Abstract
Why do patients with multiple sclerosis (MS) sometimes develop transient worsening of preexisting symptoms? The cause is often attributed to “disruption of compensatory mechanisms.” The observation—and the weak explanation—are not unique to demyelinating disease. Patients who have previously had a stroke or those with progressive dementia can have recurrence of symptoms or clinical worsening with infection. The conventional wisdom is that the same mechanisms underlie this phenomenon wherever it is encountered. While transient worsening with systemic infection is seen after stroke, it is not seen with simple elevation in temperature or routine fever as frequently as it is encountered in MS. It is a mistake of inference to suppose that the same mechanisms operate across the spectrum of neurologic disease. MS specialists are well aware that many of their patients have greater variability of symptoms than stroke patients or those with other CNS injury. In this issue of Neurology ®, Villoslada et al.1 have serendipitously discovered a pharmacologic method to recreate this clinical observation. They conducted a double-blind placebo-controlled trial of the low affinity NMDA receptor antagonist memantine in …
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