Modulating acute neuroinflammation in intracerebral hemorrhage: the potential promise of currently approved medications for multiple sclerosis

The secondary inflammatory injury following intracerebral hemorrhage (ICH) results in increased morbidity and mortality. White blood cells have been implicated as critical mediators of this inflammatory injury. Currently, no medications have been clinically proven to ameliorate or beneficially modulate inflammation, or to improve outcomes by any mechanism, following ICH. However, other neuroinflammatory conditions, such as multiple sclerosis, have approved pharmacologic therapies that modulate the inflammatory response and minimize the damage caused by inflammatory cells. Thus, there is substantial interest in existing therapies for neuroinflammation and their potential applicability to other acute neurological diseases such as ICH. In this review, we examined the mechanism of action of twelve currently approved medications for multiple sclerosis: alemtuzumab, daclizumab, dimethyl fumarate, fingolimod, glatiramer acetate, interferon beta-1a, interferon beta-1b, mitoxantrone, natalizumab, ocrelizumab, rituximab, teriflunomide. We analyzed the existing literature pertaining to the effects of these medications on various leukocytes and also with emphasis on mechanisms of action during the acute period following initiation of therapy. As a result, we provide a valuable summary of the current body of knowledge regarding these therapies and evidence that supports or refutes their likely promise for treating neuroinflammation following ICH.