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Neuropathic pain is caused by disorders of, or damage to, the nervous system. The affected nerves can induce the sensation of pain in the brain. Neuropathic pain is often associated with the sensation of burning, coldness, "pins and needles", numbness or itching.
Circulating monocytes contribute to the transition to pain chronicity but the molecular events that cause their deployment are still unclear. Using a mouse model of hyperalgesic priming, here the authors show that blood monocytes contribute to the emergence of chronic pain via a mechanism that requires a transient disruption of NAAA-regulated lipid signaling.
The primary somatosensory cortex and central nucleus of the amygdala project to the spleen via the dorsal motor nucleus of the vagus nerve and regulate the T helper 2 (TH2) immune cell response in models of neuropathic pain.
Cannabinol (CBN) is a promising compound that is suggested as an analgesic. Using electrophysiological techniques, this study determined that CBN inhibits the sodium currents associated with pain signaling, with potential application for neuropathic pain.
This study identifies a positive-feedback loop between the ACC and the VTA that mediates the mutual exacerbation between hyperalgesia and comorbid anxiodepressive-like behaviors and, thereby, the chronicity of neuropathic pain.
A new report shows that chronic pain leads to accumulation of pathological forms of tau protein in the hippocampus, resulting in neuronal atrophy and cognitive impairment.
