This is an interesting proposal for the ‘core deficit’ in dyslexia. Our perceptual systems seem to be twofold - we have parvocell and magnocell systems bringing in data from the senses. The visual system is the one in which magno- and parvocells have been studied to date, but there may be similar dual systems in other modalities (for example the auditory system). A parvocell (‘little cell’) system delivers very detailed and exact data to the mind, presenting it with clear, complete information. The trouble is that it’s slow - it takes time for the perception to reach the mind. Thus, perhaps, the magnocell (‘big cell’) system, which is much quicker. It won’t deliver so fine-grained a perception, so complete a picture, but what it does give, it gives quickly. This can be an important advantage. Your magnocell system will, for example, tell you in good time that a sizeable object is flying through the air towards your head. Your parvocell system will, rather later, tell you that it’s about 10 cm across, irregular in shape and made of rather nice grey granite with pretty patterns of reflective crystals on its surface. Horses for courses.
The speed of the magnocell system may have other, collateral advantages. When we read, our eyes stop and read, then snap along the line, then stop and read, then snap further along in the fixation/saccade routine we saw in chapter four. We need to be able to see, fixate and focus in detail, very rapidly and accurately if we are to do this quickly but competently. It has been suggested that it is the magnocell system which enables this. It has therefore been suggested that a deficit in the visual magnocell system might be a cause of reading difficulty in ‘dyslexics’. (eg Eden et al 1996, Hogben 1997, Stein & Talcott 1999) There is some debate among those favouring this explanation as to whether the deficit is innate, perhaps genetic, and present from birth or whether it might be the result of insufficient training of the eyes below about the age of seven, at which age it is thought the system becomes more fixed and less trainable. It should be noted that some research disputes the theory altogether (e.g. Goulandris et al 1998, Johannes et al 1996). It should also be noted that this theory involves only the visual system and cannot explain a phonological awareness deficit. ‘Dyslexics’, it should be further noted, are IQ/achievement discrepancy defined in these studies.
Reading large amounts of research on the extremely varied neurological aetiologies proposed for dyslexia can be like looking in on Bedlam. Extraordinarily multifarious claims reverberate against each other; findings loudly compete. Everyone hopes and believes they hold the Holy Grail. The onlooker is spun this way, then that. It leaves the unwary disoriented, even queasy. On a bad day you wonder if your eyes still point in the same direction. Such reading demands that both feet be kept consciously and conscientiously applied to the terra firma of common sense. The following is but a taste…
The doyen of writers on the subject of the neurology behind dyslexia is Albert Galaburda. Geschwind and he (1987) proposed a general, overarching theory of ‘anomalous cerebral dominance’. They suggested that this arose in utero as a result of a testosterone imbalance. Their theory, which can only be described as grand, claimed that the brain’s normal asymmetry was disturbed and that this caused a vast array of disorders including dyslexia, other language disorders, autism and disorders of the immune system. Evidence is rather small, wildly mixed and the theory remains warmly disputed (e.g. Bryden et al 1994). Problems of measurement and definition bedevil the elucidation of the theory and findings frequently absolutely contradict previous findings. ‘Dyslexics’ are also defined by the IQ/achievement discrepancy throughout.
Galaburda, and others, claim diagnostic abnormalities and even outright lesions are detectable at post-mortem examination of the brains of ‘dyslexics’ (only eight were examined, all defined by IQ/achievement discrepancy) and some laboratory rats and mice (Galaburda et al 1985, Galaburda (ed) 1993, Galaburda et al 1994, Galaburda 1999). On the whole, Galaburda and his co-workers appear to believe that dyslexia is not a genetically determined defect, but that it is induced in utero or in the neonatal period. The main, but not only, contender as aetiology is hormonal imbalance, particularly testosterone imbalance. Microscopically revealed ‘abnormalities’ are reported from a plethora of sites in the mid and fore brains, involving, for example, ‘… areas of the brain concerned with perceptual processing, as well as those involved in cognitive and meta-cognitive tasks’ and ‘… at least the visual and auditory pathways.’ (Galaburda 1999 p. 183). A recurring claim is that the planum temporale, found in the left upper temporal lobe and responsible for much language management, is ‘abnormally’ symmetrical in ‘dyslexics’. How abnormal such abnormalities really are, if at all, is very uncertain indeed and so is how, if at all, they relate to observed abilities or behaviours (Pumfrey & Reason 1991).