Abstract
Background
Following amputation, nearly all amputees report non‐painful phantom phenomena and many of them suffer from chronic phantom limb pain (PLP) and residual limb pain (RLP). The etiology of PLP remains elusive and there is an ongoing debate on the role of peripheral and central mechanisms. Few studies have examined the entire somatosensory pathway from the truncated nerves to the cortex in amputees with PLP compared to those without PLP. The relationship between afferent input, somatosensory responses and the change in PLP remains unclear.
Methods
Transcutaneous electrical nerve stimulation was applied on the truncated median nerve, the skin of the residual limb and the contralateral homologous nerve in twenty‐two traumatic upper‐limb amputees (12 with and 10 without PLP). Using somatosensory event‐related potentials, the ascending volley was monitored from the brachial plexus, the spinal cord, the brainstem and the thalamus to the primary somatosensory cortex.
Results
Peripheral input could evoke PLP in amputees with chronic PLP (7/12), but not in amputees without a history of PLP (0/10). The amplitudes of the somatosensory components were comparable between amputees with and without PLP. In addition, evoked potentials from the periphery through the spinal, subcortical and cortical segments were not significantly associated with PLP.
Conclusions
Peripheral input can modulate PLP but seems insufficient to cause PLP. These findings suggest the multifactorial complexity of PLP and different mechanisms for PLP and RLP.
from Wiley: European Journal of Pain: Table of Contents https://ift.tt/2ztxlyI
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