Hypoalgesia - Wikipedia, the free encyclopedia

10/05/15 18:05

Hypoalgesia
From Wikipedia, the free encyclopedia

Hypoalgesia or hypalgesia denotes a decreased sensitivity to painful

stimuli.

Look up hypoalgesia in
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Hypoalgesia occurs when nociceptive (painful) stimuli are interrupted or

decreased somewhere along the path between the input (nociceptors), and the places where they are processed
and recognized as pain in the conscious mind. Hypoalgesic effects can be mild, such as massaging a stubbed toe
to make it hurt less or taking aspirin to decrease a headache, or they can be severe, like being under strong
anesthesia. Hypoalgesia can be caused by exogenous chemicals such as opioids, as well as by chemicals
produced by the body in phenomena such as fear- and exercise- induced hypoalgesia. Hypoalgesia can also be
associated with diseases, such as CIPA or in less severe cases with diabetes or other diseases associated with
hypertension.

Contents
1 Chemical causes
1.1 Analgesics
1.2 Opioids
1.3 Exercise induced hypoalgesia
1.4 Fear induced hypoalgesia
2 Diseases
2.1 Hereditary neuropathies
2.2 Hypoalgesia and hypertension
3 See also
4 References

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

Opioids
Opioids refers to a specific group of analgesics - including morphine, codeine, and opium - that act on opioid
receptors, 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 include
endorphins, enkephalins, dynorphins and endomorphins. These peptides are especially important for modulating
pain in response to the environment. These can be released in response to a number of things, including
increased blood pressure, pain and danger. It has been found that endogenous opioids are at least partially
responsible for phenomena like Runner's high, hypoalgesia in the fight-or-flight response, and even for the
analgesic effects of acupuncture therapy.[2] In all these cases, there is a certain level of signal processing that
occurs in the CNS which leads to the release of these chemicals.

Exercise induced hypoalgesia

There has been a great deal of research examining the link between exercise and hypoalgesia. Many studies
have 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 that
the triggering mechanism for the hypoalgesic effects is the increase in blood pressure that accompanies a good
workout. The body senses the increased blood pressure, and it is hypothesized that in response, endogenous
opioids are released.[3] This hypothesis is well supported in human research, and it has been verified that it
plays a part, but animal research implies that other mechanisms are also involved.[4]

Fear induced hypoalgesia

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

Diseases
It has been demonstrated that many diseases can cause hypoalgesia. Some diseases, like CIPA, are hereditary
disorders where genes essential for the correct functioning of nociceptors no longer work. There are many
diseases 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 cause
hypoalgesia. This effect happens in people with diabetes and other diseases associated with hypertension.

Hereditary neuropathies
Hereditary sensory and autonomic neuropathies (HSAN), e.g. CIPA, are hereditary disorders that are
characterized by malfunctioning or nonfunctioning pain receptors.[8] Most of these diseases are also associated
with decreased temperature sensation as well. In some cases these diseases are also associated with other
symptoms like mental retardation and diminished production of sweat and tears. Diseases like this can be very
dangerous 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 they
were 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-Induced
Hypoalgesia, the increased blood pressure of hypertension works as a signal to the body to release opioids and
activate other pain modulation pathways. Also, although the area is not widely studied, there is evidence that
this is not the only cause. Diseases may lead to activation of any of these mechanisms, just like diabetes causing
hypertension. A full study of the pathways regulating pain is needed.

See also
Hyperalgesia
Hypoalgesic effect of swearing

References
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Vane, J. (2003). "The mechanism of action of anti-inflammatory drugs." Int J Clin Pract Suppl(135): 2.
Yang, J., Y. Yang, et al. (2007). "Effect of oxytocin on acupuncture analgesia in the rat." Neuropeptides 41(5): 285-92.
Koltyn, K. F. and M. Umeda (2006). "Exercise, hypoalgesia and blood pressure." Sports Med 36(3): 207-14.
Koltyn, K. F. (2000). "Analgesia following exercise: a review." Sports Med 29(2): 85-98.
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.
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.
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.
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.
Zamir, N., Shuber, E., 1980. Altered pain perception in hypertensive humans. Brain Research 201, 471474.
Edwards, L., C. Ring, et al. (2007). "Nociceptive flexion reflex thresholds and pain during rest and computer game play
in patients with hypertension and individuals at risk for hypertension." Biol Psychol 76(1-2): 72-82.

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