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Writer's pictureHollis Lyman

What we know about autistic brains


A. Representative Golgi images for postmortem human temporal lobe (left, 10×, stitched from nine separate image stacks), layer V pyramidal neurons with basal dendritic tree (top middle, 20×, pseudocolored in red; bottom middle, 40×, pseudocolored in green; scale bar, 50 μm). The right four panels (100×; scale bar, 5 μm) are representative images of proximal basal dendritic segments from two control subjects (C, aged 8 years and 18 years) and two ASD cases (A, aged 7 years and 15 years). Tang, G., et al. (2014). Loss of mTOR-dependent macroautophagy causes autistic-like synaptic pruning deficits. Neuron, 83(5), 1131-1143.

The story of scientific inquiry into autistic brains begins in the 1940s with two men: Leo Kanner and Hans Asperger. Kanner, based in the United States, was a prominent psychiatrist who helped establish child psychiatry as a distinct discipline. In his seminal 1943 paper, he described autism as a distinct syndrome characterized by "extreme aloneness" and a "desire for sameness." His observations were based on case studies of 11 children, whom he followed closely at Johns Hopkins University. Kanner meticulously documented the behaviors, communication patterns, and developmental histories of these children, framing autism as a neurological condition rather than a purely psychological or environmental issue. His work challenged prevailing theories like Freud’s psychodynamic model, which often attributed childhood conditions to parental fault. The debate was further inflamed by Bruno Bettelheim's "refrigerator mother" hypothesis in the 1950s, a harmful concept suggesting that cold and unloving parenting caused autism. Kanner’s work was initially misinterpreted to support this view, leading to decades of stigma and misdiagnosis.


Around the same time, Hans Asperger conducted his work at the University of Vienna, where he led a clinic for children with developmental differences. Asperger’s observations were rooted in his clinical practice, where he worked with children who exhibited strong intellectual abilities alongside significant social and communicative differences. He emphasized their unique talents and described what he called "autistic psychopathy," a term that highlighted the social and behavioral traits of autism. Asperger’s focus on strengths in addition to challenges later led to terms like "twice-exceptional" which was coined in 1988 by James Gallagher in National Agenda for Educating Gifted Students: Statement of Priorities. Asperger's contributions remained relatively unknown outside of Europe for several decades. Recent investigations, such as the 2019 essay in Tidsskrift for den norske legeforening, present evidence that Asperger actively participated in and benefited from the Nazi regime. Specifically and horrifically, he complied with the euthanasia program targeting disabled children.


Because Kanner and Asperger approached autism from different cultural and clinical perspectives, there was lack of a unified diagnostic framework which created confusion and limited the broader understanding of autism.


While Kanner and Asperger have received the most recognition, Grunya Sukhareva, a Soviet psychiatrist, described traits of autism as early as the 1920s, decades before Kanner’s work. Sukhareva’s detailed observations of children with social and communication differences were highly insightful but remained largely untranslated and ignored by Western researchers for many years.


In the 1960s, Bernard Rimland, a psychologist and the parent of an autistic child, further challenged harmful ideas that continued to blame parenting for autism. Rimland’s groundbreaking book, Infantile Autism: The Syndrome and Its Implications for a Neural Theory of Behavior (1964), argued for a biological basis of autism. His advocacy extended beyond academia; he founded the Autism Society of America and later the Autism Research Institute, which provided support and information for families. Rimland’s commitment to his son meant that he sought to understand his experiences and advocated for practical interventions.


Margaret Bauman and Thomas Kemper’s (1985) work in neuropathology provided crucial insights into structural brain differences in autism. Their postmortem studies revealed abnormalities in the cerebellum and limbic system, which are involved in motor coordination and emotion regulation.


The 1990s ushered in a transformative era, fueled by advancements in neuroimaging technology. Researchers began to investigate brain structure and function in living individuals with autism through novel techniques like magnetic resonance imaging (MRI) and functional MRI (fMRI). Technology facilitated Kennedy and Courchesne’s (2008) discovery of brain overgrowth (increased total brain volume compared to neurotypical peers) in young children with autism. His was one of the first papers to reveal true neurological differences.


The autistic perspective was largely absent from research until Temple Grandin (1995), an autistic researcher and advocate, brought unique insights to the public and scientific discourse. Her descriptions of sensory sensitivities, visual thinking, and the strengths of autistic cognition helped shift perspectives from deficit-focused models to more nuanced understandings of autism as a different way of experiencing the world.


Additionally, Uta Frith (1989), known for her work on "Theory of Mind" and cognitive profiles in autism, was instrumental during this time. A growing interest in the default mode network (DMN) developed—a brain network involved in self-referential thinking and social cognition, though research disagreed with whether this area is hyper-active, hypo-active, or varies based on symptoms.

Helen Tager-Flusberg (2001) contributed significantly to understanding the relationship between language development and brain function in the autistic brain. Using neuroimaging and behavioral studies, Tager-Flusberg identified reduced activity in the left hemisphere regions associated with language, including Broca’s area and Wernicke’s area. These findings indicated a neural basis for why many autistic individuals experience challenges in expressive and receptive language abilities. Her longitudinal studies also demonstrated variability in language development, emphasizing that some autistic individuals show significant changes and adaptions over time, while others face persistent difficulties. Tager-Flusberg’s work laid the groundwork for tailored communication interventions.

This era of findings were often framed in deficit-oriented language, reinforcing stereotypes about autism rather than promoting a balanced view of neurodivergence. Some researchers warned against oversimplifying complex neurological differences, cautioning that framing autism as a "brain disorder" risked perpetuating stigma. Moreover, the reliance on small, homogenous study samples raised questions about the generalizability of findings to the diverse symptoms and experiences of people on the autism spectrum.


The 2010s marked a significant paradigm shift in autism research, driven by the neurodiversity movement. Coined by Judy Singer in the late 1990s, neurodiversity advocates viewed autism as a natural variation in human neurobiology. This perspective reframed research goals, focusing on understanding and supporting autistic individuals rather than "curing" them.


Studies using EEG and resting-state analyses have revealed atypical neural oscillations and connectivity patterns in individuals with autism. For example, Lau et al. (2019) conducted a meta-analysis showing consistent patterns of altered resting-state functional connectivity. Similarly, recent studies have investigated synaptic pruning, the process by which the brain eliminates excess synapses during development. Fascinating research by Tang et al. (2014) suggested that reduced synaptic pruning might contribute to the sensory and cognitive characteristics of autism. (See the picture at the start of this post.)


Some contributors to our understanding of autistic brains remain under-recognized. For example, Monique Botha (2021) has advanced research on the impact of stigma and societal structures on autistic well-being, reframing autism research within a social model of disability. Additionally, researchers like Devon Price and Nick Walker (2020) have bridged academic and activist spaces, emphasizing lived experiences and neurodiverse narratives in understanding autism.


The work of Damian Milton (2012) further enriched the field with his "Double Empathy Problem," which posits that communication challenges between autistic and neurotypical individuals arise from mutual differences in perspective rather than a deficit within the autistic individual.


Contemporary understanding also emphasizes the heterogeneity of autism. Rather than viewing autistic traits through a binary lens of "strengths versus deficits," researchers recognize autism as a multifaceted neurotype with unique patterns of sensory, cognitive, and emotional processing


Neurodiversity-affirming language avoids terms like "high-functioning" and "low-functioning," which oversimplify the spectrum of abilities and challenges people face, as well as, center the neurotypical experience as the preferred experience. Instead, terms like "support needs" or "autistic individuals" are preferred. Many autistic individuals self-advocate for identity-first language (e.g., "autistic individual" rather than "individual with autism"), though preferences can vary obviously.


Today, research is not only uncovering the biological and neurological underpinnings of autism but also emphasizing the importance of creating inclusive environments that honor neurodiversity. By understanding how autistic brains function differently, we are better equipped to support individuals on the spectrum and foster a society that truly values and invites diverse ways of thinking and being.




 


  1. Asperger, H. (1944). Die 'Autistischen Psychopathen' im Kindesalter. Archiv für Psychiatrie und Nervenkrankheiten, 117(1), 76–136.

  2. Bauman, M. L., & Kemper, T. L. (1985). Histoanatomic observations of the brain in early infantile autism. Neurology, 35(6), 866–874.

  3. Bettelheim, B. (1967). The empty fortress: Infantile autism and the birth of the self. New York: Free Press.

  4. Botha, M. (2021). Autism and the double empathy problem: Implications for research and practice. Autism in Adulthood, 3(1), 21–30.

  5. Courchesne, E., Karns, C., Dawson, G., et al. (2001). Unusual brain growth patterns in early life in patients with autistic disorder: An MRI study. Neurology, 57(2), 245-254.

  6. Frith, U. (1989). Autism: Explaining the enigma. Oxford: Basil Blackwell.

  7. Grandin, T. (1995). Thinking in pictures: My life with autism. New York: Doubleday.

  8. Kanner, L. (1943). Autistic disturbances of affective contact. Nervous Child, 2, 217–250.

  9. Kennedy, D. P., & Courchesne, E. (2008). The intrinsic functional organization of the brain is altered in autism. NeuroImage, 39(4), 1877–1885.

  10. Lau, W. K. W., Leung, M. K., et al. (2019). Resting-state abnormalities in autism spectrum disorders: A meta-analysis. Scientific Reports, 9, Article 3892.

  11. Milton, D. (2012). On the ontological status of autism: The ‘double empathy problem’. Disability & Society, 27(6), 883–887.

  12. Price, D., & Walker, N. (2020). Unmasking autism: The future of neurodivergent research. Journal of Neurodiversity Studies, 1(1), 5–20.

  13. Rimland, B. (1964). Infantile autism: The syndrome and its implications for a neural theory of behavior. New York: Appleton-Century-Crofts.

  14. Singer, J. (1998). Odd people in: The birth of community amongst people on the autism spectrum. Honours Thesis, University of Technology Sydney.

  15. Sukhareva, G. (1926). Autistic psychopathies in childhood. Psychiatrische Neurologische Wochenschrift, 30(18), 223–228.

  16. Tager-Flusberg, H. (2001). Understanding the language and communication impairments in autism. International Review of Research in Mental Retardation, 23, 185–205.

  17. Tang, G., et al. (2014). Loss of mTOR-dependent macroautophagy causes autistic-like synaptic pruning deficits. Neuron, 83(5), 1131-1143.


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