Yup. I stand on what I've posted.
the pertinent info is given on pA3-14, AoK, Ap3 [ref. Human
Neuroanatomy, 8th Ed., 1983 [page numbers cited below]]:
"In the dorsal horn of the spinal cord, the terminations of noxious
and non-noxious sensory fibers are mapped inversely with respect to
each other (in a topologically-distributed antagonistic fashion) (p.
245, diagram p. 246).
Short fibers from spinal lamina II (substantia gelatinosa) enter the
zone of Lissauer (at the tip of the dorsal horn) and project
ipsilaterally within the spinal cord, synapsing one or more times
before projecting contralaterally into the (ascending) spinothalamic
tract (p. 275)."
the inverse topological mapping noxious and non-noxious fiber
terminations is a dead-give-away with respect to 'moving away from'
pain. [I wrote it into the paper in this way in order to show how
rigorously the internal frame of reference [IFR] maintains its
structural integrity, with respect to TD E/I-minimization,
=throughout= the CNS. This's one of numerous 'nuggets' that I put
into AoK, deliberately, to reward the reading of Professionals, even
though the paper was written as an introduction for
non-Professionals.
[does this New Scientist article mean that all the 'nuggets' have
been 'missed' by the Pros? C fibers are one of the main things
in-there. it's non-sense to attribute them exclusively to stroking's
'feel-good' stuff (no 'snide' remarks please :-).]
k. p. collins
Kenneth Collins wrote in message ...
>"Scientists reveal the secret of cuddles", 19:00 28 July 02,
>NewScientist.com news service
>>http://www.newscientist.com/news/news.jsp?id=ns99992598>>for now, i stand on what i posted. the bi-directional
inter-segmental
>relays just have to convey information to the closest intact
>spinothalamic entry-'point'.
>>interpretation that the short relays in the spinal [dorsal] gray are
>in-there solely for the purpose of 'feeling-good' as a result of
>'being stroked' is extreme. (in my case, they'd be a complete
'waste'
>:-)
>>i've always viewed them as constituting a 'pliable' pathway that's
>tunable-to-task, providing 'background', and spinal-'level'
>convergence [TD E/I-minimization].
>>i'll reread, and post a follow-up, one way or the other.
>>['interesting' that this link is getting a lot of hits today :-]
>>k. p. collins
>>Kenneth Collins wrote in message ...
>>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
>>
