European journal of pain : EJP
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Bed rest has been shown to be an ineffective treatment for non-specific low back pain (LBP). Despite this, during a new episode of pain some patients still rely on bed rest. Which patients choose bed rest is however unknown. ⋯ Patients with prolonged bed rest in an early phase of pain were still more disabled after one year (p<0.01). Based on these results we conclude that prolonged bed rest in the early phase of pain is associated with a higher long term disability level. In preventing low back disability, GP screening for catastrophizing and fear of injury in LBP patients who had prolonged bed rest merits consideration.
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Comparative Study
Painful traumatic peripheral partial nerve injury-sensory dysfunction profiles comparing outcomes of bedside examination and quantitative sensory testing.
The primary aim of this retrospective study was to focusing on the relationship between individual outcomes of bedside examination (BE) and quantitative testing of somatosensory functions (QST) in 32 patients with painful traumatic partial nerve injury. In addition, the potential presence of common sensory dysfunction denominators has been probed. Patients with a history of traumatic partial nerve injury and ongoing pain were included if pain was confined to the entire or part of the innervation territory of the severed nerve and a bedside titration of the neuron-anatomical borders confirmed sensory aberrations. ⋯ The most common dysfunction found at both BE and QST was hypoesthesia, however with no common denominators in somatosensory dysfunction. In conclusion, this study demonstrated that not infrequently the individual outcome of BE and the corresponding QST measure differed, most frequently for touch sensibility. This finding is of outmost importance when QST outcomes are used to corroborate results from BE in the diagnostic situation.
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Acceptance of pain and other associated negative private experiences has received increasing attention in recent years. This approach is in stark contrast to the traditional approach of reducing or controlling symptoms of pain. The empirical support for treatments emphasizing exposure and acceptance, such as Acceptance and Commitment Therapy, is growing. ⋯ Principal components analysis (PCA) suggests a 2-factor solution with a total of 16 items measuring avoidance of pain and cognitive fusion with pain. Results also indicate adequate reliability and validity for the scale. Implications of these findings for clinical assessment, as well as for research on pain related disability, are discussed along with suggestions for further research in this area.
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The transient receptor potential vanilloid 1 or TRPV1 is a calcium-permeable ion channel that is activated by capsaicin, the active component of hot chilli peppers, and is involved in the development of inflammatory and neuropathic hyperalgesias. Ethanol can sensitise TRPV1-mediated responses, but the pathways contributing to the potentiation of TRPV1 by ethanol have not been clearly defined. Since the mu opioid receptor (MOP) agonist morphine can inhibit TRPV1 responses potentiated by cAMP-dependent protein kinase A (PKA), and ethanol-mediated modulation of other ion channels involves activation of PKA, we aimed to assess the contribution of MOP-sensitive pathways to the potentiation of TRPV1-mediated capsaicin responses by ethanol. ⋯ Among other plausible mechanisms, such as non-specific inhibition of kinases including mTOR, DNA-PK, MLCK, MAPK and polo-like kinases, this suggests that ethanol may affect the PIP2-TRPV1 interaction. This was confirmed by inhibition of ethanol-potentiation by the PLC inhibitor U73122. The results presented here suggest that morphine may be of limited use in inhibiting nociceptive TRPV1 responses that have been sensitised by exposure to ethanol.
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Clinical Trial
Modulation of sensitized C-fibers by adrenergic stimulation in human neuropathic pain.
The chronic constriction injury model is widely used in studying mechanisms of neuropathic pain. In this model neuropathic pain can be influenced by sympathetic interventions. It is assumed that similar mechanisms as in animals are responsible for pain arising from nerve entrapment syndromes in humans. The aim of the present study was to investigate if in patients with nerve entrapment nociceptive afferents can be modulated by adrenergic stimulation. ⋯ Sympathetic-afferent interaction does not play a major role in pain generation due to nerve entrapment. Nevertheless in a subgroup of patients nociceptive afferents show sensitivity to physiological and pharmacological sympathetic stimulation. This finding is important because it emphasises that despite there is no clinical detectable effect on pain sympathetic afferent interaction can be found.