Acute ischemic stroke (AIS) is a significant contributor to both morbidity and mortality worldwide, and there is a great need to understand the pathways and structures affected by the stroke to improve management and treatment outcomes. One critical structure affected by AIS is the blood-brain barrier (BBB). Following the initial insult, the release of danger-associated molecular patterns (DAMPs) triggers the release of pro-inflammatory cytokines, neutrophils, and microglia. As a result, matrix metalloproteinases (MMPs) activate and degrade the BBB tight junctions. Evaluation of BBB dysfunction after AIS involves imaging modalities like magnetic resonance imaging (MRI) and dynamic computerized tomography (CT) which characterize changes in permeability possibly predicting complications such as hemorrhagic transformation and cerebral edema. BBB dysfunction is associated with poor long-term outcomes, and evaluating for increased BBB permeability immediately following an AIS with neuroimaging may be clinically relevant. Therapeutics may attenuate disruption of the BBB following AIS through interventions targeting inflammatory cells and junctional proteins. By characterizing the pathophysiology, neuroimaging, outcomes, and potential therapeutics, we summarized available clinically relevant information to demonstrate the importance of BBB dysfunction in the management and treatment of AIS.