Of the treatments for multiple sclerosis (MS) aimed at prevention of relapse or disease progression, there is only regulatory approval for beta interferons and glatiramer acetate. Treatment with either interferon beta-1a or interferon beta-1b is established, although their beneficial effects have been challenged by our systematic review of randomised trials in relapsing-remitting MS. 1 The alternative treatment is glatiramer acetate, a synthetic amino-acid polymer shown to suppress experimental allergic encephalomyelitis in animals. Although glatiramer acetate’s mechanism of action is not fully understood, molecular similarities to myelin basic protein suggest competition with myelin in binding to T lymphocytes; this may improve the course of the disease. Glatiramer acetate is now routinely prescribed for MS and it is the fastest growing product in its market. However, our systematic review of all randomised controlled trials of glatiramer acetate2 found little support for use of this drug in patients with MS.

The efficacy of glatiramer acetate has been assessed in only four studies with a total of 646 patients: 540 with relapsing-remitting and 106 with chronic progressive MS. Whatever the disease course, glatiramer acetate is no better than placebo in preventing clinical progression at 2 years. Furthermore, all studies assessing this outcome3–5 defined progression as an increase of at least 1 point on the Expanded Disability Status Scale (EDSS), maintained for 3 months. This is probably too short a follow-up period to exclude relapse. Research shows that at least 1 year of follow-up is needed to confirm disease progression and most clinicians would not agree with a shorter period. Other studies have characterised patients’ disability by measuring EDSS changes over time. Unfortunately, EDSS is an ordinal scale and comparison of mean scores with the baseline has limited validity as an outcome measure. Therefore a slight decrease in the mean EDSS score up to 3 years, shown by a