dys-lexic readers (Duara et al., 1991; Robichon & Habib, 1998; Rum-sey et al., 1996) is suggested to reflect differences in the path-ways connecting the angular gyri bilaterally (Duara et al., 1991).
Accordingly, callosal morphology has correlated with phonolog-ical processing (Robichon & Habib, 1998). Conflicting evidence for the size difference exists, however (e.g. Larsen, Høien, &
Ødegaard, 1992).
1.5.3 Magnocellular hypotheses of developmental dyslexia
Various hypotheses have been presented concerning the possi-ble causal role of the magnocellular system in the difficulties of developmentally dyslexic readers. What these hypotheses have in common is the notion of impaired temporal processing, which either causes the dyslexic reading difficulties (either via affect-ing the visual or laffect-inguistic processes) or only co-occurs with them.
1.5.3.1 Lovegrove & Breitmeyer: Saccadic suppression
Based on visual psychophysical contrast sensitivity tasks, Love-grove and his colleagues (LoveLove-grove, Bowling, Badcock, & Black-wood, 1980) suggested a deficit in the development of the tran-sient (that is magnocellular) visual system in dyslexia. Reading was thought to be impaired, because during a saccade the slowed transient system would not suppress the sustained (parvocellu-lar) system, that is, erase the image of a previous ‘sustained’ fix-ation (Breitmeyer, 1980; Lovegrove, Martin, & Slaghuis, 1986;
Lovegrove, Garzia, & Nicholson, 1990). As a result, the succeed-ing images would blend. It was later shown, however, that dur-ing a saccade, the previous activity of the transient, not the
sus-tained, system is inhibited (Burr, Morrone, & Ross, 1994). Love-grove (1993) has later hypothesized a more general sensory tim-ing problem behind the difficulties in developmental dyslexia.
1.5.3.2 Stein: The magnocellular theory of developmental dyslexia
Stein and his colleagues (Stein, 2001; Stein & Walsh, 1997) have broadened the original hypotheses by speculating more explicit-ly that the processing of ‘fast temporal information’ is impaired in developmental dyslexia, and is causally related to the dyslex-ic diffdyslex-iculties. They suggested that similar divisions, as found in the visual modality, also exists in the auditory and tactile modal-ities between the neural systems specialized in fast and slow stim-ulus processing (Stein & Walsh, 1997). This parallels the earlier results and suggestions of Tallal and her colleagues (Tallal, 1980), who showed that auditory temporal processing is impaired in developmental dyslexia. Stein generalizes the temporal impair-ment further to encompass processing beyond perceptual and brain areas outside those solely focusing on perceptual process-ing, however related to the magnocellular system (e.g. cerebel-lum) (Stein, 2001). In addition to temporal processing difficul-ties, Stein has also suggested that, resulting from the magnocel-lular impairment, some dyslexic readers have difficulties in sta-bilizing binocular fixation and therefore letters appear to move around (Stein & Walsh, 1997). This is supported by their finding that reading difficulties are at least partly relieved when one eye of such a dyslexic reader is occluded (Stein, Richardson, & Fowl-er, 2000).
1.5.3.3 Vidyasagar: Attentional spotlight
Vidyasagar has proposed a causal role of impaired magnocellu-lar mechanisms and attention in developmental dyslexia (Vid-yasagar, 1999). The magnocellular system has emphasized trans-mission times and spatial coding properties of object locations.
It is therefore suggested to give rise to the so-called attentional
spotlight. This pre-attentive, parallel processing, would guide the parvocellular system to focus selectively on a specific area or ar-eas for serial search. Magnocellular impairment could therefore also lead to symptoms of impaired parvocellular functioning. In reading, the communication between these two systems would enable the ordering (magno-based) of identified letters or words (parvo-based). When learning to read, the accumulative training of the sequential movement of the attentional spotlight is sug-gested to be perhaps the most important element. Other modal-ities besides vision could also be affected. This could result from a modality-specific or a more generalized impairment in the var-ious magnocellular systems. Alternatively, impaired visual mag-nocellular input could affect parietal, possibly multimodal, spa-tial representation system and therefore cause difficulties also in other modalities.
1.5.3.4 Hari: Sluggish Attentional Shifting
Hari and her colleagues (Hari & Renvall, 2001) have presented a magnocellular hypothesis concentrating on attention as well. She proposes that dyslexic readers have difficulties in engaging and disengaging attention, that is, they would suffer from ‘sluggish attentional shifting’. This would result from a weakness of atten-tional capture system, which is supported by, for instance, pari-etal functions. Because of this ‘sluggish attentional shifting’, processing of rapid stimulus sequences would be impaired, and the chunks in which input information is processed would be prolonged, possibly in every perceptual modality. This sluggish-ness is suggested to distort motor sequencing too, and perhaps cortical representation of stimulus categories, for instance, pho-nemes.
1.5.3.5 Nicolson & Fawcett: Cerebellar dysfuncion
Nicolson, Fawcett and Dean (2001) claim that a cerebellar function could cause the impairments observed in 80% of
dys-lexic readers. Their hypothesis in not ‘magnocellular’, but is in-troduced here because of its association to the hypotheses of Stein (2001). Directly, cerebellar dysfunction could cause motor diffi-culties and therefore the poor quality of handwriting and ham-pered articulation observed in dyslexic readers. Indirectly, the cerebellar dysfunction could cause difficulties in sensory feed-back processing, because articulation would require more processing capacity. Slower articulation speed would also result in less effective working memory processing and therefore diffi-culties in language acquisition. The defective articulatory repre-sentations could again lead to poor sensitivity to the sound struc-ture of spoken language, that is, poor phonological awareness.
Difficulties in spelling could be explained with over-effort in read-ing, poor phonological awareness, and impaired automatization of skills.
1.5.3.6 Galaburda: Cortical-phonological and thalamic-temporal impairments
Galaburda and his colleagues (Galaburda et al., 2001) have sug-gested that difficulties in linguistic and temporal processing could perhaps be somewhat independent of each other. In their rodent model, induced cortical injuries led, in male rats only, to second-ary thalamic MGN changes (greater number of small and fewer large cells). Temporal processing impairment was observed only in the case of animals with these secondary thalamic abnormali-ties. Impairments in tasks of more ‘cognitive’ nature (e.g. learn-ing) were related to primary cortical injuries. Accordingly, they suggest that also in humans cortical lesions would lead to diffi-culties in higher cognitive functioning, for instance, impaired phonological processing, but not directly to temporal processing difficulties. In some cases, in addition to the cortical areas, the thalamic magnocellular areas would be implicated and this sub-cortical abnormality would be related to impaired temporal processing.