Tuesday, November 13, 2007
MR Imaging Intensity Modeling of Damage and Repair In Multiple Sclerosis: Relationship of Short-Term Lesion Recovery to Progression and Disability
American Journal of Neuroradiology 28:1956-1963, November-December 2007
© 2007 American Society of Neuroradiology
D.S. Meier, Department of Radiology, Center for Neurological Imaging, Multiple Sclerosis Center, Brigham and Women's Hospital, Harvard Medical School, Boston Mass
H.L. Weiner, Department of Neurology, Multiple Sclerosis Center, Brigham and Women's Hospital, Harvard Medical School, Boston Mass
C.R.G. Guttmann, Department of Radiology, Center for Neurological Imaging, Multiple Sclerosis Center, Brigham and Women's Hospital, Harvard Medical School, Boston Mass
Please address correspondence to Dominik Meier, PhD, Center for Neurological Imaging, Brigham and Women's Hospital, 221 Longwood Ave, RF 396, Boston, MA 02115; e-mail: firstname.lastname@example.org
BACKGROUND AND PURPOSE: Formation of lesions in multiple sclerosis (MS) shows pronounced short-term fluctuation of MR imaging hyperintensity and size, a qualitatively known but poorly characterized phenomenon. With the use of time-series modeling of MR imaging intensity, our study relates the short-term dynamics of new T2 lesion formation to those of contrast enhancement and markers of long-term progression of disease.
MATERIALS AND METHODS: We analyzed 915 examinations from weekly to monthly MR imaging in 40 patients with MS using a time-series model, emulating 2 opposing processes of T2 prolongation and shortening, respectively. Patterns of activity, duration, and residual hyperintensity within new T2 lesions were measured and evaluated for relationships to disability, atrophy, and clinical phenotype in long-term follow-up.
RESULTS: Significant T2 activity was observed for 8 to 10 weeks beyond contrast enhancement, which suggests that T2 MR imaging is sensitive to noninflammatory processes such as degeneration and repair. Larger lesions showed longer subacute phases but disproportionally more recovery. Patients with smaller average peak lesion size showed trends toward greater disability and proportional residual damage. Higher rates of disability or atrophy were associated with subjects whose lesions showed greater residual hyperintensity.
CONCLUSION: Smaller lesions appeared disproportionally more damaging than larger lesions, with lesions in progressive MS smaller and of shorter activity than in relapsing-remitting MS. Associations of lesion dynamics with rates of atrophy and disability and clinical subtype suggest that changes in lesion dynamics may represent a shift from inflammatory toward degenerative disease activity and greater proximity to a progressive stage, possibly allowing staging of the progression of MS earlier, before atrophy or disability develops.