So far, we have discussed some theories that offer an alternative to the phonological theory considered by many to explain dyslexia and its manifestation. Breitmeyer’s saccadic inhibition theory explains some of the findings described by dyslexics that cannot be explained by a phonological theory (see Optician 26.02.16). However, we have also seen that there is some scientific evidence to contradict such a theory.

An alternative theory to explain the visual symptoms manifesting in dyslexia is the unstable binocular fixation (UBF) theory. This theory suggests that impaired development in specific areas of the visual pathway causes poor control and co-ordination over convergence and fixational eye movements, both of which are required in reading. This means that the two eyes are ‘wobbly’ and unable to fixate precisely on a single word, leading to an unstable visual percept.

Uncontrolled vergence eye movements are especially problematic when reading. Being uncontrolled, the visual axis of the two eyes can cross and re-cross each other leading to visual symptoms.1 The quality of a person’s binocular fixation ‘determines how steady the letters appear when they are trying to read them’. It has been suggested that subjects with lower than average fusional reserves, as is the case for most dyslexics,2 may have to work harder than usual to maintain alignment when reading. This means that they are more likely than usual to have binocular instability and are therefore more likely to suffer the associated visual symptoms.

Link between M pathway deficit theory and UBF

For many years, the UBF theory has been in direct opposition to the M pathway theory. However, recent evidence suggests that the two theories are indeed connected.2 A link has been found in dyslexic individuals between binocular instability and deficits in the M pathway. This is displayed in Figure 1, where the line of best fit demonstrates a strong correlation between log flicker threshold and vergence amplitude (r = -0.627, p = 0.0004).

[CaptionComponent="3065"]

In other words, the dyslexic subjects who were worse at perceiving flicker (regulated by M pathway) were the same people who were worse at changing vergence of their eyes (related to binocular instability). Vergence amplitude was measured optometrically via the near base OUT prism fusion range. This measures how good the eyes are at turning in at near, such as when reading.

Discussion

During my initial research, I had found dozens conflicting studies for and against the M theory of dyslexia, some of which I have regrettably been forced to omit for reasons of brevity. Opinions about the aetiology of dyslexia are highly polarized; for every paper proving one theory, another paper is released to disprove that theory. It’s all somewhat contradictory, but I have attempted some clarification in this short series.

Anatomy, Physiology and Pathophysiology

The results from the anatomical 3 and physiological 4 studies clearly reveal evidence of deficits in the M system among dyslexics, although there is controversy over how these deficits cause the visual problems which manifest in dyslexia. Breitmeyer’s theory of saccadic suppression, which was taken for many years as the gospel truth by scientists, has actually been suggested to be incorrect by Burr.5

However, using pathophysiological data,6 it has been deduced that dyslexics have abnormal neuronal processing in brain area V5-MT, which forms part of the M system and is key in motion sensitivity. Area V5-MT projects to the posterior parietal cortex (PPC) which is essential for ‘normal eye-movement control, visuospatial attention and peripheral vision – all important components of reading’.7 Small deficits in magno LGN organisation or function may consequently ‘multiply up to bigger deficits in PPC function’, a possible explanation for such processing deficits that dyslexics have to face (see Figure 2).

[CaptionComponent="3066"]

Damage to the PPC can also cause acquired reading disorders. This can be demonstrated using Figure 2, which has been divided into two separate sections. Figure 2A is an illustration of the brain; it has been shaded in a specific pattern to demonstrate the separate subareas of the PPC and the numbers in the illustration represent brain areas. Figure 2B summarises the function of various regions of the PPC and how lesions to each region can produce specific deficits, with the final column indicating the link, if any between impaired function of the PPC with dyslexia.

Contrast Sensitivity

In Livingstone and colleagues’ 1991 study, 3 it was revealed that dyslexics generate reduced responses to low contrast in comparison with high contrast stimuli, consistent with M visual processing deficits. However, Skottun’s review on various studies measuring the contrast sensitivity (CS) curve in dyslexics compared with normal readers, has established the wide range of hugely conflicting evidence.8

The shape of the CS curve in dyslexics varies between different studies, with inconsistent evidence on whether the curve’s shape is consistent with M deficits. Different studies had used different sample sizes and subjects were of different ages, a possible explanation for the varied results.

On further inspection of the data used in the review, it has become apparent that direct comparison of each individual study is impossible owing to differences in the methodology of the experiments. For example, out of the eight studies mentioned by Skottun, four were conducted using static stimulus, three were conducted using 20Hz flicker stimulus and one study was the combination of both static stimulus and flicker. Furthermore, the CS plots use different units for the contrast sensitivity axes, another reason why one is unable to directly compare absolute sensitivity between the plots.8

Thus, while there are some studies which have found CS reductions consistent with a M deficit in dyslexia, meta-analysis suggests that, ‘these studies are outnumbered by both the studies which have found no loss of sensitivity and by studies which have found contrast sensitivity reductions of a nature inconsistent with a M deficit’.8

Dyslexia Redefined

Many of the studies mentioned have used the ‘discrepancy model’ to diagnose dyslexia on the belief that there is ‘positive correlation between intelligence and reading performance.’8 However, a recent study using fMRI brain imaging to localise areas of brain activity, has found that ‘poor reading’ children have the same reduction in brain activity to sound and language stimulus’ independent of IQ thus suggesting that the entire diagnosis for dyslexia may need to be reconsidered.9

Prevalence of M Deficit in Normal Readers

According to Lovegrove,10 a ‘strikingly high’ percentage of dyslexic individuals have M deficits (75%, or 46 out of 61 dyslexics tested), indicating that M deficits are a common occurrence within the dyslexic population. However, mathematically, it was later revealed by Skoyles and Skottun 11 that the total number of non-dyslexics in the general population with M deficits is very likely to be higher. Figure 3 is a graphical interpretation of Skoyles and Skottun’s equation. As can be seen, the prevalence of dyslexia in the total population greatly influences the ratio of normal readers with M deficits to dyslexics with such deficits. This prevalence of dyslexia, depending on the study one reads can vary from 4%12 to 15%.13 The dashed horizontal line indicates a 1:1 ratio between the two groups, crossing the curve at 9.64%. Values above this dashed line indicate that there are more non dyslexics than dyslexics with magnocellular deficits.

[CaptionComponent="3067"]

In the present day, the prevalence of dyslexia is considered to be much less than 9.64% 14 meaning there are substantially more normal readers with M deficits than dyslexic readers with M deficits. This revelation concludes that deficits in the M pathway aren’t exclusive to dyslexics. Skoyles and Skottun noted that investigators had both overlooked the reality that the control group corresponds to a significantly larger percentage of the population than the dyslexic group and also decided on comparing sample groups with each other.11

When analysing these results on a larger scale, one must consider whether they apply to all studies comparing dyslexic to non-dyslexic individuals, for example the studies of Livingstone,3 Breitmeyer 15 and Eden.6 In particular, do normal readers have abnormal lateral geniculate nuclei (LGNs)? If this was the case, then the significance of these studies would be largely redundant. That said, Skoyles’ and Skottun’s formula is a mathematical prediction and therefore may or may not be entirely applicable.

Ideally, the only technique to reach a definitive conclusion on the prevalence and significance of dyslexic readers presenting with M deficits is through large epidemiological studies. Here, examiners would test and match dyslexics of various ages, wealth and intelligences and so on with controls. Currently, only small sample sizes have been used in such studies. Larger studies would reduce the risk of sampling bias and increase the reliability of tests. However, it is impractical and cost/time ineffective to perform post mortem examinations on dyslexic brains, as it is to undertake fMRI upon entire living dyslexic populations to assess brain activity. Due to the lack of large epidemiological studies published, the topic will remain something of uncertainty giving rise to further theoretical debate from scientists.

Sub-categories of dyslexia

In 1989, Stein and colleagues16 suggested that 60-70% of dyslexics suffer perceptual problems consistent with M deficits which is consistent with the proportion of SRD children noted by Lovegrove10 also suffering from a M channel deficit..

However, this means that the remaining 30-40% do not. To explain this, a model by Boder has been used;17 here, Boder has subcategorised dyslexic individuals into three separate classes based on their presenting symptoms:

  • dyseidetic (visual)

  • dysphonetic (auditory)

  • dysphoneidesia (auditory and visual)

Recent evidence 18 indicates that dysphoneidetic dyslexics have reduced sensitivity to low spatial frequencies at 10 Hz, whereas dyseidetic dyslexics do not have reduced sensitivity at either I or 10 Hz. This indicates that the type of dyslexia that one has influences whether perceptual losses, that are consistent with M deficits, are found.

General M Deficit

This review has analysed the visual implications for an M deficit in dyslexics. However, it has been postulated that M dysfunction is not restricted to the visual pathways but is generalised to all modalities (visual and auditory as well as tactile).19 This is summarised in Figure 4. Moreover, as the cerebellum, often known as the brain’s ‘autopilot’, receives extensive input from various M systems in the brain. It is also thought to be affected by a general M defect hence its under activity in many dyslexics.20

[CaptionComponent="3068"]

Through a single biological cause, the general M theory of dyslexia attempts to account for all known manifestations of dyslexia, as noted by the green circles in Figure 4. It postulates that a general M dysfunction ‘affects all sensory pathways and further spreads’ to the PPC and cerebellum, thereby ‘encompassing all the known cognitive, sensory, and motor manifestations of dyslexia’.19

Non-Visual Theories of Dyslexia

As previously noted, dyslexia is a multifactorial condition. This review has focused on one stream of evidence (visual) but there are various other theories to the aetiology of dyslexia. These are summarised in Figure 5.

[CaptionComponent="3069"]

Conclusion

I have found significant evidence both supporting and disputing the M theory of dyslexia; I feel inclined to support this theory while acknowledging it is not flawless. For the M theory to be convincing, sufferers should have an impaired M system but normal P system, something which is disputed in Skottun’s review.8

In my opinion, for the M visual processing theory of dyslexia to still be valid it has needed to evolve into the general M processing deficit theory,1 a theory that is able to account for other, non-visual symptoms of dyslexia. Interestingly, dyslexia is defined as a specific reading disability.3 However, nearly every visual task that we perform depends on M system function so if there were deficits in M processing then dyslexia should be a huge problem, and not just confined to reading.22

The phonological processing impairment theory is still the most widely accepted theory of dyslexia but, dyslexia is a complex condition and there are almost certainly a variety of factors that can contribute to it, suggesting that more than one theory can be simultaneously correct.22 For example in Figure 4, a general M dysfunction could also result in poor phonological skills. The cerebellar theory of dyslexia, something which is beyond the scope of this dissertation also has links to the general M theory.19

Conversely, improvements in scientific methods and technology, for example with the introduction of fMRIs, are producing more reliable evidence of M deficits in the dyslexic brain.

Researchers are in constant disagreement over the relative merits of these theories; I believe there is more than one correct theory due to dyslexia’s heterogeneous nature. The evidence-based approach of proving and consequently disproving theories will only better our understanding of the condition in the long term and provide better treatment for sufferers.

Jaskiran Sandhu is a hospital optometrist based in Surrey. The author would like to thank associate professor Simon Grant of City University for his review and input on this paper

References

1 Stein J, 2001. The Magnocellular theory of developmental dyslexia. Dyslexia, Volume 7, pp12-36

2 Evans B, Drasdo N, Richards IL, 1996. Dyslexia: The link with visual deficits. Opthamic and Physiological Optometry, 16(1), pp3-10

3 Livingstone MS, Rosen, GD, Drislane, FW, Galaburda AM, 1991. Physiological and anatomical evidence for a magnocellular defect in developmental dyslexia. Proceedings of the National Academy of Sciences of the United States of America, Volume 88, pp 7943-7947

4 Galaburda A, Livingstone, M, 1993. Evidence for a magnocellular defect in developmental dysleexia. Ann N Y Acad Sci, Issue 682, pp70-82

5 Burr DC, Concetta Morrone M, John R, 1994. Selective suppression of the magnocellular visual pathway during saccadic eye movements. Nature, 371(6946), pp511-513

6 Eden, GF et al, 1996. Nature. Abnormal Processing of visual motion in dyslexica revealed by functional brain imaging, 4 July, pp66-69

7 Stein J, Walsh V, 1997. To see but not to read; the magnocellular theory of developmental dyslexia. Trends Neuroscience, Volume 20, pp147-152

8 Skottun B, 2000. The magnocellular theory of dyslexia; the evidence from contrast sensitivity. Vision Research, Volume 40, pp111-127

9 Gabrieli J et al, 2011. The Brain Basis of the Phonological Deficit in Dyslexia is independent of IQ. Psychological Science, 4 November, pp1-10

10 Lovegrove W, Martin F, Slaghuis W, 1986. A theoretical and experimental case for a visual deficit in specific reading disability. Cognitive Neuropsychology, Volume 3, pp225-267

11 Skoyles J, Skottun BC, 2004. On the prevalence of magnocellular deficits in the visual system of non-dyslexic individuals. Brain and Language, Volume 88, pp79-82

12 Rutter M, Tizard J, Whitmore K, 1970. Education Health and Behaviour, New York: Longman

13 Duane D, 1974. A neurological overview of the specific language disability for the non neurologist. Bulletin of the Orton Society, Volume 24, pp5-36

14 NHS, 2009. Dyslexia. www.nhs.uk/Conditions/Dyslexia/Pages/Causes.aspx

[Accessed 10 November 2012]

15 Breitmeyer B, 1993. The Role of Sustained (P) and Transient (M) channels in Reading and Reading Disability. In: Facets of Dyslexia and its Remediation. Houston: Elesvier Science Publishers BV, pp13-31

16 Stein J, Riddell P, Fowler S, 1989. Disordered right hemisphere function in developmental dyslexia. In: v. E. In C, I. Ludenberg & G. Lenerstrand, eds. Brain and Reading. New York: Srockton Press, pp139-157

17 Boder E, 1971. Developmental Dyslexia: Prevailing Diagnostic Concepts and a new approach. In: H. Mykleburst, ed. Progress in Learning Disabilities. New York: Grune & Stratton, pp293-321

18 Borsting E et al, 1996. The Presence of a Magnocellular Deficit Depends on the type of Dyslexia. Vision Research, 36(7), pp1047-1053

19 Ramus F, 2003. Developmental Dyslexia: Specifical Phonological Deficit or sensiromotor dysfunction?. Neurobiology, 13(2), pp. 212-218

20 Stein J, 2004. Visual Dyslexia. www.brookes.ac.uk/schools/education/rescon/cfe.pdf

[Accessed 13 November 2012]

21 Ramus F, 2006. A neurological model of dyslexia and other domain-specific developmental disorders with an associated sensorimotor syndrome. In: G. Rosen, ed. The Dyslexic Brain: New Pathways in Neuroscience Discovery. Mahwah New Jersey: Lawrence Erlbaum Associates, pp75-101

22 Evans BJ, 2001. Dyslexia & Vision. 1st ed. London: Whurr Publishers