Neurology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Correspondence:
Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Correspondence are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wichman, A.
Right arrow Articles by Fauci, A. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wichman, A.
Right arrow Articles by Fauci, A. S.
NEUROLOGY 1985;35:1140
© 1985 American Academy of Neurology

Peripheral neuropathy in hypereosinophilic syndrome

Alison Wichman, MD, Fritz Buchthal, MD, Gholam H. Pezeshkpour, MD and Anthony S. Fauci, MD

National Institutes of Health. NINCDS (Drs. Buchthal and Wichman). NIAID (Dr. Fauci)., Hethesda, MD: and the Armed Forces Institute of Pathology (Dr. Pezeshkpourl, Washington, DC.

We evaluated seven patients with the hypereosinophilic syndrome (HES) to define the clinicopathologic spectrum of the peripheral neuropathy. Clinically, three had evident polyneuropathy; the others were asymptomatic, although they had electrophysiologic evidence of neuropathy. Nerve conduction studies and EMG were compatible with axonal neuropathy. Morphometry of sural nerves from four patients ranged from normal to marked axonal loss, more prominent in large myelinated fibers. Demyelination was rare, and there was no evidence of vasculitis. Neuropathy may be produced by an eosinophil-derived neurotoxin.

Address correspondence and reprint requests to Dr. Wichman, NIH. Building 10, Room 5N226. Bethesda, MD 20205.

This paper was presented in part at the thirty-sixth annual meeting of the American Academy of Neurology, Boston, MA. April 1984.

Accepted for publication November 30, 1984.




This article has been cited by other articles:


Home page
BloodHome page
J. Gotlib, J. Cools, J. M. Malone III, S. L. Schrier, D. G. Gilliland, and S. E. Coutre
The FIP1L1-PDGFR{alpha} fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and management
Blood, April 15, 2004; 103(8): 2879 - 2891.
[Abstract] [Full Text] [PDF]


Home page
BrainHome page
N. Hattori, M. Ichimura, M. Nagamatsu, M. Li, K. Yamamoto, K. Kumazawa, T. Mitsuma, and G. Sobue
Clinicopathological features of Churg–Strauss syndrome-associated neuropathy
Brain, March 1, 1999; 122(3): 427 - 439.
[Abstract] [Full Text] [PDF]


Home page
Arch DermatolHome page
N. M. DeYampert and L. A. Beck
Eosinophilia and Multiple Erythematous Indurated Plaques
Arch Dermatol, December 1, 1997; 133(12): 1584 - 1584.
[Abstract] [PDF]


Home page
NEJMHome page
M. Hayes and E. T. Hedley-Whyte
Case 40-1994- A 77-Year-Old Woman with Fever, Sweats, and Pain in the Head and Legs
N. Engl. J. Med., November 10, 1994; 331(19): 1293 - 1300.
[Full Text]


Home page
Arch NeurolHome page
J. M. Shefner and D. M. Dawson
The Use of Sensory Action Potentials in the Diagnosis of Peripheral Nerve Disease
Arch Neurol, March 1, 1990; 47(3): 341 - 348.
[Abstract] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1985 by AAN Enterprises, Inc.