Basic neurobiologic mechanisms of pain and analgesia.

Information about tissue damaging, subjectively painful stimuli is transmitted to the central nervous system by specific receptors. Histologically, they are supposed to be free nerve endings connected to the spinal cord by thin myelinated (A delta or group III) and nonmyelinated (C or group IV) fibers. Nociceptive information is transferred to secondary cells mainly in the surface layers (lamina I and II) and the neck (lamina V) of the dorsal horn; it then ascends the anterolateral funiculus contralaterally in axons of the spinothalamic tract. One portion of this tract ends in the ventroposterior and posterior thalamus. It is assumed that it mediates the discriminative component of a pain sensation. The emotional-affective component of a pain sensation is supposed to be produced by that portion of the spinothalamic tract that terminates in the intralaminar nuclei and by the spinoreticular tract. The existence of a cortical pain center has not yet been proved, nor is it clear where in the cerebrum pain is consciously felt. The descending pain inhibiting systems, originating in the brain stem, may block the transfer of nociceptive information at a spinal level, probably using enkephalin as a transmitter. It is probable that they mediate morphine-induced analgesia. Lesions of tissue release endogenous substances, such as serotonin and certain prostaglandins, which sensitize receptors. The analgesic effect of nonsteroidal anti-inflammatory drugs, such as aspirin, can be explained by the inhibition of prostaglandin synthesis and the desensitization of nociceptors.