01 NRDC Dyslexia 1-88 update - Texthelp

Developmental dyslexia in adults: a research review 65
variance in continuous rapid automatised naming provides an unmistakable refutation of the
temporal processing deficit hypothesis (Chiappe et al., 2002).
It seems unlikely that dyslexia is characterised by impaired processing of rapidly-changing
auditory stimuli.
The magnocellular deficit hypothesis
It is only one of many paradoxes in this field of investigation that a wide-ranging explanatory
hypothesis finds mixed support for its central observation of a temporal processing deficit in
reading disability. Yet the magnocellular deficit hypothesis (Stein, 2001; Stein & Talcott, 1999;
Stein et al., 2000; Stein, 1994; Stein & Walsh, 1997) is a comprehensive if not yet persuasive
attempt to explain a wide range of behaviours associated with developmental dyslexia and to
do so at every level in the three-level model (see Appendix 4).
The magnocellular deficit hypothesis starts from an observation that many dyslexic people
find that the letters they are trying to read appear to move around and cross over each other
(Stein, 2001). This phenomenon is explained in terms of impaired sensitivity to visual motion
and unstable binocular fixation, caused by atypical development of the magnocellular layers
of the lateral geniculate nucleus, a ‘processing station’ on the route from the eyes to other
parts of the brain. The atypical development of the magnocells is ascribed to geneticallydirected
antibody attack during antenatal development, together with vulnerability resulting
from diets low in essential fatty acids.
The magnocellular deficit hypothesis proposes a comprehensive account of dyslexia from
biology to behaviour.
Limitations of the magnocellular deficit hypothesis
The hypothesis is highly speculative (Stein & Talcott, 1999) and most of the evidence is still
circumstantial (Stein, 2001), so that further research is essential. The impairment in the
dyslexic visual magnocellular system is slight and is not found in all dyslexics (Stein, 2001). It
is not immediately obvious how the visual magnocellular system contributes to reading; it
might even be an epiphenomenon connected with the dyslexic phenotype but playing no
important causal role in dyslexic people’s reading difficulties (Stein, 2001). Impaired contrast
sensitivity is unlikely to be the direct cause of dyslexic reading difficulties, as print does not
normally flicker and contrast is usually high (Stein & Talcott, 1999). Measures of visual motion
sensitivity correlate with visual homophone test scores across the whole population (Stein,
2001), which implies that the differences between dyslexic and non-dyslexic are differences in
degree rather than categorical distinctions. If this proves to be the case, then the best
understanding of developmental disabilities may be achieved by investigating the causes of
population variability (Gilger & Kaplan, 2001).
Although the evidence for an association between immune disorders and dyslexia is
inconclusive (Flannery & Liederman, 1995; Galaburda, 1993; Gilger & Pennington, 1995;
Gilger et al., 1998; Taylor et al., 2001; Tønnessen et al., 1993; Vincent et al., 2002), the
question is one that merits further investigation. At the very least, the genetic evidence is
suggestive; further research on the gene loci associated with myelination (Smith et al., 2001),
for example, may or may not lead to effective interventions for enhancing information
processing by addressing problems identified elsewhere as ‘noisy neural networks’ (Fawcett