Articles: neuropathic-pain.
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Objectives: Subcutaneous injection of botulinum toxin-A (sBONT-A) is a novel treatment for peripheral neuropathic pain. While its analgesic effects are well documented, this treatment is often not comfortable and fails in patients who show signs of sensory loss but rarely allodynia. There are some case reports about perineural BONT-A injection (pBONT-A) which could be an alternative approach. ⋯ Based on these results, we suggest that future parallel design trials on pBONT-A need to include at least 84 patients. Discussion: Ultrasound-guided pBONT-A injection seems to be a safe treatment leading to a sufficient pain relief for some months without sensory changes. Surprisingly, pBONT-A showed a pronounced analgesic effect also in patients without signs of hyperalgesia.
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Cutaneous mechanical hyperalgesia can be induced in healthy volunteers in early phase analgesic studies to model central sensitization, a key mechanism of persistent pain. However, such hyperalgesia is short-lived (a matter of hours), and is used only for assessing only single drug doses. In contrast, postsurgical peri-incisional hyperalgesia may be more persistent and hence be a more useful model for the assessment of the efficacy of new analgesics. ⋯ The findings suggest that central sensitization contributes significantly to mechanical hyperalgesia at the peri-incisional site. The prolonged duration of hyperalgesia would be advantageous as a pain model, but there was considerable variability of mechanical hyperalgesia in the cohort; the challenges of recruitment may limit its use to small, early phase analgesic studies. PERSPECTIVE: Peri-incisional mechanical hyperalgesia persists for ≥4 weeks after open inguinal hernia repair and reflects central sensitization; this may have usefulness as a model of chronic pain to assess the potential of antineuropathic analgesics.
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Little is published on the prognosis of small fiber neuropathy (SFN). ⋯ Small fiber neuropathy tends to be stable and rarely affects ambulation and employment status. Effective pain control remains a challenge.
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Neurobiology of disease · Oct 2019
Upregulation of tumor necrosis factor-alpha in the anterior cingulate cortex contributes to neuropathic pain and pain-associated aversion.
Injury associated pain involves subjective perception and emotional experience. The anterior cingulate cortex (ACC) is a key area involved in the affective component of pain processing. However, the neuroimmune mechanisms underlying enhanced ACC excitability following peripheral nerve injury are still not fully understood. ⋯ Microinjection of anti-TNF-α antibody into the ACC completely eliminated c-Fos overexpression and greatly attenuated pain aversion and mechanical allodynia induced by SNI, suggesting an important role of ACC TNF-α in the pain aversiveness and pain maintenance. Furthermore, modulating ACC pyramidal neurons via a Gi-coupled human M4 muscarinic receptor (hM4Di) or a Gq-coupled human M3 muscarinic receptor (hM3Dq), a type of designer receptors exclusively activated by designer drugs (DREADD), greatly changed the ACC TNF-α level and the mechanical paw withdrawal threshold. The positive interactions between TNF-α and ACC neurons might modulate the cytokine microenvironment thus contribute to the neuropathic pain.
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Int. Immunopharmacol. · Oct 2019
Nrf2/HO-1 signaling pathway participated in the protection of hydrogen sulfide on neuropathic pain in rats.
Neuropathic pain is evoked by aberrant sensory processing in the peripheral or central nervous system, which is characterized by persistent pain, tactile allodynia, or hyperalgesia. Neuroinflammation is associated with the initiation and maintenance of persistent pain in both the peripheral and central nervous systems. Hydrogen sulfide plays important regulatory roles in different physiological and pathological conditions. ⋯ Mechanical allodynia, thermal hyperalgesia and the number of paw lifts were measured at different time points after operation. In the present research, neuropathic pain induced Nrf2 and HO-1 expression in the microglial cells of the spinal cord; Nrf2 and HO-1 were necessary to alleviate the hyperalgesia of CCI-induced rats; NaHS mitigated the hyperalgesia and allodynia induced by the CCI operation; and NaHS mitigated the excessive release of the cytokines TNF-α, IL-1β, IL-6 and HMGB1 via the Nrf2/HO-1 pathway in the microglial cells of the spinal cord. These results indicated that NaHS exhibited antinociceptive and anti-inflammatory effects that were associated with the activation of the Nrf2/HO-1 pathway in the spinal cord of rats with neuropathic pain.