European journal of pain : EJP
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In patients with localized musculoskeletal pain, spread of pain and tenderness outside the primarily painful area and sometimes even generalization of pain have been reported, the latter possibly indicating a dysfunction of endogenous pain modulatory systems. The purpose of the study was to use patients with long-term trapezius myalgia as a model to investigate the possible influence of a localized muscle pain on somatosensory processing in a remote pain-free area and the effect of heterotopic noxious conditioning stimulation (HNCS) on 'diffuse noxious inhibitory controls' (DNIC) related mechanisms. Altered somatosensory processing may indicate subclinical derangement of endogenous modulatory systems. ⋯ During HNCS, the sensitivity to pressure pain and suprathreshold heat pain decreased in patients and controls alike (p<0.02 and p<0.04 respectively) and returned to baseline following HNCS. In conclusion, in a remote non-painful area allodynia to pressure and hypoaesthesia to cold were found in conjunction with preserved function of DNIC-related mechanisms. Whether altered central somatosensory processing at rest may indicate a predisposition for further spread of pain is at present unclear.
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"He slept less and less; they gave him opium and began to inject morphine. But this did not relieve him. The dull pain he experienced in the half asleep condition at first only relieved him as a change, but then it became as bad, or even more agonizing, than the open pain."--Tolstoy, The Death of Ivan Ilyitch. ⋯ Those who work in chronic pain are unfortunately only too aware of the problems that such pains can cause. One of the hallmarks of neuropathic pain is poor or incomplete relief with opioids. As with so many things in medicine, there is nothing novel in this realization, as the Tolstoy quotation shows.
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The overarching reason that pain patients seek medical attention is because their pain interferes with some or all aspects of their quality of life (QOL). Interventions are considered successful by the patient if QOL is improved. Simple pain scores, although providing important information, do not capture the patient's total pain experience, which includes the effect on QOL. A focus on patient QOL should be adopted by all clinicians treating patients with neuropathic pain to work toward successful outcomes.
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Systemic morphine selectively depresses a thalamic link of widespread nociceptive inputs in the rat.
The lateral part of the ventromedial thalamus (VM l) relays nociceptive inputs from the whole body surface to the dorsolateral frontal cortex. The aim of the present study was to investigate the effects of systemic morphine on nociceptive activity evoked in VM l neurones either by thermal (48 degrees C) or by supramaximal percutaneous electrical stimuli. The noxious thermal evoked responses were depressed by 10.8 +/- 10.1%, 48.3 +/- 23.0% and 67.3 +/- 10.1%, 5 min after i.v. injections of 1.0, 1.73 and 3.0 mg/kg of morphine, respectively. ⋯ The dose of morphine that reduced VM l neuronal nociceptive responses by 50% (1.73 mg/kg) was around 3.5 times lower than that necessary to inhibit the responses of its spinal or medullary relays under similar experimental conditions. These results, added to the data of the literature, suggest that supraspinal effects of morphine are primarily mediated at the thalamic level. It is tempting to speculate that morphine-induced reductions of attentional or psychomotor responses related to pain may be mediated by its action on VM l.