In article <10895XTGOASUAFAQKRM at dsp.com>, <bmw at dsp.com> wrote:
>IX> In article <199503161542.AA25682 at unf6.cis.unf.edu>,
>IX> jander at UNF6.CIS.UNF.EDU ("Jo Anderson ", CSHNL) writes:
>IX> >> I think it is also important to recognize that pain can be lack of
>IX> a signal that use to be there. Phantom limb pain is a good example.
>IX> >> Ron Blue
>IX> >
>IX> >Is phantom limb pain necessarily due to the _lack_ of a signal?
>IX> >Couldn't it also be due to the _presence_ of a signal located somewhat
>IX> >in from the periphery, that is interpreted as coming from the missing
>IX> >limb?
>IX> >
>IX> >John Anderson
>IX> Excellant remark! Yes, circles in circles with the first circle be the
>IX> real arm. Once the real arm is gone other opponent signals now are
>IX> allow
>IX> through resulting in the sensation of pain. That pain message could be
>IX> blocked by creating a mild pain at the stub. The mild signal would
>IX> create
>IX> an opponent signal blocking the MAIN opponent signal created by the lack
>IX> of an arm signal. Ron Blue
>> What of the case of Reflex Sympathetic Dystrophy. Would this theory
>also work?
>bruce bmw at dsp.com
It seems we are mixing apples and oranges here: There are many origins of
pain and ways to naturally block them.
First of: Phantom limb is a pain mostly produced centrally (that means
from the spinal cord up). It is probably generated from a lack of
_peripheral_ inputs (it's not there anymore). Some have its origin in the
thalamus, others in the spinal cord. The pain can be rekindled by
manipulation (even light) of the stub.
Then what Ron seems to be confused with is either the "gate control"
theory (Melzack and Wall 1965) which proposes that, *in the same spinal
segment*, large myelinated fiber (conducting touch) when stimulated can
block the pain traveling on the C- and A-delta fibers because they can
activate a _spinal_ inhibition of the C-/A-delta inputs;
or with DNIC (diffused noxious inhibitory control) where pain from a second
insult (pinching a toe) is centrally blocked by the continuous pain from a
first insult (dipping a hand in 55oC water).
Then Bruce wants to throw in RSD. This one is tougher: it has 2 components
(at least): a peripheral one which is the activation of C-fibers by
sympathetic stimulation or norepinephrine _AFTER A PARTIAL NERVE INJURY_
and, also following that injury, a second one where a number of _central_
changes occur which result in a "sensitisation" of spinal and higher
neurons to *touch* (!) and *cold*! What is really puzzling with RSD is
that the nerve injury is invisible (if there was a trauma everything has
usually healed long ago) and the pain is excruciating (described as
stabing, burning, ...) to the point people live reclused, their limb
wraped in a damped linen.
The difference between phanton limb and RSD is in the injury: partial vs
total. I phantom limb pain the sympathetic sensitivity occurs on the
neuroma (the regenerating sprouts) whereas in RSD it occurs in the
receptive field of C-fibers which appear to change their phenotype
(possibly by displaying new adrenergic receptors).
Daniel Bossut
