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Effect of copolymer-1 on serial gadolinium-enhanced MRI in relapsing remitting multiple sclerosis

G L Mancardi1, F Sardanelli, R C Parodi

  • 1Department of Neurological Sciences, University of Genoa, Italy.

Neurology
|May 5, 1998
PubMed

Insights

Copolymer-1 (Cop1) treatment significantly reduced new gadolinium-enhancing lesions in multiple sclerosis patients. This therapy also decreased overall lesion load, suggesting Cop1 impacts MRI-visible disease activity.

Area of Science:

  • Neuroimmunology
  • Radiology
  • Clinical Neurology

Background:

  • Multiple Sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system.
  • Relapsing-remitting MS (RRMS) is characterized by distinct neurological episodes followed by recovery.
  • Magnetic Resonance (MR) imaging, particularly with gadolinium (Gd) enhancement, is crucial for monitoring MS disease activity.

Purpose of the Study:

  • To evaluate the effect of Copolymer-1 (Cop1) on MR imaging metrics in patients with RRMS.
  • To assess changes in Gd-enhancing lesions and overall lesion load during Cop1 therapy.

Main Methods:

  • Prospective study involving 10 RRMS patients.
  • Monthly Gd-enhanced MR imaging before and during Cop1 treatment (9-27 months pretreatment, 10-14 months treatment).
  • Independent, masked radiologist evaluation of MR images.

Main Results:

  • A 57% decrease in the frequency of new Gd-enhancing lesions during Cop1 treatment compared to pretreatment (0.92 vs 2.20 lesions/month).
  • A significant reduction in the mean area/month of new Gd-enhancing lesions (22 mm2 vs 43 mm2).
  • A decrease in lesion load accumulation on T2-weighted images during Cop1 treatment, significant in patients with longer pretreatment periods (p=0.05).

Conclusions:

  • Copolymer-1 treatment is associated with a reduction in new Gd-enhancing lesions and overall lesion load in RRMS patients.
  • These findings suggest Cop1 has a beneficial effect on MR-detectable disease activity in multiple sclerosis.
  • Cop1 may modulate the inflammatory processes underlying MS lesion formation.

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