01 NRDC Dyslexia 1-88 update - Texthelp

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Research Report
function are compelling. Cerebral specialisation depends as much on specific experiences as
on ‘pre-wiring’, so that researchers need to explain a complex pattern of associated
impairments, not a highly selective deficit (Bishop, 1997; Gilger & Kaplan, 2001). The
assumption of residual normality against a background of normal development is difficult to
maintain when both compensation and disruption result from initially undamaged cognitive
functions developing in untypical ways (Karmiloff-Smith, 1998; Thomas & Karmiloff-Smith,
2002).
Empirical evidence, too, suggests that the analogy is invalid (Ellis, 1985; Snowling et al., 1996).
An early study reported that developmental dyslexics resembled ‘surface’ but not ‘phonological’
alexics in that they were qualitatively similar to younger, normal readers (Baddeley et al.,
1982). Some later studies have reported a phonological-to-surface continuum (Bryant & Impey,
1986; Ellis et al., 1996; Racket al., 1993), which is also seen in ‘normal’ readers (Bryant &
Impey, 1986; Ellis, 1985) and reports of distinct phonological and surface subtypes of
developmental dyslexia (e.g. Curtin et al., 2001) might be explained as outcomes of teaching
method and strategic choice, not as outcomes of biological constraint (Hendriks & Kolk, 1997;
Manis et al., 1996; Murphy & Pollatsek, 1994; Thomson, 1999).
There is further evidence for rejecting the assumption that ‘surface’ and ‘phonological’ dyslexia
are alternative or complementary manifestations of an organic dysfunction. ‘Surface’ dyslexics
are characterised by developmental delay, whereas ‘phonological’ dyslexics are characterised
by a cognitive deficit (Griffiths & Snowling, 2002; Gustafson, 2001; Sprenger-Charolles et al.,
2000; Stanovich et al., 1997). Unlike ‘surface dyslexia’, ‘phonological dyslexia’ is associated with
naming-speed deficits (Wolf & Bowers, 1999) and also with deficits in the transient visual
system (Borsting et al., 1996; Spinelli et al., 1997).
In theory, the ‘surface dyslexia’ profile could be caused by any or all of lead exposure, prenatal
exposure to alcohol, influenza viruses and other causes of congenital malformation, or by
intensive instruction in phonological processing (Castles et al., 1999). Empirical evidence
suggests that it might be explained by insufficient exposure to print (Griffiths & Snowling,
2002; Gustafson, 2001; Sprenger-Charolles et al., 2000) and lower verbal ability (although not
necessarily less potential for intellectual development). This might offer a parsimonious
explanation for the association between ‘surface dyslexia’ and socio-economic adversity
(Bishop, 2001; Samuelsson et al., 2000), since higher and lower IQ groups of reading-disabled
children differ significantly on several home literacy variables, including parental education,
books in the home and being read to (Wadsworth et al., 2000), all of which relate to print
exposure.
Whether reading difficulties are attributable to delay (the ‘surface’ subtype) or to deficit (the
‘phonological’ subtype), they are of equally high priority for intervention. However, if the
‘phonological’ dyslexia profile alone is robust in reading-level comparisons (Sprenger-
Charolles et al., 2000; Stanovich et al., 1997), then perhaps most developmental ‘surface’
dyslexia should be thought of as ordinary poor reading, leaving only the ‘phonological’ subtype
to be properly considered as an organic dysfunction. Such a change would have important
implications for estimates of the prevalence of developmental dyslexia, should it be
conceptualised as a discrete condition. Although this change would have no implications for
estimates of the overall numbers of people with reading skills deficits, it might affect
estimates of the cost and duration of preventive measures and remedial interventions and their
probable outcomes, by a downward adjustment of the numbers estimated to require intensive
remediation over a long period or to need support in other ways.