The bulk of hos to best understand qualia and other subjective
johnh at faraway.hgmp.mrc.ac.uk
Wed Apr 14 06:58:50 EST 2004
You are correct, upon getting off my lazy arse and actually paying close
attention (damn, I even printed it out), I can appreciate some aspects of
I wish they had addressed phantom limb etc. In light on this paper, if I had
the time, I need to have another look at PL and see if I can find a way to
fit that into this. It may be the case that phantom limb pain is a result of
nerve damage - neuropathic pain, hence its excruciating nature and often it
is referred pain (ie. the pain seems to emanate from a bodily region but
actually arises elsewhere).
Another issue with the sensation of pain is that it is at least in part
mediated by the immune system; there is evidence , particularly in relation
to neuropathic pain, that microglia play a key role. Common analgesics, cox
2 inhibitors being a good eg. actually address inflammation, which is
immunologically mediated. Nerve damage can result in neuropathic pain, so
phantom pain may not be an issue here. However ... cox 2 is also essential
for NMDA transmission, at least in the hippocampus. Also, il 1b, often
released in injury, increases cox 2 and Substance P.
As to phantom limb, I just have to go back and read the material again,
which is a big ask at present because now my eyesight has restored somewhat
I have a small mountain of reading to catch up on so this goes way down the
list of priorities ... . One idea I have is that while patients may act as
if they still had the limb, are they actually conscious of still having the
limb? Eg. Do they attempt to reach out grab something with the phantom limb?
2. Alerting capacity.
Just what is being alerted? Attention is not just a matter of excitation, it
also involves the inhibition of other inputs. Centre surround inhibition in
vision is a good example of this and may well be a generic feature of
sensation. Perhaps this explains why focussing on a pain increases that
pain, a matter of contrast.
3. Headaches and toothaches
I think they have created their own dilemma here. Headaches obviously cannot
be from the brain, no receptors there, but an increasing amount of evidence
suggests it arises from the meninges or dura matter inflammation (my guess
is long lasting prsence of dendritic cells driving a localised inflammatory
response - it sounds odd but it has been demonstrated that DCs can enter the
CNS and stay there for quite some time)and subsequent changes in
circulation. Pressure may change, as sense neurons are responsive to this
(the neuron fires because of increasing pressure at the tip, these types of
pain may arise because of sustained activation leading to toxin
accumulation,increased circulation (strongly associated with inflammation
via vasodilation), increased pressure distorting tissues, and eventual pain
as a result. After all, we can injure ourselves but it can take some hours
before we begin to experience pain from that injury, during that time
inflammation ensues, it is not the actual original tissue damage that causes
pain, it is the resultant inflammation. Obviously though this is not always
the case but this may be explained by the fact that immunological mediators
of inflammation are not uniformly distributed throughout the body. Eg. The
skin has its own variety of specialised dendritic cells that are always
present, DCs are key players in driving immune responses; whereas in other
regions (eg. CNS), DCs will migrate to these regions after injury and
typically are not resident in large numbers apart from this. My point here
is to suggest that both of these pain types may involve corporality.
I liked this:
"Kohler's subjects wore goggles inwhich one sodie of th field was tinted one
coulor and the other one another color. Within a period of days the subjects
came to see colors as normal again. ... Note: poor replication of this study
but I do recall some supporting studies touching on this. Eg. as in the
examples you gave, it isn't necessarily frequency that determines color.
Hmmm, I wonder where the saying "feeling blue" comes from. Perhaps it was a
dirty old swagman who preferred cattle dogs over blondes.
Their example of inattentional blindness tends to support my idea re
attention being as much about inhibition as about orientation.
How on earth do you find this stuff?
"Peter F." <effectivespamblock at ozemail.com.au> wrote in message
news:DENec.223$_84.5076 at nnrp1.ozemail.com.au...
> "John H." <johnh at faraway.> wrote in message
> news:407a78b9 at dnews.tpgi.com.au...
> > Can't understand it Peter. Not a hope. If possible, please elucidate
> > they are on about. They seem to be focussed on the "hard problem". These
> > days I"m not even sure there is a problem.
> Am afraid one of the baiting boys one-upped me, and summed it up, before I
> saw your reply and had a chance to beat him to it. %-}
> I vaguely remember that one fairly substantial philosophical point that I
> extracted (or extrapolated?) from the first 'sensorimotor contingency
> I read by O'Regan and Noë (not the one I reffed to this time) - one
> than the idea that (e.g.) the difference between being conscious of green
> distinct from red is not just the initial difference in wavelength but
> _every_ difference in meaning such as what green is most likely to smell,
> and taste, and feel like (e.g. grass against the skin) and what one is
> likely to do with things green, as distinct from the 'likewise meaty' ;-)
> meaning of red - was that it is the actual physical existence of e.g.
> and that and how their properties have played a decisive interactive role
> the successful coping and survival of our ancestors, that makes our
> consciousness of trees such a self-evident (qualia-quashing) state of our
> (normal, human-primate) being.
More information about the Neur-sci