Asperger's Syndrome

I can get along without people thinking I'm a complete weirdo (most of the time)

So withdrawl is your main form of defense mechanism? Any others?

Presumably if you notice what other people think about you - you don't really rate on the aspergers scale

I took another test, and once again, I score as being more able to read facial clues than the average human.
Which I guess means that nearly everyone around me must have AS, and I don't.

There must be something wrong with me.

I wonder how accurate these little tests are?

But looking over the following criteria, I can't imagine not having AS:

I think AS is the creation of a bunch of bored psychiatrists.

Hi there everyone.

I'm new to this forum and I thought Id join seen as I like physics and am planning on going to university to study it eventually.

I stumbled across it after searching for information regarding Asperger's Syndrome. I thought it would be a good idea to start on this thread because I have aspergers syndrome myself and was wondering if there is anyone else on this forum who has it because it would be interesting to talk somebody who is in the same boat as me.

I've got HFA. Is that close enough?

In social interaction, many people with Asperger's syndrome demonstrate gaze avoidance and may actually turn away at the same moment as greeting another...

A physicist famously wanted to find the grand unifying equation behind the laws of nature, in a form that you could put on a t-shirt. Neuroscientists Kamilla and Henry Markram have proposed a grand unifying theory of autism, and the key to it is in this picture. I wouldn't want to be seen wearing it quite yet, but if the theory pans out, I'm sure we could come up with a more torso-friendly diagram. So what does this mean? The Markrams call their idea the Intense World Theory. Essentially, they propose that all of the diverse symptoms of autism are direct or indirect consequences of the autistic brain's being hyper-responsive to stimuli.

In certain settings, autistic individuals can fare extremely well. One such setting is scientific research. For the past seven years, I have been a close collaborator of an autistic woman, Michelle Dawson. She has shown me that autism, when combined with extreme intelligence and an interest in science, can be an incredible boon to a research lab.

To advance the understanding of introversion, I propose that it is a continuous segment of the non-clinical part of the autism spectrum, and that it is not the same as the inverse of extraversion. When introversion and autism are placed on the same continuum, the nature of the relationship of the traits becomes more apparent, and new possibilities are available for exploration of both autism and introversion.

Solitary animals are thought to eschew unnecessary social contact as part of a foraging strategy often due to scarcity and wide dispersal of food in their native environments. It is thought that the human ancestral environment was often nutritionally sparse as well, and this may have driven human parties to periodically disband. Inconsistencies in group size must have led to inconsistencies in the manner in which natural selection fashioned the social minds of humans, which in turn may well be responsible for the large variation in social abilities seen in human populations. This article emphasizes that individuals on the autism spectrum may have only been partially solitary, that natural selection may have only favored subclinical autistic traits and that the most severe cases of autism may be due to assortative mating.

In response to the "unified theory" take a look at this short article:

http://www.scientificamerican.com/ar...les-have-fewer

which focuses on the amygdala, alone. I suppose if someone could demonstrate how having fewer neurons in the amygdala would lead to it becoming hyperactive, then this study would support the "unified theory".

The proposed deficits in reading other people’s feelings and thoughts and the lack in empathizing with other people have been commonly used to explain the impairments in social interactions and communication as well as inappropriate responses in social encounters even in high-functioning forms of autism such as in an Asperger. It was suggested that these deficits are mediated by a not sufficiently activated amygdala. These and other data, such as post-mortem examinations of amygdaloid morphology , amygdala lesion studies in non-human primates , as well as comparison between amygdala- lesioned patients and autistics have led to the Amygdala Theory of autism . In its current version it implies that the amygdala is hypo-functioning, thus the autistic person does not “feel” enough or does not process socio-emotional cues sufficiently .

On the other hand there is evidence that the amygdala may be overly activated in autism. First, structurally the amygdala is enlarged in autism as early as 18 months of age and this enlargement persists throughout childhood until about 12 years of age. In adolescence the enlargement disappears and by early adulthood the amygdala may even end up smaller than in control subjects . These changes may reflect an over-activation of the amygdala in early childhood. Second, functional hyper-reactivity was demonstrated when autistic subjects are confronted with socially relevant stimuli, such as faces and eyes . For example, Kleinhans et al. (2009) showed that compared to controls the amygdala of autistic subjects exhibits attenuated habitation to facial stimuli and that increased amygdala- arousal in autistics was associated with increased social impairment. Monk et al. (2010) recently showed that right amygdala activation is enhanced in autistic subjects during face processing when controlling for attention, that is when the autistic subjects pay attention to the stimuli. Dalton et al. (2005) revealed that high-functioning autistics showed greater activation in the right amygdala when viewing familiar and unfamiliar faces and greater activation in the left amygdala and also in the left orbito-frontal cortex when viewing emotional faces. Both areas form part of the emotion circuit of the brain and increased reactivity to faces in these areas means a heightened emotional response to these stimuli.

Moreover, in autistics, but not in controls, the amount of eye gaze fixation was strongly correlated with amygdala activation when viewing both, inexpressive or emotional faces (Dalton et al., 2005). This suggests that that eye gaze fixation is associated with emotional and possibly negative arousal in autistics and this could explain why autistics have “trouble looking other people in the eye.” Eye contact and watching the facial expressions are one of the first signs of cognitively healthy infants, are natural to people, and serve to build the basis for successful navigation through a social environment. For an autistic person however, these stimuli may be just too intense or even aversive to cope with and hence they are avoided. The Intense World Theory proposes that amygdaloid hyper-reactivity and hyper-plasticity may in particular provoke a dis-proportional level of negative emotions and affect in autism, such as elevated stress responses and anxiety as well as enhanced fear memory formation. Enhanced phobias and anxiety levels were first noted by Kanner himself in his original case studies and later confirmed by population studies on children with autism. However, contrary to the deficit-oriented or disconnected Amygdala Theory and Theory of Mind of autism, we propose that the amygdala may be overtly active in autism, and hence autistic individuals may in principle be very well able to attend to social cues, feel emotions and even empathize with others or read their minds, but they avoid doing so, because it is emotionally too overwhelming, anxiety-inducing, and stressful.

Hyper-or hypo-reactivity to sensory input or unusual interest in sensory aspects of environment; (such as apparent indifference to pain/heat/cold, adverse response to specific sounds or textures, excessive smelling or touching of objects, fascination with lights or spinning objects).

I apologize in advance for just skimming all of the posts in this thread and for just clicking on some of the links. By doing so, I hope that I am not repeating any thoughts expressed in this thread.

However, have there been recent research developments in identifying genes or chromosomal regions that may potentially aid in the diagnosis/treatment of Asperger’s syndrome?

Given that there are proposals to eliminate Asperger's syndrome as a separate disorder, and instead merge it under autism spectrum disorders (ASD), I'm not sure what that will mean? Here is their justification for eliminating Asperger's from DSM-V:

February 10, 2010
Asperger's Officially Placed Inside Autism Spectrum

Asperger's syndrome is really just a form of autism and does not merit a separate diagnosis, according to a panel of researchers assembled by the American Psychiatric Association.

Even though many researchers already refer to Asperger's as high-functioning autism, it hasn't been listed under the autism category in the official diagnostic guide of mental disorders, called the Diagnostic and Statistical Manual, or DSM. The DSM serves as a guide for mental health professionals and government agencies.

But a new draft fifth edition released Wednesday moves Asperger's officially into the autism category, provoking a wide range of responses among people with Asperger's — some of whom say they do not want to be labeled as autistic.

That was done almost 2 years ago. (Feb 2010)

http://www.npr.org/templates/story/s...ryId=123527833

The DSM-5 Task Force and Work Group members have spent much of 2008-2010 formulating their proposed draft criteria. This includes conducting extensive literature reviews, performing secondary data analyses, and soliciting feedback from colleagues and professionals. Although DSM-5 will not be published until 2013, the revision experts have several important tasks ahead of them in finalizing the development of this volume. Below is a detailed summary of the DSM-5 timeline leading up to the May 2013 deadline.