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Pain Mechanisms (pain + mechanism)
Selected AbstractsNitric oxide and pain: ,Something old, something new'ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2009A. MICLESCU Challenges have emerged following the revival of nitric oxide (NO) from ,something old', a simple gas derived from nitrogen and oxygen with a role in the early stages of evolution, into ,something new', an endogenously formed biological mediator regulating a wide variety of physiological functions. Although pain is a common sensation, it encompasses multiple neurobiologic components, of which NO is only one. In pain research, the study of NO is complicated by convoluted problems related mostly to the effects of NO, which are pro- or anti-nociceptive depending on the circumstances. This dual function reflects the multi-faceted roles of the NO molecule described in physiology. This review covers current information about NO and its implications in pain mechanisms. In addition, it follows the pain pathways, demonstrating the role of NO in peripheral nociceptive transmission as well in central sensitization. This knowledge may provide the scientific basis for developing new drugs that are indicated for different types of pain, drugs that may be related to the chemical links of NO. A comprehensive approach to understanding the effects of NO will help clinicians identify novel agents that combine the pharmacological profile of native drugs with a controllable manner of NO release. Inhibitors of NO synthesis may have analgesic effects and would be of interest for treating inflammatory and neuropathic pain. Unfortunately, only a few of these compounds have reached the stage of clinical pain trials. [source] Investigations into the antinociceptive activity of Sapindus trifoliatus in various pain modelsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 5 2004D. K. Arulmozhi The effect of the aqueous extract of Sapindus trifoliatus (ST) on chemical, thermal-induced pain, nitroglycerin-induced hyperalgesia and pain on inflamed tissue was investigated. The extract (20 and 100 mg kg,1, i.p.) significantly inhibited acetic-acid-induced abdominal constrictions, formalin-induced pain licking and hotplate-induced pain in mice. Furthermore, the extract significantly increased the response latencies of nitroglycerin-induced hyperalgesia by the tail-flick method and mechanical pain on carrageenan-induced inflamed paw in rats. The data suggest that ST has an inhibitory activity on both peripheral and central pain mechanisms and has a modulatory role in NO-mediated nociceptive transmission. [source] Breakthrough pain in opioid-treated chronic non-malignant pain patients referred to a multidisciplinary pain centre: a preliminary studyACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2006J. Højsted Background:, Breakthrough pain (BTP) has not formerly been discussed as such in chronic non-malignant pain patients referred to pain centres and clinics. The purpose of the study was to investigate the prevalence, characteristics and mechanisms of BTP in opioid-treated chronic non-malignant pain patients referred to a pain centre and to assess the short-term effects of pain treatment. Methods:, Patients were assessed at referral (T0) and after a treatment period of 3 months (T3) using the visual analogue scale (VAS) of the brief pain inventory (BPI) within somatic nociceptive, neuropathic and/or visceral pain conditions, the mini mental state examination (MMSE) and the hospital anxiety and depression scale (HADS). The main treatment intervention from T0 to T3 was to convert short-acting oral opioids to long-acting oral opioids and to discontinue on demand and parenteral use of opioids. Results:, Thirty-three patients were assessed at T0 and 27 at T3. The prevalence of BTP declined significantly from T0 (90%) to T3 (70.4%). Worst, least, average and current pain intensities as well as duration of BTP were significantly reduced from T0 to T3. The majority of BTPs were exacerbation of background pain assumed to be of the same pain mechanisms. High average pain intensity (BPI) was significantly associated with high scores for both anxiety and depression (HADS). Conclusion:, BTP in chronic non-malignant pain patients seems to be surprisingly frequent and severe. Stabilizing the opioid regimen seems to reduce pain intensity in general as well as the intensity and duration of BTP. Average pain intensity was associated with anxiety and depression. [source] Nociceptin system does not affect MAC of volatile anaestheticsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2005S. Himukashi Background:, Nociceptin is the endogenous agonist of the opioid receptor-like (ORL) 1 receptor (NOP), and both nociceptin and NOP are widely expressed in the brain and spinal cord, which are target organs of general anaesthetics. As nociceptin has been reported to be involved in modulating pain mechanisms and stress responses, it is possible that the activity of the nociceptin system affects the anaesthetic potency of general anaesthetics. To address this possibility, we investigated the minimum alveolar concentrations (MACs) of various volatile anaesthetics in nociceptin receptor knockout mice (NOP,/,) and wild-type mice (NOP+/+). Methods:, We used male NOP,/, mice and NOP+/+ mice. MACs for halothane, isoflurane and sevoflurane were determined by the tail-clamp method. Results:, MACs for halothane, isoflurane and sevoflurane in NOP,/, mice were 1.60 (SD 0.06), 1.68 (0.08) and 3.36 (0.07)%, respectively. In NOP+/+ mice, MACs for halothane, isoflurane and sevoflurane were 1.59 (SD 0.07), 1.72 (0.07) and 3.38 (0.09)%, respectively. Conclusion:, MACs in NOP,/, mice did not significantly differ from those in NOP+/+ mice for halothane, isoflurane and sevoflurane. This result suggests that the nociceptin system does not affect the anaesthetic potency of volatile anaesthetics. [source] ,Protective premedication': an option with gabapentin and related drugs?ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2004A review of gabapentin, pregabalin in the treatment of post-operative pain Substantial progress has been made during the last decades in our understanding of acute pain mechanisms, and this knowledge has encouraged the search for novel treatments. Of particular interest has been the observation that tissue injury initiates a number of modulations of both the peripheral and the central pain pathways, which convert the system from a ,physiological' to a ,pathological' mode of processing afferent information. Gabapentin, which binds to the ,2, subunit of the voltage-dependent calcium channel, is active in animal models of ,pathological' but not in models of ,physiological' pain. Consequently, attention has so far been focused on neuropathic pain as a target for the clinical use of gabapentin and analogues. Recently, several reports have indicated that gabapentin may have a place in the treatment of post-operative pain. This article presents a brief summary of the potential mechanisms of post-operative pain, and a systematic review of the available data of gabapentin and pregabalin for post-operative analgesia. It is concluded that the results with gabapentin and pregabalin in post-operative pain treatment published so far are promising. It is suggested that future studies should explore the effects of ,protective premedication' with combinations of various antihyperalgesic and analgesic drugs for post-operative analgesia. [source] POST-SURGICAL NEUROPATHIC PAINANZ JOURNAL OF SURGERY, Issue 7 2008Edward Shipton Surgeons and anaesthetists are involved in Pain Medicine, as they have a responsibility to contribute to postoperative pain management and are often consulted about longer-term pain problems as well. A large component of persistent pain after surgery can be defined as neuropathic pain (NP). Nerves are injured during surgery and pain can persist after the surgical wound has healed. NP is because of a primary lesion or dysfunction of the peripheral or central nervous system. Prevalence estimates indicate that 2,3% of the population in the developed world experience NP. Persistent post-surgical NP is a mostly unrecognized clinical problem. The chronicity and persistence of post-surgical NP is often severely debilitating and impinges on the psychosocial, physical, economic and emotional well-being of patients. Options for treatment of any neuropathic factors are based on understanding the pain mechanisms involved. The current understandings of the mechanisms involved are presented. There is reasonable evidence for the efficacy of pharmacological management for NP. The aim of this article was to appraise the prevention, diagnostic work-up, the physical and particularly the pharmacological management of post-surgical NP and to provide a glimpse of advances in the field. It is a practical approach to post-surgical NP for all surgeons and anaesthetists. The take-home message is that prevention is better than waiting for post-surgical NP to become persistent. [source] Alteration of sensory neurons and spinal response to an experimental osteoarthritis pain modelARTHRITIS & RHEUMATISM, Issue 10 2010Hee-Jeong Im Objective To verify the biologic links between progressive cellular and structural alterations within knee joint components and development of symptomatic chronic pain that are characteristic of osteoarthritis (OA), and to investigate the molecular basis of alterations in nociceptive pathways caused by OA-induced pain. Methods An animal model of knee joint OA pain was generated by intraarticular injection of mono-iodoacetate (MIA) in Sprague-Dawley rats, and symptomatic pain behavior tests were performed. Relationships between development of OA with accompanying pain responses and gradual alterations in cellular and structural knee joint components (i.e., cartilage, synovium, meniscus, subchondral bone) were examined by histologic and immunohistologic analysis, microscopic examination, and microfocal computed tomography. Progressive changes in the dynamic interrelationships between peripheral knee joint tissue and central components of nociceptive pathways caused by OA-induced pain were examined by investigating cytokine production and expression in sensory neurons of the dorsal root ganglion and spinal cord. Results We observed that structural changes in components of the peripheral knee joint correlate with alterations in the central compartments (dorsal root ganglia and the spinal cord) and symptomatic pain assessed by behavioral hyperalgesia. Our comparative gene expression studies revealed that the pain pathways in MIA-induced knee OA may overlap, at least in part, with neuropathic pain mechanisms. Similar results were also observed upon destabilization of the knee joint in the anterior cruciate ligament transection and destabilization of the medial meniscus models of OA. Conclusion Our results indicate that MIA-induced joint degeneration in rats generates an animal model that is suitable for mechanistic and pharmacologic studies on nociceptive pain pathways caused by OA, and provide key in vivo evidence that OA pain is caused by central sensitization through communication between peripheral OA nociceptors and the central sensory system. Furthermore, our data suggest a mechanistic overlap between OA-induced pain and neuropathic pain. [source] | ||||||||||