Central mechanisms of chronic pain (neuralgias and certain other neurogenic pain).

Almost all supratentorial intracranial lesions which may effectively control chronic pain in man are ineffective for acute pain. There are at least 10 sites at which lesions producing no somatic sensory loss have often stopped the peculiarly agonizing chronic pain of advanced cancer. They include: (a) inferior posteromedial or subcaudate (preinnominate) frontal white matter; (b) supracallosal portion of cingulum; (c) thalamotomy of centrum medianum and parafascicularis nuclei; (d) thalamotomy of linear parasagittal type separating connections between lateral specific and medial nonspecific sensory relay nuclei; (e) thalamotomy of pulvinar; (f) amygdalotomy; (g) frontothalamic tractotomy; (h) hypothalamotomy-posteromedial nuclei; (i) hypothalamotomy-periventricular nuclei; (j) hypophysectomy. It is indeed remarkable that such diversely situated lesions may many times be so successful. We understand poorly the mechanisms by which this control is often (though at times only temporarily) achieved. Hence, we are in real need of animal models to permit critical analysis. The problem of devising an ethically acceptable modus operandi is formidable. However, an ethicist who would demand that every time an experimental animal is showing some distress the experiment must be terminated, must also bear some responsibility for continuing disabling pain in hundreds of thousands of people.