Pain
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Intramuscular injection of hypertonic saline is a good model to study human muscle pain (Kellgren 1938). The present study concerns the intramuscular (i.m.) pain mediators in saline-induced muscle pain. In experiment 1, the diffusion of infused hypertonic and isotonic saline (0.5 ml) in m. tibialis anterior was illustrated by magnetic resonance imaging (MRI) in one subject. ⋯ The i.m. pressure was not different during the infusions of hypertonic and isotonic saline but was increased between the infusions of hypertonic saline. This study has shown that i.m. infusion of hypertonic saline produced a saline-pool, causing the i.m. pressure to increase. Possibly, pain activation and cessation are related to increased intramuscular sodium and potassium content respectively.
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Clinical Trial
The effects of distraction on exercise and cold pressor tolerance for chronic low back pain sufferers.
Distraction has been found to be effective for the attenuation of experimental and acute clinical pain but its efficacy for chronic pain management remains unclear. There are even some suggestions that distraction may be a counterproductive strategy for chronic pain sufferers. In this study we found that a word shadowing distraction task increased the ability of a group of 12 female and eight male chronic low back pain (CLBP) sufferers to carry out a brief (maximum 300 s) step-up exercise that temporarily increased their pain (P < 0.05). ⋯ Interestingly, the same distraction task did not increase the cold pressor (CP) tolerance time for the CLBP group but produced a 26% increase in tolerance time for a pain-free control group consisting of nine females and nine males (P < 0.05). Also, performance on the distraction task during the CP was worse for the CLBP group than the controls (P < 0.05). Although these findings should be interpreted cautiously because of the parameters of the experiment, they do suggest that distraction is a potentially useful technique to assist chronic pain sufferers.
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Clinical Trial
The influence of psychological variables on postoperative anxiety and physical complaints in patients undergoing lumbar surgery.
Previous research has indicated that postoperative distress is influenced by diverse biographic, medical and psychological variables, such as personality, coping behaviours and anxiety. The influence of state variables, apart from anxiety and coping behaviour, has received scant attention. Furthermore, the influence of coping behaviour has remained unclear. ⋯ Preoperative anxiety and fatigue independently predicted more postoperative physical complaints. No associations were found between the coping behaviours and the postoperative variables. The implications of these results are discussed in relation to intervention strategies aimed at diminishing the stress of surgery.
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The effects of mexiletine, desipramine and fluoxetine in rat models involving central sensitization.
Drugs that are clinically effective (mexiletine and desipramine) or ineffective (fluoxetine) in the treatment of human neuropathic pain were evaluated for efficacy in rat models involving central sensitization (i.e., formalin model and the L5/L6 spinal nerve ligation model of neuropathic pain) using tests that differ in stimulus modality: noxious chemical stimulus (formalin model) as well as noxious (pin prick) and innocuous mechanical stimuli (application of von Frey filaments). Mexiletine (10-100 mg/kg, s.c.) significantly (P < 0.05) attenuated hyperalgesia in formalin-treated (60 mg/kg and 100 mg/kg) and neuropathic rats (100 mg/kg) as well as tactile allodynia in neuropathic rats (100 mg/kg). Desipramine (1-100 mg/kg, s.c.), on the other hand, reduced hyperalgesia significantly (P < 0.05) in formalin-treated (3, 10, 30 and 100 mg/kg) and neuropathic rats (10 mg/kg and 100 mg/kg), but did not reduce tactile allodynia in the neuropathic rats. ⋯ Thus, drugs which are effective in reducing human neuropathic pain consistently attenuated hyperalgesia in formalin-treated or neuropathic rats. Desipramine also distinguished mechanical hyperalgesia from tactile allodynia in rats rendered neuropathic by spinal nerve ligation. These data are consistent with the hypothesis that the neuronal mechanisms underlying these two manifestations of neuropathic pain are different.
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An animal model showing mechanical allodynia following systemic bolus injection of a human/mouse chimeric monoclonal antibody to the GD2 ganglioside (ch14.18) has been established (e.g. pain behavior generated by a light tactile stimulus). This is of clinical relevance since ch14.18 is a promising experimental treatment for pediatric neuroblastoma. The present study examined the hypothesis that allodynic effects of the anti-GD2 antibody are mediated by actions on cutaneous nerve fibers. ⋯ Mean mechanical threshold for A delta fibers in all three antibody treated groups was significantly reduced compared to the saline control; this was not observed for C-fibers in any group. Intravenous bolus injection (15 mg/kg) and infusion of lidocaine (plasma level 0.3-2.2 micrograms/ml) both reduced anti-GD2 associated BA. These data demonstrate that mechanical-allodynia could be produced by action(s) of the anti-GD2 antibody (direct or indirect) on peripheral nerves and suggest intravenous lidocaine as part of the analgesic regimen accompanying anti-GD2 antibody treatment.