Tuesday, February 9, 2010

I'm participating in cal tech emotions lab research

Today I went in for a research study on eye tracking in the Cal Tech emotions lab. They are doing research in high functioning autism and Asperger's syndrome. This involved looking at some faces and being asked to push a key depending on the gender of the face under various circumstances. I did this while wearing an eye tracking device on my head. It was rather cumbersome and uncomfortable for the duration of the experiment but I managed it. Dr. Dan Kennedy, a protege of Eric Courchesne in whose research group I have participated in, in the past is the investigator in the study. I have also written about my experiences with the Courchesne lab elsewhere Now that he has finished his doctoral work under Courchesne at UCSD, he is now a post-doctoral fellow in the lab of Ralph Adolphs, a professor of psychology and neuroscience at CIT.

It started out last month at an autism conference in Long Beach that I went to. Normally the fare at autism conferences is bland if not drab, mostly behaviorists, special educators or people pushing whatever flavor-of-the-month treatment is extant. Not to mention the Jeff Bradstreets and others who push the very questionable mercury-causes-autism hypothesis. However, this conference was somewhat a metaphorical diamond in the rough. They had Manuel Casanova, who has done autopsies of autistic brains and has demonstrated abnormal minicolumns as a possible etiology of autism. Also among the impressive lineup was a somewhat pregnant Lindsay Oberman who gave her take on mirror neurons and mu wave suppressions. It included Mirella Depratto, wife of mirror neuron maestro Marco Iacabonni,-talking about some of her work. Interesting sidenote, but least relevant to this post Donna Williams was also a scheduled speaker, but she got sick and was not able to show up in person. However, she gave a videotape of her presentation and later there was a question and answer session with her using skype, which I did not attend, leaving the conference before this.

Last but not least was a new kid on the block (at least to me) a young and up and coming brain researcher whom I had never heard of named Dan Kennedy. I had not been keeping up with a lot of the literature as of late so I missed out on reading the intriguing study about the default network that he did with Eric Courchesne. here is the study for your reading pleasure. To summarize there are a variety of areas at the brain that have a high activity at rest, i.e. when a person is not engaging in any task such as solving a mathematical problem or reading something. These areas consist of areas of the brain called the medial prefrontal cortex, rostral anterior cingulate, posterior cingulate, and precuneus. These are interconnected to each either via axons and are collectively known as the resting network or default network. Though the study is rather technical for me and I did not understand all of it, the gist of it was that an experiment was done with autistics versus normal controls in which they engaged in a task called the stroop test in which a research subject is asked to read words that describe colors but printed in a different color for example green written in blue ink. The subject is asked to name the color the word is written in rather than the word itself, in this case saying blue instead of saying green. It has been shown that the natural tendency is to say the word rather than the color of the word, so this is a more challenging test than it might appear to be superficially. When the nonautistic controls did this, their default networks shut down, that is they showed a low metabolic rate as measured in a fMRI scan showing that blood oxygen no longer went to these areas during somewhat challenging mental activity. In the autistic subjects, the default network still remained active. It was speculated that abnormalities in these processes might be part of the etiology of autism.

This is intriguing to me, because I have to wonder if this is why I have had intrusive thoughts and an inability to concentrate on my former medical transcription jobs making abnormal amounts of mistakes. Could it also have something to do with my twiddling (self-stimulatory behavior)? Perhaps in non-autistic people these areas shut down when they are not engaged in a task, and if mine won't turn off, maybe that is why I have difficult doing things and concentrating.

Dr. Kennedy also speculated that because of the high metabolic rates of certain brain areas such as the precuneus and the posterior cingulate cortex they might be more susceptible to damage due to genetic factors, infectious factors or possibly an environmental factor. It seemed to me the way Dr. Kennedy worded this in the study that he was implying that there were known factors in the environment that could cause autism. I certainly questioned this and called him on it. He stated that he meant that for example lead poisoning and mercury poisoning could cause some autistic like behaviors in children brain damaged from these things even if the children were not autistic themselves. I questioned this, because as regular readers of gadfly know, I don't really believe that heavy metal poisoning causes autism. Of course it is speculation and Dr. Kennedy conceded this. He also conceded he did not mean to say that these environmental factors could cause autism itself, just some behaviors that resembled autism such as in lead poisoned or mercury poisoned children.

Before I did the eyetracking study, I was introduced to the group's director, Dr. Ralph Adolphs. I was intrigued because Dr. Adolphs had studied under Antonio Demasio, a very well known eminent neuroscientist formerly at the University of Iowa and now at the University of Southern California. Many years ago I read a journal article that was published in the late 1970's by Dr. Demasio and his colleague, Ralph Maurer which dealt with comparisons of adult syndromes of the frontal lobes and basal ganglia and parallels and similarities to autism. The frontal lobes deal with organization and executive functioning which are often the bane of autistic people. The basal ganglia deals with motor behaviors, though I don't think it is responsible for my twiddling (self-stimulatory behavior) or fine motor coordination problems. Though it was interesting one problem is that adult lesions are probably different from developmental lesions so not sure how apt the comparisons are.

I was then interviewed by Dr. Lynn Paul, a clinical psychologist who works with the group. We took a break for lunch after that during which time Dr. Kennedy and I reminisced over mutual acquaintences of ours who worked in the Courchesne lab such as Matthew Belmonte and Greg Allen.

They wanted me to do some more stuff for them, but it was getting late and I was concerned about driving back in heavy traffic, so I guess this is a saga to be continued. It is also possible that I will have a functional MRI scan done by them at some point but still not sure, and I made a little money which is nice considering my financial situation of late has not been the best. Though I have had two structural MRI scans I have not yet had a functional one, where you do a certain type of task while undergoing a scan. Before I stopped going to the Courchesne group in 1998, Greg Allen attempted one on me, but my head was too big to fit in the apparatus along with all of the computer equipment that was in place in the scanner.

Well this is the beginning of what may be an interesting story and a new chapter in the saga of my life with autism so far. I may or may not write more about my experiences with the cal tech emotions lab stay tuned.

Addendum: The group is looking for research subjects with high functioning autism or asperger's syndrome. They pay $20/hour for the type of study I was involved in and I think $50/hour if you undergo an fMRI scan. They gave me some pamphlets and told them if I knew anyone to let them know they are looking for subjects. I think it is possible they pay out of state travel expenses to people who are not local to southern california but i am not sure, you can contact them at (626) 395-4486 or send the director, Ralph Adolphs email at radolphs@hss.caltech.edu


Stephanie said...

I hope you write about it because we need all the info we can get.

jonathan said...

Stephanie: If you are ever in the Los Angeles/Pasadena area you might be interested in being a subject in their studies. They pay $20/hour for the eye tracking studies i took part in and $50/hour for an fMRI study They are desperately seeking research subjects with high functioning autism or Asperger's syndrome.

I think it is possible they would pay your out of state travel expenses but I am not sure, so it might be possible for you to be their research subject if you were willing to travel to Southern California.

They gave me some pamphlets and asked me to tell anyone I might know who would qualify and be interested in being a subject in their studies.

Anyhow Stephanie or anyone else who may be interested can call the lab director, Ralph Adolphs at
(626)395-4486 or send him an email at: radolphs@hss.caltech.edu Think I will add an addendum to the post

SM69 said...

The paper from Kennedy you flag is interesting, I have not read it in full, but I note that the lack of desactivation (low metabolic rate) was not found to be related to differences in counting Stroop task performance amongst others similar tasks. Therefore, whilst this is interesting, it is by no mean suggestive that "abnormalities in these processes might be part of the etiology of autism". The study includes only 15 subjects, 3 of whom were excluded, so 12 total. The nature of the task implies of course that only HFA/AS can take part to the study and one cannot tell if the finding could be representative of the full spectrum. There is no indication on any medication taken by the subjects, it is possible that many are on anti-depressant of some sort, whilst the controls are healthy control.

There are alternative possible explanation to the possible relevance of these observations. I wonder what ADHD/ADD subjects would be like? I note he study makes references to others in Alzheimer disease and ageing and another one in Fragile X, in all cases, there was reduced desactivation, papers avaiable online as also in PNAS.

Stephanie said...

I'm not flying across the country to participate in a study. I don't like to travel.

If there is ever something here I might think differently...

(And I often look as a way to make a little extra $)

jonathan said...

Stephanie, if i hear of anything near south carolina where they are doing research like this I will let you know. I think University of North Carolina Chapel Hill has some sort of autism program where they may do some studies like that but I am not sure.

jonathan said...

Lorene: That is one of the great problems in autism research, the fact that the findings are limited to the higher end of the spectrum and very possibly if not probably not applicable to the lower end. There are compliance issues that preclude the use of persons at the lower end in studies such as these, since they need to sit still in an MRI scanner to avoid artifacts.

If you had any suggestions as to how to do research using lower functioning research subjects, I am sure most autism researchers would love to hear it as many persons would like to learn more about possible etiologies from this group.

I guess I will have to tell Dan Kennedy about your other criticisms of his study next time I see him.

Stephanie said...

UNC still too far for me (I have no way of getting there.)

I was thinking more along the lines of MUSC (which is about 30 min away from me). MAYBE USC (University of SC) but they are almost 2 hr away from me.

SM69 said...

Hi J,

Yes please do! These will come to no surprise to him.

Coincidently I have found an interesting article on this subject, http://www.scribd.com/doc/20645850/The-Psychologist-October-2009, see p22-24. They refer this phenomenon as an energy-guzzling default mode network (DMN), and discuss not only Alzheimer and autism, but also depression and mind-wandering, which all have also this difference in de-activation (hence, this is not an autism-specific phenomenon). There are also very interesting observations that normal subjects would have less deactivation of the DMN when engaged in a task that is well known as opposed to a novel task. Further A Damasio also reported of a stroke patient, now recovered, who had damaged DMN- After recovery she reported she had been unable to formulate her thoughts. The idea emerges therefore that the DMN could be involved in thoughts, such as for example thinking about the future. It may well be that issues in ASD relate to “attention flicking back and forth between internal and external focus”.

Please do ask D Kennedy, what would he predict ADHD and ADD to be like, also what he would expect the effect of anti-depressant to be, or even how individuals with specific short term-memory issues would do?

Regarding your question on assessing LFA- this is indeed a difficult issue- and one that I am focusing on at the moment. There are many confounding factors, you mentioned compliance, but there are many more still, motivation, attention, sensory, social, communication, cognition. I believe most traditional psychologists are less than adequate in their ability to interact with autistic individuals. If one does not know how to relate, and how to get people motivated to attend to a task etc., one stands no chance to provide a reliable assessment. On the other hand, there are many talented therapists about who are just great, hands on, and effective, but they don’t know how to administer a standardised assessment- it’s like this area is divided with no cross talk. What we are trying to do is to bridge these 2 areas of knowledge together, using standardised assessments, for example by administrating Leitcher-R cognitive assessment to LFA in a way that will be most child-centred, motivating and accurate- this needs to be delivered hands in hands with other assessment (ADOS and Vineland, SCQ) to understand better what might affect the score. As for functional brain imaging, or even eye tracking studies, for now, there is little that can be done with LFA. None the less, researchers should remain humble in their conclusions, if they study AS, they should not pretend to study autism as whole. Individuals differ greatly that this must be acknowledged in each and every report. (this sub-phenotyping is an other issue I am focusing on at the moment).

SM69 said...

I have to flag an alternative explanation to the Kennedy/ DMN observations that is raised in the article I have the link of earlier on page 838.

“Gilbert and his colleagues argued that what Mason’s group had inferred was mind-wandering activity could just they’ll only be engaged in internal processes just doesn’t accord with my subjective experience when I’ve been in a scanner,’ says Gilbert. ‘If you’re given nothing to do, especially if it’s your first time, you’re suddenly a bit anxious, you’re wondering what’s going on, there are also these beeps and strange noises, and you may be waiting for something to come up on the screen. So it’s just as plausible that you’re actually in a state where you’re really looking out for something in the environment.’

“The points of contention, the state of play, revolves around whether scanning people at rest is the way to study these intrinsic processes, and whether the DMN, as it was originally conceived, really exists at all. “

If we take this second possible explanation, then we could expect AS subjects being more active, even when engaged in a task because of an increase need to constantly assess the environment due to greater uncertainties/anxieties. That would fit well with depression too, and possibly also Alzheimer disease, in early stage, the knowledge of having the disease and awareness of assessment must cause anxiety that is greater than in control subjects.