Oxford Brookes University

Psychology Department

Is the phonological deficit theory of developmental dyslexia the only current theory that can fully account for developmental dyslexia?
Developmental dyslexia represents the most researched of the developmental disorders. Several deficit hypotheses have been proposed to explain its underlying causes, however none of these theoretical approaches has reached to an agreed theoretical framework. In the present essay the main theoretical approaches will be evaluated. The first part of the essay will briefly highlight the role of genetics in the development of the disorder. In the second part a brief overview of the phonological deficit theory will be given pointing out the main limitations that led to consider other hypothetical views. Consequently, the alternative theories proposed for dyslexia will be considered. Different approaches will be evaluated as, for example, the auditory deficit (Tallal, 1980, 1993) the visual deficit theory, the cerebellar deficit (Nicolson and Fawcett, 1990) and finally the magnocellular deficit theory (Livingstone et al., 1991; Lovegrove, 1994), pointing out the main criticisms raised for each single approach. DSM IV-R defines developmental dyslexia (or specific reading disability), as an unexpected, specific, and persistent failure to acquire efficient reading skills despite adequate intelligence, conventional instruction, and socio-cultural opportunity (American Psychiatric Association 1994). Dyslexia is a lifelong persistent and widespread disorder that affects approximately 4-10% of the population (Hari & Renvall 2001; Ramus 2003). Dyslexia is usually presented with a variety of symptoms consistent with problems in reading and phonology, but also sensory difficulties in the visual and auditory domain as well as problems with balance and motor control (Ramus et al 2003), making it difficult to establish a unique hypothesis concerning its possible cause. From a genetic perspective, it is well known that dyslexia has a genetic component. Several studies suggest that the disorder tends to run in families (Stephenson, 1907; Fisher & DeFries, 2002). It has been shown that dyslexia is significantly higher among monozygotic twins, than it is in dizygotic twins, who share only half of their segregating alleles (DeFries, Fulker & LaBuda, 1987). Specifically it has been found a concordance rate of 68% in monozygotic twins, as compared with 38% in dizygotic twins, revealing a substantial genetic component but also that other environmental

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factors could account for the development of the disorder (DeFries & Alarcn 1996; Fisher & DeFries, 2002). Additional, linkage studies have revealed at least four candidates (DYX1C1, DCDC2, KIAA0319, and ROBO1) dyslexia susceptibility genes implicated in neuronal migration and other developmental processes (axon growth) (Galaburda et al. 2006). It is held that these genes can be responsible for subtle cortical malformations that lead to abnormal cortical and cortico- thalamic pathways, which affect sensorimotor, cognitive and perceptual processes important for learning (Galaburda et al. 2006), however although several candidate genes have been identified, no specific dyslexia risk gene has been found yet and thus the disorder is mainly diagnosed by phenotypic symptoms. At a cognitive level, the mainstream view of dyslexia includes the idea that learning an alphabetic writing system requires the brain to map letters (graphemes) to mental representations of the corresponding phoneme (basic speech sound). According the phonological deficit theory, dyslexics have specific problems in recalling or representing sounds, thus a deficit in mapping sounds into letters (Ramus 2001), meaning that if the sounds are poorly stored, represented or retrieved the learning of grapheme-phoneme correspondences could be affected (Brady & Shankweiler, 1991). The phonological deficit theory therefore claims a direct connection between a cognitive deficit and the behavioural problem to be explained (Ramus et al. 2003). In support of the phonological deficit is evidence suggesting that dyslexics perform poorly on tasks that demand phonological awareness, including phoneme deletion (cat without the /k/), phoneme blending (/k/ /a/ /t/ - cat) and phoneme counting (cat 1, 2, 3) (Snowling, 1995) as well as different functional brain imaging studies suggesting a dysfunction in left-hemisphere perisylvian brain areas to be central for the phonological deficit (Temple et al., 2000; Ramus 2003). However this prevailing view of dyslexia, under the hypothesis of a phonological deficit, has been challenged by different approaches. Challengers of the phonological deficit view, uphold that phonological deficit is only one aspect of the disorder, pointing out that the disorder is more extended having its origins in more general sensory, learning and motor processes (Ramus, 2001). Based on the fact that dyslexics perform poorly in simple auditory and visual tasks (Stein 2001; Ramus et al 2003), it has been suggested that the phonological problems may result from a more fundamental deficit in the perceptual mechanisms that are responsible for rapid temporal information. According Tallal (1984) the deficit could be in the perception of short or rapidly varying sounds, suggesting that an

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auditory deficit could be the main cause in the difficulty in learning to read. Support for this rapid processing deficit theory comes from evidence that many children with Specific language Impairment had difficulties in making rapid temporal judgements for stimuli presented spatially close in time (Tallal, 1987). The children showed deficits when one stimulus rapidly came after another in both a temporal order judgement paradigm and a same-different discrimination paradigm (Richardson et al. 2004). Similar deficits were also found in dyslexic children (Tallal, 1980). In a more recent study McAnally and Stein (1996) have found that many dyslexics show a significantly impaired ability to discriminate closely spaced frequencies by phase locking, and to detect phase differences between the ears respect controls suggesting that this problem of phonological analysis could result from impairment in low-level auditory transient processing. To sum up supporters of the rapid processing deficit hypothesis argue that a rapid processing deficit could negatively influence literacy as transient information is crucial for phoneme perception, and phoneme awareness is important for reading (Richardson et al. 2004). Although the theory has been tested in several studies, however Tallals initial findings have been difficult to replicate, rising several criticism for the value of these findings (Farmer & Klein 1995). The visual theory represents another hypothetical view in the study of dyslexia. According the visual hypothesis, dyslexia is seen as a visual impairment that generates difficulties with the processing of letters and words on a written text (Ramus et al. 2003). Again this theory does not exclude the pholological deficit, however gives an emphasis to the contribution of vision in reading problems. Evidence in support of this theory come from studies suggesting neurological abnormalities in certain areas of the visual system (Galaburda & Livingstone, 1993) Specifically it has been found that the magnocellular pathway of the visual system is selectively impaired in some dyslexic children, suggesting impairments in the visual processing, and via the posterior parietal cortex (specialized for spatial perception, thus where an object is), abnormalities in visuospatial attention (Lovegrove et al. 1990; Hari et al. 2001; Ramus et al. 2003). Additionally, Lemkuhle et al. (1993) testing the spatial response characteristics of the two visual pathways (magnocellular and parvocellular) demonstrate a dysfunction in the magnocellular suggesting a physiological basis for some behavioral aspects in developmental dyslexics that cope poorly in tests requiring rapid visual processing (Galaburda et. al., 1994).

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A different view of dyslexia has been proposed from the cerebellar theory (Nicholson & Fawcett, 1990). It is well known that the cerebellum is a subcortical brain structure, involved in motor control and thus speech articulation (Ramus et al. 2003). It has been argued that a dysfunctional articulation could lead to impaired phonological representations (Ramus et al. 2003). It is also known the cerebellums role in automatization. Supporters of the cerebellum theory also argue that a reduced capacity to automatize would negatively influence the learning of grapheme phoneme correspondences. Evidence for the cerebellar hypothesis come from several studies revealing that dyslexics cerebellum is mildly dysfunctional and from evidence suggesting a poor performance for dyslexics in a number of motor tasks (Fawcett et al. 1996; Ramus et. al. 2003). In their study Nicolson and Fawcett (1990) assessing the motor competence in dyslexic children comparing them with a control group, found a relevant difference in the performances requiring motor coordination, ability in motor balance and, motor reaction between the two groups, with lower scores for dyslexic individuals (Fawcett, Nicolson & Dean, 1996). Furthermore evidence suggests structural, metabolic and activation differences in dyslexics cerebellum. Using new functional techniques in order to observe brain activity, Nicolson et al., (1999) evaluating cognitive functions (e.g reading), in tasks of learning and performance, found that the little brain was linked both with the frontal lobes, (responsible for motor tasks), and with Brocas area (involved in linguistic functions) Further, Stein et al. (2001), comparing the metabolism of dyslexics cerebellum with that of control group, found a lower ratio on the right hand side cerebellum of the dyslexics. Finally, in terms of activation, brain imaging studies have shown significant structural differences (smaller right anterior lobes) in dyslexic subjects, that could be correlated with deficits in reading, spelling and language associated with dyslexia Fawcett & Nicolson, 1994). The cerebellar theory however faces growing criticisms both because fails to account for sensory disorders and because the causal link assumed between phonology and articulation is based on the outdated view of the motor theory of speech, that suggests that the development of phonological representations relies on speech articulation (Ramus et al., 2003). Concluding, its still uncertain what proportion of dylexics has motor problems as in some studies they failed to find any (Krondichler et. al. 2002) while in others motor problems were found only in dyslexics with comorbidity with other disorders (e. g. ADHD) (Wimmer et al. 1999).

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Finally, the findings suggesting auditory and visual impairments in dyslexics have been recently integrated in a more unifying theory suggesting that the magnocellular dysfunction proposed in the visual theory, mention above, could be generalized to several different modalities (auditory, visual, motor), accounting for all symptoms of dyslexia (Fawcett & Nicholson, 1994; Tallal, Miller & Fitch, 1993; Stein & Walsh, 1997; Ramus 2001; Ramus et al., 2003). This new view of dyslexia across the magnocellular theory is supported by several evidence suggesting both cooccurrence of visual and auditory problems in some dyslexics (Ramus et al. 2003) and abnormalities in the medial and lateral geniculate nucleus in dyslexics brain (Galaburda et al. 1994). Galaburda et. al. (1994) measuring cross sectional neuronal areas in the medial geniculate nuclei (MGN) of dyslexic and control groups found dyslexics having smaller left than right MGN neurons and a different distribution of neuronal between dyslexics and controls specifically dyslexics had more small neurons and only few large neurons in the left MGN, compared to controls. In other words like visual magnocells, auditory magnocells in the MGN were also abnormal in dyslexics (Stein & Walsh 1997). These findings seem to be consistent with other findings of a left hemisphere-based phonological defect in dyslexic individuals. (Galaburda et. al. 1994).However again this theory has raised a lot of criticisms as several studies of auditory disorders not only have been difficult to replicate (Hill et. al. 1999; Mc Arthur & Hogden 2001; Ramus, 2003) but also because those revealing auditory deficits were only in a few individuals of the population studied (Ramus, 2003). Additionally, there is an inconsistency of whether the auditory deficit lies in rapid auditory processing as in some tasks rapid auditory processing was found to be intact and in others slow auditory processing was found to be impaired (Rosen & Manganari, 2001; Share et. al., 2002; Ramus, 2003) Finally, different studies (Chiappe et al., 2002; Kronbichler, Hutzler & Wimmer, 2002), looking simultaneously at auditory, visual, motor and phonological skills within the same subject, found only a partial overlap between the deficits in the different domains. To Sum up it is clear that the phonological deficit theory is not the only current theory that accounts for the developmental dyslexia. Each single theoretical approach described above does not explain all cases of developmental dyslexia. Considering that learning to read demands many cognitive processes and involves different brain areas, a difficulty in learning to read should not be seen as a condition in itself, but as a symptom of a breakdown in one or more of the different processes involved.

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Psychology Department

References
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