Articles: hyperalgesia.
-
Randomized Controlled Trial
Effects of COX inhibition on experimental pain and hyperalgesia during and after remifentanil infusion in humans.
Opioids may enhance pain sensitivity resulting in opioid-induced hyperalgesia (OIH). Activation of spinal cyclooxygenase may play a role in the development of OIH. The aim of this study was to demonstrate remifentanil-induced postinfusion hyperalgesia in an electrical pain and a cold pain model, and to investigate whether COX-2 (parecoxib) or COX-1 (ketorolac) inhibition could prevent hyperalgesia after remifentanil infusion. ⋯ These results demonstrated OIH in both models, and may suggest that COX-2 inhibition is more important than COX-1 inhibition in reducing hyperalgesia. Remifentanil-induced hyperalgesia was demonstrated for both electrically induced pain and cold-pressor pain. Both parecoxib and ketorolac prevented hyperalgesia in the electrical model, parecoxib to a larger extent.
-
The aim of this study was to analyze cutaneous pain threshold (CPT) during the interictal phase in headache patients, and the relationships between headache frequency and analgesic use. A consecutive series of 98 headache patients and 26 sex- and age-balanced controls were evaluated. Acute allodynia (AA) was assessed by Jakubowski questionnaire, and interictal allodynia (IA) by a skin test with calibrated monofilaments. ⋯ In MOH patients there were no significant differences depending on the diagnosis of starting headache (migraine or tension type headache) and, in both groups, we found the overuse of analgesics plays an important role: intake of more than one daily drug dramatically reduces the CPT (p < 0.05). Thus, when acute allodynia increases frequency, worsens or appears for the first time in patients with a long-standing history of chronic headache, it could reasonably suggest that the reduction of CPT had started, without using a specific practical skin test but simply by questioning clinical headache history. In conclusion, these results indicate that the role of medication overuse is more important than chronicization in lowering CPT, and suggest that prolonged periods of medication overuse can interfere with pain perception by a reduction of the pain threshold that facilitates the onset of every new attack leading to chronicization.
-
Anesthesiology clinics · Jun 2011
ReviewNew concepts in acute pain management: strategies to prevent chronic postsurgical pain, opioid-induced hyperalgesia, and outcome measures.
Chronic postsurgical pain (CPSP) is a pain syndrome that has attracted attention for more than 10 years. CPSP is a pain syndrome that develops postoperatively and lasts for at least 2 months in the absence of other causes for pain (eg, recurrence of malignancy, chronic infection, and so forth). Pain continuing from a preexisting disease is not considered as CPSP. In this article, the authors discuss the etiopathogenesis of CPSP and interventions that can help prevent and treat this condition.
-
Randomized Controlled Trial Comparative Study
[Clonidine for remifentanil-induced hyperalgesia: a double-blind randomized, placebo-controlled study of clonidine under intra-operative use of remifentanil in elective surgery of the shoulder].
In the postoperative period, α2-adrenergic agonists have an opioid sparing effect. In a previous, experimental study, it was also shown that clonidine attenuates remifentanil-induced hyperalgesia. In this study, we examined under clinical conditions whether early administration of a single dose of clonidine can inhibit remifentanil-induced hyperalgesia in patients undergoing elective surgery of the shoulder and with continuous intraoperative use of remifentanil. ⋯ An early single dose of 150 µg of clonidine did not reduce the postoperative morphine consumption and pain scores in patients undergoing elective surgery of the shoulder with remifentanil/propofol-based anaesthesia. After the effect of clonidine has presumably subsided the pain can even increase, therefore further studies with repetitive doses of clonidine should be carried out.
-
Journal of neurotrauma · Jun 2011
Delayed intrathecal delivery of RhoA siRNA to the contused spinal cord inhibits allodynia, preserves white matter, and increases serotonergic fiber growth.
RhoA is a key regulator of the actin cytoskeleton that is upregulated after spinal cord injury (SCI). We analyzed different methods for siRNA delivery and developed siRNAs targeting RhoA (siRhoA) for SCI treatment. Cy 3.5-labeled siRNA delivered at the time of SCI yielded fluorescence in several cell types in the injury site. ⋯ Histological analysis at 8 weeks showed significant improvement in white matter sparing with siRhoA compared to control siRNA. siRhoA treatment also resulted in less accumulation of ED1+macrophages, increased PKC-γ immunoreactivity in the corticospinal tract rostral to the injury site, and increased serotonergic fiber growth 12 mm caudal to the contusion site. The ability of siRhoA to preserve white matter and promote serotonergic axonal regrowth caudal to the injury site is likely to suppress allodynia. This provides justification for considering clinical development of RhoA inhibitors to treat SCI sub-acutely to reduce allodynia, which occurs frequently in SCI patients.