Microbleeds evolution and remote hemorrhage post-tPA

With the increasing use of MRI, treating acute stroke patients having cerebral microbleeds (CMBs) with IV thrombolysis represents a thorny clinical dilemma in vascular neurology.¹ CMBs, small round hypointense lesions detected on blood-sensitive MRI sequences, e.g., T2*-gradient echo or susceptibility-weighed imaging, are presumed to reflect minute intraparenchymal bleeding regions resulting from microvascular fragility or increased permeability.¹ Hence, much of the enduring clinical interest around CMBs focuses on whether they confer increased intracerebral hemorrhage (ICH) risk, including early symptomatic ICH after IV thrombolysis with recombinant tissue-type plasminogen activator (tPA) in acute stroke.¹ While rare, post-tPA ICH is a feared complication, associated with poor outcomes. A large-scale individual-patient data meta-analysis demonstrated that increasing CMB burden on pretreatment MRI is associated with increased ICH risk and poor 3- to 6-month functional outcome after IV thrombolysis for acute stroke.² Based on these nonrandomized data, 2018 American Stroke Association guidelines,³ while not recommending routine MRI for CMB exclusion before tPA, note the association of >10 CMBs on prior imaging with increased bleeding risk and uncertain treatment benefits. However, the heterogeneous underlying nature of CMBs and the differing patterns of post-thrombolysis ICH, including hemorrhage within the infarct and remote bleeding, leave uncertainty regarding this association. CMBs, as markers of hemorrhage-prone small vessel injury, might contribute particularly to remote ICH.