Central stimulation-induced analgesia in humans--modulation by endogenous opioid peptides

Stimulation of the endogenous opiate system produced relief of somatosensory induced pain states. Stimulation of the nonopiate system can control pain from somatosensory causes as well as damage to the nervous system. Neither of these systems in themselves are rewarding or produce self-stimulation in humans, who have free choice of whether to use stimulation or not, except to reduce discomfort. Lack of pain in general produces lack of use of the stimulation system. Apparently, the descending opiate system for somatosensory pain control involves descending norepinephrine and serotonin pathways at an intermediate step through the dorsolateral funiculus of the cord. Enhancement of the opiate system can be produced by administration of L-Tryptophan and L-Dopa due to precursor loading of serotonin and norepinephrine. The endogenous opiate system, when activated by electrical stimulation, usually produces excellent control of somatosensory induced pain, but often is not effective for centrally produced pain. Stimulation of areas that produce analgesia that are nonopiate-dependent are usually more effective in reducing pain from damage to the nervous system itself than the opiate-dependent system, but this is sometimes the converse. While cross tolerance to morphine from electrical stimulation of the endogenous opiate system exists in animals, it does not seem to be a problem clinically as the abstinence syndrome and tolerance have not been a problem in humans.