Cerebral malaria is a severe complication that occurs during Plasmodium falciparum infections in humans. Mouse models using Plasmodium berghei ANKA have been important for elucidating the precise molecular and cellular events involved in the progression of this disease. A key feature of cerebral malaria pathogenesis is the sequestration of leukocytes within the blood vessels of the brain, which is thought to contribute to vascular damage and occlusion and disease progression. Nevertheless, the precise spatio-temporal context of leukocyte behaviour in the central nervous system in vivo is poorly understood. Using intravital microscopy, we showed that both Ly6C+ monocytes and T cells are recruited to the pial vessels before the appearance of neurological signs. Within the vascular lumen, monocytes were occasionally found in close contact with regions of blood vessel associated with perivascular macrophages. Development of neurological signs was associated with increased retention of both Ly6C+ monocytes and T cells in the vascular lumen. At late stage disease, a small fraction of T cells was found to enter the brain parenchyma where they actively migrate. In contrast, monocytes were restricted to the vascular lumen. Our studies map the sequence of leukocyte accumulation in the vasculature during cerebral malaria, and highlight hitherto unknown cellular interactions between monocytes, T cells and perivascular macrophages.