TY - JOUR
T1 - Dyslexie und ihre neuronale Signatur
AU - Bartl-Pokorny, K. D.
AU - Landerl, K.
AU - Einspieler, C.
AU - Enzinger, C.
AU - Gebauer, D.
AU - Fink, A.
AU - Zhang, D.
AU - Kozel, N.
AU - Kargl, R.
AU - Seither Preisler, A.
AU - Vollmann, R.
AU - Marschik, P. B.
PY - 2011
Y1 - 2011
N2 - 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.
AB - 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.
KW - developmental dyslexia
KW - eye tracking
KW - functional imaging
KW - reading
UR - http://www.scopus.com/inward/record.url?scp=80053034597&partnerID=8YFLogxK
U2 - 10.1055/s-0031-1285905
DO - 10.1055/s-0031-1285905
M3 - Article
AN - SCOPUS:80053034597
SN - 1434-0275
VL - 42
SP - 166
EP - 171
JO - Klinische Neurophysiologie
JF - Klinische Neurophysiologie
IS - 3
ER -