Damage to the brain parenchyma is a common component of head trauma. The type, location and degree of brain injury is determined to a large extent by the physical properties of the skull and brain. The skull is very hard and rigid, and protects the brain from direct injury. However, the inner table of the skull has roughened edges and ridges of bone along the floor of the anterior cranial fossa, sphenoid wings and petrous ridges that can contuse the brain surface during the compressive forces of trauma.

      Injury of the brain parenchyma sets in motion a series of events. Tissue disruption and cell injury are associated with release of vasoactive substances and other byproducts. Subsequent increase in vascular permeability to serum proteins results in a progressive increase in interstitial fluid. Over a period of several days, the edema fluid spreads within the white matter, producing mass effect on adjacent structures and possible further damage. More serious injuries may be associated with vascular disruption and hemorrhage into contusions. Cortical contusion are usually multiple, measuring approximately 2-4 cm in size, and 30% to 50% of lesions are hemorrhagic. Approximately 50% to 75% of cortical contusions involve the frontal and temporal lobes, particularly the lateral surfaces of both lobes and the inferior surface of the frontal lobes.

      Varying signal intensity patterns are seen on MR depending on the age and amount of hemorrhage present. In several studies MR has had a decided advantage over CT in the imaging of bland contusions and has been roughly equivalent to CT in imaging hemorrhagic contusions. Overall, MR has shown approximately 90% of all cortical contusions imaged by either modality. In general, T2-weighted images are best for evaluating brain contusions. T1-


weighted images are helpful to look for any associated hemorrhage. Nonhemorrhagic contusions are hyperintense on T2 and hypointense on T1-weighted scans due to brain edema and increased water content in the lesions. The brain edema increases during the first few days, producing mass effect on adjacent brain structures. With time, the edema subsides and the dead tissues are removed, resulting in areas of encephalomalacia and compensatory focal dilatation of adjacent ventricles and sulci.

      The MR appearance of hemorrhagic contusions is more dynamic, changing over time as the internal chemistry of the hematoma changes. In fact, the signal intensities on T1 and T2-weighted images often provide clues about the approximate age of hemorrhagic contusions. The central hypointensity of acute hemorrhagic contusions on T2- weighted images is often highlighted by the surrounding edema. After a few days, methemoglobin forms and gives a mottled pattern of high signal on T1-weighted images owing to the multifocal nature of hemorrhage into cortical contusions.

      The brain stem is also subject to injury from head trauma. Although it is protected from direct injury by its location, acceleration/deceleration forces associated with impact to the head may produce displacement and twisting of the brain stem. These forces can result in tearing of penetrating arteries or veins, and compression of the brain stem against the sharp edges of the tentorium or surfaces of the clivus and petrous bones.  

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