itchsensing

Itch sensing, or pruritus perception, is the neural process by which the skin detects and transmits itch-inducing stimuli to the brain. It involves specialized free nerve endings in the skin that are sensitive to a range of mediators released during inflammation or injury, and to certain environmental irritants. The sensation is distinct from pain but can interact with pain pathways, influencing intensity and motivation to scratch.

Peripheral transduction is carried by unmyelinated C-fibers and, to a lesser extent, thinly myelinated A-delta fibers. A subset of these fibers expresses receptors that respond to histamine, as well as receptors involved in non-histaminergic itch. In humans and animals, pruriceptive neurons often express Mas-related G protein-coupled receptors (Mrgprs) and other molecular mediators that convey itch signals when activated by various mediators such as histamine, proteases, endothelins, or certain antipruritic compounds. The exact receptor repertoire and signaling pathways differ among species, but the general principle is that distinct molecular cues can selectively initiate itch.

Neural transmission proceeds from the skin to the dorsal root ganglia and into the dorsal horn of the spinal cord, where itch signals are processed and routed through the spinothalamic tract to higher brain centers. Brain regions involved in itch include areas of the somatosensory cortex that map sensory experience, as well as limbic structures related to emotion and reward. Descending pathways can modulate itch, sometimes suppressing it or enhancing it under certain states.

Chronic pruritus can arise from skin disease, systemic illness, or neurological changes, and is often maintained by the itch-scratch cycle. Clinically, itch is assessed through patient self-report and scales measuring intensity. Treatments target underlying causes and may include topical emollients, antihistamines, neuromodulators, or newer agents that modulate itch-specific pathways.