Wikipedia - Hypoalgesia (for CHECK)

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HypoalgesiaFrom Wikipedia, the free encyclopedia

Hypoalgesia or hypalgesia denotes a decreased sensitivity to painfulstimuli.

Hypoalgesia occurs when nociceptive (painful) stimuli are interrupted ordecreased somewhere along the path between the input (nociceptors), and the places where they are processedand recognized as pain in the conscious mind. Hypoalgesic effects can be mild, such as massaging a stubbed toeto make it hurt less or taking aspirin to decrease a headache, or they can be severe, like being under stronganesthesia. Hypoalgesia can be caused by exogenous chemicals such as opioids, as well as by chemicalsproduced by the body in phenomena such as fear- and exercise- induced hypoalgesia. Hypoalgesia can also beassociated with diseases, such as CIPA or in less severe cases with diabetes or other diseases associated withhypertension.

Contents1 Chemical causes

1.1 Analgesics1.2 Opioids1.3 Exercise induced hypoalgesia1.4 Fear induced hypoalgesia

2 Diseases2.1 Hereditary neuropathies2.2 Hypoalgesia and hypertension

3 See also4 References

Chemical causesAnalgesicsAnalgesics are a class of biochemicals that cause hypoalgesia. Analgesics can act on both the peripheral andcentral nervous systems to decrease pain. Certain analgesics also work to decrease the source of the pain byworking to decrease swelling and inflammation, as in the case of NSAIDs.[1]

OpioidsOpioids refers to a specific group of analgesics - including morphine, codeine, and opium - that act on opioidreceptors, which are located mainly in the central nervous system.

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Endogenous opioids are types of opioids produced by the body specifically to modulate pain. They includeendorphins, enkephalins, dynorphins and endomorphins. These peptides are especially important for modulatingpain in response to the environment. These can be released in response to a number of things, includingincreased blood pressure, pain and danger. It has been found that endogenous opioids are at least partiallyresponsible for phenomena like Runner's high, hypoalgesia in the fight-or-flight response, and even for theanalgesic effects of acupuncture therapy.[2] In all these cases, there is a certain level of signal processing thatoccurs in the CNS which leads to the release of these chemicals.

Exercise induced hypoalgesiaThere has been a great deal of research examining the link between exercise and hypoalgesia. Many studieshave shown the direct link between the two by subjecting patients to exercise and rating their pain responses,but despite the great deal of research, the mechanism of action is still poorly understood. It has been shown thatthe triggering mechanism for the hypoalgesic effects is the increase in blood pressure that accompanies a goodworkout. The body senses the increased blood pressure, and it is hypothesized that in response, endogenousopioids are released.[3] This hypothesis is well supported in human research, and it has been verified that itplays a part, but animal research implies that other mechanisms are also involved.[4]

Fear induced hypoalgesiaFear induced hypoalgesia is another example of a mechanism controlled by opioids. It is postulated that fear isa defense mechanism that has evolved over time to provide protection. In the case of hypoalgesia, a decreasedresponse to pain would be very beneficial in a situation where an organisms life was at stake, since feeling painwould be a hindrance rather than a help. It has been well documented that fear does cause a decrease in painresponse,[5] however much like the exercise induced hypoalgesia, the exact mechanisms of action are not wellunderstood. Studies have shown that opioids are definitely involved in the process, yet opiates alone do notcompletely explain the analgesic response.[6][7] What the other mechanisms of action are is still unknown.

DiseasesIt has been demonstrated that many diseases can cause hypoalgesia. Some diseases, like CIPA, are hereditarydisorders where genes essential for the correct functioning of nociceptors no longer work. There are manydiseases like this, and they all fall under the category of hereditary sensory autonomic neuropathies.Alternatively, some diseases affect other functions in your body, which can activate the pathways that causehypoalgesia. This effect happens in people with diabetes and other diseases associated with hypertension.

Hereditary neuropathiesHereditary sensory and autonomic neuropathies (HSAN), e.g. CIPA, are hereditary disorders that arecharacterized by malfunctioning or nonfunctioning pain receptors.[8] Most of these diseases are also associatedwith decreased temperature sensation as well. In some cases these diseases are also associated with othersymptoms like mental retardation and diminished production of sweat and tears. Diseases like this can be verydangerous for the patients, because they are not able to judge what hurts, and therefore when they should stop

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doing something. A child with the disease might bite their finger clean off before they realized that what theywere doing might harm them, or they might leave their hand on a hot stove without ever realizing it was on.These examples support the theory that pain is essential for life, more specifically, survival.

Hypoalgesia and hypertension

Many studies have shown that hypertension in patients can cause hypoalgesia.[9][10] Diseases like diabetes,which are associated with hypertension are also associated with hypoalgesia. Just like in Exercise-InducedHypoalgesia, the increased blood pressure of hypertension works as a signal to the body to release opioids andactivate other pain modulation pathways. Also, although the area is not widely studied, there is evidence thatthis is not the only cause. Diseases may lead to activation of any of these mechanisms, just like diabetes causinghypertension. A full study of the pathways regulating pain is needed.

See alsoHyperalgesiaHypoalgesic effect of swearing

References1. Vane, J. (2003). "The mechanism of action of anti-inflammatory drugs." Int J Clin Pract Suppl(135): 2.2. Yang, J., Y. Yang, et al. (2007). "Effect of oxytocin on acupuncture analgesia in the rat." Neuropeptides 41(5): 285-92.3. Koltyn, K. F. and M. Umeda (2006). "Exercise, hypoalgesia and blood pressure." Sports Med 36(3): 207-14.4. Koltyn, K. F. (2000). "Analgesia following exercise: a review." Sports Med 29(2): 85-98.5. Rhudy, J. L., J. S. Grimes, et al. (2004). "Fear-induced hypoalgesia in humans: effects on low intensity thermal

stimulation and finger temperature." J Pain 5(8): 458-68.6. J.M. Lichtman and M.S. Fanselow, Cats produce analgesia in rats on the tail-flick test: naltrexone sensitivity is

determined by the nociceptive test stimulus. Brain Res 533 (1990), pp. 9194.7. H.S. Hagen and K.F. Green, Effects of time of testing, stress level and number of conditioning days on naloxone

sensitivity of conditioned stress-induced analgesia in rats. Behav Neurosci 102 (1988), pp. 906914.8. Schalka, M. M., M. S. Correa, et al. (2006). "Congenital insensitivity-to-pain with anhidrosis (CIPA): a case report with

4-year follow-up." Oral Surg Oral Med Oral Pathol Oral Radiol Endod 101(6): 769-73.9. Zamir, N., Shuber, E., 1980. Altered pain perception in hypertensive humans. Brain Research 201, 471474.

10. Edwards, L., C. Ring, et al. (2007). "Nociceptive flexion reflex thresholds and pain during rest and computer game playin patients with hypertension and individuals at risk for hypertension." Biol Psychol 76(1-2): 72-82.

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Wikipedia - Hypoalgesia (for CHECK)