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Pain. 2002 Mar;96(1-2):9-12.

Intractable postherpetic itch and cutaneous deafferentation after facial shingles.

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1
Neuropathic Pain Study Group, Department of Anesthesiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. aoaklander@partners.org

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.

PMID:
11932056
[Indexed for MEDLINE]
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