The EEG is the summation of LFPs therefore phase shifts are necessarily related to connection density. However, the arrival of distant synaptic action potentials exhibits temporal dispersion whereas local excitatory connections are higher in number and temporally compact. Therefore, it is hypothesized that the ratio of distant to local connections varies as a function of distance from any Brodmann area and as a consequence longer phase shift duration occurs as the ratio shifts toward distant excitatory inputs. It is hypothesized that phase lock is inversely proportional to phase shift duration based on the spatial-temporal GABA connections and delays between excitatory neurotransmitter EPSPs (and excitatory neuromodulators) in local and long distance loops. It is also hypothesized that the physiological differences in the genesis of phase shift vs. phase lock is related to the “Gap” of time between distant and local EPSP excitation that produce the phase shift followed by long duration inhibitory synaptic potentials that contribute to phase lock duration. The collective resonance of the rebound from local inhibition and the arrival of long distant EPSPs contribute to the onset of the PR process.
