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ABSTRACT (SUBMITTED) Chaos Theory and Migraine
Pathophysiology
Lawrence Robbins, M.D. and Cameron Leith, Ph.D.
Posted: February 2007  
 


Objectives: This paper will describe in detail the probable connection between chaos theory and migraine pathophysiology.

Background: Chaos is a math-based, non-linear dynamical theory. Chaos has been used to predict the behavior of ion flow, as well as neural and biosystems. Chaos is a misnomer, as it is deterministic, not random. A key property is extreme sensitivity to initial conditions; a tiny change in initial conditions results in huge changes downstream; this has advantages for biosystems, particularly in conserving energy. Chaos has been shown to govern the beating of the heart, as well as the evolution of epileptic seizures.

Methods: To demonstrate chaos in the brain, it takes 3 to 5 billion data points; therefore, this paper will interpret and expand upon what is known about chaos and migraine.

Results: Ionic flow is governed by random, linear, or chaotic (non-linear) controls. Chaotic control means that a small change in the channel protein results in a large change in the channel protein shape. This saves energy, versus a simple linear control system. Ionic dynamics are crucial in cortical spreading depression (csd). A tiny change in K+ efflux, or Ca+ influx, will result in a large effect downstream, with csd and oligemia. Chaos has been demonstrated to play a role in K+, Ca+, and Na+ movements. Tiny perturbations, possibly brought about via weather, stress, or hormonal changes, in the hyperexcitable brain may result in csd, and eventually in plasma protein extravasation (ppe). Only chaotic dynamics could logically explain the cascade that leads from csd to ppe. The drugs that affect csd may influence the membrane thru chaotic controls. Drugs that better control chaos may inhibit csd; for instance, by affecting K+ efflux, through small effects upstream, we may prevent the events downstream that lead to headache. This has been demonstrated to be true with epileptic seizures. Peripherally, the familiar cascade of MG++ binding to NMDA, with subsequent Ca+ influx, is very sensitive to initial conditions and changes. Drugs that work thru chaotic controls peripherally may be effective in very small concentrations. With central sensitization (cs), wind-up is typical system that is probably controlled by a non-linear flexible system (chaos). Linear dynamics could not explain or control wind-up. Different aspects of cs are most likely under chaotic control from NMDA activation to nitric oxide synthesis. Thalamic recruitment involved in expansion of the pain area is best explained by chaos. The pathological shift of homeostasis seen in chronic sc, with a loss of brainstem inhibition, may actually reflect a loss of chaotic control; this is similar to the loss of control in the heart, resulting v-tachycardia. The brainstem pag, important in migraine has been shown to be under chaotic control thru p/q-type Ca+ channels. Chaos may assert its most profound affects in the brainstem.

Conclusions: This paper will define and describe chaos, and how it applies to biosystems. We will elucidate the probable role of chaotic controls with regard to migraine pathophysiology, and discuss how chaos may be controlled.