Cortical spreading depression (CSD), first described by Leão in 1944, is a slow wave of near-complete neuronal and glial depolarization that crawls across the cortical surface at roughly 2–6 mm/min — about 1000× slower than a normal action potential. It is driven by diffusion, not synaptic transmission: depolarized tissue dumps K⁺ and glutamate into the extracellular space faster than pumps can clear them, and that local rise in [K⁺]o pushes neighboring tissue over its firing threshold, which depolarizes and repeats the process outward — a self-regenerating reaction-diffusion front.
This simulator models the cortex as an excitable-medium cellular automaton on a flat map (a discretized reaction-diffusion system, in the spirit of Greenberg–Hastings models):
each cell: REST → ACTIVE → REFRACTORY → REST
REST → ACTIVE if (active neighbors) ≥ threshold (excitability)
ACTIVE → REFRACTORY after 1 step
REFRACTORY → REST after R steps (refractory duration)
- Propagation speed sets how much real biological time one lattice step represents, matching the clinically observed 2–6 mm/min range — the bright wave is played back as a time-lapse so it stays watchable.
- Refractory duration is why the wave never doubles back through tissue it just crossed: cells stay silent for R steps, forcing a strictly outward-expanding front. Shorten it enough and colliding fronts can re-invade recovered tissue, producing reentrant spiral activity — a pattern also seen in cardiac fibrillation, which is the same class of excitable-medium mathematics.
- Tissue excitability is the number of already-active neighbors a resting cell needs before it fires. At low threshold a single point ignites a wave easily. Raise it and a small focus can fail to reach the critical mass needed to self-sustain — real CSD foci also require a minimum size and metabolic push (spreading K⁺/glutamate release) before they "take"; too small or too weak a trigger simply fizzles out.
- Measured speed below is not just an echo of the slider: it is fit from the actual growth of the front radius over the last few seconds of biological time, so a focus that is failing to ignite (below critical mass) correctly reads near 0 mm/min even while the slider is set high.
Clinically, the depolarization front correlates with the scintillating, expanding zig-zag of a migraine visual aura, while the trailing refractory zone corresponds to the blind spot (scotoma) that follows a few minutes behind it. The same wave — in more severe, prolonged form — also propagates through the ischemic penumbra after stroke and traumatic brain injury, where each passing wave increases the metabolic burden on already-compromised tissue.