Abstract
A number of studies have shown that phantom limb pain is associated with plastic changes along the neuraxis, with a close correlation between changes in the cortical representation of the affected limb and phantom limb pain. Mechanisms underlying these maladaptive plastic changes are related to a loss of GABAergic inhibition, glutamate-mediated long-term potentiation-like changes and structural alterations such as axonal sprouting. These plastic changes and phantom limb pain seem to be more extensive when chronic pain precedes the amputation. Behavioral interventions, stimulation, feedback and pharmacological interventions that are designed to reverse these maladaptive memory traces and enhance extinction may be beneficial for the treatment and prevention of phantom limb pain.
Financial & competing interests disclosure
This work was supported by grants from BMBF, DLR (01EM0512, German Research Network on Neuropathic Pain, DFNS) and the European Union (EU PR6 043432).
The author has no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
Notes
+: Denotes that at least one controlled study with a positive effect of phantom limb pain is available; -: Denotes that a controlled study with no effect on phantom pain is available.
+: Denotes that at least one controlled study with a positive effect of phantom limb pain is available.