Editors' ChoiceNeurology

Modulating Intracerebral Hemorrhage

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Science Translational Medicine  20 Aug 2014:
Vol. 6, Issue 250, pp. 250ec145
DOI: 10.1126/scitranslmed.3010120

Much of the morbidity and mortality from intracerebral hemorrhage results from secondary brain injury, which is characterized by brain inflammation, ischemia, and edema. It is thought that modulation of early brain inflammation reduces perihematoma edema and subsequent secondary brain injury. Now, in a proof-of-concept open-label clinical trial, Fu et al. evaluated oral fingolimod, a sphinosine 1-phosphate receptor modulator that inhibits the movement of lymphocytes from lymph nodes. Fingolimod has been shown to reduce the inflammatory response and motor and cognitive deficits after intracerebral hemorrhage in animal models. In 23 patients with primary supratentorial intracerebral hemorrhage and hematoma volumes of 5 to 30 ml, a 3-day course of oral fingolimod was compared with a matched control cohort who did not receive the drug. Treatment with fingolimod demonstrated a marked reduction in circulating lymphocytes and perihematoma edema at 7 and 14 days compared with the control group. In addition, fingolimod treatment was associated with short-term neurological improvements and no increase in adverse effects. Despite the limitations of a small sample size and an open-label design, this study demonstrated the biological activity of fingolimod and the potential for immunomodulatory therapies in the management of intracerebral hemorrhage.

Y. Fu et al., Fingolimod for the treatment of intracerebral hemorrhage: A 2-arm proof-of-concept study. JAMA Neurol. 10.1001/jamaneurol.2014.1065 (2014). [Full Text]

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