Phantom Limp Pain Pathophysiology

While there are many theorized mechanisms for the existence of phantom limb pain (PLP), the exact 

mechanism is not known.  In this post, I will cover a few of the main theories and attempt to explain some possible origins of PLP.  However, as with most things in the human body, the mechanism that controls PLP is likely an amalgamation of mechanisms that work together to cause the symptoms of this disease.

(http://www.amazingsuperpowers.com/2012/08/en-garde/)

Three of the main theories are :

The peripheral theory, which assumes that PLP originates at the nerves around the injury.
When tissues are injured, chemicals and enzymes create an inflammatory process and sensitize the pain receptors.  Neurotransmitters are released around the site of damage, which then activates neighboring nerve endings.  This causes nerves not originally involved in the damage to become involved and expands the area of the body the pain perceives.  In normal tissue, this sensitization resolves spontaneously, but in damaged tissue it leads to neuropathic pain such as PLP.

The spinal theory, which attributes the cause to changes in the spinal cord.
Amputation damages the nerves which causes a hyperexcitability in the CNS, manifesting as an increase in neuronal firing, changes in the structure of the sensory neurons, and a reduction in the normal spinal cord inhibitory processes.
 
The central theory, which assumes that PLP is caused by some mechanism in the brain.
This theory is grounded in the idea of remapping of the somatosensory cortex of the brain.  Basically, when damage occurs and an area of the brain is no longer receiving impulses from a section (where the amputation was), the brain will "rewire" itself and interpret sensations from other parts of the body in the missing limb.  This is evident when a part of the body is touched, but the amputee feels it in their amputated limb.  


(http://kin450-neurophysiology.wikispaces.com/Phantom+Limbs+II)

References:

Chapman, S. (2011). Pain management in patients following limb amputation. Nursing Standard, 25(19), 35-40.