Developmental dyslexia and animal studies: at the interface between cognition and neurology.
Recent findings in autopsy studies, neuroimaging, and neurophysiology indicate that dyslexia is accompanied by fundamental changes in brain anatomy and physiology, involving several anatomical and physiological stages in the processing stream, which can be attributed to anomalous prenatal and immediately postnatal brain development. Epidemiological evidence in dyslexic families led to the discovery of animal models with immune disease, comparable anatomical changes and learning disorders, which have added needed detail about mechanisms of injury and plasticity to indicate that substantial changes in neural networks concerned with perception and cognition are present. It is suggested that the disorder of language, which is the cardinal finding in dyslexic subjects, results from early perceptual anomalies that interfere with the establishment of normal cognitive-linguistic structures, coupled with primarily disordered cognitive processing associated with developmental anomalies of cortical structure and brain asymmetry. This notion is supported by electrophysiological data and by findings of anatomical involvement in subcortical structures close to the input as well as cortical structures involved in language and other cognitive functions. It is not possible at present to determine where the initial insult lies, whether near the input or in high-order cortex, or at both sites simultaneously.
Galaburda
A M
AM
Department of Neurology, Beth Israel Hospital and Harvard Medical School, Boston, MA 02215.
D000818:Animals; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000473:pathology / Q000503:physiopathology*; D002648:Child; D004195:Disease Models, Animal; D004292:Dominance, Cerebral / Q000502:physiology; D004410:Dyslexia / Q000503:physiopathology* / Q000523:psychology; D005260:Female; D006801:Humans; D007360:Intelligence / Q000502:physiology*; D051379:Mice; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011603:Psychophysiology; D051381:Rats