<p>Stroke research has traditionally focused on parenchymal injury, including neuronal death, blood-brain barrier disruption, edema, and secondary neuroinflammation. Recent studies also show that central nervous system (CNS) border tissues, including perivascular spaces, meninges, and the choroid plexus, participate in immune signaling, fluid movement, and communication between the brain and peripheral immune sites after stroke. Border-associated macrophages (BAMs), also called CNS-associated macrophages (CAMs) in some studies, are resident macrophages located in these border compartments. BAMs are not a single uniform population. Recent single-cell, fate-mapping, spatial, and genetic-tool studies have shown that BAMs differ not only from microglia, but also from one another across perivascular, leptomeningeal, dural, and choroid plexus (CP) niches. This review summarizes current evidence on BAMs in stroke with emphasis on how perivascular, leptomeningeal, dural, and choroid plexus macrophages differ in location, homeostatic role, and stroke-related responses. We first describe the organization of CNS border tissues and the fluid routes that are relevant to ischemic and hemorrhagic stroke. We then discuss how BAMs can be distinguished from microglia and monocyte-derived macrophages, with emphasis on replacement patterns in perivascular, leptomeningeal, dural, and choroid plexus compartments. The main sections focus on how BAMs at different anatomical sites participate in vascular leakage, leukocyte recruitment, drainage support, and barrier responses after ischemic or hemorrhagic stroke. We also discuss how BAMs relate to meningeal lymphatic drainage, cerebrospinal fluid (CSF)-perivascular transport, arachnoid cuff exit (ACE) points, dural sinuses, and skull marrow channels. This compartment-based organization helps clarify why BAMs should not be treated as one pooled macrophage population in stroke.</p>