Chronic Traumatic Encephalopathy (CTE) is a brain disease associated with repetitive head impacts, characterized in part by perivascular phosphorylated tau (p-tau) accumulation in the depths of the cortical sulci. Increasing evidence suggests that concussive and subconcussive head impacts cause acute damage to the neurovascular unit in distinct cortical layers. Given that microvascular injuries often precede the seeding of tau aggregates near blood vessels, it has been proposed that microvascular injury is one of the primary drivers of CTE. In animal experiments of closed-head impact and blast, it has been demonstrated that microvascular damage along vessel walls is spatially heterogeneous. Similarly, tau aggregates are often localized to specific vessel walls while being absent from others in their vicinity, both in the aforementioned animal experiments and in human brain tissue with confirmed CTE. In this work, we use finite element modeling to show how the energy from a head impact damages the neurovascular unit. We built a 100 × 100 × 100 μm3 representative volume element (RVE) consisting of brain tissue and its capillary network. Applying dynamic head impact-related loading conditions to the RVE, we quantified stress and strain and are able to show that these two fields reproduce the spatially heterogeneous, "bullet-hole"-like, pattern of neurovascular injuries observed in animal experiments. Future work on this model will involve inflammatory cell recruitment to damaged sites in the neurovascular architecture, an important aspect of secondary injury following head impacts, allowing us to associate acute impacts to CTE pathologies on a longer timescale. The development of this multiscale model may allow us to assess and mitigate the risk of CTE among individuals exposed to repetitive head impacts.