The reasons for my literacy, part 3: the medical model

The following is a brief commentary of dyslexia as a medical condition. Many conditions get medicalised, but should they be? This is just one way of looking at a difficulty in acquiring literacy.

The various definitions of dyslexia (of which there are many) do not differentiate between the condition and a delay, or whether they are one and the same. There are discussions as to whether dyslexia is a form of natural difference, a discrete condition or collection of differences. Morton and Frith (cited in Reid, 2009) put forward a causal modelling framework which covers three dimensions, neurological, cognitive and educational, taking into account cultural/environmental factors and that all dimensions may overlap. There is a growing body of evidence which suggests that dyslexia is genetic in origin, however even with genetics, environment invariably plays a part. For example, a person may have a predisposition to obesity, but this can be encouraged or kept at bay through lifestyle choices. A person with a ‘dyslexia gene’ may thrive with good teaching, or disengage completely with indifferent or poor teaching. Gilger (cited in Reid, 2009) warns against making sweeping statements about heritability, although there is a suggested 40% possibility of it being so – subject to environmental factors of course.

Potentially, gene studies point to a possible site which may be in the region implicated in autoimmune diseases. Stein (cited in Reid, 2009) considers that magnocellular systems may affect the visual, phonological, kinaesthetic, sequencing, memory and motor. Stein suggests that inheriting particular mixes of different magnocellular systems gives rise to dyslexia. This is an interesting idea, and could link to the different expression of alleles making for no one-size-fits-all diagnosis, and why early intervention can lead to optimum outcomes.

Issues with procedural timing and hemispheric symmetry are two other hypotheses put forward to account for dyslexia. Both theories suggest atypical brain structures either occurring prenatally or from premature birth. Fawcett and Nicolson (cited in Reid, 2009) propose a cerebellum deficit hypothesis, which would account for the overlap between dyslexia and other disorders, affecting reading, writing and spelling. They also consider that this would account for the difficulty in acquiring automaticity in literacy. Hemispheric symmetry on the other hand theorises that misplaced cells in the left hemisphere, which associated with language, gives rise to right or left (perceptual or linguistic) hemisphere learners who require different teaching styles. Further to these hypotheses, Breznitz (cited in Reid, 2009) posits that dyslexics have problems transferring information from one hemisphere to the other due to information delay in the corpus collosum. As said before, all of this should be viewed against a backdrop of environmental influences. Can dyslexia be reductionist in nature? Can anything about human development be reduced to a few ticks in a box?

Problems with visual and temporal processing and the magnocellular system have also been put forward as a cause of dyslexia, although research only suggests between 35-40% of dyslexics are affected (Reid, 2009). The use of overlays has been found to increase reading fluency by 5% in 45% of dyslexic children (Kriss and Evans, cited in Reid, 2009). However, this is only suggestive of those with dyslexia also having visual stress. The two are not mutually inclusive – or exclusive. A small-scale study of children with autism suggested that 79% of the children also improved reading fluency by 5% (Ludlow et al, 2006). This would suggest that visual stress is not unique to dyslexia, but may crossover with other SpLDs. Does this also lend weight to genetics due to the cross-overs between conditions?

Unfortunately, the lack of clarity over the definition of dyslexia affects the selection process for research, potentially hindering the development of suitable interventions. Cynically, it could also be argued that research is also influenced by those seeking to develop interventions, so there may be financial factors behind what is being researched and why.

Rassool (cited in Soler et al, 2010) states that from the perspective of experimental psychology, literacy is viewed as a process involving phonological and graphic, morphology, and technical spelling skills. Understanding where these processes occur in the brain and whether there is atypical processing, could shed light on the origins of dyslexia and/or help inform interventions. A dual route model to the written word is proposed by Coltheart (cited in Soler et al, 2010), one route being visual where the whole word is read, and the other is through phonological processing. Neuroimaging shows that regardless of the type of language learned (alphabetic or character), it is the phonological system that underpins it (Goswami, 2009). Velluntino et al (2004) point out that you cannot have good reading comprehension if you cannot first decode the word; also lexical retrieval requires a good working memory.

Phonological awareness is acquired through language, with the syllable as the primary processing unit, working down to on-set rime then phoneme awareness. The visual system takes over when phonological decoding is established. Most neuroimaging studies have involved adults, due to radioactive tracers unsuitable for children. Scans can show which areas of the brain activate when reading real words, false fonts or nonsense words. Cognitive information processing has been shown to start 100-200ms after exposure and it takes about 160-180ms to decide if a word is real or nonsense. Goswami reports that seven year-olds perform as well as adults in false-font tasks, which could indicate that this is reflective of developmental differences rather than reading expertise. What doesn’t appear to be happening with dyslexics is the move towards left-lateralized processing seen in typical development, rather, there is continuing right hemisphere involvement. Goswami cites studies by Simos et al who consider that children with phonological difficulties rely more on articulation networks when phonological processing is needed. Remediation through intense phonological interventions showed brain activity closer to typically developing readers, although neural activity was delayed by an average of 40%.

I am constantly saddened when students walk in declaring dyslexia ‘because a teacher said so’, or similar. Dyslexia should not be assumed or casually given to a student whose reading or spelling ability is below that of peers. There are a great many other causes of poor literacy development, including a lack of quality teaching, although probably no less distressing or frustrating. The non-consensus of origin or definition is not helpful either. For many parents, a label brings funding, so it is sought. Parents may also buy-in to an idea that only a specialist can teach their child should a label be applied. Is this real or assumed? Does it depend on whether you subscribe to a medical model, social model or something else?


Goswami, U (2009) ‘Reading, Dyslexia and the Brain’ in Fletcher-Campbell, F., Soler, J. And Reid, G (eds) Approaching Difficulties in Literacy Development: Assessment, Pedagogy and Programmes Milton Keynes: The Open University/London: Sage

Gerber, P., J. And Price, L., A. (n.d.) ‘Self-disclosure and Adults with Learning Disabilities: Practical Ideas about a Complex Process’ [online] (accessed 18/04/2013)

Ludlow, A. K., Wilkins, A. J. And Heaton, P. (2006) ‘The Effect of Coloured Overlays on Reading Ability in Children with Autism’ in Journal of Autism and Development Disorders [online] (accessed 13 April 2013)

Pollak, D (2009) ‘The self-concept and dyslexia’ in Soler, J., Fletcher-Campbell, F. and Reid,G. (eds) Understanding Difficulties in Literacy Development: Issues and Concepts Milton Keynes: The Open University/London: Sage Publications Ltd

Reid, G (2009) Dyslexia: A Practitioner’s Handbook (4th edn) Chichester: Wiley-Blackwell

Soler, J., Fletcher-Campbell, F., Reid, G. And Wearmouth J. (2010) E801 Difficulties in Literacy Development Milton Keynes: The Open University

Vellutino, F. R., Fletcher, J. M., Sowling, M. J. And Scanlon, D. M., (2004) ‘Specific reading disability (dyslexia): What have we learned in the past four decades? in Journal of Child Psychology and Psychiatry Volume 45, Issue 1, pp2-40 [online] (accessed 1 March 2013)


2 thoughts on “The reasons for my literacy, part 3: the medical model

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