Abstract
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.
Highlights
Both microscopic damage, such as small-fiber neuropathy, and macroscopic trauma such as that occurring from spinal cord transection can result in neuropathic pain or itch [1]
Neuropathic pain is defined by the International Association for the Study of Pain (IASP) as pain caused by a lesion or disease of the somatosensory nervous system [2]
Pain- and itch-detecting neurons are anatomically indistinguishable. Both are sensed by small-diameter, unmyelinated C-fibers of the dorsal root ganglia (DRG) and trigeminal ganglia (TG)
Summary
Both microscopic damage, such as small-fiber neuropathy, and macroscopic trauma such as that occurring from spinal cord transection can result in neuropathic pain or itch [1]. Neuropathic itch has no consensus definition but is generally understood as itch resulting from neuronal or glial damage without skin alterations Under this definition, neuropathic itch accounts for approximately 8% to 19% of chronic pruritus conditions and include a wide variety of neurologic diseases with high medical burden and diverse pathologic mechanisms [3]. Pain- and itch-detecting neurons are anatomically indistinguishable Both are sensed by small-diameter, unmyelinated C-fibers of the dorsal root ganglia (DRG) and trigeminal ganglia (TG). Advances in molecular biology have identified itch-specific sensory neurons and allowed detailed dissection of both pain and itch circuits From these studies, a comprehensive framework of noxious sensation, from molecule to cell to circuit and perception, has emerged. Understanding how nervous damage and disease can result in pathologic itch can allow better explanation and management of the pruritus and cutaneous symptoms experienced by fibromyalgia patients. We will discuss recent advances in itch biology, the itch-specific circuit, and pathophysiologic mechanisms of neuropathic itch
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