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Name of Symptom/Sign:
Chronic pain
ICD-10 R521-R522
OMIM [2]
MedlinePlus [3]
eMedicine /
DiseasesDB [4]

Chronic pain was originally defined as pain that has lasted 6 months or longer. More recently it has been defined as pain that persists longer than the temporal course of natural healing, associated with a particular type of injury or disease process.[1]

The International Association for the Study of Pain defines pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage."[2] It is important to note that pain is subjective in nature and is defined by the person experiencing it, and the medical community's understanding of chronic pain now includes the impact that the mind has in processing and interpreting pain signals.

Functional Anatomy

The anatomy of the nociceptive system can be grossly divided into the peripheral and central nervous system. The peripheral nervous system consists of small myelinated and unmyelinated nerve fibers. These nerve fibers converge into a region of the spinal cord referred to as the dorsal horn. The dorsal horn is the first relay station in pain signal transmission. The next element of pain transmission includes nerve fibers that then travel to the thalamus. From the thalamus the next order of neurons ascend to the limbic system and sensory cortex. This accounts for the affective elements and discriminative of pain respectively.[3][4]


The experience of pain biologically is referred to as nociception. Nociception occurs in any tissue or organ in which pain signals arise secondary to a disease process or trauma. The nociception can also occur if there is dysfunction or damage to nerves themselves.[2]


Main article: Pain and nociception

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.[5]


Nociception (pain) may arise from injury or disease to visceral, somatic and neural structures in the body. More broadly pain is described as malignant or non-malignant in origin.[4]


Pain may be a response to injury or any number of disease states that provoke nociception. Advances in imaging studies and electrophysiological studies allow us to gain a deeper insight into the characteristics and properties associated with the phenomenon of chronic pain.[6][7][8]

Related sequelae

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.[9] Conversely it may itself have psychosomatic or psychogenic component to its cause.[10]


It is rare to completely achieve absolute and sustained relief of pain. Thus, the clinical goal is pain management. Pain management is often multidisciplinary in nature. A recent journal article by Gatchell and Okifuji recognizes the importance of comprehensive pain programs(CPPs) in the management of chronic pain. They summarize their findings as follows: "CPPs offer the most efficacious and cost-effective treatment for persons with chronic pain, relative to a host of widely used conventional medical treatment." [11][12]


In the treatment of chronic pain, whether due to malignant or benign processes, the three-step WHO Analgesic Ladder is often used.[5][6][7] This provides guidelines for stepping up the amount of analgesia and maintains a general basis that is used in a number of countries around the world to manage chronic pain conditions. The exact medications recommended will vary with the country and the individual treatment centre, but the following gives an example of the approach to treating chronic pain with medications. If, at any point, treatment fails to provide adequate pain relief, then the doctor and patient move onto the next step.

Mild pain

Paracetamol (acetaminophen), or a non steroidal anti-inflammatory drug such as ibuprofen

Mild to moderate pain

Paracetamol, an NSAID and/or paracetamol in a combination product with a weak opioid such as hydrocodone; used in combination, may provide greater relief than their separate use.

Moderate to severe pain

Morphine is the gold standard choice, followed by Oxycodone, Fentanyl in the form of a transdermal patch designed for chronic pain management, Diamorphine, hydromorphone or methadone are used less frequently.

Pethidine is not recommended for chronic pain management due to its low potency, short duration of action, and toxicity associated with repeated use.


Opioid medications can provide a short, intermediate or long acting analgesia depending upon the specific properties of the medication and whether it is formulated as an extended release drug. Opioid medications may be administered orally, by injection, via nasal mucosa or oral mucosa, rectal, transdermal, intravenously, epidurally and intrathecally. In chronic pain conditions that are opioid responsive a combination of a long acting or extended release medication is often prescribed in conjunction with a shorter acting medication for break through pain (exacerbations).

Most opioid treatment is oral (tablet, capsule or liquid), but suppositories and skin patches can be prescribed. An opioid injection is rarely needed for patients with chronic pain.

Although opioids are strong analgesics, they do not provide complete analgesia regardless of whether the pain is acute or chronic in origin. Opioids are efficacious analgesics in chronic malignant pain and modestly effective nonmalignant pain management. However, there are variable associated adverse effects, especially during the commencement or change in dosing and administration. When opioids are used for prolonged periods drug tolerance, chemical dependency and (rarely) addiction may occur. Chemical dependency is ubiquitous among opioid therapy after continuous administration; however, drug tolerance is not well studied in patients on long term opioid therapy. Addiction rarely occurs as a result of opioid prescription, but they are abused by some individuals, which can cause concern to health care providers. Diversion of opioid medications is another concern for health care providers.

Non-steroidal anti-inflammatory drugs

The other major group of analgesics are Non-steroidal anti-inflammatory drugs (NSAID). This class of medications does not include acetaminophen, which has minimal anti-inflammatory properties. However, acetaminophen may be administered as a single medication or in combination with other analgesics (both NSAIDs and opioids). The alternatively prescribed NSAIDs such as ketoprofen and piroxicam, have limited benefit in chronic pain disorders and with long term use is associated with significant adverse effects. The use of selective NSAIDs designated as selective COX-2 inhibitors have significant cardiovascular and cerebrovascular risks which have limited their utilization.[13][14]

Antidepressants and antiepileptic drugs

Some antidepressant and antiepileptic drugs are used in chronic pain management and act primarily within the pain pathways of the central nervous system, though peripheral mechanisms have been attributed as well. These mechanisms vary and in general are more effective in neuropathic pain disorders as well as complex regional pain syndrome.[15] Drugs such as Gabapentin have been widely prescribed for the off-label use of pain control. The list of side effects for these classes of drugs are typically much longer than opiate or NSAID treatments for chronic pain, and many antiepileptics cannot be suddenly stopped without the risk of seizure.

Interventional therapy

Pulsed radiofrequency, Injections, Neuromodulation and Neuroablative Therapy may be used to target either the tissue structures and organ/systems responsible for persistent nociception or the nerves conveying nociception from the structures implicated as the source of chronic pain.[16][17][18][19][20]

An intrathecal pump used to delivery very small quantities of medications directly to the spinal fluid. This is similar to epidural infusions used in labour and postoperatively. The major differences are that it is much more common for the drug to be delivered into the spinal fluid (intrathecal) rather than epidurally, and the pump can be fully implanted under the skin. This approach allows the drug to be delivered directly to the site of action, ie the spinal cord, and so allows a higher dose to be given with less systemic side effects.[21]

A spinal cord stimulator is an implantable medical device that creates electric impulses and applies them near the dorsal surface of the spinal cord provides a paresthesia ("tingling") sensation that alters the perception of pain by the patient.


Further information: Physical medicine and rehabilitation

As alluded to earlier there are other modalities used in the treatment of chronic pain. These include: physical modalities such as thermal agents and electrotherapy. Complementary and alternative medicine, therapeutic exercise and behavioral therapy are also utilized autonomously or in tandem with interventional techniques and conventional pharmacotherapy. This is most often structured in a multidisciplinary or interdisciplinary program.[22]

Applied Behavior Analysis for Treating Chronic Pain

From the field of applied behavior analysis has come a behavioral model of chronic pain. This model sees pain as mixture of operant and respondent behavior. Through the learning process normal tissue learns to fire pain responses in the presence of specific environmental antecedents and consequences. The model was first proposed by Fordyce [23] [24]. The behavioral model has received much research support[25][26]. Behavioral interventions often termed behavior therapy or behavior modification have growing research support [27][28] Another operant and respondent behavioral intervention is EMG bifeedback. Biofeedback based on behavioral principles has shown success for chronic pain [29][30]

See also

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



  1. Shipton EA, Tait B (2005). Flagging the pain: preventing the burden of chronic pain by identifying and treating risk factors in acute pain. European journal of anaesthesiology 22 (6): 405-12.
  2. 2.0 2.1 Merskey H (1994). Logic, truth and language in concepts of pain. Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation 3 Suppl 1: S69-76.
  3. Romanelli P, Esposito V (2004). The functional anatomy of neuropathic pain. Neurosurg. Clin. N. Am. 15 (3): 257-68.
  4. 4.0 4.1 Vanderah TW (2007). Pathophysiology of pain. Med. Clin. North Am. 91 (1): 1-12.
  5. Vadivelu N, Sinatra R (2005). Recent advances in elucidating pain mechanisms. Current opinion in anaesthesiology 18 (5): 540-7.
  6. Dunckley P, Wise RG, Fairhurst M, Hobden P, Aziz Q, Chang L, Tracey I (2005). A comparison of visceral and somatic pain processing in the human brainstem using functional magnetic resonance imaging. J. Neurosci. 25 (32): 7333-41.
  7. Geha PY, Apkarian AV (2005). Brain imaging findings in neuropathic pain. Current pain and headache reports 9 (3): 184-8.
  8. Turton AJ, McCabe CS, Harris N, Filipovic SR (2007). Sensorimotor integration in Complex Regional Pain Syndrome: a transcranial magnetic stimulation study. Pain 127 (3): 270-5.
  9. Pruimboom L, van Dam AC (2007). Chronic pain: a non-use disease. Med. Hypotheses 68 (3): 506-11.
  10. Sarno, John et al. (2006). The Divided Mind: The Epidemic of Mindbody Disorders, 11-18, New York: ReganBooks.
  11. Henningsen P, Zipfel S, Herzog W (2007). Management of functional somatic syndromes. Lancet 369 (9565): 946-55.
  12. 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.
  13. Munir MA, Enany N, Zhang JM (2007). Nonopioid analgesics. Med. Clin. North Am. 91 (1): 97-111.
  14. Ballantyne JC (2006). Opioids for chronic nonterminal pain. South. Med. J. 99 (11): 1245-55.
  15. Jackson KC (2006). Pharmacotherapy for neuropathic pain. Pain practice : the official journal of World Institute of Pain 6 (1): 27-33.
  16. Varrassi G, Paladini A, Marinangeli F, Racz G (2006). Neural modulation by blocks and infusions. Pain practice : the official journal of World Institute of Pain 6 (1): 34-8.
  17. Meglio M (2004). Spinal cord stimulation in chronic pain management. Neurosurg. Clin. N. Am. 15 (3): 297-306.
  18. Rasche D, Ruppolt M, Stippich C, Unterberg A, Tronnier VM (2006). Motor cortex stimulation for long-term relief of chronic neuropathic pain: a 10 year experience. Pain 121 (1-2): 43-52.
  19. Boswell MV, Trescot AM, Datta S, Schultz DM, Hansen HC, Abdi S, Sehgal N, Shah RV, Singh V, Benyamin RM, Patel VB, Buenaventura RM, Colson JD, Cordner HJ, Epter RS, Jasper JF, Dunbar EE, Atluri SL, Bowman RC, Deer TR, Swicegood JR, Staats PS, Smith HS, Burton AW, Kloth DS, Giordano J, Manchikanti L (2007). Interventional techniques: evidence-based practice guidelines in the management of chronic spinal pain. Pain physician 10 (1): 7-111.
  20. Romanelli P, Esposito V, Adler J (2004). Ablative procedures for chronic pain. Neurosurg. Clin. N. Am. 15 (3): 335-42.
  21. Ferrante FM, Lu L, Jamison SB, Datta S (1991). Patient-controlled epidural analgesia: demand dosing. Anesth. Analg. 73 (5): 547–52.
  22. Geertzen JH, Van Wilgen CP, Schrier E, Dijkstra PU (2006). Chronic pain in rehabilitation medicine. Disability and rehabilitation 28 (6): 363-7.
  23. Fordyce, W.E.(1976). Behavioral methods for chronic pain and illness. St Louis: Mosby
  24. Fordyce, W.E.(1988). Pain and suffering: A reappraisal. American Psychologist, 43, 276-283
  25. Romano, J.M., Jensen, M.P., Turner, J.A., Good, A.B., & Hops, H. (1990). Chronic pain patient-partner interactions: Further support for a behavioral model of chronic pain. Behavior Therapy, 31(3), 415-440.
  26. Sanders, S.H. (2006). Behavioral Conceptualization and Treatment for Chronic Pain. The Behavior Analyst Today, 7(2), 253-271 [1]
  27. Turner, J.A., & Clancy, S. (1988). Comparison of operant behavioral and cogntiive behavioral group treatment for chronic low back pain. Journal of Consulting and Clinical Psychology, 58, 573-579.
  28. Turner, J.A., Clancy, S., McQuade, K.J., & Cardanes, D.D. (1990). Effectiveness of behavior therapy for chronic low back pain: A component analysis. Journal of Consuling and Clinical Psychology, 58, 573-579.
  29. Flor, H., & Birbaumer, N. (1993). Comparison of the efficacy of cicctromyographic biofeedback, cognitive behavior therapy, and conservative medical treatment for chronic skeletal pain. Journal of Consulting and Clinical Psychology, 61, 653-658.
  30. Newton-John, T.R.O., Spence, S.H., & Schotte, D.(1995). Cognitive-behavioral therapy versus EMG biofeedback in the treatment of chronic low back pain. Behaviour Research and Therapy, 33, 691-697.

External links

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