We sought to identify and describe cases of post-TBI territorial cerebral infarction without LVO.

Cerebral infarction is a known complication of traumatic brain injury (TBI). Despite this recognition, the mechanism of territorial infarction in the absence of large vessel occlusion (LVO) remains poorly characterized.

In this single-center, retrospective descriptive study, ten years (2015 - 2024) of inpatient TBI encounters registered in an institutional database were reviewed. Radiology reports were screened by four abstracters to identify possible cases of territorial infarct. Two clinical practitioners subsequently reviewed images to confirm territorial infarct as well as absence of LVO and vasospasm. Chart data was abstracted for these cases, including infarct location, other intracranial injury, neurosurgical and medical interventions, and morbidity/mortality outcomes. Descriptive analysis was performed using SAS 9.4. 

Of 697 reviewed cases with complete brain and cerebrovascular imaging, there were 28 cases of post-TBI territorial cerebral infarction without LVO. Most occurred in Middle Cerebral Artery (MCA, n = 9, 32.1%) or Posterior Cerebral Artery (PCA, n = 9, 32.1%) territories. In 6 cases (21.4%), blunt cerebrovascular injury (BCVI) was seen. Midline shift (n = 25, 89.2%) and intracranial hemorrhage (n = 26, 92.8%) were common. 16 patients (57.1%) underwent decompressive craniectomy and 15 (53.6%) underwent extraventricular drain (EVD) placement.

Post-TBI territorial cerebral infarction without LVO is rare. Vessel injury is unlikely to be the primary etiology of these infarcts as BCVI was appreciated in only 6 cases. However, ICH and midline shift were prevalent. Furthermore, over half of these cases required surgical intervention to alleviate elevated intracranial pressure (ICP), including EVD placement or craniectomy. Together, these findings suggest that vascular compression secondary to cerebral edema may be the primary mechanism of post-TBI territorial cerebral infarction without LVO. Thus, early recognition and intervention to control intracranial pressure may be critical to mitigate this secondary injury.