The bilaterally symmetrical deafferentation syndrome in macaques after bilateral spinal lesions: evidence for dysesthesias resulting from brain foci and considerations of spinal pain pathways.

Six macaques had been subjected to chronic left thoracic anterolateral cordotomy, which released persistent self-attacks of the hypoalgesic right hind limb. One to 4 weeks later, lesions were placed in the right thoracic spinal cord, 2-5 segments apart from the left lesion. None of these second-stage spinal lesions, including spinal hemisection, affected the continued self-attacks of the right leg. Therefore, the chronic deafferentation syndrome of contralateral anterolateral cordotomy is not dependent upon the rostral conduction, via long spinal sensory tracts, of neural activity from ipsilateral lumbosacral spinal segments. Furthermore, second-stage right thoracic spinal lesions, which damaged the anterolateral tracts in 4 macaques, caused the release of the deafferentation syndrome in the left hind limb, despite extensive prior destruction of the left anterolateral tracts. Therefore, the release of the deafferentation syndrome by contralateral cordotomy is independent of the functional activity of the ipsilateral anterolateral tracts. The bilateral symmetry of this syndrome after extensive bilateral spinal lesions suggests pathophysiological foci at the level of the brain rather than the spinal cord. This syndrome is considered to be an objective index of disturbing subjective sensations.