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Amajor symptom in numerous medical conditions is pain which accounts for 80% ofthe reasons behind medical visits ( Voscopoulos & Lema., 2010). The internationalassociation for the study of pain describes pain as an uncomfortable sensationcaused by noxious stimulus or negative emotional experience (Bogduk &Merskey,1994). Pain is habitually dichotomised into chronic and acute .

Acutepain is usually caused by damage to tissues caused by harm or surgeries andusually 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 bodyagainst harm.  Although it is not alwayswelcomed, the experience of such pain serves some evolutionary purposes whichallows for survival (for example pain encourages one to change their behaviourand avoid the reoccurrence of such feeling). In term of evolution painendurance (one ability to cope with pain) is an adaptive trait which increasesone survival value (Bonavita & De Simone, 2011). Moreover, by some, pain isa positive outcome of a situation (for example someone who aims to gain muscleswould 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 thansix months (Voscopoulos & Lema, 2010).

In the 16th century painwas only thought to arise from noxious stimuli however in the 21stcentury pain such as acute pain has been reported to arise without previousinjuries. Despite having some positive connotation, the sensation of pain isoften despised when it comes to both the clinical and general population. Thereare various adverse consequences to pain, especially those that persist(Rashiq, Schopflocher, Taenzer, & Jonsson, 2008). The common negativeeffects such as  destructive impact onpsychological and physical wellbeing, lack of employment maintenance, anddinability to retain social functioning (Hadjistavropoulos et al.

,2011).Therefore studying its nature and modulation is of upmost importance. As theexperience of pain is subjective ( Aslaksen et al.,2007) , this essay is goingto 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 thebasic physiological aspect of pain processing), then it will look at thepsychological factors (focusing on attention and emotion) that modulates painand finally the essay will briefly examine areas for improvement in researchsuch as the social factors and discuss the importance of a biopsychosocialmodel when it comes to the modulation of pain. All the factors will bediscussed in conjunction with neuroscientific evidences provides by Functional MagneticResonance Imaging.TheNature of pain has been extensively debated in the literatures in the 17thand 19th century ( Moayedi & Davis.,2013 ; Melzack&Wall.

,1965). The gate control theory was formulated in the 20thcentury, 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 postulatedthat there is a linear relationship between sensory stimulus and the brainwhereby, peripheral sensory neurones specific to noxious stimulus (nociceptors& low-threshold mechanoreceptors (LTMRs)) in the body tissues produces animpulse that travel through specific pathway and projects to a specific brainarea “pain centre” in the brain (Moayedi & Davis.,2013).  Evidence supporting specificity of brain areasin pain processing has been reported by Segerdahland colleagues (2015 ).

They induced a continuing pain with capsaicin(irritant that produce burning sensation on skin tissues) and asked theparticipants to rate the intensity of their pain. They then correlated theparticipants response with the change in brain perfusion which was measure by Magnetic resonance imaging-based. The perfusion methodmeasure changes in regional cerebral blood flow without the need for a stimulus.

The results showed that as the pain intensity ratings of participants increasedso did the magnitude of cerebral blood flow in the dorsal posterior insula. Due to this activation, the researcherssuggested that dorsal posterior insula is a pain specific area in the brain.These results provide support for the relationship between noxious stimulus andthe brain as well as the gate control theory.

However, the result from thisstudy needs to be interpreted carefully as the design used lack statisticalpower as it has low sample size of seven participant and few data points duringscanning. Therefore, the analysis was underpowered and does not constitute avalid control for the pain experiment. Additionally, the proposition that thebrain has a pain centre was reported without taking into consideration thelarge number of studies examining brain mechanism relationship to pain. Neuroimagingdata has demonstrated in the past that brain areas of the brain that consist ofnociceptive neurones also contains non-nociceptive neurone and they cantherefore respond to noxious and neutral stimuli (Iannetti et al.,2013).

Contrasting evidence showing that pain is modulated indifferent brain areas has been reported (Iannetti et al.,2013; Wise et al.,2002).

Evidentially, Sprenger, Finsterbusch and Bulchel (2015) investigated thefunctional connectivity between the spinal cord and the brain during theprocessing of pain using Fmri. The experiment consisted of twenty healthyparticipants, who were stimulated by painful thermal stimuli at two different intensities(46.0 and 47.0°C)  on their left radialforearm. They used Presentation software (Neurobehavioral Systems) for stimuluscontrol and recording of pain rating.

They showed the interaction betweendorsal horn of the spinal cord and several brain structures; thalamus, primarysomatosensory cortex, and bilateral insula. More importantly, they observedsignificant functional connectivity with key structures of the descending painmodulatory system (periaqueductal gray matter, hypothalamus, and the amygdala).Whilst pain rating increased in participant, the intensity dorsal horn andperiaqueductal gray matter coupling were significant. This providephysiological evidence for the second aspect of the gate control theory wherethe pattern theory is taken into consideration. The patterntheory assumed that afferents neurones (neurones that projects to the centralnervous system) response to different type of stimuli, however whether it isperceived as a painful stimuli depends on the brain interpretation of thepattern of activity across the different nerve fibres ( Moayedi &Davis.,2013) .

The gate control theory proposes that the nociceptors and LTMRsproduces impulses that are transmitted to three regions in the spinal cords;.1) the substantia gelatinosa, 2) the dorsal column, and 3) a group of cellsthat they called transmission cells. They proposed that the substantiagelatinosa in the dorsal horn acts as a gate, which controls the transmissionof sensory information from the primary afferent neurons to transmission cellsin the spinal cord.

Therefore, the Gate Control Theory describes an ascendinggating mechanism which shows that pain can be modulated. Sprenger andcolleugues (2015) study evidence for a gatingmechanism of pain processing by the nervous system as the periaqueductal gray mattercan both facilitate or inhibit nociceptive inputs and acts as a final relay inthe control of descending pain facilitation( Millan,2002 ).This novel study is the first to measure spinal and corticalresponses to pain during the same experiment. Moreover. The gate control theorysuggests that the transmission of information can be reduces or blocked at thegate. Hence the severity of the painful stimuli is either decreased or notsensed at all.

This study showed how pain intensity can be modulated via spinalcord signalling. However, it does consist of some limitation in its sample sizeas well as methodological shortcoming such as the fact that the source of thespinal BOLD response is not fully understood yet. Although the gate theory provide an explanation for themodulation of acute pain it did not provide explanation for clinical disorderssuch as chronic pain and phantom limb pain (Melzack &Wall.,1965 ). Therefore, the theory was expanded, and it proposedthat, there are neuronal network pathways that are unique to everyone based ontheir genetic make-up and/or sensory input. The neural pathway is consistentlyproducing perceptual and motor output, however both output can be activated bystimuli or no stimuli.

This stipulates that the relationship between painexperience and actual reason for the pain is not linear (Melzack,2005). Thisexplanation changed the gate theory into the neuro-matrix theory which takesinto considerations the physiological and psychological factors that may affecton pain perception. Cognitive factors such as attention has been postulated to modulatesperception of pain intensity (Crombez, Van Ryckeghem, Eccleston, & VanDamme,2013).

The way in which attention modulate pain perception and intensityhas been demonstrated in cognitive studies (Van Ryckeghem, Crombez, Van Hulle,& Van Damme,2012; Bulcke, Van Damme, Durnez, & Crombez,2013) usingdifferent type of tasks e.g. stroop task, lazer task.The research suggests that unless an individual actively paysattention elsewhere the sensation of painful stimuli will take over that ofnon- painful ones.

The consensus of most researches is that painincreases when individual focuses on it (Quevedo & Coghill.,2007). Evidentially, Spenger and colleagues (2012) conducted a highresolution Fmri experiment on twenty participants. The participants wereintroduced to painful heat stimulation using a 30 3 30 mm3 Peltier-thermodewhile they were performing 1-back versus 2 back letter task (working memoryparadigm which assess high memory load versus low memory load). This allowedthem to investigate whether spinal cord’s BOLD response to thermal pain isassociated with attention as well as the level at which cognitive processesbegins to modify pain processing.

They found that during high working memoryload task, the pain intensity perception of the participants decreased.Moreover, the BOLD signal of the spinal cord demonstrated a decrease inresponse. Their results show that individual attention can affect their painexperience and that attention has a direct effect on the spinal cord responsehence the way in which the brain response.

This line with other neuroscientificevidence that shows that the insula along with other brain regions such as thehypothalamus and amygdala which are involved in the processing of attention arealso 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 theparticipants used. The participants used were solely males which decreases itsreliability as research has shown that male and female cope with paindifferently and their rating may depend on the experimenters’ gender (Aslaksenet al.,2007). Male subject often reports lowerpain intensity of pain when the experimenter is male.

Hence the study lacksecological validity. Despite the limitations, this type of findings has beenrobust in the attention-pain literature and posits clinical implication in thestudy of chronic pain; are chronic pain patient focusing on their pain andignoring other stimuli? and in research examining Attention deficit disorder(ADHD) whereby those who are inflicted by the disorder are more sensitive topain when off their medication (Treister, Eisenberg, Demeter, & Pud, 2013).Another common psychological factor that has an impact on oneexperience 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 anadapted version of Pavlovian delay conditioning task and Fmri. During theexperiment, the participants were given a visual signal which was alwaysfollowed by, nociceptive stimulation at low temperature to their left hand. Thesignal was used to induce expectation of pain which in turn causes mildanxiety.

In the second condition another visual signal which could either befollowed by high thermal or low thermal stimulation was presented to theparticipant with the goal of evoking high anxiety. The result of the studyshowed that anxiety related to pain increases pain intensity perception. Theevent-related Fmri measure shows that pain is modulated by anxiety. The twomain areas that showed the different changed in activation was the perigenual cingulate (affective area of anteriorcingulate cortex) (Bush, Luu, & Posner,2000) and the mid insula (shown tobe involved in the processing of anxiety attention and pain) (Wager &Barrett, 2017).

Moreover, the Hippocampal activation during pain maysignify that there are other non-pain specific processes occurs e.g. memory.There results support that as anxiety increase so did the activation in thedescending pain modulatory system. One can stipulate that the inhibitoryprocess is activated removing the analgesic effect of the system.  It has been reported that it under relatively high arousal levels that emotion canincrease pain, or decrease (Rhudy, Bartley & Williams, 2010)therefore data presented in the study may lack validity as what constitute ashigh arousal for one individual may differ for the other.

These findingshave important implications in disorders such as depression which is highlyinfluence by mood changes and body state arousal. Researches has shown thatover 50% of chronic pain sufferers suffers from depression and people that aredepressed are more likely to complain about pain without injury (Velly et al., 2011).  The effect of emotion on pain is now morediscussed in the literature and has been introduced as a cognitive treatmentplane for chronic pain.Furtherevidence for the role of emotion in pain processing comes from study examiningemotional empathy. Human has the innate ability to feel or at least empathisewith others emotion. Observing another person in pain and knowing that somethat you care about is in pain activates brain areas that processing emotionand pain (Jackson, Meltzoff & Decety,2005;Osborn & Derbyshire, 2009).

 A meta-analysisof Fmri studies where the relationship between empathy and pain were conductedby Lamm, Decety, & Singer (2011) andthey reported that bilateral anterior insula, anterior medial cingulate cortex,posterior anterior cingulate cortex constitutes a core network for painempathy, and that this pattern is observed among studies performed in differentcountries, on different MRI scanners, and using different types of paradigms. Specificevidence was reported by Decety, Echols, and Correll (2010). Using acombination of behavioural and neuroimaging measure they examined therelationship between empathy, stigma and pain. More importantly they wanted tofind out if pain perception is modulated by an individual stigmatised status orwhether they felt responsible for the stigma. The participants were scannedwhile they watch short video clips showing someone that is like the participant(healthy), a stigmatised individual who suffers from AID but is not responsiblefor their infection or someone that is stigmatised and responsible for their condition.After the MRI scanned was completed participants pain and empathy ratings wererecorded.

Their result showed that participants were more empathetic towardindividual who were accidently infected by AIDS than healthy and those who wereinfected because of their life choices. These results were further supported bytheir pain and empathy rating whilst they were watching the video as well astheir BOLD signal response which showed higher activity in brain regionsassociated with pain processing (right anterior insula, anterior midcingulatecortex, periaqueductal gray). The opposite was observed in the anteriormidcingulate cortex for individual responsible for their AID as compared withhealthy controls.  This study shows how thatone perception of pain intensity is dependant on their empathetic response. However,it does consist of some limitation is in relation to the experiment externalvalidity. The researcher postulated that their higher empathetic response AIDbias. However, the participant pool was intellectual who came from educationalbackground that endorse empathy and censure prejudice. Therefore, it ispossible that participants did not report the true extent of their emotions,therefore influencing the data collected.

 Furthermore, the participant was of young agewhich could have affect their level of stigmatisation and subsequently theirempathy rating. It has been previously reported that younger individual presentwith less stigmatisation that older ones. Additionally, this study reports effectsof attitudes and stigmatisation which are social construct on pain. Painresearches has focused on intrapersonal processes, both biological andpsychological, leaving the social dimensions out. Hence a working biopsychosocialmodel in research and practice is needed. This could help in the understandingof the full of scope of pain nature.

Pain is usually experienced in complexedsocial environments which impacts individual distress.  For example Hjern,Alfven & Östberg  (2007) conducted across-sectiona study by interviewing 2588 children between the age of 10-18. They defined psychosomatic pain asweekly recurring headache, and abdominal pain , whils school stressors weredefined as bullying, work pressure in school and being mistreated.

The foundthat the school stressors were correlated with affective emotions such asirritability , anxiety , insecurity and sadness. Bullying was a maindeterminant of such emotions. This paper shows that our social environementaffect our emotion and I viewed previously emotion affects pain.Thereforeone social situation could predict once response and perception to pain.

Furthermore the reaction of others in a patient social environment which wouldsubsequently impact on ones’ mood and behaviour of the individual need to betaken into consideration as this could have a positive implication in thetreatment program provided and cognitive therapy provided for the treatment ofchronic pain  (Gatchel, Peng, Peters, Fuchs, & Turk, 2007). Moreover thereis a lack of neuroscientific studies that examine the effect of one social environmentone emotion and pain experience.Inconclusion, Fmri Study has been widely use to study at the cortical areas thatare 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 thereforefurther electrophysiological is needed to test the Gate-control theory atneuronal level. During pain processing they all reported similar activations inthe : periaqueductal gray matter, hypothalamus, and the amygdala  .

These areas are also recruited during theprocessing of cognitive information such as attention and emotion. Overall, thedata shows us that “pain is all in the brain” is correct if it mean that painis process on both physiological and psychological levels. A painful experiencerelies on more than just the brain, it involves an individual genetic make up (neuronalconnection , personality ) , their cognitive functioning ; attention,emotion  and as well as their social environmentwhich can be a determinant in how the react/cope to the pain.

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