Controlling chimera states: The influence of excitable units.

We explore the influence of a block of excitable units on the existence and behavior of chimera states in a nonlocally coupled ring-network of FitzHugh-Nagumo elements. The FitzHugh-Nagumo system, a paradigmatic model in many fields from neuroscience to chemical pattern formation and nonlinear electronics, exhibits oscillatory or excitable behavior depending on the values of its parameters. Until now, chimera states have been studied in networks of coupled oscillatory FitzHugh-Nagumo elements. In the present work, we find that introducing a block of excitable units into the network may lead to several interesting effects. It allows for controlling the position of a chimera state as well as for generating a chimera state directly from the synchronous state.

Transient localized wave patterns and their application to migraine.

Transient dynamics is pervasive in the human brain and poses challenging problems both in mathematical tractability and clinical observability. We investigate statistical properties of transient cortical wave patterns with characteristic forms (shape, size, duration) in a canonical reaction-diffusion model with mean field inhibition. The patterns are formed by ghost behavior near a saddle-node bifurcation in which a stable traveling wave (node) collides with its critical nucleation mass (saddle). Similar patterns have been observed with fMRI in migraine. Our results support the controversial idea that waves of cortical spreading depression (SD) have a causal relationship with the headache phase in migraine and, therefore, occur not only in migraine with aura (MA), but also in migraine without aura (MO), i.e., in the two major migraine subtypes. We suggest a congruence between the prevalence of MO and MA with the statistical properties of the traveling waves' forms according to which two predictions follow: (i) the activation of nociceptive mechanisms relevant for headache is dependent upon a sufficiently large instantaneous affected cortical area; and (ii) the incidence of MA is reflected in the distance to the saddle-node bifurcation. We also observed that the maximal instantaneous affected cortical area is anticorrelated to both SD duration and total affected cortical area, which can explain why the headache is less severe in MA than in MO. Furthermore, the contested notion of MO attacks with silent aura is resolved. We briefly discuss model-based control and means by which neuromodulation techniques may affect pathways of pain formation.

Is spreading depolarization characterized by an abrupt, massive release of gibbs free energy from the human brain cortex?

In the evolution of the cerebral cortex, the sophisticated organization in a steady state far away from thermodynamic equilibrium has produced the side effect of two fundamental pathological network events: ictal epileptic activity and spreading depolarization. Ictal epileptic activity describes the partial disruption, and spreading depolarization describes the near-complete disruption of the physiological double Gibbs-Donnan steady state. The occurrence of ictal epileptic activity in patients has been known for decades. Recently, unequivocal electrophysiological evidence has been found in patients that spreading depolarizations occur abundantly in stroke and brain trauma. The authors propose that the ion changes can be taken to estimate relative changes in Gibbs free energy from state to state. The calculations suggest that in transitions from the physiological state to ictal epileptic activity to spreading depolarization to death, the cortex releases Gibbs free energy in a stepwise fashion. Spreading depolarization thus appears as a twilight state close to death. Consistently, electrocorticographic recordings in the core of focal ischemia or after cardiac arrest display a smooth transition from the initial spreading depolarization component to the later ultraslow negative potential, which is assumed to reflect processes in cellular death.