My Experiences as Eric Courchesne's Research Subject



I am a person who is a so-called "high-functioning autistic". Eric Courchesne is a neuroscientist who is studying and doing research on the neurophysiology of autism. This article details some of my experiences as his research subject and some perspectives on it, particularly having had an MRI scan of my brain.

For many years, I was frustrated by the fact that I had problems that impaired my ability to function in the world and that I had no idea about the reason why. This started many years before I thought of my problems as possibly having a neurologic etiology and before ever hearing of autism, let alone thinking of myself as possibly having this disorder. When I first learned that my problems were believed not to be emotional, but rather physical, i.e., the result of brain-damage or a brain dysfunction, I wondered what proof there was of this. The psychologist who I was seeing at the time told me that a lot of my problems were the result of a neurologic disorder. Not long after that, I began to think of myself as possibly being autistic or at least having autistic symptomatology.

In my case, the only proof seemed to be my scores on psychologic tests. On the Weschler I.Q. test, for example, I do relatively well in the academic areas such as vocabulary, arithmetic, general knowledge, etc. However, I do, poorly on the performance part of test, i.e., putting together jigsaw like puzzles, puzzles involving copying a block design, etc. This was said to be the result of a "perceptual-motor dysfunction" which was the result of brain-damage. Also, there is a test called the Bender-Gestalt. This is a test of visual motor perception that clinical psychologists are trained in the administration of. This consists of asking the person being tested to copy nine geometric designs. The manner in which the figures are copied enables psychologists to detect certain types of subtle brain-damage in some cases, for example, with reading disabilities and with the type of perceptual and fine motor coordination problems that I have. I was not really satisfied with this form of proof that my problems hhad a neurologic etiology. For years I yearned for something more.

A few doctors had diagnosed me as being autistic or at least having autistic-like symptomatology. I definitely do have certain types of autistic symptomatology in addition to the handwriting, fine motor, and perceptual-motor dysfunctions. This is somewhat of a paradox in my case as most autistic persons do not have these dysfunctions and do better on the performance part of the I.Q. test than the verbal part. They also score normally on the Bender-Gestalt. Most people seemed to believe unequivocally that autism was caused by a physical disease of the brain. However, no one could really say for sure what brain structures were involved. The only evidence was really indirect, such as certain biochemical abnormalities such as elevated serotonin in the blood platelets as well as abnormal responses on evoked brain stem response tests and a few studies showing enlarged ventricles in the brain on pneumoencephalograms and CAT scans. The results of these studies were largely mixed.

For years I wondered what was exactly going on in my brain and in college I became very interested in the brain and in possibly uncovering the etiology of my brain disorder, i.e. exactly what structures were involved or how exactly my brain was damaged or not functional. I was very cynical as to whether my brain was certainly dysfunctional or if perhaps there was some other explanation for my problem. It seemed that a brain disorder was the most likely explanation in my case so I almost accepted it as a matter of faith. It seemed to me that most if not all of the persons who were doing research about autism and writing anything in the literature were psychologists and psychiatrists who had no formal training in neuroscience as well as not having done any real research that was neurophysiologically oriented. This was a source of frustration to me. All of the physiological psychology and other types of textbooks that I had read mainly talked about schizophrenia and affective disorders and the neurophysiologic basis for those, or at least what was known about the neurophysiologic basis of these disorders. They never discussed autism and this bothered me. It seemed strange that no experimental psychologists or neurophysiologists were interested in autism. I ended up writing a letter to Neil Carlson, author of the text Physiology and Behavior , asking him why this was so and why he did not write anything about autism in his book. He wrote me back, stating that he believed that autism was a severe right hemisphere problem based on autists inability to relate to objects in the environment as well as the lack of prosodic inflections in their speech. He also wrote that he would review the literature and that if he found anything promising he would include it in his next book. He never did include anything about autism in his subsequent editions.

Some years later, I was having lunch in a Mexican restaurant on my lunch hour from work and had turned to the bottom of the front page of the Los Angeles Times. I was very intrigued to read a headline proclaiming that a major breakthrough had been made in discovering the etiology of autism. A researcher I had never heard of named Eric Courchesne had discovered that certain parts of the cerebellum were abnormally small in autistic persons as opposed to normal controls whose scans they had measured. This research continued to get media attention with headlines in Newsweek magazine proclaiming "part of the autism puzzle solved." I was absolutely intrigued by this man who supposedly had partially solved the autism puzzle. Then I found the article in the New England journal of medicine that the media had referred to. They had scanned a total of 18 autistic persons and 14 of these had cerebellar abnormalities. Also, I later found out that in less subjects, autopsies had been done showing some cerebellar abnormalities. I wished that somehow I could get an MRI scan to see if I had this abnormality or any other abnormality of my brain that it could detect. Courchesne's research seemed well done and planned out from the articles that I had read.

One day, I decided that I would call them to see if I could be a research subject in their lab. I left a message on their answering machine and then never heard back from Dr. Courchesne. About two months later, I got home from work and was surprised to hear a message on my answering machine from Rachel Courchesne, Eric's wife. When I told her I was interested in having a scan she seemed rather skeptical, thinking my problems did not seem so overt over the phone. She then said she would like to discuss my problems and situation with my parents. I complied, giving her my parent's phone number. After talking to my parents, she asked me numerous questions about my symptomatology. After I answered them to the best of my ability, she concluded that it sounded like I had enough of the symptoms to qualify as a research subject in their lab, but that I would have to take some tests and do an interview with Dr. Alan Lincoln, a psychologist who works with them. She also needed to know if I had a pin or wire of any kind from any injuries, as the magnet in the MRI scanner would pull these out and I could not have a scan if this were the case. I had no pins or wires in any bones or joints. I drove down to San Diego from Los Angeles which took a little over two hours. I stayed at the house of a friend who was living there at the time. I then went to the San Diego Children's Hospital Neuropsychology Research Lab where they do a lot of their research and testing. I was met by Natacha Akshoomoff, a graduate student in clinical psychology who worked with Alan Lincoln and Eric Courchesne. She gave me a Bender-Gestalt Test, a Weschler I.Q. test, and something called the WRAT (Wide Range Achievement Test). This is a test of various academic abilities, such as vocabulary and math. This was followed by an intake interview with Alan Lincoln, the psychologist whom I wrote about earlier. He asked me various questions to determine what my autistic symptomatology was.

After this, it would finally be time for my MRI scan the following weekend. This would consist of another two hour drive to San Diego, but I was really interested. I had been told by Rachel, that I would get to meet her husband, Eric, this neurophysiologist who had been felt to have made such a major breakthrough in the understanding of the etiology of autism. I would have a variety of questions to ask him, and I knew that this would be a golden opportunity to pick the brain (slight pun intended) of one of the greatest neuroscientific minds studying autism. His research had been published in the New England Journal of Medicine and he had made headlines worldwide. I was really uptight that I would meet him and have nothing meaningful to say or ask. After all, it had been many years since I had studied physiological psychology in college or even read very much about the brain on my own. If my understanding of neurophysiology in general and Courchesne's research in particular were greater, than I would be able to ask more meaningful questions. No matter, I would review my old physiological psychology text and also look in a neuropharmacology book to see what they had about the cerebellum. Then, I went to where they had the MRI scanner and sat in the waiting room after being greeted by the technician, an amiable late middle aged woman whose name I don't remember. Then a balding bearded man, casually dressed in a t-shirt, came in and started making jovial comments to the technician. I knew it had to be either Courchesne or the neuroradiologist who works with him; I later found out it was the latter. The technician then motioned me to come into the scanning room where I disrobed and put on a hospital gown. I went on the table where I would lay down on the device that would put me in the claustrophobic-causing tube where I would have the scan. I was then pulled into the narrow tube. I have slight claustrophobia, but this tube was not nearly as confining as I thought it might be. I was then laid down and heard the clicking of the scanner. I had been told to lie still and not move my head so that they could get the best images of my brain possible. She (the technician) kept talking to me over the intercom, asking me if I was okay. I replied that I was. I kept hearing the clicking as they were getting pictures of different parts of my brain.

Finally, the scan was over and the electronically movable table started moving again, pulling me out of the scanning tube. I saw the neuroradiologist sitting at a console with a picture of a skull with a brain in it. I did not get a really close look at this picture on the console but I saw enough of it to know vaguely what it looked like, a skull and a brain. I knew that they were my skull and my brain. The technician told me to go back to the waiting room and wait for some people to come out and see me. My body felt really strange having been cooped up in that narrow tube for so long and I needed to go sit on the couch and get my body together. I felt a really weird tingling sensation all over my body. Then Rachel emerged from the room with a man that I had never seen before. I knew that man had to be Courchesne.

"Are you Eric Courchesne?", I asked.

"Yes, I am", he replied. He extended his hand and I took it and we shook hands. Courchesne then motioned me to sit on the couch in the waiting room. He took a seat on the couch next to me.

"Do you have any questions you would like to ask me?"

"Yes, I do." What I don't understand is that autistics generally don't have really profound motor impairments. I do have a fine motor coordination problem which impairs my handwriting, but I can type very fast and have no real problems with balance and gait. So if it is the cerebellum, which controls motor behavior, that is impaired in autism then why don't autistics have profound motor problems?"

"If the damage to the cerebellum occurs early enough then there will be no motor problems. You see, developmental lesions are different than adult lesions."

This seemed to me to be a pretty good response and a fairly good explanation. I then asked him a bit more about the research he was doing and he went into a very technical explanation of the whole thing. I started to like Dr. Courchesne at this point. He seemed pretty amiable and down to earth to me in spite of all of the publicity that his research had garnered. I also liked the fact that he explained everything to me and answered my questions in a noncondescending fashion. I also asked him if the self-stimulatory behaviors I did were related to the so-called pleasure centers in the brain since "twiddling"-what I have always called the self-stimulatory behaviors that I do- seemed like a drive just like hunger, thirst, or sex. He agreed that it was very possible that this was true and pointed out to me that the vermis of the cerebellum-the area of the cerebellum in lobules VI and VII that were abnormally small in autistics- had reinforcing properties, just as did the septum-in association with sex- and the hypothalamus in association with hunger and thirst. I had also read that the superior cerebellar peduncle- one of the structures that connects the cerebellum to the rest of the brain-had reinforcing properties as well. I asked him if it would be possible to measure this structure. He then told me that the cerebellar peduncles were only a few millimeters in diameter and too small to measure comparatively between autistics and normals with any degree of real precision given the limitations of MRI scanning. He then asked me where I had obtained my knowledge of the literature on autism as well as my knowledge of neuroanatomy. I told him that since I had been about 20 I had been interested in brain research, and that I had studied the subject to some degree in college as well as having done a little bit of reading on my own. "Well, it sounds like you have read a lot.", he replied. This made me feel good, sort of. I knew that he may have just been saying this to flatter me. Of course it might have been possible that what little I did know about his work and autism and neurophysiology seemed like quite a bit for anyone who was autistic.

Several months later I found that I had a smaller cerebellar vermis than a normal person's. There was a range of sizes for persons with autism, varying between no hypoplasia, i.e. smaller cerebellar vermis, and extreme hypoplasia. I was somewhere in the middle, he said, being about "average" for someone with autism. There was apparently no relationship between degree of autism and degree of cerebellar hypoplasia, because in the article that he published in the New England journal of medicine some of the highest functioning autistics that they scanned had the most pronounced level of cerebellar hypoplasia. This was an interesting fact, someone may have actually done something physical to show that there was really something in my brain that might be causing these problems. Or had they? I remembered Rachel (Courchesne) telling me that other independent investigators had sent them scans with the measurements that they had attempted of the cerebellar vermis. These other investigators had not been able to replicate Courchesne's findings. Rachel told me that the reason for this lack of replication was that the other investigators did not know how to properly make measurements of the cerebellar vermis. Of course, there could be some other explanation that she was not telling me or even something that neither she nor her husband knew.

A few years later, I ended up having a second MRI scan of my brain, also by Courchesne and associates. The reason for the second scan was that they had developed a better method for scanning people as well as a software program that Brian, who does computer programming for them, had developed using a Silicone Graphics Computer. This program allows for more accurate measurements of various structures in the brain. Well, I subsequently had my second scan. This was done only by the technician and Courchesne himself, sans neuroradiologist Gary Press. I did not even disrobe or put on a hospital robe, just did it with my regular street clothes on. This time, Courchesne spent a fair amount of time with me, showing me the setup in the MRI room that he did not show me during my first scan. He then had a picture of a brain on a console, it was my brain. It was a sagittal view of my left hemisphere. What this means is that hypothetically, if you took an apple and sliced it at the top it would produce two pieces, a right and a left. The inside of either the left piece of the apple or the inside of the right piece of the apple can then be viewed. Similarly, an MRI image can be taken in the same manner. The view that I saw of my own left hemisphere was analogous to looking at the inside of the left piece of an apple. The left hemisphere is the part of the brain involved in speech and language in most people, rather than the right hemisphere which is involved in spatial relations, artistic ability, mathematical ability. I had seen plenty of pictures of brains in textbooks but seeing my own brain photographed as well as it could be given the current state of the art was quite astounding.

Courchesne, while I stood next to him, used this button that I guess was sort of like a mouse on a computer and pushed it while outlining the areas of my cerebellum that would be of interest in autism. They were smaller than what would be normal. To illustrate a comparison to me, he then did the same thing with my corpus callosum-another brain structure which serves to connect the right and left hemispheres of the brain-and this, he said, was the same size as in a normal person. I then asked him about other structures. He said that he also planned to do measurements of the hippocampus-a brain structure involved in short term memory-as well as other parts of the so-called limbic system to attempt to corroborate by MRI scan the results that Margaret Bauman had gotten by autopsies. I also told him that I had seen somewhere that Luke Tsai, another autism investigator had found abnormalities in portions of another brain structure, the basal ganglia, and asked him if he planned to try to replicate this work. "Basal ganglia measurements are really easy to do, Jonathan", he replied, but did not say whether or not he planned to replicate this work. I also asked Dr. Courchesne about what his wife had told me a few years previously, i.e. the lack of replication. He then stated that although some researchers had not replicated his work, two of them, namely Drs. Pivin and Cielcelsky, had replicated his work. I was also concerned about the fact that although Margaret Bauman's work, like Dr. Courchesne's work, had concentrated largely on the cerebellum in the autopsies that she had done, she had found abnormalities in different parts of the cerebellum than had Courchesne. His work had been largely concentrated on the vermis, and Bauman had specifically reported finding no abnormalities of the vermis. He then told me that he and Bauman had had strong disagreements about this, specifically which parts of the cerebellum had been affected in autism. He stated that Bauman had redone her measurements somehow (the explanation he gave was somewhat technical and did go over my head a bit) and had now corroborated his findings and now agreed with him that the vermis was indeed affected in the cerebella of the autistic brains that she had autopsied. "Margaret Bauman and I used to have arguments about that all of the time, Jonathan." I was not sure if he was exaggerating or not. I certainly did not believe that he could be completely objective. This was a concern to me and a possible shortcoming in his research. I also raised the issue that similar types of cerebellar abnormalities (although not identical) had also been found in persons with schizophrenia and I asked if he knew anything about this. He told me that he had not known about these cerebellar abnormalities in schizophrenia. I later talked about this with Jeanne Townsend, a graduate student who works with Courchesne, and she said that she had known about the similar abnormalities in schizophrenics.

He also acknowledged to me that MRI scans are quite limited in what they can actually resolve, even using the best measurement techniques. I asked him if it were possible to resolve aspects at the molecular level with either MRI or PET scans such as synaptic transmission, possible sodium-potassium pump deficiencies in persons with autistic symptomatology, deficiencies in neurotransmitters, etc. He acknowledged that it was not yet possible to identify such abnormalities in living brain tissues. I also told him about how before I was five years old and had been nonverbal and that perhaps part of the problem was a deficiency in the language centers and described the areas I thought he might like to scan. He said he felt that this might mean that I had autism per se rather than Asperger's syndrome, since persons with Asperger's generally never had the language problems associated with autism. He also told me that scanning these language centers that I expressed an interest in might not be the best bet for autism since dysfunctions in these areas were generally reflected in various types of aphasias and other language disorders occurring in persons who suffered strokes and such as adults. He pointed out to me that developmental lesions are different from adult lesions of the brain. I really don't know if this is true or not or if he was just saying that to justify the inconsistencies between cerebellar abnormalities of autism and the lack of flagrant motor impairments. Overall, it was very interesting meeting with Eric Courchesne and the people that he worked with, including his wife, Rachel. Some of the time they did seem like nice people even though at other times they did seem rather perfunctory. I did believe and still do believe that this is one of the best and most productive programs for someone with autistic symptomatology. I do not believe that there are any effective therapies for autism. Therefore, I believe that it is important to determine whether or not autism is a physical disease of the brain, and assuming it is then develop etiologically-based therapies based on these discoveries. I think that Courchesne is at least moving in the right direction in this regard. I hope that Rachel's prediction that etiologically-based therapies could be developed within the next 20 years based on the research that they are now doing comes true. I do think, however, that this is being a bit optimistic. In spite of all of this, I did have some concerns. If it is true that developmental lesions are different than adult lesions then this complicates the picture somewhat. This would make it more difficult to make inferences from what is known about adult lesions and their effects and use this knowledge to speculate about the etiology of autism in general and my problems in particular. The study of the brain concentrates on presumed functions of different nuclei such as the function of the hypothalamus in regulating hunger and thirst, the amygdala in rage, some of the basal ganglia as well as the cerebellum in motor function, etc. Dysfunctions in these nuclei produce certain types of effects in adults. If dysfunctions in these areas are congenital rather than occurring later on in life, then they will produce different effects and the problems associated with autism cannot be extrapolated from this. For example, Broca's area in the frontal lobe of the brain is known to control expressive speech. Adults who suffer strokes in this area of the brain develop language problems. Other types of adult aphasias can cause language problems that are somewhat analogous to those found in autism, e.g. echolalia. If Eric Courchesne is correct about the differences in adult vs. developmental lesions than one cannot say that autistics necessarily have an impairment in Broca's area or in other areas of the brain normally associated with speech. This is an area of frustration to me because it makes it more difficult to speculate about what areas in my brain have gone awry. Subsequently, they published some research showing evidence of parietal lobe dysfunction in persons with autism. This is of particular interest to me because it is very possible that my fine motor coordination problem and so-called perceptual motor problem which impairs my ability to put together puzzles and learn things is caused by a dysfunction of the parietal lobe, particularly the one in the right hemisphere. Of course, once again, the problem of extrapolating between the constructional apraxia of adults and my similar developmental problems may be invalid. It seems like it was worth my while to contact them in spite of what little they seemed to be able to do or tell me about the etiology of my problems. They are interesting people doing what I think is some of the best work in the business on elucidating the etiology of autism and related disorders. However, they have just pretty much explored the tip of the iceberg, probably leaving more questions than answers. It may take a while, but hopefully sometime in my lifetime I will have a genuine understanding of the etiology of my problems. I do, however, believe that the headline "part of the autism puzzle solved" is either written by someone not informed of the facts or is media hype or a combination of the two.