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Auteur: Fusa KATADA

Ludling Acquisition in Williams-Beuren Syndrome and Its Implications to Neuroplasticity for Language Development

Abstract/Résumé: Williams-Beuren syndrome (WBS) is a hemizygous multisystem disorder caused by microdeletion of 26 - 28 genes from chromosome #7 (7q11.23), most notably elastin, which is directly linked to cardiac anomalies. Individuals with WBS manifest various (neuro)physiological deficits on the one hand, and affinities for music and excellent absolute pitch perception on the other hand. The onset of speech is significantly delayed; however, the end-state of language development in WBS is relatively spared in the face of serious deficits in visuo-spatial and cognitive nonverbal tasks dealing with number, space, planning, and problem solving. WBS is marked by such asymmetries in verbal-nonverbal tasks (Lenhoff et al., 2001; Bellugi et al. 1988, 2000; Karmiloff-Smith et al. 2003). This study reports on a longitudinally observed, remarkable ability in ludling (< Latin ludus ‘game’ + lingua ‘language’) displayed by our subject KT (male, Japanese) born with Williams-Beuren syndrome. With response time averaging around 300ms, KT can instantly render words he hears backward: [toriwasa] > [sawarito], [tebagyo:za] > [za:gyobate], [keNta] > [taNke]. Aside from significance of the data to the investigation of the structure of syllables (Katada, 2013a; 2013b), I postulate that facts (1) and (2) below indicate KT’s unfading neuroplasticity of speech development and of maintenance of the ability in phonological computational aspects of language into adulthood. (1) KT’s backward lundling performance emerged abruptly, with very little (if any at all) ‘primary data’ for the play when he was 8. No one around him has never been able to play on reversing. (2) While losing agility in other verbal tasks such as story-telling and conversational turn-taking, KT’s ludling has been vivid in his adulthood (currently aged 25). The delayed onset of speech, co-occurring with the delayed onset of ambulation, in WBS is likely a physiological consequence of the identified gene deletion and does not necessarily imply the underdeveloped knowledge of language in the child’s brain. I contend that dissociation between language competence (knowledge) and speech performance (vocalization) is obvious in the atypically developing population with WBS, whereas the dissociation is less in typically developing populations.