Articles: neuralgia.
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Gut dysbiosis, defined as pathogenic alterations in the distribution and abundance of different microbial species, is associated with neuropathic pain in a variety of clinical conditions, but this has not been explored in the context of neuropathy in people with HIV (PWH). We assessed gut microbial diversity and dysbiosis in PWH and people without HIV (PWoH), some of whom reported distal neuropathic pain (DNP). DNP was graded on a standardized, validated severity scale. ⋯ Two candidate pathways for these associations, involving microbial pro-inflammatory components and microbially-produced anti-inflammatory short chain fatty acids, are discussed. Future studies might test interventions to re-establish a healthy gut microbiota and determine if this prevents or improves DNP. PERSPECTIVE: The association of neuropathic pain in people with HIV with reduced gut microbial diversity and dysbiosis raises the possibility that re-establishing a healthy gut microbiota might ameliorate neuropathic pain in HIV by reducing proinflammatory and increasing anti-inflammatory microbial products.
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Curr Pain Headache Rep · Feb 2022
ReviewDorsal Column Stimulation and Cannabinoids in the Treatment of Chronic Nociceptive and Neuropathic Pain: a Review of the Clinical and Pre-clinical Data.
The main objective of this review is to appraise the literature on the role of spinal cord stimulation (SCS), cannabinoid therapy, as well as SCS and cannabinoid combination therapy for the management of chronic neuropathic and nociceptive pain. Current research suggests that SCS reduces pain and increases functional status in carefully selected patients with minimal side effects. ⋯ As cannabinoid-based medications become a topic of increasing interest in pain management, data remains limited regarding the clinical efficacy of cannabinoids for pain relief. Furthermore, from a mechanistic perspective, although various pain treatment modalities utilize overlapping pain-signaling pathways, clarifying whether cannabinoids work synergistically with SCS via shared mechanisms remains to be determined. In considering secondary outcomes, the current literature suggests cannabinoids improve quality of life, specifically sleep quality, and that SCS decreases opioid consumption, increases functional capacity, and decreases long-term healthcare costs. These findings, along with the high safety profiles of SCS and cannabinoids overall, incentivize further exploration of cannabinoids as an adjunctive therapy to SCS in the treatment of neuropathic and nociceptive pain.
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Review
Motor Cortex Stimulation for Pain: A Narrative Review of Indications, Techniques, and Outcomes.
Motor cortex stimulation (MCS) was introduced in 1985 and has been tested extensively for different types of peripheral and central neuropathic pain syndromes (eg, central poststroke pain, phantom limb pain, trigeminal neuropathic pain, migraines, etc). The motor cortex can be stimulated through different routes, including subdural, epidural, and transcranial. ⋯ Scientific evidence supports the use of MCS for treatment of refractory neuropathic pain syndromes. Further studies are warranted to elucidate the specific indications and stimulation protocols that are most amenable to the different types of MCS.
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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.
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Curr Pain Headache Rep · Feb 2022
ReviewModulatory Effects of Stem Cells on Opioid Receptors and Neuroinflammation.
This narrative review examines stem cell therapy and its effect on opioid therapy in neuropathic pain. ⋯ Stem cell therapy has shown promise in neuropathic pain and opioid tolerance, with a notable common pathway (the P2X4 receptor). Opioid therapy frequently has poor efficacy in patients who suffer from neuropathic pain. There is evidence that the presence of neuropathic pain itself causes changes to the opioid receptor, decreasing the therapeutic potential of this modality. The efficacy of opioid therapy is further decreased in this patient population after chronic opioid exposure, which leads to opioid tolerance and in some cases opioid-induced hyperalgesia. There is growing evidence that stem cell therapy has potential to treat neuropathic pain and may simultaneously decrease opioid tolerance and hyperalgesia. Opioid-induced hyperalgesia occurs via mu-opioid receptor-dependent expression of P2X4 receptors on microglia. Intrathecal stem cell therapy provides analgesic properties due to the significant reduction of P2X4R expression in spinal cord microglia, thereby directly decreasing chronic neuropathic pain.