Traumatic Brain Injury


Nearly 2 million cases of traumatic brain injury (TBI) occur each year. Worldwide, trauma is the leading cause of death and disability in those younger than 45 years, with nearly half of fatalities resulting from TBI. In younger patients, traffic accidents are the leading cause of TBI, and in the elderly, falls are the principal cause. TBI is a heterogeneous disorder with different forms of presentation. Approximately 15% to 25% of TBIs are serious injuries requiring specialist care, but the majority are considered mild. Mortality from severe TBI has decreased substantially with protocols that depend in part on computed tomography (CT) to monitor and recognize findings that may result in further injury. Magnetic resonance imaging (MRI) is an important problem-solving tool in moderate to severe TBI and has shown increasing utility for risk-stratifying mild TBI (mTBI), which can be associated with insidious long-term cognitive impairment.

Classification of Traumatic Brain Injury

TBI is most broadly classified based on blunt or penetrating mechanism. This chapter emphasizes issues pertaining to the imaging of TBI from blunt head trauma. TBI may be intra- or extraparenchymal ; intraaxial injuries are further subdivided as focal or diffuse, the former occurring more commonly from falls in the elderly and the latter in high-velocity traffic accidents. Injury may be primary, resulting directly from external forces and structural strain to cerebral tissue at the time of the traumatic event, or secondary, representing evolution of the primary injury as well as consequences and complications of increased intracranial pressure (ICP).

Mechanism of Injury—Primary TBI

Intraaxial Lesions

Diffuse Axonal Injury, Contusions, and Intracerebral Hematomas.

TBIs usually results from either deceleration impact or impulsive acceleration and deceleration forces (e.g., “whiplash”), which cause variable degrees of compression, tension, and shear. Shear stress is caused by differential acceleration between peripheral and central portions of the brain with respect to the axis of rotation (often about the fulcrum of the cervical spine or from wave propagation through the head after direct impact. Diffuse axonal injury (DAI) is seen in approximately half of severe TBI cases and refers to the microstructural damage to white matter tracts resulting from shear injury. Injury occurs primarily at interfaces of different density such as the gray-white matter junction and the corpus callosum, and also tends to cluster where the brain can collide and splay out against dural reflections such as the falx and tentorium. This may account for the predilection of DAI to the midline of the splenium and the dorsolateral midbrain ( Fig. 13-1 ). Generally the more central the injury, the greater the overall severity, and severity is greatest when the midbrain or brainstem is involved. Contusions occur in approximately 45% of patients with TBI. Coup contusions are relatively common in falls that result in lateral and occipital blows to the calvarium. These are sometimes seen deep to the margins of depressed skull fractures ( Fig. 13-2 ). Because coup contusions tend to involve the cortex immediately subjacent to the point of impact, as in DAI, contusions extending more centrally also tend to be more severe. Stress waves resulting from motion of the buoyant brain against the fixed inelastic calvarium and skull base account for the frequent presence of both coup and contrecoup contusions. Contrecoup contusions are usually more severe and are also more common than coup contusions, possibly owing to cavitation effects as the brain reflects off the inner table of the skull and the gliding movement of the undersurface of the brain over the rough surface of the anterior and middle cranial fossae. This also explains the susceptibility of the orbitofrontal regions (especially the gyrus rectus) and anterior inferior temporal lobes to contrecoup contusions ( Fig. 13-3 ). Intraparenchymal hematomas involving deeper structures such as the thalamus, basal ganglia, hippocampus, and parahippocampal regions are distinct from cortical contusions, and like DAI can result from shear strain or may be caused by compression against the tentorium after blows to the vertex.

FIG 13-1

Axial FLAIR images show high signal in the splenium ( A ) and dorsolateral midbrain ( B ) in a 21-year-old woman following a motor vehicle accident.

FIG 13-2

Axial noncontrast CT of the head shows a depressed comminuted “eggshell”-type right parietal skull fracture ( A ) in a 28-year-old unhelmeted man after a motorcycle collision. B, A right parietal coup contusion is seen deep to the depressed skull fracture (arrow).

FIG 13-3

This 37-year-old male pedestrian was struck by a vehicle. On CT ( A ), a left posterior temporal coup contusion is seen, with edema and hemorrhage resulting in a typical “salt-and-pepper” appearance (white arrow). Hemorrhagic contrecoup contusions involve the gyri recti (black arrows). B, On the axial FLAIR image, nonhemorrhagic cortical contrecoup contusions are also demonstrated, involving the bilateral anterior inferior temporal lobes (arrows). Previously described coup-contrecoup contusions are also seen to better advantage on this image.

Extraaxial Lesions

Tensile failure of bridging veins that extend from the subarachnoid perivascular spaces to the dura accounts for the high frequency of subdural hematomas (SDH), particularly in the elderly and in children, where the vessels are maximally preloaded as a result of increased extraaxial space. The subdural space is normally occupied by fluid similar to cerebrospinal fluid (CSF). Because of this, the greatest amount of motion occurs in the subdural space, predisposing bridging veins to shearing. SDHs tend to spread out along the entire hemisphere because there is very little attachment between the inner leaflet of the dura and the arachnoid ( Fig. 13-4 ). SDHs sometimes occur as a result of isolated impulsive forces without impact for this reason. Tearing of cortical veins resulting in SDH often occurs in the same distribution as coup and contrecoup contusions, and like contusions, a large proportion of SDHs, epidural hematomas (EDHs), and subarachnoid hemorrhage (SAH) result from lateral blows.

FIG 13-4

The patient in Figure 13-3 had a hyperdense holohemispheric left subdural hematoma (arrow) on the same side as the coup contusion. There is associated bulk hemispheric swelling and subfalcine herniation (rightward shift) measuring more than 1 cm.

Knowledge of the anatomy of fluid spaces and the relationship of the meningeal layers to the brain surface and inner table of the skull is important to understand common appearances of different extraaxial hemorrhagic lesions. The pia lines the cortical gyri as well as perforating vessels (bridging veins), forming a perivascular space (Virchow-Robin space) that communicates with the subarachnoid space, lying between the arachnoid and pia. SAH can result from laceration of small cortical, pial, or subarachnoid vessels in the subarachnoid space, or the pial/subarachnoid portions of bridging veins. SAH may also result from transependymal diffusion of intraventricular hemorrhage (IVH) if the ependyma lining the ventricles is compromised, from direct migration through the ventricular outflow foramina, from direct extension of hemorrhage within a cortical contusion, from SDH with arachnoid tear, and from EDHs with dural and arachnoid tears.

EDHs are more closely correlate with skull fractures than SDH and often occur in the temporoparietal region because the middle meningeal artery, which runs within a groove in the inner table of the squamous temporal bone, or its branches are the usual source of bleeding. The dura is a two-layer membrane with an inner meningeal layer and outer periosteal layer that is tightly bound to the skull. The two layers encase the venous sinuses. The epidural space is a potential space between the periosteal layer of the dura and inner table of the skull. The periosteal layer of the dura is tightly adherent to the inner table, particularly at the sutures, preventing most EDHs from crossing sutural margins ( Fig. 13-5 ). Small EDHs without clinical deterioration can be treated conservatively but need to be followed closely because approximately one quarter enlarge within 36 hours after injury, usually within the first 5 to 8 hours ( Fig. 13-6 ). IVH may result from shearing of subependymal veins during rotational acceleration, direct extension from parenchymal hematoma, or from retrograde migration through ventricular outflow foramina.

FIG 13-5

A, Left parietal epidural hematoma confined by the lambdoid suture posteriorly and coronal suture anteriorly in a 21-year-old following a motor vehicle accident. B, Oblique off-axial nondepressed fracture is shown on thin-section coronal CT image (arrow), traversing the left parietal bone, overlying the epidural hematoma.

FIG 13-6

A, A 16-year-old with right frontal epidural hematoma measuring 1.3 cm in thickness after being hit in the head by a falling tree limb. B, Because the hematoma contained an area of low density representing active bleeding, a follow-up CT was performed 2 hours later. On this study, the hematoma had increased in size, now measuring 1.7 cm, and new areas of low density indicating continued active bleeding were seen. C, Postoperative changes of craniotomy for evacuation of the hematoma. Two burr holes are seen at the anterior and posterior margins of the craniotomy on this axial image. To create the craniotomy flap, burr holes are first made and connected with a craniotome. These were sealed with burr hole covers (solid arrow). There is a subgaleal drain (open arrow), subgaleal gas, swelling, and overlying skin staples in keeping with immediate postoperative changes.

Mechanism of Injury—Secondary TBI

TBI is not a one-time event but rather a continuously progressive injury. Secondary brain injury may refer to the evolution and enlargement of the primary injury around a “traumatic penumbra” (analogous to the ischemic penumbra in stroke) ( Fig. 13-7 ), or it may refer to the potentially preventable consequences of resultant mass effect and elevated ICP, including herniation, ischemia and infarction, and global hypoxic injury. Secondary brain injury is responsible for over 50% of deaths related to trauma within the first 48 hours after injury. Brain swelling after TBI can be the result of both cytotoxicity and vasogenic edema, which have a synergistic effect. The initial mechanical disruption results in cellular damage and cytotoxicity that progresses throughout the first week after injury. Ischemic damage after primary brain injury is most commonly perilesional, resulting from impaired cerebral perfusion and oxygenation, excitotoxic injury, focal arterial or venous microthrombi, and vasospasm. On a cellular level, traumatic injury induces a vicious cycle beginning with the release of excitatory neurotransmitters such as glutamate, which causes a massive influx of calcium and sodium into neurons, leading to cellular swelling, mitochondrial dysfunction, free radical production, and calcium-mediated proteolysis. This in turn leads to ischemic and apoptotic cell death and more neurotransmitter release. Although cytotoxic edema appears to be the primary cause of cerebral swelling after TBI ( Fig. 13-8 ), the blood-brain barrier typically becomes compromised, leading to some degree of vasogenic edema. Mass lesions and swelling cause increased ICP, with resulting herniation that can occlude vessels and cause territorial infarction ( Fig. 13-9 ). During the subacute period after the initial injury, microglial cells enter areas of focal injury and phagocytize blood products and damaged tissue. A cavitary area of encephalomalacia lined by glia results ( Fig. 13-10 ). Small lesions may heal only with a glial scar. The overall effect is widespread volume loss beyond any focal area of TBI.

FIG 13-7

A, CT of a 51-year-old with TBI after a fall. SDH, SAH, and bifrontal hemorrhagic contusions (right greater than left) are displayed. B, On follow-up CT the bifrontal contusions have both increased in size. Worsening mass effect from enlargement of contusions and SDH necessitated a wide decompressive craniectomy to allow brain parenchyma to herniate through the defect. Notice that there is essentially no midline shift after the wide craniectomy. C, On the T2-weighted MR image the corresponding mixed–signal intensity appearance is typical of hemorrhagic bifrontal contusions. Low signal intensity corresponds with acute blood product.

FIG 13-8

A, Nonhemorrhagic contusions in the frontal and temporal regions are difficult to distinguish from a background of diffuse cerebral edema and extensive SAH at CT in this 38-year-old following a motor vehicle accident. B, T2-weighted image better shows the extensive contrecoup cortical contusions. The suprasellar and quadrigeminal plate cisterns are completely effaced, consistent with uncal and descendant transtentorial herniation, respectively. C, Uncal and transtentorial herniation is seen on sagittal T1-weighted image. Basal cisterns are completely obliterated. D, DWI shows lesional and perilesional cytotoxic edema in and around the regions of contusion. E, Corresponding low ADC in the contused areas confirms the high signal on DWI is from cytotoxicity rather than T2 shine-through, which would be seen in vasogenic edema. Restricted diffusion due to concurrent DAI is also seen in the corpus callosum.

FIG 13-9

This 36-year-old bicyclist was struck by an automobile. A, At CT, extensive bilateral contusions were shown to result in complete effacement of the suprasellar cistern from uncal herniation (white arrows) and near-total obliteration of the quadrigeminal plate cistern (black arrow) from descendant transtentorial herniation. This resulted in infarction of the superior right cerebellar hemisphere from compression of the superior cerebellar artery, which arises near the tip of the basilar artery and courses around the midbrain. B, DWI shows infarct of the superior right cerebellar hemisphere, resulting from compression of the superior cerebellar artery from uncal and descendant transtentorial herniation. The infarct may have also been caused by vasospasm from large central subarachnoid hemorrhage. C, At ADC, an area of low signal intensity corresponding with the territory of high signal on DWI is seen, confirming infarct.

FIG 13-10

Evolving encephalomalacia replacing contrecoup contusions in a 41-year-old woman after motor vehicle collision (arrow). There is associated ex vacuo dilation of the right temporal horn.

Indications for Imaging

The Glasgow Coma Scale (GCS) is a ubiquitously used scoring system for clinical grading of TBI severity, with eye, verbal, and motor components added to give a sum score ranging from 3 to 15. The lowest score in the first 48 hours is used to classify TBI. Scores of 13 to 15 correspond with mild TBI, scores of 9 to 12 with moderate TBI, and scores of 3 to 8 with severe TBI. In practice, the GCS can falsely suggest brain injury in the setting of intoxication, sedation, or paralysis. Another limitation is that most patients with TBI have mild injuries and may exhibit residual neurocognitive sequelae despite having normal or near-normal GCS scores. Nevertheless, the GCS serves as a useful triage tool for determining the need for CT. CT is generally indicated for severe and moderate TBI (GCS < 13). Some argue for imaging any patient with a GCS below 15, even though less than 20% of patients with minor head trauma have positive findings on CT and only up to 5% require intervention. Additional factors, such as high-velocity mechanism, contribute to the likelihood of positive CT findings even when GCS scores are normal. Other predictors used to determine the need for head CT in otherwise clinically mild head injury include risk factors such as advanced age (>60-65 years), loss of consciousness greater than 5 minutes, worsening level of consciousness, failure to improve over time, periods of transient amnesia or confusion, and headache with episodes of vomiting. Scanning should be performed more liberally in those on anticoagulation therapy or with bleeding diatheses and should be routinely performed for depressed skull fractures. CT is also important in allowing the neurosurgeon to clear patients prior to surgical treatment of non–life-threatening extracranial injuries. In unconscious patients, fixed dilated pupils are a sign of herniation requiring urgent imaging and decompression. Deteriorating mental status and delayed development of coma may reflect evolving secondary injury with worsening ICP and herniation or brainstem compression. DAI, which may not be apparent on CT, can also be the sole source of posttraumatic coma.

Because of the time, resources, and logistics involved in MR scanning, particularly in polytraumatized patients with anesthetic and monitoring equipment, CT has long been used as the workhorse to screen patients for prognostic indicators for surgical intervention and for following the dynamics of lesion development, although MRI remains an important problem-solving tool. Any focal lesions detected on CT, regardless of size, require follow-up CT scanning. New lesions will arise in around 15% of patients, and 25% to 45% of cerebral contusions will significantly enlarge (see Fig. 13-7 ). CT progression generally occurs within 6 to 9 hours after injury. CT facilitates a preemptive approach in which surgery is used to prevent deterioration rather than treating lesions once neurologic deterioration has already occurred. This strategy has been shown to improve outcome. CT is also used to determine the need for ICP monitoring. In general, ICP should be monitored in all patients with clinical evidence of severe TBI (GCS of 3-8) and any abnormal findings on CT.

Stratifying Injury Severity with CT

CT signs that have been correlated with increased ICP, coma, and death include midline shift greater than 3 to 5 mm (see Figs. 13-4 and 13-5 ), obliterated basal cisterns (see Figs. 13-3, 13-8, and 13-9 ), diffuse hemispheric swelling, SDHs greater than 10 mm in thickness ( Fig. 13-11 ), EDHs greater than 15 mm in thickness (see Figs 13-5A and 13-6B ), SAH, and IVH. Any intracranial mass lesion may warrant surgical evacuation, whether intracerebral hematoma (ICH), hemorrhagic contusion, SDH, or EDH once the size is large enough to cause brain distortion and elevated ICP. SDHs have a higher mortality than acute EDHs, which may seem counterintuitive given that EDHs often have an arterial source. However, the force required to separate the dura from its periosteal attachment to the inner table of the calvarium is considerable, whereas SDHs can continue to increase with little restriction as additional bridging veins tear when stretched beyond their capacity. Significant improvement in mortality is seen when SDHs are evacuated less than 4 hours after injury. Intraparenchymal mass lesions typically result in less mass effect than extraaxial hemorrhagic mass lesions and are less ominous predictors of poor outcome ; contusions or ICHs, however, particularly in elderly patients with low GCS scores, are likely to benefit from prompt intervention. Classification systems relying on mass effect and mass lesions on CT are limited in patients with DAI.

FIG 13-11

A, CT in an 82-year-old after a fall from ladder shows a hemorrhagic contusion in the right frontal region (arrow) , with subdural blood (open arrow) that likely migrated from the contusion through a tear in the arachnoid into the subdural space. The holohemispheric SDH is greater than 1 cm in thickness and is associated with bulk right hemispheric swelling and marked leftward transfalcine herniation. B, Marked transfalcine herniation has resulted in entrapment of the left temporal horn (solid arrow), and there is associated locoregional transependymal spread of CSF (open arrow) .

CT Findings in Primary Injury

Cortical Contusions.

Contusions are common, occurring in 43% of closed head injuries, frequently with coexisting coup and contrecoup injuries, and can be multiple or solitary. Cortical contusions represent bruising and laceration of the brain and primarily involve gray matter. Contusions are often based at the cortical surface and extend toward the center of the brain. On noncontrast CT, contusions appear as peripheral low-attenuation areas with loss of gray-white differentiation, reflecting the combination of cytotoxic edema and vasogenic edema involved. In most cases, some hemorrhage is present at MRI, but this may not be detectable at first with CT. When contusions are nonhemorrhagic on MRI, they may also be difficult to appreciate on CT, with subtle areas of low-density edema ( Fig. 13-12 ). Hemorrhagic contusions may take the form of multiple areas of microhemorrhage interspersed with low density, giving a heterogeneous “salt-and-pepper” appearance (see Fig. 13-3A ), or they may appear as more coalescent areas of hemorrhage, giving a more uniformly hyperdense appearance (see Fig. 13-7B ). As the injury progresses, small hemorrhages may coalesce into larger hematomas.

FIG 13-12

Images of a 37-year-old male pedestrian struck by a car. A, Hypodensity is seen in the bifrontal regions, right (open arrow) greater than left. There is sulcal SAH (solid arrow), but no intraparenchymal hemorrhage is appreciated. B, On FLAIR, nonhemorrhagic cortical contusions corresponding to the areas of low density on CT are visible (open arrow). The acute subarachnoid blood appears as low signal intensity on T2/FLAIR (solid arrow). The round area of low signal intensity in the right frontal region corresponds with an extraventricular drain seen in A . C, On SWI, which is highly sensitive to para- and ferromagnetic substances in blood, the SAH is redemonstrated. Tiny foci of subarachnoid blood are also seen on the right. D, On DWI, cortical contusions are apparent in a wider distribution than what is appreciable on FLAIR.

Intracerebral Hematoma.

Whereas ICHs can result from coalescent hemorrhage in contusions ( Fig. 13-13 ), deeper lesions often result from shear-induced hemorrhage and rupture of small intraparenchymal vessels. Unlike contusions, these often occur in areas of otherwise normal-appearing brain and initially have less surrounding edema. These often occur within frontotemporal white matter, sparing the cortex. Deeper lesions may occur in the basal ganglia, but bleeding in this area may also suggest a possible hypertensive hemorrhage. ICHs can be a marker of concurrent DAI even when typical hemorrhagic foci at the gray-white matter junction are absent on CT ( Fig. 13-14 ).

FIG 13-13

Images of a 70-year-old man after a rollover motor vehicle collision. A, Right frontal intracerebral hematoma (open arrow) resulting from coalescent hemorrhage in a contusion deep to a complex skull fracture (shown with volumetric imaging in B ). There is an overlying SDH, likely resulting from active bleeding arising from the intraparenchymal hematoma, with a relatively low-density area representing liquid blood (solid arrow). There is also scattered SAH. There is a depressed “eggshell” fracture involving the vertex ( B ) and vertically oriented displaced fractures propagating down the frontal and parietal bones on the right.

FIG 13-14

Images of a 68-year-old following a motor vehicle collision. A, CT shows intraparenchymal hematoma with thin halo of edema in the left temporal region, sparing the cortex, and surrounded by otherwise normal-appearing brain parenchyma. B, Low T2 signal within the intraparenchymal hematoma on FLAIR, with surrounding high signal, corresponding with the acute hemorrhage and rim of edema seen at CT. C, On SWI, blooming artifact accentuates the deoxyhemoglobin within the intraparenchymal hematoma. Foci of hemorrhage are also seen at SWI throughout the gray-white junction of the bilateral convexities ( D ), along the septum pellucidum, splenium of the corpus callosum, and within the lateral ventricles ( E ).

Diffuse Axonal Injury.

DAI is thought to be present in over 50% of severe head injuries and in more than 85% of severe head injuries resulting from motor vehicle accidents. The key point to remember is that DAI is more the rule than the exception in severe TBI patients. DAI presents with the classic CT findings of petechial hemorrhage (an indirect sign of axonal injury) in only 10% to 50% of cases ( Fig. 13-15 ). DAI can be appreciated on CT when small hemorrhagic foci are evident, typically occurring at the gray-white junction ( Fig. 13-16 ) and, in more severe cases, in the corpus callosum complex, which includes the septum pellucidum, fornix, and choroid. Hemorrhagic DAI can also occur in the periventricular white matter at the corner of the frontal horns and in the hippocampal and parahippocampal areas, internal capsule, and cerebellum ( Fig. 13-17 ). Common areas of hemorrhage should be examined very thoroughly for minimal lesions.

FIG 13-15

Images of a 20-year-old woman following a motor vehicle collision. CT at the level of the corpus callosum ( A ) and at the level of the basal ganglia ( B ) show no visible foci of hemorrhage, but in A, there are small foci of intraventricular hemorrhage in the occipital horns. C, At SWI, numerous petechial foci of hemorrhage are seen in classic locations, including the septum pellucidum, choroid, and splenium of the corpus callosum. D, More caudally, foci of hemorrhage are also seen in the basal ganglia. E, On conventional T2*GRE, foci of hemorrhage are less conspicuous and fewer in number than at SWI. Several petechial foci are seen in the right basal ganglia and right parahippocampal region. F, On DWI, several nonhemorrhagic foci of DAI are identified in the deep white matter along the bodies of the lateral ventricles (arrows) that were not appreciated on the other sequences. These foci show restricted diffusion on the ADC map ( G ). H, On the FLAIR sequence, CSF is nulled out. The bright signal within the parietal sulci represents subacute subdural blood (arrows). I, The SAH is obscured on conventional T2-weighted imaging because the CSF is also bright.

FIG 13-16

This 22-year-old suffered DAI after a motor vehicle collision. A, At CT, a small hemorrhagic lesion is seen at the parasagittal gray-white matter junction near the vertex (arrow). B, FLAIR shows the more extensive shear injury in this region, most of which was not appreciable on CT. Additional areas of DAI are revealed with FLAIR in the left basal ganglia ( C ), right parahippocampal region ( D [open arrow] ), and dorsolateral brainstem ( D [solid arrow] ). E, Hemorrhage is more conspicuous in the same areas at SWI.

FIG 13-17

A, Several hemorrhagic lesions are seen at the corner of the right frontal horn in a 31-year-old with DAI following motor vehicle collision. B, At SWI, much more extensive hemorrhagic lesions are apparent in the same region at the corner of the right frontal horn, also involving the genu of the corpus callosum. Lesions not apparent on CT are revealed in the left basal ganglia (solid arrow) and fornix (open arrow).

Subdural Hematoma.

In general, the incidence of SDH and EDH is higher when skull fractures are present. SDHs occur along the convexities, tentorium, and falx in descending order of frequency. SDHs follow dural reflections, spreading out along the anterior or posterior falx cerebri and typically the supratentorial aspect of the tentorium cerebelli ( Fig. 13-18 ), which may be symmetric or appear as asymmetric high density ( Fig. 13-19 ). Unlike EDHs, SDHs are not restricted by suture lines. SDHs are usually described as being crescent shaped, in contradistinction to EDHs, which dissect between the dura and inner table, resulting in a biconvex (“lentiform”) appearance. The density of acute SDH is high because of clot formation and retraction (see Fig. 13-7A ). Density is highest in the first week after injury and then gradually decreases with protein degradation and liquefaction. In acute SDHs, heterogeneity can result from active bleeding (see Fig. 13-13A ). SDHs may appear isodense to brain parenchyma in the acute setting if there is severe anemia or trauma-induced coagulopathy or when there is admixture with subarachnoid fluid crossing through an arachnoid tear ( Fig. 13-20 ). Diffuse underlying cortical swelling is common with SDH ; 85% of cases of diffuse swelling and bulk enlargement of a cerebral hemisphere are associated with SDHs.

FIG 13-18

A 19-year-old with TBI following a motor vehicle accident. On CT, acute SDH is seen propagating along the posterior falx ( A [arrow] ), and tentorial leaflets ( B [arrows] ).

FIG 13-19

A 40-year-old woman with TBI following a motor vehicle accident. A, A high-density SDH is seen spreading out along the right tentorial leaflet. Unlike EDHs, SDHs may be indistinct and can blend with SAH, seen in B in the quadrigeminal plate cistern (solid arrow). A small focus of SAH is also seen in the interpeduncular cistern ( B [open arrow] ).

FIG 13-20

Images of a 25-year-old driver of a sedan that was “run over” by a tractor trailer. The patient sustained injury to multiple body regions and large-volume resuscitation. A, A thin isodense right SDH is barely perceptible on head CT, even with the use of low-level wide window settings, which accentuate subdural blood. There is resultant bulk hemispheric swelling on the right, resulting in a 3-mm leftward midline shift. B, An image from the arterial phase neck CT is shown. There is displacement of the cortical vessels away from the inner table of the calvarium (arrows). C, On the contralateral side, vessels extend all the way to the inner table (arrow).

Epidural Hematoma.

EDHs are relatively uncommon, occurring in approximately 4% of head trauma patients. EDHs mostly occur in young adults. In the elderly, the dura is more strongly affixed to the skull, and in children, plasticity of the calvarium mitigates against EDH. In 91% of EDHs, a skull fracture is seen on CT (see Fig. 13-5 ). EDH typically occurs at the site of impact (coup site) in contradistinction to SDH. As EDHs dissect along the tightly adherent inner table and dura, the shape formed by the leading edges is well defined. As with SDH, mixed density may indicate active bleeding. Areas of often central and irregular low density within hyperdense hematoma, representing admixture of liquid blood and fresh clot, has been termed swirl sign. Low-density liquid blood can also occur eccentrically or peripherally (see Figs. 13-5 and 13-6 ). Low-density liquid blood with an EDH is associated with massive hemorrhage and poor outcome. Unlike SDHs, EDHs cross dural reflections. EDHs usually do not cross suture lines unless the sutures themselves are disrupted or diastatic ( Fig. 13-21 ). The sagittal sutural line is an exception because the dura is not as tightly attached to the periosteum as it is elsewhere ( Fig. 13-22 ). Occipital EDHs, often venous in origin, can extend both across the midline and above and below the tentorium ( Fig. 13-23 ), whereas SDHs are restricted by dural reflections ( Fig. 13-24 ). Venous EDHs may cause the dural sinuses to be displaced away from the inner table of the calvarium (see Fig. 13-21C ). Venous EDHs (representing only 15% of EDHs overall) typically occur in three locations: the posterior fossa from torcular injury, middle cranial fossa from sphenoparietal sinus injury, and vertex from injury to the superior sagittal sinus. Venous EDH also occurs in the regions of the transverse and sigmoid sinuses. These EDHs tend to enlarge less quickly than arterial EDHs.

FIG 13-21

A 21-year-old after a fall while skateboarding. A, A biconvex epidural hematoma is seen, which crosses the lambdoid suture. An indentation of the dura (arrow) is seen immediately over the suture, likely representing the prior point of sutural attachment. B, Diastatic lambdoid suture is shown on bone window (arrow). C, CT venogram shows a distorted extrinsically narrowed left transverse sinus displaced off the inner table of the calvarium (arrow), with overlying (likely venous) EDH and sutural diastasis.

FIG 13-22

A 21-year-old after a fall from height. A, EDH is seen over the vertex on coronal CT. B, This crosses the midline and results in sagittal suture and coronal suture diastasis, seen on volumetric 3D CT image.

FIG 13-23

This 17-year-old sustained an occipital bone fracture after a fall from height and was found to have an EDH ( A ), which enlarged on short-interval follow-up CT ( B ). The EDH extended above ( A ) and below ( B ) the tentorium. Areas of low density correspond with active bleeding.

FIG 13-24

A, Occipital SDH in a 71-year-old woman after a fall from standing. Unlike occipital EDHs, SDHs do not cross dural reflections. B, Sagittal reformatted image shows the SDH coursing along the inferior aspect of the tentorium.

Intraventricular Hemorrhage.

IVH is uncommon, occurring in approximately 3% of newly diagnosed cases of TBI, but it contributes significantly to morbidity and mortality, with half of patients with IVH developing increased ICP, and 10% requiring ventricular drainage. IVH usually appears as a hyperdense blood-fluid level layering dependently in the ventricular system. In small hemorrhages this can be subtle, with punctate foci appearing in the tips of the occipital horns (see Fig. 13-15A ). Occasionally IVH may appear tumefactive as a cast within the ventricle ( Fig. 13-25 ).

FIG 13-25

TBI and skull base fracture in a 28-year-old following a motorcycle collision. Patient had previously undergone decompressive frontotemporoparietal craniectomy. Two weeks after the initial injury, he developed delayed intraparenchymal hematoma ( A ) and substantial IVH, which formed casts within the lateral, third, and fourth ventricles. B, Tumefactive IVH in the third ventricle is shown (arrow). C, A repeat CT angiogram revealed the source of hemorrhage to be a newly formed pseudoaneurysm of the right anterior cerebral artery (arrow). D, Skull base fracture extending through the sphenoid is shown.

Subarachnoid Hemorrhage.

SAH occurs in 40% of cases of moderate to severe head injury and is usually associated with other types of intracranial hemorrhage. The volume of extravasated blood is rarely as large or extensive as in aneurysmal SAH and more often has a peripheral distribution, sometimes adjacent to areas of cortical contusion. Acute SAH is readily identified on noncontrast CT as linear and serpentine areas of high attenuation extending into and con­forming to the cerebral sulci and sylvian fissures without mass effect ( Fig. 13-26 ; see also Fig. 13-12A ). SAH along the convexity, tentorium, or falx can be difficult to differentiate from SDH. Small foci of SAH at the interpeduncular cistern may be easily missed without conscious attention to this area (see Fig. 13-19B ). Although SAH is usually associated with other findings, it may be the sole finding in a minority of cases. In the subacute setting, SAH becomes isodense and may be very subtle; effacement of sulci may be the only imaging clue. The reason for increased mortality is uncertain but is hypothesized to be related to vasospasm.

Aug 20, 2019 | Posted by in MAGNETIC RESONANCE IMAGING | Comments Off on Traumatic Brain Injury

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