Articles: neuropathic-pain.
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Pancreatitis-associated proteins (PAPs) display multiple functions in visceral diseases. Previous studies showed that the expression level of PAP-I was low in the DRG of naive rats but was de novo expressed after peripheral nerve injury. However, its role in neuropathic pain remains unknown. ⋯ Here we reveal that, after peripheral nerve injury, PAP-I can be transported to the spinal dorsal horn and is crucial in the progression of neuropathic pain. Importantly, we prove that PAP-I mainly functions through activating the spinal microglia via the CCR2-p38 MAPK pathway. Furthermore, we confirm that the proinflammatory effect of PAP-I is more prominent after the establishment of neuropathic pain, thus indicating that microglia also participate in the maintenance phase of neuropathic pain.
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Voltage-gated T-type Ca2+ (CaV3) channels regulate diverse physiological events, including neuronal excitability, and have been linked to several pathological conditions such as absence epilepsy, cardiovascular diseases, and neuropathic pain. It is also acknowledged that calcium/calmodulin-dependent protein kinase II and protein kinases A and C regulate the activity of T-type channels. Interestingly, peripheral nerve injury induces tactile allodynia and upregulates CaV3.2 channels and cyclin-dependent kinase 5 (Cdk5) in dorsal root ganglia (DRG) and spinal dorsal horn. ⋯ The present work shows that the exacerbated expression of Cdk5 in a preclinical model of neuropathic pain increases the functional expression of CaV3.2 channels. This finding is relevant for the understanding of the molecular pathophysiology of the disease. Additionally, this work may have a substantial translational impact, since it describes a novel molecular pathway that could represent an interesting therapeutic alternative for neuropathic pain.
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Neuropathic pain can be generated by chronic compression of dorsal root ganglion (CCD). Stimulation of primary motor cortex can disrupt the nociceptive sensory signal at dorsal root ganglion level and reduce pain behaviors. But the mechanism behind it is still implicit. ⋯ In vivo extracellular recording of the ventral posterolateral thalamus, viral expression in the primary motor cortex, and protein kinase C gamma expression in dorsal root ganglion were investigated. So, optical cortico-thalamic inhibition by motor cortex stimulation can improve neuropathic pain behaviors in CCD animal, and knocking down of protein kinase C gamma plays a conducive role in the process. This study provides feasibility for in vivo optogenetic stimulation on primary motor cortex of dorsal root ganglion-initiated neuropathic pain.
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Journal of pain research · Jan 2020
ReviewUltrasound-Guided Nerve Hydrodissection for Pain Management: Rationale, Methods, Current Literature, and Theoretical Mechanisms.
Nerve hydrodissection (HD), a technique used when treating nerve entrapments, involves the injection of an anesthetic, saline, or 5% dextrose in water to separate the nerve from the surrounding tissue, fascia, or adjacent structures. Animal models suggest the potential for minimal compression to initiate and perpetuate neuropathic pain. Mechanical benefits of HD may relate to release of nervi nervorum or vasa nervorum compression. ⋯ The in-plane technique is the predominant and safest method for nerve HD. Five percent dextrose may be favored as the preferred injectate based on preliminary comparative-injectate literature, but additional research is critical. Literature-based hypotheses for a direct ameliorative effect of dextrose HD on neuropathic pain are presented.
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Chemotherapy-induced peripheral neuropathy (CIPN) is a major, dose-limiting side effect of treatment with neurotoxic cancer treatments which can result in long-term impairment. Deficits often reflect a large fiber polyneuropathy, however small fiber involvement resulting in neuropathic pain and autonomic dysfunction can occur. Quantification of both CIPN and small fiber neuropathy (SFN) remains a challenge. ⋯ Accurately identifying subgroups of patients with neuropathic symptoms which may respond to existing pain medication may reduce the impact of CIPN and improve long-term quality of life as well as provide better categorization of patients for future clinical trials of neuroprotective and treatment strategies for CIPN. PERSPECTIVE: This review provides a critical analysis of SFN associated with neurotoxic cancer treatments and the assessment tools for evaluating small fiber dysfunction in cancer patients. Quantification of small fiber involvement in CIPN will assist in identifying subgroups of patients with neuropathic symptoms which may respond to existing pain medications.