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March 8, 2010

Ring and nodular multiple sclerosis lesions
A retrospective natural history study

M. Davis, BS, S. Auh, PhD, M. Riva, MD, N. D. Richert, MD, PhD, J. A. Frank, MD, H. F. McFarland, MD, and F. Bagnato, MD, PhDAuthors Info & Affiliations
March 9, 2010 issue
74 (10) 851-856
https://doi.org/10.1212/WNL.0b013e3181d31df5
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Abstract

Background: In patients with multiple sclerosis (MS), contrast-enhancing lesions (CELs) on postcontrast MRI are considered markers of the inflammatory responses associated with blood-brain barrier breakdown. Based upon shape, CELs may be defined as nodular (nCEL) or ring (rCEL) lesions. Several short-term studies pointed towards the assumption that rCELs represent areas of a more aggressive inflammatory process.
Methods: In the present long-term (i.e., 2 years) retrospective natural history study, we used monthly imaging to follow rCEL and nCELs evolution in 16 patients with MS during the natural history. New CELs were identified monthly on month 4–9 MRIs, using month 1–3 MRIs to ensure that all CELs were not previously enhancing. Chronic black holes (cBHs) were counted monthly upon CEL disappearance up to the 24th MRI. Generalized estimating equation methods investigated within-patient differences between rCELs and nCELs in volume and likelihood to convert into cBHs. Kaplan-Meier survival curves estimated differences in the length of persistence between cBHs originating from nCELs and cBHs deriving from rCELs.
Results: Fifty-two new rCELs and 281 nCELs were identified. rCELs had larger mean (z = 5.06, p ≤ 0.0001) volumes than nCELs. The proportion of cBHs from rCELs was similar (z = 1.81, p = 0.0710) to the proportion of cBHs from nCELs. Likewise, the length of persistence of cBHs deriving from rCELs was similar (χ12 = 2.339, p = 0.1262) to the duration of cBHs from nCELs.
Conclusions: Our data suggest that worse radiologic characteristics associated with the acute phase of ring contrast-enhancing lesions and nodular contrast-enhancing lesions do not necessarily reflect a poorer lesion outcome over time.

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Information & Authors

Information

Published In

Neurology®
Volume 74 • Number 10 • March 9, 2010
Pages: 851-856
PubMed: 20211910

Copyright

© 2010.

Publication History

Published online: March 8, 2010
Published in print: March 9, 2010

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M. Davis, BS
From the Neuroimmunology Branch (NIB) (M.D., M.R., N.D.R., H.F.M., F.B.) and Office of the Clinical Director Biostatistics Unit (S.A.), National Institute of Neurological Disorders and Stroke (NINDS), NIH, Bethesda; Frank Laboratory, Radiology and Imaging Sciences Clinical Canter (J.A.F.), NIH, Bethesda; and Intramural Research Program (J.A.F.), National Institute of Biomedical Imaging and Bioengineering, NIH, Bethesda, MD.
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S. Auh, PhD
From the Neuroimmunology Branch (NIB) (M.D., M.R., N.D.R., H.F.M., F.B.) and Office of the Clinical Director Biostatistics Unit (S.A.), National Institute of Neurological Disorders and Stroke (NINDS), NIH, Bethesda; Frank Laboratory, Radiology and Imaging Sciences Clinical Canter (J.A.F.), NIH, Bethesda; and Intramural Research Program (J.A.F.), National Institute of Biomedical Imaging and Bioengineering, NIH, Bethesda, MD.
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M. Riva, MD
From the Neuroimmunology Branch (NIB) (M.D., M.R., N.D.R., H.F.M., F.B.) and Office of the Clinical Director Biostatistics Unit (S.A.), National Institute of Neurological Disorders and Stroke (NINDS), NIH, Bethesda; Frank Laboratory, Radiology and Imaging Sciences Clinical Canter (J.A.F.), NIH, Bethesda; and Intramural Research Program (J.A.F.), National Institute of Biomedical Imaging and Bioengineering, NIH, Bethesda, MD.
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N. D. Richert, MD, PhD
From the Neuroimmunology Branch (NIB) (M.D., M.R., N.D.R., H.F.M., F.B.) and Office of the Clinical Director Biostatistics Unit (S.A.), National Institute of Neurological Disorders and Stroke (NINDS), NIH, Bethesda; Frank Laboratory, Radiology and Imaging Sciences Clinical Canter (J.A.F.), NIH, Bethesda; and Intramural Research Program (J.A.F.), National Institute of Biomedical Imaging and Bioengineering, NIH, Bethesda, MD.
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J. A. Frank, MD
From the Neuroimmunology Branch (NIB) (M.D., M.R., N.D.R., H.F.M., F.B.) and Office of the Clinical Director Biostatistics Unit (S.A.), National Institute of Neurological Disorders and Stroke (NINDS), NIH, Bethesda; Frank Laboratory, Radiology and Imaging Sciences Clinical Canter (J.A.F.), NIH, Bethesda; and Intramural Research Program (J.A.F.), National Institute of Biomedical Imaging and Bioengineering, NIH, Bethesda, MD.
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H. F. McFarland, MD
From the Neuroimmunology Branch (NIB) (M.D., M.R., N.D.R., H.F.M., F.B.) and Office of the Clinical Director Biostatistics Unit (S.A.), National Institute of Neurological Disorders and Stroke (NINDS), NIH, Bethesda; Frank Laboratory, Radiology and Imaging Sciences Clinical Canter (J.A.F.), NIH, Bethesda; and Intramural Research Program (J.A.F.), National Institute of Biomedical Imaging and Bioengineering, NIH, Bethesda, MD.
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F. Bagnato, MD, PhD
From the Neuroimmunology Branch (NIB) (M.D., M.R., N.D.R., H.F.M., F.B.) and Office of the Clinical Director Biostatistics Unit (S.A.), National Institute of Neurological Disorders and Stroke (NINDS), NIH, Bethesda; Frank Laboratory, Radiology and Imaging Sciences Clinical Canter (J.A.F.), NIH, Bethesda; and Intramural Research Program (J.A.F.), National Institute of Biomedical Imaging and Bioengineering, NIH, Bethesda, MD.
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Notes

Address correspondence and reprint requests to Dr. Francesca Bagnato, NIB–National Institute of Neurological Disorders and Stroke–NIH Building 10, Room 5C103, 10 Center Drive, Bethesda, MD, 20892-1400 [email protected]

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