Articles: neuralgia.
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Refractory to most types of treatment, neuropathic pain (NP) is a major problem for people living with spinal cord injury (SCI). The underlying mechanisms among problems related to treatment are poorly understood. The aim of the present study was to investigate the association between cortical reorganization and NP after SCI. Twenty-four individuals with sensorimotor complete and incomplete paraplegia and tetraplegia (12 with NP, 13 pain free) and 31 healthy individuals were examined. Functional magnetic resonance imaging was used to assess activation in primary somatosensory and motor cortices in response to motor (ie, active and passive wrist extension) and sensory (ie, heat and brushing) tasks applied on the dorsum of the hand. In individuals with SCI, there were no group-level differences in task-related activation (ie, movement or sensory) compared with the healthy controls. However, based on the Euclidean distance measure, individuals with SCI demonstrated a lateral shift of peak activity in primary sensory and motor cortices (P < .05). Among those with NP, chronic pain intensity inversely correlated with the magnitude of the shift in the primary motor cortex during active wrist extension. The findings reveal that NP in motor and sensory tasks at or above the level of the lesion is not associated with increased plasticity. In line with previous studies, changes in somatotopy and activation after SCI are rather limited and the influence of NP on plasticity remains controversial. ⋯ Using functional magnetic resonance imaging, we have provided novel evidence that reorganization (i.e., topographical shifts in peak activity) in the primary motor cortex after spinal cord injury is limited to individuals without neuropathic pain.
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To determine the association of self-report use of metformin and pain intensity. ⋯ In a clinic sample of patients with diabetes, the use of metformin at an average dose of 1,432 mg (SD = 596 mg) was not associated with lower pain scores. Given the anti-nociceptive effects of metformin in the animal models of pain, and the relative safety of metformin, future research should evaluate the effect of the higher dose of metformin as a potential analgesic.
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Painful diabetic neuropathy is a common complication of diabetes produced by mechanisms that as yet are incompletely defined. The aim of this study was to investigate the roles of nuclear factor-κB (NF-κB) in the regulation of purinergic receptor P2X ligand-gated ion channel 3 (P2X3R) plasticity in dorsal root ganglion (DRG) neurons of rats with painful diabetes. Here, we showed that hindpaw pain hypersensitivity in streptozocin-induced diabetic rats was attenuated by treatment with purinergic receptor antagonist suramin or A-317491. ⋯ The inhibition of p65 signaling using the NF-κB inhibitor pyrrolidine dithiocarbamate or recombinant lentiviral vectors designated as lentiviral vector-p65 small interfering RNA remarkably suppressed P2X3R activities and attenuated diabetic pain hypersensitivity. Insulin treatment significantly attenuated pain hypersensitivity and suppressed the expression of p65 and P2X3Rs. Our findings suggest that the p2x3r gene promoter DNA demethylation and enhanced interaction with p65 contributes to P2X3R sensitization and diabetic pain hypersensitivity.
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Previous studies have demonstrated that glutamate plays an important role in the development of pathological pain. This study investigates the expression changes of glutamate and the roles of different types of glutamate receptors in the red nucleus (RN) in the development of neuropathic allodynia induced by spared nerve injury (SNI). Immunohistochemistry indicated that glutamate was constitutively expressed in the RN of normal rats. ⋯ However, microinjection of the non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3(1H,4H)-dione or the mGluR antagonist (±)-α-methyl-(4-carboxyphenyl) glycine into the RN significantly increased the PWT and alleviated SNI-induced mechanical allodynia. These findings suggest that RN glutamate is involved in regulating neuropathic pain and facilitates the development of SNI-induced neuropathic allodynia. The algesic effect of glutamate is transmitted by the non-NMDA glutamate receptor and mGluRs.
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Case Reports
Spinal Cord Stimulation for the Treatment of Neuropathic Pain Associated With Leprosy: A Case Report.
Leprosy is a major source of nerve damage and may lead to neuropathic pain as well as complex regional pain syndrome (CRPS). Spinal cord stimulation is an effective treatment for CRPS, but there are no reports of this treatment in a patient with leprosy. ⋯ Spinal cord stimulation may be a valuable intervention for patients with leprosy-induced CRPS.