Articles: neuralgia.
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Prospective, observational cohort study. ⋯ 2.
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Neuropathic pain in cancer patients is often difficult to treat, requiring a combination of several different pharmacological therapies. We describe two patients with complex neuropathic pain syndromes in the form of phantom limb pain and Brown-Sequard syndrome who did not respond to conventional treatments but responded dramatically to the addition of levorphanol. ⋯ It bypasses hepatic first-pass metabolism and thereby not subjected to numerous drug interactions. Levorphanol's unique profile makes it a potentially attractive opioid in cancer pain management.
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Global burden of disease studies measure the impact of disability and premature death resulting from specific diseases and injuries. Recently, these studies have highlighted the leading contribution of regional pain conditions (low back pain and neck pain in particular) to the global burden of disability. However, to date, there has not been a systematic approach to measuring the global burden of disease attributable to neuropathic pain (NP) conditions. This article gives a brief overview of the concept of burden of disease, the underlying drivers, and dynamics of disease burden at a population level and proposes an agenda in relation to NP for developing the conceptual and empirical evidence base necessary for estimating the global burden of NP.
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Letter Case Reports
The Relationship of Auriculotemporal Neuralgia and Epicrania Fugax.
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Voltage-gated sodium channels NaV1.7, NaV1.8 and NaV1.9 have been the focus for pain studies because their mutations are associated with human pain disorders, but the role of NaV1.6 in pain is less understood. In this study, we selectively knocked out NaV1.6 in dorsal root ganglion (DRG) neurons, using NaV1.8-Cre directed or adeno-associated virus (AAV)-Cre mediated approaches, and examined the specific contribution of NaV1.6 to the tetrodotoxin-sensitive (TTX-S) current in these neurons and its role in neuropathic pain. We report here that NaV1.6 contributes up to 60% of the TTX-S current in large, and 34% in small DRG neurons. ⋯ Although NaV1.8-Cre driven NaV1.6 knockout does not alter acute, inflammatory or neuropathic pain behaviors, AAV-Cre mediated NaV1.6 knockout in adult mice partially attenuates SNI-induced mechanical allodynia. Additionally, AAV-Cre mediated NaV1.6 knockout, mostly in large DRG neurons, significantly attenuates excitability of these neurons after SNI and reduces NaV1.6 accumulation at nodes of Ranvier at the neuroma. Together, NaV1.6 in NaV1.8-positive neurons does not influence pain thresholds under normal or pathological conditions, but NaV1.6 in large NaV1.8-negative DRG neurons plays an important role in neuropathic pain.