Dysesthesias and self-mutilation in humans and subhumans: a review of clinical and experimental studies.

The chronic deafferentation syndrome includes a complex pattern of abnormal self-directed behavior and a stress response. Subhuman self-mutilation is a secondary consequence of the chronic deafferentation syndrome. The evidence indicates that the chronic deafferentation syndrome in subhumans is a valid model for the induced and the spontaneous dysesthesias in humans. Objective criteria for the definition of subhuman dysesthesias have been derived from independent sources of evidence, in neurally intact subjects; those criteria are then found to match the subhuman syndrome of deafferentation. Support for the validity of the inference of subhuman dysesthesias derives from the parallels with the various facts of the human dysesthesias. The credibility of this argument is significantly strengthened by reports of morphological and excitatory physiological abnormalities, in central somatosensory structures, in response to deafferentation. There is no independent subhuman evidence in support of alternate interpretations of the deafferentation syndrome, and those interpretations seem to be inadequate in several aspects. Doubts concerning the validity of this animal model have been allayed by reports of dysesthesias in humans with spinal posterior rhizotomies or ganglionectomies, and also those with congenital analgesia. Moreover, the occurrence of this syndrome in hypoalgesic areas as a consequence of anterolateral cordotomy in monkeys, can best be interpreted as a reflection of dysesthesias. This syndrome is released by neuropathological or neurosurgical lesions in the peripheral or central nervous system; lesions which involve small caliber peripheral afferents or the spinothalamic tract. Variability in the release of this syndrome has been associated with several different factors. So far, the chronic syndrome is intractable. Evidence relates the abnormalities of this syndrome to pathophysiological foci in central relays of the somatosensory system, and suggests that the chronic abnormalities of this syndrome can be sustained at brain levels.