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Pain has been a major medical problem from the beginning of recorded history. Since the earliest medical writings, there have been innumerable procedures designed to relieve pain and its suffering. In this study, we have reviewed both the early medical writings of various civilizations and the first modern publications, to compile a history of neurosurgical procedures for the relief of pain.
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The effect of peripheral transcutaneous electrical nerve stimulation (TENS) on the reaction to experimental pain in human volunteers has been assessed. Placebo stimulation and electrical stimulation at moderate intensities failed to modify the response to the pain produced by conducted thermal stimuli. TENS at very high intensities did however elevate both the thermal pain threshold and the tolerance temperature. TENS at moderate intensities failed completely to alter the response to graded mechanical stimuli. The subjective pain assessment and the maximum pain tolerance produced by ischaemic pain after a submaximal effort tourniquet test were significantly modified by peripheral electrical stimulation at non-noxious intensities. The response to experimental pain can therefore be altered in man by peripheral electrical stimulation in a manner partly dependent on the sensory modality used for producing the experimental pain and on the intensity of the electrical stimulation.
Experimental C-fiber pain caused by radiant heat was applied to the skin area supplied by the left sural nerve of 20 subjects. Percutaneous electrical stimulation (PNS) was performed on the left sural nerve, the left superficial peroneal nerve and the right superficial radial nerve. Stimulation frequencies were: 3, 50, 100, 300, 500 and 1000 Hz. The analgesia resulting at the different stimulation sites was recorded according to a preset scale of estimation. Without considering the influence of the different frequencies, the best analgesic effects were reached if noxious heating and PNS were both performed on the left sural nerve; the anatomical conditions prevented us from distinguishing between the effects of possible peripheral blockade or spinal modification of pain. PNS of the superficial peroneal nerve seems to indicate spinal, possibly polysegmental, interactions between C-fiber pain and electrical stimulation of thick myelinated fibers. However, long loop effects may also play a part in local analgesia as demonstrated by PNS of the right radial nerve.
Phantom urinary phenomena are a relatively rare disease entity. Literature search has revealed only one case following cystectomy, seven cases following spinal cord injury and several other cases in hemodialysis patients. This report presents a case of painful phantom bladder following cystectomy for chronic kidney and urinary tract infection. Treatment was directed toward sensory hyperstimulation for suppression of the subjective experience of the painful phantom. Lumbar sympathetic blocks and transcutaneous electrical stimulation were used. Competent coping mechanisms were increased through relaxation training and assertiveness training to deal with a medical problem which has no standard solution. The patient's response to the Comprehensive Pain Control Program was excellent with an estimated 75% reduction in painful phantom perceptions. A brief discussion of the medical literature on the subject is presented.
In a series of 13 cats the effect of electrical stimulation of peripheral nerve on the mechanism of fast axoplasmic transport was studied. Electrical stimulation was used for varying time periods at parameters reported in the range of those used to produce electroanalgesia in man. Our results indicate that at these parameters, electrical stimulation produced no effect on this important aspect of nerve function, and, therefore, our work lends support to the safety of these devices in pain states.
Levels of beta-endorphin immunoreactivity in cerebrospinal fluid were measured in 12 chronic pain patients undergoing the surgical implantation of an electrode into the periventricular gray matter. Cerebrospinal fluid fractions were collected following placement of a cannula into the third ventricle, following injection of metrizamide contrast medium into the ventricles, following implantation of the electrode, and following electrical stimulation. A second set of samples was collected on a non-surgical day before and after stimulation. Levels of beta-endorphin immunoreactivity increased significantly from baseline levels to post-electrode implantation in one group of patients, but no significant change was seen following the onset of stimulation. Immunoreactivity increased significantly following metrizamide injection in a second group and was still elevated, in comparison to baseline, following electrode placement, but no increase was seen following the onset of stimulation. Levels of immunoreactive beta-endorphin did not increase in either group after stimulation on a post-surgical day, despite consistent reports of pain relief. Addition of metrizamide or a related contrast medium, iothalamate meglumine (Conray) to the beta-endorphin radioimmunoassay revealed that both compounds interfered with antigen-antibody binding and also quenched the gamma radiation emitted by iodinated peptide ligands. Due to these combined effects, the contrast media alone produced results similar to those of the beta-endorphin standard. Moreover, similar observations were made when contrast media were incorporated into radioimmunoassays for met-enkephalin, dynorphin and cholecystokinin octapeptide. These findings indicate that increased levels of beta-endorphin in cerebrospinal fluid are not directly associated with patient report of pain relief following periventricular gray stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult male rats, which had electrodes chronically implanted in the periaqueductal gray (PAG), were immunized with sheep red blood cells (SRBCs). The number of direct and indirect plaque-forming cells (PFCs) in the group receiving PAG stimulation after immunization did not differ significantly from that in the unstimulated group. Thus, the results indicate that short-term PAG stimulation does not suppress antibody-producing activity in the rat.
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A marked expression of the c-fos proto-oncogene has been recently reported in cells of the anterior lobe of the pituitary gland in rats subject to electroacupuncture or noxious thermal stimulation under pentobarbital anaesthesia. The present study was undertaken to identify the activated pituitary cells. Following both kinds of stimulation, most Fos-immunoreactive anterior lobe cells showed colocalization with adrenocorticotropic hormone or beta-endorphin immunoreactivity. No c-fos expression occurred in pituitary cells immunoreactive for growth hormone, prolactin, luteinizing hormone, or thyrotropin-stimulating hormone. A marked rise of adrenocorticotropic hormone and beta-endorphin concentrations occurred in plasma. In the hypothalamus, c-fos expression was increased in the mediobasal nuclei-namely, the arcuate nucleus-and in the paraventricular nucleus, but more in the former. It is suggested that somatosensory noxious input, or the partly noxious input evoked by electroacupuncture, activate the hypothalamo-pituitary-adrenocortical axis as in common forms of stress, but with a specific activation of the mediobasal hypothalamic nuclei and no stimulation of intermediate lobe cells. Opiate release from the pituitary gland may contribute to acupuncture analgesia or the intrinsic antinociceptive reactions triggered by noxious stimulation.
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Potent analgesia results from electrical stimulation of the periaqueductal grey matter in several species including man. Electrophysiological experiments indicate that this electrical analgesia could result from the activation of descending influences which inhibit the activity of dorsal horn interneurons in the transmission of painful messages. Numerous physiological, behavioral and pharmacological studies mention that the descending serotoninergic Bulbo-spinal system plays a major role in electrical analgesia. Several studies suggest that both electrical and morphine analgesia share, at least in part, a common site and mechanism of action. This possibility is mainly supported by the fact that analgesia induced by electrical stimulation is suppressed or reduced by a specific opiate antagonist (Naloxone).