01 NRDC Dyslexia 1-88 update - Texthelp

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Research Report
(Moffatt et al., 1998), including experiences associated with childhood deprivation (De Bellis,
2001).
However, reports of anatomical differences between ‘dyslexic’ and ‘non-dyslexic’ brains must
not be taken to imply that they are causes rather than consequences of reading problems.
People who have never learned how to represent speech in writing cannot perform mental
functions requiring an ability to spell (Castro-Caldas & Reis, 2003). These mental functions
have a biological counterpart in the anatomical development of the brain (Carr & Posner,
1995; Castro-Caldas & Reis, 2003). A developmental pattern can thus be the consequence
rather than the cause of atypical learning activity and not only in the representation of speech
(Hsieh et al., 2001).
Consider two examples. Exceptional developments in the brain area associated with spatial
awareness have been shown in London taxi-drivers, who need to master ‘the knowledge’ of
routes and destinations in the capital (Maguire et al., 2000) and both functional and structural
differences have been shown between the brains of musical instrumentalists and nonmusicians
(Schlaug, 2001). In each case, it is a reasonable assumption that these differences
develop as adaptations to experience; for, although the ability to adapt is present in the
cradle, the taxi-driver’s ‘knowledge’ and the abilities to play the xylophone or spell its name
are not.
The structural imaging literature contains many inconsistent findings. They can be accounted
for by the use of a variety of scanning protocols and image analysis methods, by small study
populations, by wide variations in the diagnostic criteria used to define dyslexia, by
heterogeneous samples, by non-uniform matching of controls and by lack of routine analysis
for sex, handedness, socio-economic status, psychiatric co-diagnoses, intellectual ability and
educational background (Filipek, 1995, 1999).
There are two further grounds for caution when the findings from structural imaging are
interpreted. To begin with, simple comparisons between ‘dyslexic’ and ‘non-dyslexic’ subjects
may imply categorical distinctions where the differences are really points on a continuum.
Then, the abnormalities seen in ‘dyslexic’ brains might be assumed to be typical of dyslexia,
or exclusive to dyslexia, when they are neither.
Structural findings from the imaging studies, like those from the post-mortem studies, are at
best suggestive, not definitive. Indeed, it is possible that the neurological anomalies in
developmental dyslexia are task-specific; that is to say, they are not structural at all but
functional (McCrory et al., 2000).
Evidence from in vivo studies: functional differences
Certainly, the most compelling evidence for neurological anomalies in dyslexia comes from
functional imaging. Both positron emission tomography (PET) and functional magnetic
resonance imaging (fMRI) techniques directly relate behaviour to brain activity. They allow
researchers to contrast patterns of brain activation in impaired and unimpaired readers.
Functional neuroimaging has demonstrated that reading entails much more complex patterns
of activation than had been suspected on the basis of findings from post-mortem studies of
stroke and brain injury patients. Formerly, reading was conceptualised in terms of two
localised and self-contained components, known as Broca’s area and Wernicke’s area, in the
dominant cerebral hemisphere (Pickle, 1998). Now, reading is known to entail a wider