Pain
is an essential part of everyday human life, ensuring that people don’t heavily
wound themselves and indicating that there is a problem in the one’s body.
However pain, and especially chronic pain, can also be a, sometimes
debilitating, problem in itself. Furthermore, our current methods to deal with
pain can be addictive and not always helpful. Therefore, pinpointing the cause
of pain within the human brain could revolutionize the pain response system by
enabling the provision of targeted pain-response mechanisms that numb the pain
without the large side effects or addictiveness of drugs such as morphine.
However, if pain is a more complicated, dispersed reaction within the brain,
the production of methods to control pain would be similarly more complicated.
Thus, determining the method of pain response within the brain has direct,
human impacts.

            Researchers
have long hypothesized that there exists a “pain matrix” that (is the primary
area that) codes primarily for pain responses. However, there is a debate
within the neuroscience community regarding whether this pain matrix only
encodes painful stimuli or if it also encodes other non-pain, salient, and
somatosensory stimuli. Additionally, due to its simplicity and usefulness the
hypothesis of having a pain-specific region very seductive meaning that the
neuroscience community may have assumed for the pain matrix to exist without
very compelling evidence. Recent articles have been produced arguing both sides
and there also exist critiques of articles arguing for a specific area of the
brain encoding pain. For this reason, it is important and pertinent to look
into the existence of a pain matrix within the brain.

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Evidence
for a Pain-only Encoding Pain Matrix

One
study by Baliki et al. looked at the location of pain perception within the
brain and the difference in activation due to pain stimuli of different levels.
Using fMRI, analyzed with blood oxygenated level-dependent signal, on pain and
visual stimuli, fourteen people were asked to either estimate the magnitude of
a painful stimulus based or the length of visual stimulus. The pain stimuli
were related to increased brain activity in a large portion of the brain, specifically activating the
bilateral anterior insula, amygdalae, thalami, basal ganglia, and anterior
portions of anterior commissure as well as the ventral striatum much more than
the visual stimuli (1). Additionally, both stimuli activated the bilateral
insula, dementia pugilistica, ventral posterior nucleus, posterior parietal
cortex, and medial temporal cortices (likely activated as both of these stimuli
had a visual component), and had midline activations in the middle portions of
the  anterior commissure and
supplementary motor area (1). These results indicated that, although not all
areas that coded for pain were specific to pain, part of the insular cortex was
coded specifically for painful activity (1). However, it was simultaneously
found that, with regards to activation related to extracting estimated sizes,
the pain and visual stimuli activated the same regions (indicating that there
are specific regions that code for size estimates) (1). This study’s small
number of subjects as well as its lack of a different salient cue with which
the pain response could be compared leads to its findings holding slightly less
significance.

Another recent study by Segerdahl et al.
specifically implicated the posterior insula as an area specific to pain using
arterial spin-labeling quantitative perfusion imaging and MRI. This study used
seventeen subjects, scanned in two phases. First, the subjects scanned at a
baseline for seven minutes, followed by being scanned for twenty eight minutes
while capsaicin cream was applied (to stimulate pain)–the onset period–,
seven of which were at the pain peak–the peak period–and then being taken out
of the room. In the second phase (directly following the break at the end of
the first phase), the patients were scanned first without any adjustments for
seven minutes–the habituation period–, then with a warm water bottle applied
to the site upon which the capsaicin was applied for seven minutes–the
rekindle period–, and finally with a cold water bottle applied to the site
upon which the capsaicin was applied for seven minutes–the relief period.
Throughout the experiment, pain ratings were verbally taken. These same periods
were repeated using vibration stimuli (salient stimuli) instead of pain stimuli
for the purpose of determining if the activated areas of the brain were
activated due to saliency or pain. This study found that the dorsal posterior
insula specifically coded for pain response (and not other somatosensory
responses), making it one of the first studies to strongly come out stating
specifically that one area of the brain encoded only for pain responses (2).

 

Evidence Against a Pain-only Encoding
Pain Matrix

Due
to the high claims of Segerdahl et al.’s article, the neuroscientific community
highly critiqued the methods of the article and put the results into question.
The main problems they found with the article are as follows: (1) there is not
enough evidence in the article that the control stimulus was as salient as the
pain stimulus (3), (2) the intensity of the control stimulus, unlike that of
the pain stimulus, did not vary with time, not allowing for the response to be
measured against the intensity of the stimulus (3),  (3) not enough control subjects were used
(4), (4) there were no direct comparisons between the control and the pain (4),
(5) the researchers looked for a specific “spot” dedicated to pain, which is
questionable due to the large variability in “brain maps” between people (4),
and (6) the researchers neglected the wide body of research implying that pain
is, like most other bodily sensations, coded throughout the brain (4).

            In
a study similarly comparing a vibratory, non-pain stimulus to a painful heat
stimulus (in this case, with the addition of a neutral control), both the pain
and control stimuli activated similar regions of the primary and, to a lesser
extent, secondary somatosensory cortices. However, the pain stimulus activated
“a number of cortical and subcortical areas-including anterior cingulate
cortex, SMA, anterior insula, and basal thalamus-all contralateral to the
stimulated arm” (5). In general, the pain and vibration conditions activated
similar regions except for the activation of the anterior portion of the
contralateral insular cortex (5). The researchers reached the conclusion that
pain produces distributed activation. The pain stimulation was found to be
“more widely dispersed across both cortical and thalamic regions” than that of
the control stimulation (5). This research used PET scans alongside ratings of
stimuli from 1 to 100, with 50 being the pain threshold and 100 being extreme
pain. While this study found different results than Segerdahl et al.’s study,
it suffers from similar problems: the painful stimuli applied were more salient
than the vibratory, non-painful stimuli and there were few (in this case even
fewer-only 9) subjects. This study also brought up a separate potential
complicating factor for the research: patients feel anxiety prior to the
application of the stimuli. This study used the control (no stimulus) to
mitigate this problem, but this should still be noted as a potential reason for
some of the study’s results.    

            In
a different study, Mouraux et al. investigated if any parts of the pain matrix
were activated only by pain. This study took fMRI data, analyzed with blood
oxygenated level-dependent signal, on people experiencing painful stimuli,
other somatosensory stimuli, auditory stimuli, and visual stimuli during
stimulation and rating periods (of 8 and 2 minutes in duration respectively).
The study additionally rated the saliency of the four stimuli, finding that the
painful stimuli were 20% more salient than the non-painful stimuli (all of
which had approximately the same levels of saliency). While the majority of the
areas activated similar areas of the brain, the somatosensory areas activated
additionally areas of the brain (located in the post-central gyrus) (6).
Additionally, after separating the people into two groups and giving them more
or less salient stimuli, the researchers found that the activation was more
correlated to the saliency of the response than whether the response was a pain
response (6). All stimuli tested activated the thalamus, secondary
somatosensory cortex, the insula, and the anterior cingulate cortex in very similar
ways (6). In general, the researchers took this data to mean that the pain
matrix actually processes all somatosensory stimuli, not just pain stimuli (6).
They also concluded that due to their findings about the saliency of the
stimuli, “the “pain matrix” is partly, if not entirely, related to bottom–up
cognitive processes involved in saliency detection, arousal, and/or attentional
capture” (6).  Despite these rigorous
findings, this study also faces the problem of having very few participants (in
this case, fourteen people).

Conclusion

Having
evaluated the data both supporting and against a pain-specific part of the
brain, I find the evidence for a distributed network of pain-coding areas more
compelling. The studies that found that painful and nonpainful stimuli were
coded in similar ways had, to me, better methodologies–as they used more and
better non-pain stimuli to measure the pain stimuli against–and were larger in
number. That the main study showing that pain was specifically coded in one
area had multiple, valid criticisms also implies that the theory of specific
areas for pain is not fully true. Additionally, the acquisition of data
supporting the theory (that painful stimulation is not the only stimulation
that activates the pain matrix) occurs in multiple papers not specifically
investigating this information, lending more credence to this theory. This
theory additionally makes intuitive sense after learning about the fundamental
interconnectedness of the brain. Additionally, it seems that more recent
studies have argued against against the existence of a pain-encoding specific
region than have argued against it. This falls in line with the shifting
conception of the brain from that with regions that all have very specific and
unique functions to that with regions working together to encode specific
stimuli.

With
regards to the general methods of the studies, I found the use of vibrotactile
stimulation as either a control for or a comparison to pain stimulation to be
interesting, but not fully understandable as none of the articles explained the
reason for this useage. That the one study comparing salience between different
stimulation types found that pain stimulation was non-negligibly more salient
than other somatosensory stimulation leads me to question if vibrotactile
stimulation is a good counterweight to painful stimulation. Therefore, I hope
that more studies are conducted in this area specifically using more salient
non-painful stimulations. I also found the studies in which different levels of
salience were studied to be of particular interest and use. Especially
considering that the primary question regarding the coding of the pain matrix
is whether it codes for pain or salience, differentiating between levels of
stimulus and levels of activity within this region is of large importance. In
addition to more studies of this nature, having more studies with a larger
number of participants would allow for a larger ability to determine whether
the data gathered is generalizable to the whole population.

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