Pain
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Two studies are presented that investigated 'fear of movement/(re)injury' in chronic musculoskeletal pain and its relation to behavioral performance. The 1st study examines the relation among fear of movement/(re)injury (as measured with the Dutch version of the Tampa Scale for Kinesiophobia (TSK-DV)) (Kori et al. 1990), biographical variables (age, pain duration, gender, use of supportive equipment, compensation status), pain-related variables (pain intensity, pain cognitions, pain coping) and affective distress (fear and depression) in a group of 103 chronic low back pain (CLBP) patients. ⋯ Furthermore, subjects who report a high degree of fear of movement/(re)injury show more fear and escape/avoidance when exposed to a simple movement. The discussion focuses on the clinical relevance of the construct of fear of movement/(re)injury and research questions that remain to be answered.
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The clinical, electrophysiological and haemodynamic effects of precentral gyrus stimulation (PGS) as a treatment of refractory post-stroke pain were studied in 2 patients. The first patient had a right hemibody pain secondary to a left parietal infarct sparing the thalamus, while the second patient had left lower limb pain developed after a right mesencephalic infarct. In both cases, spontaneous pain was associated with hyperpathia, allodynia and hypoaesthesia in the painful territory involving both lemniscal and extra-lemniscal sensory modalities in patient 1, extra-lemniscal sensory modality only in patient 2. ⋯ PGS analgesic efficacy may be mainly related to increased synaptic activity in the thalamus and brainstem while changes in cingulate gyrus and orbito-frontal cortex may be rather related to attentional and/or emotional processes. The inhibitory control on pain would involve thalamic and/or brainstem relays on descending pathways down to the spinal cord segments, leading to a depression of nociceptive reflexes. Painful dysesthesiae during stimulation have to be distinguished from other innocuous sensory side effects, since they may compromise PGS efficacy.
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Supraspinally mediated antinociception has been clearly established for agonists acting via both micro- and delta-opioid receptors. The present experiments were undertaken to further characterize the role of supraspinal opioid delta receptors in the mediation of antinociception in rats and to examine the possible role of putative delta1- and delta2-opioid receptors in the antinociceptive effect. Cannulae directed at the right lateral ventricle, the periaqueductal gray (PAG), or the medullary reticular formation (MRF) were implanted in adult male, Sprague-Dawley rats for the microinjection of [D-Ala2,Glu4]deltorphin (delta2 agonist), [D-Pen2,D-Pen5]enkephalin (DPDPE, delta1 agonist), [D-Ser2,Leu5,Thr6]enkephalin (DSLET, mixed delta/micro agonist) or morphine (reference micro-opioid). ⋯ Morphine anticociception was not antagonized by either DALCE or Cys-DELT. These data demonstrate that supraspinal delta-opioid receptors can be activated to elicit antinociception in the rat and that opioid delta2 receptors predominate in this effect. Further, these effects may occur predominately via inhibition of supraspinally organized behavior without activation of descending systems such as those mediating the TF response in the rat.