Chronic pain was originally defined as pain that has lasted 6 months or longer. It is now defined as pain that persists longer than the normal course of time associated with a particular type of injury. This constant or intermittent pain has often outlived its purpose, as it does not help the body to prevent injury.

Causes

Chronic pain is essentially caused by the bombardment of the central nervous system (CNS) with nociceptive impulses, which causes changes in the neural response. The pain subsequently provokes changes in the behavior of the patient, and the development of fear-avoidance strategies. As a result, the patient may also become physically atrophied and deconditioned. However, it is important to remember that chronic pain is multifactorial, with the underlying biological changes affecting physical and psychosocial factors.

Pain is usually elicited by the activation of specific nociceptors ('nociceptive pain'). However, it may also result from injury to sensory fibres, or from damage to the CNS itself ('neuropathic pain'). Although acute and subchronic, nociceptive pain fulfils a warning role, chronic and/or severe nociceptive and neuropathic pain is maladaptive.

Types

It  discusses chronic pain in two categories: malignant and non-malignant.

• Pain associated with malignancy can be caused by the cancer itself or by treatment.
• Non-malignant pain includes a variety of causes: arthritis, neuropathy/neuralgia, back pain from injury or disorders (cervical stenosis, degenerative disc disease, other disc disorders, etc), migraines and other types of headaches, abdominal pain from chronic pancreatitis, bowel disorders, etc; pelvic pain from various conditions (endometriosis, interstitial cystitis, etc); and also diffuse conditions such as fibromyalgia, reflex sympathetic dystrophy, lupus and other systemic autoimmune/connective tissue conditions, multiple sclerosis and some other neuromuscular conditions.

Chronic pain can occur anywhere in the body; this list includes only a few examples of conditions that can cause chronic pain.

The most common symptoms are a tingling sensation near or around the area where the operation was performed, sharp shooting pains, severe aches after much movement, constant 'low ache' all day and sometimes a general 'weak' feeling.

Contrary to popular belief, all pain is real. This may seem like an obvious statement, but people with chronic pain are sometimes treated as if their chronic pain is either imaginary or exaggerated. In some cases, they feel like they have to prove their chronic pain to their friends, family and doctors. Some patients are told by their doctor that there is no reason for the chronic pain and therefore “it cannot be that bad”.

Chronic pain  is a personal experience and cannot be measured like other problems in medicine, such as a broken leg or an infection. For instance, a broken leg can be confirmed by an X-ray and an infection by a blood test measuring white blood cell count. Unfortunately, there is no medical test to measure chronic pain levels.

To make matters more challenging for the patient, for many chronic pain problems there is no objective evidence or physical findings to explain the pain. Thus, many chronic pain sufferers go from one doctor to the next searching for explanations. This process can lead to unnecessary evaluations and treatments, in addition to putting the patient at risk for actually being harmed or made worse by the healthcare profession.

Everyone experiences and expresses pain differently. Two people with the exact same injury will feel and show their pain in unique ways depending on a number of things such as:

• The situation in which the pain occurs
• Thoughts about the chronic pain, such as “this is nothing serious” versus “this pain could kill me”
• Emotions associated with the chronic pain, such as depression and anxiety versus hopefulness and optimism
• Cultural influences determining whether a person is to be more stoic or more dramatic in showing pain to others

The newest theories of chronic pain can now explain, on a physiological level, how and why people experience pain differently.

Modern theories of chronic pain

The specificity theory of pain

In the 16th century, the French philosopher and mathematician Rene Descartes proposed one of the original theories of pain. His theory proposed

This theory - the “specificity theory” - is generally accurate when applied to certain types of injuries and the acute pain associated with them.

Problems with specificity theory of pain

Various clinical observations have proven the specificity theory to be inadequate to explain chronic pain. Dr. Henry Beecher, who worked with severely wounded soldiers during World War II, was one of the first doctors to question the theory. He observed that only one out of five soldiers carried into a combat hospital complained of enough pain to require morphine. These soldiers were not in a state of shock, nor were they unable to feel pain—indeed, they complained when the IV lines were placed.  They found that severity of wound was not related to the intensity of pain. Also he found that the pain depends upon the meaning attached to the injury. It was found that the civilian with the same amount of injury as the soldier in war was having, the civilian required more morphiene. Also ,how hypnosis can be used as anesthesia is not been explained by this theory .

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Modern Ideas: The Gate Control Theory of chronic pain

Due to the observations that raised questions, a new theory of pain was developed in the early 1960s to account for the clinically recognized importance of the mind and brain in pain perception. It is called the gate control theory of pain, and it was initially developed by Ronald Melzack and Patrick Wall.

Although the theory accounts for phenomena that are primarily mental in nature - that is, pain itself as well as some of the psychological factors influencing it - its scientific beauty is that it provides a physiological basis for the complex phenomenon of pain. It does this by investigating the complex structure of the nervous system, which is comprised of the following two major divisions:

• Central nervous system (the spinal cord and the brain)
• Peripheral nervous system (nerves outside of the brain and spinal cord, including branching nerves in the torso and extremities, as well as nerves in the lumbar spine region)

Gates open or closed depending upon the number of factors

In the gate control theory, before they can reach the brain these pain messages encounter “nerve gates” in the spinal cord that open or close depending upon a number of factors (possibly including instructions coming down from the brain). When the gates are opening, pain messages “get through” more or less easily and pain can be intense. When the gates close, pain messages are prevented from reaching the brain and may not even be experienced.

Although no one yet understands the details of this process or how to control it, the following concepts are presented to help explain why various treatments are effective and how to find solutions to chronic back pain.

Sensory nerves bring information about pain, heat, cold and other sensory phenomena to the spinal cord from various parts of the body. At least two types of nerve fibers are thought to carry the majority of pain messages to the spinal cord:

• A-delta nerve fibers, which carry electrical messages to the spinal cord at approximately 40 mph (“first” or “fast” pain).
• C-fibers, which carry electrical messages at approximately 3 mph to the spinal cord (“slow” or “continuous pain”)

A good example of how these respective nerve fibers work is the activation of the A-delta nerve fibers followed by the activation of the slower C-fibers. The activation of other types of nerve fibers can modify or block the sensation of pain.

Sensory nerve fibres faster than A- delta fibres prevents pain

After hitting one’s elbow or head, rubbing the area seems to provide some relief. This activates other sensory nerve fibers that are even “faster” than A-delta fibers, and these fibers send information about pressure and touch that reach the spinal cord and brain to override some of the pain messages carried by the A-delta and C-fibers.

The action of these other types of nerve fibers helps to explain why treatments such as massage, heat or cold packs, transcutaneous nerve stimulation, or even acupuncture are often effective in treating back pain..

Factors determining how the spinal nerve gates will manage pain

Many factors determine how the spinal nerve gates will manage the pain signal. These factors include the intensity of the pain message, competition from other incoming nerve messages (such as touch, vibration, heat, etc), and signals from the brain telling the spinal cord to increase or decrease the priority of the pain signal. Depending on how the gate processes the signal, the message can be handled in any of the following ways:

• Allowed to pass directly to the brain
• Altered prior to being forwarded to the brain (for instance, influenced by expectations)
• Prevented from reaching the brain (for instance, by hypnosis-induced anesthesia)

Once a pain signal reaches the brain, a number of things can happen. Certain parts of the brain stem (which connects the brain to the spinal cord) can inhibit or muffle incoming pain signals by the production of endorphins, which are morphine-like substances that occur naturally in the human body. Stress, excitement, and vigorous exercise are among the factors that may stimulate the production of endorphins. The impact of endorphins is why athletes may not notice the pain of a fairly serious injury until the “big” game is over. It is also why regular low-impact aerobic exercise (e.g. a riding stationary bike) can be an excellent method to help control chronic back pain.

Pain messages may also be directed along a variety of pathways in the brain.

• For instance, a “fast” pain message (A-delta fiber) is relayed by the spinal cord to specific locations in the brain, namely the thalamus and cerebral cortex. The cortex is the portion of the brain where higher thinking takes place. A fast pain message reaches the cortex quickly and prompts immediate action to reduce the pain or threat of injury.
• In contrast, chronic pain tends to move along a “slow” pathway (C-fiber). Slow pain tends to be perceived as dull, aching, burning, and cramping. Initially, the slow pain messages travel along the same pathways as the fast pain signals through the spinal cord. Once they reach the brain, however, the slow pain messages take a pathway to the hypothalamus and limbic system. The hypothalamus is responsible for the release of certain stress hormones in the body, while the limbic system is responsible for processing emotions. This is one reason why chronic back pain is often associated with stress, depression, and anxiety. The slow pain signals are actually passing through brain areas that control these experiences and emotions.

The brain also controls pain messages by attaching meaning to the personal and social context in which the pain is experienced. This occurs in the cortex. As we have seen previously, soldiers who are wounded in combat may display much less pain than similarly wounded civilians involved in accidents. The meaning attached to the situation seems to be the important difference.

Opening and closing the pain gates for chronic pain

. The brain can send signals down the spinal cord to open and close the nerve gates.

In times of anxiety or stress, descending messages from the brain may actually amplify the pain signal at the nerve gate as it moves up the spinal cord. Alternatively, impulses from the brain can “close” the nerve gate, preventing the pain signal from reaching the brain and being experienced as pain.

The events and conditions that may open the pain gates and cause more suffering include:

• Sensory factors, such as injury, inactivity, long-term narcotic use, poor body mechanics, and poor pacing of activities
• Cognitive factors, such as focusing on the chronic pain, having no outside interests or distractions, worrying about the pain, and other negative thoughts
• Emotional factors, such as depression, anger, anxiety, stress, frustration, hopelessness, and helplessness.

Alternatively, influences that can close the pain gates and reduce suffering include:

• Sensory factors, such as increasing activities, short-term use of pain medication, relaxation training and meditation.
• Cognitive factors, including outside interests, thoughts that help the patient cope with the pain, and distracting oneself from the chronic pain.
• Emotional factors, such as having a positive attitude, overcoming depression, feeling reassured that the pain is not harmful, taking control of one’s chronic pain and life, and stress management

Chronic pain is a subjective experience and has not only physical, but also psychological and social dimensions Among the different factors relevant to the psychological assessment and treatment of chronic pain, those of a cognitive nature play a prominent role, due in large part to the fact that pain is a perceptual phenomenon. Indeed, cognitive factors are largely responsible for the final (cortical) part of the perception process, so that, without subtracting importance from the more sensorial and even emotional aspects of pain, the final integrating point is cognitive in character.

Of the different cognitive variables that can mediate in the experience of pain,  few variables are selected that have greatest relevance to chronic pain.

Pain prevalence and impaired cognition:

Pain prevalence did not differ between the communicative resident with normal cognition (48.7%), mildly impaired cognition (46.5%), or severely impaired cognition (42.9%). However, the latter 2 groups reported more acute pain than those with normal cognition (7.9% to 14.1% vs. 2.5%). Those with impaired cognition reported constant pain more often, reported fewer total sites of pain, and had more frequent and more severe pain. Regardless of cognitive status, 73.3% to 100% of residents had significant scores on depression or anxiety measures when they reported pain-related mood disturbance. Pain-related reduction in activity was associated with a lower Human Activities Profile score. Sixteen of 36 uncommunicative residents had pain on the Pain Assessment in Advanced Dementia and at least 12 of them had significant mood disturbance.  They found that  Cognitive status does not affect pain prevalence; however, it affects the chronicity and characteristics of reported pain. Self-report of pain-related mood involvement is associated with significant mood scores.( Leong and Nuo ,2007)

Older adults with chronic low back pain demonstrated impaired neuropsycholgical performance as compared with pain-free older adults. Further, pain severity was inversely correlated with Neuropsycholgical performance, and Neuropsychological performance mediated the relationship between pain and physical performance ( Weiner et al.,2006).

In a subset of chronic pain disorder patients there were disturbances of mood , sleep, energy, libido, memory/concentration, behaviour and stress tolerance.( Rome and Rome , 2000)

Cancer pain and cognitive functions:

 Cancer survivors did not differ from persons without cancer on the cognitive functions.( Keating et al., 2005).

 Chronic pain in rats impaired spatial learning and memory function

Chronic pain stress induced by CFA impairs the spatial learning and memory function in neonatal rats. These effects might exert through down-regulating Bcl-2 and BDNF mRNA expression in the hippocampus (Li et al , 2005)

Causal attributions and beliefs about pain

Causal attributions and   beliefs that the pain is caused by external factors like luck or organic  causes increases the perception of pain ( Demjen and Bakel, 1981; ). The patients who believed that pain is a mysterious phenomenon apart from poor adherence of treatment also presented low self esteem and high level of somatization( Williams and Thorn, 1989). Also they used lower coping strategies

( Williams and Keefe, 1991)

Locus of control and pain

High internal locus of control present active coping strategies with regard to their pain (Brown and Nicassio, 1987; Crisson and Keefe, 1988) while patients with strong beliefs in the luck presented higher level of psychological  unease, feel more helplessness and tend to use more passive strategies with pain ( Crisson and Keefe.,1988).

Impaired attention and pain

Glass (2006) found that fibromyalgia patients have impaired control of attention, due to chronic pain. Neuroimaging studies demonstrated cerebral abnormalitites and pattern of increases neural recruitment during cognitive tasks. Some chronic pain patients did show scores suggestive of attentional impairment( Etherton et al 2006). There is a poor attention to chronic pain due to osteoarthritis in community-dwelling elders with cognitive impairment.( Cornali et al, 2006)

Chronic non-malignant pain patients (N=91) treated in a multidisciplinary pain centre were compared with age and sex matched healthy volunteers (N=64).It was found that Continous reaction time and Finger tapping test  were impaired in the total patient sample. Treatment with opioids was associated with poorer performance of paced auditory serial addition task. ( Sijogren et al 2005).  Dick et al (2002) found that the patients with fibromyalgia, rheumatoid arthritis and musculoskeletal pain patients have impaired cognitive functioning on the test sensitive to attention.

 Decrease in attention in the rats with colotis( chronic visceral inflammatory state of pain).

In  a study colitis was induced in rats by an emema containing 2,4,6 trinitorbenzen sulfunic acid and it was found that rats with colitis had decreased attention level but there was no change in their locomotor activity and interest in the environment on memory encoding. ( Mellicamps et al, 2004)

Slow information processing and pain

Patients with chronic fatigue syndrome  have slow information processing as found in the study by Glass (2006). The results  of a study highlighted (Moseley et al , 2005)that the differences between acute and chronic pain and may reflect a bias in information processing in acute pain toward the affected part. Both pain and the expectation of pain increased response time  to recognize the opposite hand. The findings are consistent with a bias in information processing toward the painful or impending painful hand.( Hudson et al, 2006).

In  a study, it was found that diagnosed chronic pain patients demonstrated a recall bias away from depression related  stimuli while the non – diagnosed chronic patients did not. The diagnosed ankylosing spondylitis also showed a bias toward sensory stimuli perhaps reflecting the presence of an enduring and over-riding pain.( Wells et al 2003).

In a study it was found that processing biases extend beyond the healing and adaptive processes to enmesh the self schema with pain and illness schemas could maintain or exacerbate distress and illness behavior in patients with chronic pain( Pincus and Morley, 2001)

Memory impairment and Pain

Fibromyalgia patients showed significant deficits on memory and vocabulary deficits while they were intact in information processing (Park et al ,2001). This indicated that the cognitive deficits were not global.

In a study it was found that the patients with fibromyalgia had  more complaints of memory and reported more fatigue, pain and depression than with the other groups. However, after controlling for fatigue, pain and depression neuropsychological tests did not vary.  (Suhr, 2003).

In a study the results indicated that patients with Fibromyalgia Syndrome  performed more poorly on tests of immediate and delayed recall, and sustained auditory concentration, and their ratings of both their memory abilities and sleep quality were lower than those of controls( Grace et al 1999).

            Ling et al (2007) compared  50 patients of chronic pain and 50 pain free patients . They found that participants with chronic pain had significantly impaired short term memory, which was evident even after the use of analgesic and drugs.

Grisart et al(2006) found that the process of attention demanding cognitive processes such as recollection is significantly lower in patients with chronic pain as compared to controls.

In a study on a questionnaire designed to be more specific to memory complaint in chronic pain patients, differences in memory complaint between pain patients and controls were found, even after the effects due to depression were statistically removed. Although pain patients often attribute their memory problems to codeine use and/or psychoactive medications, there was no support for this in the present study. Within the limitations of this study, these findings suggest that memory complaints may be related not only to depression but also to the presence of chronic pain. Further research in this area is needed.(Schnurr and MacDonald, 1995)

 The topo-kinesthetic memory test seemed to discriminate medication overuse headache  patients and chronic tension type headache patients from healthy volunteers and found  to be related to pain scores .( Pini et al, 2005)

Reports of memory functioning by patients with chronic pain.

In a study the regression analyses showed that depression accounted for the largest proportion of variance in memory complaints (35%) followed by anxiety (6%) and rumination (2%). The results of this study support the hypothesis that emotional distress (depression and anxiety) plays an important role in memory complaints in patients with chronic pain, as well as rumination, the intrusive component of catastrophizing.

Auotobiographical memory for previously painful events

 Kelly et al (2006) revealed that a putative neural mechanism for the retrieval of autobiographical memories of previously painful events , may provide a means of cognitive reappraising a painful episode without physically re -experiencing it

Selective memory for pain

 Cognitive bias , such as selective memory for pain related information is frequently observed in chronic patients. ( Edwards et al ,1992; Pincus et al.1993))|However , Busch et al (2006) found that on pain related tasks patients performed significantly worse than controls although they performed equally well on neutral pictorial  memory game. They explained that perhaps they were cognitively avoiding the painful stimuli.

Experimental muscle pain does not affect dexterity:

In a study it was found that there was no significant difference in the performance of either task (a modified Purdue pegboard test and the precision grip-lift task), when the muscle was painful, indicating that acute experimental muscle pain does not affect dexterity. (Smith et al , 2006)

Conscious and automatic uses of memory in chronic pain patients

 In a study the procedure permitted  to separate the contribution of controlled processes from automatic processes operating within a memory task. The results showed a significant decrease of controlled processes in chronic pain patients. Furthermore for both groups, automatic processes contribute in a similar extent to the memory performance. The estimates of controlled processes in the chronic pain patients are significantly related to the fear of pain and catastrophic beliefs.( Grisart, Van der Linden, 2001)

Controlled processes are more strongly affected in fibromyalgia patients related to the group with localized pain. ( Grisart et al ,2002).

Patients with fibromyalgia reported lower memory capacity and more detoriation than the control group.( Glass et al , 2005)

Hypervigilance and attentional fixedness in chronic musculoskeletal pain

In a study it was  found that  participants had difficulty disengaging attention from affective pain and health catastrophe words but there were no significant interactions between clinical status and threat word type observed for any of the indices of selective attention derived from the dot-probe task . Findings were not influenced by individual differences in mood, anxiety, or fear of pain. Correlational analyses of the standard (unmasked) Stroop interference index and dot-probe indices of selective attention revealed a consistent lack of significant association, suggesting that the 2 tasks might be measuring different phenomena. Taken together, these findings provided evidence that chronic pain patients and healthy control participants do not differ in the way they attend to threatening linguistic stimuli.( Asmudson et al, 2005).

 In another study it was revealed that there was no evidence of pain related selective attention  as a function of pain ,although they did reveal hyper vigilance of all word types on dot probe task, when compared with low fear of pain patients. The authors concluded that fear of pain can be used to categorise people into groups more or less vulnerable to disabling effects of pain. ( Asmundson and Hadjustavropoulos, 2007).

 Andersson and Haldrup (2003) found  in a study  that the patients’s showed a weak  stroop interference effect with slower reaction time  to pain words in the patient group, but they did not differ significantly from control. Both the groups , patients and normals were slower on threat words and displayed the classical stroop interference effect for color words  ( Andersson and Haldrup,2003)

The relationship between pain and mental flexibility in older adult pain clinic patients.

In community dwelling older adults, neither pain nor mood was associated with measures of short-term memory or information-processing speed. However, pain severity was associated with decreased performance on a test of number-letter switching, indicating a relationship between pain and mental flexibility.( Karp et al, 2006)

Enhanced presynaptic neurotransmitter release in the anterior cingulate cortex of mice with chronic pain

The anterior cingulate cortex (ACC) is a forebrain structure known for its roles in learning and memory. Recent studies show that painful stimuli activate the prefrontal cortex and that brain chemistry is altered in this area in patients with chronic pain. Zhao et al ( 2006) found  strong evidence that presynaptic alterations caused by peripheral inflammation contribute to memory impairments after injury in mice.

Effect of chronic nonmalignant pain on highway driving performance.

The results  of a study demonstrated that a subset of chronic nonmalignant pain patients had standard deviation of lateral positions that were higher than the matched healthy controls, indicating worse highway driving performance. Overall, there was a statistically significant difference in highway driving performance between the groups. Further, chronic nonmalignant pain patients rated their subjective driving quality to be normal, although their ratings were significantly lower than those of the healthy controls. No significant effects were found on the laboratory tests.( Veldhuijzen et al, 2006)

Predictors of neurocognitive performance in chronic pain patients

The full model predicting attention and concentration was found to be significant in a study where as, there was no significant contribution of pain severity, psychological distress, or the Pain Severity x Psychological Distress interaction to the prediction of attention and concentration scores after controlling for the effect of years of formal education.( Iezzi et al ,2004)

Chronic pain and emotional decision making task

Since human brain imaging studies show that brain regions critical for emotional decision making task are also involved in chronic pain so Apkarian et al (2004) hypothesized that the performance on this will be impaired. They found that the patient’s performed poorly as compared to the normal controls on the emotional decision making task. However  other cognitive abilities such as attention, short term memory and general intelligence was found to be normal in chronic pain patients.

Memory distortion during acute and chronic pain recalling.

 Matera et al(2003) proposed  that the patients do not remember initial pain correctly- either they under estimate it or overestimate it. They found in a study that it was inversely related  to the initial pain intensity.

Memories of chronic pain and perceptions of relief

In a study it was found that ratings of relief increased over time but true changes in pain were not related to  relief scores. Almost all patients have reported relief even those whose pain was increased. Hence it was concluded that perceived relief do not necessarily reflect  true changes in pain.( Feine et al, 1998).

Neuroendochrine functions and fibryomyalgia:

 Sephton et al (2003) found that neuroendochrine function and depression had significant independent associations with memory functions. Their findings suggested that a basic disorder of endochrine stress responses may contribute to the cognitive symptoms experienced by fibromyalgia patients.

Cognitive function and Migraine:

There are contradictory reports in literature concerning the neuropsychological functioning of migraine headache patients. Bell et al (1999) compared headache patients with the non headache and mild traumatic brain injury patients. The results revealed that the two pain group patients were within the normal cut off scores. They concluded that the results did not reveal the significant link between the cognitive dysfunction and migraine.

Cognition and chronic psychogenic pain versus somatic pain patients

 In a study it was reported that patients with psychogenic pain reported higher levels of bodily discomfort but less concentration and memory difficulties as compared with the patients with somatic pain.( Binzer et al , 2003).

Do chronic pain patients 'Stroop' on pain stimuli?

In two studies.( Pincus et al 1998) it was  found  that there is no evidence for an attentional bias, although a memory recall bias was demonstrated. They found Interference in attending to emotionally salient stimuli appears to be related to measures of anxiety and depression rather than pain per se. When added to the findings of other investigators, these results suggest that the presence of attentional biases in chronic pain patients can best be accounted for as arising from mood state rather than pain-patient status.

 In a study  repeated-measures ANOVA indicated that patients with chronic pain but not healthy volunteers had delayed color-naming latencies to both sensory and affect pain words in the unmasked condition. Color-naming latency differences were not evident for other word types in the unmasked condition or for any word types in the masked condition . Correlational and regression analyses indicated that the delayed color-naming latencies to pain words in the unmasked condition observed for the chronic pain patients were, in part, associated with high pain-specific cognitive anxiety and interference and lower levels of anxiety sensitivity. Individuals with chronic pain selectively process pain-related cues at the strategic level but not at the automatic level. Implications of the findings and future research directions are discussed (Snider et al , 2000).

Anticipatory electroencephalography alpha rhythm predicts subjective perception of pain intensity.

The suppression of the alpha power before the painful stimulation [as reflected by the event-related desynchronization (ERD)] indexed the anticipatory cortical processes. Results showed maximum (negative) correlations between the alpha 2 and alpha 3 ERD amplitude at the left central area and the subjective evaluation of pain intensity (P < .001). The stronger the anticipatory alpha 2 and alpha 3 ERD, the higher the subjective evaluation of pain intensity. For alpha 3, that correlation was confirmed even when the effect of habituation across the recording session was taken into account. These results suggest that the anticipatory suppression of the alpha rhythms over the contralateral primary sensorimotor cortex predicts subsequent subjects' evaluation of pain intensity, in line with its crucial role for the discrimination of that intensity. This electroencephalographic study showed that anticipatory activation/deactivation of sensorimotor cortex roughly predicts subjective evaluation of pain. This motivates further investigation on possible implications for the understanding of central chronic pain. Chronic pain patients might exaggerate the anticipatory activation of sensorimotor cortex to negligible pain stimuli.

Conclusion

Chronic pain syndromes are characterized by altered neuronal excitability in the pain matrix. The ability to rapidly acquire and store memory of aversive events is one of the basic principles of nervous systems throughout the animal kingdom. These neuroplastic changes take place e. g. in the spinal cord, in thalamic nuclei and cortical and subcortical (limbic) areas integrating pain threshold, intensity and affective components. Chronic inflammation or injury of peripheral nerves evokes the reorganisation of cortical sensory maps. Neurons conveying nociceptive information are controlled by various sets of inhibitory interneurons. The discharge activity of these interneurons counteracts long-term changes in the pain matrix following nociceptor activation, i. e. it prevents the transition of acute pain signaling to chronic pain states. The  most recent research suggests that pain states may be sensitive to novel families of agents and therapeutic measures not predicted by traditional preclinical pain models as well as human pain states. The endogenous cannabinoid system plays a central role in the extinction of aversive memories. It is proposed  that endocannabinoids facilitate extinction of aversive memories via their selective inhibitory effects on GABAergic networks in the amygdala.

( Azad and Zieglagansberger, 2003)

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