shapeofsoup
  • Monotropic Expansion
  • 1. Introduction
    • 1.1 Prevailing Deficit Framework
    • 1.2 Purpose and Goals
    • 1.3 Monotropic Expansion Model
    • 1.4 Addressing Accessibility
    • 1.5 Paper Overview
    • 1.6 Positionality and Rationale
  • 2. Model Mechanism
    • 2.1 Anchoring
    • 2.2 Iterative Context Building
    • 2.3 Cognitive Inertia
    • 2.4 Directionality and Precision
    • 2.5 Scalability and Flexibility
  • 3. Neurological Foundation
    • 3.1 Salience Anchoring and Internal Relevance
    • 3.2 Attentional Modulation and Cognitive Inertia
    • 3.3 Predictive Coding and Inside-Out Construction
    • 3.4 Neurodevelopmental Trajectories and Structural Divergence
    • 3.5 Implications for Structural Modeling and Neuroethical Practice
  • 4. Theoretical Alignment
    • 4.1 Monotropism (Murray, Lesser, Lawson, 2005)
    • 4.2 Executive Dysfunction and Attentional Flexibility
    • 4.3. Weak Central Coherence (Frith, 1989)
    • 4.4. Theory of Mind (ToM) and the Assumption of Deficiency
    • 4.5. Language Processing and Internal Narrative
    • 4.6. Trauma, Inertia, and Pattern Reinforcement
    • 4.7. Double Empathy Problem (Milton, 2012)
    • 4.8. DSM-5 Framing and Pathologized Comparison
  • 5. Implications
    • 5.1. Diagnostic Framing and the Myth of Functioning Labels
    • 5.2. Coexisting Neurodivergent Conditions and Inertial Structures
    • 5.3. Rethinking Support and Accommodation
    • 5.4. Therapy Approaches, Cognitive Models, and Ethical Misalignment
    • 5.5. Self-Perception, Identity, and Communication Disconnects
    • 5.6. Social Systems, Education, and Institutional Friction
  • 6. Reframing Autism
    • 6.1. The Structural Model of Divergence
    • 6.2. Moving Beyond Developmental Language
    • 6.3. Implications for Language, Ethics, and Research
  • 7. Conclusion
  • 8. Update Log
  • Contact & Support
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1.1 The Prevailing Deficit Framework

For decades, autism research and diagnosis have predominantly operated within a deficit-based framework. Clinical definitions, most notably in the DSM-5, characterize autism as a developmental disorder defined by observable impairments in social interaction, restricted behaviors, and sensory sensitivities. This diagnostic approach emphasizes behavioral divergence from neurotypical expectations, prioritizing external observation over internal cognitive mechanisms. This paper challenges this prevailing approach, operating under the foundational assumption that what is currently broadly understood as "autism" is to a significant extent an artifact of deficit-based pathology. It critiques the very notion of a categorically "normal" behavior, arguing that current clinical definitions pathologize autistic cognition by failing to recognize its inherent validity and coherence. What if these observed behaviors are not indicative of dysfunction, but rather manifestations of an internally coherent, structurally distinct cognitive system?

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