Neuropathic / sensitised pain read as a firing-threshold shift on the shared R19 nociceptor, and the three improvement levers that raise the threshold back, derived on this volume own engine

Neuropathic pain is, on the shared substrate, an acquired firing-threshold shift: peripheral nerve injury up-regulates depolarising channels (e.g. Na_V1.3) and the NGF/CGRP drive lowers the nociceptor threshold, so an innocuous input now fires the cell (allodynia) and it fires un-provoked (spontaneous pain). On this volume R19 engine a sensitisation bias b raises the afferent gain chi = 1/(3s*²−g) — ×1.6822 at b = 0.6×spinodal. Each of the three inherited levers lowers the effective bias, so the firing threshold rises and the gain falls monotonically back to the baseline 1/(2g). That is the improvement: raise the threshold, by any of three doors.

This is this volume native disease reading (VP_FRAMEWORK_MAP ownership): the primary somatosensory nociceptor is a neuro entity, and neuropathic pain is an acquired, dynamics-key condition, so it is owned here by dynamics (the monogenic pain channelopathies are gene-key entities owned by disease_wp and cross-referenced in sec.23). One R19 element, nothing fitted: from the quiescent rest s0 = −√g a peripheral sensitisation bias b ≥ 0 slides the operating point toward yield, and two locked readings of the SAME element are the firing-threshold margin T(b) = spinodal(g) − b and the afferent gain chi(b) = 1/(3s*²−g), which diverges at the R19 spinodal (allodynia/hyperalgesia as a saddle-node critical gain). At b = 0.6×spinodal the gain is 0.600188 — ×1.6822 above the baseline 0.356786 = 1/(2g). Applying each lever at increasing structural strength δ lowers b_eff = b − δ: for ALL THREE the firing threshold rises monotonically and the gain falls monotonically back toward the baseline, and a full reversal returns the gain exactly to 1/(2g). The de-sensitisation, the monotone behaviour, and the baseline return are [V]/[F]; δ is structural (not a dose) and every clinical magnitude is [O]; the felt/affective pain is the Felt Cognition volume.

The three levers, read on the sensitised nociceptor, do one thing. Take an afferent sensitised to b₀ = 0.6×spinodal (gain raised ×1.6822 above baseline); apply a lever at increasing structural strength δ (a fraction of the sensitisation removed — not a dose). For every lever the firing-threshold margin T = spinodal − b_eff rises and the gain χ = 1/(3s*²−g) falls monotonically back toward the baseline 0.356786 = 1/(2g):

This makes the inherited map a drug-class pointer for the neuro-native pain disorders — which lever, and which cited validated agent class realises it. It does not prescribe: it points to the mechanism class an effective agent moves.

Improvement, stated as a mechanism class. The single improvement these readings converge on is to raise the nociceptor firing threshold; the three levers are three structural doors onto the same axis, each pointing to a cited validated drug class. The realised peripheral case is the Na_V1.8 closed-state stabiliser (an L1 move, approved 2025); the most-prescribed adjuvant is the αδ-1 gabapentinoid (also L1); migraine/trigeminal pain is the L3 (anti-CGRP) door; refractory central pain is the N-type Ca_V2.2 (intrathecal) door. The model says which door; it never says how far to open it — δ is structural and every clinical magnitude is [O].

The firewall is kept verbatim: this layer moves only the peripheral afferent firing-threshold term; the felt / affective pain is the Felt Cognition volume; δ is structural, not a dose; potency, dose, in-vivo selectivity and efficacy are [O]. No molecule is designed and nothing diagnoses, treats, or prescribes — it is a proposal-only target hypothesis.