Other Theories of Dyslexia

The phonological theory postulates that 'dyslexic students' have a specific impairment in the representation, storage and retrieval of phonemes; that is, speech sounds. Learning to read an alphabetic system requires learning the grapheme – phoneme correspondence (the correspondence between letters and their constituent sounds of speech). If these sounds are poorly represented, stored or retrieved, the learning of grapheme – phoneme correspondences, the foundation of reading for alphabetic systems, will be affected. While theorists have different views about the nature of the phonological problems, they agree on the central and causal role of phonology in dyslexia (Bradley and Bryant, 1978; Vellutino, 1979;

52

Snowling, 1981; Brady and Shankweieler, 1991; Anthony and Francis, 2005). Snowling (2000) as well supports the phonological theory by stating that dyslexic individuals perform particularly poorly on tasks requiring phonological awareness; for example, conscious segmentation and manipulation of speech sounds, and poor verbal short-term memory and slow automatic naming. Anthony and Francis (2005) and Gathercole

et al

(2006) agree with Snowling's (2000) support and claim that severity of reading difficulties is significantly associated with phonological awareness abilities. 'Basically, individuals who have difficulty detecting or manipulating sounds in words will struggle with learning to read' Anthony and Francis (2005, p 255).

Another theory is the rapid auditory processing theory which specifies that the deficit lies in the perception of short or rapidly-varying sounds. Tallal

et al

(1993, 2004) claim that the phonological deficit is secondary to a more basic auditory deficit. Support for this theory arises from evidence that 'dyslexic students' show poor performance on a number of auditory tasks including frequency discrimination (MacAnally and Stein 1996, Ahissar

et al

, 2000) and tone-in-noise detection (Boets

et al

, 2006). The failure to represent short sounds and fast transitions correctly causes further difficulties in particular when such acoustic events are the cues to phonemic contrasts, as in /

ba

/ versus /

da

/. In this view, Serniclaes

et al

(2001), claim that the auditory deficit is therefore the direct cause, in the course of development, of the phonological deficit, and hence of the difficulty in learning to read.

The visual theory reflects another long-standing tradition in the study of dyslexia, whereby dyslexia is considered a visual impairment causing difficulties with the processing of letters and words. It may take the form of unstable binocular fixations and poor vergence as Eden

et al

(1994) claim, or increased visual crowding as Spinelli

et al

(2002) pointed out.

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The visual theory does not exclude a phonological deficit, but emphasises a visual contribution to the reading problems.

When Nicolson and Fawcett first presented their cerebellar theory on the role of the cerebellum in dyslexia in 1990, the concept was quite novel. They claimed that the cerebellum of people with dyslexia is mildly dysfunctional and a number of cognitive difficulties ensue. First, the cerebellum plays a role in motor control and therefore in speech articulation. It is postulated that retarded or dysfunctional articulation would lead to deficient representations. Secondly, the cerebellum plays a role in the automatisation of over-learned tasks, such as driving, typing and reading. A weak capacity to automatise would affect, among other things, the learning of grapheme-phoneme correspondences (Fawcett

et

al

, 1996). Evidence of poor performance of 'dyslexic students' in a large number of motor tasks, supports the cerebellar theory. Support to this theory is also found in brain imaging studies which show anatomical, metabolic and activation differences in the cerebellum of 'dyslexic students' (Nicolson

et al

, 1999; Brown

et al

, 2001; Leonard

et al

, 2001).

An additional theory is the magnocellular theory which attempts to integrate all the findings mentioned in the phonological theory, the rapid auditory processing theory, the visual theory and the cerebellar theory, all of which were discussed above. The magnocellular theory assumes that magnocellular dysfunction is not restricted to the visual pathway but is generalised to all modalities, including visual, auditory and tactile. Furthermore, according to Stein

et al

(2001), as the cerebellum receives massive input from various magnocellular systems in the brain, it is also predicted to be affected by general magnocellular defect.

When comparing and contrasting the different theories, the magnocellular theory manages to account for all known manifestations of dyslexia which

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include visual, auditory, tactile, motor and, consequently phonological deficits. While the phonological theory does not explain the sensory and motor disorders that occur in a significant proportion of 'dyslexic students', the magnocellular theory suffers does not account for the absence of sensory and motor disorders in a significant proportion of 'dyslexic students'. However, the cerebellar theory does deal with both types of problems.

Yet, it can be argued that it might be possible that all theories are true of different individuals. There could be, for instance, four partially overlapping subtypes of dyslexia, each being an independent contributor to reading difficulties (phonological, auditory, visual and cerebellar). On the other hand, it could also be that each case of dyslexia is accounted for by a different theory, and that the other manifestations mentioned are associated without causation.

Ramus

et al

(2003) conducted a multiple case study where they assessed the leading theories of developmental dyslexia: the phonological theory, the magnocellular theory (including the auditory and visual theory) and the cerebellar theory. The study results suggest that a phonological deficit can appear in the absence of any other sensory or motor disorder, and is sufficient to cause literacy impairment. Auditory disorders, when present, aggravate the phonological deficit, hence the literacy impairment. Ramus

et al

(2003) also found that auditory deficits cannot be characterised simply as rapid auditory processing problems, as would be predicted by the magnocellular theory. Nor are they restricted to speech. They claim that:

Contrary to the cerebellar theory, we find little support for the notion that motor impairments, when found, have a cerebellar origin or reflect an automaticity deficit. Overall, the present data support the phonological theory of dyslexia, while acknowledging the presence of additional

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sensory and motor disorders in certain individuals (Ramus

et al

, 2003, p 841).

The variety of imaging methods, from magneto encephalography to functional MRI (fMRI) and positron emission topography (PET), not only assisted in drawing conclusions to the vast directions of research mentioned before, but also highlighted the important information obtained through the different theories of dyslexia (the phonological theory, the rapid auditory processing theory, the visual theory, the cerebellar theory and the magnocellular theory).

Moreover, the variety of imaging methods has contributed to the observation that, at a microscopic level, a meticulous analysis of serial coronal slices disclosed specific cortical malformations including ectopias, mainly distributed across both frontal regions and in the left language areas (Kaufmann and Galaburda, 1989). This finding will be discussed in some depth in the next section in which reading disabilities are discussed.

In document A case study of a reading intervention programme for 'dyslexic students' in Israel (Page 63-67)