Australasian Science Magazine

By Tim Hannan

Leading scholars argue for the abandonment of a flawed concept.

Since it was first recognised that some children experience significant difficulty learning to read, much academic ink has been spilled in the battle over the concept of dyslexia, with its nature, cause, neuropathology, diagnosis and treatment all furiously debated. Now, a new book by two leading scholars argues that current approaches to dyslexia are largely incoherent, and that the battle should simply be abandoned.

First used in 1887 to describe the reading problems exhibited by some adult patients after a stroke, the term “dyslexia” was later employed to refer to the difficulties exhibited by those children who, despite possessing age-appropriate intellectual and linguistic abilities and having experienced sufficient educational opportunities, nevertheless failed to learn to read. While early theories held that this was due to a primary visual pathology, research over the past several decades has demonstrated that reading difficulties are associated with deficits in phonological skills – specifically the ability to discriminate, manipulate and reproduce the sounds of one’s native language.

Being conceptualised as a specific problem with reading, the diagnosis of dyslexia was traditionally restricted to those children who possess at least average intellectual abilities. In practice, this required a clear discrepancy between scores on standardised tests of intelligence and reading skills. Those poor readers who scored low on intelligence tests were labelled non-discrepant, so they were not considered to have dyslexia. It was presumed that their reading difficulties resulted from different causes to those seen in dyslexics, who were believed to have a specific neurobiological abnormality that required a different type of educational intervention.

In their book The Dyslexia Debate, Julian Elliott and Elena Grigorenko demonstrate that many of the key assumptions of the traditional understanding of dyslexia are false. First, the use of an intelligence–reading discrepancy as a diagnostic criterion for dyslexia has lost favour due to a host of theoretical and methodological problems. In brief, while discrepancy approaches assume that the reading problems of dyslexics differ from those of non-discrepant poor readers in terms of aetiology, underlying cognitive processes and/or response to intervention, studies over several decades have failed to support any of these assumptions. It is now well-established that distinguishing between dyslexic and non-discrepant children does not help to predict either the presence of phonological deficits or the response to intervention, and the intelligence–reading discrepancy has been removed as a diagnostic criterion.

But if the traditional intelligence–reading discrepancy approach is abandoned, how should dyslexia be conceptualised? Some researchers define dyslexia as a genetically inherited neurobiological disorder, but this is of little use for diagnostic practice. While a genetic contribution to reading is well-established, specific markers remain elusive, and though certain brain abnormalities have been associated with reading difficulties, there is no convenient means by which these may be detected in individuals.

Others equate dyslexia with the lowest end of the reading spectrum, such as labelling the weakest 5% of readers at any age as dyslexic. This avoids the problematic notion that dyslexic children are categorically different from non-discrepant poor readers, but in reducing dyslexia to a statistical range the concept is effectively rendered meaningless.

As no coherent definition of dyslexia has met with the agreement of the scientific and professional community, Elliott and Grigorenko argue that the term has outgrown its conceptual and diagnostic utility. This is not to imply that the problems labelled by this term are not real or significant: there is clear agreement that a proportion of children have significantly more difficulty with reading than the majority of their peers; that some have a specific neurobiological cause for their reading problems; and that these children do not respond well to standard reading instruction.

It is also possible that future advances may yet identify a genetically inherited, neurobiologically mediated condition that can be treated by novel educational interventions. At present, however, the enterprise of distinguishing between a biologically based dyslexic and an environmentally determined poor reader appears flawed.

The demise of dyslexia has been predicted for around 40 years, but the concept has proven remarkably resilient. This may be because it enables families and schools to affirm that their child’s reading difficulties do not result from low intelligence, laziness or poor teaching, and it provides a defensible means of identifying those who should receive funded educational support.

Being so deeply entrenched in professional practice and public understanding, dyslexia well may be a meme whose power to replicate will remain undiminished by rigorous scientific debate.

Tim Hannan is an Associate Professor of Clinical Psychology at Charles Sturt University, and the President of the Australian Psychological Society.