01 NRDC Dyslexia 1-88 update - Texthelp

Developmental dyslexia in adults: a research review 29
repertoire of distributed processes in both cerebral hemispheres (Binder et al., 1997; Price,
2000), functioning as neural networks in which Broca’s and Wernicke’s areas might be
analogues of Crewe and Clapham junctions in the railway network. It is also evident that
patterns of activation emerge and are transformed in the course of learning to read and write
(Booth et al., 2001; Petersson et al., 2000).
It appears that the normal process of reading has a characteristic neural signature —or
rather, that each linguistic subprocess has a neural signature of its own (Cabeza & Nyberg,
1997; Wise et al., 2001). For example, normal silent reading activates the left inferior parietal
cortex, the right posterior temporal cortex, both sensorimotor cortices and the
supplementary motor areas (Cossu, 1999). Additionally, non-word reading activates the left
inferior temporal region the left inferior frontal area, and the supramarginal gyrus (Cossu,
1999). Viewing words in alphabetic script (by contrast with viewing word-like forms in false
fonts) activates bilateral language areas, including the left inferior prefrontal regions and the
left posterior temporal cortex (Cossu, 1999). Reading aloud and making lexical decisions also
entail bilateral activation of the mid-to-posterior temporal cortex and mainly left-hemisphere
activation of the inferior parietal cortex (Cossu, 1999).
Evidence for a neural signature of reading impairment is provided by studies reporting
differential activation patterns in three key areas: the inferior frontal gyrus (Broca’s area); the
dorsal parieto-temporal region, incorporating the superior temporal gyrus (Wernicke’s area)
and angular and marginal gyri; and the left posterior inferior temporal area, incorporating the
fusiform gyrus and middle temporal gyrus (McCrory, 2003).
However, these neural studies of reading impairment are not without interpretational
problems (McCrory, 2003). One study reports reduced activation in Wernicke’s area (Rumsey
et al., 1997b), but leaves open the possibility that the same reduction might be seen in
ordinary poor readers, in which case it could be interpreted as secondary to some other
difficulty (McCrory, 2003). A similar reduction in activation (Shaywitz et al., 1998) might be
explained as a reflection of lower levels of reading accuracy, again leaving open the possibility
that it might also be characteristic of ordinary poor readers, a possibility made all the more
likely in this case by a lower level of intellectual ability in the group designated as ‘dyslexic’
(McCrory, 2003).
Reduced activation reported in the parietal-temporal-occipital association cortex (Brunswick
et al., 1999) may indicate a more robust difference (McCrory, 2003), and this finding has been
replicated in a cross-linguistic comparison (Paulesu et al., 2001).
Across these and other studies, the most consistent discrepancies between the activation
patterns of dyslexic and non-dyslexic participants have been in three areas: the posterior
inferior temporal cortex, the left angular gyrus and the left inferior frontal cortex (McCrory,
2003).
Reduced neural activation by dyslexics in the posterior inferior temporal cortex is consistent
with difficulty in retrieving phonological forms from visual stimuli, perhaps including
dyslexics’ frequently-reported difficulty in picture-naming (McCrory, 2003). Reduced neural
activation by dyslexics in the left angular gyrus, however, might possibly be a secondary and
nonspecific effect of inefficient phonological processing (McCrory, 2003). In the left frontal and
precentral regions, the neural activation seen in dyslexics is greater, not less, than that seen
in efficient readers and may correspond to effortful compensatory strategies involving inner