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    There are several different theories on what causes dyslexia; mainly biological and cognitive theories. In this section, we are going to look at 3 main biological theories.

    5.1 Cerebellar Theory

    Nicolson and Fawcett (2004) postulate that the dyslexic’s cerebellum is mildly dysfunctional, resulting in a spectrum of cognitive difficulties that includes speech processing and articulation problems. This theory is also sometimes known as the Cerebellar Deficit Hypothesis (CDH).

    The cerebellum is a deeply folded sub-cortical brain structure located at the back of the brain, sometimes known as the “hind brain” (Fawcett & Nicolson, 2004). As it plays a huge role in general motor control, damage to this area can result in retarded speech articulation, which in turn, can possibly lead to deficiency in phonological representations. In addition, the cerebellum controls automatisation of over-learned tasks such as cycling, typing and reading. Thus, a weak capacity to automatise would affect, among other things, the learning of letter-sound correspondences. As such, it is harder for dyslexics to acquire language dexterity.

    5.2 Magnocellular Theory

    The magnocellular theory proposes that literacy difficulties faced by dyslexics may be a consequence of impaired development of a system of large neurons in the brain called the magnocells (magno meaning larger in Latin) that is responsible for timing sensory and motor events. The visual demands of reading require the capabilities of this visual magnocellular system and any weakness in this area can cause one to have unstable binocular control that may lead to visual confusion of letter order and poor visual memory for the written word (Stein, 2001).

    Although the magnocellular theory largely applies to the visual aspect, research by Stein & Walsh in 1997 has shown that magnocellular dysfunction is not restricted to the visual pathways, but is generalised to all modalities (that includes auditory as well as tactile). That is to say, a weak magnocellular network can lead to a range of other cognitive difficulties such as delayed auditory processing, which can in turn result in certain behavioural manifestations of dyslexia (e.g. weak sound discrimination).

    5.3 Genetic Linkage Theory

    In addition to the neurological theories, there seems to be strong evidence to show that there is truly a genetic origin to dyslexia. Among all, Orton (1925) was one of the first to propose that spoken language difficulties tend to run in families. According to a research done by Gilger, Pennington and DeFries in 1991, the estimated risk of dyslexia for an individual is higher if there is a family member with the same condition. To be more specific, an offspring’s risk was elevated 2 to 80 times over population expectancies if there was an affected parent.

    Together with the results from the research (cited in Miles, 1993) conducted on twelve pairs of monozygotic dyslexic twins (where the result shows 100% concordance), it is very possible that dyslexia could be due to a single heritable gene, or the interaction between several genes, particularly the long arm of chromosome 15 and the short arm of chromosome 6 (Grigorenko et al., 1997). As these gene markers are found to be linked to phonological awareness and single-word reading respectively, differences on these gene markers can affect language abilities.


    Written by

    Ms. Cara Tan

    Specialist Tutor


    Fawcett, A.J. & Nicolson, R.I. 2004, ‘Dyslexia: the role of the cerebellum’, Electronic Journal of Research in Education Psychology, vol. 2, no. 2, pp. 35-58.

    Stein, J. 2001, ‘The Magnocellular Theory of Developmental Dyslexia’, Dyslexia: An International Journal of Research and Practice, vol. 7, no. 2, pp. 12-36.

    Stein, J. & Walsh, V. 1997, ‘To see but not to read: the magnocellular theory of dyslexia’, Trends in Neurosciences, vol. 20, pp. 147-52.

    Orton, S. T. 1925, ‘‘Word blindness’ in schoolchildren’, Archives of Neurology and Psychiatry, vol. 14, pp. 581-615.

    Gilger, J.W., Pennington, B.F. & DeFries, J.C. 1991, ‘Risk for reading disabilities as a function of parental history in three samples of families’, Reading and Writing, vol. 3, pp. 205-217.

    Pernet, C.R., Poline, J.B., Demonet, J.F. & Rousselet, G.A.  2009, ‘Brain classification reveals the right cerebellum as the best biomarker of dyslexia’, BMC Neuroscience, vol. 10, no. 67

    Grigorenko, E.L., Wood, F.B., Meyer, M.S., Hart, L.A., Speed, W.C., Shuster, A. & Pauls, D.L. 1997, ‘Susceptibility loci for distinct components of developmental dyslexia on chromosomes 6 and 15’, The American Journal of Human Genetics, vol. 60, pp. 27-39.