Articles: hyperalgesia.
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In certain patients with neuropathic pain, the pain is dependent on activity in the sympathetic nervous system. To investigate whether the spared nerve injury model (SNI) produced by injury to the tibial and common peroneal nerves and leaving the sural nerve intact is a model for sympathetically maintained pain, we measured the effects of surgical sympathectomy on the resulting mechanical allodynia, mechanical hyperalgesia, and cold allodynia. Decreases of paw withdrawal thresholds to von Frey filament stimuli and increases in duration of paw withdrawal to pinprick or acetone stimuli were observed in the ipsilateral paw after SNI, compared with their pre-SNI baselines. Compared with sham surgery, surgical lumbar sympathectomy had no effect on the mechanical allodynia and mechanical hyperalgesia induced by SNI. However, the sympathectomy significantly attenuated the cold allodynia induced by SNI. These results suggest that the allodynia and hyperalgesia to mechanical stimuli in the SNI model is not sympathetically maintained. However, the sympathetic nervous system may be involved, in part, in the mechanisms of cold allodynia in the SNI model. ⋯ The results of our study suggest that the SNI model is not an appropriate model of sympathetically maintained mechanical allodynia and hyperalgesia but may be useful to study the mechanisms of cold allodynia associated with sympathetically maintained pain states.
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Randomized Controlled Trial
Sleep deprivation is hyperalgesic in patients with gastroesophageal reflux disease.
Studies have demonstrated that gastroesophageal reflux disease (GERD) can cause sleep deprivation because of nighttime heartburn or short, amnestic arousals during sleep. Sleep deprivation has been associated with reports of increased GERD severity. Our aim was to determine whether sleep deprivation enhances perception of intraesophageal acid in patients with GERD vs healthy controls. ⋯ Sleep deprivation is hyperalgesic in patients with GERD and provides a potential mechanism for increase in GERD symptom severity in sleep-deprived patients.
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Eur. J. Nucl. Med. Mol. Imaging · Dec 2007
Controlled Clinical TrialFollow-up of pain processing recovery after ketamine in hyperalgesic fibromyalgia patients using brain perfusion ECD-SPECT.
The aim of this study was to determine whether the follow-up of pain processing recovery in hyperalgesic fibromyalgia (FM) could be objectively evaluated with brain perfusion ethyl cysteinate dimer single photon computerized tomography (ECD-SPECT) after administration of ketamine. ⋯ This prospective study suggests that blockade of facilitatory descending modulation of pain with ketamine can be evaluated in the periaqueductal grey with brain perfusion SPECT.
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Pharmacol. Biochem. Behav. · Dec 2007
Milnacipran attenuates hyperalgesia and potentiates antihyperalgesic effect of tramadol in rats with mononeuropathic pain.
Milnacipran is a non-tricyclic antidepressant drug which selectively inhibits serotonin and noradrenaline re-uptake and is recommended in the treatment of various chronic pain syndromes. Many studies have shown that compounds known to block monoamine uptake potentiate the antinociceptive effects of opioids. This study investigates the effect of milnacipran alone or in combination with an opiodergic drug, i.e. tramadol, on hyperalgesia in a rat model of neuropathic pain. ⋯ Intraperitoneal acute injection of milnacipran 60 mg/kg produced an antihyperalgesic effect which was prevented by pretreating systemically with alpha-methyl-p-tyrosine, an inhibitor of noradrenaline synthesis; parachlorophenylalanine, an inhibitor of serotonin synthesis; and naloxone, an antagonist of opioidergic receptors. Co-administration of milnacipran 40 mg/kg with tramadol (20 and 40 mg/kg) potentiated the antihyperalgesic effect of tramadol. Milnacipran has an antihyperalgesic effect mediated by serotonergic, noradrenergic and opioidergic systems and the combined use of tramadol with milnacipran potentiates the effect of tramadol in the management of neuropathic pain.
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We have previously demonstrated that gabapentin supraspinally activates the descending noradrenergic system to alleviate neuropathic pain. In this study, we investigated whether pregabalin, an antiepileptic and analgesic drug that is also designed as a structural analogue of gamma-aminobutyric acid (GABA), exhibits supraspinal analgesic effects similar to those of gabapentin involving the descending noradrenergic system. Both systemically (intraperitoneally; i.p.) and locally (intracerebroventricularly or intrathecally; i.c.v. or i.t.) injected pregabalin reduced thermal and mechanical hypersensitivity in a murine chronic pain model that was prepared by partial ligation of the sciatic nerve (the Seltzer model), suggesting that pregabalin acts at both supraspinal and spinal loci. ⋯ Depletion of spinal noradrenaline (NA) or pharmacological blockade of spinal alpha(2)-adrenoceptors with yohimbine (i.p. or i.t.), but not alpha(1)-adrenoceptors with prazosin (i.p.), reduced the analgesic effects of pregabalin (i.p. or i.c.v.) on thermal and mechanical hypersensitivity. Moreover, i.c.v.-administered pregabalin dose-dependently increased the spinal 4-hydroxy-3-methoxyphenylglycol (MHPG) content and the MHPG/NA ratio only in mice with neuropathic pain, whereas the concentrations of NA, serotonin, 5-hydroxyindoleacetic acid and dopamine were unchanged, demonstrating that supraspinal pregabalin accelerated the spinal turnover of NA. Together, these results indicate that pregabalin supraspinally activates the descending noradrenergic pain inhibitory system coupled with spinal alpha(2)-adrenoceptors to ameliorate neuropathic pain.