Chronic pain

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Chronic pain
ICD-10 R52.1-R52.2
ICD-9 338.2

Chronic pain is defined as pain that has lasted longer than three to six months,[1][2] though some theorists and researchers have placed the transition from acute to chronic pain at 12 months.[3] Others apply acute to pain that lasts less than 30 days, chronic to pain of more than six months duration, and subacute to pain that lasts from one to six months.[4] A popular alternative definition of chronic pain, involving no arbitrarily fixed duration, is "pain that extends beyond the expected period of healing".[2]

Classification[edit]

Chronic pain may be divided into "nociceptive" (caused by activation of nociceptors), and "neuropathic" (caused by damage to or malfunction of the nervous system).[5]

Nociceptive pain may be divided into "superficial" and "deep", and deep pain into "deep somatic" and "visceral". Superficial pain is initiated by activation of nociceptors in the skin or superficial tissues. Deep somatic pain is initiated by stimulation of nociceptors in ligaments, tendons, bones, blood vessels, fasciae and muscles, and is dull, aching, poorly-localized pain. Visceral pain originates in the viscera (organs). Visceral pain may be well-localized, but often it is extremely difficult to locate, and several visceral regions produce "referred" pain when damaged or inflamed, where the sensation is located in an area distant from the site of pathology or injury.[6]

Neuropathic pain is divided into "peripheral" (originating in the peripheral nervous system) and "central" (originating in the brain or spinal cord).[7] Peripheral neuropathic pain is often described as "burning", "tingling", "electrical", "stabbing", or "pins and needles".[8]

Pathophysiology[edit]

Under persistent activation nociceptive transmission to the dorsal horn may induce a wind up phenomenon. This induces pathological changes that lower the threshold for pain signals to be transmitted. In addition it may generate nonnociceptive nerve fibers to respond to pain signals. Nonnociceptive nerve fibers may also be able to generate and transmit pain signals. The type of nerve fibers that are believed to propagate the pain signals are the C-fibers, since they have a slow conductivity and give rise to a painful sensation that persists over a long time.[9] In chronic pain this process is difficult to reverse or eradicate once established.[10]

Chronic pain of different etiologies has been characterized as a disease affecting brain structure and function. Magnetic resonance imaging studies have shown abnormal anatomical[11] and functional connectivity, even during rest[12][13] involving areas related to the processing of pain. Also, persistent pain has been shown to cause grey matter loss, reversible once the pain has resolved.[14][15]

These structural changes can be explained by the phenomenon known as neuroplasticity. In the case of chronic pain, the somatototic representation of the body is inappropriately reorganized following peripheral and central sensitization. This maladaptative change results in the experience of allodynia and/or hyperalgesia. Brain activity in individuals suffering from chronic pain, measured via electroencephalogram (EEG), has been demonstrated to be altered, suggesting pain-induced neuroplastic changes. More specifically, the relative beta activity (compared to the rest of the brain) is increased, the relative alpha activity is decreased, and the theta activity both absolutely and relatively is diminished.[16]

Management[edit]

Main article: Pain management

Complete and sustained remission of many neuropathies and most idiopathic chronic pain (pain that extends beyond the expected period of healing, or chronic pain that has no known underlying pathology) is rarely achieved, but much can be done to reduce suffering and improve quality of life.[17]

Pain management is the branch of medicine employing an interdisciplinary approach to the relief of pain and improvement in the quality of life of those living with pain.[18] The typical pain management team includes medical practitioners (particularly anesthesiologists), clinical psychologists, physiotherapists, occupational therapists, physician assistants, and nurse practitioners.[19] Acute pain usually resolves with the efforts of one practitioner; however, the management of chronic pain frequently requires the coordinated efforts of the treatment team.[20][21][22]

Psychological treatments including cognitive behavioral therapy[23][24] and acceptance and commitment therapy[25][26][27] have been shown effective for improving quality of life in those suffering from chronic pain. Clinical hypnosis, including self-hypnosis, has been shown effective not only for improving quality of life, but for direct improvement of chronic pain symptoms.[28][29][30]

The emergence of studies relating chronic pain to neuroplasticity also suggest the utilization of neurofeedback rehabilitation techniques to resolve maladaptive cortical changes and patterns.[16] The proposed goal of neurofeedback intervention is to abolish maladaptive neuroplastic changes made as a result of chronic nociception, as measured by abnormal EEG, and thereby relieve the individual's pain. However, this field of research lacks randomized control trials, and therefore requires further investigation.

Epidemiology[edit]

In a recent large-scale telephone survey of 15 European countries and Israel, 19% of respondents over 18 years of age had suffered pain for more than 6 months, including the last month, and more than twice in the last week, with pain intensity of 5 or more for the last episode, on a scale of 1(no pain) to 10 (worst imaginable). 4839 of these respondents with chronic pain were interviewed in depth. Sixty six percent scored their pain intensity at moderate (5–7), and 34% at severe (8–10); 46% had constant pain, 56% intermittent; 49% had suffered pain for 2–15 years; and 21% had been diagnosed with depression due to the pain. Sixty one percent were unable or less able to work outside the home, 19% had lost a job, and 13% had changed jobs due to their pain. Forty percent had inadequate pain management and less than 2% were seeing a pain management specialist.[31]

In a systematic literature review published by the International Association for the Study of Pain (IASP), 13 chronic pain studies from various countries around the world were analyzed. (Of the 13 studies, there were three in the United Kingdom, two in Australia, one each in France, the Netherlands, Israel, Canada, Scotland, Spain, and Sweden, and a multinational.) The authors found that the prevalence of chronic pain was very high and that chronic pain consumes a large amount of healthcare resources around the globe. Chronic pain afflicted women at a higher rate than men. They determined that the prevalence of chronic pain varied from 10.1% to 55.2% of the population.[32]

In the United States, the prevalence of chronic pain has been estimated to be approximately 30%. According to the Institute of Medicine, there are about 116 million Americans living with chronic pain, which suggests that approximately half of American adults have some chronic pain condition.[1][33] The Mayday Fund estimate of 70 million Americans with chronic pain is slightly more conservative.[34] In an internet study, the prevalence of chronic pain in the United States was calculated to be 30.7% of the population: 34.3% for women and 26.7% for men.[35] These estimates are in reasonable agreement and indicate a prevalence of chronic pain in the US that is relatively comparable to that of other countries.[citation needed]

Comorbidities and sequelae[edit]

Chronic pain is associated with higher rates of depression and anxiety.[36] Sleep disturbance, and insomnia due to medication and illness symptoms are often experienced by those with chronic pain.[37] Chronic pain may contribute to decreased physical activity due to fear of exacerbating pain, often resulting in weight gain.[36] Such comorbid disorders can be very difficult to treat due to the high potential of medication interactions, especially when the conditions are treated by different doctors.

Severe chronic pain is associated with increased 10 year mortality, particularly from heart disease and respiratory disease.[38] Several mechanisms have been proposed for the increased mortality, e.g. abnormal endocrine stress response.[39] Additionally, chronic stress seems to affect cardiovascular risk by acceleration of the atherosclerotic process. However, further research is needed to elucidate the relationship between severe chronic pain, stress and cardiovascular health.[38]

Psychology[edit]

Psychosocial factors[edit]

Those who have a tendency to "catastrophise" in response to pain report greater pain levels induced by an ice bath (Sullivan et al., 1995).[40] A study by Crombez et al. (1998) showed that those with unhealthy catastrophising pain beliefs experienced greater impairment in performance in an auditory discrimination task when a painful stimulus was applied then those with more healthy pain beliefs.[41] In addition there was a perception of pain at greater intensity during the experiment. This indicates that there is an increase in attention to pain at the expense of other somatosensation. Indeed Crombez et al. (2005) postulated that in chronic pain patients are thought to display a “hyper-vigilance” to pain.[41] In addition, pain inhibited visual attention disengagement in those with a tendency to catastrophise though not in non-catastrophisers (Van Damme et al., 2004).[42]

Personality[edit]

Two of the most frequent personality profiles found in chronic pain patients by the Minnesota Multiphasic Personality Inventory (MMPI) are the conversion V and the neurotic triad. The conversion V personality, so called because the higher scores on MMPI scales 1 and 3, relative to scale 2, form a "V" shape on the graph, expresses exaggerated concern over body feelings, develops bodily symptoms in response to stress, and often fails to recognize their own emotional state, including depression. The neurotic triad personality, scoring high on scales 1, 2 and 3, also expresses exaggerated concern over body feelings and develops bodily symptoms in response to stress, but is demanding and complaining.[43]

Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to chronic pain causing neuroticism. When long term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety fall, often to normal levels.[44][45][46][47] Self-esteem, often low in chronic pain patients, also shows striking improvement once pain has resolved.[47]

Social Support[edit]

Social support has important consequences for individuals with chronic pain. In particular, pain intensity, pain control, and resiliency to pain has been implicated as outcomes influenced by different levels and types of social support. Much of this research has focused on emotional, instrumental, tangible and informational social support. Research has examined a wide range of social support including, but not limited to, online social networks, romantic partners, friends, and even complete strangers. A meta-analysis conducted by Zaza and Baine (2002) revealed moderate effect sizes between chronic pain variables and social support. [48] Across a majority of studies investigated, there was a direct significant association between social activities and/or social support and pain. Higher levels of pain were associated with a decrease in social activities, lower levels of social support, and reduced social functioning.

Recent neuroimaging studies have supported this link between the experience of pain and social support. Eisenberger and colleagues (2011) conducted a study that investigated the role attachment figures serve as safety signals for individuals experiencing pain. [49] The researchers had participants view pictures of a significant other while receiving painful stimuli during an fMRI procedure. The study demonstrated that viewing partner pictures during a painful experience led to reductions in self-reported pain intensity and reductions in pain-related neural activity as indicated by dorsal anterior cingulate cortex, and anterior insula activity and increased activity in the ventromedial prefrontal cortex (VMPFC) compared to individuals who did not view a picture of a partner. Activity in the VMPFC has been shown to be related to safety signaling and fear extinction, and greater activity was associated with the participant’s perception that the significant other was a greater source of support. Additionally, it has been shown that interaction with a romantic partner activates several reward-processing regions of the brain including the caudate head, nucleus accumbens, lateral orbitofrontal cortex, amygdala, and dorsolateral PFC. [50] While distraction tasks such as word association tasks were also shown to significantly reduce perceived pain, the tasks did not activate these reward areas. Taken together, these results suggest that companionship support may buffer the pain experience such that the greater the perceived sense of support the less intensity an individual will rate their pain.

In addition to the above findings, recent studies have demonstrated that the size and quality of a person’s social network also impacts pain sensitivity. Molton and Terrill (2014) discussed research conducted by Martin and colleagues (2012) demonstrating that smaller social networks are more sensitive to losses and strain. [51] [52] According to their study, those with persistent pain conditions tend to rely on their social support as a coping mechanism and therefore have better outcomes when they are a part of larger more supportive social networks. Brown and colleagues (2003) further demonstrated that both passive and active forms of social support reduce experimental pain.[53] The aforementioned work was extended by Vigil and colleagues (2013) who demonstrated sex differences in how social networks and intimate relationships influence experimental pain sensitivity. [54] Females displayed higher pain sensitivity when their social networks contained a higher proportion of more intimate relationships while males displayed patterns in the opposite direction. Males displayed lower pain sensitivity when they received higher levels of support from their social networks.

A common way an individual with chronic pain communicates their pain is by catastrophizing as a way to elicit emotional and/or tangible support from others. [55] Pain catastrophizing has been associated with greater levels of supportive solicitation and higher observer ratings of pain behaviors in the presence of painful stimuli. [56] While pain catastrophizing often functions as a way to communicate pain, it has also been consistently shown to be associated with punishing responses from significant others. [57] These punishing responses (i.e., irritation or frustration) have been shown to be related to higher levels of pain severity and depressed mood. [58] Quartana, Campbell, & Edwards (2009) point out that individuals with chronic pain may be attempting to solicit supportive responses, yet may unintentionally causing interpersonal stress and difficulty. [59] Further research on social support and chronic pain has shown that too much sympathy and help may lead to increased pain and disability. [60] This indicates that there is an optimal level of interpersonal effectiveness for social support for individuals with chronic pain.

The type of support an individual with chronic pain receives has also been shown to be associated with pain controllability. A study by Cho, Zunin, Chao, Heiby, and McKoy (2012) attempted to determine differences in social support for individuals with high and low pain controllability for patients seeking treatment at two outpatient pain management clinics. [61] The results showed that individuals with low pain controllability had greater preference for informational, instrumental, and emotional social support. This demonstrates that individuals with lower pain control attempt to seek support, but may not be effective in doing so. Thus, these individuals may indirectly communicate their desire for support and fail to obtain their preferred level of support.

It is also important to consider the strong associations the have been demonstrated between social support and chronic pain resilience (i.e., the ability to cope with adversity and adjust to chronic pain symptoms). Newton-John, Mason, and Hunter (2014) conducted a study investigating the role of resilience in adjustment and coping with chronic pain.[62] The results of their study revealed positive associations between the ability to recover from adversity and/or stress and social support in individuals from a pain rehabilitation clinic. The researchers also found that resilient individuals were more likely to be employed compared to less resilient individuals. This finding indicates that integration into social systems and having support resources are valued aspects of chronic pain adjustment and coping. These findings also support previous research conducted by Sturgeon and Zautra (2010) who explained that social engagement noticeably improves the ability cope with pain among those who suffer from chronic pain. [63] They also suggest that those who are more proactive in their efforts to engage with their social networks demonstrate higher levels of resilience to pain.

Effect on cognition[edit]

Chronic pain's impact on cognition is an under-researched area, but several tentative conclusions have been published. Most chronic pain patients complain of cognitive impairment, such as forgetfulness, difficulty with attention, and difficulty completing tasks. Objective testing has found that people in chronic pain tend to experience impairment in attention, memory, mental flexibility, verbal ability, speed of response in a cognitive task, and speed in executing structured tasks. In 2007, Shulamith Kreitler and David Niv advised clinicians to assess cognitive function in chronic pain patients in order to more precisely monitor therapeutic outcomes, and tailor treatment to address this aspect of the pain experience.[64]

See also[edit]

References[edit]

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