Developmental Dyslexia Simone Löhndorf Developmental dyslexia (DD), also known as a specific reading disorder, is a complex cognitive disorder. It is the most carefully studied of the childhood learning disabilities (Shastry, 2007). The disorder affects a large number of people, and its prevalence in school age children is approximately 5-10% (Shaywitz et al.1992). It has been studied by linguists, educationalists, psychologists, geneticist and neuroscientists, and neurolinguists (Shastry 2007). A number of theories have been proposed for the disorder. The four current main theories are called phonological deficit theory (PDT), the visual magnocellular theory (MDT), the auditory magnocellular theory (auditory MDT - also called the auditory rapid processing theory), and the cerebellar deficit theory (CDT) (A. A. Reid et al. 2006). In accordance with these theories, studies have, among other things, shown deficit in verbal memory and phonological coding, suggesting involvement of the left hemisphere (Rumsey 1992). The visual magnocellular theory The auditory magnocellular theory (MDT) The magnocellular theory claims that the underlying cause of literacy problems in dyslexia is not language specific, but a more general impairment of the visual / auditory magnocellular system. The visual magnocellular system specializes in processing fast visual temporal information, whereas the auditory magnocellular system specializes in fast auditory temporal information. Stein and Walsh (1997) suggest that the magnocellular temporal processing deficit extends to other systems, such as the vestibular and motor. The main types of evidence cited in support of the visual magnocellular system are: unsteady binocular fixation (e.g. Stein, 2001), reduced motion sensivity (e.g. Hansen et al. 2001) and reduced contrast sensivity (e.g. Lovegrove et al.1980). The argument linking deficits in the auditory magnocellular system to dyslexia, is that impairment in low-level sensory temporal processing degrades sensory input for proper phonological coding which is important for reading. In support of this theory, training techniques aimed at improving dyslexics’ auditory temporal processing abilities have shown improvements in their language and possibly reading abilities (Petkov et al. 2005). The cerebellar deficit theory (CDT) Originally this theory was formulated as an automatization deficit theory. It was supported by the findings from a dual task paradigm, which involved balancing, defined as maintaining one’s body in a state of equilibrium, while performing a secondary task. The results revealed that although under optimal conditions dyslexics could balance as well as controls, in a dual task dyslexics balanced significantly worse than the controls (Nicolson & Fawcett, 1990). More recently, the automatisation deficit has been linked to impaired function of the cerebellum. Dyslexics have shown deficits in a range of functions, which rely on cerebellar processing. Converging biological evidence of cerebellar impairment has come from a histological study (Finch, Nicolson & Fawcett, 2002) that re-analysed the brain specimens of people with dyslexia originally investigated by Galaburda and colleagues (e.g. Galaburda et al.,1994). The results showed significant differences in the numbers of large and small cerebellar neurons in dyslexics and controls (see also Rae et al.1998). On the basis of findings implicating cerebellar impairment in dyslexia, Nicolson et al. (2001) proposed a hypothetical causal chain linking cerebellar impairment with phonological processing deficits, and problems with reading and spelling. The phonological deficit theory (PDT) Phonological theories claim that irregularities in parts of the brain associated with language processing underlie dyslexics’ difficulties to properly represent, store and/or retrieve the constituent sounds of written words. The difficulty in properly mapping the constituent sounds of oral language would affect the phoneme to grapheme mapping for reading. Proponents of phonological theories view dyslexia as a language specific impairment (A. A. Reid et al. 2007). It is claimed that the phonological deficit is manifested by problems in several closely related subdomains: phonological awareness (difficulties with analysing, blending and manipulating the sound structures of words), verbal short-term memory (difficulties with recall of words and nameable visual stimuli, and repetition of pseudowords and sentences), word retrieval (reduced verbal fluency and naming speed), and recoding in reading and spelling (evident especially when processing unfamiliar words or pseudowords)(A. A. Reid et al. 2006). It has been established that phonological impairment persists until adulthood and also in compensated dyslexics – individuals who despite their difficulties achieve almost normal reading and writing abilities (Paulesco et al. 1996). Brain mechanisms in dyslexic readers Recent Neuroimaging studies have shown that across ages, languages, and methodologies, dyslexics have a disrupted temporoparietal brain resonse to phonological demands; dyslexics have a disruption in left frontal brain responses to rapid auditory processing demands, and they have abnormalities in the white matter connecting temporoparietal cortex to other cortical regions. These results give continued support for hypothesis suggesting that DD has a neurobiological etiology. What the studies do not yet address is the issue of causality – more research is required to determine the realtionships between the disruptions in brain function and structure (Temple, 2002). (Temple, 2002) Different cognitive profiles? A. A. Reid et al. (2007) conducted a study with the aim to establish cognitive profiles of dyslexic adults on tests developed within three main theories of developmental dyslexia: PDT, visual MDT and cerebellar and to investigate which theory can account for these profiles. 9 out of 15 dyslexics exhibited only a phonological deficit; one a phonological and a visual magnocellular deficit; a further three a phonological and a cerebellar deficit; two either a cerebellar or a visual magnocellular deficit. None of the main theories of dyslexia can account for all the cases studied here. It is suggested that the best account of these data is in terms of different sub-types of dyslexia with different underlying causes, such as phonological, visual magnocellular and cerebellar, or a combination of these (Reid, A.A. 2007). References: - Galaburda et. al.1994. Evidence for aberrant auditory anatomy in developmental dyslexia. Proceedings of the National Academy of Science of the USA, 91, 8010–8013– Finch et. al. 2002. Evidence for a neuroanatomical difference within the olivo-cerebellar pathway of adults with dyslexia. Cortex, 38, 529–539. – Hansen et al. 2001. Are dyslexics’ visual deficits limited to measures of dorsal stream function? Neuroreport, 12, 1527–1530. - Lovegrove et. Al. 1980. Specific reading disability: differences in contrast sensitivity as a function of spatial frequency. Science, 210:439-440. - Nicolson, R. I., & Fawcett, A. J. (1990). Automaticity: A new framework for dyslexia research? Cognition, 35, 159–182. - Nicolson, R. I., Fawcett, A. J., & Dean, P. (2001). Developmental dyslexia: The cerebellar deficit hypothesis. Trends in Neurosciences, 24(9), 508–511. - Paulesu et. al.: Is developmental dyslexia a disconnection syndrome? Evidence from PET scanning. Brain 1996, 119:143-157. – Petkov et al. 2005. Auditory perceptual grouping and attention in dyslexia. Brain Res. 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