01 NRDC Dyslexia 1-88 update - Texthelp

Developmental dyslexia in adults: a research review 19
People can be described as ‘dyslexic’ on a variety of criteria, not all of which are compatible.
What kind of causal process might result in dyslexia?
Once more, the theoretical pathway divides. There might be either one cause or more than
one cause of ‘dyslexia’. If there is only one cause, it has to be either biological or experiential.
However, if there is more than one cause, the causes might be either biological, or
experiential, or part biological and part experiential. If there is more than one cause, the
causes might take effect separately or in combination. If the causes take effect in
combination, they might do so independently, in a ‘main effect’ model; or one cause might
mediate the effect of another cause, whether by exacerbating it or by alleviating it, in a static
‘interactional’ model; or there might be continuing and progressive interplay over time
between biological and experiential causes, in a dynamic ‘transactional’ model (Gottlieb &
Halpern, 2002; Gottlieb et al., 1998; Sameroff & Chandler, 1975).
These causes may take effect at different developmental stages. They may be immediate or
remote, with respect to learning how the alphabet encodes the spoken language. A cause at
one stage in development might be supplemented by a second cause at a later stage. One
cause might mediate the effect of another. At every stage from conception onwards, some
event might affect a person’s acquisition of alphabetic skills, to their benefit or detriment.
There can be many different courses of individual development before a learner reaches the
final common pathway of failure to acquire alphabetic skills at the expected age and with a
fluency that makes reading for meaning both informative and enjoyable.
In short, there may be no single causal process. If it turns out that there is indeed no single
causal process, then no single theory of reading failure can explain every individual failure.
Indeed, it might be that no single theory could fully explain any individual failure or, at the
extreme, that a fully-developed theory might explain one case only.
This analysis has used the metaphor of a dividing pathway. In an ideal world, there would be
only a single pathway. On the landscape of ‘dyslexia’, however, there are many pathways, and
it seems that almost every one is—rightly or wrongly— signposted to our destination.
Samples of the evidence for these observations can be found in Appendices 1 and 2.
Dyslexia might be a final pathway common to many causal processes.
What is the prevalence of dyslexia?
Although people sometimes speak of the ‘incidence’ of dyslexia, incidence is the frequency
with which new cases occur and are diagnosed over a period of time (Barker et al., 1998). The
proportion of dyslexic individuals in a population at any one time is properly called the
‘prevalence rate’ (Everitt & Wykes, 1999), although ‘prevalence’ is the term in general use.
The previous section implies that any estimate of the prevalence of dyslexia will reflect the
chosen definition and how it is operationalised. No two of those definitions could possibly
identify the same individuals, or the same number of individuals, in any population. It has
been shown that prevalence estimates for dyslexia are susceptible to definitional
manipulation over a wide range (Snowling et al., 2000a). In the absence of a definition that
provides unequivocal identification criteria, all statements about prevalence are guesses; they
are value judgements, not scientific facts (Kavale & Forness, 2000). All the same, there can be
no doubt that the higher the estimate is, the more likely it will be to confound dyslexia with
ordinary reading difficulty.