Article Neuroscience · Excitable Media · ⏱ 9 min read

FitzHugh-Nagumo: Spike Nucleation & Propagation of Excitation

Hodgkin-Huxley has four coupled equations and five parameters per ion channel — accurate, but hard to reason about geometrically. In 1961 Richard FitzHugh (and independently, in a circuit realisation, Jin-ichi Nagumo) reduced it to just two variables, cheap enough to simulate on a whole 2D tissue and simple enough to draw the entire dynamics as a phase portrait.

TL;DR: FitzHugh-Nagumo collapses Hodgkin-Huxley's four-variable neuron model into just two variables, plotted as a phase plane with two crossing nullclines. This reveals why nerves fire all-or-nothing above a threshold, why they can oscillate as pacemakers, and — once diffusion couples neighbouring cells — how spikes become travelling waves and cardiac spiral arrhythmias.

1. From four equations to two

The Hodgkin-Huxley model tracks membrane voltage V plus three gating variables m, h, n — each with its own voltage-dependent rate functions. It reproduces real axon data almost perfectly, but its five-dimensional-ish structure hides the qualitative reason why a nerve spikes at all.

FitzHugh noticed that m (Na⁺ activation) is much faster than h and n, and that h and n move roughly in lockstep. Collapsing the fast variables into one "activator" and the slow variables into one "recovery" variable gives a 2-variable relaxation oscillator — the same mathematical family as the Van der Pol oscillator used to describe vacuum-tube circuits.

The payoff: the entire state of a FitzHugh-Nagumo (FHN) neuron is a single point (v, w) in a 2D plane, and its dynamics are just two nullcline curves crossing at an equilibrium. You can see excitability instead of only computing it.

Two independent routes to the same equations

FitzHugh (1961) arrived at the model by simplifying Hodgkin-Huxley analytically. Nagumo, Arimoto and Yoshizawa (1962) built the exact same equations as an electronic tunnel-diode circuit — which is why the model is credited to both and often just called "FitzHugh-Nagumo" or "Nagumo's equation".

2. The FitzHugh-Nagumo equations

The classical dimensionless form couples a fast activator v (playing the role of membrane voltage) with a slow recovery variable w:

FitzHugh-Nagumo system dv/dt = v − v³/3 − w + Iext
dw/dt = ε · (v + a − b·w)

where the parameters have this role:

  • v — fast variable: excitation / membrane voltage analogue
  • w — slow variable: recovery / net (Na⁺ inactivation + K⁺ activation)
  • Iext — external stimulus current
  • ε (epsilon, typically 0.08) — time-scale separation; small ε ⇒ w moves much slower than v
  • a, b (typically a = 0.7, b = 0.8) — shape and position of the recovery nullcline

The cubic term v − v³/3 is what makes the system excitable rather than simply damped: it creates an S-shaped (N-shaped) nullcline with three intersections with any nearly-flat line, which is the geometric root of the threshold behaviour below.

3. Phase plane and nullclines

A nullcline is the set of points where one derivative is zero. Setting dv/dt = 0 and dw/dt = 0 gives two curves in the (v, w) plane:

Nullclines v-nullcline: w = v − v³/3 + Iext  (cubic "N" shape)
w-nullcline: w = (v + a) / b  (straight line)

Where the two curves cross is a fixed point — the resting state, if it is stable. Because the v-nullcline is fast and the w-nullcline is slow, trajectories snap almost horizontally onto the cubic curve, then crawl slowly along it, jumping to the other branch whenever they reach a fold (the local max/min of the cubic). This fast-jump / slow-crawl pattern is the shape of an action potential: depolarisation (fast jump up), plateau (slow crawl), repolarisation (fast jump down), refractory recovery (slow crawl back).

Reading the phase portrait

If you plot v(t) against w(t) instead of against time, a single spike traces a large elongated loop around the fixed point — the same loop, every time, regardless of exactly how the neuron was stimulated. That loop-independent-of-details property is called a limit cycle when it repeats forever (periodic firing).

4. Threshold and excitability

Because the v-nullcline is cubic, a small perturbation from rest that stays on the "near" branch simply decays back — the system is sub-threshold. But a perturbation that pushes v past the local fold point (the threshold) gets picked up by the fast dynamics and launched onto the far branch: a full spike fires, independent of exactly how big the extra push was, as long as it crossed the fold. This is the mathematical version of the all-or-nothing law of nerve firing.

Depending on parameters, the FHN system exhibits three regimes:

  • Excitable — single stable resting point; a supra-threshold stimulus fires exactly one spike, then relaxes back.
  • Oscillatory — the resting point becomes unstable (crosses a Hopf bifurcation) and the system fires spontaneously and periodically — a simple model of a pacemaker cell.
  • Bistable — for some parameter ranges, two stable fixed points coexist, giving switch-like behaviour instead of spiking.

5. Spatial coupling: travelling waves

A single FHN unit is a point. Real tissue — nerve axon, cardiac muscle — is spatially extended, and neighbouring cells are electrically coupled (gap junctions or the axoplasm itself). Add a diffusion term to the fast variable and you get a reaction-diffusion PDE that supports self-sustaining travelling pulses:

Spatially extended FitzHugh-Nagumo ∂v/∂t = D·∇²v + v − v³/3 − w + Iext(x, t)
∂w/∂t = ε · (v + a − b·w)

The diffusion coefficient D sets how far the fast jump spreads to neighbours before they, too, cross threshold and fire — this is exactly how an action potential propagates along an axon, or how a depolarisation wave sweeps across cardiac tissue during a heartbeat. Because the recovery variable w lags behind, the tissue just behind the wavefront is refractory (temporarily unexcitable) — this is what prevents the wave from immediately reversing on itself and what allows stable spiral waves to form in 2D tissue, a mechanism believed to underlie cardiac arrhythmias such as atrial fibrillation.

Why medicine cares

The same equations that describe a single nerve spike, when solved over a 2D sheet, reproduce the rotating spiral waves seen in fibrillating heart tissue. FHN is popular in cardiac electrophysiology precisely because it is cheap enough to run over a full anatomical mesh while still capturing excitability, refractoriness and wave propagation.

6. Pseudocode

One explicit-Euler step of the spatially coupled system on a 2D grid:

function stepFHN(v, w, dt, dx):
  // v, w are 2D arrays (grid), same shape
  const a = 0.7, b = 0.8, eps = 0.08, D = 1.0

  for each cell (i, j):
    // 5-point Laplacian (diffusion of the fast variable)
    lap = (v[i+1][j] + v[i-1][j] + v[i][j+1] + v[i][j-1]
           - 4*v[i][j]) / (dx*dx)

    dv = D*lap + v[i][j] - v[i][j]**3/3 - w[i][j] + Iext(i, j)
    dw = eps * (v[i][j] + a - b*w[i][j])

    v_new[i][j] = v[i][j] + dv*dt
    w_new[i][j] = w[i][j] + dw*dt

  return v_new, w_new

Stability requires D·dt/dx² < 0.25 in 2D (standard explicit-diffusion CFL condition). For real-time browser simulation, dt ≈ 0.05–0.1 with a coarse grid (100–200 cells per side) is usually enough to see clean spiral waves and pulse annihilation on collision.

🧠 Try the excitation-propagation simulation

Watch a FitzHugh-Nagumo wave nucleate, propagate and collide on a 2D excitable sheet — the same mechanism that drives nerve spikes and cardiac arrhythmias.

Related: Hodgkin-Huxley Neuron →