| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
From the Neuroimmunology Branch (Drs. Morgen, Martin, Kadom, and McFarland, and R.D. Stone) and Cognitive Neuroscience Section, National Institute of Neurological Disorders and Stroke (Dr. Grafman); National Institute of Infectious Diseases and Allergies, National Institutes of Health (Dr. Marques), Bethesda, MD; and Department of Neurology (Dr. Morgen), Justus–Liebig University, Giessen, Germany.
Address correspondence and reprint requests to Dr. Roland Martin, Cellular Immunology Section, Neuroimmunology Branch, NINDS, Building 10, Room 5B16, 10 Center Drive, MSC 1400, Bethesda, MD 20892-1400; e-mail: martin{at}ninds.nih.gov
Objective:— To determine patterns of abnormalities on cerebral MRI that may characterize subgroups of patients with post-treatment Lyme disease syndrome (PTLDS) and to help identify pathomechanisms of disease.
Methods:— The authors analyzed the distribution of cerebral lesions in a cohort of 27 patients with PTLDS. A subgroup of eight patients with PTLDS was further studied using whole-brain magnetization transfer ratio measures to identify abnormalities not seen on T2-weighted images.
Results:— Four patients had focal neurologic deficits, relapsing–remitting disease, and lesions in a distribution typical of MS. Twenty-three patients presented with nonfocal symptoms such as fatigue, subjective memory deficits, and mood disturbance. Twelve of these patients had normal MRI, including the more sensitive fluid-attenuated inversion recovery sequence, 10 had primarily punctate and subcortical lesions, and one patient had multiple periventricular lesions.
Conclusions:— In a portion of patients with post-treatment Lyme disease syndrome, white-matter hyperintensities tend to occur in subcortical arteriolar watershed areas and are not specific. Magnetization transfer ratio analysis did not provide evidence for structural abnormalities of the brain parenchyma in patients with nonfocal disease.
This article has been cited by other articles:
|
|
 |
|
  P. Hildenbrand, D.E. Craven, R. Jones, and P. Nemeskal Lyme Neuroborreliosis: Manifestations of a Rapidly Emerging Zoonosis AJNR Am. J. Neuroradiol., June 1, 2009; 30(6): 1079 - 1087. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. A. Fallon, R. B. Lipkin, K. M. Corbera, S. Yu, M. S. Nobler, J. G. Keilp, E. Petkova, S. H. Lisanby, J. R. Moeller, I. Slavov, et al. Regional Cerebral Blood Flow and Metabolic Rate in Persistent Lyme Encephalopathy Arch Gen Psychiatry, May 1, 2009; 66(5): 554 - 563. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. M. Feder Jr., B. J.B. Johnson, S. O'Connell, E. D. Shapiro, A. C. Steere, G. P. Wormser, and the Ad Hoc International Lyme Disease Group A Critical Appraisal of "Chronic Lyme Disease" N. Engl. J. Med., October 4, 2007; 357(14): 1422 - 1430. [Full Text] [PDF]
|
|
|
|
|
|
F. Agosta, M.A. Rocca, B. Benedetti, R. Capra, C. Cordioli, and M. Filippi MR imaging assessment of brain and cervical cord damage in patients with neuroborreliosis. AJNR Am. J. Neuroradiol., April 1, 2006; 27(4): 892 - 894. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. P. Steinbach, A. Melms, M. Skalej, and J. Dichgans Delayed resolution of white matter changes following therapy of B burgdorferi encephalitis Neurology, February 22, 2005; 64(4): 758 - 759. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
