Traumatic brain injury (TBI) encompasses heterogeneous insults and presentations resulting from blunt or penetrating mechanisms that disrupt normal cerebral function. While the primary injury may demand emergent intervention, secondary injury due to hypotension, hypoxia, edema, and ischemia can significantly worsen outcomes. Post-traumatic cerebral infarction (PTCI) remains an underrecognized but potentially preventative cause of deterioration. PTCI may arise through various systemic and brain-related factors, including those due to post-traumatic vasospasm. The clinical significance, mechanisms, and management of vasospasm after TBI are controversial and bring to question whether vasospasm is merely a marker of injury or a separate, modifiable contributor to ischemia. Thus, in this review, we examine the evidence regarding incidence, etiology, and consequence of PTCI with an emphasis on vasospasm. We highlight diagnostic challenges, therapeutic interventions, and opportunities for future clinical use directed toward improving outcomes after TBI.
Manners et al. (Mon,) studied this question.