Similarly, a related group of researchers maintain that there is an abnormality in the visual magnocellular system of dyslexics. The re-establishment of visual deficits in dyslexia has arisen due to several studies that have reported dyslexics exhibiting impairments in visual processing that are functions of the dorsal visual pathway, a system dominated by magnocellular cells in the lateral geniculate nucleus and is involved in the detection of transient visual information.
For instance, Lovegrove and his colleagues (1990) demonstrated that developmental dyslexics had slightly reduced contrast sensitivity at the low spatial frequencies and low luminance levels favoured by the magnocellular system, particularly during flicker. Stein and Walsh (1997), also committed proponents of the visual magnocellular hypothesis and has argued that dyslexic individuals have difficulties with binocular vision. Eden, Vanmeter, Rumsey, Maisog, Woods and Zeffiro (1996) reported a brain-imaging study in which a small sample of dyslexics showed impairments in judging the relative velocity of movement of visual stimuli. In addition they also exhibited abnormal activation in area V5/MT, part of the magnocellular system (Rayner, Foorman, Perfetti, Pesetsky & Seidenberg, 2001).
It should be emphasised that these supporters of the magnocellular theory do not dispute the phonological deficit hypothesis. Rather, they challenge that phonological problems are caused by a basic deficiency in hearing sounds, and that a visual deficit might independently contribute to reading problems. Therefore, on the basis of the two alternative approaches discussed so far: the phonological deficit and magnocellular deficit, it can be seen that dyslexia researchers agree that a phonological deficit is a cause of developmental dyslexia. However differences in the exact degree of centrality of the phonological deficit in explaining the reading retardation and about the importance of apparent sensory impairments in the dyslexic population reduce the strength of the consensus and give rise to an alternative magnocellular account of dyslexia.
Recently, Roderick Nicolson and his colleagues have criticised that “in spite of extensive research, these approaches have failed to account for the full range of difficulties established for dyslexic children” (Nicolson, Fawcett, Dean, 2001, p.508), specifically the more recently established impairments in balance and motor skills. Initial cognitive level arguments (Nicolson & Fawcett, 1990) emphasised an all-encompassing difficulty in skill automatisation, an inability to become completely fluent in cognitive and motor skills to the extent that they no longer need conscious control. The same researchers have now implicated abnormal function of the cerebellum, a system long known to be responsible for motor skill execution and more recently thought to play a central role in skill automatisation and skills relating to language.
Following this, Nicolson et al (2001) claim to account for the full range of difficulties established for dyslexic children in their cerebellar deficit hypothesis. Cerebellar abnormality at birth is hypothesised to lead to problems in skill (motor and articulation), fluency and automaticity. More specifically, the lack of articulatory fluency is seen to lead to impoverished representation of the phonological characteristics of speech, which in turn may lead directly to impaired sensitivity to onset, rime and the phonemic structure of language – that is a deficit in phonological awareness, which leads to the subsequent problems in learning to read.
Cerebellar impairment therefore causes by direct means the phonological core deficit. Again at a cognitive level of explanation, proponents of the cerebellar deficit account of dyslexia agree with the vast majority of researchers that a phonological core deficit is a “…fruitful explanatory framework for many aspects of dyslexia…” (Nicolson et al, 2001, p.510), but disagree that it is the sole cognitive dysfunction and also highlight an automatisation deficit. In relation to the theoretical formulation for dyslexia based on a magnocellular deficit, the cerebellar deficit also highlights an underlying neural substrate but is an alternative mechanism to the magnocellular abnormality and addresses a general motor deficit as opposed to a sensory impairment.
Remediation of dyslexia
Regarding the remediation of developmental dyslexia, proposed interventions have been largely based on these theoretical approaches and have therefore varied along with the specific claims concerning the mechanisms responsible for the disorder. However the general agreement among researchers that a lack of phonological skills does somehow or the other play a causal role in dyslexia, transfers to the issue of remediation, specifically that this insufficiency should be addressed, directly or indirectly, in all interventions designed to overcome the disorder. The vast majority of researchers solely in support of the phonological deficit hypothesis, exclusively advocate direct training in aspects of phonology.
Systematic phonics instruction, for example has successfully been implemented and teaches the dyslexic the major grapheme-phoneme correspondences and how to use these to decode and spell words. Also it teaches phonemic awareness which is as noted before the ability to analyse and manipulate phonemes in speech, for example, how to break the spoken word ‘beach’ into three phonemes, /b/-/e/-/ch/, or how to blend these phonemes to say the whole word. Acquiring a reasonable grasp of phonics, the dyslexic reader is in a better position to make progress because he or she will be better equipped to identify words encountered in print for the first time (Snowling, 2000).
Although there is widespread use of phonics instruction that has led to direct benefits in helping to overcome dyslexia, the researchers who have recently highlighted the theoretical paradox in dyslexia disagree that phonology should be the primary target of remediation,. Instead they have developed interventions specifically to remediate the sensory and motor impairments in dyslexia. In remediating these difficulties phonology is also seen to improve.
For example, based on her discovery that many children with specific language impairment show a significantly impaired ability to sequence auditory tones presented close together, a difficulty attributed to the auditory magnocellular system, Tallal and her colleagues have developed the ‘Fast ForWord’ remediation training programme (Tallal, Mezenich, Miller & Jenkins, 1998). To overcome this specific difficulty, the programme’s primary focus is on training the children to discriminate rapid auditory signals. Speech, with artificially slowed consonant transition is presented, the idea being that it is possible for the brain to be retrained to become sensitive to the transition.
Although the primary focus of the training programme is elsewhere, it too emphasises training in phonological processing. Regarding an abnormality in the visual magnocellular system, proposals for remediation have included wearing coloured glasses or an eye patch. More specifically, Stein, Richardson and Fowler (2000) advocated treatment of difficulties with binocular vision via the occlusion technique.