The global prevalence of the disorder has increased between 20 and 30 times since the late 1960s and early 1970s, CDC researchers wrote in the new report, published March 27 in the CDC's journal, Morbidity and Mortality Weekly Report.
(Typed from text of DSM V)
Autism spectrum disorder is a new DSM-5 disorder encompassing the previous DSM IV autistic disorder (autism), Asperger's disorder, childhood disintegrative disorder, Rett's disorder, and pervasive developmental disorder not otherwise specified. It is characterized by deficits in two core domains: 1) deficits in social communication and social interaction and 2) restricted repetitive patterns of behavior, interests, and activities.
Conclusions In this small, explorative study, we found focal disruption of cortical laminar architecture in the cortexes of a majority of young children with autism. Our data support a probable dysregulation of layer formation and layer-specific neuronal differentiation at prenatal developmental stages. (Funded by the Simons Foundation and others.)
reply to post by watchitburn
Autism has a direct genetic cause. There is added material to specific genes and even a doubling in some cases. There is a very real chance that autism is simply a part of our genetic heritage that has become more successful in contemporary society than it was in the past, so there is a breeding reinforcement of this trait. This could be very simple and everyone is so busy looking for that one particular tree that they can't see the forest for the distraction.
reply to post by Nyiah
Could be all the extra radio waves effecting brains of fetuses and infants. All the Wi-fi, microwaves, radio waves, cell phone signals, radar. It could have a cumulative effect that has compounded over generations?
If you're gonna quote it shouldn't you link it?
For anyone interested in the actual conclusion of the NEJM original article:
No it wasn't, according to the article. One sample from the kids with autism did not have the abnormal structure. One might question "how autistic" that child was.
The abnormal brain structure they are citing was also found in one of the normal kids brain tissue.
There were 22.
There were only 11 samples.
For the latest study, Courchesne and colleagues got brain samples from 11 children with autism who died young, mostly from accidents such as drowning, when aged 2 to 15. They compared their samples to brain tissue of 11 kids without autism who also died suddenly.
To their surprise, they found extremely similar changes in 10 out of the 11 children with autism. They found “patches” of abnormal development in the tissue taken from the brain regions important for social development, communication and language. The visual cortex was unaffected.
Was just thinking about this.
Since 2002, autism cases have seen an increase of over 100%.
Since 2000, our wifi and 3G now 4G data streams have increased substantially.
The symptoms of autism may not be obvious until a child is a toddler, but the disorder itself appears to begin well before birth.
Brain tissue taken from children who died and also happened to have autism revealed patches of disorganization in the cortex, a thin sheet of cells that's critical for learning and memory, researchers report in the New England Journal of Medicine. Tissue samples from children without autism didn't have those characteristic patches.
Organization of the cortex begins in the second trimester of pregnancy. "So something must have gone wrong at or before that time," says Eric Courchesne, an author of the paper and director of the Autism Center of Excellence at the University of California, San Diego.
The finding should bolster efforts to understand how genes control brain development and lead to autism. It also suggests that treatment should start early in childhood, when the brain is capable of rewiring to work around damaged areas.
Context Autism often involves early brain overgrowth, including the prefrontal cortex (PFC). Although prefrontal abnormality has been theorized to underlie some autistic symptoms, the cellular defects that cause abnormal overgrowth remain unknown.
Objective To investigate whether early brain overgrowth in children with autism involves excess neuron numbers in the PFC.
Design, Setting, and Cases Postmortem prefrontal tissue from 7 autistic and 6 control male children aged 2 to 16 years was examined by expert anatomists who were blinded to diagnostic status. Number and size of neurons were quantified using stereological methods within the dorsolateral (DL-PFC) and mesial (M-PFC) subdivisions of the PFC. Cases were from the eastern and southeastern United States and died between 2000 and 2006.