Introduction: There is broad consensus that dyslexia is associated with phonological deficits. However, it is still a matter of debate how these deficits are brought about and the meaning of additional deficits observed in subjects with dyslexia. One theory postulates that a phonological deficit is sufficient to explain the delayed reading acquisition. Two other major competing theories propose that the phonological deficit and the delayed reading acquisition are the result of a more basic disorder either of the magnocellular visual and auditory systems or of the cerebellum. The observation of a systematic co-morbidity of these disorders would reinforce the motion that multiple deficits contribute to the poor reading performance of the subjects with dyslexia. However, the majority of the imaging studies have investigated only one variable in the same sample of subjects. Our aim was to re-assess the co-morbidity issue in dyslexia using both behavioural and imaging techniques in the same subjects. Methods: 23 healthy adults and 8 dyslexics were tested with tasks tackling non-word reading, phonological awareness, visual motion perception and motor learning skills. The same subjects were also tested with fMRI tasks tackling the same skilled previously assessed at the behavioral level: non-word reading, phonological awareness for auditorially presented syllables; visual motion perception and motor learning. The fMRI experiments conformed to block designs. The behavioural data of the subjects with dyslexia were compared with those of the normal controls by calculating Z-score values. fMRI data were assessed using SPM. Main effects of the tasks for each group were calculated as well as group by task interaction effects. Results: The behavioural tests confirmed a phonological deficit in all dyslexics, a deficit occasionally associated with “visual/magnocellular” or “motor/cerebellar” soft signs. fMRI showed a reduced activation of the left inferior-temporal and ventral occipito-temporal cortices for reading, suggesting that our subjects with dyslexia are representative of the populations described across different cultures in previous studies. Dyslexics also showed reduced activations in the occipito-temporal cortex for rhyming and motion detection tasks, and in the cerebellum for the motor learning task. These reduced activations were associated with hyperactivations in domain specific regions and in prefrontal cortex, a possible sign of compensations or of compensatory attempts. Interestingly, these differences were not accompained by significant behavioural deficits at a group level for the simple rhyming task, for the visula motion perception task, nor for the motor learning task. Further analyses showed that the left occipito-temporal cortex could be normally fractionated into: (1) a ventral anterior region of overlap between rhyming and reading (2) a lateral posterior occipital region of shared activation between motion detection and reading (3) one area, corresponding to the VWFA, specifically activated by reading. Reduced activations in dyslexics involved both a visual/phonological interface area called LIMA by some and, visual magnocellular areas. Interestingly, the Z scores of reading performance across controls and dyslexics correlated with specific activation areas in all fMRI tasks explored. This analysis further suggest a tight link between reading performance and the systems explored in this study. Conclusions: Our data suggest that phonological, magnocellular and cerebellar disorders may co-occurs in adult dyslexics. However, the phonological and the reading speed deficit stands above other difficulties being evident at both behavioural and physiological level, while the other systems may have undergone a more successful compensation because of a more redundant neuronal architecture. References Frith. U. Paradoxes in the definition of dyslexia. Dyslexia 1999; 5: 192-214. Paulesu E, Demonet JF, Fazio F, Mc Crory E, Chanoine V, Brunswick N, et al. Dyslexia: cultural diversity and biological unity. Science 2001; 291: 2165-2167. Ramus F, Rosen S, Dakin SC, Day BL, Castellote JM, White S, et al. Theories of developmental dyslexia: insights from a multiple case study of dyslexic adults. Brain; a Journal of Neurology 2003; 126: 841-65.
Paulesu, E., Danelli, L., & Bottini, G. (2010). How many deficits in the same dyslexic brains? Behavioral and fMRI assessment of competing theories. In 16th Annual Meeting of the Organization for Human Brain Mapping.
|Citazione:||Paulesu, E., Danelli, L., & Bottini, G. (2010). How many deficits in the same dyslexic brains? Behavioral and fMRI assessment of competing theories. In 16th Annual Meeting of the Organization for Human Brain Mapping.|
|Tipo:||abstract + poster|
|Carattere della pubblicazione:||Scientifica|
|Presenza di un coautore afferente ad Istituzioni straniere:||No|
|Titolo:||How many deficits in the same dyslexic brains? Behavioral and fMRI assessment of competing theories|
|Autori:||Paulesu, E; Danelli, L; Bottini, G|
|Data di pubblicazione:||9-giu-2010|
|Nome del convegno:||Annual Meeting of the Organization for Human Brain Mapping|
|Appare nelle tipologie:||02 - Intervento a convegno|