الفهرس 
Neurodevelopmental disorders and the whiteOnly 14 pages are availabe for public view
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Abstract
White matter growth is the main source of increased brain volume during child development and continues well into the second decade for some regions.
Maturation of brain white matter pathways is an important factor in cognitive, behavioral, emotional and motor development during childhood and adolescenceChildhood and adolescence is a period of dynamic behavioral, cognitive and emotional development. This development parallels significant changes in white matter structure.
Diffusion tensor imaging (DTI) provides quantitative indices of the diffusion of water within tissue and is an excellent technique for measuring age-related changes in the biological properties of white matter in vivo. Such information is necessary to quantify subtle changes in white matter organization with maturation and relate those changes to behavior. Both the magnitude of water diffusion, expressed as apparent diffusion coefficient, and the directionality, expressed as the degree of anisotropy provide indices of white matter organization. Decreased magnitude and increased directionality of water diffusion across multiple white matter pathways are associated with increased age in children and adolescents.
Neurodevelopmental disorders are impairments of the growth and development of the brain or central nervous system. Neurodevelopmental disorders are associated with widely varying degrees of difficulty, which may have significant mental, emotional, physical, and economic consequences for individuals, and in turn their families and society in general.
There are many causes of neurodevelopmental disorder, which can range from deprivation, genetic and metabolic diseases, immune disorders, infectious diseases, nutritional factors, physical trauma, and toxic and environmental factors.
Neurodevelopmental psychiatric disorders are Autism, attention deficit hyperactivity disorder (ADHD), learning disabilities, communication disorders(stuttering disorder), motor disorder (tourette disorder), obsessive–compulsive disorder (OCD), early-onset schizophrenia (EOS) and adolescent bipolar.
Identical brain regions appear to be sensitive to a wide range of developmental abnormalities, in particular prefrontal cortex, pari¬etal lobes, the basal ganglia, thalamus and the cerebellum. However, specific differences between the different psychiatric disorders have emerged in either the development of these brain abnormalities (progressive decline in schizophrenia, non-progres¬sive changes in ADHD), the exact localization (abnormalities in predominantly orbitofrontal cortex in OCD, in inferior prefrontal cortex in ADHD, in dorsolateral prefrontal cortex in EOS and in anterior cingulate in depression), the laterality of abnormalities (predominantly right hemispheric abnormalities in ADHD, bilat¬eral abnormalities in OCD, left predominance of abnormalities in depression and schizophrenia) or the sign of the functional abnor¬malities (increased fronto-striatal brain activation during symptoms or rest in OCD, reduced frontal-striatal activation in ADHD).
The biological evidence so far suggests that neurodevelopmental psychiatric disorders suffer from abnormalities in disorder-specific fronto-striatal, fronto-parietal and fronto-cerebellar networks that are crucial for the fine-tuning of normal behaviour.
The corpus callosum plays a crucial role in communicating perceptual, cognitive, learned and volitional information, and its alterations might affect the interhemispheric integration of these functions. Mounting evidence from structural studies has implicated the CC in the pathophysiology of autism. Therefore, the examination of these developmental activities might help in elucidating the neurobiology of CC abnormalities in PDD. The anterior third transcallosal fiber tracts are mostly connected to the bilateral frontal lobe. A neuroimaging study using DTI has confirmed earlier post-mortem findings of CC topographical organization and has shown that the anterior third of CC connect the frontal regions, while the body and splenium connect parietal, temporal, and occipital regions. The dorsolateral prefrontal cortex plays a crucial role in mediating executive control, behavioral inhibition, implementation of control and decision making. It is possible that a transcallosal fibers deficit could be secondary to corticocortical disconnection or could result in underconnectivity among cortical regions in the two hemispheres. Most of the fibers in the anterior third of the CC are small diameter fibers that are thought to be important in maintaining the balance between excitation and inhibition in the cerebral hemispheres. Early neurodevelopment is associated with synaptic pruning and axonal myelination processes, which are linked to the executive function and social cognition. The neurocognitive profile in autistic disorder has been referred to as the frontal cortex unconsciously “talking only to itself” accompanying by loss of language and impaired social cognition.
Repetitive/stereotyped behaviors, social deficits, and sensory abnormalities were associated with smaller CC volumes, these relationships might not be specific to autism. Decreased CC size has been reported in children with OCD, a finding which was also correlated with compulsive behaviors. Smaller CC size has also been reported in individuals with Tourette’s disorder and this reduction was correlated with tics severity. Social deficits and sensory abnormalities have also been described in individuals with agenesis of the CC.
Functional neuroimaging studies demonstrate that reading involves a widespread network of cortical regions, predominantly in the left hemisphere. Individuals with dyslexia, however, fail to produce this typical activation pattern. Both children and adults with dyslexia show hypo activation of the left temporoparietal and occipito-temporal areas during phonological processing and reading tasks.
In addition dyslexic readers demonstrate a greater engagement of right hemisphere homologues and bilateral prefrontal dorsal sites (i.e. the inferior frontal gyrus), which was interpreted as compensatory activity for dysfunctions in the left posterior reading areas.
Recent studies reported that the overall area of the corpus callosum (CC) and anterior portion of the CC was larger in adults who stutter (AWS) compared to normally fluent adults. Generally, a larger CC is associated with right hemisphere dominance or reduced hemispheric asymmetry for speech, which is consistent with neurological reports of increased right hemisphere activation or a lack of left hemisphere dominance in stuttering.
The overall midsagittal cross-sectional area of the corpus callosum (CC) has been reported to be smaller in subjects with Tourette syndrome and to be correlated inversely in children with both symptom severity and prefrontal volumes. These studies have thus suggested that interhemispheric axons in children with TS, together with prefrontal cortices, successfully reorganize in order to enhance regulatory control of motor and phonic tics. This interpretation is consistent with the known functional characteristics of the CC, which involves primarily transfer of information between the two hemispheres, as well as modulation of attention, and inhibition of cortical activity and plastic reorganization of the brain.