Articles: neuropathic-pain.
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Brain Behav Immun Health · Aug 2020
Persistent pain induces mood problems and memory loss by the involvement of cytokines, growth factors, and supraspinal glial cells.
Lesions of peripheral nerves lead to pain, hyperalgesia, and psychological comorbidities. However, the relationship between mood disorders and neuropathic pain is unclear, as well as the underlying mechanisms related to these disorders. Therefore, we investigated if nerve injury induces depression, anxiety, and cognitive impairment and if there were changes in cytokines, growth factors, and glial cell activation in cortical sites involved in processing pain and mood in animals with nerve injury. ⋯ There were increases in proinflammatory cytokines as well as Brain-Derived Neurotrophic Factor (BDNF) in the injured nerve. In the spinal cord, there were increases in both pro and anti-inflammatory cytokines, as well as of BDNF and Nerve Growth Factor (NGF). Further, in our data was a decrease in the density of microglia and astrocytes in the hippocampus and increased microglial density in the prefrontal cortex, areas associated with neuropathic pain conditions.
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Brain Behav. Immun. · Aug 2020
In vivo intrathecal IL-1β quantification in rats: Monitoring the molecular signals of neuropathic pain.
Neuropathic pain, or pain after nerve injury, is a disorder with a significant reliance on the signalling of cytokines such as IL-1β. However, quantifying the cytokine release repeatedly over time in vivo is technically challenging. ⋯ For the first time we have established that the SS based immunosensing platform technology can repeatedly sample the intrathecal space for bioactive peptides, such as IL-1β. Using this novel approach, we have been able to establish the correlation of the intrathecal concentration of IL-1β with the extent of mechanical allodynia, providing a molecular biomarker of the degree of the exaggerated pain state.
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Meta Analysis Comparative Study
Meta-analysis comparing placebo responses in clinical trials of painful HIV-associated sensory neuropathy and diabetic polyneuropathy.
Background and aims The placebo response has been identified as one factor responsible for the lack of therapeutic trials with positive outcomes in neuropathic pain. Reviews have suggested that certain neuropathic pain conditions, including HIV-associated sensory neuropathy (HIV-SN), exhibit a greater placebo response than other neuropathic aetiologies. If true, such a finding could substantially affect clinical trial design and therapeutic developments for these conditions. ⋯ Too few studies were available that reported the necessary information to clarify potential differences in the magnitude of placebo response or to elucidate parameters that could be contributing such differences. Implications The placebo response is one factor that may contribute to a lack of positive trials in neuropathic pain; some etiologies may display larger responses than others. This meta-analysis found no significant difference in placebo response between trials of HIV-associated sensory neuropathy and painful diabetic polyneuropathy, although limited data were available.
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Curr Pain Headache Rep · Jul 2020
ReviewNeuropathic Pain and Sickle Cell Disease: a Review of Pharmacologic Management.
Sickle cell disease (SCD) remains among the most common and severe monogenic disorders present in the world today. Although sickle cell pain has been traditionally characterized as nociceptive, a significant portion of sickle cell patients has reported neuropathic pain symptoms. Our review article will discuss clinical aspects of SCD-related neuropathic pain, epidemiology of neuropathic pain among individuals with SCD, pain mechanisms, and current and future potential pharmacological interventions. ⋯ Neuropathic pain in SCD is a complicated condition that often has a lifelong and significant negative impact on life; therefore, improved pain management is considered a significant and unmet need. Neuropathic pain mechanisms are heterogeneous, and the difficulty in determining their individual contribution to specific pain types may contribute to poor treatment outcomes in this population. Our review article outlines several pharmacological modalities which may be employed to treat neuropathic pain in SCD patients.
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Cannabinoid CB2 receptor (CB2) agonists are potential analgesics void of psychotropic effects. Peripheral immune cells, neurons and glia express CB2; however, the involvement of CB2 from these cells in neuropathic pain remains unresolved. We explored spontaneous neuropathic pain through on-demand self-administration of the selective CB2 agonist JWH133 in wild-type and knockout mice lacking CB2 in neurons, monocytes or constitutively. ⋯ Interestingly, CB2-positive lymphocytes infiltrated the injured nerve and possible CB2transfer from immune cells to neurons was found. Lymphocyte CB2depletion also exacerbated JWH133 self-administration and inhibited antinociception. This work identifies a simultaneous activity of neuronal and lymphoid CB2that protects against spontaneous and evoked neuropathic pain.