Articles: hyperalgesia.
-
J Manipulative Physiol Ther · Sep 2003
Onset and recovery of hyperalgesia and hyperexcitability of sensory neurons following intervertebral foramen volume reduction and restoration.
To investigate the relationships between L4 and L5 intervertebral foramen (IVF) stenosis (IVFS), as well as the restoration and onset and recovery of behavioral hyperalgesia and alterations in primary sensory neuron excitability. ⋯ The present study demonstrates that hyperalgesia and hyperexcitability of the primary sensory neurons can be induced following the IVF volume reduction produced by insertion of a stainless steel rod and mostly relieved by the rod withdrawal. The recovery of excitability of DRG cells to normal levels is associated with the abatement of hyperalgesia. These results support the hypothesis that increased excitability of DRG neurons is associated with the generation and maintenance of hyperalgesia and suggest that relief of the IVF stenosis, which could compress all of the normal constituents within the IVF (ie, DRG, nerve root, blood and lymph vessels, adipose, etc.), may help to alleviate chronic pain in humans.
-
Psychosomatic medicine · Sep 2003
Clinical Trial Controlled Clinical TrialPlacebo and Nocebo responses, cortisol, and circulating beta-endorphin.
The experiment tested whether the placebo and nocebo responses could be mediated via modulation of stress. ⋯ A placebo response, ie, a reduced pain level, was seen in the Placebo group at 15 minutes after the injection. The placebo response was not related to stress or to beta-endorphin. Expectation of a pain increase in the Nocebo group led to an increase in cortisol, but the expectation of pain increase and the resultant cortisol increase had no effect on pain.
-
Anesthesia and analgesia · Sep 2003
Clinical TrialIntravenous remifentanil produces withdrawal hyperalgesia in volunteers with capsaicin-induced hyperalgesia.
Opioids administered during surgery may be beneficial by preempting postoperative pain or detrimental by causing acute tolerance. We used a stable model of hyperalgesia in volunteers to test whether acute opioid exposure also results in such pain sensitization over a period of hours in humans. Ten healthy volunteers were studied. ⋯ Areas of hyperalgesia and allodynia continuously enlarged 4 h after remifentanil was stopped, to 180% +/- 47% and 180% +/- 86%, respectively. This study demonstrates that acute opioid exposure enhances hypersensitivity for hours after exposure. If applicable to the surgical setting, this could increase the dose of opioid required for postoperative analgesia and enhance, rather than inhibit, postoperative pain.
-
1. Anticonvulsant agents are commonly used to treat neuropathic pain conditions because of their effects on voltage- and ligand-gated channels in central pain pathways. However, their interaction with ion channels in peripheral pain pathways is poorly understood. ⋯ Hill slope coefficients for the tested anticonvulsants indicate that the dose-response curve was less steep for gabapentin than for phenytoin, carbamazepine and ethosuximide. 5. Our data strongly suggest that cellular targets like voltage-gated Na+ and Ca2+ channels, similar to those that mediate the effects of anticonvulsant agents in the CNS, may exist in the peripheral nerve endings of rat sensory neurons. Thus, peripherally applied anticonvulsants that block voltage-gated Na+ and Ca2+ channels may be useful analgesics.
-
Comparative Study
Avulsion injury of the rat brachial plexus triggers hyperalgesia and allodynia in the hindpaws: a new model for the study of neuropathic pain.
In the present study, we sought to characterise a behavioural model of persistent peripheral neuropathic pain produced by avulsion of the right brachial plexus in rats. In addition, we compared the effects of avulsion with those of ligation or crush injury of the brachial plexus. Avulsion and, to a lesser extent, ligation and crushing of brachial plexus caused a long-lasting (up to 90 days) and highly reproducible mechanical hyperalgesia, in both ipsilateral and contralateral hindpaws. ⋯ The avulsion and, to a lesser extent, ligation and crushing of the brachial plexus elicited a significant and long-lasting (up to 90 days) ipsilateral and contralateral cold and mechanical allodynia. Furthermore, the brachial plexus injury caused a significant decrease in functional activity of the forepaws as assessed in the grasping strength test, but did not alter the locomotor activity of the rats in the open field test in comparison with control or sham groups. Taken together these results show that avulsion of the brachial plexus in rat produces persistent mechanical and cold allodynia and mechanical hyperalgesia, and might represent a valuable method for understanding the mechanisms underlying the aetiology of neuropathic pain.