Abstract:We applied calcitonin in a single-shot treatment to 10 patients with persistent or acute phantom limb pain. Nine patients responded immediately and noted a clear analgesic effect. In contrast a group of non-phantom pain patients of heterogeneous composition did not respond at all, except 1 patient with chronic stump pain. We believe that this could be an exciting new approach to the treatment of phantom limb pain.
“…Direct epidural or subarachnoidal injection of CT has also shown án analgesic effect [82,83]. Besides pain management in osteoporosis [77,[84][85][86] CT has shown analgesic action in painful conditions such as phantom limb pain [87,88], diabetic neuropathy [89], complex regional pain syndrome [90], adhesive capsulitis [91,92], rheumatoid arthritis [93], vertebral crush fractures [94,95], spondylitis, tumor metastasis [96], cancer pain [97], migraine [98,99], Paget's disease of bone [100]) as well as post-operative pain [101].…”
Section: Does Calcitonin Improve Bone Quality?mentioning
The oral formulation of salmon calcitonin provides additional benefits and increased efficacy on bone based on Phase I and II clinical trials data, as compared with the nasal formulation. Hence, the results on the ongoing Phase III fracture trial are awaited with great interest.
“…Direct epidural or subarachnoidal injection of CT has also shown án analgesic effect [82,83]. Besides pain management in osteoporosis [77,[84][85][86] CT has shown analgesic action in painful conditions such as phantom limb pain [87,88], diabetic neuropathy [89], complex regional pain syndrome [90], adhesive capsulitis [91,92], rheumatoid arthritis [93], vertebral crush fractures [94,95], spondylitis, tumor metastasis [96], cancer pain [97], migraine [98,99], Paget's disease of bone [100]) as well as post-operative pain [101].…”
Section: Does Calcitonin Improve Bone Quality?mentioning
The oral formulation of salmon calcitonin provides additional benefits and increased efficacy on bone based on Phase I and II clinical trials data, as compared with the nasal formulation. Hence, the results on the ongoing Phase III fracture trial are awaited with great interest.
“…For example, parenteral salmon calcitonin was significantly more effective than placebo in reducing the frequency of pain episodes in migraine [147,148]. Likewise, calcitonin was able to reduce the pain score in patients with the phantom limb pain syndrome in the early postoperative period [149,150] and in mild cases of lumbar spinal stenosis [146]. In this condition, calcitonin has also been reported to improve physical performance and lengthen the walking distance [151].…”
“…83 This is in contrast to studies in OVX and CCI rats, which showed that repeated systemic administration of CT is needed to produce analgesia. 3,4,18,76,97–99 Therefore, other unknown factors may be involved in the underlying mechanism of CT in relieving oxaliplatin- and paclitaxel-induced neuropathy (Figure 5). Figure 4.Proposed mechanism of inhibition of abnormal expression of 5-HT 1A -like receptors and sodium channels by CT in OVX rats.…”
Section: Site Of Action Of Ct In Other Modelsmentioning
The polypeptide hormone calcitonin is well known clinically for its ability to relieve osteoporotic back pain and neuropathic pain such as spinal canal stenosis, diabetic neuropathy, chemotherapy-induced neuropathy, and complex regional pain syndrome. Because the analgesic effects of calcitonin have a broad range, the underlying mechanisms of pain relief by calcitonin are largely unknown. However, recent studies using several types of chronic pain models combined with various methods have been gradually clarifying the mechanism. Here, we review the mechanisms of the analgesic action of calcitonin on ovariectomy-induced osteoporotic and neuropathic pain. The analgesic action of calcitonin may be mediated by restoration of serotonin receptors that control selective glutamate release from C-afferent fibers in ovariectomized rats and by normalization of sodium channel expression in damaged peripheral nerves. Serotonin receptors are reduced or eliminated by the relatively rapid reduction in estrogen during the postmenopausal period, and damaged nerves exhibit hyperexcitability due to abnormal expression of Na+ channel subtypes. In addition, in chemotherapy-induced peripheral neuropathy, inhibition of signals related to transient receptor potential ankyrin-1 and melastatin-8 is proposed to participate in the anti-allodynic action of calcitonin. Further, an unknown calcitonin-dependent signal appears to be present in peripheral nervous tissues and may be activated by nerve injury, resulting in regulation of the excitability of primary afferents by control of sodium channel transcription in dorsal root ganglion neurons. The calcitonin signal in normal conditions may be non-functional because no target is present, and ovariectomy or nerve injury may induce a target. Moreover, it has been reported that calcitonin reduces serotonin transporter but increases serotonin receptor expression in the thalamus in ovariectomized rats. These data suggest that calcitonin could alleviate lower back pain in patients with osteoporosis or neuropathic pain by the alteration in receptor or channel expression.
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