My 8 Year old son has bladder problems and he is obsessed with masterbation(masturbation) is this common is aspergers?

[muddymae]

My son was normal and healthy until he received his vaccinations when he was 2 years old, I had at first associated this with terrible twos. But his personality changed so much, he was such a happy boy and gentle and inquisitive, he was also very aware of people around him and was very calm. Then I took him for vaccinations, I held off until he was two because I was worried about the shots. He became very ill, with a very high fever and vomiting. The doctor told me it was all normal reactions to the vaccine. But he became very aggressive, he bit a chunk out of my daughters stomach and began head butting me and other alot. He also had regressed from being fully potty trained to how he was when he was only a baby, he is now 8 years old, been twice diagnosed with adhd, and with attachment disorder. His bladder has been checked and found to be normal, but he still urinates in his pants and bed frequently at times.
My biggest concern is he plays with his penis frequently and forgets that he is suppposed to only do that in the tub or his room. He makes people uncomfortable when they catch him and he often does not notice when someone enters the room or even if they always were there.
He does not know how to tell a lie, or how to know when he has been insulted, or if something is inappropriate.
He differs from many autistic children in the fact that he loves cuddles, and he requires them frequently.
I am glad that his teacher this year is a wonderful and intelligent woman who has helped him to develope some friendships, two of which are children also suspected of having aspergers. My son and I are still waiting to see another pediatrician, it is taking forever.

[William H Ahearn, Ph.D., BCBA]

There is no evidence that vaccines cause autism.  Many caregivers feel there is a correlation in the timing of the 2 year old vaccines and autism because that is the age at which the developmental impairments associated with autism become most apparent.  As to mastrubation, "self-stimulatory" behavior is more common in persons with autism than typically developing persons or persons with other disabilities.  

As to the cause of autism, I've written extensively on this topic but evidence does not usually presuade those people that want to believe vaccines cause autism and there is a great deal of recall bias (not correctly remembering the timing of events) with this issue.  Because the popular media perpuates this vaccine-autism myth and no new notable evidence supporting this causal hypothesis exists, I will focus on actual evidence of the cause of autism.

Previous research suggests that autism may be the product of “genetically determined prenatal alterations in brain development” (Acosta & Pearl, 2003).  Neuroimaging work has found that children with autism aged 2 to 4 had larger brains with more cerebral and cerebellar white matter and more cerebral cortical grey matter than typically developing children of the same age (Courchesne et al., 2001).  However, Carper and colleagues (e.g., Carper et al., 2002) found that children with autism gain substantially less grey and white matter in the frontal lobes from early to late childhood relative to typically developing children.  Acosta and Pearl feel that current evidence points to abnormal timing and amount of brain growth and that growth in some areas may end prematurely.

A number of genetics researchers have been working towards identifying the genetic mechanisms that may underlie such abnormal brain development.  Autism spectrum disorders (ASD) have long been known to have genetic origins and approximately 10% of persons with an ASD have a known genetic anomaly such as Fragile X syndrome.  One recent large scale study found that persons with autism were much more likely to have a parent who had been diagnosed with schizophrenia or a mother diagnosed with either depression or a personality disorder than unaffected individuals (Daniels et al., 2008).  Such work helps to confirm suspicions as to the genetic origins of autism but other recent work has been looking to identify specific genetic mechanisms.

A study conducted by the Autism Consortium (headed by researchers at Children’s Hospital Boston) was published earlier this year in the New England Journal of Medicine.  It was found that the genes of 1% of persons with autism had a specific region on chromosome 16 in which there was either a duplication or deletion of a sequence of genes on a part of the chromosome (Weiss et al., 2008).  Genetic problems in chromosome 16 have been identified as a suspected mechanism that may underlie intellectual disabilities in general.  Finding this anomaly in persons with autism without impaired cognitive functioning will help to clarify the significance of this finding.

Another study has honed in on a specific gene region in chromosome 7, which is thought to be involved in language development.  Alarcon and colleagues (2008) identified a suspect gene on chromosome 7, CNTNAP2.  CNTNAP2 produces a protein involved in brain cell communication.  Mutations of this gene are speculated as potential sources for abnormal brain development.  The variant form of this gene was found significantly more often in persons with autism but this finding was gender specific.  That is, the scientists found that statistical evidence for the gene was strongest in families with boys diagnosed with an ASD relative to families with affected boys and girls, or in families with affected girls only. This genetic problem may be one reason associated with the higher incidence of ASDs in males.

Sebat and colleagues (2007) detected a higher likelihood of spontaneous mutations that were present in a child diagnosed with an ASD but the mutation was not present in either parent.  Among the children with autism who had the mutations, 12 out of 14 of them were the only affected members of their family.  The rate of such mutations was much lower in families with more than one affected member, the researchers propose that "two different genetic mechanisms contribute to risk: spontaneous mutation and inheritance, with the latter being more frequent in families that have multiple affected children." The two mutations detected in the typical control subjects were duplications, while the majority of those in people with autism were deletions. Relatively more females had the mutations, suggesting that the anomalies may contribute more equally across gender than other causes of autism.

Though there has been much learned from genetics research within the past few years, the genetic mechanisms responsible for the majority of cases of autism have not yet been identified.  One application of findings such as those reported above is the development of tests to screen for specific genetic presentations.  The autism community has generally supported this type of research and the participation of many families is helping scientists better understand how autism develops.



Acosta, M.T. & Pearl, P.L. (2003).  The neurobiology of autism: New pieces of the puzzle.
Current Neurology and Neuroscience Reports, 3, 149-156.

Alarcon, M., et al. (2008).  Linkage, association, and gene-expression analyses identify
CNTNAP2 as an autism-susceptibility gene.  The American Journal of Human Genetics,
82 (1), 150-159.

Carper, R.A., et al. (2002). Cerebral lobes in autism: Early hyperplasia and abnormal age effects.
Neuroimaging, 16, 1038.

Courchesne, E. et al. (2001). Unusual growth patterns in early life in patient with autistic
disorder.  Neurology, 57, 245-254.

Daniels, J. et al. (2008). Parental psychiatric disorders associated with autism spectrum disorders
in the offspring. Pediatrics, 121, e1357 - e1362.

Sebat et al. (2007).  Strong association of de novo copy number mutations with autism. Science,
316, 445-449.

Weiss, L.A. (2008). Association between microdeletion and microduplication at 16p11.2 and
autism. New England Journal of Medicine, 358, 667-675.

[sweet92]

how ang why fallopian tube's swollen??