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  M OUNT  S INAI  J OURNAL OF  M EDICINE  76:145–162, 2009  145 Neuroimaging of Traumatic Brain Injury  Tuong H. Le, MD, PhD, and Alisa D. Gean, MD Department of Radiology, Brain and Spinal Cord Injury Center, San Francisco General Hospital, SanFrancisco, CA  ABSTRACT In this article, the neuroradiological evaluation of traumatic brain injury is reviewed. Different imag-ing strategies in the assessment of traumatic braininjury are initially discussed, and this is followedby a review of the imaging characteristics of both primary and secondary brain injuries. Com-puted tomography remains the modality of choicefor the initial assessment of acute head injury because it is fast, widely available, and highly accu-rate in the detection of skull fractures and acuteintracranial hemorrhage. Magnetic resonance imag-ing is recommended for patients with acute trau-matic brain injury when the neurological findingsare unexplained by computed tomography. Mag-netic resonance imaging is also the modality of choice for the evaluation of subacute or chronictraumatic brain injury. Mild traumatic brain injury continues to be difficult to diagnose with cur-rent imaging technology. Advanced magnetic reso-nance techniques, such as diffusion-weighted imag-ing, magnetic resonance spectroscopy, and mag-netization transfer imaging, can improve the iden-tification of traumatic brain injury, especially inthe case of mild traumatic brain injury. Furtherresearch is needed for other advanced imagingmethods such as magnetic source imaging, singlephoton emission tomography, and positron emis-sion tomography.  Mt Sinai J Med 76:145–162,2009.  © 2009 Mount Sinai School of Medicine   Address Correspondence to: Alisa D. Gean, MD Department of Radiology Brain and Spinal Cord Injury CenterSan Francisco General HospitalSan Francisco, CAEmail: Key Words:  brain herniation, cerebral edema, dif-fuse axonal injury, epidural hematoma, intracerebralhematoma, intraventricular hemorrhage, subarach-noid hemorrhage, subdural hematoma, traumaticbrain injury. Traumatic brain injury   (TBI) refers to an injury to the intracranial structures following physicaltrauma to the head. The term  head injury   is preferred when we are addressing injuries that encompassboth intracranial and extracranial structures, includingthe scalp and skull. Clinical classification of theseverity of TBI is usually based on the Glasgow Coma Scale (GCS; mild: 12  >  GCS  ≤  15; moderate:8  >  GCS  ≤  12; severe: GCS  ≤  8). 1 In theneuroradiological evaluation of head trauma, TBIis usually classified into primary and secondary injuries (Table 1). Primary injuries are the directresult of trauma to the head. Secondary injuriesarise as complications of primary lesions. Thisclassification is important because secondary injuriesare potentially preventable, whereas primary injuries,by definition, have already occurred by the time thepatient first presents for medical attention. TBI canbe further divided according to location (intra-axialor extra-axial) and mechanism (penetrating/open orblunt/closed). The goal of neuroimaging is to identify treatable injuries to prevent secondary damage and toprovide useful prognostic information. In this article,a discussion of the different imaging options for TBIis followed by a review of the imaging characteristicsof primary and secondary TBI. METHODS  A search was performed at (National Center for Biotechnol-ogy Information and National Library of Medicine)using ‘[Text Word]’ search with the search terms  trau-matic  AND  brain , AND ‘[Title]’ search with searchterm  imaging  , which resulted in 240 articles pub-lished in English since 1978. Among these 240 articles, Published online in Wiley InterScience ( ©  2009 Mount Sinai School of Medicine  146  T. H. L E AND  A. D. G EAN : N EUROIMAGING OF  T RAUMATIC  B RAIN  I NJURY   Table 1.  Imaging Classification of Traumatic Brain Injury  .Primary injury Extra-axial injury Epidural hematomaSubdural hematomaSubarachnoid hemorrhageIntraventricular hemorrhageIntra-axial injury  Axonal injury Cortical contusionIntracerebral hematoma Vascular injury DissectionCarotid cavernous fistula Arteriovenous dural fistulaPseudoaneurysmSecondary injury  AcuteDiffuse cerebral swelling/dysautoregulationBrain herniationInfarctionInfectionChronicHydrocephalusEncephalomalaciaCerebrospinal fluid leakLeptomeningeal cyst 39 were review articles. Abstracts from the 240 arti-cles were examined. Selected articles from the 240abstracts and key articles referenced by some of theselected articles, relevant to the objectives of ourarticle, were reviewed. These articles include bothpediatric and adult populations.Most images published in our article werederived from the Teaching File Server (, which is the property of the Departmentof Radiology, University of California. Images on theserver have been submitted over the years by theattendings, fellows, and residents in the Departmentof Radiology at Moffit-Long Hospital, the VA MedicalCenter, and San Francisco General Hospital. Patientdemographics were removed in compliance with theHealth Insurance Portability and Accountability Act. IMAGING OPTIONS Skull Films Skull films are poor predictors of intracranialpathology and should not be performed to evaluateTBI. 2–4 In mild TBI, skull films rarely demonstratesignificant findings. In severe TBI, the lack of abnormality on skull films does not exclude majorintracranial injury. 5 Negative findings may evenmislead medical management. Patients who are athigh risk for acute intracranial injury must be imagedby computed tomography (CT). Computed Tomography  CT is indicated for moderate and severe TBI (GCS ≤  12) and for patients with mild TBI and agegreater than 60 years, persistent neurological deficit,headache or vomiting, amnesia, loss of consciousnesslonger than 5 minutes, depressed skull fracture, pene-trating injury, or bleeding diathesis or anticoagulationtherapy. 6–12 CT is the modality of choice because itis fast, widely available, and highly accurate in thedetection of skull fractures and intracranial hemor-rhage. Life-support and monitoring equipment can bemore easily accommodated in the CT scanner suitethan in the magnetic resonance (MR) suite. In addi-tion, CT is superior to magnetic resonance imaging(MRI) in revealing skull fractures and radio-opaqueforeign bodies. Intravenous contrast administrationshould not be performed without a prior noncontrastexamination because contrast can both mask andmimic underlying hemorrhage. In suspected vascu-lar injury, CT angiography can be performed at ahigh (submillimeter) resolution, especially on mul-tidetector CT. However, even with the tremendousadvances in CT over the last 3 decades, the majority of mild TBI cases still show no visible abnormality on CT. 13 Magnetic Resonance Imaging  MRI may be indicated in patients with acute TBI whenthe neurological findings are unexplained by the CTfindings. MRI is also the preferred imaging modality for subacute and chronic TBI. MRI is comparable toCT in the detection of acute epidural hematoma(EDH) and subdural hematoma (SDH). 14,15 How-ever, MRI is more sensitive to subtle extra-axialsmear collections, nonhemorrhagic lesions, brain-stem injuries, and subarachnoid hemorrhage (SAH) when fluid attenuated inversion recovery (FLAIR) isused. 16,17 Fluid Attenuated Inversion Recovery  FLAIR imaging improves the detection of focalcortical injuries (eg, contusions), white mattershearing injuries, and SAH by suppressing the brightcerebrospinal fluid (CSF) signal typically seen onroutine T2-weighted images. Sagittal and coronalFLAIR images are particularly helpful in the detectionof diffuse axonal injury (DAI) involving the corpuscallosum and the fornix, 2 areas that are difficultto evaluate on routine axial T2-weighted images.DOI:10.1002/MSJ  M OUNT  S INAI  J OURNAL OF  M EDICINE  147 However, an abnormally high signal in the sulciand cisterns of ventilated patients receiving a highinspired oxygen fraction ( > 0 . 60) can be observed inuninjured patients and should not be mistaken forhemorrhage. 18 Gradient-Recalled-Echo T2 ∗ -Weighted Magnetic Resonance Imaging  Gradient-recalled-echo (GRE) T2 ∗ -weighted MRI ishighly sensitive to the presence of ferritin andhemosiderin, 2 breakdown products of blood. Thepresence of hemosiderin and ferritin alters the localmagnetic susceptibility of tissue, resulting in areas of signal loss on GRE T2 ∗ -weighted images. Becausehemosiderin can persist indefinitely, its detectionon GRE T2 ∗ -weighted images allows for improvedevaluation of remote TBI. Unfortunately, GRE imagesare limited in the evaluation of cortical contusionsof the inferior frontal and temporal lobes because of the inhomogeneity artifact induced by the paranasalsinuses and mastoid air cells. This limitation is evenmore problematic at higher magnetic field strengthsunless parallel imaging is used. 19,20 Diffusion-Weighted Imaging  Diffusion-weighted imaging (DWI) measures therandom motion of water molecules in brain tissue.Because of its improved sensitivity to foci of acuteshearing injury, DWI has been particularly useful forthe detection of DAI. 21–24 DWI reveals more DAIlesions than fast spin-echo T2-weighted or GRE T2 ∗ - weighted images in patients imaged within 48 hoursof injury. The apparent diffusion coefficient, whichmeasures the magnitude of water diffusion averagedover a 3-dimensional space, is often reduced in acuteDAI. The fractional anisotropy, which measures thepreferential motion of water molecules along the white matter axons, is frequently reduced in chronicDAI. The integrity of white matter tracts can beevaluated with diffusion tensor imaging. Magnetic Resonance Spectroscopy  Magnetic resonance spectroscopy (MRS) measuresthe relative amount of metabolites in brain tissue.Common neurochemicals that are measured withproton MRS include  N  -acetylaspartate (NAA), crea-tinine (Cr), choline, and myoinositol. In brief, NAA isa marker of neuronal health, and Cr is a marker of energy metabolism. A reduction in the NAA/Cr ratiohas been found in patients with a history of TBI,and this finding has been correlated with a poorerprognosis. 25 Magnetization Transfer Imaging  Magnetization transfer imaging exploits the longi-tudinal (T1) relaxation coupling between bound(hydration) protons and free water (bulk) protons. When an off-resonance saturation (radiofrequency)pulse is applied, it selectively saturates protons thatare bound in macromolecules. These protons sub-sequently exchange longitudinal magnetization withfree water protons. The magnetization transfer ratioprovides a quantitative measure of the structuralintegrity of tissue. A reduction of the magnetizationtransfer ratio correlates with worse clinical outcomein a patient with a history of TBI. 25 Magnetic Source Imaging  Magnetic source imaging (MSI) uses magnetoen-cephalography to localize weak magnetic signalsgenerated by neuronal electrical activity. In 2 stud-ies, MSI showed excessive abnormal low-frequency magnetic activity in mild TBI patients with postcon-cussive syndromes. 26,27 TBI research using MSI hasbeen limited, and the practical application of MSI inthe evaluation of TBI has not been very successful. Single Photon Emission Tomography  Single photon emission tomography (SPECT) is anuclear medicine study that measures cerebral bloodflow (CBF). It can potentially provide a betterlong-term prognostic predictor in comparison withCT or conventional MRI. 28 Specifically, a worseprognosis has been associated with multiple CBFabnormalities, larger CBF defects, and defects thatinvolve the basal ganglia, temporal and parietal lobes,and brainstem. However, SPECT is less sensitive indetecting smaller lesions that are visible on MRI.Therefore, SPECT imaging is complementary for MRI,but not a replacement, in the evaluation of TBI. Positron Emission Tomography  Positron emission tomography measures regionalbrain metabolism with 2-fluoro-2-deoxy-d-glucose.In animal studies, acutely injured brain cells show increased glucose metabolism following severe TBIdue to intracellular ionic perturbation. Following theinitial hyperglycolysis state, injured brain cells show aprolonged period of regional hypometabolism lastingup to months. 29 Human studies in TBI have hadlimited success in demonstrating consistent resultsregarding regional glucose metabolism. Because of the heterogeneous nature of TBI, studies have foundboth hypermetabolism and hypometabolism in thesame regions across different TBI patients. 30 TheDOI:10.1002/MSJ  148  T. H. L E AND  A. D. G EAN : N EUROIMAGING OF  T RAUMATIC  B RAIN  I NJURY  metabolic abnormalities can also be found extendingfar beyond the lesions, especially with SDHs andEDHs. 31 Cortical contusion, intracerebral hematoma,and encephalomacia tend to show more regionalmetabolic abnormalities confined to the specificlesions. PRIMARY EXTRA-AXIAL INJURY IMAGING FINDINGS Epidural Hematoma  EDH develops within the potential space locatedbetween the inner table of the skull and the dura.The developing hematoma dissects the dura fromthe inner table of the skull, forming an ovoid massthat displaces the adjacent brain. Because the EDHis located in the potential space between the duraand inner table of the skull, it rarely crosses cranialsutures, where the periosteal layer of the dura isfirmly attached at sutural margins (Figure 1). At the vertex, where the periosteum is not tightly attachedto the sagittal suture, the EDH can cross the midline.The majority of EDHs are associated with a skullfracture, commonly in the temporal squamosa, wherethe fracture disrupts the middle meningeal artery. 12 Inchildren, EDHs may occur from stretching or tearingof meningeal arteries without an associated fracture.On CT, an acute EDH appears as a well-defined, hyperdense, biconvex extra-axial collection(Figures 2 and 3). Mass effect, sulcal effacement, andmidline shift are frequently seen with large EDHs. An important imaging finding that predicts rapidexpansion of an arterial EDH is the presence of low-density areas within the hyperdense hematoma (theso-called swirl sign), which is thought to represent Fig 1. Coronal diagram of EDH and SDH. The EDH islocated above the outer dural layer (ie, the periosteum),and the SDH is located beneath the inner (meningeal)dural layer. The EDH does not cross sutures. TheSDH does not directly cross the falx or the tentorium.  Abbreviations:  EDH, epidural hematoma; SDH, subduralhematoma. Reprinted with permission from Williams & Wilkins-Lippincott. 44 Copyright 1994, Williams & Wilkins-Lippincott. active bleeding. 32,33 It is an ominous sign that needsto be followed closely. Venous EDHs are less common than arterialEDHs and tend to occur at 3 common locations:the posterior fossa from rupture of the torculaor transverse sinus, the middle cranial fossa fromdisruption of the sphenoparietal sinus (Figure 3),and the vertex from injury to the superior sagittalsinus. 34  Venous EDHs can be difficult to diagnoseon axial CT imaging but are readily confirmed oncoronal reformatted CT images or multiplanar MR images. Subdural Hematomas SDHs usually develop from laceration of bridgingcortical veins during sudden head deceleration. They can also arise from injury to pial vessels, pacchioniangranulations, or penetrating branches of superficialcerebral arteries. Because the inner dural layerand arachnoid are not firmly attached, SDHs arefrequently seen layering along the entire hemisphericconvexity from the anterior falx to the posteriorfalx (Figure 4). In elderly patients with cerebralatrophy, the increase in extra-axial space allows forincreased motion between the brain parenchyma andthe calvarium, resulting in an increased incidence of SDH in these patients. Another cause of SDH is rapiddecompression of obstructive hydrocephalus. In thissetting, the brain surface recedes from the dura morequickly than the brain parenchyma can re-expandafter being compressed by the distended ventricles,and this causes disruption of the bridging cortical veins.On CT, the acute SDH appears as a hyperdense,homogeneous, crescent-shaped extra-axial collection(Figure 5A). Most SDHs are supratentorial andare located along the convexity. They are alsofrequently seen along the falx and tentorium(Figure 5B). Because the SDH is often associated with parenchymal injury, the degree of mass effectseen frequently appears more severe with respect tothe size of the collection.In comparison with a normal brain, the density (attenuation) of the acute SDH is higher becauseof clot retraction. The density of the SDH willprogressively decrease as protein degradation occurs.Rebleeding during the evolution of the SDH appearsas a heterogeneous mixture of fresh blood andpartially liquefied hematoma (Figures 4 and 6). Asediment level or hematocrit effect may be seenfrom rebleeding or in patients with clotting disorders.The chronic SDH has density similar to, but slightly higher than, that of CSF (Figure 6). The chronicSDH can be difficult to distinguish from prominentDOI:10.1002/MSJ
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