k.p.collins at worldnet.att.net
Thu Aug 1 11:48:16 EST 2002
"Scientists reveal the secret of cuddles", 19:00 28 July 02,
NewScientist.com news service
for now, i stand on what i posted. the bi-directional inter-segmental
relays just have to convey information to the closest intact
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 ...
>there're several 'pathways involved in what's been referred to as
>[for those who have it, there is a basic overview of these pathways,
>their topological-mapping [within a larger 'enumeration', with
>more than 'pain'], in AoK, Ap3.]
>one of these 'pathways' occurs via many bi-directional relays within
>'gray-matter' of the spinal column.
>any divergence from 'normal' activation within this pathway is
>as 'pain' be-cause it constitutes a TD E/I-up condition within this
>which is part of the 'pain' sub-system.
>the 'many-relay' nature of this pathway is 'engineered' with
>sort of tissue-damage that you've described, and the overall
>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
>inherent topology of the resultant "tuning-precision void" [TD
>=still=, carries the correct [topologically-mapped] information into
>CNS, which enables survival-enhancing behavioral manifestation. [in
>way as is discussed in the 'sprained-ankle example in AoK's "Short
>section [footnote 11 in the paper version].
>we experience 'pain' as an inducement to redistribute the activation
>effectors during behavior. such 'strategic' redistribution of
>activation 'shifts-the-burden' away from injured tissue,
>allowing what remains fully-functional to work in attempts to
>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
>if you don't have AoK, and want a copy, msg. privately [runs under
>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
>>understanding the mechanism in which the sensation of pain can be
>>experienced in areas where there's no other sensory activity. For
>>if a peripheral nerve is severed and a limb or digit then becomes
>>all forms of sensory activity, how then can pain still be detected
>>More specifically, about 2 weeks ago I was in an accident where I
>>a rather deep laceration in the upper wrist / lower hand resulting
>>ulnar nerve becoming severed, as well as part of the median nerve
>>tendon and artery, which were also repaired). The nerves were
>>but theres no feeling (proprioreceptive or cutaneous) in 3 fingers
>>of the upper palm. However, there's the sensation of "shooting
>>fingertips and elsewhere in these areas. How is that possible?
>>a result of feedback with adjacent nerves in the relay sites and
>>about distal portions of the nerve beginning to regain function but
>>being "remapped" after reattachment? As you can see, I have no
>>Kandel's book touches on this sort of phenomenon, but nothing
>>enough to answer this type of question.
>>Any insights are appreciated.
>>- Mark Zarella
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