[Interaction between the systems involved in fast pain perception and in slow, persistent pain (author's transl)]

A single pinprick triggers both a pang, the "1st pain" and after a pause of 0.5 s, a spreading burning feeling, the "2nd pain". The 2nd pain is delayed because it is conducted by unmyelinated C-fibers at a rate of less than 1 m/s, 20 times slower than conduction of the 1st pain. In the spino-thalamic tract the myelinated fibers of the 1st pain conduct much faster than those of the 2nd pain, and terminate in the parvocellular ventroposterior (VP) thalamic nucleus, which projects to area 3b in the postcentral gyrus. The slow C-fibers of the 2nd pain terminate in cortex-independent thalamic nuclei like limitans, which project to the outer segment of the pallidum. This subcortical pain pathway is disinhibited after destruction of the cortical pathway of the 1st pain, so that the patients suffer from spontaneous agonizing pain feeling (thalamic pain). Unbearable pain in cases of thalamic softening, in anaesthesia dolorosa and in phantom pain can be relieved by stereotactic coagulation of the thalamic nuclei involved in the 2nd pain. Normally they are inhibited by the cortical pathway of the 1st pain.