Pain
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Randomized Controlled Trial Multicenter Study
Effect of local anesthesia on atypical odontalgia--a randomized controlled trial.
The aim of the study was to evaluate the analgesic effect of lidocaine in a double-blind, controlled multi-center study on patients with atypical odontalgia (AO)--a possible orofacial neuropathic pain condition. Thirty-five consecutive AO patients (range 31-81 years) with a mean pain duration of 7.2 years (range 1-30 years) were recruited from four different orofacial pain clinics in Sweden. In a randomized cross-over design, 1.5 ml local anesthesia (20mg/ml lidocaine and 12.5 microg/ml adrenaline) or 1.5 ml saline (9 mg/ml NaCl solution) (placebo) was injected to block the painful area. ⋯ All patients demonstrated significant disturbances in somatosensory function on the painful side compared to the non-painful side as revealed by quantitative sensory tests, however, only one significant inverse correlation was found between percentage pain relief and the magnitude of brush-evoked allodynia (Spearman: P<0.01). In conclusion, AO patients experienced significant, but not complete, pain relief from administration of local anesthetics compared with placebo. The findings indicate that the spontaneous pain in AO patients only to some extent is dependent on peripheral afferent inputs and that sensitization of higher order neurons may be involved in the pathophysiology of AO.
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Comparative Study
Can pain can be more or less neuropathic? Comparison of symptom assessment tools with ratings of certainty by clinicians.
Chronic pain is generally regarded as being divided into two mutually exclusive pain mechanisms: nociceptive and neuropathic. Recently, this dichotomous approach has been questioned and a model of chronic pain being 'more or less neuropathic' has been suggested. To test whether such a spectrum exists, we examined responses by patients with chronic pain to validated neuropathic pain assessment tools and compared these with ratings of certainty about the neuropathic origin of pain by their specialist pain physicians. ⋯ There were also significant differences between many S-LANSS and NPS item scores between groups. We have shown that higher scores on both the S-LANSS and the NPS are indicative of greater clinician certainty of neuropathic pain mechanisms being present. These data support the theoretical construct that pain can be more or less neuropathic and that pain of predominantly neuropathic origin may be a useful clinical concept.
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Paclitaxel chemotherapy frequently induces neuropathic pain during and often persisting after therapy. The mechanisms responsible for this pain are unknown. Using a rat model of paclitaxel-induced painful peripheral neuropathy, we have performed studies to search for peripheral nerve pathology. ⋯ Comparable to the pain behaviour, these mitochondrial changes had resolved by day 160. Our data do not support a causal role for axonal degeneration or dysfunction of axonal microtubules in paclitaxel-induced pain. Instead, our data suggest that a paclitaxel-induced abnormality in axonal mitochondria of sensory nerves contributes to paclitaxel-induced pain.
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Temporal summation (TS) is usually evoked by repetitive mechanical or electrical stimuli, and less commonly by tonic heat pain. The present study aimed to examine the TS induction by repetitive-phasic versus tonic heat pain stimuli. Using 27 normal volunteers, we compared the extent of summation by three calculation methods: start-to-end pain rating difference, percent change, and double-logarithmic regression of successive ratings along the stimulation. ⋯ The extent of TS induced by both paradigms was found to be associated with anxiety level and pain catastrophizing. Despite some dissimilarity between the repetitive-phasic and the tonic paradigms, the many similarities suggest that the two represent a similar physiological process, even if not precisely the same. Future clinical applications of these tests will determine the clinical relevance of the TS paradigms presented in this study.
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The Communal Coping Model of pain catastrophizing proposes that pain catastrophizers enact pain behaviors in order to solicit support or empathy from their social environment. By this account, pain catastrophizers might be expected to engage in behavior aimed at maximizing the probability that their pain will be perceived by others in their social environment. To test this prediction, 40 undergraduates were videotaped during a cold pressor procedure. ⋯ The relation between cold pressor participants' level of pain catastrophizing and observer inferences of pain intensity was mediated by the cold pressor participants' pain behavior. Although pain catastrophizing was associated with observers' inferences of more intense pain, cold pressor participants' level of pain catastrophizing was not associated with observers' accuracy in inferring self-reported pain. Implications of the findings for theory and clinical practice are addressed.