Articles: neuropathic-pain.
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Randomized Controlled Trial
Treatment of Postherpetic Neuralgia with Gastroretentive Gabapentin: Interaction of Patient Demographics, Disease Characteristics, and Efficacy Outcomes.
To understand how patient demographics and patient-reported disease characteristics relate to successful management of postherpetic neuralgia (PHN), integrated data from phase 3 and phase 4 studies of patients with PHN (n = 546) who received once-daily gastroretentive gabapentin (G-GR, 1800 mg) were analyzed. There were widespread, networked, positive correlations among efficacy end points--pain qualities on the visual analog scale (VAS) and Brief Pain Inventory (BPI), measures of pain interference on the BPI, and Patient Global Impression of Change (PGIC)--most likely characterized by positive feedback loops, in which pain interferes with patient functioning, and poor functioning enhances pain. VAS scores at baseline or at week 2 were the strongest predictors of being "much" or "very much" improved on the PGIC; BPI sleep interference scores were the strongest predictors of percent changes in BPI pain qualities and in the average of BPI interference scores, whereas age, sex, and race were not important predictors. In addition to VAS, BPI sleep interference and PGIC assessments appeared to be key co-strategic factors important for successful treatment outcomes, and should be considered as co-primary end points in future clinical trials of PHN. This could improve detection of true positive efficacy responses and guide successful transition to real-world clinical practice. ⋯ This study describes complex relationships among measures of pain intensity, pain interference with daily activities, and demographics of patients with PHN treated with G-GR. Such comprehensive characterization provides important insight into how different variables contribute to successful treatment, and may lead to better management of neuropathic pain.
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Neuropathic pain is notoriously variable in its severity and impact on patients, as well as in its response to treatment. Certain therapies for neuropathic pain have better evidence for their use; however, it is apparent that although some therapies provide relief for only a minority of patients, the relief may be significant. Without a trial of therapy, there is no way to know if that relief is achievable. ⋯ While opioid medications, particularly methadone, can be effective in treating neuropathic pain, they are best used only in refractory cases and by experienced clinicians, due to concerns for both short- and long-term safety. Some therapies have a long history of successful use for certain syndromes (e.g., carbamazepine for trigeminal neuralgia pain), but these should not be considered to the exclusion of other more recent, less-supported therapies (e.g., botulinum toxin A for the same), particularly in refractory cases. We find the principles of palliative care highly applicable in the treatment of chronic neuropathic pain, including managing expectations, mutually agreed-upon meaningful outcomes, and a carefully cultivated therapeutic relationship.
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Observational Study
Topical ambroxol for the treatment of neuropathic pain : An initial clinical observation. English version.
Neuropathic pain is difficult to treat, and the available options are often inadequate. The expectorant ambroxol also acts as a strong local anaesthetic and blocks sodium channels about 40 times more potently than lidocaine. It preferentially inhibits the channel subtype Nav 1.8, which is expressed especially in nociceptive C-fibres. In view of the low toxicity of ambroxol, it seemed reasonable to try using it for the treatment of neuropathic pain that failed to respond to other standard options. ⋯ Ambroxol acts as a strong local anaesthetic and preferentially inhibits the nociceptively relevant sodium channel subtype Nav 1.8. For the first time, we report below on a relevant pain relief following topical ambroxol 20% cream in patients with neuropathic pain. In view of the positive side effect profile, the clinical benefit in patients with pain should be investigated further.
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J. Peripher. Nerv. Syst. · Dec 2015
Caffeine prevents antihyperalgesic effect of gabapentin in an animal model of CRPS-I: evidence for the involvement of spinal adenosine A1 receptor.
This study was designed to determine whether 3 weeks of gabapentin treatment is effective in alleviating neuropathic pain-like behavior in animal models of complex regional pain syndrome type-I and partial sciatic nerve ligation (PSNL). We investigated the contribution of adenosine subtypes to the antihyperalgesic effect of gabapentin by examining the effect of caffeine, a non-selective adenosine A1 and A2 receptor antagonist or 1,3-dipropyl-8-cyclopentylxanthine (DPCPX), a selective adenosine A1 subtype receptor antagonist on this effect. Neuropathic pain was produced by unilateral prolonged hind paw ischemia and reperfusion (I/R) or PSNL procedures which resulted in stimulus-evoked mechanical hyperalgesia. ⋯ Mice were tested for tactile mechanical hyperalgesia at 1, 2, and 3 weeks following procedures. Gabapentin produced dose-related inhibition of mechanical hyperalgesia over a 3-week period, and this effect was blocked by concomitant caffeine or DPCPX administration 1 week after injuries. The results of this study demonstrated that the mechanism through which gabapentin produces its effect may involve the activation of adenosine A1 subtype receptor.
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Neuropathic pain, which is characterized by hyperalgesia, allodynia and spontaneous pain, is one of the most painful symptoms that can be experienced in the clinic. It often occurs as a result of injury to the peripheral nerves, dorsal root ganglion (DRG), spinal cord or brain. The renin-angiotensin system (RAS) plays an important role in nociception. ⋯ Compared with the sham control groups, CCI significantly decreased the paw withdrawal latency and threshold, and this was markedly improved and aggravated by intrathecal injection of the selective Mas agonist Ang-(1-7) and the selective Mas inhibitor D-Pro7-Ang-(1-7), respectively. In conclusion, this study has provided the first evidence, to the best of our knowledge, that the Mas expression in DRG neurons is time-dependently induced by chronic nerve injury and that the intrathecal activation and inhibition of Mas can improve and aggravate CCI-induced neuropathic pain, respectively. This study has provided novel insights into the pathophysiological process of neuropathic pain and suggests that the Ang-(1-7)/Mas axis could be an effective therapeutic target for neuropathic pain, warranting further study.