Information provided by The International Dyslexia Association
DYSLEXIA: IS IT ALL IN YOUR MIND?
Recent neurological research provides newinsight into the mechanisms and etiology of developmental dyslexia, although there isstill much to learn and discover. In thisarticle, we will consider the latestneuroanatomical findings that may, in part,be responsible for the functional difficultiesthat challenge individuals with dyslexia. Theconjecture explored here is that there is adisruption of the cerebral architecture duringgestation that sets in motion a cascade of events resulting in reorganization of neuronal circuits and networks. Thisreorganized anatomical substrate is notoptimally organized for language acquisitionand does not flourish in the typicalenvironment/education system. Learningdifficulties may result depending on theseverity and location of brain alterations, theneural plasticity of the system, availablecompensatory cognitive strategies, andenvironmental conditions.
In 1979, Albert Galaburda and ThomasKemper examined a brain removed duringan autopsy from a 20-year-old man withdyslexia and reported that there were nervecells in unusual parts of the cerebral cortex.Subsequent studies at the Dyslexia ResearchLaboratory at Beth Israel Hospital inBoston, MA, of four dyslexic males andthree dyslexic females showed that in themales (less so in females) clusters of “ectopic” neurons are consistently seen inthe outside layer of the cerebral neocortex.This layer usually is devoid of nerve cellbodies. Most ectopias were in the frontal andperisylvian language regions. Ectopias areproduced before six months of gestationwhen there is a breach in the pial-glialborder which normally prevents neuronsfrom migrating too far. Although femaledyslexics had only a few ectopias, largenumbers of gliotic regions representingareas of neuronal loss were present in thecortex.
Etiology of the Anatomical Changes
Ectopias result from the disruption of thedeveloping cerebral cortex before neuronalmigration ends at mid-gestation. The focalgliotic regions in female dyslexics may bethe outcome of a similar pathologicalprocess acting during the third trimester of early postnatal period after neuronalmigration is completed. An insult spanningthe two periods could produce both ectopiasand areas of neuronal loss. Becauseautoimmune disorders (work begun by thelate Dr. Norman Geschwind in 1982) maybe increased in individuals with dyslexia, itwas suggested that maternal auto-antibodiesmight injure the developing brain duringgestation, leading to the type of neuropathology seen in dyslexia. This viewis not supported by work in experimentalanimal models. Further, new findings in thehuman and in experimental models point tothe importance of genetic factors. Anexciting finding recently by Dr. BrucePennington and colleagues is that a regionon chromosome 6 may be related todyslexia. It is intriguing that this areacontains many genes related to immunefunction.