[ExI] putting the qual into qualia
gts_2000 at yahoo.com
Tue May 7 19:53:16 UTC 2013
I find this study below interesting, Eugen. Thanks for posting it.
This is the kind of work that I think will eventually lead to an understanding of the neurological processes associated with conscious experience (the NCC). Study 4, in which the signature response was substantially reduced after the administration of an analgesic, seems to confirm that they have identified the neural correlates of this sort of pain.
Study 3, in which they looked at the relationship between physical and social pain, reminds me of an abstract I read recently about a study that found that the administration of acetaminophen (Tylenol) changes one's social outlook. Though not a barbiturate, Tylenol seems to cause people to have a more relaxed attitude about life. I would not be surprised to learn that other ordinary analgesics have similar effects.
An fMRI-Based Neurologic Signature of Physical Pain
Tor D. Wager, Ph.D., Lauren Y. Atlas, Ph.D., Martin A. Lindquist, Ph.D.,
Mathieu Roy, Ph.D., Choong-Wan Woo, M.A., and Ethan Kross, Ph.D.
N Engl J Med 2013; 368:1388-1397April 11, 2013DOI: 10.1056/NEJMoa1204471
Persistent pain is measured by means of self-report, the sole reliance on
which hampers diagnosis and treatment. Functional magnetic resonance imaging
(fMRI) holds promise for identifying objective measures of pain, but brain
measures that are sensitive and specific to physical pain have not yet been
In four studies involving a total of 114 participants, we developed an
fMRI-based measure that predicts pain intensity at the level of the
individual person. In study 1, we used machine-learning analyses to identify
a pattern of fMRI activity across brain regions — a neurologic signature —
that was associated with heat-induced pain. The pattern included the
thalamus, the posterior and anterior insulae, the secondary somatosensory
cortex, the anterior cingulate cortex, the periaqueductal gray matter, and
other regions. In study 2, we tested the sensitivity and specificity of the
signature to pain versus warmth in a new sample. In study 3, we assessed
specificity relative to social pain, which activates many of the same brain
regions as physical pain. In study 4, we assessed the responsiveness of the
measure to the analgesic agent remifentanil.
In study 1, the neurologic signature showed sensitivity and specificity of
94% or more (95% confidence interval [CI], 89 to 98) in discriminating
painful heat from nonpainful warmth, pain anticipation, and pain recall. In
study 2, the signature discriminated between painful heat and nonpainful
warmth with 93% sensitivity and specificity (95% CI, 84 to 100). In study 3,
it discriminated between physical pain and social pain with 85% sensitivity
(95% CI, 76 to 94) and 73% specificity (95% CI, 61 to 84) and with 95%
sensitivity and specificity in a forced-choice test of which of two
conditions was more painful. In study 4, the strength of the signature
response was substantially reduced when remifentanil was administered.
It is possible to use fMRI to assess pain elicited by noxious heat in healthy
persons. Future studies are needed to assess whether the signature predicts
clinical pain. (Funded by the National Institute on Drug Abuse and others.)
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