Neurologic insults as varied as inflammation, stroke, and fibromyalgia elicit neuropathic pain and itch. Noxious sensation results when aberrantly increased afferent signaling reaches percept-forming cortical neurons and can occur due to increased sensory signaling, decreased inhibitory signaling, or a combination of both processes. To treat these symptoms, detailed knowledge of sensory transmission, from innervated end organ to cortex, is required. Molecular, genetic, and behavioral dissection of itch in animals and patients has improved understanding of the receptors, cells, and circuits involved. In this review, we will discuss neuropathic itch with a focus on the itch-specific circuit.
Keyphrases
- neuropathic pain
- atopic dermatitis
- spinal cord
- end stage renal disease
- spinal cord injury
- induced apoptosis
- oxidative stress
- ejection fraction
- chronic kidney disease
- healthcare
- atrial fibrillation
- genome wide
- cell cycle arrest
- functional connectivity
- cell death
- brain injury
- gene expression
- dna methylation
- signaling pathway
- patient reported
- patient reported outcomes
- endoplasmic reticulum stress
- cerebral ischemia