Schizophrenia — the over-ignition mirror of autism

Schizophrenia is the over-ignition mirror of autism-T on the same R19 ignitability axis: a disinhibitory bias lowers the fold so irrelevant assemblies ignite (aberrant salience). Its positive, negative and cognitive symptoms sit on the threshold, output and wiring axes; a gain-reducing antipsychotic reverses the positive domain only, which is why dopamine blockade spares the rest. efficacy=0.

Part II opens its atlas extension with the condition the autism engine separates most cleanly: schizophrenia. On the one shared ignitability axis — the M3 R19 fold, spinodal(g) = 2(g/3)^1.5 = 0.3849 — schizophrenia is the opposite pole from autism-T: where autism's inhibitory bias raises the fold and loses relevant ignitions, a disinhibitory/excitatory bias lowers it, so weak, in-health-sub-threshold assemblies now ignite — aberrant salience. The pair (ignition-direction, aberrant-vs-lost) separates HEALTH / AUTISM-T / SCHIZOPHRENIA uniquely. Then the three symptom domains are placed on the three axes — positive → threshold, negative → output, cognitive → wiring — and a single gain-reducing antipsychotic-class operator is shown to reverse the positive domain only: a mechanistic account of why dopamine blockade relieves positive but not negative or cognitive symptoms. Every value is an in-silico coupling state, not a clinical measure — efficacy = 0.

schizophrenia = the over-ignition mirror of autism-T on the same R19 axis = excitatory bias lowers the fold → aberrant ignition; antipsychotic restores it and worsens autism-T — on the one shared ignitability axis (the M3 R19 fold = spinodal(g) = 2(g/3)^1.5 = 0.3849, measured-grounded), schizophrenia is the opposite pole from autism-T: a disinhibitory/excitatory E/I bias LOWERS the fold (ignition threshold 0.245 vs health 0.395) so weak, in-health-sub-fold assemblies (candidates 2,3) now ignite — aberrant salience with no loss of the relevant ones — where autism-T's inhibitory bias RAISES the fold and loses relevant ignitions. The pair (ignition-direction, aberrant-vs-lost) separates HEALTH / AUTISM-T / SCHIZOPHRENIA uniquely. A uniform gain-reducing / threshold-raising antipsychotic-class push restores the healthy selective set (4,5) and worsens autism-T; the gain-raising stimulant that helped autism-T worsens schizophrenia — one handle, opposite signs at the two poles. The therapeutic sign aligns with sleep-need (arousal down), the mirror of autism. Which pole a given psychosis is, is OWED [O]. efficacy=0; not medical advice. [V mech]. this chapter

positive / negative / cognitive symptoms sit on the threshold / output / wiring axes = one gain-reducing operator reverses positive only; negative and cognitive are not reached → axis-structured — the three symptom domains map onto the three T/O/W axes. POSITIVE = the threshold over-ignition pole (excitatory bias lowers the fold → aberrant ignition of irrelevant assemblies); the gain-reducing antipsychotic raises the fold back and removes them (REACHED). NEGATIVE = an output/gain DEFICIT (R = 0.354 < health 0.390); the antipsychotic is itself a gain reduction, so it pushes output even lower (to 0.309 — wrong direction, NOT reached). COGNITIVE = a long-range WIRING fault (locality 0.842 > health 0.794; the dysconnection hypothesis); a scalar gain operator leaves the locality imbalance EXACTLY invariant (NOT reached). One gain-reducing operator reverses POSITIVE only → the differential antipsychotic response is AXIS-structured, not dose-structured: the mechanistic account of why D2 blockade relieves positive but not negative/cognitive symptoms. It retires more D2 blockade as a route to negative/cognitive benefit (an in-silico mechanistic null). Which domain dominates a given illness is OWED. efficacy=0. [V mech]. this chapter

The same axis, the opposite pole

Autism's threshold fault (D8 T) is an inhibitory bias: it raises the R19 ignition fold, so genuinely relevant assemblies fail to ignite — under-ignition, a narrowed gate. Schizophrenia is the mirror. A disinhibitory / excitatory E/I bias (the engine reads it as a raised effective coupling, grounded in NMDA hypofunction and the parvalbumin/GABA-interneuron deficit) lowers the same fold. With the ignition threshold dropped from the healthy 0.395 to 0.245, candidate assemblies that sit below the fold in health — the weak, the irrelevant — now cross it and ignite. The relevant ones are not lost; the gate has not narrowed, it has leaked. That is the engine's image of aberrant salience: meaning attaching to noise.

A three-way fingerprint

This gives a clean discriminant that no single scalar could. Read two signs — the direction the fold moved, and whether ignitions were recruited (irrelevant added) or lost (relevant dropped) — and the three states are uniquely identified. HEALTH: normal ignition, nothing recruited, nothing lost. AUTISM-T: fold raised, ignition lowered, relevant assemblies lost, none recruited. SCHIZOPHRENIA: fold lowered, irrelevant assemblies recruited, none lost. The same pair of signs that told autism-T apart from health now tells schizophrenia apart from both — the discriminant generalises beyond the condition it was built on, which is the point of the atlas.

One handle, opposite signs at the two poles

Because the two conditions sit at opposite ends of one axis, an intervention that helps one must, by the same mechanism, harm the other. A uniform gain-reducing / threshold-raising push — mechanistically the antipsychotic class (D2 antagonism dampening dopaminergic gain, in Kapur's framing dampening the salience of aberrant signals) — raises the lowered fold back up and restores the healthy selective set; applied to autism-T, the same push raises an already-high fold and makes the under-ignition worse. Conversely the gain-raising stimulant that recovered relevant ignitions in autism-T worsens schizophrenia, recruiting yet more aberrant ignitions — the attested direction of stimulant-precipitated psychosis. One handle, opposite therapeutic signs at the two poles. The therapeutic direction for schizophrenia (gain down, sedating) even aligns with sleep-need — the mirror of autism, whose arousal-raising therapy ran against it.

Why dopamine blockade spares the negative and cognitive domains

The second result places schizophrenia's three symptom domains on the three T/O/W axes and asks which the antipsychotic operator can reach. POSITIVE symptoms are the threshold over-ignition pole above — and the gain-reducing antipsychotic reverses them, raising the fold and removing the aberrant ignitions. NEGATIVE symptoms (avolition, blunted affect, alogia) are an output/gain deficit: the in-silico order parameter sits at 0.354, below health's 0.390. Here the antipsychotic — itself a gain reduction — pushes output lower still (to 0.309): the wrong direction, the domain is not reached. COGNITIVE symptoms are a long-range wiring fault (the dysconnection hypothesis): the engine's locality imbalance rises to 0.842 against health's 0.794, and a scalar gain operator leaves that imbalance exactly invariant — it cannot re-route geometry. So one operator reverses the positive domain only.

The differential antipsychotic response is therefore axis-structured, not dose-structured: dopamine blockade relieves positive symptoms because they sit on the axis a gain operator can move, and spares the negative and cognitive domains because they sit on axes it cannot. This is exactly the atlas's third deliverable — a mechanistic null that retires a wasted approach: more D2 blockade is not a route to negative or cognitive benefit, and a non-responder stuck on the output or wiring axis is identifiable as such. Which domain dominates a given illness, and which pole a given psychosis is, remain OWED [O] — they need per-individual external data (spectral E/I markers, connectomics, genetics); the model asserts only the fingerprints and the reversibility signs. The secondary global-integration rise the disinhibition produces is engine-internal and is not the defining fingerprint — real schizophrenia is dysconnective. Loss of the selective gate is a mechanism boundary, not a claim about the disorganised subjective state (Axis-A firewall; consciousness_claim = 0). Every number here is an in-silico coupling state, not a dose or a response rate — efficacy = 0; this is a mechanism-level result about schizophrenia as represented in the VP framework, not medical advice, a diagnosis, a treatment protocol, or a cure.