I already discussed this two days ago, but probably a repetition is needed in
view of the follow up on this issue:
When a limb is amputated the sensory neurons *are not* destroyed. Their cell
bodies are in the dorsal root ganglia and start to react to the injury. Only
their normal peripheral terminations have dissapeared and now the peripheral
branch of the dorsal root ganglion neuron ends in a neuroma. This is the
cut end of the nerve and contains all the peripheral branches ending now in
an abnormal fashion. However their central connections still map to the
central representation of the missing limb. One thing neuromas are well
known for is producing an unregulated tonic discharge of APs in the fibers
terminating in them. So the spinal cord *does* receive a signal and this is
very abnormal and unregulated and can produce all short of long term changes
in the spinal cord network and also in the networks of upper brain relay
centers. Much of this mechanisms are as yet not exactly known, but clinically
manipulations of the stump (e.g. with anesthetics, ion channel blockers....)
or of the peripheral sensory fibres relieve phantom limb pain. In
other occassions the process has already gone very far centrally and the
central networks spinal and/or supraspinal are sensitized to the extent that
they also contribute to form the phantom limb sensation even with little
peripheral input. Similar central sensitization mechanisms also occur and
contribute to other hyperalgesic states where an abnormal peripheral input
occurs (e.g. peripheral neuropathies, immflamation....) Much is still under
research. If you are interested in the phantom limb phenomena I suggest this
reading:
By the way, not al phantom limbs are necessarily painfull.
Phantom limb and other phenomena after amputation
by T.S. Jensen and P. Rasmussen
In Textbook of Pain, 1994 (ed Wall and Melzack) Chapter 36 pp 651-666
Francisco J. Alvarez
Wright State University
