Articles: neuralgia.
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Spinal Cord Ser Cases · May 2019
Pulse article: opioid prescription for pain after spinal cord damage (SCD), differences from recommended guidelines, and a proposed algorithm for the use of opioids for pain after SCD.
Online questionnaire of spinal cord injury (SCI) physicians. ⋯ Most physicians who responded to this survey prescribe opioids for intractable pain after SCD. A significant proportion of respondents believed that there should not be a specific upper limit of opioid dose prescribed if the drug is tolerated; this does not align with current recommendations. Most physicians do not feel influenced in their prescribing habits by regulatory bodies. If physicians decide to taper an opioid that is being tolerated well, it is most commonly related to a fear of the patient developing an opioid-use disorder. The authors propose an algorithm that may help align practice patterns with current recommended practice guidelines.
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Current diabetes reports · May 2019
ReviewPainful and Painless Diabetic Neuropathies: What Is the Difference?
The prevalence of diabetes mellitus and its chronic complications are increasing to epidemic proportions. This will unfortunately result in massive increases in diabetic distal symmetrical polyneuropathy (DPN) and its troublesome sequelae, including disabling neuropathic pain (painful-DPN), which affects around 25% of patients with diabetes. Why these patients develop neuropathic pain, while others with a similar degree of neuropathy do not, is not clearly understood. This review will look at recent advances that may shed some light on the differences between painful and painless-DPN. ⋯ Gender, clinical pain phenotyping, serum biomarkers, brain imaging, genetics, and skin biopsy findings have been reported to differentiate painful- from painless-DPN. Painful-DPN seems to be associated with female gender and small fiber dysfunction. Moreover, recent brain imaging studies have found neuropathic pain signatures within the central nervous system; however, whether this is the cause or effect of the pain is yet to be determined. Further research is urgently required to develop our understanding of the pathogenesis of pain in DPN in order to develop new and effective mechanistic treatments for painful-DPN.
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Postherpetic neuralgia, a persistent pain condition often characterized by allodynia and hyperalgesia, is a deleterious consequence experienced by patients after an acute herpes zoster vesicular eruption has healed. The pain associated with postherpetic neuralgia can severely affect a patient's quality of life, quality of sleep, and ability to participate in activities of daily living. Currently, first-line treatments for this condition include the administration of medication therapies such as tricyclic antidepressants, pregabalin, gabapentin, and lidocaine patches, followed by the application of tramadol and capsaicin creams and patches as second- or third-line therapies. As not all patients respond to such conservative options, however, interventional therapies are valuable for those who continue to experience pain. ⋯ Interventional treatment, postherpetic neuralgia, botulinum toxin, steroid, stellate ganglion block, peripheral nerve stimulation, paravertebral block, radiofrequency, spinal cord stimulation.
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While evidence indicates that sigma-1 receptors (Sig-1Rs) play an important role in the induction of peripheral neuropathic pain, there is limited understanding of the role that the neurosteroidogenic enzymes, which produce Sig-1R endogenous ligands, play during the development of neuropathic pain. We examined whether sciatic nerve injury upregulates the neurosteroidogenic enzymes, cytochrome P450c17 and 3β-hydroxysteroid dehydrogenase (3β-HSD), which modulate the expression and/or activation of Sig-1Rs leading to the development of peripheral neuropathic pain. Chronic constriction injury (CCI) of the sciatic nerve induced a significant increase in the expression of P450c17, but not 3β-HSD, in the ipsilateral lumbar spinal cord dorsal horn at postoperative day 3. ⋯ Co-administration of the Sig-1R agonist, PRE084 restored the development of mechanical allodynia originally suppressed by the ketoconazole administration. However, ketoconazole-induced inhibition of thermal hyperalgesia was not affected by co-administration of PRE084. Collectively these results demonstrate that early activation of P450c17 modulates the expression and activation of astrocyte Sig-1Rs, ultimately contributing to the development of mechanical allodynia induced by peripheral nerve injury.
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Neuropathic pain significantly reduces an individual's quality of life and places a significant economic burden on society. As such, many cost-effectiveness analyses (CEAs) have been published for treatments available for neuropathic pain. ⋯ Though many pulished studies have evaluated the cost-effectiveness of treatments for neuropathic pain, significant heterogeneity between CEAs prevented synthesis of the results. Standardized methodology and improved reporting would allow for more reliable comparisons across studies.