Articles: neuralgia.
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Cochrane Db Syst Rev · Apr 2019
Meta AnalysisHerbal medicinal products or preparations for neuropathic pain.
Neuropathic pain is a consequence of damage to the central nervous system (CNS), for example, cerebrovascular accident, multiple sclerosis or spinal cord injury, or peripheral nervous system (PNS), for example, painful diabetic neuropathy (PDN), postherpetic neuralgia (PHN), or surgery. Evidence suggests that people suffering from neuropathic pain are likely to seek alternative modes of pain relief such as herbal medicinal products due to adverse events brought about by current pharmacological agents used to treat neuropathic pain. This review includes studies in which participants were treated with herbal medicinal products (topically or ingested) who had experienced neuropathic pain for at least three months. ⋯ There was insufficient evidence to determine whether nutmeg or St John's wort has any meaningful efficacy in neuropathic pain conditions.The quality of the current evidence raises serious uncertainties about the estimates of effect observed, therefore, we have very little confidence in the effect estimate; the true effect is likely to be substantially different from the estimate of effect.
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We attempted to determine whether clinical features could differentiate painful small-fiber neuropathy related to primary Sj€ogren's syndrome (pSS-SFN) from idiopathic SFN (idio-SFN). ⋯ Our results suggest that idio-SFN more specifically involved small sensory fibers than pSS-SFN, in which subtle dysfunction of larger sensory fibers and damage of distal autonomic sudomotor innervation may occur. A practical algorithm is proposed to help to differentiate SFN associated with pSS from idio-SFN, based on information very easy to obtain by clinical interview.
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Post-traumatic neuropathic pain in the head and face is a condition that is often refractory to medical management. Peripheral nerve stimulation (PNS) can be an effective treatment. Successful implantation of a novel minimally invasive wireless device is reported here. ⋯ High-frequency stimulation with an external pulse generator and minimally invasive, percutaneous, and bilateral placement of 2 passive INSs on the supraorbital nerves resulted in a significant pain relief in this patient with post-traumatic SON. The device was safe and effective, and the cosmesis was satisfactory.
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Although the first publications on clinical use of peripheral nerve stimulation for the treatment of chronic pain came out in the mid-1960s, it took 10 years before this approach was used to stimulate the occipital nerves. The future for occipital nerve stimulation is likely to bring new indications, devices, stimulation paradigms, and a decrease in invasiveness. As experience increases, one may expect that occipital nerve stimulation will eventually gain regulatory approval for more indications, most likely for occipital neuralgia, migraines and cluster headaches. This process may require additional studies, at least for approval from the US Food and Drug Administration.
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Activation of cannabinoid CB1 receptors suppresses pathological pain but also produces unwanted side effects, including tolerance and physical dependence. Inhibition of fatty-acid amide hydrolase (FAAH), the major enzyme catalyzing the degradation of anandamide (AEA), an endocannabinoid, and other fatty-acid amides, suppresses pain without unwanted side effects typical of direct CB1 agonists. However, FAAH inhibitors have failed to show efficacy in several clinical trials suggesting that the right partnership of FAAH inhibition and pathology has yet to be identified. ⋯ Both FAAH inhibitors synergized with paclitaxel to reduce 4T1 and HeyA8 tumor cell line viability without reducing viability of non-tumor HEK293 cells. Neither FAAH inhibitor reduced viability of non-tumor HEK293 cells in either the presence or absence of paclitaxel, suggesting that nonspecific cytotoxic effects were not produced by the same treatments. Our results suggest that FAAH inhibitors reduce paclitaxel-induced allodynia without the occurrence of CB1-dependence in vivo and may, in fact, enhance the anti-tumor actions of paclitaxel in vitro.