>
> --- In [email protected], "sparaig" <sparaig@> wrote:
[...]
> > Probably not due to the same mechanism --not even remotely.
> Witnessing waking,
> > dreaming and sleeping likely don't have any effect on the
> functioning of the rostral
> > anterior cingulate cortex. Any in CC "not minding" of pain isn't
> due not feeling or "caring"
> > about the pain, but simply due to the strength of the connections
> that give rise the CC
> > state in the first place.
>
> I'm not sure what you're referring to by "connections,"
> but I don't know why shutting down the rACC couldn't be
> a side effect of CC. I wasn't suggesting that disabling
> the rACC somehow invoked CC, but rather the reverse.
>
"Connections" as in neural connections. CC doesn't appear to have anything to do with
shutting down any specific part of the brain, but rather with strengthening the long-
distance communications of the various parts of the brain in such a way as to support
what TMers call "witnessing." OTHER forms of meditation appear to often reduce (or
increase'0 the activity of spec ific parts of the brain beyond the normal range of activity
outside of meditation, but TM doesn't appear to have that effect. It has the effect of
*balancing* the activity of various parts of the brain. During TM, there appears to be some
effect of reducing sensory processing, but that isn't one of the correlates of witnessing
during waking, but rather the way in which TM enhances restfulness DURING meditation.
Any change in how the brain handles pain in someone in CC probably has nothing to do
with changes in how the brain processes pain _per se_, but in how the brain processes
ANY strong stimulus: the strong stimulus doesn't overwhelm the brain's ability to maintain
the long-distance coherent state that apparently characterizes CC-witnessing. The brain
still "feels" pain the same as always --it just doesn't overshadow the global coherence
state.
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