link to Home Page

Autism Factors

Dr. Grace Baranek, et. al. at UNC-Chapel Hill conducted a review of home videos from early childhood (9-12 months) of infants who were later diagnosed with autism. Such children already show developmental irregularities at that age. ... Also, thimerosol has largely been phased out in the U.S., with no change in autism rates. ... Autism rates are also correlated with the age of the mother.

Experts Find No Vaccine-Autism Link
May 19, 2004
http://www.adhdnews.com/testforum/test14456.htm
Especially convincing were a Danish study showing no difference in the rate of autism between children who got thimerosal-containing vaccines and those who did not and a British study showing no relationship between the introduction of MMR and autism rates, or between the timing of a vaccination and the onset of autism symptoms.
 
http://www.asw4autism.org/Madison/Madisonjune99.htm
What is different about the cerebellums of individuals with autism? The whole posterior cerebellum is small, and the cerebellar vermis is reduced by 10-15%. According to a study by Ritvo, there is a 40-50% loss of Purkinje cells in individuals with autism. The inferior olive sends "climbing fibers" to the Purkinje cells, capturing them for specific cerebellar functions, such as motor functioning, speech, attention, etc. In neurologically typical people, there are plenty of Purkinje cells to allow the cells to specialize for these different functions. But in individuals with autism there are far fewer Purkinje cells, so each cell may have lots of climbing fibers for several different functions. Since each Purkinje cell may receive conflicting messages about what it should be doing at any time, the individual may experience difficulty performing the kinds of activities controlled by these cells. These abnormalities start very early in development, before birth. ... The overgrowth of the frontal lobes starts at some point between birth and age two, and continues until about age five or six.
 
http://www.sciencenews.org/articles/20041113/bob8.asp
In the Jan. 1, 2003, Journal of Neuroscience, scientists led by Paul H. Patterson of the California Institute of Technology in Pasadena reported that when pregnant mice were infected with a modified human-flu virus, they produced offspring that, as adults, behaved in ways similar to those of many autistic children. Compared with a control group, the affected mice interacted less and were unusually anxious under mildly stressful situations and around unfamiliar objects. The scientists also found unusually low numbers of critical signaling components, called Purkinje cells, in brain tissue of the affected mice. Autopsies of people with autism have revealed fewer than normal of these cells. In an upcoming International Journal of Developmental Neuroscience, Patterson's group reports that altered brain development in the mice doesn't appear to occur as a direct result of viral infection in the fetus. Instead, "there's evidence it's related to a natural immune response in the mother, [but the] mechanism is something we're still working on," says Patterson. Some of the molecules that the mother uses to fight the virus may be crossing the placenta and affecting brain development in the fetus, he explains. If so, the problem wouldn't be specific to the flu virus. "Lots of kinds of infection could lead to the same effects," Patterson says. [Note: it has long been known that pregnancies during a flu epidemic result in more schizophrenia among the offspring.]
 
http://www.autism.org/temple/visual.html
Autism is a neurological disorder that is not a result of psychological factors. A complex inheritance of many interacting genetic factors cause most cases of autism. There is a continuum from normal to abnormal. Autistic traits often show up in a mild degree in the parents, siblings, and close relatives of an autistic child (Narayan et al. 1990; Landa et al. 1992). Some of the traits that seemed to be associated with autism are: intellectual prowess, shyness, learning disabilities, depression, anxiety, panic attacks, Tourettes (tic disorder), and alcoholism (Narayan et al. 1990; Sverd 1991). There is a high correlation between Asperger's syndrome and manic depression (Delong and Dyer 1988). Possibly a small amount of these genetic traits confers an advantage, such as high intelligence or creativity; too many of the traits will cause problems (Clark 1993) Other causes of autism are the Fragile X gene, insults to the fetus, such as Rubella or other viruses, and high fevers at a young age.

Brain autopsy research (Bauman 1991, Bauman and Kemper 1994) and MRI studies (Courchesne et al. 1988; Hashimoto et al. 1992) indicate that people with autism have structural abnormalities in the brain. Certain areas of the brain, such as the limbic system and cerebellum are immature. Other studies have shown that lower functioning people with autism also have abnormally slow transmission of nerve impulses through the brain stem (McClelland et al. 1993) and immature EEG patterns (Cantor et al. 1986).
Dr. Patricia Rodier (2000) explains that the brain abnormalities that cause autism occur very early in the developing embryo. Her research has shown that there are defects in the developing brain stem that happened near the end of the first month of pregnancy. A structure called 'the superior olive' is missing in the brain stem. This may explain the lack of cerebellum development in autism. In summary, autism is a disorder in which some parts of the brain are underdeveloped and other parts may be overdeveloped. This may be a possible explanation for why some autistic people have enhanced visual and savant skills.
Weighted Blanket Guides
A detailed article and guide about ASD and ADHD.