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Abstract. Cannabinoids have been reported to have analgesic properties in animals of acute nociception or of inflammatory and neuropathic pain models, but the mechanisms by which they exert such alleviative effects are not yet fully understood. We investigated whether the CB 1 -cannabinoid-receptor agonist HU210 modulates the capsaicin-induced 45 Ca 2+ influx and substance P like-immunoreactivity (SPLI) release in cultured rat dorsal root ganglion (DRG) cells. HU210 attenuated the capsaicin-induced 45 Ca 2+ influx and this effect was reversed by the CB 1 antagonist AM251. Treatment of DRG cells with 100 nM bradykinin for 3 h potentiated capsaicin-induced SPLI release accompanied with the induction of cyclooxygenase-2 mRNA expression. The potentiation of SPLI release by bradykinin was reversed by HU210 or the protein kinase A (PKA) inhibitor H-89. HU210 also reduced forskolin-induced cyclic AMP production and forskolin-induced potentiation of SPLI release. These results suggest that CB 1 could inhibit either the capsaicin-induced Ca 2+ influx or the potentiation of capsaicin-induced SPLI release by a long-term treatment with bradykinin through involvement of a cyclic-AMP-dependent PKA pathway. In conclusion, CB 1 -receptor stimulation modulates the activities of transient receptor potential vanilloid receptor 1 in cultured rat DRG cells.

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Aims: Somatoform pain disorder is associated with psychosocial dysfunction, and psychotherapies, such as cognitive behavioral therapy (CBT), are thought to provide useful interventions to address such dysfunction as well as the pain itself. However, little is known about whether CBT for somatoform pain disorder is effective, including the long-term course of the illness, in non-Western populations. We therefore tailored such a program based on an existing CBT protocol and examined its effectiveness in Japan.Methods: Thirty-four Japanese participants (22 women; mean age = 52.5 years) enrolled in a weekly 12-session group treatment, with 32 completing both wait-list and treatment conditions. The primary outcome measure was pain intensity. Secondary outcome measures included pain characteristics, as measured by pain catastrophizing and psychometric evaluations, including depression, anxiety, and quality of life. The patients were followed up for 12 months after treatment. Results:We found that pain intensity, anxiety, depressive symptoms, and social functioning all significantly improved after treatment compared with the wait-list period, and the improvements in pain intensity, depressive symptoms, and social functioning were sustained at 12 months following the completion of CBT. There were strong positive correlations (P < 0.01) among pre-and post-treatment changes in the affective dimension of pain, depression, anxiety, and pain catastrophizing. Conclusions:These results show that the present CBT program was effective for Japanese patients with somatoform pain disorder and that gains were maintained over the long term. More work is needed to further clarify the effects of CBT interventions on somatoform symptoms, particularly in Japan.

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For difficult to treat neuropathic pain from cancer, adjuvant analgesics are often used with opioids. We present the case of a 5-year-old girl who was diagnosed with meningitis caused by malignant T-cell lymphoma. She had severe neuropathic pain not relieved by increasing doses of a fentanyl infusion. Intravenous administration of ketamine and lidocaine in combination with fentanyl provided excellent analgesia without significant side effects. Ketamine and lidocaine can be safely infused together with concomitant opioids for the treatment of refractory neuropathic pain caused by cancer.

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