Intercellular adhesion molecule–1 (ICAM-1) is an adhesion molecule of the immunoglobulin family expressed on endothelial cells that is upregulated in brain as part of the acute inflammatory response to traumatic brain injury (TBI). ICAM-1 mediates neurologic injury in experimental meningitis and stroke; however, its role in the pathogenesis of TBI is unknown. We hypothesized that mutant mice deficient in ICAM-1 (−/−) would have decreased neutrophil accumulation, diminished histologic injury, and improved functional neurologic outcome versus ICAM-1 +/+ wild type control mice after TBI. Anesthetized ICAM-1 −/− mice and wild-type controls were subjected to controlled cortical impact (CCI, 6 m/sec, 1.2 mm depth). Neutrophils in brain parenchyma and ICAM-1 on vascular endothelium were assessed by immunohistochemistry in cryostat brain sections from the center of the contusion 24 h after TBI (n = 4/group). Separate groups of wild-type and ICAM-1–deficient mice (n = 9–10/group) underwent motor (wire grip test, days 1–5) and cognitive (Morris water maze [MWM], days 14–20) testing. Lesion volume was determined by image analysis 21 days following TBI. Robust expression of ICAM-1 was readily detected in choroid plexus and cerebral endothelium at 24 h in ICAM-1 +/+ mice but not in ICAM-1 −/− mice. No differences between groups were observed in brain neutrophil accumulation (9.4 ± 2.2 versus 11.1 ± 3.0 per × 100 field, −/− versus +/+), wire grip score, MWM latency, or lesion volume (7.24 ± 0.63 versus 7.21 ± 0.45 mm³, −/− versus +/+). These studies fail to support a role for ICAM-1 in the pathogenesis of TBI.