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DOI: 10.1055/s-0031-1285905
Dyslexie und ihre neuronale Signatur
Dyslexia and its Neural SignaturePublikationsverlauf
Publikationsdatum:
14. September 2011 (online)
Zusammenfassung
Dyslexie, als eine der häufigsten umschriebenen Entwicklungsstörungen, ist eine schwerwiegende und persistierende Problematik schriftsprachlicher Verarbeitungsprozesse. Ursächlich für Dyslexie werden phonologische, auditive oder visuelle Defizite, Schwierigkeiten beim schnellen Benennen sowie Automatisierungsdefizite diskutiert. Aufgrund der familiären Häufung der Dyslexie gilt eine genetische Grundlage für diese Störung als gesichert. Post-mortem Untersuchungen fanden bei Dyslektikern Ektopien und Dysplasien im sprachassoziierten perisylvischen Cortex. Ob die Plana temporalia bei Dyslektikern im Vergleich zu Nicht-Dyslektikern symmetrisch sind, wird noch kontroversiell diskutiert. Neben neuroanatomischen Auffälligkeiten wurden mittels funktioneller bildgebender Verfahren auch neurofunktionelle Abweichungen bei Dyslektikern nachgewiesen: Teile der parieto-temporalen und okzipito-temporalen Strukturen der linken Hemisphäre sind bei spezifischen Aufgaben vermindert aktiviert, während linker und rechter Gyrus frontalis inferior und rechtshemisphärische okzipito-temporale Strukturen eine vermehrte Aktivierung aufweisen. Eye-Tracking Studien zeigten bei Dyslektikern häufig längere Fixationen, kleinere Sakkaden und mehr Regressionen als bei normal entwickelten Lesern. Noch immer sind neurofunktionelle und -strukturelle Ergebnisse inkonsistent, was unter anderem mit unterschiedlichen Messverfahren, Altersunterschieden der Probanden, geringer Sample-Größe, uneinheitlicher Definition der Dyslexie und der Heterogenität der Störung selbst zusammenhängt.
Abstract
Dyslexia is one of the most common specific developmental disorders. Dyslexics exhibit a profound and persistent reading disorder, frequently accompanied by spelling difficulties. Current theories assume dyslexia to be caused by phonological, auditory or visual deficits, or by deficits in rapid naming and automatisation. Due to the familial risk of this developmental disorder, a genetic origin is being discussed as well. Post-mortem studies revealed ectopias and dysplasias in the language-associated perisylvian cortex of dyslexics. Whether the plana temporalia are symmetrically distributed or asymmetric as in non-dyslexics is still the subject of controversial discussion. In neurofunctional studies dyslexics showed underactivated left-hemispheric parieto-temporal and occipito-temporal structures. However, there was an overactivation of the left and right inferior frontal gyri and of the right-hemispheric occipito-temporal structures. Various eye-tracking studies revealed longer fixations, shorter saccades and more frequent regressions in dyslexics than in normal readers. Neuroanatomic and neurophysiological results are still inconsistent, which is certainly due to the diversity of methodological approaches, to age differences between the participants, small sample sizes, heterogeneous definitions of dyslexia, and to the phenotypic heterogeneity of the disorder itself.
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