This Article  • References  • Full text PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

Andrew R. Pachner, MD; Paul Duray, MD; Allen C. Steere, MD

Arch Neurol. 1989;46(7):790-795.

Abstract
• We studied six patients with central nervous system manifestations of Lyme disease. Weeks to years after the initial infection, behavioral changes, ataxia, and/or weakness in bulbar or peripheral muscles developed. Four of the six patients had a lymphocytic pleocytosis in the cerebrospinal fluid, and two of them had magnetic resonance imaging scans suggestive of demyelination. In a patient with a subacute encephalitis, a brain biopsy specimen showed microgliosis without an inflammatory infiltrate and spirochetes morphologically compatible with Borrelia burgdorferi. All six patients had elevated antibody titers to B burgdorferi in serum, but none had selective concentration of specific antibody in the cerebrospinal fluid. All six patients were treated with high-dose intravenous penicillin; four had complete recoveries and two did not. Lyme disease may affect the central nervous system causing organic brain disease or syndromes suggestive of demyelination.

Author Affiliations
From the Department of Neurology, Georgetown University School of Medicine, Washington, DC (Dr Pachner); the Department of Pathology, Fox Chase Cancer Institute, Philadelphia, Pa (Dr Duray); and the New England Medical Center, Division of Rheumatology/Immunology, Tufts University School of Medicine, Boston, Mass (Dr Steere).

Footnotes
Accepted for publication December 14, 1988.

Reprint requests to Department of Neurology, Georgetown University Hospital, 3800 Reservoir Rd NW, Washington, DC 20007 (Dr Pachner).

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Lyme Neuroborreliosis: Manifestations of a Rapidly Emerging Zoonosis
Hildenbrand et al.
Am. J. Neuroradiol. 2009;30:1079-1087.
ABSTRACT | FULL TEXT  

Borrelia burgdorferi Surface-Localized Proteins Expressed during Persistent Murine Infection Are Conserved among Diverse Borrelia spp.
Hughes et al.
Infect. Immun. 2008;76:2498-2511.
ABSTRACT | FULL TEXT  

Immunohistochemical Analysis of Lyme Disease in the Skin of Naive and Infection-Immune Rabbits following Challenge
Chong-Cerrillo et al.
Infect. Immun. 2001;69:4094-4102.
ABSTRACT | FULL TEXT  

The Cost-effectiveness of Vaccination Against Lyme Disease
Shadick et al.
Arch Intern Med 2001;161:554-561.
ABSTRACT | FULL TEXT  

Classic diseases revisited: Overdiagnosis and overtreatment of Lyme neuroborreliosis are preventable
Prasad and Sankar
Postgrad. Med. J. 1999;75:650-656.
ABSTRACT | FULL TEXT  

Case 37-1995- A 6-year-old boy with a rash, meningismus, and diplegia
Hafler and Hedley-Whyte
NEJM 1995;333:1485-1493.
FULL TEXT  

The biological and social phenomenon of Lyme disease
Barbour and Fish
Science 1993;260:1610-1616.
ABSTRACT  

Current Perspective on Lyme Borreliosis
Kaslow
JAMA 1992;267:1381-1383.
ABSTRACT  

Nervous System Lyme Borreliosis--Revisited
Finkel and Halperin
Arch Neurol 1992;49:102-107.
ABSTRACT  

Borrelia Rhombencephalomyelopathy
Kuntzer et al.
Arch Neurol 1991;48:832-836.
ABSTRACT  

Cerebrospinal Fluid Interleukins, Immunoglobulins, and Fibronectin in Neuroborreliosis
Weller et al.
Arch Neurol 1991;48:837-841.
ABSTRACT  

Lyme Disease: Recommendations for Diagnosis and Treatment
Rahn and Malawista
ANN INTERN MED 1991;114:472-481.
ABSTRACT