EMPIRICAL STUDIES OF MEDITATION: DOES A SLEEP RHYTHM HYPOTHESIS EXPLAIN THE DATA?

This article reviews the findings of important empirical studies of meditators and shows that these findings can be explained by the hypothesis that meditation is generated by induction of slow wave sleep rhythms. This hypothesis explains why radionucleide imaging (PET, SPECT, and fMRI) studies report increases in neuronal activity in the thalamus (where sleep rhythms are generated) and in the hippocampus (which receives a barrage of vision-related signals caused by manipulations of attention and sleep rhythm activity). It also explains the diverse findings of EEG/QEEG studies, for example, the observed short-term increases in alpha band frequencies and coherence, the subsequent shifts to slower theta/delta frequencies, and the reports of a sudden frequency-splitting and amplitude-doubling concurrent with ecstatic raptures. The author suggests that existing studies of meditation do not account for the likelihood that the theta/delta frequency distribution associated with meditation can be generated by two very different mechanisms: (1) by induction of a drowsy, hypnagogic state ("stage 1" NREMS), an experience familiar to many people and thus easily achievable by novice meditators, and alternatively, (2) by inducing the full progression of thalamic sleep rhythms, an option available only to advanced meditators who are able to move beyond "stage 1" NREMS ro induce thalamic spindle-burst typical of "stage 2" NREMS, then beyond that to induce delta waves typical of "stage 3" NREMS. These thalamic delta waves, after augmentation by intracortical circuits, register in the cortical EEG as low-theta/high-delta band activity, making it easy to mistake the underlying mechanism as stage 1 NREMS