Friday, February 6, 2009

an interesting lecture by Nancy Minshew

Today I attended a rather interesting lecture by autism researcher Nancy Minshew. Dr. Minshew is a professor of psychiatry and neurology at the University of Pittsburgh and is one of the people currently doing research into the neurophysiology of autism. She talked about autism being "synapseopathy". I guess that might mean lack of connections between synapses. Also she talked about autism being a disconnection syndrome, various areas of the brain being disconnected from each other. What, of course, was most interesting about this idea was that she stated that it had implications for someday making good interventions a reality for autistic people. She stated that one of the most interesting questions to her about autism was the heterogeneity between autistic persons. She used the book about social skills co-written by Temple Grandin and Sean Barron as an example of this phenomena. She read the blurbs on the flap of the book, one from Grandin and one from Barron. She contrasted the differences between these two persons with autism. Temple had no emotion in her blurb, just approached social situations logically, whereas Sean was the opposite.

She discussed the fact since autism seemed to result in a problem of migration of neurons to various places during fetal development that this suggested that the mercury/vaccines causes autism people were mistaken. She quoted a toxicologist who worked at the CDC who had an autistic son stating that he had studied this and the evidence of toxicological factors and this showed that autism was not caused by anything toxicological. She then gave Paul Offit's book a plug. She also plugged a book that has just come out by someone named Andrew Zimmerman, though I don't remember the name of the book or she never gave it.

One interesting anecdote that she discussed was how rules could override concepts in autistic individuals. She talked of a story about an autistic boy who was an eagle scout trained in first aide who liked to ice skate. One day he went ice skating with his mother and then skated a bit too fast and knocked his mother over who became unconscious. Though the boy was trained in first aide, someone else ended up administering it to her and not her son. After she was administered the first aide and taken to the hospital the boy's mother inquired as to why he had not given her first aide since he was an Eagle scout and had been trained and given a first aide badge. His reply was, "my first aide badge expired".

She talked about some studies of amygdala-cortical interactions.

One interesting thing that she talked about was functioning in Broca's and Wernicke's areas in autistics versus normal controls. Broca's area is the part of the brain in the frontal lobe that is involved in expressive speech. Persons who have lesions in this area as adults become aphasic and are not able to speak. Wernicke's area is in the temporal lobe of the brain and it involves receptive language or the ability to understand language and adults with lesions in this area have trouble understanding language. Minshew talked about a study in which the autistic group had less activation in Broca's than the normal control group whereas they had more activation in Wernicke's area. These results are consistent with poorer comprehension of complex sentences yet good reading and spelling ability among autistics. What I found most interesting about this study is perhaps this could be the reason that autistics do not always develop expressive speech. Perhaps there is some dysfunction in Broca's area that is analogous to adult aphasics. This would contradict what Eric Courchesne told me years ago when I was his research subject in some MRI scans and event related potential studies. He claimed that studying Broca's area would probably not be fruitful in autistics as developmental lesions were different than adult lesions. When I first asked him about why if autistics have damaged cerebellums they have no obvious motor impairments this was along the lines of his explanation that because the damage to the cerebellum was early enough there were not the same types of motor impairments that took place when an adult had damage to the cerebellum.

I don't remember much more about the lecture but overall a very interesting lecture.

4 comments:

Stephanie Lynn Keil said...

Thank you for this. The evidence that autism is a neurological disorder is overwhelming and is what I find most fascinating about the causes of the disorder.

I don't find the heterogeneity between autistic persons too fascinating as each individual has a unique personality and ideas of how to approach the world regardless of illness. People with autism all have the same symptoms (as do people with bipolar, schizophrenia, etc.) but how they manifest and how the individual deals with them is what makes the difference. Therefore, I do not believe the heterogeneity between autistic people has too much to do with the brain but rather with each individual, at least when comparing HFA/AS to others of the same type and those with LFA to those like themselves.

I think it's more interesting to look at the personality of those with AS/HFA and compare personality types and how they react. My symptoms of autism are very similar to Temple Grandin's but we have very different personalities, thus I interpret the world quite differently and cope my autism in very different way.

JediKnight2 said...

Very good post!

Now I have a greater in-depth understanding on why I have a Mixed Expressive-Receptive Language Disorder along with my PDD-NOS label I was given as a toddler where it's currently known I have HFA.

Now besides my obvious damaged Broca's area, Wernicke's area, lack of communication among my synapses, a damaged cerebellum that was treated greatly through occupational therapy and a bit at speech therapy by placing me on a tire swing, my likely enlarged amygdala among other brain dysfunction, my theory is that I have more activity in my brain taking place as a way of compensating for my brain dysfunction. This is the cause of my third co-morbid condition, ADHD.

Now I realize 98 percent of people on the autism spectrum have problems with executive functioning according to my speech pathologist, but we read over a section asking 20 different questions from a book entitled "Driven to Distraction", and I had 17 out of 20 'yes' answers. My pathologist even guided me through them.

Boo yeah!!! I'm innocent after many years of misunderstandings.
The many people I've met on the Internet and at support groups suck at supporting each other because of their own impairments and denial due to not knowing they could be getting the same help I'm getting. Only a neurologist and speech pathologist know this stuff.

What's the point of being an autistic advocate if one is only able to help others and share advice based on the life experiences of that individual if he/she doesn't even know every detail about how differently an autistic's brain functions. Almost no one gets their facts straight when they discuss disablities and labels, especially the bipolar asspies, because all they can do is take a mixture of facts from the Internet and be naive about it all, especially through other contacts. Not to mention, they typically don't have language problems, so they could be easily influencing lower-functioning autistics.

How much do you want to bet many autistics do not realize the neurologist mainly studies the brain and performs brain surgery occasionally while the pathologist has to ability to change an individual's brain chemistry as if he/she was performing brain surgery using a remote control? Well, I'm sure there's a few out there who know about this, but they could never tell me the truth.

As for the rest of the spectrum, many of them could not possibly be interested in or be slow to understand Nancy Minshew's lecture. The only stuff they're interested in is their limited, nerdy interests/obsessions.

SM69 said...

Hi that’s a good post- I would agree with Eric Courchesne (for once) when he says that developmental lesions are different than adult lesions. In fact there is no consensus amongst all fMRI, MRI, SPECT studies done- not one, other than they show something different each time. What is also important is who constituted the study group, which type of autism do they have, are how old are they, are they on medication? Are they institutionalized? HFA or lower end of the spectrum? Which co morbidity symptoms do they have? Etc. Martha Hebert (Harvard Medical school) proposes that autism is a integration dysfunction- irrespectively of the specific brain abnormality, what matters would be a lack of integration of brain sub-regions with one another- that impairment could take place at key stages of development, pre-natal, as well as post natal, but during the earlier years of development. Development of symptoms of autism after a period of normal development has been seen in reported in children till age 10). There are a few cases also reported in teenagers and adults as consequence of brain herpes encephalitis. This is Gillberg’s work. But we also have to highlight the findings that abnormalities can be with regard to inflammatory processes not necessarily cause brain structure abnormalities. But there has not been any fMRI done of such individuals. Plus final point, some SPECTY studies reported the same hypoperfusion abnormalities in autistic people than in siblings or parents, showing that an abnormalities does not necessarily equal a dysfunction. Complex stuff.

Anonymous said...

Interesting. I have Chronic Fatigue Syndrome, and recently I realized I probably have Asperger's too. In CFS, exercise results in less activity in Wernicke's area (Spanish researcher Montoya). But I do not know if this research was done on the same subset of CFS that I am in. There seem to be a lot of similarities between CFS and Aspergers e.g. the sensory problems with noise and light. I think I also have Aspergers because of the social difficulties I have, and the way I have of thinking. I had those problems in childhood before I felt ill with CFS and post-exertional malaise.