Chronic pain

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

Chronic pain has several different meanings in medicine. Traditionally, the distinction between acute and chronic pain has relied upon an arbitrary interval of time from onset; the two most commonly used markers being 3 months and 6 months since the initiation of pain,[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

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 somatic" and "deep", and deep pain into "deep somatic" and "visceral". Superficial somatic 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 injured, 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" (originiting in the brain or spinal cord).[6] Peripheral neuropathic pain is often described as “burning,” “tingling,” “electrical,” “stabbing,” or “pins and needles.” [7] Bumping the "funny bone" elicits peripheral neuropathic pain.

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 [10] 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. [11]

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.

Pain management (also called pain medicine) is that branch of medicine employing an interdisciplinary approach to the relief of pain and improvement in the quality of life of those living with pain.[12] The typical pain management team includes medical practitioners, clinical psychologists, physiotherapists, occupational therapists, and nurse practitioners.[13] 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.[14][15][16]

Behavioral model

The behavioral model of chronic pain comes from the applied behavior analysis literature. The model focuses on decreasing pain behaviors [17]. This model has shown effectiveness in reducing pain responses though operant based interventions.[18]. More recently a [behavioral activation] model has been generated for pain [19]. This model has research support and has been replicated[20]

Prognosis

Chronic pain may cause other symptoms or conditions, including depression and anxiety. It may also contribute to decreased physical activity given the apprehension of exacerbating pain.[21] Very little work has been done on the cognitive effects of chronic pain, with most of the publications focussing on the effects of cognition on pain but only 5% examining the effects of pain on cognition.[22]

People with high-intensity chronic pain have significantly reduced ability to perform attention-demanding tasks.[23] Pain appears to strongly capture the attention of people with chronic pain; tests assessing the ability to attend show poorer performance than pain-free people on all tests demanding attention.[24] The exception is found with tasks that are highly demanding of attention, where performance between the two groups is equivalent.[24] In experimental testing, two-thirds of individuals with chronic pain demonstrate clinically significant impairment of attention, independent of age, education, medication and sleep disruption. Individuals with the highest levels of pain showed greatest disruption of memory traces, suggesting that pain diminishes working memory.[25]

Psychology

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.[26]

See also

Conditions related to pain
Drugs
Other approaches in Physical medicine and rehabilitation (Physiatry)
Alternative therapies
Surgery

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 0683304623. http://books.google.com.au/books?id=TyNEicOiJqQC&pg=RA1-PA18&dq=Pain+terms+and+taxonomies&cd=1#v=onepage&q=Pain%20terms%20and%20taxonomies&f=false. 
  2. ^ Main, C.J.; Spanswick, C.C. (2001). Pain management: an interdisciplinary approach. Elsevier. p. 93. ISBN 0-443-05683-8. http://books.google.com/?id=wcEQPzTOEAoC&pg=PA93&dq=chronic+acute+subacute+pain&cd=48#v=onepage&q=chronic%20acute%20subacute%20pain. 
  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. http://books.google.com.au/books?id=lg7sIgP9D3kC&pg=PA28&dq=chronic+acute+subacute+pain+idiopathic&lr=&client=firefox-a&cd=1#v=onepage&q=chronic%20acute%20subacute%20pain%20idiopathic&f=true. 
  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. http://books.google.com.au/books?id=IeElgT1clUcC&pg=PA303&lpg=PA303&dq=%22definitions+of+pain+and+its+central+representation%22&source=bl&ots=mKVpvW_2gA&sig=gs3Z5lQMiMHg2tT7Fc1D2RSzbHI&hl=en&ei=DlpAS83FE8uHkQWOnon1Bg&sa=X&oi=book_result&ct=result&resnum=1&ved=0CAoQ6AEwAA#v=onepage&q=%22definitions%20of%20pain%20and%20its%20central%20representation%22&f=true. 
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  7. ^ Paice, JA (2003). "Mechanisms and management of neuropathic pain in cancer". Journal of supportive oncology 1 (2): 107–20. PMID 15352654. http://www.supportiveoncology.net/journal/articles/0102107.pdf. 
  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. 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. http://www.jneurosci.org/cgi/content/full/28/6/1398. 
  11. ^ 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. 
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  13. ^ Main, Chris J.; Spanswick, Chris C. (2000). Pain management: an interdisciplinary approach. Churchill Livingstone. ISBN 0 443 05683 8. 
  14. ^ 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. http://books.google.com/?id=L2CSdeiMZi4C&pg=PA27&dq=%22the+classification+of+pain%22+thienhaus&q=%22chronic%20pain%20frequently%20requires%20the%20coordinated%20efforts%20of%20a%20broadly%20based%20treatment%20team%22. 
  15. ^ 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. 
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  19. ^ Duane A. Lundervold, Chris Talley & Michael Buermann (2008).Effect of Behavioral Activation Treatment on Chronic Fibromyalgia Pain: Replication and Extension. Internationa Journal of Behavioral Consultation and Therapy, 4(2), 146-157 [1]
  20. ^ Duane A. Lundervold, Chris Talley & Michael Buermann (2008).Effect of Behavioral Activation Treatment on Chronic Fibromyalgia Pain: Replication and Extension. Internationa Journal of Behavioral Consultation and Therapy, 4(2), 146-157 [2]
  21. ^ 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. 
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