Eight Independent Computational Constraints on Parallel Signal Conduction in Myelinated Axons, and a Quantified Study Design for the Real Modulatory Channels

Background: Several recent proposals suggest that myelinated axons may conduct neural signals through a parallel optical or electromagnetic channel — via biophoton emission, cavity-enhanced generation, node-enriched gain chemistry, neuro-antennae, displacement currents, or opsin-based phototransduction — in addition to classical saltatory conduction. Methods: We constructed six independent computational falsification modules, each using measured material constants and deliberately generous upper-bound assumptions: (1) a photon-budget analysis; (2) a full-wave optical transmission sweep through the myelin wall (400 nm–10 um); (3) a Purcell-factor estimate for the myelin cavity; (4) a fluorophore-gain audit of all known neural chromophores; (5) a neuro-antenna radiation and displacement-current decomposition; and (6) an opsin audit across all endogenous photopigments; and (7) a decoherence audit of every quantum claim (thermal occupation, cavity coherence time, vibrational T2 vs emission lifetime). We further quantified the detectability of a hypothetical parallel channel via a stochastic jitter experiment (20,000 trials) and mapped the ephaptic-coupling regime with a two-axon dose-response simulation. Finally, we designed and power-analysed a dual-channel (biophoton-count and gamma-coherence) music-intervention study with head-to-head piece contrasts. Results: All eight constraints falsify an efficient parallel channel: mid-infrared transmission through the myelin wall is approximately 4 x 10^-97 per internode at the C-H stretch band; the Purcell factor is approximately 1.3 x 10^-6 (suppression, not enhancement); every neural fluorophore is a net absorber or at least 2.4 orders of magnitude short of required gain; neuro-antenna radiation is approximately 40 orders of magnitude below the required energy; and no endogenous opsin combines the required presence, kinetics and photon flux; and the thermal emitters' coherence time (approx 1 ps) collapses to essentially zero first-order coherence over any useable path, while lamellar path-length roughness accumulates pi-rad RMS phase error within a fraction of one internode — chaotic, mutually incoherent light carries no phase-locked information. The decoherence audit shows the cavity coherence time (Q/omega, 1-3 fs at biological Q) is approximately 2,000 times shorter than the internode transit, and vibrational T2 (approximately 2 ps) is 10^9 times shorter than the emission lifetime, so any cascade pair is emitted by a fully dephased classical source: the quantum version of the hypothesis is falsified independently of the classical one. A 5% photon-channel contribution is electrically invisible (jitter test), and ephaptic coupling transitions sharply from sub-threshold timing nudges to merged circuits near kappa = 0.1 with no intermediate 'separate-and-fast' window. In the study design, the photon channel requires approximately 10 subjects for 80% power while gamma coherence requires > 60, and head-to-head piece contrasts (sacred vocal vs classical) require 55–113 subjects. Conclusions: Fast parallel signal conduction in myelinated axons is excluded computationally across every physical mechanism proposed to date. What survives — ephaptic synchrony, volume transmission, and externally powered photobiomodulation — are modulatory, not conduction, channels, and we provide a power-quantified design for their experimental study.