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Opioid-induced hyperalgesia (OIH) or opioid-induced abnormal pain sensitivity, also called paradoxical hyperalgesia, is an uncommon condition of generalized pain caused by the long-term use of high dosages of opioids [1] such as morphine, [2] oxycodone, [3] and methadone. [4] [5] OIH is not necessarily confined to the original affected site. [6]
However, since opioid antagonists also block the beneficial effects of opioid analgesics, they are generally useful only for treating overdose, with use of opioid antagonists alongside opioid analgesics to reduce side effects, requiring careful dose titration and often being poorly effective at doses low enough to allow analgesia to be maintained.
Morphine is a phenanthrene opioid receptor agonist – its main effect is binding to and activating the μ-opioid receptor (MOR) in the central nervous system. Its intrinsic activity at the MOR is heavily dependent on the assay and tissue being tested; in some situations it is a full agonist while in others it can be a partial agonist or even ...
Tomycz’s research group is among the first in the nation to look at this deep brain stimulation therapy as a possible treatment for opioid addiction and have embarked on a small study to test ...
The first attempt to purify the receptor involved the use of a novel opioid antagonist called chlornaltrexamine that was demonstrated to bind to the opioid receptor. [10] Caruso later purified the detergent-extracted component of rat brain membrane that eluted with the specifically bound 3 H -chlornaltrexamine.
Naloxone is an opioid antagonist and reverses the central nervous depressive effects seen in opioid overdose. [6] In the setting of a colonoscopy, naloxone is rarely administered but when it is administered, its half-life is shorter than some common opioid agonists. Therefore, the patient may still exhibit central nervous system depression ...
[30] [31] [32] Another long-term adaptation to opioid use can be upregulation of glutamate and other pathways in the brain which can exert an opioid-opposing effect, so reduce the effects of opioid drugs by altering downstream pathways, regardless of MOR activation. [33] [34]
Permanent brain damage: Causes: Opioids (morphine, codeine, heroin, fentanyl, tramadol, methadone, etc.) Risk factors: Opioid dependence, metabolic disorders, use of high doses of opioids, injection of opioids, use with antidepressants, alcohol, benzodiazepines and cocaine. [1] [2] Diagnostic method: Based on symptoms [3] Differential diagnosis