mechanism: separate BCI role from performance velocity

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+# Oral-B recovery: temporal-difference somato-dendritic innovation
+
+This branch follows the complete negative result in `ORAL_B.md`; it does not
+reinterpret or overwrite that preregistration. It is motivated by Fig. 5 and
+Extended Data Fig. 13 of Francioni et al. (2026): P+ versus P- SD residuals
+separate epochs by the sign of recent error change, whereas absolute error
+magnitude alone does not separate the populations.
+
+## Structural diagnosis
+
+The failed model always calibrated its vectorizer against the instantaneous
+squared-loss descent direction `e_t s_i`. Its P+ minus P- residual contrast is
+therefore proportional to current error magnitude. Conditional on lower
+current error during improving epochs, the preregistered sign-inversion index
+must be negative. Supplying error velocity as a second regressor cannot alter
+the target being regressed. All 36 negative signs are consistent with this
+structural mismatch.
+
+## Candidate mechanism
+
+The recovery factorizes the instruction into two locally obtainable terms:
+
+1. a slowly learned per-cell causal-role coefficient `m_i`, estimated from
+   sparse antithetic perturbations and the scalar BCI cursor difference;
+2. the within-episode performance innovation
+   `delta_t = |e_(t-1)| - |e_t|`, reset at episode boundaries.
+
+The task instruction is `m_i delta_t`. Ordinary soma-predictable apical
+traffic is added before the same per-cell neutral predictor, so the plasticity
+signal remains the somato-dendritic innovation rather than a directly supplied
+role label. Forward updates use only current presynaptic context, local
+postsynaptic gain, and that innovation. The first recovery is plasticity-only
+(`kappa=0`): the empirical residual points along observed performance change,
+not necessarily a corrective online-control direction.
+
+For perturbation vector `xi`, the role target is
+
+```text
+q_i = [(z(h + sigma xi) - z(h - sigma xi)) / (2 sigma)] xi_i,
+```
+
+whose expectation is the unknown causal role `s_i`. This consumes scalar
+cursor observations rather than gradients or reverse-mode differentiation.
+
+## R0 mechanics gate
+
+R0 generates no task endpoint and touches no development or confirmation
+environment. It passes only if deterministic checks establish all of:
+
+- the mean perturbation role target has cosine above 0.99 with the analytic
+  role used only by the diagnostic;
+- the local vectorizer update moves toward that role without reading it;
+- the neutral predictor exactly removes affine soma traffic in the controlled
+  synthetic check;
+- episode-initial performance velocity is zero;
+- perfect role identification gives a strictly positive P+/P- error-change
+  sign-inversion index; and
+- all original BCI pairing, lesion-mask, decoder, and finite checks still pass.
+
+R0 is implemented by `performance_velocity` in `sdil/bci.py` and audited by
+`experiments/bci_smoke.py` plus `experiments/verify_theory.py`. Passing R0
+only permits a separately committed training-only structural screen after the
+D4 accept confirmation closes. No success-rate endpoint, hyperparameter
+selection, or oral-B score change is authorized by R0.
+
+## Boundary for the next gate
+
+Before any recovery task run, R1 must freeze its development-only task seeds,
+forward/vectorizer rates, role-estimator cadence, cost accounting, and a stop
+rule requiring both positive derivative sign and actual learning. A sign that
+is positive merely because `delta_t` was inserted is not evidence of credit
+assignment. Confirmation seeds 10--15 from the original oral-B protocol
+remain untouched unless an R1 candidate passes every frozen learning,
+innovation, role-vectorization, and plasticity-lesion requirement.