Time-delayed feedback control of unstable periodic orbits near a subcritical Hopf bifurcation

We show that Pyragas delayed feedback control can stabilize an unstable periodic orbit (UPO) that arises from a generic subcritical Hopf bifurcation of a stable equilibrium in an n-dimensional dynamical system. This extends results of Fiedler et al. [PRL 98, 114101 (2007)], who demonstrated that such feedback control can stabilize the UPO associated with a two-dimensional subcritical Hopf normal form. Pyragas feedback requires an appropriate choice of a feedback gain matrix for stabilization, as well as knowledge of the period of the targeted UPO. We apply feedback in the directions tangent to the two-dimensional center manifold. We parameterize the feedback gain by a modulus and a phase angle, and give explicit formulae for choosing these two parameters given the period of the UPO in a neighborhood of the bifurcation point. We show, first heuristically, and then rigorously by a center manifold reduction for delay differential equations, that the stabilization mechanism involves a highly degenerate Hopf bifurcation problem that is induced by the time-delayed feedback. When the feedback gain modulus reaches a threshold for stabilization, both of the genericity assumptions associated with a two-dimensional Hopf bifurcation are violated: the eigenvalues of the linearized problem do not cross the imaginary axis as the bifurcation parameter is varied, and the real part of the cubic coefficient of the normal form vanishes. Our analysis of this degenerate bifurcation problem reveals two qualitatively distinct cases when unfolded in a two-parameter plane. In each case, Pyragas-type feedback successfully stabilizes the branch of small-amplitude UPOs in a neighborhood of the original bifurcation point, provided that the phase angle satisfies a certain restriction.Comment: 35 pages, 19 figure

Anesthetic action on the transmission delay between cortex and thalamus explains the beta-buzz observed under propofol anesthesia

In recent years, more and more surgeries under general anesthesia have been performed with the assistance of electroencephalogram (EEG) monitors. An increase in anesthetic concentration leads to characteristic changes in the power spectra of the EEG. Although tracking the anesthetic-induced changes in EEG rhythms can be employed to estimate the depth of anesthesia, their precise underlying mechanisms are still unknown. A prominent feature in the EEG of some patients is the emergence of a strong power peak in the β–frequency band, which moves to the α–frequency band while increasing the anesthetic concentration. This feature is called the beta-buzz. In the present study, we use a thalamo-cortical neural population feedback model to reproduce observed characteristic features in frontal EEG power obtained experimentally during propofol general anesthesia, such as this beta-buzz. First, we find that the spectral power peak in the α– and δ–frequency ranges depend on the decay rate constant of excitatory and inhibitory synapses, but the anesthetic action on synapses does not explain the beta-buzz. Moreover, considering the action of propofol on the transmission delay between cortex and thalamus, the model reveals that the beta-buzz may result from a prolongation of the transmission delay by increasing propofol concentration. A corresponding relationship between transmission delay and anesthetic blood concentration is derived. Finally, an analytical stability study demonstrates that increasing propofol concentration moves the systems resting state towards its stability threshold

Stability Analysis of Systems with Delay-Dependent Coefficients Subject to Some Particular Delay Structure

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