Reorganization of primary afferent nerve terminals in the spinal dorsal horn of the primate caudal to anterolateral chordotomy.

A primate model has been used to explore the possibility that anterolateral chordotomy may produce intraspinal sprouting or rearrangement of primary afferent nerve terminations that could account for delayed postoperative recovery of sensory function. Monkeys were trained to limit the duration of an electrical stimulus, and the vigor and frequency of their escape responses were used to differentiate painful from nonpainful levels of stimulation. Behavioral testing after chordotomy revealed: 1) contralateral hypalgesia in all animals, with sensory recovery in half of the group, and 2) bilateral decreases in reflexive force in all animals, with reflex recovery in the majority of monkeys. At the terminal experiment, dorsal rootlets caudal to the spinal lesion were labeled bilaterally with HRP, and the distribution of labeled synaptic complexes was determined within the dorsal horn. When compared to controls, animals undergoing chordotomy showed a loss of terminals in the superficial dorsal horn and an increase of synaptic enlargements in deeper layers. These effects were bilateral, but were most pronounced on the side contralateral to chordotomy. Animals with diffuse spinal lesions showed a completely different change in the distribution of primary afferent terminals. Animals with sensory recovery demonstrated a more normal terminal distribution pattern than persistently hypalgesic monkeys, but there was considerable variability in the data, and analysis by different statistical tests yielded varying results.