Pain medicine : the official journal of the American Academy of Pain Medicine
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It has been hypothesized that serotonin reuptake inhibitor antidepressants (ADs) are only weakly antinociceptive but augment noradrenergic (NA) antinociception. Thus, ADs with combined serotonergic (SN) and NA activity, (i.e., the serotonergic/noradrenergic (SN/NA) ADs) should have greater antinociceptive activity versus the NA ADs, which in turn should have more antinociceptive activity than the SN ADs. The objective of this structured review was to test this hypothesis by reviewing relevant basic science literature on the treatment of experimental pain with the above different types of ADs. DESIGN, SETTING, PARTICIPANTS, OUTCOME, MEASURES: Animal or human experimental AD pain treatment studies were located by the usual search methods. For animal studies only placebo-controlled studies were included for review. For human studies only double blind placebo-controlled studies were selected for review. The animal and human studies were then sorted according to the pain model represented, e.g., neuropathic pain model. Studies were then characterized according to the type of AD utilized, and the antinociceptive outcome of the AD trial. ⋯ Overall, the results of this structured review support the above hypothesis.
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Immune responses are an input source of modulation/modification for the peripheral nervous system that can result in pain and/or peripheral neuropathy. The resulting pain can be a significant debilitating component of many diseases as well as an untoward side effect of treatment. This paper briefly describes three sources of peripheral neuropathy generated in the presence of, or associated with, an immune response. ⋯ The body, in an attempt to rid itself of a tumor or an invading bacterial infection or virus, attacks its nervous system due to molecular mimicry; this results in, respectively, paraneoplastic neuropathy or inflammatory polyneuropathy. The third neuropathic pain syndrome is iatrogenic and occurs after administration of an antibody to GD2 ganglioside as an immunotherapy for neuroblastoma. This paper will attempt to point out some common elements in their neuropathologies and mechanisms.
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Intravenous lidocaine is used to treat various neuropathic pain states. Systemic local anesthetics have been reported to cause behavioral alteration via limbic system activation. This case report describes a dramatic behavioral change in a patient receiving intravenous lidocaine and suggests a possible use of lidocaine to discriminate somatic and affective pain characteristics.
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Although bone cancer pain can be severe and is relatively common, very little is known about the basic mechanisms that generate and maintain this debilitating pain. To begin to define the mechanisms that give rise to bone cancer pain, a mouse model was developed using the intramedullary injection and containment of osteolytic sarcoma cells in the mouse femur. These tumor cells induced bone destruction as well as ongoing and movement-evoked pain behaviors similar to that found in patients with bone cancer pain. ⋯ To determine whether this mouse model of bone cancer could be used to define the basic mechanisms giving rise to bone cancer pain, we targeted excessive osteoclast activity using osteoprotegerin, a secreted decoy receptor that inhibits osteoclast activity. Osteoprotegerin blocked excessive tumor-induced, osteoclast-mediated bone destruction, and significantly reduced ongoing and movement-evoked pain, and the neurochemical reorganization of the spinal cord. These data suggest that this model can provide insight into the mechanisms that generate bone cancer pain and provide a platform for developing and testing novel analgesics to block bone cancer pain.