Chronic Pain

Chronic pain

From Wikipedia, the free encyclopedia

Jump to: navigation, search

Chronic pain

ICD-10

R52.1-R52.2

ICD-9

338.2

Chronic pain is pain that has lasted for a long time. In medicine, the distinction between acute and chronic pain has traditionally been determined by an arbitrary interval of time since onset; the two most commonly used markers being 3 months and 6 months since onset,[1] though some theorists and researchers have placed the transition from acute to chronic pain at 12 months.[2] 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.[3] A popular alternative definition of chronic pain, involving no arbitrarily fixed durations is “pain that extends beyond the expected period of healing.”[1]

Contents
[hide] 1 Classification
2 Pathophysiology
3 Management
4 Epidemiology
5 Comorbidities and sequelae
6 Psychology 6.1 Personality
6.2 Effect on cognition

7 See also
8 References
9 External links

[edit] Classification

Main article: Pain#Classification

Chronic pain may be divided into “nociceptive” (caused by activation of nociceptors), and “neuropathic” (caused by damage to or malfunction of the nervous system).[4]

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.[5]

Neuropathic pain is divided into “peripheral” (originating in the peripheral nervous system) and “central” (originating in the brain or spinal cord).[6] Peripheral neuropathic pain is often described as “burning,” “tingling,” “electrical,” “stabbing,” or “pins and needles.”.[7]

[edit] Pathophysiology

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. In chronic pain this process is difficult to reverse or eradicate once established.[8]

Chronic pain of different etiologies has been characterized as a disease affecting brain structure and function. Magnetic resonance imaging studies have shown abnormal anatomical[9] and functional connectivity, even during rest [10][11] 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.[12][13]

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.[14]

[edit] Management

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.[15]

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.[16] The typical pain management team includes medical practitioners, clinical psychologists, physiotherapists, occupational therapists, and nurse practitioners.[17] 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.[18][19][20]

Psychological treatments including cognitive behavioral therapy[21][22] and acceptance and commitment therapy[23] 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.[24][25][26]

The emergence of studies relating chronic pain to neuroplasticity also suggest the utilization of neurofeedback rehabilitation techniques to resolve maladaptive cortical changes and patterns.[14] 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.

[edit] Epidemiology

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.[27]

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.[28]

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.[29] The Mayday Fund estimate of 70 million Americans with chronic pain is slightly more conservative.[30] 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.[31] 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]

[edit] Comorbidities and sequelae

Chronic pain is associated with higher rates of depression and anxiety.[32] Sleep disturbance, and insomnia due to medication and illness symptoms are often experienced by those with chronic pain.[33] Chronic pain may contribute to decreased physical activity due to fear of exacerbating pain.[32]

[edit] Psychology

[edit] Personality

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.[34]

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.[35][36][37][38] Self-esteem, often low in chronic pain patients, also shows striking improvement once pain has resolved. [38]

[edit] 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.[39]

[edit] See also
Chronic pain syndrome
Suffering
Conditions related to pain Arthritis
Temporomandibular joint disorder
Back pain
Cancer
Chronic Fatigue Syndrome
Clinical depression
Complex Regional Pain Syndrome
Fibromyalgia
Headache
Interstitial Cystitis
Irritable Bowel Syndrome
Myofascial Pain Syndrome
Neuropathic pain
Pelvic pain
Neuropathy
Post-Vasectomy Pain Syndrome
Restless Leg Syndrome
Sciatica
Lumbar spinal stenosis and cervical spinal stenosis
Drugs Analgesia
Antiepileptics Gabapentin
Pregabalin
Levetiracetam
Topiramate
Lamotrigine
Zonisamide

Antidepressants Duloxetine
Amitryptiline
Nortriptyline
Milnacipran

Local anesthetics Ketamine

Acetaminophen (Paracetamol)
NSAIDs
Opioids
Medical cannabis
Other agents: Clonidine
Ziconotide
Tizanidine

Other approaches in Physical medicine and rehabilitation (Physiatry) Cryotherapy
Exercise
Hot pack
Occupational therapy
Physical therapy
TENS
Alternative therapies Acupuncture
Chiropractic
Massage therapy
Hypnosis
Behavioral therapy
Prolotherapy
Structural Integration
Surgery Spinal cord stimulation

[edit] References

1.^ 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.
2.^ Main, C.J.; Spanswick, C.C. (2001). Pain management: an interdisciplinary approach. Elsevier. p. 93. ISBN 0-443-05683-8.
3.^ 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.
4.^ 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 089603.
5.^ 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.
6.^ 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.
7.^ Paice, JA (Jul-Aug 2003). “Mechanisms and management of neuropathic pain in cancer”. Journal of supportive oncology 1 (2): 107–20. PMID 15352654.
8.^ Vadivelu N, Sinatra R (2005). “Recent advances in elucidating pain mechanisms”. Current opinion in anaesthesiology 18 (5): 540–7. doi:10.1097/01.aco.0000183109.27297.75. PMID 16534290.
9.^ 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. doi:10.1016/j.neuron.2008.08.022. PMC 2637446. PMID 19038215.
10.^ 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. doi:10.1523/JNEUROSCI.4123-07.2008. PMID 18256259.
11.^ 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. doi:10.1016/j.neulet.2010.08.053. PMC 2954131. PMID 20800649.
12.^ May A (2009). “Chronic pain may change the structure of the brain”. Pain 137 (1): 7–15. doi:10.1016/j.pain.2008.02.034. PMID 18410991.
13.^ 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. doi:10.1523/JNEUROSCI.5280-10.2011. PMID 21593339.
14.^ a b 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
15.^ Chou R, Huffman LH (2007). “Ann Intern Med. 2007 Oct 2;147(7):505-14”. Annals of internal medicine 147 (7): 505–14. PMID 17909211.
16.^ Hardy, Paul A. J. (1997). Chronic pain management: the essentials. U.K.: Greenwich Medical Media. ISBN 1-900151-85-5.
17.^ Main, Chris J.; Spanswick, Chris C. (2000). Pain management: an interdisciplinary approach. Churchill Livingstone. ISBN 0-443-05683-8.
18.^ 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.
19.^ Henningsen P, Zipfel S, Herzog W (2007). “Management of functional somatic syndromes”. Lancet 369 (9565): 946–55. doi:10.1016/S0140-6736(07)60159-7. PMID 17368156.
20.^ 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. doi:10.1016/j.pmr.2005.12.004. PMID 16616276.
21.^ “Assessing the role of cognitive behavioral therapy in the management of chronic nonspecific back pain.”. Journal of Pain Research. 2012. PMID 23091394.
22.^ . PMID 23175199. http://www.ncbi.nlm.nih.gov/pubmed/23175199.
23.^ “Acceptance and commitment therapy for fibromyalgia: A randomized controlled trial.”. European Journal of Pain. 2012. PMID 23090719.
24.^ “Cognitive Hypnotherapy for Pain Management”. American Journal of Clinical Hypnosis. 2012. doi:10.1080/00029157.2011.654284.
25.^ “Pain Reduction is Related to Hypnotizability but Not to Relaxation or to Reduction in Suffering: A Preliminary Investigation”. American Journal of Clinical Hypnosis. 2005. doi:10.1080/00029157.2005.10401512.
26.^ “Hypnotic Self-Regulation of Chronic Pain”. American Journal of Clinical Hypnosis. doi:10.1080/00029157.1977.10403912.
27.^ 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. doi:10.1016/j.ejpain.2005.06.009. PMID 16095934.
28.^ 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.
29.^ 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.
30.^ A Call to Revolutionize Chronic Pain Care in America: An Opportunity in Health Care Reform. The Mayday Fund. 2009.
31.^ 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. doi:10.1016/j.jpain.2010.07.002.
32.^ a b Pruimboom L, van Dam AC (2007). “Chronic pain: a non-use disease”. Med. Hypotheses 68 (3): 506–11. doi:10.1016/j.mehy.2006.08.036. PMID 17071012.
33.^ Ferini-Strambi L (2011). “Sleep disorders in multiple sclerosis”. Handb Clin Neurol.. Handbook of Clinical Neurology 99: 1139–46. doi:10.1016/B978-0-444-52007-4.00025-4. ISBN 978-0-444-52007-4. PMID 21056246.
34.^ Leo, Raphael (2007). Clinical manual of pain management in psychiatry. Washington, DC: American Psychiatric Publishing. p. 58. ISBN 978-1-58562-275-7.
35.^ 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. doi:10.1111/j.1526-4637.2006.00239.x. Retrieved 25 September 2011.
36.^ 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. doi:10.1080/00365529850172151.
37.^ 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.
38.^ a b Melzack, R; Wall, PD (1996). The Challenge of Pain (2 ed.). London: Penguin. pp. 31–32. ISBN 0-14-025670-9.
39.^ 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.

[edit] External links
Chronic Pain Syndromes at the Open Directory Project
Chronic Pain Australia
American Chronic Pain Association
American Pain Foundation
International Association for the Study of Pain- IASP
Media related to pain at Wikimedia Commons
Reproducibility of tender point examination in chronic low back pain patients as measured by intrarater and inter-rater reliability and agreement: a validation study.

Jensen OK, Callesen J, Nielsen MG, Ellingsen T.

Source

Spine Center, Diagnostic Center, Regional Hospital Silkeborg, Silkeborg, Denmark.

Abstract

OBJECTIVES:

To evaluate the reliability and agreement of digital tender point (TP) examination in chronic low back pain (LBP) patients.

DESIGN:

Cross-sectional study.

SETTINGS:

Hospital-based validation study.

PARTICIPANTS:

Among sick-listed LBP patients referred from general practitioners for low back examination and return-to-work intervention, 43 and 39 patients, respectively (18 women, 46%) entered and completed the study.

MAIN OUTCOME MEASURES:

The reliability was estimated by the intraclass correlation coefficient (ICC), and agreement was calculated for up to ±3 TPs. Furthermore, the smallest detectable difference was calculated.

RESULTS:

TP examination was performed twice by two consultants in rheumatology and rehabilitation at 20 min intervals and repeated 1 week later. Intrarater reliability in the more and less experienced rater was ICC 0.84 (95% CI 0.69 to 0.98) and 0.72 (95% CI 0.49 to 0.95), respectively. The figures for inter-rater reliability were intermediate between these figures. In more than 70% of the cases, the raters agreed within ±3 TPs in both men and women and between test days. The smallest detectable difference between raters was 5, and for the more and less experienced rater it was 4 and 6 TPs, respectively.

CONCLUSIONS:

The reliability of digital TP examination ranged from acceptable to excellent, and agreement was good in both men and women. The smallest detectable differences varied from 4 to 6 TPs. Thus, TP examination in our hands was a reliable but not precise instrument. Digital TP examination may be useful in daily clinical practice, but regular use and training sessions are required to secure quality of testing.

PMID: 23444448 [PubMed – in process]

Home
Journals

Books

Madame Curie Database
Contact
Support
For Librarians
iPad

Login

by Author by Title
Advanced

Cell Cycle Home
Editorial Board
Subscribe
Search
Archive
Online First
Contact
For Authors
eTOC Alerts
RSS Feeds

Report

TIPE2 deficiency accelerates neointima formation by downregulating smooth muscle cell differentiation

Purchase or Subscribe

Purchase article for $29

Subscribe to Cell Cycle

Recommend this Publication

Subscriber Login

Volume 12, Issue 3 February 1, 2013
Pages 501 – 510
http://dx.doi.org/10.4161/cc.23325
Keywords: TNFAIP8L2 (TIPE2), atherosclerosis, cell cycle, phenotypic switching, vascular smooth muscle cell

Authors: Guizhong Zhang, Wenqian Zhang, Yunwei Lou, Wenjin Xi, Jian Cui, Minghong Geng, Faliang Zhu, Youhai H. Chen and Suxia Liu

View affiliations

Abstract:
Phenotypic switching of vascular smooth muscle cells (VSMCs) is known to play a key role in the development of atherosclerosis. However, the mechanisms that mediate VSMC phenotypic switching are unclear. We report here that TIPE2, the tumor necrosis factor (TNF) α-induced protein 8-like 2 (TNFAIP8L2), plays an atheroprotective role by regulating phenotypic switching of VSMCs in response to oxidized low-density lipoprotein (ox-LDL) stimuli. TIPE2-deficient VSMCs treated with ox-LDL expressed lower levels of contractile proteins such as SMαA, SM-MHC and calponin, whereas the proliferation, migration and the synthetic capacity for growth factors and cytokines were increased remarkably. Furthermore, TIPE2 inhibited VSMCs proliferation by preventing G1/S phase transition. Interestingly, these effects of TIPE2 on VSMCs were dependent on P38 and ERK1/2 kinase signals. As a result, neointima formation was accelerated in the carotid arteries of TIPE2-deficient mice. These results indicate that TIPE2 is a potential inhibitor of atherosclerosis.

Preview:

National Institute of Dental and Craniofacial Research (NIDCR)
National Institutes of Health, DHHS
31 Center Drive, Room 5B-55
Bethesda, MD 20892
nidcrinfo@mail.nih.gov
http://www.nidcr.nih.gov
Tel: 301-496-4261

American Chronic Pain Association (ACPA)
P.O. Box 850
Rocklin, CA 95677-0850
ACPA@theacpa.org
http://www.theacpa.org
Tel: 916-632-0922 800-533-3231
Fax: 916-652-8190

American Headache Society Committee for Headache Education (ACHE)
19 Mantua Road
Mt. Royal, NJ 08061
achehq@talley.com
http://www.achenet.org
Tel: 856-423-0043
Fax: 856-423-0082

National Headache Foundation
820 N. Orleans
Suite 411
Chicago, IL 60610-3132
info@headaches.org

Home

Tel: 312-274-2650 888-NHF-5552 (643-5552)
Fax: 312-640-9049

Arthritis Foundation
P.O. Box 7669
Atlanta, GA 30357
help@arthritis.org
http://www.arthritis.org
Tel: 800-283-7800 404-872-7100 404-965-7888
Fax: 404-872-0457

Related NINDS Publications and Information

BACKGROUND: Chronic pain is recognised as an important problem in the community but our understanding of the epidemiology of chronic pain remains limited. We undertook a study designed to quantify and describe the prevalence and distribution of chronic pain in the community. METHODS: A random sample of 5036 patients, aged 25 and over, was drawn from 29 general practices in the Grampian region of the UK and surveyed by a postal self-completion questionnaire. The questionnaire included case-screening questions, a question on the cause of the pain, the chronic pain grade questionnaire, the level of expressed needs questionnaire, and sociodemographic questions. FINDINGS: 3605 questionnaires were returned completed. 1817 (50.4%) of patients self reported chronic pain, equivalent to 46.5% of the general population. 576 reported back pain and 570 reported arthritis; these were the most common complaints and accounted for a third of all complaints. Backward stepwise logistic-regression modelling identified age, sex, housing tenure, and employment status as significant predictors of the presence of chronic pain in the community. 703 (48.7%) individuals with chronic pain had the least severe grade of pain, and 228 (15.8%) the most severe grade. Of those who reported chronic pain, 312 (17.2%) reported no expressed need, and 509 (28.0%) reported the highest expressed need. INTERPRETATION: Chronic pain is a major problem in the community and certain groups within the population are more likely to have chronic pain. A detailed understanding of the epidemiology of chronic pain is essential for efficient management of chronic pain in primary care.

Content referenced by

http://en.wikipedia.org/wiki/Chronic_pain
http://www.ncbi.nlm.nih.gov/pubmed?term=chronic%20pain
http://www.landesbioscience.com/journals/cc/article/23325/
http://www.ninds.nih.gov/disorders/chronic_pain/chronic_pain.htm
http://scholar.google.ca/scholar?hl=en&q=chronic+pain&btnG=&as_sdt=1%2C5&as_sdtp=