Abstract

Various types of brain pathology may be associated with neuropathic pruritus. While the mechanisms behind neuropathic itch is not well understood, damage to the itch processing centers and circuits of the brain may lead to changes in signaling in both top-down and bottom-up pathways that results in the distortion of itch sensation. Patients with brain pathologies such as such as stroke, brain tumors, spongiform encephalopathies, multiple sclerosis, trigeminal trophic syndrome, and systemic diseases such as end-stage renal diseases and primary biliary cholangitis have reported neuropathic itch of different characteristics. Commonly involved areas of the brain that, when damaged, are associated with neuropathic itch are the primary somatosensory cortex, precuneus, hippocampus, amygdala, periaqueductal gray, thalamus, insula, nucleus accumbens, Gasserian ganglion, cerebellum, cingulate cortex, prefrontal cortex, medulla, frontotemporal, and parietal lobe. Treatments for neuropathic pain, depression and seizures, such as kappa opioids, gabapentinoids, tricyclic antidepressants, and ketamine, are commonly used to treat neuropathic pruritus and are found to be effective.

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