Personal Perspective: What my brother taught me about the etiology of autism.
When I was a doctoral student in developmental psychology in the early 1970s at the University of Rochester, there was a big, federally funded, longitudinal study going on that examined the relative contribution of genetics and family pathology to the later onset of schizophrenia in children enrolled in the study.
One of my professors, noted infancy researcher Arnold Sameroff, opened my eyes (and the eyes of other study investigators) to the increased frequency of perinatal anoxia or hypoxia (cut-off or reduction in oxygen during the birth process) in the birth histories of children and adults who develop severe psychopathology.  
This information made me aware of two facts which many psychologists and psychiatrists seem oblivious to even today, namely that: (a) organicity is routinely missed as a causative factor in developmental and psychopathology conditions, and (b) even when organicity is suspected, in almost all cases it is assumed to be genetic in nature, and non-genetic forms of “organicity” (such as perinatal anoxia) are typically overlooked.
I have a younger brother who, around 1958, when he was 10, was diagnosed with “childhood schizophrenia,” a term that later was replaced by autism. In 1948, three or four days after he was born, he was dropped on his head by a baby nurse. My parents, especially my mother, were tarred for the rest of their lives by the “refrigerator mother” theory of autism causation at that time espoused by Leo Kanner, the father of American child psychiatry and autism research.
Kanner, who evaluated my brother, later abandoned that theory, but it was taken up by others, especially Bruno Bettelheim (an art historian who took only four psychology courses and falsely claimed to have both a doctorate and psychoanalytic training) whose extreme psychogenic treatment for autistic children when he was a professor at the University of Chicago and director of its affiliated Orthogenic School for Disturbed Children was to try and separate them from their parents.
Interestingly, when I was doing a postdoc in developmental disabilities at UCLA Medical School in 1976–1977, the first symposium I attended was a lecture by Sir Michael Rutter, the father of child psychiatry in Great Britain and Kanner’s successor as the dean of international autism scholarship. The focus of his talk was on the increased incidence of autism in children who in early infancy suffered closed head injuries.  In other words, he was talking about children such as my brother. This was despite the fact that much of Rutter’s scholarly work had been on the role of attachment disorders in causing mental illness in children.
Thus, Rutter, unlike many of his colleagues, was able to keep in mind the principle of “equifinality,” namely that the same outcome (in this case autism) could have different developmental precursors and pathways. According to some researchers, the connection between early head injury and autism is explained by a marked decrease in the migration during the first year of life of Purkinje cells, a class of GABAergic inhibitory neurons located in the cerebellum.  Autopsy, followed by microscopic examination of brain tissue, of autistic individuals who died young in accidents such as drownings show such a cerebellar pattern.
The fact that organicity still tends to be viewed as another word for “genetics” is seen in the feature article in a fundraising newsletter that I recently received from a university-affiliated children’s hospital in the Bay Area. The title of the article, by a professor of neurology at the hospital, was “Investigating the Genetics of Autism.” Certainly, that is a worthwhile research topic, but I was put off by the first sentence in the article: “Autism is a relatively common genetic disorder.” Undoubtedly, there is a genetic pathway for many cases (although multiple autistic sibs in the same family is relatively rare). But where is there room in such a characterization of the disorder for someone like my brother?
The focus of the author of the newsletter article and his team is on autistic children with agenesis (absence or thinning) of the corpus callosum (an important mid-brain structure) and its association with mutation in a protein-coding gene called DDX3X. This mutation hypothesis could explain why autism might only be found in one child and not their siblings. But I assume the researcher, a neurologist, is aware of the fact that agenesis of the corpus callosum is an extremely common finding in the brains of individuals with fetal alcohol spectrum disorder (FASD), a developmental disorder caused solely by excessive consumption of alcohol by pregnant women. 
FASD is the main known cause of preventable cases of intellectual disability  and also has a high degree of co-occurrence with autism . A colleague and I are working on a paper in which we shall argue that FASD should be viewed as a “syndromic subtype of autism.” The term syndromic subtype is used to refer to a subordinate condition that overlaps behaviorally (such as in social unintelligence, my main topic over the years) in a substantial but not necessarily perfect way with a superordinate condition, and that has a biological cause that is shared by a subset of people with the superordinate condition.
Given the strong genetic bias among developmental disability scientists and practitioners, the focus in identifying syndromic subtypes of autism has until now been entirely on genetic conditions such as Angelman and Prader-Willi syndromes (both involving chromosome 15) with little or no appreciation of non-genetic biological causes of autism or related disorders. The list of non-genetic causes of autism (the cause of which for most individuals is unknown) is fairly long and, besides FASD, perinatal anoxia and infant TBI includes such things as infections (in pregnancy and early childhood), severe malnutrition, lead exposure and pregnancy complications. (I have not included the MMR vaccine theory of autism causation espoused by anti-vaxxers, as it has not received empirical support). Part of my purpose in exploring this issue is to inform mental health professionals of something that I learned from Arnold Sameroff and my brother, which is that a condition which often is genetic can have an organic etiology that does not involve heritability or defective genes.
 Eaton, W.W., Mortensen, P.B., Thomsen, P.H. & Freyberg, M. (2001). Obstetric complications and risk for severe psychopathology in childhood. J. of Autism and Developmental Disorders, 31279-31285.
 Burstyn, I., Wang, X., Yasui, Y., Sithole, F. & Zwaigenbaum, L. (2011). Autism spectrum disorders and fetal hypoxia in a population-based cohort. BMC Med Res Methodology. 11: 2.
 Rutter, M. (1977). Brain damage syndromes in childhood: Concepts and findings. Journal of Child Psychology and Psychiatry, 18(1):1-21
 Arin DM, Bauman ML, Kemper TL. The distribution of Purkinje cell loss in the cerebellum in autism. Neurology. 1991;41(Suppl):307
 Riley, E., Mattson, S.N., Sowell, E.R. et al. (1995). Abnormalities of the corpus callosum in children prenatally exposed to alcohol. Alcohol: Clinical and Experimental Research, 19 (5) 198-1202.
Reprinted with permission of FASD Now member, Stephen Greenspan. Original article can be found on Psychology Today.