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The onset location of multiple sclerosis predicts the location of subsequent relapses
  1. E M Mowry1,
  2. S Deen1,
  3. I Malikova2,
  4. J Pelletier2,
  5. P Bacchetti3,
  6. E Waubant1
  1. 1
    Multiple Sclerosis Center, Department of Neurology, University of California, San Francisco, USA
  2. 2
    Marseille Multiple Sclerosis Center, Pole de Neurosciences Cliniques, Department of Neurology, Marseille, France
  3. 3
    Department of Epidemiology and Biostatistics, University of California, San Francisco, USA
  1. Dr E M Mowry, University of California, San Francisco MS Center, 350 Parnassus Ave, Suite 908, San Francisco, CA 94117, USA; ellen.mowry{at}


Background: Demyelinating events in relapsing-remitting multiple sclerosis (RRMS) can involve several locations in the central nervous system. We sought to determine if initial clinical demyelinating event (IDE) location predicts subsequent clinical relapse locations in early RRMS.

Methods: We identified all RRMS patients from two large MS clinics who were seen within 1 year of disease onset. Logistic regression was performed with the outcome defined as the second or third exacerbation location and the predictor defined as IDE±second event location.

Results: 195 patients with at least two clinical exacerbations were identified. There was an increased odds of a patient’s second relapse occurring in the spinal cord if the IDE was in the spinal cord (odds ratio (OR) = 3.79, 95% CI 2.06 to 7.00, p<0.001). There was more than a sixfold increase in the odds of a patient’s second relapse occurring in the optic nerve if the IDE was in the optic nerve (OR = 6.18, 95% CI 2.90 to 13.18, p<0.001). These associations remained similar after adjusting for treatment and patient characteristics. If the IDE and second event were both in the same location (spinal cord, optic nerve or brainstem/cerebellum), the third event was likely to remain in that location.

Conclusion: Patients with RRMS have relatively localised clinical relapses. It remains to be determined if genetic or biological processes are responsible for this pattern.

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  • Competing interests: None.

  • Funding: EW has received research support from Biogen Idec, Genentech, Pfizer and Sanofi-Aventis, and honorarium for one educational presentation from Teva and Biogen. JP and IM have received research support from Biogen Idec, Schering Bayer, Serono Merck and Sanofi-Aventis. This study was supported by the NMSS (RG-3692A), a Clinical Fellowship Award from the Partners MS Center, and the Nancy Davis Foundation.

  • Ethics approval: Ethics approval was provided by the University of California, San Francisco and Marseille Committees on Human Research.