English: "Hypoxia-induced surge of PAC in the dying brain. (A) Cross-frequency coupling between the phase of lower frequency bands (0 to 50 Hz) and amplitude of higher frequency waves (30 to 250 Hz) in the right anterior-mid temporal lobe (T4) in Pt1. (B) Spatial and temporal distribution of phase-amplitude coupling (PAC) between gamma (gamma1 and gamma2) and lower frequency (delta, theta, alpha, and beta) bands in Pt1 at baseline (S1) and near-death (S2 to S11). (C) Temporal changes of theta/gamma1 and beta/gamma2 coupling in Pt1 in 16 cortical regions at near-death. (D) Beta-gamma2 PAC in somatosensory cortices (C3 and C4) and right dorsal lateral prefrontal cortex (F4) in both Pt1 and Pt3 at baseline (S1) and during the early dying phase (S2, S3)." "In the right anterior-mid temporal lobe (T4) of Pt1, the amplitude of gamma oscillations (>50 Hz) showed intense coupling to the phase of lower frequency bands (<50 Hz), whose coupling strength varied dynamically across the dying stages (Fig. 2A). Coupling was undetectable in S1 but showed marked increases in S4, S6, S7, and S9. In S6 and S9, extensive coupling was found between the phase of frequency bands (8 to 40 Hz) and amplitude of all frequency bands above 50 Hz. The frequency of coupled gamma oscillations peaked above 150 Hz. In this study, we restricted our focus on the coupling between the amplitude of gamma1 (25 to 55 Hz), gamma2 (80 to 150 Hz) and the phase of lower frequency bands (theta, alpha, and beta). The phase-amplitude coupling (PAC) was nearly absent at baseline (S1) for any of the frequency combinations (Fig. 2B) across the brain for Pt1. It became evident as early as in S2 for all displayed PAC types, except delta/gamma1 PAC (Fig. 2B). Interestingly, while PAC of all types rose only on the right SSC (C4) and right DLPFC (F4) in S2, the further rise of PAC in S3 was detected only in the left SSC (C3; Fig. 2B) for gamma1-associated PAC (theta/gamma1 and alpha/gamma1). For gamma2-associated PAC coupling (alpha/gamma2 and beta/gamma2), elevated coupling was expanded to both hemispheres in S3 that included the left SSC (C3), as well as the right DLPFC (F4) and right SSC (C4) (Fig. 2 B and C). During the periods when the external atrial pacemaker was triggered (S4, S6, S7) by the persistent decline of heart rate in S3, high levels of PAC clustered in the right anterior (Fp2, F8, F4, C4) and left posterior (T3, T5, P3, O1) areas for theta/gamma2, alpha/gamma2, and beta/gamma2 PACs (Fig. 2B). In S8 and S9 when the atrial pacemaker was off, PAC was detected mainly in the left temporal (T3 and T5 in S8) and right frontal, central, parietal, and temporal lobes (F4, F8, C4, T4, T6, P4 in S9) (Fig. 2 B and C). The surge of beta/gamma2 PAC, ranging 1- to 188-fold over S1 in S2 or S3, was detected in the right DLPFC (F4) and SSCs in both Pt1 (Fig. 2 C and D) and Pt3 (Fig. 2D and SI Appendix, Fig. S3B). Phase-amplitude coupling between gamma2 and lower frequency bands was absent in Pt2 (SI Appendix, Fig. S3A) and largely undetectable in Pt4 (SI Appendix, Fig. S3C)."