Developmental dyslexia is a specific learning difficulty that primarily affects the acquisition of word reading (and spelling). During early schooling, individuals may display difficulty in acquiring adequate reading skills, reading more slowly or less accurately than expected. The following description of the subject of an early case study of dyslexia captures the challenging paradox faced by the wide variety of researchers of this developmental disorder. “He has always been a bright and intelligent boy…in no way inferior to others of his age. His great difficulty has been…his inability to learn to read….” (Morgan, 1986, cited in Brown, 2003).
Why is it that these articulate, intelligent people show such a problem in what seems like one of our most routine skills? Due to this unexpectedness in reading failure and its high incidence in Western populations (between 5% and 15%), dyslexia research has instigated great passion and controversy. Early pioneers in dyslexia research, Morgan, Hinshelwood, and Orton believed that visual problems underlay an apparent ‘wordblindness’. Orton (1925) introduced the term ‘strephosymbolia’ to specify that, although the problem was believed to be primarily visual, it was not one of blindness as such, but one of ‘twisted symbols’, a difficulty in distinguishing the order of letters. However, around a quarter of a century ago, there was a gradual realisation that problems of language must be, at least in part, responsible for the reading deficits (Vellutino, 1979).
This general hypothesis has been refined over the years to provide what is arguably the consensus theoretical belief of most dyslexia researchers, namely that dyslexic children suffer from an early impairment in their phonological skills, and this impairment prevents them from acquiring the word decoding and blending skills that are essential for the acquisition of skilled reading. Following on from this consensus, systematic phonics instruction, as a remediation for dyslexia has become largely popular. In addition to this consensus concerning the causes and remediation of developmental dyslexia, this essay will also discuss more recent paradoxical research which highlights how despite this large consensus, there are disagreements among theoreticians over the exact neurological and cognitive basis of the disorder.
Causes of developmental dyslexia
Dyslexia researchers, especially those with a background in psychology have focused on cognitive analyses of the disorder in order to determine the direct cause of the learning failure. A consensus has emerged among the majority of these researchers that the specific reading retardation characteristic of dyslexia is directly and exclusively caused by a cognitive deficit that is specific to the representation and processing of speech sounds: this is the phonological theory of dyslexia or the phonological deficit hypothesis. In line with this view is recent reading-related research that has placed a strong emphasis on understanding the acquisition of reading skill as building upon already developed representations of spoken language (De Gelder & Morais, 1995).
Furthermore, ample evidence suggests various phonological variables, especially the ability to consciously manipulate sound units smaller than the whole world (e.g. in the size of phonemes and syllables), labelled phonological awareness, are good predictors of future reading ability and are already poor in would be dyslexics (Pennington & Lefty, 2001). Indeed, there is strong evidence showing that, in addition to the more obvious reading and writing problems, diagnosed dyslexic individuals do display impairments in tasks that involve phonological processing (Snowling, 2000).
For example the metaphonological deficit of phonological awareness, specifically phonemic awareness has been measured in dyslexics using tasks such as phoneme elision. This involves the repetition of a heard word while omitting the first or last sound of that word, for example “cat” without the first sound becomes “at” (McDougall, Hulme, Ellis & Monk, 1994). Dyslexics consistently perform with great difficulty on such tasks, therefore displaying an impairment in the ability to segment words into the single speech sounds.
Other phonological processing skills that are frequently shown to be impaired in dyslexics are rapid naming and poor verbal short-term memory. The lack of phonological skills affects the reading of dyslexics through its interaction with the demands of learning to read an alphabetic writing system such as English. Normal reading development of such a system requires the acquisition of phonemic awareness “…if children are to abstract how written words relate to spoken words, and to develop the alphabetic principle” (Snowling, 2000, p.54), the idea that written units (graphemes) can be mapped onto a small set of elements (phonemes) of a language.
A deeper understanding of dyslexia and its’ deficits in phonology has been provided by the medical perspective. As emphasised by Morton and Frith (1995), in trying to understand a developmental disorder such as dyslexia, links between biological and cognitive levels of explanation are needed. Observable behaviour can be explained by a cognitive dysfunction: the cognitive dysfunction can be explained by a (genetic) brain dysfunction. Indeed since its familial aggregation, suggesting a genetic basis, was identified, large scale twin and familial studies (e.g., Smith, Kimberling, Pennington & Lubs, 1983) have established specific abnormalities both of chromosome 15 and, more recently, chromosome 6 (Lubs, Duara, Levin, Jallad, Lubs, Rabin, Kusch, & Gross-Glenn, 1991).
So, at the level of the brain, the cognitive deficit in the phonological system of dyslexia can be seen to arise from a congenital dysfunction of certain cortical areas involved in phonological decoding and reading comprehension. Evidence of this is provided by Galaburda and his colleagues (Galaburda, 1994; Galaburda & Kemper, 1978) who were also interested in the biological substrates of the disorder. Microscopic examinations throughout the perisylvian region of the left hemisphere of dyslexic brains, presented intriguing abnormalities in the form of scarred neurons. Furthermore, it was found that the dyslexic individual’s planum temporale, a part of the Wernicke’s area, were abnormally symmetrical. Since it is well established that the left hemisphere, particularly, the Wernicke’s area, subserve language processing, it is reasonable to infer that the dysfunction of these regions is the origin of what many have now labelled as a core phonological deficit (Snowling, 2000).
Although a deficit in phonological processing as a cause of developmental dyslexia has a wide consensus among researchers and remains the most consistent finding in all psychological studies of dyslexia, the basis of the deficit remains less clear. Largely attributable to an increasingly significant proportion of dyslexics presenting sensory deficits, which the phonological deficit hypothesis is unable to account for, an increasing group of researchers have deviated from this approach and focused on a magnocellular account of dyslexia. This holds that the reading problems derive from impaired sensory processing, caused by abnormal auditory and/or visual magnocellular pathways.
Tallal, Miller and Fitch (1993) for example, are a subset of such researchers who agree with the idea of a phonological deficit but see it as secondary to a more basic auditory impairment. This proposal derived from early studies (Tallal, 1980), which identified impairments in reproducing the order of rapidly presented temporal events. Specifically “a deficit in auditory processing of rapid auditory sounds that are entering the nervous system in the 10’s of millisecond are thought to impact language and subsequently reading because phonemes differ only in frequency changes that in the first 40-50 ms of the sound”(Temple, 2003, p.1). Without this ability to detect rapid auditory signals the child presents problems in phonological discrimination, and thus to reduced phonological skills. These researchers have now linked these problems to underlying abnormalities in the auditory magnocellular system.