‘Abnormalities’ are reported among ‘dyslexics’ in numerous living brain structures and behaviours using brain scan techniques. Hynd et al (1995), for example, found the genu of the corpus callosum significantly smaller in ‘dyslexic’ children. Duara et al (1991) found another area in the corpus callosum, the splenium, to be larger in ‘dyslexics’ than ‘normals’. Larsen et al (1990) found ‘abnormal’ symmetry in the planum temporale in ‘dyslexic’ adults, 70 per cent of whom showed symmetry compared to only thirty per cent in ‘normals’. (Why the figure is not one hundred per cent is unclear. Nor was it shown that any of the apparent ‘abnormalities’ in any of these studies actually related to any difference in performance or behaviour.)

Brain scans appear to show exciting, if crude, differences between ‘dyslexics’ and ‘normals’. A recent popular science text on dyslexia, for example, relies heavily upon them (Shaywitz 2005). However, the normal but literate brain will differ from the normal but less literate brain in important functional ways which will show up on a brain scan. This is absolutely unremarkable - they have had radically different experiences and we know that brain architecture is profoundly affected by experience. (Robertson 1999.) (And remember Castro-Caldas 1998, Gaser & Schlaug 2003, Maguire et al 2000, Schlaug 2001, those large straws-in-the-wind.) As we have seen, Adams (1990) Siegel & Himel (1998) and Stanovich (1991), for example, all write that reading well, and often, enhances IQ while reading poorly and little does the reverse. Remember also the Matthew effect, of which more later. We need not, in fact, invoke neuropathology to explain these apparently neuropathological findings. There are other more parsimonious and credible explanations, of which more later.

It is also important to point out that scans, although they produce wonderful (and marvellously expensive) pictures cannot really tell us about the detailed procedures within so subtle an organ as the brain. Scans are excellent for gross anatomy and visualising lesions and materially assist in medical diagnosis thereby. Their value in cognitive psychology, however, is much smaller. They may rather generally point to broadly interesting ideas on occasion, but they cannot be expected to do better than that. We cannot expect a scan, or even a series of scans, to show us the procedures which we suspect go on in our heads. These remain invisible – we have yet to film mental processes such as literacy, or love!

It is not at all clear, anyway, how far such weights-and-measures approaches to an organ as outrageously complicated, subtle and individually variable as the brain actually take us. Carts and horses are almost certainly also involved. Sample sizes, particularly when for post-mortem examinations, have been very small (or composed of rats or mice) and ‘dyslexics’ defined by the discredited IQ/achievement discrepancy criterion.

Two Sheffield researchers claim, on the basis of educational, intelligence and adapted clinical assessment of ‘dyslexics’ (discrepancy defined) to have demonstrated severe defects ‘… across the entire cerebellum.’ (Nicolson & Fawcett 1999 p. 166). They claim, flatly, that ‘Dyslexia is genetic in origin …’ (ibid. p.155) and that it is ‘… characterised as problems in skills automatisation’ (ibid. p. 171). Their battery of tests for screening adults for dyslexia includes a test of postural stability which consists of ‘… a calibrated push in the back.’ (Nicolson & Fawcett 1997 p. 78). They claim that ‘dyslexics’ showed ‘… severe and persistent problems’ with literacy but also with ‘… balance and motor skill’ (Nicolson & Fawcett 1999 p. 156). Many celebrated ‘dyslexics’ would dispute this finding (not least, perhaps, Jackie Stewart, three times formula one racing world champion and a crack clay pigeon shot) as many researchers have. This research spawned a ‘therapy’ to ‘cure’ ‘dyslexia’ (and more) by improving motor coordination (the DDAT treatment - Dyslexia, Dyspraxia, Attention Deficit Treatment). Many claim this therapy has proved, on dispassionate examination, to be an expensive chimera, as with so many other cures which have come and gone (Nicolson & Reynolds 2003, McPhillips 2003, Rack 2003, Rack et al 2007, Reynolds et al 2003, Reynolds & Nicolson 2007, Richards et al 2003, Singleton & Stuart 2003, Stein 2003, Snowling & Hulme 2003).