Articles: hyperalgesia.
-
Experimental studies suggest that surgical injury may up- or down-regulate nociceptive function. Therefore, the aim of this clinical study was to evaluate the effect of elective arthroscopically assisted knee surgery on nociceptive responses to a heat injury. ⋯ Arthroscopic knee surgery did not modify nociceptive responses to a contralaterally applied experimental burn injury.
-
Randomized Controlled Trial Clinical Trial
Short-term infusion of the mu-opioid agonist remifentanil in humans causes hyperalgesia during withdrawal.
Numerous animal studies suggest that acute and chronic exposure to opioids can be associated with the development of hyperalgesia, i.e. an increased sensitivity to noxious stimuli. Hyperalgesia has been documented during withdrawal and on occasion while animals were still exposed to opioids. A pivotal role in the genesis of opioid-associated hyperalgesia has been attributed to a pain facilitating system involving the N-methyl-D-aspartate (NMDA)-receptor. ⋯ Co-administration of the NMDA-receptor antagonist S-ketamine abolished observed enlargement of the hyperalgesic skin area. This study provides direct evidence in humans that short-term administration of an opioid can enhance hyperalgesia as observed during withdrawal and points to a potential role of the NMDA-receptor system in mediating such a hyperalgesic response. This study also points to a differential susceptibility of different pain modalities for the expression of hyperalgesia associated with opioid administration.
-
We report a case of a patient with metastatic testicular cancer and intractable pain refractory to massive doses of oral, intravenous, and intrathecal (IT) opioids supported by analgesic adjuvants. During our efforts to control his pain, the patient exhibited opioid-induced hyperalgesia, an uncommon but important phenomenon seen with high-dose opioid therapy. With appropriate opioid adjustment--in this case reduction of intrathecal morphine dosage by a factor of 100--the condition rapidly resolved and the patient became pain-free and remained so until his death six weeks later. The keys to identifying this uncommon, but treatable, opioid side effect are recognizing it as a possibility when aggressive efforts to control pain with high doses of opioids, especially when administered neuraxially, are met with increasing pain.
-
Joint manipulation has long been used for pain relief. However, the underlying mechanisms for manipulation-related pain relief remain largely unexplored. The purpose of the current study was to determine which spinal neurotransmitter receptors mediate manipulation-induced antihyperalgesia. ⋯ NAN-190 also blocked manipulation-induced antihyperalgesia suggesting that effects of methysergide are mediated by 5-HT1A receptor blockade. However, spinal blockade of opioid or GABAA receptors had no effect on manipulation induced-antihyperalgesia. Thus, the antihyperalgesia produced by joint manipulation appears to involve descending inhibitory mechanisms that utilize serotonin and noradrenaline.
-
Randomized Controlled Trial Clinical Trial
Withdrawal hyperalgesia after acute opioid physical dependence in nonaddicted humans: a preliminary study.
Hyperalgesia has been demonstrated to be a cardinal sign of physical withdrawal from opioids in preclinical models for more than 30 years, although few empirical data exist to support its occurrence in humans. In this preliminary study we used the acute opioid physical dependence (APD) model to test for the presence of hyperalgesia to experimental cold-pressor pain in 4 healthy non-opioid-dependent men via 3 different pretreatment opioid administration protocols previously demonstrated to induce APD (morphine 18 mg/70 kg intramuscular, morphine 10 mg/70 kg intravenous, hydromorphone 2 mg/70 kg intravenous), repeated on 2 separate occasions, and placebo. ⋯ Paired t tests comparing change scores between the opioid pretreatments and placebo showed that pain threshold and tolerance to the cold-pressor uniformly decreased across all APD induction methods, and the effect size was large (approximately 70% of baseline) and reproducible. These findings provide initial support for the existence of opioid-induced hyperalgesia, which has been conceptualized as a coexisting opponent process to opioid-induced analgesia and proposed to be an alternative explanation for the development of analgesic tolerance to opioids.