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A number of investigators have suggested that the early and late phases of the formalin test are mediated by separate neural systems. Evidence is presented which suggests that in addition to a dissociation between the two phases based on nociceptor stimulation and inflammation, the late phase of the formalin test is also dependent upon plasticity in the central nervous system which occurs during the transient early phase. Selectively blocking neural activity during the early phase with local anesthetics given peripherally, or in the cingulum bundle or fornix, prevents the development of these changes. Locally anesthetizing the cingulum bundle, fornix or medial bulboreticular formation prior to testing in the late phase produces analgesia which exceeds the duration of the anesthetic. It was also demonstrated that a thermal injury to the hindpaw or electrical stimulation of the sciatic nerve prior to neurectomy produces changes in the pattern and severity of self-mutilation following peripheral neurectomy, suggesting that the injury is encoded and maintained in central structures.

The four studies in this thesis deal with peripheral and central factors in phantom limb phenomena. Study 1 documents sensations referred to the phantom limb during transcutaneous electrical nerve stimulation (TENS) applied at the outer ears, face, and torso. The results suggest that some phantom sensations are maintained by activity of sympathetic fibers in the stump. Other sensations appear not to involve a peripheral mechanism. Studies 2 and 3 focus on sympathetic nervous system correlates of phantom sensations reported during TENS applied at the outer ears and contralateral leg. The results indicate that TENS significantly reduces the intensity of phantom limb paresthesias whereas a placebo control has no effect. Significant relationships between (a) phantom limb intensity and (b) stump skin conductance and temperature suggest that a cycle of sympathetic-efferent-somatic-afferent activity explains phantom limb paresthesias. Skin temperature was significantly lower at the stump than the intact limb in amputees with phantom limb pain (PLP), but not in those with a painless phantom, or no phantom limb at all, indicating that PLP is associated with reduced blood flow to the stump. Study 4 examines PLP that resembles pain experienced in the limb before amputation. These somatosensory memories constitute compelling evidence of a purely central component of PLP. Finally, amputees with and without PLP could not be differentiated by scores on personality, depression, or anxiety inventories. The results of the four studies indicate that the experience of phantom limb paresthesias involves a central mechanism that acts on peripheral structures whereas others qualities of experience depend exclusively on activation of central neural structures. Implications for treatment, research, and clinical practice are discussed.

No description available.