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The findings of this study suggest that duloxetine may be an effective treatment of broad neuropathic pain states, including neuropathic low back pain. The analgesic effects of duloxetine might be mediated by alterations of the descending pain modulatory pathways in the spinal cord, independent of the antidepressant effects.

The blunt probe method is useful for evaluating bladder pain signalling in mice, and revealed the involvement of an NGF-sensitive pain pathway in chronic cystitis pain. This assessment method may be useful for studying the pathophysiology of bladder pain and for developing therapeutic strategies for non-ulcerative IC/PBS in patients.

de-Lacerda99m Tc-MDP bone uptake in secondary hyperparathyroidism: comparison of the mandible, cranium, radius, and femur Abstract Objectives. To evaluate the bone involvement of the mandible, cranium, radius, and femur in secondary hyperparathyroidism (SHPT) using 99m Tc-MDP uptake correlated with the serum intact parathyroid hormone (PTHi). Methods. In a prospective study of 54 patients with SHPT due to chronic renal disease and 15 normal individuals (control group), all patients had elevated serum PTHi and positive 99m Tc-MDP bone scintigraphy. Bone uptake was measured in regions of interest (ROIs) in the mandible, posterior cranium, distal radius, and proximal femur. In addition, soft tissue uptake was measured in one ROI in the soft tissues of the medial thigh (BG). The ROI-BG ratio was used as an index of the normalized bone uptake. Results. The uptake differences in the SHPT and control groups were statistically signifi cant for the mandible (P = 0.001) and cranium (P = 0.002). When the SHPT group was subclassifi ed according to serum PTHi levels, the bone uptake increased with the serum PTHi level. All mandibles of the patients with SHPT were abnormal, and 33% had focal lesions. Conclusions. The bone uptake in the SHPT group was abnormal in all areas evaluated, and a high uptake of 99m Tc-MDP was correlated with an increased serum PTHi.

Bladder pain is a most prominent feature of interstitial cystitis ⁄ painful bladder syndrome (IC ⁄ PBS), but unfortunately the efficacy of current analgesic s was thought to be insufficient in many patients with IC. Despite the clinical significance of bladder pain, there have been only a few research efforts to elucidate the mechanisms of this chronic pain and its pathophysiology remains poorly understood. One of the reasons is the lack of well-characterized experimental animal models of bladder pain. Hence, the present study was conducted to establish a novel bladder pain model in mice and examined whether nerve growth factor (NGF), a major pain mediator, was involved in bladder pain. Repeated injections of cyclophosphamide (150 mg/kg) for 4 days induced persisting mechanical hypersensitivity in mouse abdomen, decreased the threshold gradually from day 1, peaked at day 4 and persisted for at least day 7 after the first injection. The treatments also altered the levels of bladder impairment markers such as heparin binding-epidermal growth factor-like growth factor and glycosaminoglycan without apparent inflammatory signs on day 4. Peroral administrations of amitriptyline (2.5 -10 mg/kg) and gabapentin (10 and 30 mg/kg) suppressed the mechanical hypersensitivity on day 4 in these cystitis mice, but indometha cin (10 and 30 mg/kg) did not affect it. Bladder NGF levels were significantly increased in these cystitis mice and an intravenous injection of anti-NGF serum reversed mechanical hypersensitivity. These results show that this chronic cystitis model induced by repeated cyclophosphamide treatments has less inflammatory elements and NGF-sensitive pain mechanism, which are similar to some features observed in IC patients. Recently, anti-NGF antibody tanezumab has been reported to show the signifi cant efficacy in relieving bladder pain of IC patients and is now working on clinical stage. This model may be useful for not only the mechanism study of chronic bladder pain but also the development of novel therapies for IC patients. 162 E. Kasai, et al. PAIN RESEARCH Vol.29 2014

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