Summary of Traumatic Brain and Vascular Injuries

## Introduction Traumatic brain injury (TBI) is damage to the brain resulting from an external mechanical force. It ranges from mild concussion to severe injury with permanent neurologic deficits. Imaging—especially CT and MRI—helps determine injury type, guide treatment, and predict outcome. ## Mechanisms of Injury ### Acceleration–Deceleration and Rotational Forces - Rotational acceleration produces shear forces that commonly cause widespread axonal damage. - Direct impact is not required for many primary neuronal injuries; skull fractures and epidural hematomas typically need a direct blow. > Definition: Diffuse axonal injury (DAI) is widespread disruption of axons from acceleration or deceleration forces, often produced by rotational shear. ### Influence of Force Duration - Short, abrupt acceleration/deceleration favors cortical contusions and intracranial hematomas. - Longer-duration acceleration/deceleration favors DAI and gliding contusions. - Example: High-speed motor vehicle collisions more commonly produce DAI; simple falls are more likely to cause contusions or hematomas. ## Major Injury Types: Clinical and Imaging Features ### Diffuse Axonal Injury (DAI) - Pathology: Shearing of axons in white matter tracts due to rotational forces. - Typical locations: gray–white junction, parasagittal frontal regions, periventricular temporal regions, corpus callosum (posterior body and splenium), dorsolateral midbrain and upper pons in severe cases. - Clinical: Immediate and often prolonged loss of consciousness; more severe impairment than isolated contusions. - Imaging: - CT: May be subtle or show small petechial hemorrhages at gray–white junction or corpus callosum. - MRI: Better sensitivity—FLAIR/T2 shows small foci of hyperintensity for nonhemorrhagic lesions; diffusion-weighted imaging (DWI) and low ADC indicate cytotoxic injury or restricted diffusion; GRE/SWI shows low signal for hemorrhagic foci. - Advanced: Diffusion tensor imaging and tractography improve detection of white matter disruption. Fun fact: DAI lesions may be underestimated on CT but revealed by MRI techniques such as SWI and DTI, which can change prognosis and management. ### Cortical Contusions - Pathology: Focal injury of superficial gray matter; often hemorrhagic and adjacent to bony protuberances. - Typical sites: temporal lobes above the petrous bone, posterior to the greater sphenoid wing, frontal lobes above the cribriform plate and planum sphenoidale; cerebellar involvement <10%. - Clinical: Less likely to have immediate loss of consciousness than DAI; generally better prognosis than DAI. - Imaging: - CT: Hemorrhagic contusions appear as high-attenuation foci within superficial gray matter; surrounding vasogenic edema appears hypodense. Nonhemorrhagic contusions can be initially subtle and become evident during the first week as edema increases. - MRI: FLAIR/T2 hyperintensity, SWI/GRE low signal for blood products; chronic contusions may show encephalomalacia. - Complications: May require surgical decompression for mass effect. ### Intracerebral Hematoma - Pathology: Focal intraparenchymal hemorrhage from rupture of small vessels; may occur without cortical contusion. - Typical locations: frontotemporal white matter and basal ganglia. - Clinical: Patients can remain lucid unless hematoma expands; clinical deterioration commonly results from mass effect or delayed hemorrhage. - Imaging: - CT: High-attenuation focal mass; intraventricular extension can occur. - CTA: Active contrast extravasation into the hematoma ("spot sign") predicts expansion and worse outcome. ### Subcortical Gray Matter (Basal Ganglia/Thalamus) Petechial Hemorrhages - Pathology: Microscopic perivascular collections of blood from disrupted perforating vessels. - Clinical: Typically associated with severe trauma. - Imaging: Multiple small hemorrhages in basal ganglia and thalamus, best seen on SWI/GRE and CT for acute bleeding. ### Vascular Injuries (Dissec