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Cutaneous innervation in hereditary sensory and autonomic neuropathy type IV


Verzé, L; Viglietti-Panzica, C; Plumari, L; Calcagni, M; Stella, M; Schrama, L H; Panzica, G C (2000). Cutaneous innervation in hereditary sensory and autonomic neuropathy type IV. Neurology, 55(1):126-128.

Abstract

The authors investigated immunocytochemically the innervation of a skin biopsy in a rare case of hereditary sensory and autonomic neuropathy type IV. A few protein gene product 9.5-, growth-associated protein 43-, calcitonin gene-related peptide-, and substance P-immunoreactive nerve fibers were observed in the deeper regions of the dermis. Neuropeptide Y-, nitric oxide-, and vasoactive intestinal polypeptide-immunoreactive fibers were completely absent. Their observations support the hypothesis that the sensory and autonomic defects reported in hereditary sensory and autonomic neuropathy are based on profound developmental alterations of the peripheral nervous system.

Abstract

The authors investigated immunocytochemically the innervation of a skin biopsy in a rare case of hereditary sensory and autonomic neuropathy type IV. A few protein gene product 9.5-, growth-associated protein 43-, calcitonin gene-related peptide-, and substance P-immunoreactive nerve fibers were observed in the deeper regions of the dermis. Neuropeptide Y-, nitric oxide-, and vasoactive intestinal polypeptide-immunoreactive fibers were completely absent. Their observations support the hypothesis that the sensory and autonomic defects reported in hereditary sensory and autonomic neuropathy are based on profound developmental alterations of the peripheral nervous system.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Reconstructive Surgery
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Health Sciences > Neurology (clinical)
Language:English
Date:2000
Deposited On:19 Mar 2009 10:10
Last Modified:25 Jun 2022 22:46
Publisher:American Academy of Neurology
ISSN:0028-3878
OA Status:Closed
Publisher DOI:https://doi.org/10.1212/WNL.55.1.126
PubMed ID:10891921