosome 6 which helps to control the production of antibodies. The development of magnocells may be impaired by autoantibodies affecting the developing brain. Magnocells also need high amounts of polyunsaturated fatty acids to preserve the membrane flexibility that permits the rapid conformational changes of channel proteins which underlie their transient sensitivity. But the genes that underlie magnocellular weakness would not be so common unless there were compensating advantages to dyslexia. In developmental dyslexics there may be heightened development of parvocellular systems that underlie their holistic, artistic, ‘seeing the whole picture’ and entrepreneurial talents.

Stein, J. and S. Fowler (1985). “Effect of monocular occlusion on visuomotor perception and reading in dyslexic children.” Lancet 2(8446): 69-73.

101 (68%) of 148 dyslexic children had unstable vergence eye movement control (unfixed reference) in the Dunlop synoptophore test. These children tended to make visual rather than phonemic errors when reading and writing; the opposite was true for those with stable control (fixed reference). The 148 dyslexic children were given plano spectacles to wear for 6 months when reading and writing and were randomised to receive either spectacles that had the left lens occluded or untreated ones. The trial was double blind. Conversion from unfixed to fixed reference occurred in 51% of the children who wore occluded spectacles, compared with 24% of those who wore plain spectacles. In the former group increase in reading ability improved by almost 6 months relative to change in age, whereas in those who wore plain spectacles and whose reference did not become fixed reading ability regressed by 0.4 months. The children with unfixed reference who did not benefit from occlusion were those who made not only visual but also phonemic and sequencing errors. Monocular occlusion may thus help one-sixth of dyslexic children to develop reliable vergence control and thereby to read.

Stein, J. F. (1989). “Unfixed reference, monocular occlusion, and developmental dyslexia–a critique.” Br J Ophthalmol 73(4): 319-320.

Stein, J. F., P. M. Riddell, et al. (1988). “Disordered vergence control in dyslexic children.” Br J Ophthalmol 72(3): 162-166.

By means of a synoptophore vergence eye movements were recorded in dyslexic and normal children while they were attempting to track small targets moving in simulated depth. Of the dyslexic children 64% were unable to make proper vergence movements when macular sized fusion targets (2 1/2 degrees) were employed, but their vergence control was better for larger (7 degrees) targets. The normal readers and the remaining dyslexics showed normal vergence responses for both large and small moving fusion stimuli. The results suggest that many dyslexics suffer a disorder of visuomotor control and perception for stimuli falling on the macula; this may explain their characteristic visual problems when reading. Hence recording vergence eye movement responses to small moving fusion stimuli may be useful in the investigation and treatment of children with reading difficulties.

Tunmer, W. and K. Greaney (2010). “Defining dyslexia.” J Learn Disabil 43(3): 229-243. In 2007, the New Zealand Ministry of Education formally recognized the condition of dyslexia for the first time and has subsequently developed a working definition of the condition. The aim of this article is to draw on contemporary theory and research on reading development, reading difficulties, and reading intervention to describe what the authors believe are four key components of a definition of dyslexia/reading disability.They begin by discussing some preliminary factors that need to be considered in developing a definition of dyslexia. The authors then present the four components of their proposed definition, drawing on a framework for conceptualizing reading

difficulties derived from the simple view of reading. They conclude by comparing their definition of dyslexia with the working definition put forward by the ministry.

Young, B. S., Collier-Gary, D., Schwing, S. (1994). “Visual Factors: A primary cause of failure in beginning reading.” Journal of Optometry and Visual Development(25): 276-288.