Autism Spectrum Disorders are marked by impairments in the ability to communicate and interact socially and by the presence of repetitive behaviors or restricted interests. These conditions appear to be ever more prevalent. There are many ways to define them, but in general the condition affects everyday function and interferes with early childhood development in a pervasive way.
People with ASD may communicate, interact, behave, and learn in ways that are different from most other people. Intellect and cognition can vary from gifted to severely challenged. The diagnosis of ASD now includes several conditions that used to be diagnosed separately: autistic disorder, pervasive developmental disorder not otherwise specified (PDD-NOS), and Aspergers Syndrome.
In January 2005, Hughes & Melyn reported their study on autistic children: it “found 46% with seizures and also a relatively high prevalence of 20% with epileptiform discharges but without any clinical seizures.” In other words, 66% of the children had clearly abnormal EEG’s. Shortly thereafter, Hughes was able to report that: “The evidence is now clear that one major finding in autism is the under-connectivity within the brain. This finding is consistent with the behavior of these children, who tend to concentrate on some object, rather than on any person, but without any significant relationship to other sensory modalities, as may be expected from disconnected cerebral circuits.”
Later in the same article, Hughes summarized his review of the medical literature: “Possible etiologies included metallic elements, although the mercury in thimerosal, a preservative previously used in vaccines, is likely not involved. Many chromosomes and genes (especially MECP2) have been implicated, but autism is likely polygenic with a complex genetic architecture. Parental conditions that may be significant include vitamin D deficiency, anti-thyroid medication, advanced age, and relatives with learning and mood disorders. Central nervous system conditions are varied, but considerable evidence exists for under-connectivity of cortical regions. Especially involved are the frontal cortex, amygdala, hippocampus, and temporal cortex. An increase in radiating white matter volume has also been reported, as has serotonergic hypoactivity. Mini-columns in the cortex are likely diminished, as are mirror neurons that are active not only during one’s own movements but also during the movements of others. (These factors refer to the theory of mind explanation of autism, that these children have a deficient appreciation of the thoughts and feelings of others.) Many examples can be given of global deficiencies in the brains of autistic children, including an increase in inhibitory synaptic transmission, delay in brain-derived neurotropic factor, global lack of integration from brain enlargement, and many structural abnormalities. There is some evidence for the involvement of autoimmune, hormonal, and electrolyte factors. Oxidative stress and toxicity have also been mentioned. One view of autism is that it represents an extreme male brain with high testosterone levels.”
In 2014 van Elst opined that: “Against the background of these observations, the increased Glx (glutamate + glutamine) signals reported in children and adolescents with ASD could be understood as an indicator of anterior cingulate cortex over-excitation. Whereas the decreased anterior cingulate cortex Glx signals we and others measured in adults might point to over-inhibition of this brain area. From this perspective, the magnetic resonance spectroscopy Glx signal might serve as a surrogate marker of the functional equilibrium of anterior cingulate cortex networks, with increased signals pointing to pathological over-activation and decreased signals hinting at over-inhibition.”and
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