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A
major symptom in numerous medical conditions is pain which accounts for 80% of
the reasons behind medical visits ( Voscopoulos & Lema., 2010). The international
association for the study of pain describes pain as an uncomfortable sensation
caused by noxious stimulus or negative emotional experience (Bogduk &
Merskey,1994). Pain is habitually dichotomised into chronic and acute . Acute
pain is usually caused by damage to tissues caused by harm or surgeries and
usually last for a short period of time ranging from a few weeks to six months.
Acute pain is a mechanism of defence which allows the protection of one body
against harm.  Although it is not always
welcomed, the experience of such pain serves some evolutionary purposes which
allows for survival (for example pain encourages one to change their behaviour
and avoid the reoccurrence of such feeling). In term of evolution pain
endurance (one ability to cope with pain) is an adaptive trait which increases
one survival value (Bonavita & De Simone, 2011). Moreover, by some, pain is
a positive outcome of a situation (for example someone who aims to gain muscles
would see muscle pain as a sign of reward for their work at the gym)
(Meeusen,2009). Chronic pain can result from acute pain but lasts longer than
six months (Voscopoulos & Lema, 2010). In the 16th century pain
was only thought to arise from noxious stimuli however in the 21st
century pain such as acute pain has been reported to arise without previous
injuries. Despite having some positive connotation, the sensation of pain is
often despised when it comes to both the clinical and general population. There
are various adverse consequences to pain, especially those that persist
(Rashiq, Schopflocher, Taenzer, & Jonsson, 2008). The common negative
effects such as  destructive impact on
psychological and physical wellbeing, lack of employment maintenance, and
dinability to retain social functioning (Hadjistavropoulos et al.,2011).
Therefore studying its nature and modulation is of upmost importance. As the
experience of pain is subjective ( Aslaksen et al.,2007) , this essay is going
to discuss the different factors that affect and modulates one pain experience.
First the essay is going to look at the gate-control theory which provide the
basic physiological aspect of pain processing), then it will look at the
psychological factors (focusing on attention and emotion) that modulates pain
and finally the essay will briefly examine areas for improvement in research
such as the social factors and discuss the importance of a biopsychosocial
model when it comes to the modulation of pain. All the factors will be
discussed in conjunction with neuroscientific evidences provides by Functional Magnetic
Resonance Imaging.

The
Nature of pain has been extensively debated in the literatures in the 17th
and 19th century ( Moayedi & Davis.,2013 ; Melzack
&Wall.,1965). The gate control theory was formulated in the 20th
century, and revolutionised research in the field of pain (Melzack
&Wall.,1965). The theory was inspired from aspects of past theories; e.g.
Specificity theory and the pattern theory. The specificity theory postulated
that there is a linear relationship between sensory stimulus and the brain
whereby, peripheral sensory neurones specific to noxious stimulus (nociceptors
& low-threshold mechanoreceptors (LTMRs)) in the body tissues produces an
impulse that travel through specific pathway and projects to a specific brain
area “pain centre” in the brain (Moayedi & Davis.,2013).  Evidence supporting specificity of brain areas
in pain processing has been reported by Segerdahl
and colleagues (2015 ). They induced a continuing pain with capsaicin
(irritant that produce burning sensation on skin tissues) and asked the
participants to rate the intensity of their pain. They then correlated the
participants response with the change in brain perfusion which was measure by Magnetic resonance imaging-based. The perfusion method
measure changes in regional cerebral blood flow without the need for a stimulus.
The results showed that as the pain intensity ratings of participants increased
so did the magnitude of cerebral blood flow in the dorsal posterior insula. Due to this activation, the researchers
suggested that dorsal posterior insula is a pain specific area in the brain.
These results provide support for the relationship between noxious stimulus and
the brain as well as the gate control theory. However, the result from this
study needs to be interpreted carefully as the design used lack statistical
power as it has low sample size of seven participant and few data points during
scanning. Therefore, the analysis was underpowered and does not constitute a
valid control for the pain experiment. Additionally, the proposition that the
brain has a pain centre was reported without taking into consideration the
large number of studies examining brain mechanism relationship to pain. Neuroimaging
data has demonstrated in the past that brain areas of the brain that consist of
nociceptive neurones also contains non-nociceptive neurone and they can
therefore respond to noxious and neutral stimuli (Iannetti et al.,2013).

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Contrasting evidence showing that pain is modulated in
different brain areas has been reported (Iannetti et al.,2013; Wise et al.,2002).
Evidentially, Sprenger, Finsterbusch and Bulchel (2015) investigated the
functional connectivity between the spinal cord and the brain during the
processing of pain using Fmri. The experiment consisted of twenty healthy
participants, who were stimulated by painful thermal stimuli at two different intensities
(46.0 and 47.0°C)  on their left radial
forearm. They used Presentation software (Neurobehavioral Systems) for stimulus
control and recording of pain rating. They showed the interaction between
dorsal horn of the spinal cord and several brain structures; thalamus, primary
somatosensory cortex, and bilateral insula. More importantly, they observed
significant functional connectivity with key structures of the descending pain
modulatory system (periaqueductal gray matter, hypothalamus, and the amygdala).
Whilst pain rating increased in participant, the intensity dorsal horn and
periaqueductal gray matter coupling were significant. This provide
physiological evidence for the second aspect of the gate control theory where
the pattern theory is taken into consideration. The pattern
theory assumed that afferents neurones (neurones that projects to the central
nervous system) response to different type of stimuli, however whether it is
perceived as a painful stimuli depends on the brain interpretation of the
pattern of activity across the different nerve fibres ( Moayedi &
Davis.,2013) . The gate control theory proposes that the nociceptors and LTMRs
produces impulses that are transmitted to three regions in the spinal cords;.
1) the substantia gelatinosa, 2) the dorsal column, and 3) a group of cells
that they called transmission cells. They proposed that the substantia
gelatinosa in the dorsal horn acts as a gate, which controls the transmission
of sensory information from the primary afferent neurons to transmission cells
in the spinal cord. Therefore, the Gate Control Theory describes an ascending
gating mechanism which shows that pain can be modulated. Sprenger and
colleugues (2015) study evidence for a gating
mechanism of pain processing by the nervous system as the periaqueductal gray matter
can both facilitate or inhibit nociceptive inputs and acts as a final relay in
the control of descending pain facilitation
( Millan,2002 ).This novel study is the first to measure spinal and cortical
responses to pain during the same experiment. Moreover. The gate control theory
suggests that the transmission of information can be reduces or blocked at the
gate. Hence the severity of the painful stimuli is either decreased or not
sensed at all. This study showed how pain intensity can be modulated via spinal
cord signalling. However, it does consist of some limitation in its sample size
as well as methodological shortcoming such as the fact that the source of the
spinal BOLD response is not fully understood yet.

Although the gate theory provide an explanation for the
modulation of acute pain it did not provide explanation for clinical disorders
such as chronic pain and phantom limb pain (Melzack &Wall.,1965 ). Therefore, the theory was expanded, and it proposed
that, there are neuronal network pathways that are unique to everyone based on
their genetic make-up and/or sensory input. The neural pathway is consistently
producing perceptual and motor output, however both output can be activated by
stimuli or no stimuli. This stipulates that the relationship between pain
experience and actual reason for the pain is not linear (Melzack,2005). This
explanation changed the gate theory into the neuro-matrix theory which takes
into considerations the physiological and psychological factors that may affect
on pain perception. Cognitive factors such as attention has been postulated to modulates
perception of pain intensity (Crombez, Van Ryckeghem, Eccleston, & Van
Damme,2013). The way in which attention modulate pain perception and intensity
has been demonstrated in cognitive studies (Van Ryckeghem, Crombez, Van Hulle,
& Van Damme,2012; Bulcke, Van Damme, Durnez, & Crombez,2013) using
different type of tasks e.g. stroop task, lazer task.

The research suggests that unless an individual actively pays
attention elsewhere the sensation of painful stimuli will take over that of
non- painful ones. The consensus of most researches is that pain
increases when individual focuses on it (Quevedo & Coghill.,2007). Evidentially, Spenger and colleagues (2012) conducted a high
resolution Fmri experiment on twenty participants. The participants were
introduced to painful heat stimulation using a 30 3 30 mm3 Peltier-thermode
while they were performing 1-back versus 2 back letter task (working memory
paradigm which assess high memory load versus low memory load). This allowed
them to investigate whether spinal cord’s BOLD response to thermal pain is
associated with attention as well as the level at which cognitive processes
begins to modify pain processing. They found that during high working memory
load task, the pain intensity perception of the participants decreased.
Moreover, the BOLD signal of the spinal cord demonstrated a decrease in
response. Their results show that individual attention can affect their pain
experience and that attention has a direct effect on the spinal cord response
hence the way in which the brain response. This line with other neuroscientific
evidence that shows that the insula along with other brain regions such as the
hypothalamus and amygdala which are involved in the processing of attention are
also activated during processing of painful stimuli (Bantick et al., 2002; Valet et al.,2004). One of the main limitation of the paper is the gender of the
participants used. The participants used were solely males which decreases its
reliability as research has shown that male and female cope with pain
differently and their rating may depend on the experimenters’ gender (Aslaksen
et al.,2007). Male subject often reports lower
pain intensity of pain when the experimenter is male. Hence the study lacks
ecological validity. Despite the limitations, this type of findings has been
robust in the attention-pain literature and posits clinical implication in the
study of chronic pain; are chronic pain patient focusing on their pain and
ignoring other stimuli? and in research examining Attention deficit disorder
(ADHD) whereby those who are inflicted by the disorder are more sensitive to
pain when off their medication (Treister, Eisenberg, Demeter, & Pud, 2013).

Another common psychological factor that has an impact on one
experience of pain is emotion (especially negative ones and memories) (Villemure,
& Bushnell,2009). For example, Ploghaus and colleagues
(2001) examine the modulating effect of anxiety on pain perceptions using an
adapted version of Pavlovian delay conditioning task and Fmri. During the
experiment, the participants were given a visual signal which was always
followed by, nociceptive stimulation at low temperature to their left hand. The
signal was used to induce expectation of pain which in turn causes mild
anxiety. In the second condition another visual signal which could either be
followed by high thermal or low thermal stimulation was presented to the
participant with the goal of evoking high anxiety. The result of the study
showed that anxiety related to pain increases pain intensity perception. The
event-related Fmri measure shows that pain is modulated by anxiety. The two
main areas that showed the different changed in activation was the perigenual cingulate (affective area of anterior
cingulate cortex) (Bush, Luu, & Posner,2000) and the mid insula (shown to
be involved in the processing of anxiety attention and pain) (Wager &
Barrett, 2017). Moreover, the Hippocampal activation during pain may
signify that there are other non-pain specific processes occurs e.g. memory.
There results support that as anxiety increase so did the activation in the
descending pain modulatory system. One can stipulate that the inhibitory
process is activated removing the analgesic effect of the system.  It has been reported that it under relatively high arousal levels that emotion can
increase pain, or decrease (Rhudy, Bartley & Williams, 2010)
therefore data presented in the study may lack validity as what constitute as
high arousal for one individual may differ for the other. These findings
have important implications in disorders such as depression which is highly
influence by mood changes and body state arousal. Researches has shown that
over 50% of chronic pain sufferers suffers from depression and people that are
depressed are more likely to complain about pain without injury (Velly et al., 2011).  The effect of emotion on pain is now more
discussed in the literature and has been introduced as a cognitive treatment
plane for chronic pain.

Further
evidence for the role of emotion in pain processing comes from study examining
emotional empathy. Human has the innate ability to feel or at least empathise
with others emotion. Observing another person in pain and knowing that some
that you care about is in pain activates brain areas that processing emotion
and pain (Jackson, Meltzoff & Decety,2005;
Osborn & Derbyshire, 2009).  A meta-analysis
of Fmri studies where the relationship between empathy and pain were conducted
by Lamm, Decety, & Singer (2011) and
they reported that bilateral anterior insula, anterior medial cingulate cortex,
posterior anterior cingulate cortex constitutes a core network for pain
empathy, and that this pattern is observed among studies performed in different
countries, on different MRI scanners, and using different types of paradigms. Specific
evidence was reported by Decety, Echols, and Correll (2010). Using a
combination of behavioural and neuroimaging measure they examined the
relationship between empathy, stigma and pain. More importantly they wanted to
find out if pain perception is modulated by an individual stigmatised status or
whether they felt responsible for the stigma. The participants were scanned
while they watch short video clips showing someone that is like the participant
(healthy), a stigmatised individual who suffers from AID but is not responsible
for their infection or someone that is stigmatised and responsible for their condition.
After the MRI scanned was completed participants pain and empathy ratings were
recorded. Their result showed that participants were more empathetic toward
individual who were accidently infected by AIDS than healthy and those who were
infected because of their life choices. These results were further supported by
their pain and empathy rating whilst they were watching the video as well as
their BOLD signal response which showed higher activity in brain regions
associated with pain processing (right anterior insula, anterior midcingulate
cortex, periaqueductal gray). The opposite was observed in the anterior
midcingulate cortex for individual responsible for their AID as compared with
healthy controls.  This study shows how that
one perception of pain intensity is dependant on their empathetic response. However,
it does consist of some limitation is in relation to the experiment external
validity. The researcher postulated that their higher empathetic response AID
bias. However, the participant pool was intellectual who came from educational
background that endorse empathy and censure prejudice. Therefore, it is
possible that participants did not report the true extent of their emotions,
therefore influencing the data collected.  Furthermore, the participant was of young age
which could have affect their level of stigmatisation and subsequently their
empathy rating. It has been previously reported that younger individual present
with less stigmatisation that older ones. Additionally, this study reports effects
of attitudes and stigmatisation which are social construct on pain. Pain
researches has focused on intrapersonal processes, both biological and
psychological, leaving the social dimensions out. Hence a working biopsychosocial
model in research and practice is needed. This could help in the understanding
of the full of scope of pain nature. Pain is usually experienced in complexed
social environments which impacts individual distress.  For example Hjern,
Alfven & Östberg  (2007) conducted a
cross-sectiona study by interviewing 2588 
children between the age of 10-18. They defined psychosomatic pain as
weekly recurring headache, and abdominal pain , whils school stressors were
defined as bullying, work pressure in school and being mistreated. The found
that the school stressors were correlated with affective emotions such as
irritability , anxiety , insecurity and sadness. Bullying was a main
determinant of such emotions. This paper shows that our social environement
affect our emotion and I viewed previously emotion affects pain.Therefore
one social situation could predict once response and perception to pain.
Furthermore the reaction of others in a patient social environment which would
subsequently impact on ones’ mood and behaviour of the individual need to be
taken into consideration as this could have a positive implication in the
treatment program provided and cognitive therapy provided for the treatment of
chronic pain  (Gatchel, Peng, Peters, Fuchs, & Turk, 2007). Moreover there
is a lack of neuroscientific studies that examine the effect of one social environment
one emotion and pain experience.

In
conclusion, Fmri Study has been widely use to study at the cortical areas that
are involved in pain processing (Sprenger,
Finsterbusch and Bulchel (2015) ;Sprenger et al.,2012; Ploghaus et al.,2001)
. However one down side of Fmri , is that it cannot measure neuronal activity  due to its limited spatial resolution therefore
further electrophysiological is needed to test the Gate-control theory at
neuronal level. During pain processing they all reported similar activations in
the : periaqueductal gray matter, hypothalamus, and the amygdala  . These areas are also recruited during the
processing of cognitive information such as attention and emotion. Overall, the
data shows us that “pain is all in the brain” is correct if it mean that pain
is process on both physiological and psychological levels. A painful experience
relies on more than just the brain, it involves an individual genetic make up (neuronal
connection , personality ) , their cognitive functioning ; attention,
emotion  and as well as their social environment
which can be a determinant in how the react/cope to the pain.

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