REDEFINIENDO LA DISLEXIA: EXPLICANDO LA VARIABILIDAD (Re-Defining Dyslexia: Accounting for variability)

Cyril

Description

RESUMEN
La efervescencia científica que reina en torno a la dislexia evolutiva se explica por el difícil desafío que implica atribuir esta dificultad a una causa simple al tiempo que se observan pacientes disléxicos con múltiples perfiles. En este capítulo, empezamos presentando la hipótesis neurocognitiva principal que persigue explicar la dislexia. Revisaremos la naturaleza multidimensional de la dislexia y discutiremos la necesidad de utilizar un criterio diagnóstico común para mejorar nuestra comprensión de su verdadera naturaleza. Concluiremos con la presentación de un trabajo prometedor que conecta endofenotipos cerebrales y fenotipos conductuales, resaltando la necesidad de un enfoque multifactorial más que monoteórico de la dislexia evolutiva.
ABSTRACT
The scientific effervescence that reigns around developmental dyslexia is explained by the difficult challenge that consists of ascribing this handicap to a single cause whilst multiple profiles of dyslexic patients can be observed. In this chapter, we start by presenting the main neuro-cognitive hypotheses that aim to explain dyslexia. We then review the multidimensional nature of dyslexia, and discuss the necessity of using a common diagnostic criteria to improve our understanding of its true nature. We then conclude by presenting promising work connecting cerebral endophenotypes and behavioral phenotypes highlighting the need for a multi-factorial rather than mono-theoretical account of developmental dyslexia.

Sujets

• Révision
• Dyslexia
• Review

Informations

• Publié par: erevistas
• Publié le: 01 janvier 2011
• Nombre de lectures: 52

Extrait

Escritos de Psicología, Vol. 4, nº 2, pp. 17-24 Copyright © 2011 Escritos de Psicología
Mayo-Agosto 2011 ISSN 1989-3809 DOI: 10.5231/psy.writ.2011.24072
Re-Defning Dyslexia: Accounting for variability
Redefniendo la dislexia: explicando la variabilidad
1 2 3Cyril R. Pernet , Olivier Dufor , Jean-Francois Démonet
1 Division of Clinical Neurosciences. University of Edinburgh. Scotland, UK
2 Department of Cognitive Science. Johns Hopkins University. Baltimore. USA
3 Neuroscience Department. Toulouse University Hospital. Toulouse. France
Disponible online 31 de agosto de 2011
The scientifc effervescence that reigns around developmental dyslexia is explained by the diffcult challenge that
consists of ascribing this handicap to a single cause whilst multiple profles of dyslexic patients can be observed. In
this chapter, we start by presenting the main neuro-cognitive hypotheses that aim to explain dyslexia. We then review
the multidimensional nature of dyslexia, and discuss the necessity of using a common diagnostic criteria to improve
our understanding of its true nature. We then conclude by presenting promising work connecting cerebral endophe-
notypes and behavioral phenotypes highlighting the need for a multi-factorial rather than mono-theoretical account
of developmental dyslexia.
Keywords: Developmental dyslexia; Multi-factorial defcit; Review .
La efervescencia científca que reina en torno a la dislexia evolutiva se explica por el difícil desafío que implica
atribuir esta difcultad a una causa simple al tiempo que se observan pacientes disléxicos con múltiples perfles. En
este capítulo, empezamos presentando la hipótesis neurocognitiva principal que persigue explicar la dislexia. Re-
visaremos la naturaleza multidimensional de la dislexia y discutiremos la necesidad de utilizar un criterio diagnóstico
común para mejorar nuestra comprensión de su verdadera naturaleza. Concluiremos con la presentación de un trabajo
prometedor que conecta endofenotipos cerebrales y fenotipos conductuales, resaltando la necesidad de un enfoque
multifactorial más que monoteórico de la dislexia evolutiva.
Palabras clave: Dislexia Evolutiva; Défcit Multifactorial; Revisión.
Correspondence concerning this article should be addressed to: Dr Cyril Pernet. Brain Research Imaging Center. Division of Clinical Neurosciences.
University of Edinburgh. Western General Hospital. Crewe Road. Edinburgh. EH4 2XU. Scotland, UK. E-mail: [e-mail], dufor-at-
[e-mail]. Authors’ E-mails: Oliver Dufor: [e-mail]; Jean-Francois Démonet: demonet@toulouse.
inserm.fr
17CYRIL R. PERNET, OLIVIER DUFOR, JEAN-FRANCOIS DÉMONET
Back to basic: what is dyslexia? or allophonic representations (Serniclaes et al., 2001). These
According to the World Health Organization (WHO, 1997 - hypotheses are supported by the frequently observed presence
ICD 10), dyslexia is a specifc reading disorder: “The main fea - of phonological disorders in dyslexic readers as for instance re-
ture is a specifc and signifcant impairment in the development duced performances for short-term verbal memory tasks, pho-
of reading skills that is not solely accounted for by mental age, nemic awareness (Ramus et al., 2003) and/or defcits in phone -
visual acuity problems, or inadequate schooling. Reading com- mic categorization (Serniclaes et al., 2001). Such behavioural
prehension skill, reading word recognition, oral reading skill, defcits have been linked with abnormalities of the left posterior
and performance of tasks requiring reading may all be affected. temporal cortex, the supramarginal gyrus and the inferior fron-
Spelling diffculties are frequently associated with specifc tal cortex (Dufor et al., 2007; Dufor et al., 2009).
reading disorder and often remain into adolescence even after By contrast with the phonological hypothesis, the auditory
some progress in reading has been made. Specifc developmen - processing defcit theory proposes that phonological defcits
tal disorders of are commonly preceded by a history are secondary to a more basic impairment in rapid acoustic
of in speech or language development. Associated transition perception (Tallal, 2004; Tallal et al., 1985). Such
emotional and behavioural disturbances are common during the defcits have been linked with microscopic abnormalities in the
school age period.” Strikingly, this defnition relies mainly on auditory cortex (Galaburda & Kemper, 1979), the frontal and
exclusion criteria, i.e. dyslexia is not diagnosed because of the perisylvian areas (Kaufman & Galaburda, 1989) and soma atro-
reading impairment per se but because the learning diffculties phies of magnocells in the medial geniculate nuclei of the tha-
cannot be explained otherwise; that is reading disorder cannot lamus (Galaburda et al., 1994). Abnormal functional responses
be explained by basic sensory defcits, evident brain abnormali - to speech sounds have also been observed in the brainstem and
ties, or primary psychological defcits. Importantly, the ICD 10 the left inferior frontal cortex. For instance, Banai et al. (2009)
defnition does not exclude those defcits: it points out that they showed abnormal timing and harmonic information contents
cannot ‘solely’ explain the reading disorder. Indeed, specifc in the brainstem response to the sound /da/. Such abnormal
reading disorders have been associated with defcits in related response is likely to be due to an interaction with other sub-
domains such as oral language (dysphasia and Specifc Language cortical (thalamus) and cortical (auditory cortex) structure via
Impairment), writing skills (dysgraphia), mathematical abilities cortico-fugal projections since no ‘basic’ defcits are observed
(dyscalculia), motor coordination (dyspraxia), temporal orien- when using clicks rather than complex sounds (Song et al.,
tation (dyschronia), visual abilities, Attention-Defcit/Hyperac - 2006). Those defcits in temporal and spectral coding of com -
tivity-Disorder (Habib, 2000) and increased internalizing, anx- plex auditory stimuli would thus explain phonological defcits.
ious and depressive symptomatology (Mugnaini et al., 2009). This hypothesis is further supported by the fact that (1) slowing
down the acoustic features in rolling /ma na/ /na ma/ stimuli
Multiple defcits in dyslexia? (vs. /ma ma/ /na na/) enhances the left inferior frontal cortex re-
There are many competing neuro-cognitive hypotheses sponse of dyslexic subjects to a level comparable to controls in
aiming at explaining dyslexia, each one highlighting one type normal situation (Ruff et al., 2002) and (2) training in auditory
of behavioural defcit in relation with abnormal brain structures temporal processing improves reading performances (Merzen-
and/or functional responses. Among those hypotheses, one can ich et al., 1996).
identify three major approaches (Démonet et al., 2004; Pernet
& Démonet, in press). A frst approach relates reading to pho - Visual hypotheses
nology, an essential part of the reading process. A second ap- The visual hypothesis posits the existence of low level vis-
proach relies on identifying subtle visual or visuo-attentional ual disorders related to abnormal thalamic magno-cells. These
defcits which would explain the specifc reading disorder. cells are involved in the processing of low contrast information
Finally, a third approach is to conceive dyslexia as a specifc and fast moving stimuli and would thus be important for read-
learning / memory disorder. ing activities related to saccadic eye movements. Histological
studies revealed soma atrophies of magno-cells in the lateral
Phonological and auditory hypotheses geniculate nuclei of the thalamus (Livingstone et al., 1991) and
The phonological hypothesis, which is the most infuential cyto-architectonic abnormalities of the primary visual cortex
account for reading problems, postulates defcits related to the (Jenner et al., 1999) have been observed alongside abnormal
access or the manipulation of phonemic information, or both, functional brain responses of visual areas receiving magnocel-
preventing effcient learning of graphemes/phonemes corre - lular inputs (i.e. MT and dorsal regions - Demb et al., 1997,
spondences that are crucial to reading (e.g. Bradley & Bryant, 1998). Favouring this hypothesis, behavioural studies also
1983; Ramus, 2004; Shaywitz & Shaywitz, 2005). One pos- showed increased thresholds on detection of low contrast, low
sible explanation for those defcits and in particular the def - spatial or high temporal frequencies (Lovegrove et al., 1980),
cit in phonemic categorization is that dyslexic subjects have and poor sensitivity to visual motion (Demb et al., 1998) in
too many representations, i.e. they have many non-pertinent dyslexic readers (see however, Skotun, 2000).
18RE-DEFINING DYSLEXIA
As an alternative or complementary explanation, the visuo- ful for the control participants to correctly process the stimuli.
attentional hypothesis situates the impairment in the encoding Another account of this theory comes from a study which dis-
of letter sequences. For instance, Valdois and collaborators cusses the existence of phonological troubles when the context
showed that dyslexic readers have a shorter visuo-attentional of the experimental condition does not suffciently load the