Autism or Autisms: What should be our Default Position?

I recently gave a lecture for the Autism Research Institute. The same dealt with whether autism should be considered a single condition or a conglomerate of multiple disorders. My position approaches the problem from the perspective of somebody with experience in the fields of neurology and neuropathology. In the lecture I argue that there is enough evidence to indicate the presence of one basic mechanism underlying autism. I also argue that differences in susceptibility for an individual person (e.g. genetic makeup), environmental exigencies, and timing during brain development may all interact in various ways thus accounting for the observed clinical heterogeneity of autism. Thus despite many causative factors (e.g., risk genes, congenital viruses, use of drugs during gestation) they all seem to act through the same mechanism yet still provide for a clinical heterogeneous disorder. The lecture and findings are of importance in regards to the ongoing debate about neurodiversity. People claiming that autism falls under the purview of the normal variability of traits within the general population are hard pressed to explain brain findings that are evidently pathological and whose manifestations (e.g., seizures) are in need of treatment.

I apologize in advance for the audio quality of the recording, this is something that went beyond my control. The same was taped from a Skype session in my office. However, if you liked the video, please share the same with your social contacts and leave a like on YouTube. You can also leave comments on this blog. The link to the lecture is:

10 responses to “Autism or Autisms: What should be our Default Position?

  1. There are definitely multiple subtypes and different underlying causes.There is a growing body of evidence there is an inherited autoimmune encephalopathy than can cause autism in children of mothers with systemic autoimmune diseases,like lupus,MS,or type 1 diabetes.This is is completely different from autism due metabolic and mitochondrial disease.Both are different from someone with autism due to a genetic malformation of the brain.To say nothing of someone who developed autism due to chemical or drug exposures in the womb.How are all these the same condition with the same mechanism?No,I have not listened to your talk yet.


    • Thanks for the comment. I think you have a logical question. It is interesting that the mechanism proposed in the lecture is the same one by which autoimmune disorders appear to mediate their effects in autism (Martinez Cerdeno V, Cerebral Cortex 2014). Also, viruses (ribella, CMV0 and drugs (cocaine, thalidomide) when expressing an autism phenotype appear to act through the same mechanism. I think I took the position of the devil’s advocate in trying to say that the null hypothesis had not been dis-proven.


  2. I liked it very much so far, I am about 47 minutes in. I am a housewife, no medical background…but I have followed research for about 18 years because of my son.
    At ~47.50, I noticed the nodular heterotopias and ectopic cells…tying in with Tuberous Sclerosis to be sure, but I wondered if other than TSC and NF, heterotopias are present in brain tissues of autistic individuals? Also, I loved the terminology of a short circuit or shower curtain …and the sense it made that the presence in the cerebral cortex would lead to atypical sensory processing.
    Again, my questions: How common are herterotopias outside of TS and NF among people with ASD? Are they more common among autistics who need 24/7 care for their lifetime? Do they exist among autistics of high IQ? Only answer if you have time.


    • Depending on the series (the level of resolution and the type of screening) heterotopias may be found in about 75% of autistic individuals. Cortical dysplasias may be more prevalent and found in about 85% of individuals. However, taken both together they suggest a defect in neuronal migration early on during gestation. They abnormalities are still more common in syndromic cases. Thanks for the question and more so, for your patience in listening to the lecture.


  3. Sorry…is it possible for hetorotopias to be be subclinical? Are they generally localized, or primarily systemic? Would localization lead to different behavioral manifestations? I think of sensory defensiveness and sensory under-repsonsivity, as well as craving. I wonder if the location of the nodules, if they are localized, could be an indication of the particular sense affected. Sounds too simple to be the answer. Sorry…I think so much of autism research these days is advantageous—find a way to use your lab to get money by putting the word autism in your research grant appllications—or exceedingly complicated to the effect that the researcher is totally ignorant outside of his finite area of expertise, and misses profoundly simple possibilities because of it.


  4. Autism seems to be closest defined as a “syndrome” in which multiple factors are at play. Factors with a wide range of affect that likely are interdependent like shades of purple as opposed to red or blue… Gary S


  5. I am sorry…I have just never seen so many causes of autism put together in an idea, except in my own brain. I know Rubella, CMV, TS, Ehlers-Danlos, genetic anomalies and prematurity are involved, but to see them put together, with an idea of the correlation they may have to each other. You know, we hear, “We don’t know what causes autism”….BUT WE DO! We know hundreds of conditions that end up with a behavioral manifestation of autism. Good luck, I hope people listen. This is fantastic.


    • That was the original idea. There are many conditions that express an autism phenotype for which the pathology is known (syndromic autism). What is common to all of them, if anything? See Med Hypothesis 83(1):32-8, 2014.


  6. This talk is very hard to understand to someone who not a neuroscientist.I have become fairly adept at understanding medical journal articles,and I had a hard time keeping up.I am guessing this was over the heads of many people in the audience at ARI.

    That said,I think you may have hit upon a very interesting theory.I had to watch the section of the video where you explain it,a number of times to get it.I think your theory is that there can be any number of stressors during brain development in the womb,that can lead to an out of place alignment of cells in the development of the hindbrain,but the result is always the same,because this misalignment always occurs in the same place.These stressors can be anything from genetic disorders to prenatal/anenatal drug exposure.I had never seen the theory you talk about presented as a cause of before as a cause of autism.

    I had never heard the terms rhombic lip or germinal zones before.I am still not clear on what these are.I did a little reading online,and I was able to piece together a fuzzy picture of the prenatal development of the ventricular and sub ventricular systems,but I still do not quite get it.You should have explained this to the audience.

    What layer or what ventricle are we talking about here?

    Is the problem you discuss here linked to neural tube development or defects? Could it then be caused by a prenatal folate deficiency?


    • Sorry about the difficult terminology, etc. When I spoke about the Rhombic lip it was just to say that besides the periventricular germinal layer (in the brain) there could be other germinal cells affected. Those in the rhombic lip would help explain abnormalities of the brainstem and cerebellum. Other germinal cells outside of the CNS could also be affected. The ventricles of the brain (primarily the frontal horns) is surrounded by a germinal layer that is very vascular and lacks connective tissue. It is very similar to granulation tissue (the tissue that forms in response to a cut or a wound) and it is transitory. Probably the article that I wrote expressing this as a hypothesis would clarify things a little bit: Med Hypotheses. 2014 Jul;83(1):32-8.


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