Psychiatric Failure Modes as Architectural States

Emergent from EXQ-237a LONG_HORIZON condition. Seed=42. First observed 2026-04-06.

Overview

The REE architecture produces psychiatric phenomenology as emergent failure modes, not by design. When specific architectural components fail or are absent, the resulting behavioural patterns correspond structurally to recognised clinical syndromes. This document catalogues the 2x2 motivational state taxonomy, the three missing serotonergic mechanisms that define the V4 treatment model, and the predictions that follow.

The key insight from EXQ-237a is that the LONG_HORIZON condition (3 hazards, 1 resource, 150 steps) produced goal_norm=0.004 in the PLANNED condition, with resource_rate and harm_rate identical between HABIT and PLANNED modes. The goal-directed planning system was structurally intact, but behaviourally silent – the environment had collapsed the motivational terrain that planning requires.

2x2 Psychiatric State Taxonomy

The motivational state of the agent at any time can be characterised by two independent variables: the level of z_harm_a (aversive arousal) and the status of z_goal (wanting signal).

	z_goal INTACT	z_goal ABSENT
z_harm_a ELEVATED	GAD-like state	Anxious depression (INV-053 attractor)
z_harm_a LOW	Healthy goal-directed behaviour	Melancholic depression (burnt-out)

Cell descriptions

Healthy (z_harm_a low, z_goal intact) Normal goal-directed behaviour. Planning and habitual modes diverge: PLANNED achieves higher resource_rate, lower harm_rate. The architecture functions as designed.

GAD-like (z_harm_a elevated, z_goal intact) Goals exist but are repeatedly interrupted by threat responses. z_harm_a fires during goal pursuit, triggering avoidance that displaces goal-directed sequences before completion. The agent wants but cannot sustain action sequences long enough to succeed. Anxiety without motivational collapse: the planning system is engaged but constantly derailed.

Anxious depression (z_harm_a elevated, z_goal absent) – INV-053 attractor This is the state observed in EXQ-237a LONG_HORIZON. Chronic harm exposure has suppressed benefit_exposure below the SD-012 seeding threshold. z_goal cannot form. The VALENCE_WANTING terrain in the residue field has collapsed to near-zero. HABIT and PLANNED modes are behaviourally identical because the planning system has no motivational signal to act on. Aversive arousal is elevated (harm_rate=0.14) but wanting is absent (goal_norm=0.004). This corresponds structurally to anxious depression: the patient is activated (aroused, vigilant, distressed) but cannot initiate or sustain goal pursuit.

Melancholic depression / burnt-out attractor (z_harm_a low, z_goal absent) A further evolution of the anxious depression attractor: z_harm_a has habituated to the chronic aversive environment, leaving flat affect (low aversive arousal) combined with absent wanting. The agent is neither distressed nor motivated. This corresponds to melancholic depression: psychomotor retardation, anhedonia, flat affect, absent initiative. Both depressive cells share the z_goal=0 foundation; they differ in whether aversive arousal remains active.

The Three-Stage Motivational Pipeline

Goal-directed behaviour in aversive environments requires tonic regulation at three stages (INV-052):

Stage 1: TERRAIN         Stage 2: TRANSDUCTION    Stage 3: MAINTENANCE
VALENCE_WANTING floor    benefit -> z_goal gain    z_goal persistence
(MECH-186)               (MECH-187)                (MECH-188)

Stage 1 – Terrain maintenance (MECH-186)

A slow-accumulating tonic signal (serotonergic analog) maintains a non-zero floor on VALENCE_WANTING entries in the residue field even when phasic benefit events are sparse. Without this, a chronic harm-dominated environment suppresses the benefit gradient until it is flat. The agent has no terrain to navigate toward resources.

Failure mode: benefit terrain collapse. Agent cannot orient toward goals because the residue field contains no WANTING gradient. HABIT and PLANNED modes become equivalent.

Stage 2 – Gain regulation (MECH-187)

The serotonergic system modulates the gain on the benefit->z_goal transduction function. Currently SD-012 implements a hard threshold: benefit_exposure must exceed a floor to produce any z_goal seeding. MECH-187 converts this to an adaptive graded function.

Failure mode: anhedonia as wanting failure. Benefit events occur (liking is intact), but z_goal is not seeded (gain is suppressed). This is the Berridge dissociation (MECH-117): liking preserved, wanting abolished. The agent can enjoy resources when it encounters them reactively but does not seek them.

Stage 3 – Goal persistence (MECH-188)

Once z_goal has been seeded, a PFC-mediated working memory mechanism (modulated by 5-HT projections from DRN to dlPFC) maintains the representation through periods of elevated harm or temporarily reduced benefit exposure.

Failure mode: goals form but cannot be held. z_goal collapses at the first harm event. This is the “cannot hold a plan” phenomenology: the patient articulates goals but fails to sustain them against distraction, threat, or delay. Architecturally distinct from the GAD-like state (where goals are present but interrupted by z_harm_a) because here z_goal itself collapses, not just execution sequences.

The Depressive Maintenance Loop (INV-054)

Once the INV-053 attractor is established, it is self-maintaining:

VALENCE_WANTING terrain collapses
         |
         v
Benefit-oriented exploration reduces (no gradient to follow)
         |
         v
Benefit encounters reduce
         |
         v
benefit_exposure stays below SD-012 threshold
         |
         v
z_goal seeding remains blocked
         |
         v
VALENCE_WANTING terrain cannot recover  <-- closed loop

This closed negative feedback loop predicts:

Chronicity: the depressive attractor is self-maintaining once established; environmental improvement alone may be insufficient.
Phase transition recovery: the transition from depressive attractor to normal function requires a threshold crossing (sufficient benefit_exposure to cross the SD-012 seeding threshold), not a gradual linear improvement. This maps to the clinical observation that antidepressant response is often non-linear.
Behavioural activation as first-line treatment: externally scaffolding benefit encounters (behavioural activation therapy) directly targets the maintenance loop by restoring benefit_exposure above threshold, rebuilding the terrain gradient, allowing z_goal to re-form.

Q-034: The Hazard/Resource Ratio Prediction

EXQ-237a revealed the depressive attractor by varying environment structure (3 hazards, 1 resource). Q-034 asks whether the relevant parameter is the ratio of harm exposure to benefit exposure opportunity, not absolute stress intensity.

Prediction: a fixed hazard_harm level with sufficient resource density never produces the INV-053 attractor; the same hazard_harm with insufficient resources does.

Testable: CausalGridWorldV2, hold hazard_harm constant, vary num_resources (or hold num_hazards constant, vary num_resources). Sweep the ratio.

Implications if confirmed:

Depression is a resource-availability disorder as much as a stress disorder
The same stressor produces depression or not depending on available positive affordances
Interventions targeting benefit availability (not just stress reduction) are therapeutic
Environmental enrichment (adding positive affordances) has mechanistically distinct effects from anxiolytic treatment

Frame-Tag Failure Modes: Developmental Etiology (INV-061, MECH-200, MECH-201, MECH-202)

Registered 2026-04-06. Extends MECH-094 (hypothesis tag loss = psychosis mechanism) with a developmental pathway via MECH-198 (pretend play as frame-distinction training).

Common Architectural Substrate (INV-061)

The REE architecture distinguishes real from synthetic/hypothetical frames via two co-operating tag systems: the hypothesis tag (MECH-094, agent-internal, marks simulation/replay as non-real) and the play frame tag (ARC-049, bilateral, marks play episodes as authorized-synthetic). Pretend play (MECH-198) is the developmental phase where these two systems first co-operate.

When pretend play is absent or insufficient, the frame-distinction mechanism is undertrained. The resulting adult failure modes are not independent disorders but different failure signatures of the same undertrained mechanism, varying by:

Direction of confusion: real→synthetic (derealization cluster) vs synthetic→real (delusion cluster)
Affected subsystem: frame tag, commitment gate, or threat evaluation

This provides a unified developmental etiology for conditions that are clinically distinct but architecturally related.

MECH-200: Real→Synthetic Confusion (Derealization Direction)

The agent treats real consequences as if they were synthetic. The frame tag reads “play” when the environment is real.

Mechanism: the real/synthetic distinction was never properly calibrated during pretend play. The agent defaulted to tagging ambiguous frames as synthetic (the safer error during play, where real consequences are absent). In adulthood, this default persists: when frame signals are ambiguous, the agent discounts real harm signals as if they were play-harm.

Behavioral signatures:

Actions under real-harm conditions with play-appropriate (i.e. absent) defensive responses
Commitment without adequate threat evaluation
Harm signals discounted or experienced as distant/unreal

Psychiatric mappings:

Signature	Clinical analogue	REE mechanism
Real harm experienced as unreal	Derealization	Frame tag stuck on “synthetic”; z_harm_s fires but is discounted
Elevated commitment, reduced consequence-sensitivity	Manic episodes	Play frame leaks into real operation; commitment gate fires without harm-gate check
Actions feel consequence-free	Dissociative states	Frame tag intermittently flips to “synthetic” under stress

MECH-201: Synthetic→Real Confusion (Delusion Direction)

The agent treats internally generated or simulated representations as real. The hypothesis tag (MECH-094) fails to suppress real-consequence responses during simulation, replay, or imagination.

Mechanism: during pretend play, the hypothesis tag must be active (the stick is not really a sword) while the play tag is also active (the fight is not really dangerous). If pretend play was insufficient, the hypothesis tag was never properly co-exercised with the play tag. In adulthood, internally generated representations — simulation, replay, imagination — lack the hypothesis tag marker and are processed through the real-consequence pipeline.

Behavioral signatures:

Internally generated scenarios trigger full emergency responses
Replay episodes experienced as happening now, not as memory
Pre-commit simulation generates real threat responses

Psychiatric mappings:

Signature	Clinical analogue	REE mechanism
Internal representations experienced as external	Delusion formation	Hypothesis tag absent; E3 treats simulated trajectories as real percepts
Replay triggers full emergency response	PTSD flashback	SWR replay (MECH-121) lacks hypothesis tag; experienced as real re-occurrence
Simulation generates real threat	Anxiety disorders	Pre-commit simulation (normally hypothesis-tagged) triggers z_harm_a as if real
Imagined social scenarios feel real	Paranoid ideation	Simulated other-agent threat (MECH-127 counterfactual) processed without hypothesis tag

MECH-202: Commitment Gate Developmental Failure

The commitment gate (E3 commit boundary) is undertrained because it was never exercised in synthetic mode during pretend play. Two failure directions:

Direction A — Insufficient inhibition (impulsivity): The gate fires without completing E3 evaluation. During pretend play, the gate would have been exercised in a low-stakes context where premature commitment has no real consequences, allowing calibration. Without this calibration, the gate threshold is set too low.

Signature	Clinical analogue	REE mechanism
Commits without evaluation	Impulsivity	Commitment gate fires before E3 harm/benefit evaluation completes
Elevated commitment + reduced harm sensitivity	Mania (commitment component)	Gate threshold too low + MECH-200 frame confusion compound
Cannot delay gratification	Impulse control disorders	Gate does not wait for E2 rollout to complete

Direction B — Excessive inhibition (paralysis): The gate never fires even when evaluation is complete. Without pretend play calibration, the gate threshold was never lowered from the infant default (very high commit threshold, INV-055). The agent remains in perpetual pre-commit evaluation.

Signature	Clinical analogue	REE mechanism
Endless re-evaluation without commitment	OCD (checking/rumination)	Gate threshold never calibrated down from infant default; E3 loops without committing
Complete inability to initiate action	Catatonia	Gate frozen at maximum threshold
Decision paralysis despite completed evaluation	Severe indecision	Commitment gate signal never reaches threshold

Developmental Evidence

The frame-confusion etiology predicts that pretend play deficits in early childhood should correlate with later frame-distinction failures. Existing evidence is consistent:

Reduced pretend play predicts later psychotic symptoms (Cannon et al. 2002)
Children with autism show reduced pretend play AND elevated psychosis risk
Pretend play → theory of mind → reality testing are developmentally linked
Imaginative play correlates with later impulse control (Diamond & Lee 2011)

Relationship to MECH-094

MECH-094 identifies hypothesis tag loss as a psychosis mechanism. The frame-confusion cluster (MECH-200/201/202) extends this by explaining WHY the tag system might be fragile: because pretend play (MECH-198) is where the real/synthetic frame distinction is first calibrated. MECH-094 describes the proximal mechanism (tag loss); MECH-198/200/201 describe the developmental etiology (insufficient calibration during childhood).

Claims Covered

ID	Label	Stage
MECH-186	5HT_tonic.benefit_gradient_maintenance	Terrain (Stage 1)
MECH-187	5HT.incentive_salience_gain_regulation	Transduction (Stage 2)
MECH-188	5HT_PFC.goal_persistence_under_adversity	Maintenance (Stage 3)
INV-052	tonic_regulatory_system_for_goal_persistence	All three stages required
INV-053	computational_depression_attractor	Anxious depression cell
INV-054	depressive_maintenance_loop	Chronicity mechanism
Q-034	hazard_resource_ratio_depression_threshold	Open testable question

INV-061	frame_confusion_unified_developmental_etiology	All frame-tag failures share common substrate
MECH-200	frame_confusion_real_as_synthetic	Derealization, mania, dissociation
MECH-201	frame_confusion_synthetic_as_real	Delusions, PTSD flashbacks, anxiety
MECH-202	commitment_gate_developmental_failure	Impulsivity, OCD, catatonia

Updated claims:

INV-034: added clinical inverse note (goal maintenance failure = depression, EXQ-237a)
MECH-117: added clinical note (Berridge dissociation as architectural consequence of MECH-187 failure)
MECH-094: developmental etiology added via MECH-198/200/201 (pretend play calibrates the tag system)

Implementation Status

All three serotonergic mechanisms (MECH-186, 187, 188) are V4 scope. They are not present in the current V3 substrate. The depressive attractor state (INV-053) is therefore an emergent property of the V3/current architecture under adversarial environment conditions.

V4 design will need to specify:

Tonic accumulator separate from phasic DA signals in the residue field update rule
Gain parameter on the SD-012 seeding function, modulated by tonic 5-HT level
PFC working memory module for z_goal maintenance between benefit events

Serotonergic Cross-State Architecture (MECH-203, MECH-204)

Registered 2026-04-06. The serotonergic system operates across waking and sleep states. The three waking mechanisms (MECH-186/187/188) are incomplete without their sleep-state counterparts.

The Incomplete Substrate Problem

MECH-186/187/188 model tonic regulatory systems during waking behavior. But serotonin’s architectural role spans the wake-sleep boundary:

During waking: tonic 5-HT maintains the benefit gradient (MECH-186), regulates incentive salience gain (MECH-187), and supports goal persistence (MECH-188).
During SWS: the tonic 5-HT level tags which experiences get prioritized for replay. High-5-HT experiences (benefit-salient) should be replayed alongside harm-salient experiences from the residue field. (MECH-203)
During REM: 5-HT withdrawal (dorsal raphe quiescence) defines the zero-point for precision recalibration. Without this, MECH-123 has no reference state to recalibrate against. (MECH-204)

MECH-203: Serotonergic Replay Salience Tagging

The residue field marks harm-dense experiences for preferential NREM replay (MECH-099, MECH-121). But benefit-salient experiences are equally important for consolidation – particularly missed opportunities (high benefit_exposure, low z_goal_norm) where the agent could have formed a goal but failed to.

Tonic 5-HT level at time of experience serves as the benefit-salience tag:

High tonic 5-HT -> experience tagged for benefit-replay
Low tonic 5-HT (depressive state) -> benefit-experiences under-tagged

Psychiatric prediction: Depressed agents show reduced benefit-replay density during SWS relative to harm-replay density. This creates a consolidation asymmetry: harm knowledge is maintained (the world remains threatening in memory) while benefit knowledge degrades (opportunities are forgotten). This contributes to the depressive maintenance loop (INV-054) via a sleep-mediated pathway.

MECH-204: Serotonergic REM-Gate Zero-Point

MECH-123 (REM precision recalibration) currently has no specification for how the recalibration target is established. This claim proposes: 5-HT withdrawal during REM actively sets the zero-point by removing the benefit gradient that biases waking precision. The system recalibrates against a neutral reference.

This makes REM recalibration not merely “allowed by” 5-HT withdrawal but “calibrated by” it. Connects to:

INV-045 (phase ordering): SWS needs active benefit gradient (for MECH-203 tagging); REM needs gradient absent (for MECH-204 zero-point). The serotonergic state transition implements the SWS-to-REM computational boundary.
MECH-178: noradrenergic REM suppression blocks 5-HT withdrawal, disrupting both replay salience (MECH-203) and recalibration zero-point (MECH-204) – a double hit explaining rigidity rather than just reduced recalibration.

Pharmacological prediction: 5-HT agonists administered during REM should impair precision recalibration quality specifically (not SWS consolidation), because they prevent the zero-point from being established.

Architecture note: EXQ-237a LONG_HORIZON condition (3 hazards, 1 resource, 150 steps), seed=42. Full replication pending seeds 7 and 13.

Dream Phenomenology as Diagnostic and Treatment-Response Marker (INV-062, MECH-205–210)

The four-type dream taxonomy (INV-062) follows directly from the offline pipeline architecture and provides a clinically accessible window into which process is running, whether it converged, and whether the pipeline is intact.

The four types and their computational signatures

Dream type	Process	Phase	Key phenomenological marker
Type 1: Stress/escape frustration	Harm-contrastive replay not converging (MECH-205)	SWS / early REM	Agent trying to escape; everything fails systematically; no resolution
Type 2: Joy/goal frustration	Goal-contrastive replay not converging (MECH-205)	SWS / early REM	Agent trying to reach goal; everything fails systematically; no resolution
Type 3: Procedural superposition	NREM SWR semantic consolidation (MECH-121, MECH-209)	NREM2 / SWS	No agent; one thing as all instances simultaneously; all angles, scales, times at once; peaceful
Type 4: Detailed story, close to reality	REM E1 world-model free-running (MECH-210, MECH-123)	REM	Agent in coherent novel world; narrative arc; close to plausible; super interesting

The frustration in Types 1 and 2 is not incidental affect — it is the convergence failure signal. The dream continues because the termination criterion (causally relevant features extracted) has not been met. Non-resolution is a direct phenomenological report of the replay loop still running. The self-dissolution in Type 3 is the signature of episodic context being stripped during semantic abstraction. The narrative coherence and novelty in Type 4 is E1’s world model generating in-distribution but never-experienced sequences — interesting because E1 is surfacing latent structure from its prior.

Psychiatric predictions

PTSD (MECH-205, MECH-094, MECH-208): Recurring non-resolving Type 1 dreams are a direct marker of convergence failure on harm-contrastive replay. The causal features of the threatening episode have not been extracted; the residue field update is incomplete. The intrusive quality of PTSD nightmares follows from MECH-094 hypothesis tag degradation under high-affect replay load — the replay loses its simulation marker and is processed as real re-occurrence rather than a search procedure.

Treatment-response prediction: Successful trauma therapy should produce a shift from non-resolving to resolving Type 1 dreams before the patient reports conscious relief. The dream convergence precedes the waking resolution because the offline process completes before the waking narrative catches up. This is testable with prospective dream diaries alongside standard clinical outcome measures.

Anxiety disorders (MECH-208): Elevated harm-weighting (z_beta / residue field) allocates excess replay budget to Type 1 at the expense of Types 3 and 4. Anxious individuals are predicted to report:

Predominantly Type 1 dreams, longer and more intense
Reduced frequency of Type 3 (insufficient budget for semantic consolidation)
Reduced frequency or degraded quality of Type 4 (insufficient budget for world model exploration)

The self-reinforcing loop (MECH-208): elevated harm-weighting → more harm-path replay → more harm-predictive feature extraction → more avoidance → less corrective evidence → maintained harm-weighting. Dream diary composition (ratio of Type 1 to Types 3+4) is a potential proxy for the state of this loop.

Depression (MECH-203, INV-054): Reduced benefit-replay density during SWS relative to harm-replay density (MECH-203 disruption under low tonic 5-HT) predicts a specific Type 2 deficit: the joy-frustration goal dreams should be reduced or absent, while Type 1 may be maintained. This is the replay-mediated maintenance of the depressive maintenance loop — the system has insufficient approach-side contrastive replay to extract goal-predictive features, while harm-side replay continues normally.

Dementia (MECH-210, MECH-178, INV-046): As E1’s world model degrades through the noradrenergic rigidity pathway (MECH-178), Type 4 dreams should degrade in a predictable sequence:

Type 4 becomes less interesting (prior no longer surfaces novel structure — repetitive familiar patterns)
Type 4 collapses toward habit-like sequences (the world model can only generate well-worn paths)
Type 4 disappears entirely (REM integrity too disrupted to sustain free-running)

This gradient may precede other detectable symptoms. Prospective dream diary tracking in cognitively healthy individuals over-65 may identify early E1 degradation before standard neuropsychological tests reach threshold.

REM-suppressing medications (MECH-173, MECH-210): Any medication that suppresses REM (anticholinergics, MAOIs, most antidepressants, benzodiazepines) should selectively eliminate Type 4 while leaving Types 1–3 relatively intact. Type 3 (NREM SWS process) may actually increase if the replay budget freed from REM is redistributed, but Types 1/2 (early REM contrastive replay) may also be affected by REM suppression. A testable cross-over design: measure dream-type composition before and after REM-suppressing medication, with and without sleep-stage verification.

Epistemic status

The four-type taxonomy is first-person phenomenological data from one observer (DG), noted as definite types but not claimed to be exhaustive. The mapping to computational processes is an interpretation requiring corroboration from other observers and eventual connection to polysomnographic sleep-stage measurement. Dream diaries from multiple individuals, classified by structural type (agent/no-agent, resolving/non-resolving, sequential/simultaneous), would allow initial corroboration without sleep-lab equipment.

Self-Model Failure Modes: E1 Schema Poverty and E2 Capacity Degradation (INV-064, MECH-214, MECH-215)

Registered 2026-04-07. A class of failure modes distinct from motivational/reward pathology: the preconditions for coherent goal-directed agency are absent, not the motivational system itself.

The Architectural Distinction

The motivational failure modes above (INV-052–054, 2x2 taxonomy) assume that the agent has a functioning self-model and an accurate model of its own capabilities. These failures are located in the goal-seeding and terrain-maintenance pipeline — the agent could form goals but the signal is absent or degraded.

A separate class of failure exists upstream of that pipeline: the self-model required to be the subject of goal-directed action is itself degraded. This produces a superficially similar phenomenology (absence of goal-directed behaviour, motivational flatness, inability to plan) but through a different architectural pathway with different treatment implications.

The distinction maps onto three claims:

INV-064: E1 schema differentiation → E2 transition differentiation → E3 evaluative capacity is a strict computational dependency. E3 cannot productively train until its inputs (z_world from E1, action_objects from E2) carry sufficient information. The biological fact that the prefrontal cortex myelinates last is an architectural necessity, not a developmental accident.
MECH-214: Goal content is constituted by E1 schema space. A goal aimed at an E1-unrepresented state is a random vector in E3’s operating space — it cannot generate coherent viability terrain or trajectory proposals. Goal coherence co-develops with E1 schema richness.
MECH-215: Goal pursuit requires E2 self-transition accuracy. The “I” that makes a goal first-personal — I can reach that — is constituted by E1’s self-schemas (who I am, what I feel, what my body is) and E2’s self-transition model (what I can do, how my actions transform my state). Without both, E3’s viability estimates have no coherent subject.

Two Failure Modes

Mode A — Goal incoherence (MECH-214 failure):

E1 schema differentiation is insufficient. The agent cannot form stable representations of the states it nominally wants. Goal-directed behaviour appears absent or directionless — not because the wanting system is suppressed (MECH-187 failure) but because there is no representationally coherent object for wanting to point at.

Signature	Clinical mapping	REE mechanism
Wanting without object — diffuse, undirected motivation	Certain anhedonic/dysthymic presentations	z_goal seeded but referent E1-unrepresented; z_goal is effectively noise
Goals stated but behaviorally inert	Alexithymia, emotional-cognitive disconnection	Goal object not grounded in affective E1 schema; E3 evaluates an abstract token
Difficulty identifying what one wants at all	Schizoid features, depersonalisation	E1 self-schema and world-schema both poorly differentiated; goal space is near-empty
Repeated pursuit of goals that produce no satisfaction	Compulsive achievement without hedonic gain	Goal object represented abstractly (status, money) but E1 has no schema for the hedonic state they were proxies for

Crucially, this failure is not dopaminergic. The wanting system (MECH-187 gain) may be intact; there is simply no coherent target for it to amplify. Standard antidepressants and dopamine agonists do not address E1 schema poverty.

Mode B — Capacity estimate failure (MECH-215 failure):

E2 self-transition accuracy is degraded. The agent’s model of what it can do — how its actions transform its own z_self state — is systematically wrong. E3 receives a corrupted capacity model and produces viability estimates that are either catastrophically pessimistic (the world looks unnavigable) or unrealistically optimistic (the agent overestimates its reach).

Direction	Signature	Clinical mapping	REE mechanism
Pessimistic	Cannot start — world appears unnavigable	Learned helplessness, agoraphobia, avoidance	E2 self-transitions predict action → no change or harm; E3 viability estimates uniformly low
Pessimistic	Knows the goal, cannot move toward it	Depression (action-initiation subtype)	E2 capacity model: I cannot do what this goal requires
Optimistic	Overestimates capability, repeatedly fails	Manic planning, grandiosity	E2 self-transitions inflated; E3 produces unreachable viability trajectories
Noisy	Variable, unpredictable capacity	Chronic fatigue, chronic pain, episodic illness	E2 self-transition model trained on inconsistent data; capacity estimates unreliable across days

The pessimistic direction is particularly important: avoidance, agoraphobia, and learned helplessness may be E2 failures rather than E3 over-valuations of harm. The standard cognitive framing — the patient overestimates threat — aims treatment at E3’s harm evaluation. But if E2’s capacity model is degraded (I cannot do what is required to be safe), E3’s output is not biased — it is responding correctly to a broken capacity input. Correcting E3’s output directly (cognitive restructuring) will fail if E2 remains inaccurate.

Developmental Etiology (INV-064)

Both failure modes have a developmental pathway: early-life disruption of E1 and E2 differentiation constrains E3 training quality permanently. E3 trains on E1/E2 outputs. If those outputs carry low information during the critical developmental window, E3 learns to evaluate degraded inputs — and its harm/goal representations are noise-fitted to the actual structure of the world.

Early-life adversity that disrupts sensory schema formation (sensory deprivation, trauma that narrows the experienced world, chronic unpredictability that prevents schema stabilisation) therefore does not merely cause emotional injury. It degrades the representational substrate from which coherent goals and accurate capacity estimates can ever be drawn. The downstream effects on executive function and goal-directed behaviour persist into adulthood not because of stored trauma but because E3 was trained on impoverished inputs.

This is consistent with the empirical finding that early adversity produces deficits in goal-directed behaviour and executive function that are disproportionate to, and dissociable from, the emotional sequelae of the same adversity.

Treatment Implications

The treatment target for Mode A (MECH-214 failure) is E1 schema enrichment: expanding the experiential vocabulary, building representational differentiation. Novel high-entropy environments, arts, movement, practices developing fine perceptual discrimination, and (carefully) psychedelic experiences that temporarily dissolve existing schema boundaries can expand the space of coherent goals available to E3. This is not symptom management — it is enlarging the space from which goals can form.

The treatment target for Mode B pessimistic direction (MECH-215 failure) is E2 self-transition recalibration via action in the world. This is why exposure-based therapies show consistent superiority over purely cognitive approaches in phobias and PTSD. Cognitive restructuring addresses E3’s harm estimates directly; exposure-based therapy rebuilds E2 self-transitions through direct experience of what the agent can actually do. The capacity model is updated from below, not argued into shape from above.

Somatic and interoception-focused therapies (body-based trauma approaches, movement practices, breathwork) operate at the correct architectural level: they rebuild E1 self-schemas (who I am, what my body is) and E2 self-transitions (what I can do) directly, restoring the preconditions for coherent agency rather than targeting E3 output.

Claims Covered

ID	Label	Failure type
INV-064	e1_e2_e3_maturational_sequence_necessity	Developmental: E3 cannot train on degraded E1/E2 inputs
MECH-214	goal_referent_e1_representability	Mode A: goal content requires E1 schema differentiation
MECH-215	self_model_prerequisite_for_agentive_prediction	Mode B: goal pursuit requires E1 self-schema + E2 capacity model