More MS news articles for March 2000

Glatiramer Acetate (Copaxone) Treatment in Relapsing-Remitting MS: Quantitative MR Assessment

February 2000 (Volume 54, Number 4)
Ge Y, Grossman RI, Udupa JK, et al.
Neurology. 2000;54:813-817

Many studies have used functional scales like the Expanded Disability Status Scale (EDSS) to measure the clinical progression of disease and subsequent disability in patients with multiple sclerosis (MS). Some investigators have suggested using MRI to directly quantify and measure pathologic changes within the CNS. The ability to quantify the MS lesions might impart the capacity to detect subclinical activity and assist with the prediction of subsequent progression and disability.

Glatiramer acetate has been approved for the treatment of relapsing-remitting MS (RRMS) and has been shown to reduce the frequency of relapses by an average of 30%. Ge and colleagues conducted a study to determine the efficacy of glatiramer acetate in patients with RRMS by using MRI-based measurements.

Twenty-seven patients (23 women and 4 men) with clinically defined RRMS were studied. The patients' disease duration was 1 to 17 years. Baseline EDSS ranged from 1.0 to 5.0. Participants were randomized to receive either 20 mg of glatiramer acetate by daily subcutaneous self-injection (n=14) or placebo (n=13). The treatment was administered over a period of 24 months. Four patients in the placebo group did not complete the 2-year protocol (study time between 0.54 and 1.39 years). The 2 groups were similar in age, EDSS score, disease duration, and number/volume of T1- and T2-weighted lesions.

The main outcome measures were the number of gadolinium-enhanced T1 and T2 lesions demonstrated on MRI and their volume. To analyze the effect of therapy on the development of brain atrophy, investigators determined the total volume of brain parenchyma. Axial dual-echo fast spin-echo T2- and T1-weighted images were obtained at 1.5 T before and after gadolinium.

The MRI-based measurements demonstrated an advantage of treatment with glatiramer acetate over placebo. The MRI measurements in the glatiramer acetate group revealed a decrease in the number of T1-enhanced lesions (P=.03) and a significant percentage annual reduction in their volume.

No significant difference was found between the 2 groups in the number of T2 lesions and their volumes. The degree of brain loss was significantly higher in the placebo group. The evidence suggests that glatiramer acetate might slow the progression of brain loss in RRMS. The use of MRI-based measurements to quantify the number of lesions and volume of tissue might help in the evaluation of clinical progression. A combination of disability scores and MRI-based measurements might help future trials evaluate the degree of disease activity and assist in the identification of patients at risk for significant disease progression.