Pain
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In this study, we developed a rat model of incisional pain. A 1-cm longitudinal incision was made through skin, fascia and muscle of the plantar aspect of the hindpaw in halothane-anesthetized rats. Withdrawal responses were measured using von Frey filaments at different areas around the wound before surgery and for the next 6 days. ⋯ Even remote sites as much as 10 mm from the wound showed persistent mechanical hyperalgesia. Selective denervations of the rat hindpaw prior to foot incision revealed both the sural and tibial nerves were responsible for transmitting input from the incision that produces hyperalgesia. This model should allow us to understand mechanisms of sensitization caused by surgery and investigate new therapies for postoperative pain in humans.
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Supraspinal opioid analgesia is mediated in part by connections between the periaqueductal gray (PAG) and rostral ventromedial medulla (RVM). Morphine analgesia elicited from the PAG is respectively decreased by selective serotonergic and opioid receptor antagonists administered into the RVM, and increased by RVM neurotensin antagonists. Since glutamate and excitatory amino acid (EAA) receptors are also active in the RVM, the present study evaluated whether either competitive (AP7) or non-competitive (MK-801) N-methyl-D-aspartate (NMDA) antagonists or a kainate/AMPA (CNQX) antagonist microinjected into the RVM altered morphine (2.5 micrograms) analgesia elicited from the PAG as measured by the tail-flick and jump tests. ⋯ In contrast, small but significant reductions in mesencephalic morphine analgesia occurred on the jump test following CNQX (0.5 microgram, 2.2 nmol) in the RVM. NMDA antagonists did not markedly alter either basal nociceptive thresholds following RVM administration, or mesencephalic morphine analgesia following administration into medullary placements lateral or dorsal to the RVM. These data implicate EAA and particularly NMDA receptors in the RVM in modulating the transmission of opioid pain-inhibitory signals from the PAG.
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Randomized Controlled Trial Clinical Trial
The influence of low back pain on muscle activity and coordination during gait: a clinical and experimental study.
Chronic low back pain (CLBP) is a major clinical problem with a substantial socio-economical impact. Today, diagnosis and therapy are insufficient, and knowledge concerning interaction between musculoskeletal pain and motor performance is lacking. Most studies in this field have been performed under static conditions which may not represent CLBP patients' daily-life routines. ⋯ The clinical and experimental findings indicate that musculoskeletal pain modulates motor performance during gait probably via reflex pathways. Initially, these EMG changes may be interpreted as a functional adaptation to muscle pain, but the consequences of chronic altered muscle performance are not known. New possibilities to monitor and investigate altered motor performance may help to develop more rational therapies for CLBP patients.
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Randomized Controlled Trial Comparative Study Clinical Trial
A double-blind randomised comparison of the effects of epidural clonidine, lignocaine and the combination of clonidine and lignocaine in patients with chronic pain.
Twenty patients with chronic pain who previously had obtained analgesia from epidural clonidine and lignocaine agreed to participate in a double-blind crossover study of lumbar epidural clonidine (150 micrograms), lignocaine (40 mg) and the combination of clonidine (150 microgram) and lignocaine (40 mg), all drugs were given in a volume of 3 ml. There were 11 women and 9 men with a mean age 53 years (range: 23-78 years); 9 patients had low back and leg pain, 9 had neuropathic pain, 1 had pelvic pain and 1 Wegner's granulomatosis. Pain intensity and pain relief, as well as sensory and motor blockade, were assessed for 3 h following each injection. ⋯ Overall there was no relationship between neurological blockade and analgesia. The reported side effects appeared to be related to clonidine. These data indicate that in these patients with chronic pain epidural clonidine had a supra-additive effect and behaved more like a co-analgesic than a pure analgesic.
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Randomized Controlled Trial Comparative Study Clinical Trial Controlled Clinical Trial
NMDA receptor blockade in chronic neuropathic pain: a comparison of ketamine and magnesium chloride.
Ten patients (4 female, 6 male) aged 34-67 years suffering from peripheral neuropathic pain participated in a double-blind placebo-controlled study where ketamine or magnesium chloride were administered by a 10 min bolus infusion (ketamine: 0.84 mumol/kg = 0.2 mg/kg, magnesium: 0.16 mmol/kg) followed by a continuous infusion (ketamine: 1.3 mumol/kg/h = 0.3 mg/kg/h, magnesium: 0.16 mmol/kg/h). Ongoing pain determined by VAS score, area of touch-evoked allodynia, detection and pain thresholds to mechanical and thermal stimuli were measured before and during drug infusion. Ketamine produced a significant reduction of spontaneous pain (57%) and of the area of allodynia (33%). ⋯ Following ketamine there was a significant correlation between the reduction in ongoing pain and reduction in area of touch-evoked allodynia. Detection and pain thresholds to mechanical and thermal stimuli were not significantly changed by the drugs. These findings suggest that both ongoing pain and touch-evoked pain (allodynia) in neuropathic pain are inter-related phenomena, which may be mediated by the same mechanism and involving a N-methyl-D-aspartate receptor.