Auricular acupuncture can be an effective treatment for acute anxiety, but there is a lack of direct comparisons of acupuncture to proven standard drug treatments. In this study we compared the efficacy of auricular acupuncture with intranasal midazolam, placebo acupuncture, and no treatment for reducing dental anxiety. Patients having dental extractions (n = 67) were randomized to (i) auricular acupuncture, (ii) placebo acupuncture, and (iii) intranasal midazolam and compared with a no treatment group. Anxiety was assessed before the interventions, at 30 min, and after the dental extraction. Physiological variables were assessed continuously. With the no treatment group as control, the auricular acupuncture group, and the midazolam group were significantly less anxious at 30 min as compared with patients in the placebo acupuncture group (Spielberger Stait-Trait Anxiety Inventory X1, P = 0.012 and <0.001, respectively). In addition, patient compliance assessed by the dentist was significantly improved if auricular acupuncture or application of intranasal midazolam had been performed (P = 0.032 and 0.049, respectively). In conclusion, both, auricular acupuncture and intranasal midazolam were similarly effective for the treatment of dental anxiety.
Introduction We previously described the presence of nerve growth factor receptors in the inflamed synovial compartment. Here we investigated the presence of the corresponding nerve growth factors, with special focus on nerve growth factor (NGF).
Previous studies reported that respiratory feedback (RFB) aids in alleviating chronic pain. However, to date, this adjunct treatment has not been rigorously tested against non-contingent (placebo) feedback. Forty-two patients with chronic low back pain were randomized to either RFB or non-contingent RFB. Both groups performed a daily 30-min home training for 15 consecutive days. A respiratory associated relaxation index (RI) was measured. Pain levels and a somatosensory profile were assessed before and after intervention. Additionally, pain levels were assessed 3 months after the end of intervention. Secondary outcome parameters included daily functioning, psychopathology, and suggestibility. T-tests showed higher and significant pain reductions for RFB, compared to non-contingent RFB. Between-group comparisons reached no significance. However, changes were more pronounced in the RFB condition, which was also true for the course of the RI and the psychopathological scores. This is the first study using a non-contingent respiratory placebo feedback in a randomized, controlled design. Within this design previous positive findings of symptom reductions in patients treated with RFB could partially replicated. Nonetheless, tendencies suggest that contingent feedback patients compared to placebo patients profit more from RFB in the long run regarding reduction of chronic pain and psychological distress.
Cytokines, particularly tumor necrosis factor-alpha, may play an important role in the mediation of mechanical hyperalgesia and autonomic signs in complex regional pain syndrome 1. We performed an IV regional block with low-dose administration of the tumor necrosis factor-alpha antibody, infliximab, in a patient with typical clinical signs of complex regional pain syndrome 1 (moderate pain, edema, hyperhidrosis, elevated skin temperature compared with the contralateral side). A significant improvement of clinical variables was observed 24 h after infliximab treatment. Almost complete remission was reached within 8 wk, but sensory signs improved only after 6 mo. No adverse events were observed.
Background: In contrast to psychological interventions the usefulness of acupuncture as an adjuvant therapy in rheumatoid arthritis (RA) has not yet been demonstrated. Objective: The efficacy of auricular electroacupuncture (EA) was directly compared with autogenic training (AT). Methods: Patients with RA (n = 44) were randomized into EA or AT groups. EA and lessons in AT were performed once weekly for 6 weeks. Primary outcome measures were the mean weekly pain intensity and the disease activity score 28 (DAS 28); secondary outcome measures were the use of pain medication, the pain disability index (PDI), the clinical global impression (CGI) and pro-inflammatory cytokine levels, which were assessed during the study period and 3 months after the end of treatment. Results: At the end of the treatment and at 3-month follow-up a clinically meaningful and statistically significant improvement (p < 0.05) could be observed in all outcome parameters and both groups. In contrast to the AT group, the onset of these effects in the EA group could already be observed after the 2nd treatment week. In the 4th treatment week the EA group reported significantly less pain than the AT group (p = 0.040). After the end of treatment (7th week) the EA group assessed their outcome as significantly more improved than the AT group (p = 0.035). The erythrocyte sedimentation rate in the EA group was significantly reduced (p = 0.010), and the serum concentration of tumor necrosis factor-alpha was significantly increased compared to the AT group (p = 0.020). Conclusions: The adjuvant use of both EA and AT in the treatment of RA resulted in significant short- and long-term treatment effects. The treatment effects of auricular EA were more pronounced.
Many extracellular factors sensitize nociceptors. Often they act simultaneously and/or sequentially on nociceptive neurons. We investigated if stimulation of the protein kinase C epsilon (PKCe) signaling pathway influences the signaling of a subsequent sensitizing stimulus. Central in activation of PKCs is their transient translocation to cellular membranes. We found in cultured nociceptive neurons that only a first stimulation of the PKCe signaling pathway resulted in PKCe translocation. We identified a novel inhibitory cascade to branch off upstream of PKCe, but downstream of Epac via IP3-induced calcium release. This signaling branch actively inhibited subsequent translocation and even attenuated ongoing translocation. A second 'sensitizing' stimulus was rerouted from the sensitizing to the inhibitory branch of the signaling cascade. Central for the rerouting was cytoplasmic calcium increase and CaMKII activation. Accordingly, in behavioral experiments, activation of calcium stores switched sensitizing substances into desensitizing substances in a CaMKII-dependent manner. This mechanism was also observed by in vivo C-fiber electrophysiology corroborating the peripheral location of the switch. Thus, we conclude that the net effect of signaling in nociceptors is defined by the context of the individual cell's signaling history.
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