This page is intended for psychologists, therapists, and cognitive researchers. It outlines a mental configuration I call Signal Blindness or Pure A-salience

Overview

See FAQ, Disclaimer and Objective – understand how I developed this information and why.

I didn’t know I was neurodivergent until I was 53 years old (see Everybody is the Same and History). Although externally I present similar to ASD Level 1 (see Not Autism), and indeed this was the first clue to my neurodivergence, I do not experience any distress or anxiety from my condition (or generally with life). This is primarily due to lack of Social Salience. I do not receive the social signal and coincidentally, that is the same mechanism that would make me care about the social signal and social situations. For example, I experience No Shame. I am not a-social, but I also do not crave social interaction, see Loneliness.

That isn’t to say that those around me don’t experience anxiety – Communication problems with my wife are common. Now that we understand the mechanism I am able to apply some Mitigation strategies and knowing what is going on does help.

Core Hypothesis

The signal blind architecture is defined by a primary input deficit: the Social Salience network provides zero output (see My Experience).

This is not Hyposalience – that is a weak signal or potentially signal, but the social salience network is intact (thus high social desire). This is also not noisy salience, which is common in autism (see Autism Experience). It is complete lack of both the social signal and the salience information – social norms and position are meaningless and invisible.

This gives high overlap with ASD Category A but a complete lack of social anxiety (category B).

To distinguish this from common clinical diagnoses (Autism, Alexithymia, SCD), I have the following evidence:

• Zero Social Lag: because I don’t attempt to decode the social signal (or use Theory of Mind to “mindread”) there is no delay in social interaction.
• No social anxiety or Shame: without a functioning social salience network, the biological triggers for shame are never pulled. I don’t know how others feel about me and do not care.
• Functional Success: I am a high level software engineer at a top software company and have been there over 20 years. My logical processing and even keel are Benefits in that situation.

  Statement of Clinical Utility

I am not seeking diagnosis, medication, or affordance at work. My condition does not cause internal distress, though it does cause relational friction with my wife (unnoticed by me, but obvious to my wife).

My goals are:

• System Mapping: to understand my own mechanism so I can understand my experience and be accountable for my conduct.
• Friction Reduction: improve the quality of life for my wife and family by using Mitigation to bridge the gap.
• Phenotype Identification: to document this architecture in case somebody else like me finds it and finds it useful (see Where Are My People?).

  Curated Path

For those wishing to evaluate the logic of this model, I suggest the following sequence:

Input Layer (Root Cause)

• Social Salience – the missing receiver and why I am signal blind.
• Hypophantasia – a compounding factor.
• Theory of Mind – often cited as a key cause for autism behaviors.

Processing Stack (Mechanism)

Seems like that should be trouble, right? How I make it work.

• Functional Cognitive Architecture – breakdown of how I think I process things, with contrast to NT and autism.
• Manual Frame Construction – how I see the world and why I don’t get stuck.
• Functional Logic Modeling – how I understand situations and people when I need to.
• Examples – examples of how I think.

Affective Profile

• Alexithymia – I don’t think I have alexithymia. I have emotions and can describe them.
• Semantic Divergence – but my experience of emotions is quite different since there is no social component.
• Anger and Sadness – two examples that I think demonstrate both the experience and how it differs from both NT and autistic people.

Differential Analysis

• Not Autism and Not SCD – comparison with ASD and SCD.
• Overlaps – overlap with various other conditions.
• Checklist – perhaps the strongest evidence for this specific architecture, a differential diagnosis checklist.
  • By answering “No” to the standard stressors of neurodivergence, the checklist isolates a-salience as a distinct functional state rather than a state of high-effort compensation.
• Where Are My People? – a review of literature and why research might miss this particular phenotype.

  Due Diligence

I used triangulation to build this model:

1. Introspection: Capturing raw thought processes shortly after social interactions. Reflecting on my own thoughts and why I thought that way.
2. External Telemetry: Using feedback from my wife and therapist to identify gaps between my perception and theirs. Initially I thought Everybody is the Same but seeing the contrast let me see myself.
3. Machine-Assisted Synthesis: Utilizing LLMs to perform “Falsification Probes” against my hypotheses and to explain the NT “Vibe-based” experience I cannot perceive.

Read History and Discovery to see how I got here. Read System Prompt for more information about using LLMs to explore. I want to emphasize that these words are my own: I got clues and descriptions from various sources, but when I write about myself I believe these are true words.

While I may be wrong in the clinical details, this model has achieved its primary success metric: it accurately predicts my behavioral outputs and has reduced relational friction.