Skip to content

← Back to Model

Q-Factor Spectrum

One damped oscillator equation governs seven neural pathways. The only variable is γ — the net GABAergic damping coefficient. When γ decreases, Q increases, and the system becomes susceptible to resonance-driven spreading depolarization.

The Q-factor model is a theoretical framework that unifies seven neurological conditions under a common calcium-dependent oscillation mechanism. This is not established medical guidance. Current standard treatments remain appropriate.

Q-Factor Spectrum

Seven neural pathways, one damped oscillator equation

Q = ω₀ / (2γ)

where γ is the net GABAergic damping coefficient

High Q (underdamped)Low Q (overdamped)FatalSevereModerateNormal→ ∞0120–500215–300310–20048–15055–150610–2007

Select a pathway to explore

The governing equation

All seven pathways map onto a single damped harmonic oscillator. Q determines whether a perturbation (including EMF at biological resonance frequencies) triggers pathological oscillation:

Q = ω₀ / (2γ), where ω₀ = natural oscillation frequency, γ = net GABAergic damping

Q → ∞: no damping (neonatal brain, GABA excitatory) — any resonant input amplifies fatally

Q ~ 20–50: low damping — threshold easily exceeded → seizures

Q ~ 5–15: moderate damping — CSD propagates but stops at sulci → migraine aura

Q ~ 1–5: robust damping (normal adult) — oscillations self-terminate within 2–3 cycles

Clinical validation

The Q-factor model makes a specific, testable claim: every effective neurological drug for these seven conditions should modify either γ (damping) or the resonant input. This is confirmed across all drug classes — see the neurological spectrum evidence page for the complete antiepileptic drug calcium map.

EMF as resonant input

The Q-factor model explains why EMF bioeffects are frequency-dependent and why ICNIRP SAR limits fail to predict biological effects:

  • López-Martín 2006/2009: GSM + subconvulsive picrotoxin → seizures in adult rats. Neither alone sufficient. Picrotoxin reduces γ; GSM provides resonant input.
  • Pulse-modulated GSM (217 Hz) is more effective than continuous wave — the pulsation pattern matches biological resonance, not the carrier frequency.
  • ELF-priming: chronic 50/60 Hz exposure upregulates α2δ-1 (CACNA2D1) → more VGCCs at synapses → lower Q threshold → increased susceptibility to all seven conditions.
  • Neonatal prediction: the neonatal brain has endogenously reduced γ (NKCC1 > KCC2). EMF alone — without pharmacological GABA reduction — should be sufficient to trigger CSD in neonates. This is the SIDS mechanism.
Full clinical evidence: Neurological Spectrum →Drug cross-map: Pharmacological Evidence →Testable predictions →