01 NRDC Dyslexia 1-88 update - Texthelp

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Research Report
By stressing the importance of normal reading acquisition as a benchmark for reading
difficulties, the model anticipates not one but several different patterns of cognitive and
reading deficits. Whether the pattern is ‘nonalphabetic’, ‘compensatory’, ‘nonautomatic’, or
‘delayed reading’ will depend upon the point at which students go astray in reading
acquisition. However, this is not to propose a new theory of causal ‘subtypes’. The model
illustrates not ‘causes’ but developmental outcomes. It holds that any individual instance of
reading difficulty will involve multiple causes as an outcome of interaction between the
environment and the student’s individual characteristics.
The cognitive process model of reading disability differs from the explicitly biological theories
of dyslexia reviewed in Part two by acknowledging that developmental outcomes are a
consequence of complex interactions between the individual and the environment.
The model does not assume a biological abnormality as the default explanation for reading
difficulties.
It details a sequence of stages in cognitive processing through which people pass when they
learn to read.
At each stage, the model explains the conceptual nature of reading difficulties and it offers
guidance on appropriate teaching strategies.
A self-organising systems model of reading disability
A challenge to the notion of specificity in dyslexia comes from a self-organising systems
model of learning disability (Zera, 2001; Zera & Lucian, 2001), which derives from systems
theory and nonlinear dynamics (see below). It has much in common with other concepts of
developmental causality, whether they are general (Bronfenbrenner & Ceci, 1994; Cairns,
1996; Cicchetti & Cannon, 1999; Elman et al., 1996; Fischer & Bidell, 1998; Gottlieb &
Halpern, 2002; Karmiloff-Smith, 1998; Sameroff, 1995; Sameroff & Chandler, 1975; Sroufe,
1997; Thelen & Smith, 1994; Thomas & Karmiloff-Smith, 2002) or specific to reading
(Snowling, 2000). That is to say, the model is located within mainstream developmental
psychology and its concept of ‘epigenesis’, in which both new structures and new functions
are understood to arise in the course of individual development (Gottlieb, 1992).
The self-organising systems model states three main propositions about cognitive
development.
First, the system is not modular but distributed. That is to say, complex behaviours like
reading and writing are subserved by multifocal neural systems, not by specific anatomical
sites within the brain, even though single-focus lesions may impair them. Whereas the
specific learning disability concept suggests a more localised dysfunction, a self-organising
systems model suggests widespread, diffuse outcomes. If this is really the case, then the
notion of a ‘specific’ learning disability is mistaken.
Second, the system is not static but dynamic. Learning disabilities do not stay confined to
specific brain areas. Dysfunction is not focal and constrained but far more pervasive, as a