European journal of pain : EJP
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The innervation of the temporomandibular joint (TMJ) has attracted particular interest because of the close association with complex mandibular movement. Although the pathological changes of disk innervation may have a crucial role in the development of TMJ pain, the innervation of the TMJ disk by experimentally induced arthritis has rarely been examined in detail. Arthritic rats were induced by injection with 0.1ml solution of Complete Freund's adjuvant (CFA). ⋯ In addition, the ratio of trkA- and p75-positive small- and medium-sized cells increased in trigeminal ganglia. It is assumed that increasing innervation of the TMJ disk may be important for the pathophysiology of TMJ pain. NGF and its receptors are likely involved in pathological changes of the TMJ disk.
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Comparative Study
Experimental muscle pain provokes long-lasting alterations of thermal sensitivity in the referred pain area.
This study explores thermal sensitivity and thermal nociception for signs of central sensitization in the area of referred muscle pain. Two groups of 24 healthy subjects (ss) each, and with mean ages of, respectively, 27 and 55 years, were first trained in quantitative sensory testing and pain rating. Then, in a second session, referred pain was evoked by injection of 6% hypertonic saline into the infraspinatus muscle. ⋯ The decrease of cold pain threshold or SHT in subgroups of ss may indicate central sensitization. However, the observed changes in this experiment do not provide an unambiguous indicator for central sensitization which seems to be rather individual and might depend on pain intensity and proneness to express central mechanisms of sensitization. Therefore in clinical pain states the individual pattern of sensory abnormalities has to be analysed and interpreted in addition to the pain parameters to assess central involvement.
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The increased use of quantitative sensory testing in the study of pain raises the need to characterize various aspects of psychophysical response to noxious stimulation in healthy subjects. The present study aims to address several issues regarding the use of heat pain stimuli: (a) Are pain scores for short-term repeated phasic stimuli consistent? (b) Does an exposure to tonic heat pain stimulus cause sensitization and change the scores for subsequent phasic stimuli? and (c) Are pain scores for phasic and tonic heat pain correlated? To address these questions, a series of four phasic heat pain stimuli of 47 degrees C were given to the forearms of 70 healthy volunteers, over the course of an hour. Pain scores by Visual Analog Scale (VAS) were obtained for each stimulus. In 50 subjects, a tonic heat pain of 70s duration at 47.5 degrees C was given between the first and second phasic stimuli. Pain scores were obtained at four points along this tonic stimulus. Repeated measures ANOVA and a sensitive post hoc analysis indicated that, while the pain perception was reduced on the second, nearly immediate trial, subsequent VAS scores of pain perception were not different from the first (#1: 35.2+/-19.2; #2: 31.4+/-20.2, #3: 33.0+/-21.6; and #4: 33.2+/-20.1, respectively), with strong correlation among the phasic tests. The average tonic pain score was 53.7+/-23.1. Administration of tonic pain stimuli did not result in different VAS scores of subsequent phasic pain stimuli, compared to those subjects who did not receive tonic pain stimuli. Tonic and phasic pain were positively correlated (e.g., r=0.45,p<0.001 for the first phasic stimuli). However, no relation was found between the level of perceived pain, either for phasic or for tonic stimuli, and presence or absence of temporal summation during the tonic pain. ⋯ (i) phasic pain scores assessments at 30' and 60' after baseline is consistent; (ii) tonic heat pain, despite relatively high VAS scores, does not cause a change in the scoring of subsequent phasic stimuli; and (iii) phasic and tonic pain scores correlate with each other. Thus, the normal pattern of pain perception is stable and not altered by single tonic pain stimulation.
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Epidural opioids have been reported to provide superior analgesia in acute pain management. Despite the fact that the required doses are low, major side effects such as respiratory depression may still occur. In an effort to maximize analgesia and to minimize the rate of side effects, epidural NMDA receptor antagonists, especially ketamine, may be co-administered with opioids. ⋯ Moreover, increasing doses of ketamine tended to decrease the MPE of various doses of fentanyl. These data confirm that ketamine, contrary to opioids, does not possess important antinociceptive properties in an acute test such as the TWR test. Furthermore, these data indicate that additive drugs such as ketamine may have different effects on different opioids.
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L5 and L6 spinal nerve ligation (SNL) in rats leads to behavioral signs of neuropathic pain including mechanical allodynia. The purposes of this study were to investigate the role of the intact L4 spinal nerve in the development of mechanical allodynia following L5 and L6 SNL and, as a result, to develop a modified model of neuropathic pain. As a first set of experiments, in addition to tight ligation of the left L5 and L6 spinal nerves, the intact L4 spinal nerve was manipulated either (1) by gentle repeated stretching of the L4 spinal nerve immediately after L5 and L6 SNL or (2) by intermittent mechanical stimulation to the ipsilateral paw during the first week after SNL. ⋯ These results suggest that afferent activity of the intact L4 spinal nerve aids in the development of mechanical allodynia in the SNL model of neuropathic pain. The addition of a chromic gut loop around the intact L4 spinal nerve can augment the development of mechanical allodynia following SNL of L5. We propose this latter as a useful and practical animal model of neuropathic pain.