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. Cogn Brain Res 24:343-354. – Rae et. al.1998. Metabolic abnormalities in developmental dyslexia detected by 1H
magnetic resonance spectroscopy. Lancet, 351(9119), 1849–1852. - Reid A. A et.al. 2007. Cognitive profiles of adult developmental
dyslexics: theoretical implications. Dyslexia vol.13. 1: 1-24. – Rumsey, J.M. 1992. The biology of developmental dyslexia. JAMA 268:912915 - Shastry, B.S. 2007. Developmental Dyslexia: an update. The Japan Society of Human Genetics and Springer 52:104-109 –
Shaywitz et al. 1992. Discrepancy compared to low achievement definition of reading disability. J Learn Disabil 25:634-648. Stein J: The
magnocellular theory of developmental dyslexia. Dyslexia 2001, 7:12-36. Stein, J., & Walsh, V. (1997). To see but not to read: The
magnocellular theory of dyslexia. Trends in Neuroscience, 20, 147–152. Temple, E. 2002. Brain mechanisms in normal and dyslexic
readers. Current opinion in Neurobiology 12:178-183.
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Developmental Dyslexia