Previous research implicates an endogenous central pain inhibitory mechanism in opiate analgesia, analgesia produced by focal electrical stimulation of the brain, and acupuncture analgesia. This investigation evaluates the possibility that analgesia produced by hypnosis is also mediated by such a mechanism. Results suggest that hypnotic analgesia is unlikely to involve this central pain inhibitory mechanism since hypnotic analgesia is not altered by naloxone hydrochloride, a specific narcotic antagonist.
The controversy about acupuncture is familiar to us since its recent reintroduction into this country. Much of its philosophical concepts were taken at their face values as the bases for condemnation. Since I last reviewed these antiquated concepts in the light of modern medicine, much has developed. It seems that if the effects of acupuncture were transmitted along the peripheral nerves to the central nervous system, it would be more effective if applied segmentally to the site of noxious stimulation. Disruption of extralamniscal pathways would abolish its analgesic effect.
In this study the hypothesis that hypnotic analgesia under conditions of stress is mediated through a neurochemical mechanism involving the release of opioid peptides in the CNS was investigated. Ten highly hypnotizable subjects participated in a 2 x 2 factorial design, which involved hypnotic analgesia, stress and double blind administration of naloxone (an opiate antagonist) or placebo. Analysis of post-hypnosis results indicates that hypnotic analgesia was significantly reversed by the interactive effects of stress and naloxone.
Previous research has shown that animal hypnosis (tonic immobility) in the rabbit may be elicited in a condition of prolonged nociceptive stimulation. These experiments show that long-lasting irritative pain, produced within 15 min of formalin injection, potentiates the duration of hypnosis. Morphine, in the absence of painful stimuli, also potentiates hypnosis duration and this effect is antagonized by naloxone. Naloxone reduces hypnosis duration, but only at high doses (15 mg/kg). In a condition of irritative pain, the potentiation of hypnosis duration is abolished by naloxone (5 mg/kg).
The effects of naltrexone on the increase in locomotor activity induced by a low dose (1.35 g/kg IP) of ethanol and on the duration of loss of righting reflex after a high dose (3.5 g/kg) of ethanol were studied in BALB/c, DBA/2, and C57BL/6 mice. Ethanol increased locomotor activity in DBA and BALB mice, but not in C57BL mice. Naltrexone, at a dose of 0.1 mg/kg, antagonized the ethanol-induced increase in locomotion similarly in DBA and BALB mice. The duration of loss of righting reflex was, however, differentially affected in all three strains by naltrexone.
The hypothesis that the alleviation of chronic pain with hypnosis is mediated by endorphins was tested. Six patients with chronic pain secondary to peripheral nerve irritation were taught to control the pain utilizing self-hypnosis. Each subject was tested at 5-min intervals during four 1-h sessions for the amount of reduction of pain sensation and suffering associated with hypnosis while being given, in a random double-blind crossover fashion, an IV injection of either 10 mg naloxone or a saline placebo through an indwelling catheter.
This study is an attempt to detect the most important modifications of physiological parameters occurring during pressure immobility in rabbits and to compare them with those recorded during animal hypnosis. Like the latter, pressure immobility is characterized by the development of high voltage slow waves in the EEG, reduction in frequency and amount of rhythmic slow activity in the hippocampus (RSA) and depression of spinal polysynaptic reflexes. Systolic and diastolic blood pressures are not modified. Duration of two types of immobility is positively correlated within individuals.
We investigated how repeated agonistic confrontations affect the hypnotic effect of pentobarbital (PB) in male mice, using a resident-intruder paradigm. PB concentrations in the cortex, midbrain and brainstem were determined. Agonistic confrontations were terminated after 10 or 20 attack bites, and were repeated for 5 consecutive days. Immediately after the last encounter, PB (55 mg/kg, IP) was administered to both resident and intruder mice.