Phantom limb pain in the human brain: Unraveling neural circuitries of phantom limb sensations using positron emission tomography

Abstract

Pain and other phantom limb (PL) sensations have been proposed to be generated in the brain and to be reflected in activation of specific neural circuits. To test this hypothesis, hypnosis was used as a cognitive tool to alternate between the sensation of PL movement and pain in 8 amputees. Brain activity was measured using positron emission tomography. PL movement and pain were represented by a propagation of neuronal activity within the corresponding sensorimotor and pain‐processing networks. The sensation of movement was significantly (corrected for multiple comparisons) related to activity in the supplementary motor area and the primary sensorimotor cortex. The sensation of a painful PL posture activated the same brain areas but was weaker and less extended in the supplementary motor area. In contrast to the sensation of movement, pain was significantly related to activity in the thalamus, anterior cingulate, and lateral prefrontal cortex. Subjectively rated PL pain sensation correlated positively to activations in the anterior and posterior cingulate. These findings provide evidence that PL sensations are produced by the same central nervous processes that underlie the experience of the body when it is intact and that the corporeal awareness of PL pain is encoded in a thalamocortical network. Ann Neurol 2000;48:842–849

Repetitive low‐energy shock wave application without local anesthesia is more efficient than repetitive low‐energy shock wave application with local anesthesia in the treatment of chronic plantar fasciitis

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Phantom percepts: Tinnitus and pain as persisting aversive memory networks

“…Nonpainful phantom phenomena have been shown to be more closely related to activation of S1 and the posterior parietal cortex, without activation of the secondary somatosensory cortex (63) and without cortical reorganization (64), whereas phantom limb pain is related to activation of the thalamus, the ACC, and the lateral prefrontal cortex (65), similarly to neuropathic pain in general (6), and is associated with plastic changes in S1 (50,64). The reorganization of A1 in tinnitus (20) and the activation of the ACC and the lateral prefrontal cortex in bothersome tinnitus (9) therefore suggest that distressing tinnitus and phantom pain are more similar than nonbothersome tinnitus and nonpainful phantom phenomena.…”

Supernumerary phantom limbs in spinal cord injury

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