Increased touch‐evoked itch (punctate hyperknesis) in postherpetic itch: Implications of reduced intraepidermal nerve fibers representing small fiber neuropathy

Abstract

Chronic itch conditions are often accompanied by neural itch sensitization, known as hyperknesis (excessive itch induced by stimuli that would normally induce only mild itching or pain) and alloknesis (considerable itch evoked by light tactile stimuli). Herpes zoster (shingles) can cause neuropathic itch (postherpetic itch), although it is unknown whether hyperknesis accompanies postherpetic itch. The authors report five patients with postherpetic itch who showed increased touch‐evoked itch (punctate hyperknesis) in the affected skin areas compared with the contralateral site. Collected skin biopsy specimens from two patients showed histopathologically detected reduced intraepidermal nerve fibers in the affected skin areas, reflective of small C/Aδ fiber neuropathy. In one case, improvement in itching and comparable levels of touch‐evoked itch on the affected and contralateral sites were noted after 6 months without any medication, accompanied by restored intraepidermal nerve fibers proven through rebiopsy of the affected site. Reduced intraepidermal nerve fibers could be one of the precipitating factors for postherpetic itch and its associated punctate hyperknesis.

Reverse underwear sign as an indicator of alloknesis

“…6 In SSS the IENFD was found to be reduced, 7 but the exact relationship between IENFD and alloknesis remains unclear. Interestingly, in prurigo nodularis 8 and post-herpetic pruritus, 9 the itchy sensations can subside once the IENFD is normalized; thus, it can be hypothesized that a similar effect could result in the context of SSS.…”

Increased sensitivity to touch‐evoked itch (punctate hyperknesis) in prurigo nodularis and type 2 inflammation: A cross‐sectional pilot study

“…C/Aδ small sensory nerves innervating the epidermis carry punctate hyperknesis sensations. 3 PN patients are reported to show altered epidermal neural structures in PN lesions, accompanied by increased responsiveness to pinprick pain stimuli (gain of function of Aδ fibres). 8 This finding indicates that the altered epidermal neural structures might contribute to punctate hyperknesis in PN patients.…”