European journal of pain : EJP
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Deep tissue pain can be related to reduced muscle blood flow, which comprises the metabolic demand under muscle work. The tissues and receptors involved in nociception after ischaemic muscle contractions are not known. The concentration of adenosine is increased after ischaemic contractions and might act as an algesic substance. ⋯ During hypertonic saline infusions, the pressure pain threshold was decreased compared with before and immediately after the pain had vanished. The present study shows that pharmacological levels of adenosine in skeletal muscle did not induce pain. Excitation of muscle nociceptors by hypertonic saline evoked hyperalgesia, larger areas of pain, and a different quality of pain compared with ischaemic contractions, suggesting that the pain after ischaemic contractions is mediated by other populations of nociceptors in muscle and/or other tissues than excited by hypertonic saline.
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Continuous sensory analgesia of brachial plexus (CSA BP) was only occasionally reported to have been used in the treatment of CRPS. In the past four years, we have treated 21 patients with a working diagnosis of CRPS. The treatment was instituted one to six months after inciting injury. ⋯ In 16 cases, no evident improvement was observed and CSA BP was introduced. At follow-up (3-36 months), the results were: 13/16 (81%) had at least good results (excellent 2, good without any sequelae 5, good with sequelae of initial injury 6, and poor 3). The results were judged as follows: excellent (completely normal hand); good (only temporary pain up to 2 on a 0-10 numeric rating scale; no signs of dysfunction of sympathetic nervous system; ROM of wrist over 50% of normal hand; ROM of fingers excellent or good; and the strength of hand grasp and key pinch over 50% of normal hand measured with dynamometer) and if any of the former criteria was missing, the result was defined as poor.
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One of the most prominent features of secondary hyperalgesia is touch-evoked pain, i.e., pain evoked by dynamic tactile stimuli applied to areas adjacent or remote from the originating injury. It is generally accepted that the neurobiological mechanism of this sensory alteration involves the central nervous system (CNS) so that incoming impulses in low-threshold mechanoreceptors from the area of secondary hyperalgesia can evoke painful sensations instead of touch. ⋯ Here we review the evidence gathered in support of this model in the intervening years with special reference to experimental studies of antidromic activity (Dorsal Root Reflexes--DRRs) in nociceptive afferents and on the acquisition of low-threshold inputs by nociceptor-specific neurons in the spinal dorsal horn. We also discuss and identify potential molecular mechanisms that may underlie the presynaptic interaction model and therefore that could be responsible for the development of secondary hyperalgesia.
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Attentional bias in patients with chronic pain was investigated using the emotional Stroop task with personalized pain words. A group of 20 chronic pain patients with 20 matched controls participated in the experiment. Before administration of the emotional Stroop patients were asked to select the five best descriptors of their pain from a list of 19 sensory pain descriptors. ⋯ Results showed a weak Stroop interference effect with slower reaction times to pain words in the patient group, but they did not differ significantly from the controls. Both groups were slower on the threat words and displayed the classical Stroop interference effect for color words. The overall pattern of results are in line with previous Stroop studies on pain patients showing weak support for the attentional bias hypothesis.
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Randomized Controlled Trial Clinical Trial
Suppression of motor evoked potentials in a hand muscle following prolonged painful stimulation.
Earlier investigations have shown that stimulation of peripheral afferent nerves induces prolonged changes in the excitability of the human motor cortex. The present study compared the effect of experimental pain and non-painful conditioning stimulation on motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) in the relaxed first dorsal interosseous (FDI) and flexor carpi ulnaris (FCU) muscles. The MEPs were measured in 10 healthy subjects, and stimulus-response curves were generated before and after each of four stimulation paradigms conducted in random order on separate occasions: (a) control; (b) "dual stimulation" consisting of electrical stimulation of the FDI motor point paired with TMS; (c) painful infusion of hypertonic saline in the FDI muscle; and (d) pain combined with dual stimulation. ⋯ In two additional subjects, the responses evoked in FDI by direct stimulation of the descending corticospinal tracts were significantly depressed following painful stimulation of the FDI, although the ulnar-evoked M-waves remained constant. It is concluded that muscle pain is followed by a period with profound depression of MEPs amplitudes in the resting muscle, but that these changes are at least in part due to a lasting depression of the excitability of the motoneurones in the spinal cord. Hence, painful stimulation differs from non-painful, repetitive stimulation, which facilitates the corticomotor pathway.