01 NRDC Dyslexia 1-88 update - Texthelp

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Research Report
speech (McCrory, 2003). Nevertheless, activation in Broca’s area is not specific to dyslexia: all
poor readers work harder to uncover the gestures underlying the phonological structure of
words (Mody, 2003).
Differences in brain activation observed in functional imaging studies could occur for a variety
of reasons (McCrory, 2003; Pennington, 1999). Even where there are consistent differences
across studies, a causal association with dyslexia cannot be taken for granted (McCrory,
2003). Atypical functioning may point to nothing more ‘pathological’ than an unusual brain
organisation set up earlier, adaptively, in response to atypical experience (Locke, 1997). An
individual might exhibit contrasting responses to the same stimulus by attending to different
aspects of it on separate occasions (Kuhl et al., 2001). Group differences may reflect primary
cognitive deficits, but they might also reflect secondary consequences of those deficits,
compensatory processing, some other behavioural impairment, or more general differences
such as intelligence (McCrory, 2003). The cross-sectional nature of most functional imaging
studies might also invite misinterpretation, as the pattern of impairments at an early stage of
development may not resemble any pattern observed at a later stage (Bishop, 1997).
Nonetheless, functional neuroimaging is an invaluable technique for evaluating cognitive
theories of dyslexia and testing their implications (McCrory, 2003). Importantly, the dynamic
changes in regional cerebral blood flow challenge the established notion that phonological
representations are ‘located’ in a particular brain area and thus sequentially accessed, as
opposed to being ‘activated’ in parallel computational processes that are distributed across a
number of brain areas (McCrory, 2003). This insight into the competitive nature of the
computational process in reading, where many prospective candidates may need to be
considered before a word is finally identified (Pulvermüller, 2003), suggests that the central
difficulty in dyslexia could be conceptualised as a difficulty in resolving the phonological
competition (McCrory, 2001).
What do the brain studies tell us?
Many adult education practitioners have grown up at a time when ‘nurturism’ prevailed over
‘nativism’—except (paradoxically) in linguistics (e.g. Chomsky, 1957). Now, it is well
understood that individual differences are joint and interactive outcomes of random genetic
recombination at conception and subsequent experience (Gottlieb, 1992; Michel & Moore,
1995; Rutter, 2002). In this process as in so much else, timing is all: ‘The effects of a
particular set of genes depend critically on the environment in which they are expressed,
while the effects of a particular sort of environment depend on the individual’s genes’
(Bateson & Martin, 1999).
The differences between ‘dyslexic’ and ‘non-dyslexic’ brains revealed by the autopsy and
imaging studies are unquestionably biological in nature. This does not amount to proof that
the differences are biological in origin. There are grounds for caution in our understanding of
the brain’s ‘plasticity’—its capacity for adaptation and development. This understanding
should lead us to prefer a ‘neuroconstructivist’ view of language development (Bates, 1999;
Johnson, 2003; Karmiloff-Smith, 1998) to a ‘nativist’ view (Pinker, 1994); that is to say, to
prefer a view of language ability emerging in the course of development to a view of language
as an innately modular capacity. A neuroconstructivist approach to developmental disabilities
(e.g. Snowling, 2000) is supported by the interpretation of findings from imaging studies that
‘learning to read and write during childhood influences the functional organisation of the
adult human brain’ (Castro-Caldas & Reis, 2003).