These symptoms are triggered by attacks on cells in the central nervous system by the body's own immune system. Specifically, these attacks damage cells called myelin which form the "insulation" around nerve fibers. When this insulation is damaged, communication in the central nervous system is delayed, disrupted, and even blocked. It is believed that fampridine improves the transmission of signals in the central nervous system of some multiple sclerosis patients by blocking potassium ion channels in nerve cells and restoring signal conduction.
Goodman and his colleague Steven Schwid, M.D., who passed away in November 2008, have been evaluating fampridine for multiple sclerosis since the mid 1990s.
Progress began to accelerate when the license to develop the drug was acquired by Acorda Therapeutics. The primary obstacle then was that the process of evaluating the drug's impact required researchers to devise a new way to think about clinical trial methodology. Most multiple sclerosis drugs are measured by their ability to prevent relapses or slow the progression of the disease, not reverse symptoms once they became established. Goodman and Schwid developed methods for assessing functional outcomes in multiple sclerosis patients such as measuring walking speed over a 25 foot distance.
In the Lancet study, they reported that 35% of patients taking the drug were responders who consistently improved their walking speed by an average of about 25%. While walking was the primary measure, patients also reported that they could walk farther distances, climb stairs better, and stay on their feet longer. In prior research, they a
|Contact: Mark Michaud|
University of Rochester Medical Center