Cerebral Contusions and Lacerations

Cerebral contusions are the most common of the intraaxial injuries. True brain lacerations are rare and typically occur only with severe (often fatal) head injury.TerminologyCerebral contusions are basically "brain bruises". They evolve with time and often more apparent on delayed scans than at the time of initial imaging. Cerebral contusions are alsa called gyral "crest" injury (2-57). The term "gliding" contusion is sometimes used to describe parasagital contusion.EtiologyMost cerebral contusions result from non-missile or blunt head injury. Closed head injury induces abrupt changes in angular momentum and deceleration. The brain is suddenly and forcibly impacted against an osseus ridge or the hard, knife-like edges of the falx cerebri and tentorium cerebelli. Less commonly, a depressed skull fracture directly damages the underlying brain.PathologyLOCATION. Contusions are injuries of brain surface that involve the gray matter and contiguous subcortical white matter (2-57) (2-58) (2-59). They occur in very characteristic, highly predictable locations. Nearly half involve the temporal lobes. The temporal tips, as well as the lateral and inferior surface and the perisylvian gyri, are most commonly affected (2-60). The inferior

(orbital) surface of the frontal lobes are also frequently affected (2-61).Convexity gyri, the dorsal corpus callosum body, dorsolateral midbrain, and cerebelum are less common sites of cerebral contusions. The occipital poles are rarely involved even with relatively severe closed head injury.SIZE AND NUMBER. Cerebral contusions vary in size from tiny lesions to large confluent hematoma (2-59). They are almost always multiple and often bilateral (2-62) contusions that occur at 180 opposite the site of direct impact (the "coup") are common and are called "contre-coup" lesions.GROSS PATHOLOGY. Contusions range in appearance from small petechial to large confluent hemorrhages. Cortical contusions are usually associated with. traumatic subarachnoid hemorrhage in adjacent sulci.

MICROSCPIC FEATURES. Perivaskular micro-hemorrhage rapidly form and coalesce over time into more confluent hematomas. Edema surrounding the hemorrhages develops. Activations and proliferation of astrocytes together with macrophage infiltration ensues.Necrosis with neuronal loss and astrogliosis as well as hemosiderin-laden macrophages are present in subacute and chronic lesions.Clinical IssuesEPIDEMIOLOGY AND DEMOGRAPHICS. Cerebral contusions account for approximatbely half of all traumatic parenchymal lesions. They occur at all ages, from infants to the elderly. The

pea age is from 15-24 years, and the M : F ratio 3 : 1.PRESENTATION. Inital symptoms vary from none to confusion, seizure or obtundation. Compared to diffuse axonal injuries (see below), cerebral contusions are less frequently associated with immediate loss of consciousness unless they extensive or occure with other traumatic brain liesions (e.g. brainsterm trauma or axonal injury). NATURAL HISTORY. Neurologic deterioration is more common in older patients. Patients with large contusions, initial low Glasgow Coma Score (GCS), coagulopathy, and presence of coexisting subdural hematoma are prone to clinical deterioration. Those with small contusions, good initial GCS, and absence of clinical deterioration in the first 48 hours are unlikely to require surgery. Hematoma expansion requiring surgical intervention occurs in approximately 20% of conservatively managed patients. Patients with unexplained clinical deterioration should have repeat imaging.TREATMENT OPTIONS. Treatment options vary from conservative (observation with repeat imaging if the patient deteriorates) to surgical evacuation of large focal focal hematomas. Craniectomy is perfomed in patients with severe brain swelling to present fatal brain herniation. ImagingGENERAL FEATURES. With time, cortical contusions become more apparent on imaging studies. Radiologic progression is the rule, not the exception. Nearly half of all patients show increase in lesion size and number over the first 24-48 hours. In the absence of clinical

deterioration, though, the relevance of documenting this progression is debutable.CT FINDINGS. Initial scans obtained soon after a closed head injury may be normal. The most frequent abnormality is the presence of petechial hemorrhages along gyral crest immediately adjacent to the calvaria (2-63). A mixture of petechial hemorrhages surrounding by patchy illdefined hypodense areas of edema is common. Lesions "blooming" over time is frequent and is seen with progressive increase in hemorrhages, edema, and many effect. Small lesion may coalesce' formng larger focal hematomas. Developement of new lesions that were not present on initial is also common.MR FINDINGS. MR is much more sensitive that CT in detecting cerebral contusions but is rarely obtained in the acte stage of traumatic brain injury. T1 scans may show only mild inhomogeneous isointensites and mass effect.

T2 scans show patchy hyperintense area (edema) surrounding hypointense foci of hemorrhage (2-64A).FLAIR scan are most sensitive for detecting cortical edema and associated traumatic subarachnoid hemorrhages, both of which appear as hyperintense foci on FLAIR. T2* (GRE' SWI) is the most sensitive sequence for imaging parenchymal hemorrhages. Significant "blooming" is typical in acute lesions (2-64B).Hemorrhagic contusions follow the expected evolution of parenchymal hematomas, with T1 shortening developing over time. Atrophy, demyelination, and microglial scarring are seen on FLAIR and T2W1. Parenchymal volume loss with ventricular enlargement and sulcal prominsence is common.DWI in patients with cortical contusions shows diffuse restriction in areas of cell death. DTI may disclose coexisting white matter damage in minor head trauma even when standars MR sequences are normal. Differential DiagnosisThe major diffrential diagnosis of cortical contusions Diffuse Axonal Injury (DAI). Both cerebral contusions and DAI are often present in patients who have sustained moderate to severe head injury. Contusions tend to be superficial, located along gyral crests. DAI is most commonly found in the corona radiata and along compact white matter tracts such as the internal capsule and corpus callosum.Severe corical contusion with confluent hematomas may be difficult to distinguish from brain laceration on imaging studies. Brain laceration occurs when severe trauma disrupts the pia and literally tears the under apart.A "burst lobe" is the most severe manifestation of frank brain laceration (2-65) (2-66). Here the affected lobe is grossly disruptes, with large hematoma formation and adjacent traumatic subarachnoid hemorrhage. In some cases, especially those with depressed skull fracture, the arachnoid is also lacerated and hemorrhage from the burst lobe extends to communicate directly with the subdural space, forming a coexisting subdural hematoma.