Pain
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Randomized Controlled Trial Clinical Trial
Intraarticular morphine versus dexamethasone in chronic arthritis.
Intraarticular morphine inhibits pain after knee surgery without overt toxicity. This study examined intraarticular morphine in chronic arthritis. We undertook a randomized double-blind comparison between intraarticular morphine (3 mg), dexamethasone (4 mg) and saline (3 ml) in 44 patients with chronic inflammatory arthritis or osteoarthritis of the knee. ⋯ No patient displayed untoward side effects. Synovial leukocyte counts were lower after morphine than after saline. In conclusion, intraarticular morphine produces analgesia of similar magnitude to dexamethasone and it may have antiinflammatory actions in chronic arthritis.
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Tricyclic antidepressants and carbamazepine have become the mainstay in the treatment of neuropathic pain. Within the last decade, controlled trials have shown that numerous other drugs relieve such pain. We identified all placebo-controlled trials and calculated numbers needed to treat (NNT) to obtain one patient with more than 50% pain relief in order to compare the efficacy with the current treatments, and to search for relations between mechanism of pain and drug action. ⋯ There were no clear relations between mechanism of action of the drugs and the effect in distinct pain conditions or for single drug classes and different pain conditions. It is concluded that tricyclic antidepressants in optimal doses appear to be the most efficient treatment of neuropathic pain, but some of the other treatments may be important due to their better tolerability. Relations between drug and pain mechanisms may be elucidated by studies focusing on specific neuropathic pain phenomena such as pain paroxysms and touch-evoked pain.
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The objective of this study was to investigate the central processing of dynamic mechanical allodynia in patients with mononeuropathy. Regional cerebral blood flow, as an indicator of neuronal activity, was measured with positron emission tomography. Paired comparisons were made between three different states; rest, allodynia during brushing the painful skin area, and brushing of the homologous contralateral area. ⋯ This finding is consistent with previous studies suggesting attentional modulation and a central coping strategy for known and expected painful stimuli. Involvement of the medial pain system has previously been reported in patients with mononeuropathy during ongoing spontaneous pain. This study reveals a bilateral activation of the lateral pain system as well as involvement of the medial pain system during dynamic mechanical allodynia in patients with mononeuropathy.
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Considerable research indicates increased experience of clinical pain among females relative to males, and females also demonstrate enhanced responses to experimentally-induced pain. However, previous research has not investigated the relationship between clinical and experimental pain responses in healthy females and males. This experiment examined recent clinical pain as well as thermal pain thresholds and tolerances in 209 (117 female, 92 male) healthy young adults. ⋯ The differences remained significant after correcting for psychological variables including hypervigilance and sex role expectancies. These results indicate that experimental pain responses may be more clinically relevant for females than males. Potential explanations and implications for this pattern of results are discussed.
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Expression of bradykinin receptors was analyzed in freshly isolated dorsal root ganglion neurons of the ipsi- and contralateral segments L4/L5, L2/L3, and T12/T13 two to twenty days after unilateral injury of the adult rat sciatic nerve using gold labeled bradykinin. The number of infiltrating leucocytes was investigated by flow cytometry. Sciatic nerve injury transiently increased the proportion of neurons expressing bradykinin receptors not only in the ipsilateral ganglia L4/L5, but also in the homonymous contralateral ganglia and also bilaterally in the adjacent ganglia L2/L3. ⋯ No increase was observed prior to day ten and only in ipsilateral ganglia L4/L5, not contralaterally and not in adjacent ganglia L2/L3 and T12/T13. The experiments show that the induction of bradykinin receptors following a unilateral nerve lesion is not restricted to neurons projecting into the damaged nerve but is (i) bilateral, (ii) different in time course between injured and uninjured neurons, and (iii) locally confined to neurons of the adjacent ganglia. Macrophages and lymphocytes are increased after ten day ligation only in the affected ganglia and are probably not involved in the induction of bradykinin receptors.