While correlations between reading and performance on movement perception tasks are interesting, they do not tell us how a magnocellular deficit might lead to difficulties in learning to read and to spell. Breitmeyer and Ganz (1976) suggested that in the brief interval between successive fixations of a visual scene, when the eyes move and vision is impaired (although we are not usually aware of this), the M pathway suppresses or masks activity in the P pathway. This would ensure that the images received during each fixation would not interfere with each other. Any anomalous operation of the suppression mechanism in relation to the
M system would thus be expected to have consequences for reading. However, recent research has provided evidence for the opposite effect, namely that during saccades the magnocellular system is selectively suppressed (Burr, Morrone, & Ross, 1994; see also review by Ross, Burr, & Morrone, 1996) which rather undermines Breitmeyer's theory.
Talcott et al. (1998) suggested that impaired M pathway functions do not interfere directly with reading, but rather indirectly, perhaps via effects on persistence of retinal images, visual stability, or eye movements. Stein (2000) recently expressed the argument as follows:
One problem that constantly bedevils the hypothesis that dyslexics have impaired mag-nocellular function is that people find it very difficult to understand how a system devoted to detecting visual motion could possibly be relevant to reading. After all, we don't usually have to track moving targets when reading; the page is usually kept stationary. In fact, the retinal images of print are not stationary, and many dyslexic children complain that letters seem to move around when they are trying to read, i.e. their visual world is highly unstable. This is because during reading visual images are actually very far from being stationary on the retina, and dyslexics fail to compensate for this . .. We believe that their unstable visual perceptions are the result of the insensitivity of their visual magnocellular systems (p. 111).
In an earlier review, Stein and Walsh (1997) argued that "Slight impairments of mLGN (magnocellular laminae of the LGN) performance or organization might... multiply up to greater deficits in PPC (posterior parietal cortex) function. The PPC is known to be important for normal eye movement control, visuo-spatial attention and peripheral vision—all important components of reading" (p. 149).
They are not the only authors to implicate eye movements. Borsting et al. (1996) suggested an abnormal saccade mechanism could adversely affect reading (p. 1052). It is also possible that attentional factors might be relevant. Certainly, the frequent co-occurrence of dyslexia and attentional problems poses a methodological challenge to those attempting to investigate visual deficits in dyslexia.
The magnocellular deficit hypothesis of dyslexia has generated considerable scepticism and controversy (see Hayduk, Bruck, & Cavanagh, 1996; Hulme, 1988; Lovegrove, 1991; Skottun, 1997, 2000; Walther-Muller, 1995) and there have been a number of failures to support it. Skottun (2000) reviewed nearly two dozen studies involving measurement of contrast sensitivity. He concluded that only 4 out of 22 studies support the magnocellular deficit hypothesis, 11 provide evidence against it, while 7 studies have provided inconclusive results. Even with regard to experiments involving moving stimuli, Skottun notes that random dots can stimulate both M and P pathways and therefore any deficit cannot be unambiguously attributed to the magnocellular pathway. The conclusion of Skottun's review is that there is little compelling evidence for a deficit in dyslexia that can be related exclusively to the magnocellular system. This does not, of course, invalidate those findings said to support the hypothesis even if their interpretation is in doubt. The findings themselves still have to be explained.
Some of the early research reported in the scientific journals was sloppily executed or carried out with inadequate methodological control procedures or with unmatched participant groups. However, not all the research was flawed (see, e.g., Evans, Drasdo, & Richards, 1994) and this is unlikely to be the reason why the idea of a magnocellular deficit has met with so much resistance (as with so much in the field of dyslexia!). The predominant view (see Ramus et al., 2003) of dyslexics' difficulties is that they are caused by phonological problems; the idea that visual problems might be crucial has been largely rejected by many researchers (if not by practitioners).
As always, much hangs on the meaning attributed to a particular word, in this case "visual." All sorts of phenomena can be and have been classified under this heading, including visuo-spatial perception, ocular factors, memory for visually presented events and so on (see Chapter 1 in this volume by Bruce Evans). Many people are reluctant to accept that "visual" problems contribute to dyslexic difficulties. Yet there is no necessary incompatibility between phonological problems on the one hand and M system problems on the other, especially, as we shall see, if the designation "M system" is broadened to include sensory systems other than vision.
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