Investigation of a pain syndrome of spinal origin (on the concept of the generator mechanism of the pain syndrome).

A pain syndrome was induced in rats by means of a microinjection of purified tetanus toxin into the posterior horns of gray matter of the lumbosacral segments of the spinal cord. The toxin was used as a means of disturbing inhibitory mechanisms. Investigation showed that a pain syndrome can be reproduced if afferent stimulation from the periphery is blocked (by division of the nerves of the hind limbs or division of the dorsal lumbosacral roots on the side of injection of the toxin). Under these conditions the latent period of onset of the syndrome was lengthened and the degree of its development weakened a little in the initial stages by comparison with animals with intact afferentation. In many animals with blocked afferentation from the hind limb general manifestations (restlessness, aggressiveness, crying, etc.) were accompanied by a localized response in the form of increased licking, biting, or even chewing the tissues of the deafferented limb at the site of projection of the pain (the phantom syndrome). In some animals only the general reaction was observed without localization of the pain (protopathic pain). In all cases the attacks of pain arose paroxysmally. In animals with intact limb innervation the zones of licking were trigger zones of facilitated induction of an attack of pain. Injection of glycine into the affected posterior horns of the spinal cord abolished the pain syndrome during the time of action of the glycine. It is concluded that the pain syndrome is based on the formation of a generator of pathologically intensified excitation, as a result of disturbance of inhibitory processes, in the system of neurons connected with pain sensation. These mechanisms are evidently those principally concerned in the pathogenesis of all pain syndromes.