Supraspinal factors

Amputation produces a cascade of events in the periphery and in the spinal cord. It is reasonable to assume that these changes will eventually sweep more centrally and alter the neuronal activity in cortical and subcortical structures.

Animal studies have demonstrated functional plasticity of the primary somatosensory cortex after amputation. After dorsal rhizotomy, a lowered threshold to evoked activity in the thalamus and cortex can be demonstrated, and adult monkeys display cortical reorganization in which the mouth and chin invade cortices corresponding to the representation of the arm and digits that have lost their normal afferent input.73,74

Studies in humans have also documented a cortical reorganization after amputation using different cerebral imaging techniques. In a series of studies, Flor et al.75, 76 showed a correlation between phantom pain and the amount of reorganization in the somatosensory cortex. Birbaumer etal.77 studied the effect of regional anesthesia on cortical reorganization in upper limb amputees and found that a brachial plexus blockade abolished pain and reorganization in three out of six amputees. Huse et al.78 showed in a small group of amputees that cortical reorganization and pain were reduced during treatment with morphine.

At more subcortical levels, changes have also been observed. Using neuronal recording and stimulation techniques, thalamic neurons that normally do not respond to stimulation in amputees begin to respond and show enlarged somatotopic maps.79,80 In addition to functional plasticity, structural alterations also follow amputation. Draganski et al81 recently demonstrated a decrease in the gray matter of the thalamus in 28 amputees. The decrease was correlated with the time span after the amputation and explained as a structural correlate of the loss of afferent input.

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