ABSTRACT
Although there is a great deal of evidence supporting the efficacy of hypnosis for pain management, there is much less research evidence regarding the mechanisms that underlie the beneficial effects of hypnosis. The slow wave hypothesis proposes that hypnotic analgesia operates by utilizing neuronal assemblies that fire in the theta and alpha frequencies to control the activity of neuronal assemblies that underlie the experience of pain, including those that fire in the faster (gamma) frequencies. Three findings would be anticipated based on the slow wave hypothesis: (1) baseline (i.e., pre-hypnosis) levels of slow oscillation activity should be positively associated with response to hypnotic analgesia, (2) interventions or strategies that increase slow oscillation activity should enhance response to hypnotic analgesia, and (3) when changes in brain oscillation bandwidth power are observed, pain reduction in response to hypnotic analgesia should be mediated by increases in slower oscillation and decreases in faster oscillation power. Although more research is needed to provide definitive conclusions, preliminary evidence is consistent with the slow wave hypothesis. If supported, the slow wave hypothesis provides some specific guidelines that clinicians can follow that would enhance outcomes when using hypnosis to treat individuals with chronic pain.
