Mark N. Rubin, MD
As we’ve discussed over, and over, and over again, intracerebral hemorrhage (ICH) is bad disease. Although it represents only ~10-20% of all strokes, it is accountable for upwards of 50% of stroke mortality and is typically quite disabling. We have no targeted therapies available in clinical practice, for the acute or chronic phases, that definitely change the neurologic and/or mortality outcome.
These investigators had previously published their observation that early mortality after ICH was associated with absolute monocyte count (AMC) independent of ICH volume, with the putative mechanism being inflammatory neuronal apoptosis and/or a contribution to cerebral edema. The current publication highlights similar findings in a larger, more ethnically diverse population: those enrolled in Ethnic/Racial variations of IntraCerebral Hemorrhage (ERICH) cohort. In brief, they found that independent of the most important confounders including age, NIHSS, ICH volume and location, AMC was not associated with ICH volume but was associated with 30 day mortality. From these results, they concluded that the association of AMC with mortality may be generalizable and its lack of association with ICH volume suggests a mechanism beyond ICH-related mass effect and neuronal destruction.
As the authors correctly address in their discussion, this represents a potential target for early neuroprotection in ICH. With immunomodulatory therapies directed at monocyte action, we may be able to mitigate whatever role (assuming this finding is causal and not associational) monocytes play in the process. Clinical trials will likely depend on the elucidation of the mechanism prior to attempting (potentially dangerous) immunomodulatory therapy in already typically gravely ill patients.
