Duke ACE Keynote
Understanding Hostile Attribution Bias in Autism
in PlanSpeak Plain Language for Lay Reader
Hostile Attribution Bias is when someone thinks others are being mean or hostile, even when their actions are unclear or accidental. For example, if a person with this bias gets accidentally bumped into, they might believe it was done on purpose. This can lead to more misunderstandings because they react as if they are being threatened.
Hostile Attribution Bias and Autism.
But because autistic people often struggle with social cues and communication, it's possible they might also experience this bias.
Studies have found that autistics are more likely to see ambiguous situations as hostile compared to non-autistics. This can lead to higher levels of social anxiety and problematic behaviors like aggression or self-injury.
The Role of Society However, this bias in autistic people might not just be due to their difficulty with social cues. It can also come from a lifetime of facing social stigma, exclusion, and misunderstanding. When someone is repeatedly treated negatively, they can become more sensitive to potential threats. They lose trust that others will treat them well. This sensitivity means they might see even innocent actions as harmful.
Challenges Faced by Autistics. Autistics often face unique social challenges and stigma, which can make interpreting social cues even harder. They are frequently misunderstood and rejected. This is even worse for those with more noticeable behaviors or communication issues. From a young age, they might be placed in educational systems with low expectations, reinforcing a belief that they can't succeed. The very people (professional/educators) put in place to support them can often end up limiting opportunities and discriminating againsst them. This cycle of negative experiences can make them more likely to develop hostile attribution bias.
Impact on Mental Health. The combination of social difficulties inherent in autism and external societal stigma can create a strong foundation for developing hostile attribution bias. This not only affects their social interactions but also adds to their mental health struggles.
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Read more on Hostile Attribution Bias: [Version for Scientific/Academic Audience], [PlainSpeak for the Lay Reader], [A Simple Definition]
Related Posts on [Neuroception], [Negative Attribution Bias]
April events
My events this April include
- Keynote at Duke's ACE event (Apr 3)
- TedX talk (Apr 20)
- Two Panels Mar 27 (Mary Ann Libert) & Apr 17 (Lancet).
Keynote at Duke ACE Autism Seminar Series
Public Voices Fellowship Year One
Positive Psychology and Autism
Citation:
Wright, P., Moseley, R., Tomasulo, D., Srinivasan, H., Wilson, J., Woods, S., & Rashid, T. (2024). Integrating Positive Psychology and Autism: A Roundtable. Autism in Adulthood.
Wright, Patricia, Rachel Moseley, Dan Tomasulo, Hari Srinivasan, Jodie Wilson, Sara Woods, and Tayyab Rashid. "Integrating Positive Psychology and Autism: A Roundtable." Autism in Adulthood (2024).
Wright, P., Moseley, R., Tomasulo, D., Srinivasan, H., Wilson, J., Woods, S. and Rashid, T., 2024. Integrating Positive Psychology and Autism: A Roundtable. Autism in Adulthood.
Wright P, Moseley R, Tomasulo D, Srinivasan H, Wilson J, Woods S, Rashid T. Integrating Positive Psychology and Autism: A Roundtable. Autism in Adulthood. 2024 Aug 14
Cognitive Theories and Sensorimotor Explanations for Autism
- Active Sensing
- Alexithymia
- Apraxia
- Asset Framing
- Attribution Errors
- Autistic Burnout
- Autistic Inertia
- Blindsight
- Body Schema
- Camoflauging
- Catatonia
- Cocktail Party Effect
- Cognitive Dissonance Theory
- Depersonalization
- Double Empathy Problem
- Dyspraxia
- ECCT - Executive and Contextual Control Theory
- E-I Imbalance Theory
- EPF - Enhanced Perceptual Functioning Model
- ES Theory of Autism
- Executive Dysfunction Theory
- Exteroception
- Flat Effect
- Fluid & Crystallized Intelligence
- Hostile Attribution Bias
- Implicit and Explicit Bias
- Intense World Theory
- Interoception
- Linear & Non Linear Thinking
- Local and Distributed Information
- Lucid Dreaming
- Masking
- Mental Age
- Mental Time Travel
- Monotropism
- Multiple Intelligences
- Neuronal Pruning Theory
- Negative Attribution Bias
- Neuroception
- Peripersonal Space (My area of research)
- Predictive Coding Theories
- Predictive Homeostatis Theory
- Propagnosia
- PV Neuron Hypothesis
- Sensory Processing (see #Sensorimotor)
- Social Motivation Theory
- Special Interests (SPIN)
- Spoon Theory
- Stimming
- Synesthesia
- Temporal Binding Window
- Theory of Mind
- Triple Bind and Masking
- Weak Central Coherence Theory
PV hypothesis of autism
Background and Rationale
The Parvalbumin (PV) hypothesis of autism proposes that dysfunction in PV-expressing interneurons (INs) underlies many of the core features of autism. Despite the heterogeneity in genetic and environmental factors contributing to autism, there is a remarkable similarity in the atypical behaviors observed, suggesting a common pathophysiology across brain regions (Contractor et al., 2021).
The Parvalbumin hypothesis of autism underscores the critical role of PV+ interneurons in maintaining neural circuit balance. Their dysfunction leads to various neurological and behavioral abnormalities observed in autism, such as sensory hypersensitivity and seizures.
Evolution of the E/I Imbalance Theory
Initially, the theory of excitation/inhibition (E/I) imbalance was proposed, suggesting that reduced GABAergic inhibition leads to an increased E/I ratio, which correlates with delayed cortical maturation in autism (Hussman, 2001; Rubenstein & Merzenich, 2003). This model explains the co-occurrence of seizures in autism but has limitations due to the involvement of various cell types in regulating E/I balance, making it difficult to identify specific therapeutic targets. A more nuanced approach involves examining different IN subtypes under behaviorally relevant brain states.
Evidence for PV+ Cell Hypofunction in Autism
Recent findings highlight several key aspects of PV+ cell hypofunction in autism:
- Reduced density of PV INs: Lower expression of PV protein and decreased density of perineuronal nets (PNNs) around INs.
- Increased power of baseline gamma oscillations: Gamma oscillations, regulated by PV and somatostatin (SST) INs, show increased power in autism.
- Decreased activity of PV INs: Reduced visually-evoked activity in PV INs.
PV INs are the most prevalent IN subtype in the cortex, but this does not exclude the possibility that other IN subtypes are involved.
Hyperexcitability and Hypersynchrony
PV hypofunction leads to hyperexcitability and hypersynchrony, predisposing individuals to seizures and exaggerated sensory-evoked responses in pyramidal (Pyr) neurons of sensory cortices. For instance, whisker-evoked responses are suppressed in Layer 2/3 neurons of the primary somatosensory cortex (S1) in Fmr1 knockout (KO) mice, a model of autism.
Sensory Hypersensitivity
A failure of neurons to adapt to ongoing stimulation, observed in Fmr1 KO mice and autistic humans, may contribute to sensory hypersensitivity. This lack of neuronal adaptation can prevent individuals from tuning out irrelevant stimuli (Green et al., 2015).
Role of PV+ Neurons in Visual Processing
PV+ neurons are crucial for modulating the tuning of Pyr neurons in the primary visual cortex (V1), thereby improving visual discrimination.
Gamma Oscillations and Other Brain Rhythms
Increased power of resting-state gamma band oscillatory activity (> 30 Hz) is associated with sensory processing and communication deficits in autism and fragile X syndrome (FXS). PV INs are critical in generating gamma rhythms. PV hypofunction, as seen after PV cell-specific deletion of the NR1 subunit of NMDA-type glutamate receptors, results in increased broadband gamma power due to decreased synchronicity (Guyon et al., 2021).
2 Versions of this Post
For the Science/Academic Reader
References
- Contractor, A., Klyachko, V. A., & Portera-Cailliau, C. (2021). Reduced density and activity of parvalbumin interneurons in autism. Journal of Neurodevelopmental Disorders, 13(1), 1-15.
- Green, S. A., & Gu, Y. (2015). Sensory hypersensitivity in autism spectrum disorders. Current Biology, 25(18), R876-R879.
- Guyon, N., & Nahmani, M. (2021). Role of parvalbumin interneurons in gamma oscillations and sensory processing in autism. Frontiers in Neuroscience, 15, 692872.
- Hussman, J. P. (2001). Suppressed GABAergic inhibition as a common factor in suspected etiologies of autism. Journal of Autism and Developmental Disorders, 31(2), 247-248.
- Rubenstein, J. L., & Merzenich, M. M. (2003). Model of autism: Increased ratio of excitation/inhibition in key neural systems. Genes, Brain and Behavior, 2(5), 255-267.
Keynote Speaker at Duke
Autism Acceptance Month Keynote Presentation: "Redefine the Table"
April 3, 2024 | 4:00pm - 5:00pm ET
Zoom Webinar
Please join us for a special event in our 2023-24 Duke Center for Autism Seminar Series! Our Autism Acceptance Month Keynote presenter will be Hari Srinivasan. A self-advocate, Mr. Srinivasan is a PhD student in neuroscience at Vanderbilt University, an alumnus of the University of California, Berkeley, a Paul & Daisy Soros Fellow, a NISE fellow at the Frist Center for Autism & Innovation at Vanderbilt University, and a public member of the Interagency Autism Coordinating Committee. At UC Berkeley, Mr. Srinivasan majored in psychology with a minor in disability studies and graduated as a University Medal Finalist, along with a Departmental Citation Award, Highest Honors, Phi Beta Kappa, and Psi Chi. He was an undergraduate Haas Scholar and carried out a year-long study on awe and empathy in autism. He was also lead student instructor for a weekly class on autism, creating and teaching content that covered a myriad of issues across the lifespan. As a student journalist at The Daily Californian, he wrote over 50 articles on both disability and non-disability topics. As part of his graduate program, he will research the sensorimotor space, specifically peripersonal space (PPS), which has practical implications on multiple fronts for autism. He has autism and ADHD. His autism includes limited speaking ability, sensorimotor issues, health issues, OCD, mood dysregulation and social anxiety. His non-academic affiliations span law and policy to research arenas such as IACC, DREDF, ASAN, ASA, INSAR, Autism Europe and The Brain Foundation. PLEASE REGISTER IN ADVANCE AT THE LINK PROVIDED.
Speaker(s): Hari Srinivasan
Duke Event Series: Duke Center for Autism Seminar Series
Duke Event Co-Sponsor(s): Duke Center for Autism and Brain Development, Department of Psychiatry and Behavioral Sciences, Duke Global Health Institute (DGHI), Duke Institute for Brain Sciences (DIBS)
Duke Event Type(s): Diversity/Inclusion, Lecture/Talk, Webcast