Loss and recovery of reactivity to noxious stimuli in monkeys with primary spinothalamic cordotomies, followed by secondary and tertiary lesions of other cord sectors.

Cebus albifrons monkeys were trained to escape electrical stimulation of either leg at five intensities, spanning a range from mild tingle to intense but tolerable pain, as judged by human observers who experienced the same stimuli. The average duration of stimulation received by the animals at each intensity was plotted for each leg during the period required for recovery of responsiveness to noxious electrical stimulation following ventrolateral spinal cordotomy. Recovery of escape responding was observed similarly following subsequent lesions to the spinal cord, in an attempt to define the pathways that subserve pain conduction after readjustment from cordotomies that produced substantial deficits of escape behaviour. The most enduring elevations of duration of stimulation by lesion I (left cordotomy) were produced by lesions that involved all of the ventrolateral column and most or all of one or both ventral columns. Secondary lesions of the dorsal columns, Lissauer's tract and the dorsolateral columns, in various combinations, did not produce long-term effects on escape responding. In contrast, a complete ventral hemisection produced a pronounced bilateral deficit that did not recover fully over three hundred and five post-operative days. The major conclusions are: (1) that the dorsal pathways do not play a major role in the rostral conduction of information critical for pain perception in monkeys, even though these pathways receive input from high threshold receptors; and (2) in order to produce a lasting decrease of pain sensitivity in primates by spinal surgery, the lesion must be bilateral and must involve both the ventrolateral and ventral columns.