This chapter highlights the clinical, pathophysiologic, and biochemical links between inflammatory bowel disease (IBD) and ischemic stroke. Deep venous thrombosis (DVT) and pulmonary embolism (PE) account for the overwhelming majority of thrombotic events in patients with IBD. Descriptions of IBD-associated central nervous system (CNS) vasculitis are based on angiography showing segmental narrowing in the small to medium-sized arteries. Of the many IBD-related hypercoagulable state manifestations, an estimated 10 percentage are ischemic strokes. Hyperhomocysteinemia has recently emerged as an independent risk factor for stroke; homocysteine is a sulfur-containing amino acid formed during the demethylation of the amino acid methionine. The mechanism for ischemic strokes in IBD patients is multifactorial, but likely secondary to an abnormal coagulability profile and, in rare situations, cerebral vasculitis. Better management of IBD flares, improved compliance with newer IBD medications, and quicker surgical interventions might lead to better outcomes and stroke risk reduction.