A review by Lindsey Tucker, MD. Phantom Limb Pain. Incidence. An estimated 1.7 million people in the US are living with limb loss. Each year 158,000 persons undergo an amputation The incidence of phantom pain is 60-80% among amputees.
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After nerve injury, C-fibers and A delta-afferents gain access to secondary pain signaling neurons (mediated by glutamate and neurokinins). This is manifested by mechanical hyperalgesia and expansion of peripheral receptive fields. (Doubell, et al 1999)
Increased activity of NMDA receptor; central sensitization can be reduced by NMDA antagonists such as ketamine. (Eichenberger, et al 2008)
Peripheral nerve damage can lead to degeneration of C-fiber afferent terminals in laminae II. As a result, central terminals of Aβ-mechanoreceptive afferents (which normally terminate in laminae III and IV) sprout into laminae I and II. (Woolf, et al 1992)
Ultimately, this results in increased general excitability of spinal cord neurons.
TCA’s and sodium channel blockers are currently considered the drug treatments of choice for neuropathic pain, but a 2004 study of 39 patients demonstrated no benefit of TCA’s over placebo in PLP after 6 weeks. (Robinson et al 2004)
One study showed that mexiletine produced pain relief in 18 of 31 patients with PLP. (Davis 1993)
Opioids (MST) produced pain relief in 42% of patients and showed evidence of reduced cortical reorganization in 12 patients with PLP. (Huse E 2001)
There have been mixed results in studies using memantine to treat chronic pain, but it may be successful in treating PLP if initiated in early post-amputation period. (Hackworth, et al 2008)