hi, Mark.
there're several 'pathways involved in what's been referred to as 'pain'.
[for those who have it, there is a basic overview of these pathways, and
their topological-mapping [within a larger 'enumeration', with respect to
more than 'pain'], in AoK, Ap3.]
one of these 'pathways' occurs via many bi-directional relays within the
'gray-matter' of the spinal column.
any divergence from 'normal' activation within this pathway is experienced
as 'pain' be-cause it constitutes a TD E/I-up condition within this pathway
which is part of the 'pain' sub-system.
the 'many-relay' nature of this pathway is 'engineered' with precisely the
sort of tissue-damage that you've described, and the overall 'engineering'
of the nervous system as a =generalized= processor is Obvious.
this is a pathway that 'calculates' with respect to =any= possible
tissue-damage, and performs its function, regardless.
if there's something 'normal' that's 'missing', the pathway 'calculates' the
inherent topology of the resultant "tuning-precision void" [TD E/I(up)], and
=still=, carries the correct [topologically-mapped] information into the
CNS, which enables survival-enhancing behavioral manifestation. [in the same
way as is discussed in the 'sprained-ankle example in AoK's "Short Paper"
section [footnote 11 in the paper version].
we experience 'pain' as an inducement to redistribute the activation of our
effectors during behavior. such 'strategic' redistribution of muscular
activation 'shifts-the-burden' away from injured tissue, simultaneously
allowing what remains fully-functional to work in attempts to survive, and,
over a longer 'time' course, allowing the injured tissue a
relatively-optimized opportunity to 'heal'.
as is discussed in AoK, all of this is made-possible via the elegant
topological 'twists and turns' of the nervous system's "special topological
homeomorphism".
if you don't have AoK, and want a copy, msg. privately [runs under DOS or
Windows].
k. p. collins
Mark Zarella wrote in message <82tZ8.572162$cQ3.54221 at sccrnsc01>...
>Even after rereading the analgesia chapter in Kandel, I'm having trouble
>understanding the mechanism in which the sensation of pain can be
>experienced in areas where there's no other sensory activity. For
instance,
>if a peripheral nerve is severed and a limb or digit then becomes numb to
>all forms of sensory activity, how then can pain still be detected in these
>areas?
>>More specifically, about 2 weeks ago I was in an accident where I sustained
>a rather deep laceration in the upper wrist / lower hand resulting in the
>ulnar nerve becoming severed, as well as part of the median nerve (and a
>tendon and artery, which were also repaired). The nerves were reattached,
>but theres no feeling (proprioreceptive or cutaneous) in 3 fingers and
parts
>of the upper palm. However, there's the sensation of "shooting pain" at
the
>fingertips and elsewhere in these areas. How is that possible? Could it
be
>a result of feedback with adjacent nerves in the relay sites and cns? What
>about distal portions of the nerve beginning to regain function but not yet
>being "remapped" after reattachment? As you can see, I have no ideas.
>Kandel's book touches on this sort of phenomenon, but nothing specific
>enough to answer this type of question.
>>Any insights are appreciated.
>>- Mark Zarella
>>
