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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

While laparoscopic cholecystectomy has become the standard procedure for symptomatic gallstones, it is likely that 10% of patients will require an open cholecystectomy whether owing to contraindications to the laparoscopic approach or because conversion to the open technique became necessary following laparoscopy. Although the trend towards smaller open cholecystectomy incisions has led to a reduced hospital stay, much of the postoperative morbidity can be ascribed to wound pain. Muscle splitting incisions tend to be less painful than muscle dividing incisions. This randomized consecutive study of elective and emergent open cholecystectomies compared a muscle splitting incision with the traditional muscle dividing technique. The muscle splitting technique was significantly (P < 0.001) less painful than the muscle dividing method as evaluated by the short form of the McGill pain questionnaire. Similarly, a significantly greater proportion of patients were fully mobile on the first and second postoperative day in the muscle splitting group compared with the muscle dividing group. Analgesia requirements, however, were not statistically significant between the two groups. We recommend that when open cholecystectomy is necessary the muscle splitting technique should be employed.
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PMID:Open cholecystectomy: muscle splitting versus muscle dividing incision: a randomized study. 767 3

We have evaluated the level of state and trait anxiety, neuroticism, extroversion and coping style as predictors of the effectiveness of patient-controlled analgesia (PCA) in 110 patients undergoing total abdominal hysterectomy. After operation patients were allocated to receive pain control with either PCA or i.m. injections (IMI). Pain was assessed using the short form McGill pain questionnaire at 6, 18 and 24 h after operation, and by recording the amount of analgesic consumed in the first 24 h after surgery. Both state anxiety and coping style were significant predictors of postoperative pain, irrespective of the method of analgesia used. Patients using PCA experienced significantly better pain control than those receiving IMI. However, it was those with high levels of state anxiety who experienced the greatest reduction in pain with PCA. In addition to achieving better pain control, patients who received PCA used significantly less analgesia and were discharged earlier than patients who received IMI.
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PMID:Psychological characteristics and the effectiveness of patient-controlled analgesia. 771 70

Knowledge of the incidence and significance of postoperative pain is essential for the establishment of effective pain treatment programmes. Detailed investigations on the incidence, severity and quality of postoperative pain from the surgeon's perspective are scarce in German hospitals. It was the aim of our study to investigate postoperative pain in general surgery under routine conditions. PATIENTS AND METHODS. A total of 168 patients scheduled for abdominal, vascular and orthopaedic surgery were investigated in a prospective trial. Pain was assessed by means of a 100-point visual analogue scale (VAS), a 5-point verbal rating scale (VRS), the original version of the McGill Pain Questionnaire (MPQ) and the short form of the McGill Pain Questionnaire (SFMPQ). These were applied preoperatively and daily thereafter up to the 7th postoperative day. Patients were randomly assigned into two groups with different sequences of application of the instruments. The pain treatment programme included intravenous analgesia with tramadol/metamizol (max. tramadol 400 mg+metamizol 5 g in any 24 h) after major surgery and additional administration of piritramide as needed (max. 60 mg/24 h.i.v.). After minor surgery ibuprofen was routinely given for analgesia (3 x 500 mg). RESULTS. All patients had pain on the days 1 and 2 postoperatively. The mean intensity of pain was 44 VAS points on day 1 and 6.8 points on day 7. The mean intensity of pain measured by the VRS on the 1st postoperative day was between "mild" and "moderate". The quality of pain showed a constant pattern concerning the mean scale values of descriptors of each subgroup (sensory, evaluative, affective, mixed) for both the original and the short form of the McGill Pain Questionnaire up to the 7th postoperative day. Sensory descriptors were reported more frequently than affective descriptors. Typical pain patterns were identified for different operations. After subtotal thyroidectomy, for example, patients perceived a high intensity of pain of short duration. In contrast, patients still have a high intensity of pain up to 7 days after abdominal and rectal operations. CONCLUSIONS. We conclude from our results that patients perceive significant postoperative pain under current standardized pain treatment in our department. Effective programmes for pain relief should take account of the different patterns of pain after different operations, as identified in this study.
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PMID:[The incidence of postoperative pain on general surgical wards. Results of different evaluation procedures]. 836 24

In order to establish effective postoperative analgesia we studied the incidence and significance of pain following maxillofacial surgery. The trial included 102 patients undergoing one of six different surgical procedures. Postoperative pain was assessed using a visual analogue scale (VAS) and the short form of the McGill Pain Questionnaire (SF-MPQ) up to the third postoperative day. Postoperative pain intensity was significantly correlated to operating time, the frequency of analgesic demand and the type of surgery (orthognathic surgery > TMJ surgery > osteosynthetic surgery > osteotomy of impacted third molars > tumor resection > removal of osteosynthetic materials). Patient's age, sex and ethnic origin did not significantly affect the severity of postoperative pain.
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PMID:[Postoperative pain after interventions in the area of the mouth-jaw-face]. 941 Jun 33

The peptide neurotransmitter substance P modulates sensitivity to pain by activating the neurokinin-1 (NK-1) receptor, which is expressed by discrete populations of neurons throughout the central nervous system. Substance P is synthesized by small-diameter sensory 'pain' fibres, and release of the peptide into the dorsal horn of the spinal cord following intense peripheral stimulation promotes central hyperexcitability and increased sensitivity to pain. However, despite the availability of specific NK-1 antagonists, the function of substance P in the perception of pain remains unclear. Here we investigate the effect of disrupting the gene encoding the NK-1 receptor in mice. We found that the mutant mice were healthy and fertile, but the characteristic amplification ('wind up') and intensity coding of nociceptive reflexes was absent. Although substance P did not mediate the signalling of acute pain or hyperalgesia, it was essential for the full development of stress-induced analgesia and for an aggressive response to territorial challenge, demonstrating that the peptide plays an unexpected role in the adaptive response to stress.
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PMID:Altered nociception, analgesia and aggression in mice lacking the receptor for substance P. 953 17

Substance P (SP) receptors in the ventral tegmental area (VTA) play a critical role in mediating the stress-induced activation of midbrain ascending dopamine (DA) neurons. Interestingly, SP acting in the VTA induces analgesia in the formalin test for tonic pain. Because exposure to stress inhibits pain in this test, we speculated that SP receptors in the VTA might mediate stress-induced analgesia. The present study explored this idea by examining the effect of blocking tachykinin NK-1 receptors in the VTA on footshock stress-induced analgesia in the formalin test. Intra-VTA infusions of the novel tachykinin NK-1 receptor antagonist, RP-67580, prevented this response. This finding suggests that exposure to stress inhibits tonic pain through the release of endogenous SP in the VTA.
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PMID:The tachykinin NK-1 receptor antagonist, RP-67580, infused into the ventral tegmental area prevents stress-induced analgesia in the formalin test. 1038 19

Although opioids can reduce stimulus-evoked efflux of Substance P (SP) from nociceptive primary afferents, the consequences of this reduction on spinal cord nociceptive processing has not been studied. Rather than assaying SP release, in the present study we examined the effect of opioids on two postsynaptic measures of SP release, Fos expression and neurokinin-1 (NK-1) receptor internalization, in the rat. The functional significance of the latter was first established in in vitro studies that showed that SP-induced Ca(2+) mobilization is highly correlated with the magnitude of SP-induced NK-1 receptor internalization in dorsal horn neurons. Using an in vivo analysis, we found that morphine had little effect on noxious stimulus-evoked internalization of the NK-1 receptor in lamina I neurons. However, internalization was reduced when we coadministered morphine with a dose of an NK-1 receptor antagonist that by itself was without effect. Thus, although opioids may modulate SP release, the residual release is sufficient to exert maximal effects on the target NK-1 receptors. Morphine significantly reduced noxious stimulus-induced Fos expression in lamina I, but the Fos inhibition was less pronounced in neurons that expressed the NK-1 receptor. Taken together, these results suggest that opioid analgesia predominantly involves postsynaptic inhibitory mechanisms and/or presynaptic control of non-SP-containing primary afferent nociceptors.
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PMID:Spinal opioid analgesia: how critical is the regulation of substance P signaling? 1053 66

The neuropeptide substance P (SP), apart from its traditional role in spinal nociceptive processing, is an important regulatory effector of opioid-dependent analgesic processes. The present study stems from our original findings indicating that 1) pharmacologically administered SP mediates a strong inhibitory activity on the development of morphine tolerance in rats, and that 2) a novel SP-opioid peptide chimera YPFFGLM-NH(2), designated ESP7, produces opioid-dependent analgesia without tolerance development. To further examine the effects of simultaneous activation of two distinct opposing spinal systems on opioid tolerance and the mechanisms underlying chimeric peptide function, a second SP-opioid chimera was synthesized. This chimera, designated ESP6 (YPFFPLM-NH(2)), contains overlapping domains of endomorphin-2 and SP, respectively. ESP6 is distinguished from ESP7 by a glycine to proline substitution at position 5. Intrathecal administration of morphine sulfate (MS) with ESP6 leads to a prolongation of MS analgesia over a 5-day period. The analgesia produced by ESP6 and MS is opioid receptor-dependent, due to the ability of naltrexone to block the analgesic response. Furthermore, when ESP6 and MS are administered with concurrent NK-1 receptor blockade, a decay in analgesic potency similar to that seen with MS alone results. The presence of a proline in ESP6 appears to reduce its conformational flexibility, limit its potency at the micro-opioid receptor, and hinder its analgesic effectiveness alone. However, ESP6 represents a novel adjuvant for the maintenance of opioid analgesia over time and provides a means to predict the pharmacological properties of a chimera from its structure.
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PMID:Inhibition of morphine tolerance development by a substance P-opioid peptide chimera. 1108 51

Substance P (SP) levels in the spinal cords of very old rats are less than the levels in younger rats (Bergman et al., 1996). After injury to a peripheral nerve in young rats, immunoreactivity (ir) to the SP receptor, NK-1 (neurokinin-1), increases in the spinal cord ipsilateral to the injury and the increases are correlated with the development of thermal hyperalgesia (Goff et al., 1998). Thus we postulated that aged rats might display an increased sensitivity to thermal stimulation before peripheral nerve injury and that they might respond differently to injury than do younger rats. To test this hypothesis, we used the Bennett and Xie model (1988) of chronic constriction injury (CCI) to the sciatic nerve to induce a neuropathic pain condition. We investigated the effect of age on changes in NK-1 ir in superficial layers of the dorsal horn and on numbers of NK ir cells in deeper laminae at the L4-L5 levels of the spinal cord after CCI. NK-1 receptors were tagged immunohistochemically and their distribution quantified by use of computer-assisted image analysis. NK-1 ir changes were related to alterations in thermal and tactile sensitivity that developed after CCI in young, mature and aged (4-6, 14-16, and 24-26 months) Fischer F344 BNF1 hybrid rats. No differences in thermal or tactile sensitivity of young and aged rats were seen in the absence of nerve injury. After injury, aged rats developed thermal hyperalgesia and tactile allodynia more slowly than did the younger rats. NK-1 receptor ir and numbers of NK-1 ir cells in the dorsal horn increased with time post-injury in all three groups. NK-1 ir increases were correlated with the development of thermal hyperalgesia in those rats that displayed hyperalgesia. However, some rats developed an increased threshold to thermal stimuli (analgesia) and that also was correlated with increases in NK-1 ir. Thus NK-1 ir extent, while correlated with thermal sensitivity in the absence of injury, is not a specific marker for disturbances in one particular sensory modality; rather it increases with peripheral nerve injury per se.
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PMID:Effect of aging on the substance P receptor, NK-1, in the spinal cord of rats with peripheral nerve injury. 1132 73

Noradrenaline (NA), a key neurotransmitter of the endogenous pain inhibitory system, acutely inhibits nociceptive transmission (including that mediated by substance P), potentiates opioid analgesia, and underlies part of the antinociceptive effects of the widely prescribed tricyclic antidepressants. Lesions of noradrenergic neurons, however, result in either normal or reduced pain behavior and variable changes in morphine antinociception, undermining the proposed association between noradrenaline (NA) deficiency and chronic pain (hyperalgesia). We used mice lacking the gene coding for dopamine beta-hydroxylase, the enzyme responsible for synthesis of NA from dopamine, to reexamine the consequences of a lack of NA on pain behavior. Here, we show that absence of NA in the central nervous system results in a substance P-mediated chronic hyperalgesia (decreased nociceptive threshold) to thermal, but not mechanical, stimuli and decreased efficacy of morphine. Contrary to studies that show substance P-mediated hyperalgesia requires intense stimuli, we found that even a mild stimulus is sufficient to evoke substance P-dependent hyperalgesia in the NA-deficient mice. Restoring central NA normalized both the nociceptive threshold and morphine efficacy, which is consistent with a tonic inhibitory effect of NA on nociceptive transmission. Unexpectedly, however, antagonists to the substance P receptor (the NK1 receptor) could achieve the same effect as NA replacement. We conclude that when unopposed by NA, substance P acting at the NK1 receptor causes chronic thermal hyperalgesia, and that the reduced opioid efficacy associated with a lack of NA is due to increased NK1-receptor stimulation.
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PMID:The NK1 receptor mediates both the hyperalgesia and the resistance to morphine in mice lacking noradrenaline. 1180 10


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