Leucocytes appear to potentiate stroke injury by clogging the microcirculation and infiltrating into the brain where they release free radicals and other substances that are toxic to neurons. Through the use of specific monoclonal antibodies directed against leucocyte adhesion receptors, both the microcirculation obstruction and the leucocyte infiltration can be decreased. Experimental studies have found reduced stroke damage through the use of antibodies that bind to either the CD18 leucocyte adhesion receptor or the corresponding endothelial cell receptor, intercellular adhesion molecule-1 (ICAM-1). These studies have shown the most benefit when anti-adhesion monoclonal antibodies are used in experimental models in which reperfusion follows an initial period of ischaemia. Based on these encouraging experimental results, a clinical trial using an anti-ICAM-1 adhesion agent has just been completed, with final results expected soon.