Chronic pain

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]

There is little evidence for treating most types of chronic pain with opioids.[5] An exception is chronic pain due to cancer. While they may improve pain in the short term there is no evidence of improved long term pain or functioning.[6] Risks include overdose and addiction.[6] In the United States about 100 million people have chronic pain, with 25% of those having more or severe chronic pain.[5]


Chronic pain may be divided into "nociceptive" (caused by activation of nociceptors), and "neuropathic" (caused by damage to or malfunction of the nervous system).[7]

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.[8]

Neuropathic pain is divided into "peripheral" (originating in the peripheral nervous system) and "central" (originating in the brain or spinal cord).[9] Peripheral neuropathic pain is often described as "burning", "tingling", "electrical", "stabbing", or "pins and needles".[10]


Under persistent activation nociceptive transmission to the dorsal horn may induce a pain 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.[11] In chronic pain this process is difficult to reverse or eradicate once established.[12] In some cases, chronic pain can be caused by genetic factors which interfere with neuronal differentiation, leading to a permanent reduction in the threshold for pain.[13]

Chronic pain of different etiologies has been characterized as a disease affecting brain structure and function. Magnetic resonance imaging studies have shown abnormal anatomical[14] and functional connectivity, even during rest[15][16] 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.[17][18]

These structural changes can be explained by the phenomenon known as neuroplasticity. In the case of chronic pain, the somatotopic representation of the body is inappropriately reorganized following peripheral and central sensitization. This maladaptive change results in the experience of allodynia and/or hyperalgesia. Brain activity in individuals with 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.[19]


Main article: Pain management

Complete and sustained remission of many types of chronic pain is rare, though some can be done to improve quality of life.[20]

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.[21] The typical pain management team includes medical practitioners (particularly anesthesiologists), clinical psychologists, physiotherapists, occupational therapists, physician assistants, and nurse practitioners.[22] 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.[23][24][25]

Psychological treatments including cognitive behavioral therapy[26][27] and acceptance and commitment therapy[28][29][30] have been shown effective for improving quality of life in those with chronic pain.

Alternative medicine

Hypnosis, including self-hypnosis, has tentative evidence.[31] Evidence does not support hypnosis for chronic pain due to a spinal cord injury,


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.[32]

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.[33]

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][34] The Mayday Fund estimate of 70 million Americans with chronic pain is slightly more conservative.[35] 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.[36] 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]


Chronic pain is associated with higher rates of depression and anxiety.[37] Sleep disturbance, and insomnia due to medication and illness symptoms are often experienced by those with chronic pain.[38] Chronic pain may contribute to decreased physical activity due to fear of exacerbating pain, often resulting in weight gain.[37] 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.[39] Several mechanisms have been proposed for the increased mortality, e.g. abnormal endocrine stress response.[40] 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.[39]



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.[41]

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.[42][43][44][45] Self-esteem, often low in chronic pain patients, also shows striking improvement once pain has resolved.[45]

Social Support

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.[46] 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.[47] 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.[48] 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.[49][50] 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.[51] 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.[52] 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 (a tendency to misinterpret and exaggerate situations that may be threatening) as a way to elicit emotional and/or tangible support from others.[53] Pain catastrophizing has been associated with greater levels of supportive solicitation and higher observer ratings of pain behaviors in the presence of painful stimuli.[54] 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.[55] These punishing responses (i.e., irritation or frustration) have been shown to be related to higher levels of pain severity and depressed mood.[56] 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.[55] Further research on social support and chronic pain has shown that too much sympathy and help may lead to increased pain and disability.[57] 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.[58] 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.[59] 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 to cope with pain among those who suffer from chronic pain.[60] 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

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.[61]


  1. ^ a b Debono, DJ; Hoeksema, LJ; Hobbs, RD (August 2013). "Caring for Patients with Chronic Pain: Pearls and Pitfalls". Journal of the American Osteopathic Association 113 (8): 620–627. PMID 23918913. doi:10.7556/jaoa.2013.023. 
  2. ^ a b Turk, D.C.; Okifuji, A. (2001). "Pain terms and taxonomies". In Loeser, D.; Butler, S. H.; Chapman, J.J. et al. Bonica's management of pain (3 ed.). Lippincott Williams & Wilkins. pp. 18–25. ISBN 0-683-30462-3. 
  3. ^ Main, C.J.; Spanswick, C.C. (2001). Pain management: an interdisciplinary approach. Elsevier. p. 93. ISBN 0-443-05683-8. 
  4. ^ Thienhaus, O.; Cole, B.E. (2002). "Classification of pain". In Weiner, R.S. Pain management: A practical guide for clinicians (6 ed.). American Academy of Pain Management. ISBN 0-8493-0926-3. 
  5. ^ a b Reuben, DB; H Alvanzo, AA; Ashikaga, T; Bogat, GA; Callahan, CM; Ruffing, V; Steffens, DC (13 January 2015). "National Institutes of Health Pathways to Prevention Workshop: The Role of Opioids in the Treatment of Chronic Pain.". Annals of internal medicine 162: 295–300. PMID 25581341. doi:10.7326/M14-2775. 
  6. ^ a b Franklin, GM; American Academy of, Neurology (30 September 2014). "Opioids for chronic noncancer pain: a position paper of the American Academy of Neurology.". Neurology 83 (14): 1277–84. PMID 25267983. doi:10.1212/wnl.0000000000000839. 
  7. ^ Keay, KA; Clement, CI; Bandler, R (2000). "The neuroanatomy of cardiac nociceptive pathways". In Horst, GJT. The nervous system and the heart. Totowa, New Jersey: Humana Press. p. 304. ISBN 978-0-89603-693-2. 
  8. ^ Coda, BA; Bonica, JJ (2001). "General considerations of acute pain". In Loeser, D; Bonica, JJ. Bonica's management of pain (3 ed.). Philadelphia: Lippincott Williams & Wilkins. ISBN 0-443-05683-8. 
  9. ^ Bogduk, N; Merskey, H (1994). Classification of chronic pain: descriptions of chronic pain syndromes and definitions of pain terms (second ed.). Seattle: IASP Press. p. 212. ISBN 0-931092-05-1. 
  10. ^ Paice, JA (Jul–Aug 2003). "Mechanisms and management of neuropathic pain in cancer" (PDF). Journal of supportive oncology 1 (2): 107–20. PMID 15352654. 
  11. ^ Hansson P (1998). Nociceptive and neurogenic pain. Pharmacia & Upjon AB. pp. 52–63. 
  12. ^ Vadivelu N, Sinatra R (2005). "Recent advances in elucidating pain mechanisms". Current Opinion in Anesthesiology 18 (5): 540–7. PMID 16534290. doi:10.1097/ 
  13. ^ Rusanescu G, Mao J (2014). "Notch3 is necessary for neuronal differentiation and maturation in the adult spinal cord". J Cell Mol Med 18 (10): 2003–16. PMID 25164209. doi:10.1111/jcmm.12362. 
  14. ^ Geha PY, Baliki MN, Harden RN, Bauer WR, Parrish TB, Apkarian AV (2008). "The brain in chronic CRPS pain: Abnormal gray-white matter interactions in emotional and autonomic regions". Neuron 60 (4): 570–581. PMC 2637446. PMID 19038215. doi:10.1016/j.neuron.2008.08.022. 
  15. ^ Baliki MN, Geha PY, Apkarian AV, Chialvo DR (2008). "Beyond feeling: chronic pain hurts the brain, disrupting the default-mode network dynamics". J of Neurosci 28 (6): 1398–1403. PMID 18256259. doi:10.1523/JNEUROSCI.4123-07.2008. 
  16. ^ Tagliazucchi E, Balenzuela P, Fraiman D, Chialvo DR (2010). "Brain resting state is disrupted in chronic back pain patients". Neurosci Lett 485 (1): 26–31. PMC 2954131. PMID 20800649. doi:10.1016/j.neulet.2010.08.053. 
  17. ^ May A (2009). "Chronic pain may change the structure of the brain". Pain 137 (1): 7–15. PMID 18410991. doi:10.1016/j.pain.2008.02.034. 
  18. ^ DA, Wideman TH, Naso L, Hatami-Khoroushahi Z, Fallatah S, Ware MA, Jarzem P, Bushnell MC, Shir Y, Ouellet JA, Stone LS (2011). "Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function". Journal of Neuroscience 31 (20): 7540–50. PMID 21593339. doi:10.1523/JNEUROSCI.5280-10.2011. 
  19. ^ Jensen, M.P., Sherlin, L.H., Hakiman, S., Fregni, F. Neuromodulatory approaches for chronic pain management: research findings and clinical implications. Journal of Neurotherapy 2009, 13:196–213
  20. ^ Chou, Roger; Huffman, LH; American Pain, Society; American College of, Physicians (2 October 2007). "Medications for Acute and Chronic Low Back Pain: A Review of the Evidence for an American Pain Society/American College of Physicians Clinical Practice Guideline". Annals of Internal Medicine 147 (7): 505–14. PMID 17909211. doi:10.7326/0003-4819-147-7-200710020-00008. 
  21. ^ Hardy, Paul A. J. (1997). Chronic pain management: the essentials. U.K.: Greenwich Medical Media. ISBN 1-900151-85-5. 
  22. ^ Main, Chris J.; Spanswick, Chris C. (2000). Pain management: an interdisciplinary approach. Churchill Livingstone. ISBN 0-443-05683-8. 
  23. ^ Thienhaus, Ole; Cole, B. Eliot (2002). "The classification of pain". In Weiner, Richard S,. Pain management: A practical guide for clinicians. CRC Press. p. 29. ISBN 0-8493-0926-3. 
  24. ^ Henningsen P, Zipfel S, Herzog W (2007). "Management of functional somatic syndromes". Lancet 369 (9565): 946–55. PMID 17368156. doi:10.1016/S0140-6736(07)60159-7. 
  25. ^ Stanos S, Houle TT (2006). "Multidisciplinary and interdisciplinary management of chronic pain". Physical medicine and rehabilitation clinics of North America 17 (2): 435–50, vii. PMID 16616276. doi:10.1016/j.pmr.2005.12.004. 
  26. ^ Sveinsdottir, Vigdis; Eriksen, Hege R; Reme, Silje Endresen (2012). "Assessing the role of cognitive behavioral therapy in the management of chronic nonspecific back pain.". Journal of pain research 5: 371–80. PMC 3474159. PMID 23091394. doi:10.2147/JPR.S25330. 
  27. ^ Castro, MM; Daltro, C; Kraychete, DC; Lopes, J (November 2012). "The cognitive behavioral therapy causes an improvement in quality of life in patients with chronic musculoskeletal pain.". Arquivos de neuro-psiquiatria 70 (11): 864–8. PMID 23175199. doi:10.1590/s0004-282x2012001100008. 
  28. ^ Wicksell, RK; Kemani, M; Jensen, K; Kosek, E; Kadetoff, D; Sorjonen, K; Ingvar, M; Olsson, GL (1 April 2013). "Acceptance and commitment therapy for fibromyalgia: a randomized controlled trial.". European journal of pain (London, England) 17 (4): 599–611. PMID 23090719. doi:10.1002/j.1532-2149.2012.00224.x. 
  29. ^ "APA website on empirical treatments". Retrieved 2009-09-01. 
  30. ^ Ruiz, F. J. (2010). "A review of Acceptance and Commitment Therapy (ACT) empirical evidence: Correlational, experimental psychopathology, component and outcome studies". International Journal of Psychology and Psychological Therapy 10 (1): 125–62. 
  31. ^ Elkins, Gary; Johnson, Aimee; Fisher, William (1 April 2012). "Cognitive Hypnotherapy for Pain Management". American Journal of Clinical Hypnosis 54 (4): 294–310. PMID 22655332. doi:10.1080/00029157.2011.654284. 
  32. ^ Breivik H, Collett B, Ventafridda V, Cohen R, Gallacher D (May 2006). "Survey of chronic pain in Europe: prevalence, impact on daily life, and treatment". Eur J Pain 10 (4): 287–333. PMID 16095934. doi:10.1016/j.ejpain.2005.06.009. 
  33. ^ Harstall C and Ospina M (June 2003). "How Prevalent Is Chronic Pain?". Pain Clinical Updates, International Association for the Study of Pain XI (2): 1–4. 
  34. ^ Institute of Medicine of the National Academies Report (2011). Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research. Washington DC: The National Academies Press. 
  35. ^ A Call to Revolutionize Chronic Pain Care in America: An Opportunity in Health Care Reform. The Mayday Fund. 2009. 
  36. ^ Johannes C, Le T, Zhou X, Johnston J, Dworkin R (Nov 2010). "The Prevalence of Chronic Pain in United States Adults: Results of an Internet-Based Study". J Pain 11 (11): 1230–1239. PMID 20797916. doi:10.1016/j.jpain.2010.07.002. 
  37. ^ a b Pruimboom L, van Dam AC (2007). "Chronic pain: a non-use disease". Med. Hypotheses 68 (3): 506–11. PMID 17071012. doi:10.1016/j.mehy.2006.08.036. 
  38. ^ Ferini-Strambi L (2011). "Sleep disorders in multiple sclerosis". Handb Clin Neurol. Handbook of Clinical Neurology 99: 1139–46. ISBN 978-0-444-52007-4. PMID 21056246. doi:10.1016/B978-0-444-52007-4.00025-4. 
  39. ^ a b Torrance N, Elliott AM, Lee AJ, Smith BH (April 2010). "Severe chronic pain is associated with increased 10 year mortality. A cohort record linkage study". European Journal of Pain 14 (4): 380–6. PMID 19726210. doi:10.1016/j.ejpain.2009.07.006. 
  40. ^ McBeth J, Chiu YH, Silman AJ et al. (2005). "Hypothalamic-pituitary-adrenal stress axis function and the relationship with chronic widespread pain and its antecedents". Arthritis Research & Therapy 7 (5): R992–R1000. PMC 1257426. PMID 16207340. doi:10.1186/ar1772. 
  41. ^ Leo, Raphael (2007). Clinical manual of pain management in psychiatry. Washington, DC: American Psychiatric Publishing. p. 58. ISBN 978-1-58562-275-7. 
  42. ^ Fishbain, David A.; Cole, Brandly; Cutler, R. Brian; Lewis, J.; Rosomoff, Hubert L.; Rosomoff, R. Steele (1 November 2006). "Chronic Pain and the Measurement of Personality: Do States Influence Traits?". Pain Medicine 7 (6): 509–529. PMID 17112364. doi:10.1111/j.1526-4637.2006.00239.x. 
  43. ^ JESS,, P.; T. JESS; H. BECK; P. BECH (1 January 1998). "Neuroticism in Relation to Recovery and Persisting Pain after Laparoscopic Cholecystectomy". Scandinavian Journal of Gastroenterology 33 (5): 550–553. PMID 9648998. doi:10.1080/00365529850172151. 
  44. ^ Jess, P; Bech, P (1994). "The validity of Eysenck's neuroticism dimension within the Minnesota Multiphasic Personality Inventory in patients with duodenal ulcer. The Hvidovre Ulcer Project Group.". Psychotherapy and psychosomatics 62 (3–4): 168–75. PMID 7846260. doi:10.1159/000288919. 
  45. ^ a b Melzack, R; Wall, PD (1996). The Challenge of Pain (2 ed.). London: Penguin. pp. 31–32. ISBN 0-14-025670-9.
  46. ^ Zaza, C.; Baine, N. (2002). "Cancer pain and psychological factors: A critical review of the literature". Journal of Pain and Symptom Management 24 (5): 526–542. doi:10.1016/s0885-3924(02)00497-9. 
  47. ^ Eisenberger, N. I.; Master, S. L.; Inagaki, T. K.; Taylor, S. E.; Shirinyan, D.; Lieberman, M. D.; Naliboff, B. D. (2011). "Attachment figures activate a safety signal-related neural region and reduce pain experience.". Proceedings of the National Academy of Sciences 108 (28): 11721–6. doi:10.1073/pnas.1108239108. 
  48. ^ Younger, J.; Aron, A.; Parke, S.; Chatterjee, N.; Mackey, S. (2010). "Viewing pictures of a romantic partner reduces experimental pain: Involvement of neural reward systems". PLOS ONE 5 (10): e13309. doi:10.1371/journal.pone.0013309. 
  49. ^ Molton, I. R.; Terrill, A. L. (2014). "Overview of persistent pain in older adults". American Psychologist 69 (2): 197–207. doi:10.1037/a0035794. 
  50. ^ Martin, K. R.; Schoster, B.; Woodard, J.; Callahan, L. F. (2012). "What community resources do older community-dwelling adults use to manage their osteoarthriris? A formative examination.". Journal of Applied Gerontology 31: 661–684. doi:10.1177/0733464810397613. 
  51. ^ Brown, J. L.; Sheffield, D.; Leary, M. R.; Robinson, M. E. (2003). "Social support and experimental pain.". Psychosomatic Medicine 65: 276–283. doi:10.1097/01.psy.0000030388.62434.46. 
  52. ^ Vigil, J. M.; Rowell, L. N.; Chouteu, S.; Chavez, A.; Jaramillo, E.; Neal, M.; Waid, D. (2013). "Sex differences in how social networks and relationship quality influence experimental pain sensitivity.". PLoS ONE 8 (11): e78663. doi:10.1371/journal.pone.0078663. 
  53. ^ Sullivan, M. J.; Thorn, B.; Haythornthwaite, J. A.; Keefe, F.; Martin, M.; Bradley, L. A.; Lefebvre, J. C. (2001). "Theoretical perspectives on the relation between catastrophizing and pain". The Clinical Journal of Pain 17 (1): 52–64. doi:10.1097/00002508-200103000-00008. 
  54. ^ Sullivan, M. J.; Martel, M. O.; Tripp, D.; Savard, A.; Crombez, G. (2001). "The relationship between catastrophizing and the communication of pain experience". Pain 122 (3): 282–288. doi:10.1016/j.pain.2006.02.001. 
  55. ^ a b Quartana, P. J.; Campbell, C. M.; Edwards, R. R. (2009). "Pain catastrophizing: A critical review". Expert Review of Neurotherapeutics 9 (5): 745–758. doi:10.1586/ern.09.34. 
  56. ^ Waxman, S. E.; Tripp, D. A.; Flamenbaum, R. (2008). "The mediating role of depression and negative partner responses in chronic low back pain and relationship satisfaction". The Journal of Pain 9 (5): 434–442. doi:10.1016/j.jpain.2007.12.007. 
  57. ^ Romano, J. M.; Jensen, M. P.; Turner, J. A.; Good, A. B.; Hops, H. (2000). "Chronic pain patient-partner interactions: Further support for a behavioral model of chronic pain.". Behavior Therapy 31: 415–440. doi:10.1016/s0005-7894(00)80023-4. 
  58. ^ Cho, S.; Zunin, I. D.; Chao, P. J.; Heiby, E. M.; McKoy, J. (2012). "Effects of pain controllability and discrepancy in social support on depressed mood among patients with chronic pain". International Journal of Behavioral Medicine 19: 270–279. doi:10.1007/s12529-011-9175-4. 
  59. ^ Newton-John, T. R. O.; Mason, C.; Hunter, M. (2014). "The role of resilience in adjustment and coping with chronic pain.". Rehabilitation Psychology 99 (3): 360–365. 
  60. ^ Sturgeon, J. A.; Zautra, A. J. (2010). "Resilience: A new paradigm for adaptation to chronic pain". Current Pain and Headache Reports 14: 105–112. doi:10.1007/s11916-010-0095-9. 
  61. ^ Kreitler S; Niv D (2007). "Cognitive impairment in chronic pain" (PDF). Pain: Clinical Updates (International Association for the Study of Pain) XV (4): 1–4. Retrieved 2008-04-15. 

External links

ru:Хроническая боль