Articles: neuralgia.
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Research suggests that the prognosis of chronic nonspecific low back pain is poor when there is an alteration in the central pain processing pathway. This alteration creates a cascade of events, leading to poor outcomes. An overview of the predictors which increase this heightened pain perception is needed. ⋯ This review identified the predictors for altered central pain modulation in chronic nonspecific low back pain. This alteration could be responsible for the suspected poor outcomes even post treatment. Furthermore, the knowledge of predictors could potentially aid the therapist in planning a treatment regime when poor outcomes are suspected.
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This review is aimed to summarize the pain-relieving effect of non-drug substances, mostly prescribed as integrators in treatment of pain, including especially in chronic postoperative pain (CPSP) and in chronic back pain after acute episodes. Their use reflects the fact that the current treatments for these syndromes continue to pose problems of unsatisfactory responses in a significant portion of patients and/or of an excess of side effects like those noted in the present opioid crisis. As integrators are frequently introduced into the market without adequate clinical testing, this review is aimed to collect the present scientific evidence either preclinical or clinical for their effectiveness. ⋯ In particular, examining their putative mechanisms of action it emerges that combinations of few of them may exert an extraordinary spectrum of activities on a large variety of pain-associated pathways and may be eventually used in combination with more traditional pain killers in order to extend the duration of the effect and to lower the doses. Convincing examples of effective combinations against pain are vitamin B complex plus gabapentin for CPSP, including neuropathic pain; vitamin B complex plus diclofenac against low back pain and also in association with gabapentin, and ALA for burning mouth syndrome. These as well as other examples need, however, careful controlled independent clinical studies confirming their role in therapy.
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Dorsal root ganglion stimulation (DRGS) is a neuromodulation therapy for chronic pain that is refractory to conventional medical management. Currently, the mechanisms of action of DRGS-induced pain relief are unknown, precluding both our understanding of why DRGS fails to provide pain relief to some patients and the design of neurostimulation technologies that directly target these mechanisms to maximize pain relief in all patients. ⋯ Here, we summarize the leading hypotheses of the mechanisms of DRGS-induced analgesia, and propose areas of future study that will be vital to improving the clinical implementation of DRGS. PERSPECTIVE: This article synthesizes the evidence supporting the current hypotheses of the mechanisms of action of DRGS for chronic pain and suggests avenues for future interdisciplinary research which will be critical to fully elucidate the analgesic mechanisms of the therapy.
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Neuropathic pain and other pain disorders have received attention as potential indications for use of cannabis-based medicines or medical cannabis (CBM/MC). Evidence regarding the efficacy and safety of CBM/MC for pain disorders is, however, insufficient. Denmark introduced a pilot programme of medical cannabis in January 2018. We aimed to evaluate efficacy, safety, and non-specific effects of CBM/MC used under the pilot programme compared with controls. ⋯ Patients with neuropathic pain may benefit from treatment with cannabis-based medicines or medical cannabis (CBM/MC), particularly in terms of reduced use of gabapentin and fewer days admitted to hospitals, compared with propensity score matched controls. CBM/MC did not, however, reduce the use of opioids. We did not find evidence that CBM/MC were effective for patients with other pain disorders.
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Mechanistic studies principally focusing on primary afferent nociceptive neurons uncovered the upregulation of collapsin response mediator protein 2 (CRMP2)-a dual trafficking regulator of N-type voltage-gated calcium (Cav2.2) as well as Nav1.7 voltage-gated sodium channels-as a potential determinant of neuropathic pain. Whether CRMP2 contributes to aberrant excitatory synaptic transmission underlying neuropathic pain processing after peripheral nerve injury is unknown. Here, we interrogated CRMP2's role in synaptic transmission and in the initiation or maintenance of chronic pain. ⋯ Conditional knockout of CRMP2 in neurons reversed established mechanical allodynia induced by a spared nerve injury in both male and female mice. In addition, the development of spared nerve injury-induced allodynia was also prevented in these mice. Our data strongly suggest that CRMP2 is a key regulator of glutamatergic neurotransmission driving pain signaling and that it contributes to the transition of physiological pain into pathological pain.