Pain
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Evidence indicates that excitatory amino acids (EAAs) like glutamate and aspartate are important in the processing of nociceptive information in the dorsal horn of the spinal cord. Recently, the role of particular EAA receptors in pain transmission and facilitated pain states has been examined utilizing spinal administration of specific receptor antagonists. Most investigators have studied the involvement of N-methyl-D-aspartate (NMDA) EAA receptors in hyperalgesia and nociception; less is known about the importance of non-NMDA EAA receptors in animal models of persistent pain. ⋯ Intrathecal NBQX also inhibited non-evoked pain behavior. In conclusion, non-NMDA receptor antagonists produced a marked decrease in pain behaviors in this model of postoperative pain. Thus, non-NMDA receptors are important for the maintenance of short-term pain behaviors caused by an incision and drugs blocking these receptors may be useful for the treatment of postoperative pain in patients.
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Spinal cord stimulation reduces pain of critical ischaemia in patients with severe inoperable coronary artery and peripheral vascular disease by increasing microvascular flow. Patients with cardiac pacemaker may be denied a spinal cord stimulator (SCS) implant because of the risk of compromising pacemaker function by inhibition or reversion to asynchronous noise-pacing mode. We describe the management of a patient with an SCS implant for lower limb ischaemia who required a pacemaker. We suggest that with modern pacemakers it is safe to implant a spinal cord stimulator simultaneously with a pacemaker provided adequate precautions are taken to prevent interdevice interference.
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Randomized Controlled Trial Clinical Trial
Dose-response relationship of opioids in nociceptive and neuropathic postoperative pain.
The treatment of neuropathic pain with opioid analgesics is a matter of controversy among clinicians and clinician scientists. Although neuropathic pain is usually believed to be only slightly responsive to opioids, several studies show that satisfactory analgesia can be obtained if adequate doses are administered. In the present study, we tested the effectiveness of buprenorphine in 21 patients soon after thoracic surgery (nociceptive postoperative pain) and 1 month after surgery in the same 21 patients who developed postthoracotomy neuropathic pain with a burning, electrical and shooting quality. ⋯ In fact, if the AD50 soon after surgery was low, the AD50 increase in the long-term neuropathic pain was threefold. By contrast, if the AD50 soon after surgery was high, the AD50 in neuropathic pain was only slightly increased. This suggests that, though neuropathic pain is indeed less sensitive to opioids, in some neuropathic patients a large amount of opioid resistance is already present in other painful conditions.
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Factors influencing natural history and clinical course of pain in temporomandibular disorders (TMD) are largely unknown. Physical, psychological and behavioral data from a population-based epidemiologic study of TMD were examined in 234 cases of persons reporting TMD pain. The cases were assigned to one of five pain pattern groups based on changes in average TMD pain from baseline to 5-year follow-up: (i) remitted (49% of the sample), (ii) high-improvement (14%), (iii) low-improvement (9%), (iv) same (13%), and (v) worse (16%). ⋯ The three psychological variables, anxiety, depression, and somatization, displayed similar change patterns, but these patterns were distinctly different from those of the physical variables in that the remitted pain group was at the population mean at baseline for these psychological variables and remained there; significant improvement in psychological status was observed only in the pain group showing high improvement. The other three pain change groups exhibited elevated psychological distress scores at both baseline and 5 years. These results indicate that although the relationships among the course of pain, of physical variables, and of psychological variables are complicated, the 5-year outcome in pain is largely independent of readily discernible changes in clinical signs.
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Temporal summation of pain occurs when repeated stimuli become increasingly painful in spite of unchanged stimulus intensity. Summation can be quantified as the difference in pain between the first and the last stimulus in a train of stimuli. The aim of the study was to compare temporal summation of pain in normal skin with summation of pain in skin with primary and secondary hyperalgesia evoked by a heat injury. ⋯ Temporal summation at high stimulus intensities was more pronounced than at lower intensities (P < 0.0002). We found no correlation between either temporal summation and area of secondary hyperalgesia, or temporal summation and pain intensity during the induction of heat injury. We conclude that the development of primary and secondary mechanical hyperalgesia after heat injury in man was not associated with changes in temporal summation of painful electrical stimuli.