DYSLEXIA - GENETICS/BRAIN PATHOLOGY
VI. Genetics, the Brain Pathology
More prevalent among first-degree biologic relatives of individual with Learning Disabilities (DSM-IV, 1994).
Numerous genetic loci have been located, specifically chromosome 6 and chromosome 15. No consistent pattern has been located as to which chromosome is chosen and why (National Institute of Child Health and Human Development--Human Learning and Behavior Branch, Center for Mothers and Children, 1992).
Phonological coding (the ability to represent and access the sound of a word in order to help remember the word) has been found to be significantly heritable, while orthographic coding (the ability to put letters together to form whole words) appears to be more strongly related to environmental influences (National Institute of Child Health and Human Development-- Human Learning and Behavior Branch, Center for Mothers and Children, 1992).
Several types of brain pathology are related to dyslexia:
ectopias: congenital displacements of organs or parts,
cell loss, hippocampal anomalies: abnormalities in the enfolding of the cerebral cortex into the lateral fissure of a cerebral hemisphere, congenital hydrocephalus: accumulation of fluid within the brain since birth, often causing the head to swell, abnormalities of the corpus callosum: the corpus callosum is the great band of fibers that unite the two halves of the cerebrum. (National Institute of Child Health and Human Development--Human Learning and Behavior Branch, Center for Mothers and Children, 1992)
Brain electrical imaging mapping has shown evidence that left-hemisphere functioning in dyslexics is qualitatively different from that in normal readers. This is particularly prominent in adjacent regions of the left parietal and temporal lobes, areas of the brain known to support speech, language and related linguistic activities. (Vellutino, 1987).
At least a portions of children with dyslexia show evidence of abnormal neural development in the posterior (back) left hemisphere (Rosenhan, et. al., 1989).