Cerebral amyloid angiopathy (CAA) is a small vessel disease marked by the deposition of β-amyloid in cortical and leptomeningeal vessels. This condition is commonly linked to lobar intracerebral hemorrhage, cortical superficial siderosis, and convexity subarachnoid hemorrhage. Ischemic events may also occur as a result of impaired vasoreactivity and subsequent hypoperfusion. The concurrent presence of ischemic and hemorrhagic strokes in biopsy-confirmed cerebral amyloid angiopathy poses significant diagnostic and treatment difficulties, particularly regarding antithrombotic therapy.

A 74-year-old female patient with type 2 diabetes mellitus and dyslipidemia initially manifested transient focal neurological deficits, later with a left parietal convexity subarachnoid hemorrhage and multiple acute infarcts in the left parietal, temporal, and centrum semiovale regions, prompting the initiation of aspirin and rivaroxaban therapy. Over the following years, she developed progressive cognitive impairment. She also presented with lobar ICH in the right frontotemporoparietal region 3 years from her ischemic stroke and subsequently developing another ischemic stroke for which she was started on cilostazol. 

This case illustrates the dual ischemic and hemorrhagic pathology in cerebral amyloid angiopathy (CAA). Recurrent lobar hemorrhage is well recognized; however, ischemic events may complicate the clinical course and adversely affect prognosis. The absence of definitive guidelines for antithrombotic therapy in CAA complicates management strategies. Our patient was treated with cilostazol, an antiplatelet with favorable safety data in patients at high hemorrhagic risk, as demonstrated in subgroup analyses of the PICASSO trial. This therapeutic approach emphasizes the need for individualized treatment strategies in CAA.