Research papersIntractable postherpetic itch and cutaneous deafferentation after facial shinglesOaklander, Anne Louisea,∗; Cohen, Steven P.b,1,1; Raju, Shubha V.Y.a,c,2,2Author Information aNeuropathic Pain Study Group, Departments of Anesthesiology, Neurology, Neuropathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA bDepartment of Anesthesiology and Critical Care, Massachusetts General Hospital, Boston, MA, USA cM.S. Ramaiah Medical College, Bangalore, India ∗Corresponding author. Massachusetts General Hospital, 55 Fruit Street/Clinics 3, Boston, MA 02114, USA. Tel.: +1-617-726-4656; fax: +1-617-726-5845 E-mail: email@example.com 1Present address: Anesthesia Service, Walter Reed Army Medical Center, 6825 16th Street NW, Washington, DC 20307-5001, USA. 2Present address: 891 Massachusetts Ave., Apt #2, Cambridge, MA 02139, USA. Submitted May 25, 2001; accepted August 6, 2001. ☆ This manuscript is dedicated to the memory of Professor Patrick D. Wall whose own work on itch provided a foundation for this study, and whose interest in this manuscript was inspirational. Pain: March 2002 - Volume 96 - Issue 1 - p 9-12 doi: 10.1016/S0304-3959(01)00400-6 Buy Metrics Abstract Some patients develop chronic itch from neurological injuries, and shingles may be a common cause. Neuropathic itch can lead to self-injury from scratching desensate skin. A 39-year-old woman experienced severe postherpetic itch, but no postherpetic neuralgia, after ophthalmic zoster. Within 1 year, she had painlessly scratched through her frontal skull into her brain. Sensory testing and skin biopsies were performed on itchy and normal scalp to generate preliminary hypotheses about mechanisms of neuropathic itch. Quantitation of epidermal neurites in PGP9.5-immunolabeled skin biopsies demonstrated loss of 96% of epidermal innervation in the itchy area. Quantitative sensory testing indicated severe damage to most sensory modalities except itch. These data indicate that in this patient, severe postherpetic itch was associated with loss of peripheral sensory neurons. Possible mechanisms include electrical hyperactivity of hypo-afferented central itch-specific neurons, selective preservation of peripheral itch-fibers from neighboring unaffected dermatomes, and/or imbalance between excitation and inhibition of second-order sensory neurons. © 2002 Lippincott Williams & Wilkins, Inc.