Understanding dyslexia
Understanding dyslexia

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Understanding dyslexia

2.4 Differences in brain architecture

2.4.1 Organisation of brain cells

Some findings that do appear to be more specific to dyslexia are various microscopic anomalies in the actual organisation of brain cells, reported from post-mortem studies (Galaburda et al., 1985). These include collections of slightly ‘misplaced’ cells (called ectopias) and some minor disordering of the regular layering of cells in the cortex. They are often particularly concentrated in left hemisphere regions involved in language processing, although their distribution varies considerably between individual cases. Another interesting feature of these ectopias is that they are typically accompanied by an unusually rich and diverse pattern of connections to other brain regions, which may account for the apparent increased creativity that is sometimes observed in people with dyslexia.

These minor disturbances of brain architecture are known to arise during prenatal development, and although the reasons for their origin are still unclear, it is thought that they could reflect unusual immune system effects on the developing brain. Research into their significance for brain function suggests that they could interfere with the coding of rapidly changing auditory stimuli, like sounds in speech. If so, this could be relevant to the phonological deficits already discussed. However, it is particularly interesting to note that these anomalies have so far only been associated with auditory processing problems in males (Herman et al., 1997).

The discovery of minor structural differences in the brains of people with and without dyslexia would support the idea that the predisposition to dyslexia is constitutional, particularly if these differences are present before birth. However, a major difficulty is that these differences can only be observed post-mortem, so only a limited number of brains have so far been studied in this way. This means that we should be very cautious about generalising these findings to all people with dyslexia.

If these anomalies do have any causal significance for dyslexia, then the fact that their regional distribution varies so much between individuals could help to explain some of the variation observed in behavioural symptoms. For example, if this unusual brain micro-architecture were to occur in left hemisphere areas important for auditory or language processing, would we expect a more ‘phonological’ form of dyslexia than if it occurred in right hemisphere areas important for rapid visual processing?

Finally, some speculation can also be offered regarding these apparent differences in the ‘hardware’ of the dyslexic brain. Two points seem particularly relevant:

  • the brain symmetry associated with dyslexia may reflect an increase in the total number of neurons

  • the microscopic disturbances of cellular organisation are associated with greater connectivity between different regions.

There is evidence from the study of artificial ‘neural networks’ that this kind of arrangement (i.e. one with more cells and more interconnections) may be disadvantageous for some tasks – such as learning associative ‘rules’ – but it may actually be more efficient at tasks which require less automatisation and more creativity.

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