Articles: neuralgia.
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Journal of neurotrauma · Nov 2015
Predicting the Risk for Central Pain Using the Sensory Components of the International Standards for Neurological Classification of Spinal Cord Injury.
Central neuropathic pain (CP) after spinal cord injury (SCI) is excruciating and difficult to manage. Pre-emptive treatment could be initiated in patients at risk for CP providing that it can be predicted. A combination of psychophysical tests could predict CP, but the process necessitates sophisticated equipment and constant monitoring. ⋯ At-level delta LT-PP score>1 best predicted CP; the odds of developing CP with LT-PP>1 was 24.4 times that of the reverse category (LT-PP<1). Heat-pain and touch thresholds significantly correlated with PP and LT. We conclude that the SC-ISNCSCI can be used as a clinical biomarker of CP with high probability.
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The activation of mitogen-activated protein kinases (MAPKs) have been observed in synaptic plasticity processes of learning and memory in neuropathic pain. Cerebrospinal fluid-contacting nucleus (CSF-CN) has been identified with the onset and persistence of neuropathic pain. However, whether extracellular signal-regulated protein kinase 5 (ERK5), a member of MAPKs, in CSF-CN participates in neuropathic pain has not been studied yet. ⋯ These findings suggest activation of ERK5 in CSF-CN might contribute to the onset and development of neuropathic pain and its role might be partly accomplished by p-CREB.
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Herpes zoster (HZ), a common vesiculo-erythematous skin disease associated with reactivation of varicella zoster virus in the cranial nerve, dorsal root, and autonomic ganglia, is accompanied by several related symptoms represented by postherpetic neuralgia. Among them, involvement of vesicorectal dysfunction is relatively rare. The vesicorectal symptom can usually be recovered in transient course, but is quite important in terms of impaired quality of life. ⋯ Average treatment term for pain relief of sacral HZ accompanied by voiding dysfunction (91.3 ± 76.44 days) was significantly longer than that of sacral HZ without urinary symptom (18.9 ± 20.42 days) (P = 0.032). These results suggested that zoster-related voiding dysfunction would mainly be involved in sacral HZ and closely associated with severity of zoster-related pain. Dermatologists should be aware that severe zoster-related pain accompanied by sacral HZ, which is related to prolonged treatment of pain relief, can be a predictive factor of voiding dysfunction.
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Experimental neurology · Nov 2015
Bulleyaconitine A depresses neuropathic pain and potentiation at C-fiber synapses in spinal dorsal horn induced by paclitaxel in rats.
Paclitaxel, a widely used chemotherapeutic agent, often induces painful peripheral neuropathy and at present no effective drug is available for treatment of the serious side effect. Here, we tested if intragastrical application of bulleyaconitine A (BLA), which has been approved for clinical treatment of chronic pain in China since 1985, could relieve the paclitaxel-induced neuropathic pain. A single dose of BLA attenuated the mechanical allodynia, thermal hyperalgesia induced by paclitaxel dose-dependently. ⋯ Spinal or intravenous application of BLA depressed the spinal LTP, dose-dependently. Furthermore, patch clamp recordings in spinal cord slices revealed that the frequency but not amplitude of both spontaneous excitatory postsynaptic current (sEPSCs) and miniature excitatory postsynaptic currents (mEPSCs) in lamina II neurons was increased in paclitaxel-treated rats, and the superfusion of BLA reduced the frequency of sEPSCs and mEPSCs in paclitaxel-treated rats but not in naïve ones. Taken together, we provide novel evidence that BLA attenuates paclitaxel-induced neuropathic pain and that depression of spinal LTP at C-fiber synapses via inhibiting presynaptic transmitter release may contribute to the effect.
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The function of microRNAs (miRNAs or miRs) in regulating neuropathic pain has attracted increasing attention in recent years. However, the precise mechanism of miRNAs in neuropathic pain remains largely unknown. In the present study, an important role of miR‑141 and its putative target gene, high‑mobility group box‑1 (HMGB1), was demonstrated in a rat model of neuropathic pain induced by chronic constriction injury (CCI). ⋯ Overexpression of miR‑141 significantly suppressed the expression of HMGB1 in vitro and in vivo. Furthermore, overexpression of HMGB1 apparently abrogated the beneficial effect of miR‑141 on inhibiting neuropathic pain. Taken together, the data suggest that overexpression of miR‑141 alleviates neuropathic pain development via targeting and inhibiting HMGB1, implying that blocking HMGB1 by miR‑141 could be a useful therapeutic strategy for the treatment of neuropathic pain.