Keywords

FormalPara Learning Objectives

  • Review imaging techniques used to help diagnose and evaluate patients with CNS trauma.

  • Compare the utility of CT vs MRI in evaluating TBI patients with a spectrum of brain injuries.

  • Show various forms of surgical vs non-surgical intracranial abnormalities resulting from head trauma.

FormalPara Key Points

  • CT is the primary imaging modality utilized to assess patients following CNS trauma in the urgent setting due to availability, speed, and few contraindications.

  • Initial CT findings can assist in the appropriate triage of patients that require urgent surgical management and those that would benefit from non-surgical monitoring.

  • MRI is useful in patients who suffer from neurologic symptoms out of proportion to initial CT imaging findings and to assist in the detection of brain injuries below the sensitivity of CT.

1 Introduction

Traumatic brain injury (TBI) is a leading health concern with approximately 2.8 million reported emergency department visits in 2014 in the United States. Of these, there is an estimated 288,000 TBI-related hospitalizations and 56,800 TBI-related deaths [1]. The majority of these cases involve elderly adults over age 75 years followed by young children [2] with a global incidence estimate of 100–749 cases per 100,000 [3]. These staggering numbers are themselves likely to be underestimates as mild severity TBI and head injury in developing areas of the world are generally under-reported and others are not counted among emergency room visits as they may be assessed in outpatient clinics. Regardless, medical imaging is crucial for diagnosis, management, and risk stratification of this important public health problem. This article provides an overview of important imaging findings for various TBI classifications as divided by anatomic location, types of injury, and severity as well as imaging findings of trauma-related intervention. Examples provided also showcase different mechanisms of injury and touch on imaging research in the field of TBI. Overall, this review aims to provide a systematic guide for imaging evaluation and interpretation in TBI-related injuries.

2 TBI Clinical Grading

Clinical grading for TBI most commonly uses the Glasgow Coma Scale (GCS), which separates injuries based on three main criteria: eye response (1–4 points), verbal response (1–5 points), and motor response (1–6 points) [4]. Scores are summed and then categorized as mild (13–15), moderate (9–12), and severe (3–8). GCS is shown to be highly correlative with patient morbidity and mortality in the moderate/severe category and helps with initial triage [5]. Despite widespread use across severity categories, GCS is limited in the mild category where a score of 15 does not necessarily indicate an absence of TBI-related symptoms or TBI-related injury. Mild TBI patients may have post-concussive symptoms that are typically self-limited without intervention, although a subgroup can suffer prolonged symptoms.

3 Imaging Use and Techniques

3.1 Computed Tomography (CT)

The essential initial imaging modality for head trauma is non-contrast computed tomography (CT). For moderate to severe TBI, the American College of Radiology (ACR) deems the non-contrast head CT scan a class 1 recommendation [6]. There are several, commonly used medical decision-making tools including the Canadian CT head rule, New Orleans Criteria, and National Emergency X-Radiography Utilization Study II (NEXUS-II) that help to determine whether a CT scan of the head is indicated in the case of mild TBI [7]. The Pediatric Emergency Care Applied Research Network (PECARN) Head Injury Decision Rule (PR) was published in 2009 by the Pediatric Emergency Care Applied Research Network; this rule is applied in pediatric patients to identify those at low risk for clinically important TBI, so that CT scan can be safely avoided and therefore reduce exposure to ionizing radiation.

Benefits of CT over other imaging modalities include speed, availability, and high sensitivity for significant injuries requiring immediate intervention or close observation such as intracranial hemorrhage, infarction, herniation, cerebral edema, and skull fracture [8]. Modern CT scans can be performed within just a few seconds and are readily available at essentially all hospital systems on an emergent basis as well as many satellite care centers. The recommended protocol includes using a multidetector CT (MDCT) with axial views, head tilt/gantry angling to reduce ocular lens radiation exposure, 120 kVP, 240 mAs, 22 cm-field of view, with a 2.5- or 5-mm slice thickness. Radiation exposure and dose have been markedly diminished with advances in CT technology. Modern scanners incorporate the use of automatic exposure control systems to optimize acquisition parameters on an individual basis and advanced techniques for image reconstruction to maintain image quality. Typically, CT images are reconstructed and displayed in a multiplanar way using both soft tissue and bone kernels at ~2.5-mm slice thicknesses. Additional 3D reconstructions may also be performed for the calvarial/skull base with axial 0.625 mm sections. Routine use of multiplanar reconstructed (MPR) images has also been supported in the literature to increase CT accuracy in detecting intracranial hemorrhage, especially adjacent to bony surfaces [9]. Comparison with prior relevant imaging is useful to help accurately identify acute findings.

3.2 Magnetic Resonance Imaging (MRI)

MRI may be considered for patients with persistent neurologic symptoms but absence of positive findings on nonenhanced CT [10]. Compared with CT, MRI has higher sensitivity for detection of small cortical/parenchymal contusions, axonal injury, and can help age intracranial hemorrhage (acute, subacute, chronic) [6, 11,12,13,14,15]. However, emergent MRI is not as readily available in various hospital systems, takes longer to scan, costs more, requires safety screening prior to scanning, and gives rise to some difficulties in patient monitoring and access during the scan. Recommended routine scanning techniques for nonenhanced brain MRI in cases of head trauma include the following: diffusion-weighted (DWI), T2* gradient recall echo (GRE) or susceptibility-weighted imaging (SWI), T2-weighted fluid-attenuated inversion-recovery (FLAIR), and T2-weighted and T1-weighted sequences. Susceptibility-weighted imaging has been shown to have high sensitivity to hemorrhage, significantly higher than the traditional T2* GRE sequences [16], and DWI can be useful in detecting non-hemorrhagic acute axonal injury [17]. Contrast enhancement is not routinely used; however, contrast may be useful to assess arterial and venous vascular injury as well as other types of meningeal injury [18].

3.3 CT or MR Angiography (CTA or MRA)

CTA and MRA are recommended in cases with mechanism of penetrating injury and suspected vascular injury. Such techniques can help detect traumatic pseudoaneurysms, dissection, post-traumatic arteriovenous fistula, venous sinus thrombosis, or other vascular sequela of injury [19,20,21]. Some hemorrhage patterns on imaging may be signs of serious, underlying injuries such as subarachnoid blood isolated to the basilar cistern, sylvian fissure, or anterior interhemispheric fissures as described later.

3.4 Diffusion Tensor Imaging (DTI) and Diffusion Kurtosis Imaging (DKI)

More sophisticated diffusion imaging models including Diffusion Tensor Imaging (DTI) and Diffusion Kurtosis Imaging (DKI) that quantify directional diffusion of water [22] as well as non-Gaussian diffusion [23] can provide information about white matter tracts and other brain tissue microstructure. While diffusion tensor models have been utilized for group-based comparisons in the research arena, there are numerous barriers that have prevented their application in individual patients. For example, DTI has been shown to be very sensitive to axonal microstructural changes; however, the results lack specificity. Changes in mean diffusivity and/or fractional anisotropy may be interpreted as changes in the interrogated white matter microstructural integrity; however, these same types of changes can be visualized in any number of comorbidities or even demographic variation. As a result, accurate and meaningful interpretation of individual DTI examinations is not currently feasible.

3.5 Outcome Prediction with Imaging Parameters

Imaging is essential for patients to help with diagnosis, prognosis, and guiding management for various types of traumatic brain injuries. Initial CT or MRI offers rapid evaluation of brain anatomy and helps guide treatment, follow-up imaging monitors recovery or progression of disease, and additional assessment with more advanced techniques better elucidates specify aspects of brain and cerebrovascular physiology and metabolism. CT perfusion, MR perfusion, SPECT, functional MRI (fMRI), PET, and MR spectroscopy (MRS) are only some of the methods where ongoing research is underway to better understand TBI, identify and monitor injury and recovery, and help better predict long-term effects and outcome [12].

4 Scalp Lesions

Scalp lacerations, hematomas, or other subcutaneous injuries are common in head trauma patients. Although isolated scalp injury is not often clinically significant, there is 20% association with intracranial injuries even in patients with mild TBI [24]. A visible scalp lesion on cross-sectional imaging directs attention to the site of impact for interpreting radiologists and assists in the detection of minor intracranial bleeds, fractures, or contusions [25]. Location and type of scalp blood (caput succedaneum, subgaleal hematoma, subgaleal hygroma, or cephalohematoma) are important to understand the potential for hemorrhage extension (Table 7.1) [26]. Use of CT soft tissue reconstruction kernel can assess scalp abnormalities with appropriate adjustments in image window and level to differentiate density differences between normal tissue, blood, fluid, and fat. Scalp injuries often also provide a visual clue to mechanism of injury and aid in the search for related intracranial injuries (Fig. 7.1).

Table 7.1 Overview of pediatric scalp fluid collections/hematomas
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Fig. 7.1
2 medical scans of the brain and a 3-D reconstructed image of the skull. Left. An arrow points to a bright, extended mass on the left lobe. Center. An arrow points to a dark spot in the left parietal bone. Right. The fracture at the left parietal bone and left squamosal suture are highlighted.

Axial non-contrast head CT demonstrating a small left parietal scalp hematoma (left image, arrow) associated with a subtle underlying non-displaced left parietal bone fracture (center image, arrow) in a young child. 3D volume rendered reconstructions, which increase sensitivity for identifying non-displaced fractures, better depict the linear left parietal bone fracture (right image, arrow) that extends through the left squamosal suture (right image, arrowhead). No intracranial hemorrhage was present

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5 Skull Fractures

Skull fractures may result from both penetrating and blunt trauma and may be categorized in various ways based on mechanism of injury, topography, complications, and management. Classification can be broken down into the following parameters:

  • Shape: linear, comminuted, stellate.

  • Depression: depressed, non-depressed, open.

  • Anatomic location and extent: skull vault, skull base, craniofacial junction.

The most common fracture shape is linear, often seen in the young pediatric population (<5 years old), typically involving the parietal or basilar skull [27]. Extension of the fracture to suture lines can result in suture diastasis. Fracture complications are dependent on location, extent, and depression. Depressed skull fractures are defined by displacement of the inner and outer tables of the skull on either side of the fracture line. Displacement of the outer table on the one side of the fracture line to or beyond the level of inner table on the other side of the fracture line is particularly concerning for additional intracranial complications. These occur primarily in the frontoparietal region and are often open, meaning associated with lacerations more superficially and can result in a host of issues including dural tearing, parenchymal contusions, wound infection, and seizure [28]. Comminuted anterior cranial fossa fractures are also associated most highly with CSF leaks [29]. Venous compromise is seen in two thirds of fractures near the dural venous sinus or jugular bulb and can relate to frank laceration of the sinus, mass effect from adjacent extra-axial hematoma, or dural venous sinus thrombosis [19, 30]. Temporal bone and skull base fractures often have more severe complications such as damage to cranial nerves, the craniocervical junction, and middle and inner ear structures [31].

Patients who sustain skull fractures from head trauma are reported to have a 2–5× increased risk of intracranial hemorrhage compared with those without fracture [25, 32]. CT is more sensitive than either skull radiograph or MRI in the detection of fractures. In particular, the combination of excellent depiction of osseous detail, high resolution, and the ability to render maximum intensity projections and surface rendered 3D reconstructions makes CT an optimal tool for the detection of skull fracture [33, 34] (Fig. 7.2).

Fig. 7.2
2 medical scans of the brain. Left. An arrow points to a fracture at the right parietal bone. Right. An arrow points to a less dense region above the right parietal bone indicating hematoma.

Axial non-contrast head CT demonstrates a focal comminuted depressed posterior right parietal bone fracture (left image, arrow) associated with a small overlying scalp hematoma (right image, arrow) following an assault with a hammer

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6 Extra-Axial Lesions

Trauma may affect four main extra-axial compartments: epidural, subdural, subarachnoid, and intraventricular spaces.

6.1 Epidural Hematoma (EDH)

An epidural hematoma (EDH) is an extracerebral hemorrhagic collection occurring between the superficial dura and inner table of the skull. Because the superficial dura is closely opposed to the inner table, it takes some force to separate them, creating a potential space in which blood may collect. EDHs are commonly associated with fractures that can disrupt and tear the superficial dura, causing damage to meningeal arterial branches embedded in the dura. EDHs classically assume a lenticular shape and typically do not cross suture lines [35, 36] as the dura is invested within the suture. Exceptions to this rule include the vertex EDH that may traverse the sagittal suture as well as pediatric skull fractures with suture diastasis. There is a higher incidence with overlying skull fractures on the same or “coup” side of injury [37,38,39]. CT is the recommended initial imaging modality as it can show both the extracerebral collection and fractures with highest sensitivity. The lentiform or biconcave shape can cause mass effect on the adjacent brain parenchyma as hemorrhage accumulates. Clinically, an EDH may be associated with a lucid window, a period of normal neurological function between the time of injury and neurological deterioration. The so-called swirl sign on CT is associated with active bleeding and is characterized by hypodense non-coagulated blood mixed with hyperdense coagulated blood. This radiologic finding is important to communicate to treating providers as patients may undergo rapid decompensation from active arterial bleeding [33, 39].

While classically associated with arterial bleeding, EDHs can arise from either arterial or venous injuries (Table 7.2). Arterial bleeding is most often from the middle meningeal artery, reported in the temporoparietal region in 75% of cases [38]. Bleeding from arterial injury may result in a rapidly expanding hematoma with progressive mass effect, increased intracranial pressure, and potential infarcts which can be surgical emergencies. Treatment often requires urgent decompressive craniotomy in severe cases or embolization of the middle meningeal artery in non-surgical small−/medium-sized EDH cases (Fig. 7.3). Venous origin of EDH is seen in cases of fractures crossing the dural venous sinuses, and bleeding can be seen on either side of the falx cerebri or tentorium cerebelli [40]. Common locations of venous EDH include the anterior middle cranial fossa, vertex, or occiput resulting from injuries to the sphenoparietal sinus, superior sagittal sinus, and transverse sinus, respectively [38] (Fig. 7.4).

Table 7.2 Epidural versus subdural hematoma common characteristics
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Fig. 7.3
3 medical scans of the brain. Left. An arrow points to a less dense region at the left temporal bone. Center. An arrow points to a hypodense region that is surrounded by a hyperdense region on the left lobe. Right. It highlights the less-dense region, indicating the compression in the sulci.

Axial non-contrast head CT demonstrates a jagged non-displaced left temporal bone fracture (left image, arrow) that lacerated the middle meningeal artery. This fracture is associated with a large acute underlying lentiform epidural hematoma with internal “swirl sign” (central image, arrow) compatible with active internal bleeding. The coronal reformation depicts the mass effect on the left parietal lobe, causing compression of the regional sulci and the left ventricular atrium (right image, arrow) as well as mild right-ward subfalcine herniation

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Fig. 7.4
3 medical scans. Left. An arrow points to a high-intense region at the right occipital bone. Center. It highlights a less dense region below the right occipital bone and a round, bright mass in the left frontal lobe. Right. It highlights a narrow, bright region indicating the right transverse sinus.

Axial reconstructed bone windows from a CT angiogram of the head demonstrate a non-displaced right occipital bone fracture (left image, arrow) that lacerated the right transverse sinus. This fracture is associated with a moderately sized acute underlying venous epidural hematoma (central image, arrow) that compresses the cerebellum, effaces the fourth ventricle, and causes non-communicating hydrocephalus that requires emergent ventricular shunting. The angiographic source images show compression and elevation of the co-dominant right transverse sinus (right image, arrow) by the venous epidural hematoma. Additional note is made of a focal contrecoup hemorrhagic brain contusion within the anteromedial left frontal lobe (central image, arrowhead)

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The location of the EDH is crucial to decision-making and management. For instance, posterior fossa EDH can result in early cerebellar compression, effacement of the fourth ventricle, non-communicating hydrocephalus, and/or brainstem compression necessitating emergent decompressive craniectomy and surgical evacuation [41]. Conversely anterior temporal EDH is often indolent, less likely to expand, and thus may be treated well with non-surgical stabilization and monitoring [42].

6.2 Subdural Hematoma (SHD)

Subdural hematomas (SDHs) are extracerebral hemorrhagic collections located between the dura and arachnoid membranes. They often arise from tears in bridging cortical veins at the site of crossing the dura. SDH is common in head trauma and seen in up to a third of cases [37]. They are often found on the opposite or contrecoup side of injury and are not generally associated with skull fractures [38]. SDH collections cross sutures but are limited by dural reflections such as the falx or tentorium, giving them the classic concave or crescentic shape [43] (Fig. 7.5).

Fig. 7.5
2 C T scans of the brain. Left. Arrows point to a crescent-shaped, less-dense region under the dura mater on the temporal lobes of both sides, indicating the hematoma. Right. The arrows highlight the less dense region on both sides of the pons.

Axial non-contrast head CT demonstrates bilateral crescentic acute SDHs, larger on the right (left image, arrows) causing regional mass effect, sulcal effacement, and mild ventricular compression, without frank subfalcine herniation. Coronal reformations show the SDHs extending inferiorly along the cerebellar tentorium (right image, arrows)

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The imaging appearance of SDHs may range from hyper to hypoattenuating crescentic collections along the inner table of the calvarium. Although acute bleeds are mostly hyperattenuating, mixed iso- or hypoattenuating blood is not always chronic and may represent hyperacute or unclotted blood, particularly in patients with underlying coagulopathies [44]. Looking for layering hematocrit levels can help identify such patients. MRI has better sensitivity in staging the time of bleed especially for subacute/chronic blood products as hemoglobin becomes deoxidized, denatured, and enters the extracellular space. A large meta-analysis comparing CT and MRI appearances showed hyperattenuating SDH after a median of 1–2 days; isoattenuation SDH after 11 days; and hypoattenuating SDH after 14 days [45]. Subacute bleeds have T1 and T2 hyperintense signal on MRI due to presence of extracellular methemoglobin [46]. Chronic SDH may have variable signal and may retain T1 or FLAIR hyperintensity depending on age and internal rebleeding. These chronic collections may also develop enhancing, capillary-rich membranes that help to resorb blood [46]. The vascular membranes are often friable and can lead to development of repeated internal hemorrhage resulting in “acute on chronic” bleeding with mix signal intensity and a complex appearance [47]. Peripheral calcifications may also form in the chronic state.

Subdural hygromas are acute low density extra-axial collections that can mimic chronic subdural hematomas. However, the etiology of hygromas is different since they result from arachnoid damage/tearing causing CSF accumulation in the subdural space. Low density hygromas may occur immediately with trauma but most reports show development days following the initial insult [48, 49] (Fig. 7.6). Hygromas also displace the cortical veins in the subarachnoid space from the inner table of the skull; this finding is particularly important for their diagnosis, as the fluid will be isoattenuating and isointense relative to CSF on CT and MRI, respectively. A combination of subdural hematoma and hygroma (hematohygromas) may also occur, most commonly in children, and the two can be difficult to distinguish on imaging.

Fig. 7.6
2 medical scans. Left. It highlights the less-dense regions indicating the hemorrhage. Right. It highlights the dark region below the dura mater on both sides of the brain, indicating hygromas and a small, less dense spot in the right frontal lobe.

Coronal non-contrast head CT performed on an elderly patient immediately following a fall demonstrates scattered regions of post-traumatic subarachnoid hemorrhage along the right cerebral convexity (left image, arrow) and a small subcortical hemorrhagic axonal injury at the left frontal gray-white interface (left image, arrowhead). The follow-up coronal non-contrast head CT performed the next day again demonstrates stable right frontal subarachnoid hemorrhage and a mild interval increase in the subcortical hemorrhage in the left frontal lobe (right image, arrowhead). In the interim, small bihemispheric subdural hygromas have developed most likely related to occult arachnoid tears (right image, arrows)

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Management for SDHs depends on size of bleed with common surgical techniques such as burr hole drainage, craniotomy, or port system placement [50]. For smaller and recurrent bleeds, middle meningeal artery embolization may be considered [51]. Differences in imaging features between subdural and epidural hematomas are detailed in Table 7.2.

In pediatric patients, abusive head trauma (AHT) can result in multicompartmental intracranial hemorrhage, classically manifesting as hemorrhages with blood products of varying age, indicating repeated head trauma. Subdural hematomas with internal membranes are particularly characteristic in babies suffering from AHT, usually associated with brain infarctions and retinal hemorrhages. However, non-contrast CT scans are relatively unreliable in determining the age of blood products within subdural hematomas and therefore simply reporting the attenuation of these hematomas rather than attempting to determine their age at initial examinations may be more prudent. Change in the attenuation characteristics of a subdural hemorrhage over time may be more valuable in deciphering the age of the hematoma. AHT should also consider when the clinical history and degree of injury severity are highly discordant. If AHT is suspected, survey imaging of the rest of the body should be pursued to look for prior fractures and other injuries and careful history should be done. Important to note that pediatric patients such as those with coagulopathy or connective tissue disorder can be prone to repeated bleeds and confound diagnosis. When considering AHT, underlying disorders must be excluded carefully.

6.3 Traumatic Subarachnoid Hemorrhage (SAH)

Subarachnoid hemorrhage (SAH) after head trauma has a reported incidence of 9–25 cases per 100,000 people annually [52, 53]. This occurs when bleeding is seen between the arachnoid and pia matter usually at the site of injury (coup) (Fig. 7.7) or site opposite of the injury (contrecoup). CT imaging shows nodular or curvilinear foci of hyperattenuation typically along the convexity sulci with decreasing intensity as blood products redistribute over time and are cleared through the arachnoid granulations [54]. On MRI, failure of the normal CSF suppression on T2-weighted FLAIR sequences is useful to detect superficial SAH while SWI can detect the presence of superficial siderosis indicative of prior SAH with hemosiderin staining of the pial surface of the brain. SWI is also sensitive for the detection of central SAH in the basilar cisterns, interpeduncular fossa, or within the ventricles with high sensitivity where T2-weighted FLAIR can be somewhat limited due to pulsation artifact [55]. In general, the presence of SAH without other forms of intracranial hemorrhage has less risk of rapid clinical deterioration and need for surgical intervention [56]; however, midline SAH (interhemispheric or peri-mesencephalic) has been reported to have worse outcomes and can be associated with diffuse axonal injury [57].

Fig. 7.7
2 C T scans of the brain. An arrow and an arrowhead in both scans point to a small and large, less-dense region, indicating the hematoma.

Axial and sagittal images from a non-contrast head CT in an elderly patient with brain atrophy demonstrate a large right frontal scalp hematoma with multifocal underlying “coup” subarachnoid hemorrhage (arrows) in the subjacent right frontal lobe

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Even in the setting of trauma, isolated SAH in the basilar cisterns should trigger a search for underlying aneurysmal rupture with either CT or MR angiography. Clinically it can be difficult to determine if a ruptured aneurysm led to a fall and subsequent head trauma or if primary head trauma has resulted in subarachnoid hemorrhage. SAH in the interpeduncular or perimesencephalic cisterns may indicate injury to the brainstem [48] or large vessel injury. As blood products are irritating to the vessels, vasospasm can result from traumatic SAH and is more common in severe TBI, reported in about a third of patients [58, 59].

Needless to say, some patients can have a combination of hematomas in different cranial spaces (Fig. 7.8).

Fig. 7.8
2 axial C T, a sagittal C T, and a sagittal non-contrast C T scans of the head. They highlight a less-dense region indicating subdural hematoma, the bright region denotes the left parietal bone fracture, and a dark region denotes the edema.

Axial non-contrast head CT demonstrates focal acute SAH within the left parieto-occipital sulcus (top left and right images, arrows) at presentation in a “coup” pattern. This SAH underlies a mildly comminuted depressed left parietal bone fracture (bottom right image, arrow) that indicates the site of the blunt head injury. An associated hemorrhagic contusion with surrounding edema centered within the left cuneus increased in size over time on the 24-h follow-up CT scan (bottom left image, arrow). Lastly, a left hemispheric acute subdural hematoma is present (top left and right images, arrowheads)

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6.4 Traumatic Intraventricular Hemorrhage (IVH)

Intraventricular hemorrhage (IVH) is reported in about 1–3% in blunt trauma and 10–25% in severe head injury [60, 61]. IVH may result from several mechanisms including injury to subependymal or cortical veins, retrograde reabsorption, or reflux of SAH, or extension of intraparenchymal hemorrhage. Large cohort regression analyses have shown strong correlation between IVH and diffuse axonal injury to the corpus collosum with poor clinical outcomes [57, 62].

On CT, hyperdense layering blood in the ventricles is compatible with IVH. MRI is more sensitive for the identification of subtle IVH using T2-weighted FLAIR or SWI sequences. In the first 48 h, blood products appear hyperintense on the FLAIR sequence then variable in signal as blood becomes more subacute/chronic and SWI shows hypointense area of susceptibility [63, 64]. Both subarachoid and intraventricular hemorrhage can result in hydrocephalus (Fig. 7.9).

Fig. 7.9
A C T scan of a brain highlights the wavy bright regions on the temporal lobes of both hemispheres of the brain and a small, less-dense spot at the occipital lobe of the left hemisphere, indicating the hemorrhage.

Axial non-contrast head CT performed on a patient extricated from a vehicle following a high-speed motor vehicle collision demonstrates diffuse acute SAH (arrowheads) and a small amount of IVH layering within the occipital horn of the left lateral ventricle (arrow). Also present on this scan is early hydrocephalus related to the SAH

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7 Intra-Axial Lesions

7.1 Hemorrhagic Cerebral Contusions, Coup Versus Contrecoup

Cerebral contusions contribute significantly to morbidity and mortality in the setting of a TBI and constitute about 35% of TBI-related injuries [65]. Brain contusions are focal parenchymal injuries that result from the impact of the brain against the inner table of the skull and can be considered a “bruise” to the brain. The most common locations are at the same (coup) (Fig. 7.10) and opposite (contrecoup) sides of the insult, at areas of irregular bony protrusions mostly involving the anterior and middle cranial fossa [66]. Contusions in the temporal lobe have the worst reported functional outcomes compare to other types of intra- and extra-axial injuries [67].

Fig. 7.10
4 medical scans of the brain highlight a narrow, dark region in the left frontal bone indicating a fracture, a large, dense region indicating hemorrhage, and a small, dark region indicating interhemispheric air.

Thin targeted axial bone algorithm images from a maxillofacial CT scan depict a complex comminuted fracture through the left frontal bone and sinus (top left image, arrow). The corresponding non-contrast head CT scan demonstrates a large underlying “coup” hemorrhagic contusion (top right image, arrow) with associated SAH (top right and bottom right images, arrowheads). Contrast is noted within the arteries of the circle of Willis due to the concurrently performed whole body contrast-enhanced trauma CT scan, although a small SAH was also suspected within the suprasellar cistern (top right image). The fracture line extended into the sphenoid bone (bottom left image, arrow) causing a suspected CSF leak in this patient. A focus of interhemispheric air was also present, due to the fracture extending through the air-filled sinuses (bottom right, arrow)

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Essentially all contusions have some component of hemorrhage, but sensitivity in detecting blood varies by imaging technique and protocol. In the hyperacute setting, contusions can appear primarily hypodense on CT indicating edema. Hyperdense cortical and subcortical hemorrhage may also be present. CT is often used to follow contusions over time that can become more evident as the amount of hemorrhage increases (Fig. 7.11). After the initial 24 h, MRI is more sensitive than CT for the detection of small contusions and defining the extent of hemorrhage and edema, important predictors for clinical outcome. MRI shows a “salt and pepper” appearance of hemorrhagic contusions that may increase in size or “bloom” over the first 48 h following injury [68]. The T2-weighted FLAIR sequence is best for evaluation of contusions mostly involving cerebral edema [38, 66]. SWI or T2* gradient recall echo (GRE) sequences are very sensitive for the detection of hemorrhagic contusions [8], with SWI being far more sensitive than T2* GRE. Contusions are often associated with SAH and must be followed with serial imaging to assess progression of hemorrhage and resulting mass effect/herniation to determine need for surgical intervention [69]. Over time, chronic contusions appear hypodense and atrophic on CT due to the resultant encephalomalacia and gliosis. On MRI, susceptibility artifact within the chronic contusion will persists within the region of encephalomalacia and gliosis due to hemosiderin/ferritin deposition [70] (Fig. 7.12).

Fig. 7.11
2 axial C T scans of the brain. The left scan highlights a small hypodense region at the left lateral temporal lobe, indicating the contusion. The right scan displays a large and bright opacity in the left temporal lobe.

Following a fall from a ladder, a non-contrast CT scan was performed in the emergency department that demonstrates multicompartmental post-traumatic intracranial hemorrhage including a subdural hematoma, SAH, and a small contusion (left image, arrows) within the left lateral temporal lobe. A CT scan performed 12 h later demonstrates a marked interval increase in size of the inferolateral left temporal lobe hemorrhagic contusion (right image, arrow)

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Fig. 7.12
2 M R I scans of the brain. An arrow and an arrowhead in both scans point to less dense and dark opacities, respectively.

T2-weighted FLAIR (left image) and SWI (right image) MR sequences demonstrate extensive chronic hemorrhagic encephalomalacia within the lateral right temporal lobe (arrows) in a patient with a severe TBI following a high-speed motor vehicle collision. There is associated ex-vacuo dilatation of the temporal horn of the right lateral ventricle (left image, arrowhead). Additionally, there is evidence of chronic hemorrhagic axonal injury involving the superior cerebellar peduncles (right image, arrowheads)

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Contusions may occur on both the coup and contrecoup sides of blunt traumatic head injury related to the directional force of the trauma. Translational forces from acceleration/deceleration cause the brain to impact the calvarium on the contrecoup side of injury, and these lesions can be larger and more extensive than coup lesions [70].

Table 7.3 provides a review of sequential signal intensity changes that intracranial hemorrhage undergoes on MRI. MRI signal of blood products is largely dependent on three main factors: (1) the fact that hemoglobin is a ferrous (iron-containing) molecule, (2) the number of unpaired electrons associated with the hemoglobin state that dictates its magnetism, and (3) the relative heterogeneity of distribution of hemoglobin (within or outside of red blood cells) which contribute to susceptibility-related local magnetic field distortions.

Table 7.3 Sequential signal intensity changes of intracranial hemorrhage on MRI (1.5 T)
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7.2 Diffuse Axonal Injury (DAI)

Diffuse axonal injury (DAI) is a relatively common type of neuronal damage from severe closed head trauma [71, 72]. DAI is clinically defined as head trauma with resulting loss of consciousness 6 h or more that can lead to neurologic degeneration or death. Damage from shear-strain forces in DAI is believed to cause injury to the brain across interfaces where tissue densities differ (e.g., gray and white matter junction) or tissue anchored to adjacent structures (cerebral/cerebellar peduncles or corpus callosum) [72, 73]. The most affected areas of DAI in order of frequency are as follows: gray–white matter junctions, corpus callosum, basal ganglia, brainstem, and mesencephalon. Classification of DAI was first described in 1982 by Adams and colleagues based on location of lesions. DAI grade I (mild) involves microscopic changes in the cerebral cortex, corpus callosum, brainstem, and cerebellum; grade II (moderate) are gross focal lesions in the corpus callosum; and grade III (severe) are focal lesions in the dorsolateral portions of the brainstem involving the superior cerebellar peduncle [74]. Axonal injury in the brainstem is an important indicator for clinical degeneration to coma in DAI patients [73]. Thalamic injury may also occur and are not included in the initial grading system but may result in worse clinical outcomes [75].

Given the clinical importance of DAI and higher associated morbidity and mortality compared to other types of extra-axial injuries or hemorrhagic brain contusions, imaging plays a crucial role in detection and prognosis. As always, non-contrast head CT is the modality of choice in the acute trauma setting but often underestimates DAI extent especially for non-hemorrhagic lesions [72]. Only around 10% of patients with DAI show hemorrhagic lesions initially (Fig. 7.13), which then can become more apparent in weeks following injury as these areas begin to atrophy and undergo gliosis with ex-vacuo ventricular dilatation [76]. Thus, when patients have clinical findings discrepant with initial CT imaging, MRI is often used to improve sensitivity in evaluation. In the acute setting, DWI sequences can show non-hemorrhagic lesions in areas of cytotoxic or vasogenic edema [17]. Greater degrees of signal abnormality in the corpus callosum and brainstem (grade II and III lesions) have been shown to correlate with length of comatose state [77]. For hemorrhagic lesions, susceptibility-weighted sequences can detect microhemorrhages with some reports showing SWI to be six times as sensitive as T2* GRE imaging [78] (Fig. 7.14). Bland T2 hyperintense white matter lesions may be present in patients with DAI but are nonspecific findings and can also be seen in nontraumatic causes such as ischemia, demyelination, migraines, vasculopathies, etc. A linear pattern along the vectors of the force applied to the brain and an association of these T2 hyperintensities with regions of diffusion restriction and microhemorrhage are important to distinguish DAI from other nonspecific causes [79]. More focal regions of traumatic axonal injury (TAI) which may be seen on MRI are also now understood to occur in less severe clinical cases.

Fig. 7.13
6 medical scans of the brain. Top left and right scans mark a bright opacity and linear dark hemorrhage region. Middle left and right scans highlight the hypodense region on the left lobe, indicating edema. Bottom right and left scans highlight dark spots indicating hemorrhagic contusion.figure 13

Axial non-contrast head CT images performed on a comatose patient with a severe TBI demonstrate bilateral frontal lobe acute hemorrhagic contusions in the frontal lobes (top left and right images, arrowheads) as well as multifocal punctate acute microhemorrhages in a linear pattern in the left superior frontal gyrus compatible with traumatic hemorrhagic axonal shear injuries (top left image, arrow). T2-weighted FLAIR demonstrates multifocal regions of white matter edema within the left superior frontal gyrus (middle left image, arrow) associated with numerous foci of microhemorrhage on SWI within the bilateral superior frontal gyri (lower left image, arrows) confirming the hemorrhagic axonal shear injuries. The T2-weighted FLAIR sequence also depicts a focal region of cortical/subcortical edema (middle right image, arrow) corresponding to cortical hemorrhage on the SWI (lower right image, arrow) within the posterolateral left frontal lobe confirming a hemorrhagic contusion

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Fig. 7.14
3 axial medical scans of the brain highlight dark spots on the left frontal lobe and the corpus callosum.

SWI demonstrates numerous punctate and linear foci of susceptibility compatible with traumatic hemorrhagic axonal shear injuries within the subcortical white matter of the left frontal lobe and the corpus callosum (arrows) in a young male patient that suffered a moderate TBI following a motorcycle accident

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Diffusion tensor imaging (DTI) has emerged as an MRI technique that can study white matter and potential white matter injury. DTI uses orthogonal diffusion vectors and can measure directional diffusion. In group studies, DTI has been shown to demonstrate anisotropy changes in white matter in patients with TBI compared with controls even in the absence of T2 FLAIR and susceptibility abnormalities [80, 81]. Changes in fractional anisotropy after TBI can be confusing (elevated vs depressed compared with normal), and this inconsistency is now believed to relate to timing after injury. Clinical use of DTI as a TAI biomarker remains challenging due to heterogeneity in data acquisition and analysis methods, variance across the normal population, and heterogeneity of head injuries. Ongoing research is still underway to better understand and characterize white matter injury using multicompartment diffusion modeling and to try to identify potential clinical uses.

8 Vascular Injury

Vascular injuries may occur with head trauma including arterial dissection, pseudoaneurysm, active extravasation, vascular occlusion, carotid cavernous fistula, dural arteriovenous fistula, and venous thrombosis. Patients with severe DAI and cerebral edema may also develop diffuse vascular injury, which is shown when dark areas of SWI susceptibility artifact surround engorged veins indicating areas of venous stasis [82]. Several guidelines exist for imaging use when vascular injury is suspected including the Denver and Western Trauma Association criteria. Consensus is that any head trauma with a skull base fracture or penetration neck injury extending through the carotid canal, particularly zone III (through superior angle of mandible) should be further evaluated with angiography [83].

8.1 Carotid Artery-Cavernous Sinus Fistula (CCF)

Carotid artery-cavernous sinus fistula (CCF) can have different etiologies but occur in the setting of trauma when the cavernous segment of the internal carotid artery is injured result in a direct communication between the arterial system and the venous system of the cavernous sinus. This fistulous connection may lead to dilation of the cavernous sinus and secondary enlargement of the superior ophthalmic vein (SOV) and inferior petrosal sinus [8]. Characteristic imaging shows enlarged cavernous sinus or ipsilateral SOV with multiple flow voids on MRI and clinical symptoms include injected conjunctiva, pulsatile exophthalmos, and periorbital edema (Fig. 7.15).

Fig. 7.15
4 scans. The two axial M R I scans highlight the dark-shaded dilated veins. The coronal M R I scan highlights bright opacities and a less dense region, indicating subdural hygromas and hemorrhagic contusion. The angiogram highlights a dark opacity in the cavernous sinuses and ophthalmic veins.

A young male patient developed bilateral ocular proptosis and chemosis while hospitalized for a recent severe TBI with non-displaced skull base fracture. The axial T1-weighted MR image demonstrates enlargement of the bilateral superior ophthalmic veins, left more than right (top left image, arrows). The coronal T2-weighted image demonstrates small bilateral post-traumatic subdural hygromas (bottom left image, arrowheads) and a small inferior left frontal hemorrhagic contusion (bottom left image, arrow). The time-of-flight gradient echo MRA demonstrates arterialized flow-related enhancement within the bilateral cavernous sinuses and left superior ophthalmic vein (top right image, arrows). The left ICA arterial phase digital subtraction catheter angiogram (anteroposterior projection) confirmed the presence of a direct carotid cavernous fistula with pronounced early arterial phase opacification of the cavernous sinuses and ophthalmic veins (bottom right image, arrows)

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8.2 Traumatic Aneurysms

Post-traumatic intracranial aneurysms are rare, accounting for <1% of all aneurysms and occur most commonly in children [84]. Common locations include the cavernous and infraclinoid internal carotid artery as well as the anterior cerebral artery. As with all intracerebral aneurysms, standard assessments include CTA/MRA and catheter digital subtraction angiography.

8.3 Traumatic Vascular Dissection

Damage to the intimal layer of an artery may result in the creation of a false lumen with blood diverting into the media through the dissection flap. Sometimes even minor neck injury can result in cervical vascular dissections with resultant potential vascular compromise of the brain. Intracranial dissection is less common, and severe cases can be associated with adjacent fractures causing direct damage to the vessels or result from rotational force in blunt head trauma [85]. The incidence of internal carotid and vertebral artery dissections in the setting of head trauma is 0.86% and 0.53%, respectively [86].

CTA and MRA are the most commonly utilized imaging modalities and are highly accurate in the assessment of the integrity of the cervical arteries and to assess for luminal narrowing. Anatomic black-blood MRI sequences may also show a high intensity “crescent sign” on T1-weighted and T2-weighted sequences indicating an intramural hematoma at the site of the dissection with a concomitant flow void or abnormal contour on MRA [87] (Fig. 7.16). Ultrasound is also being increasingly used for detection, particularly with B mode and color flow doppler. Conventional catheter angiography remains a useful tool for diagnosing cervical and intracranial arterial dissections and may show features such as the “string sign” or “flame shaped tapering,” however in current practice is reserved primarily for endovascular therapy.

Fig. 7.16
3 medical scans of the neck. Left. An arrow points to a round-shaped dense region. The top right and bottom right scans highlight a bright, crescent-shaped opacity on the left side.

CTA was performed in a young patient complaining of left neck pain following a concussion while playing ice hockey. The CTA demonstrates a linear intimal flap and pseudoaneurysm of the distal left internal carotid artery located directly below the skull base compatible with a traumatic dissection and pseudoaneurysm (left image, arrows). Crescentic T1 and T2 hyperintensity are also present on the anatomic T1-weighted and T2-weighted sequences performed through the upper neck that represented the subintimal hematoma and confirmed a traumatic ICA dissection (right images, arrows)

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9 Secondary Complications

9.1 Definition

Secondary intracranial complications are worth discussing and can be clinically critically important. These are sequelae that result as a series of pathophysiologic events triggered by the initial injury that then may lead to further tissue injury and neuron loss.

9.2 Intracranial Hypertension

Intracranial hypertension may result after head trauma due to swelling, edema, or hemorrhage and can continue to increase in the initial days after injury, leading to progressive and sometimes precipitous decline. Suspicious imaging findings include diffuse sulcal effacements, compression of the ventricles, enlarging hematomas, and/or herniation. These findings have been found to have a linear relationship with increased intracranial pressure and can help guide management including placement of ICP monitors, need for neuro ICU care with close ICP monitoring, surgical intervention such as CSF drainage, hematoma evacuation, or decompressive craniotomy [98].

9.2.1 Brain Herniation

Profound intracranial hypertension may lead to multiple secondary injuries of which brain herniation is the most dangerous. The mass effect from increased pressure can result in obliteration of the basal cisterns, subarachnoid spaces, and non-communicating hydrocephalus if ventricular outflow is obstructed. Compression of important vascular structures can lead to brain infarction thus leading to a cascade of neurologic damage. Herniation patterns are described in Table 7.4.

Table 7.4 Cerebral herniation types
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9.2.2 Secondary Brainstem Hemorrhage (Duret Hemorrhage)

Rapid downward cerebral herniation can lead to a devastating effect, hemorrhage within a compressed brainstem. CT findings show hyperdense blood in the brainstem typically in the lower midbrain/ventral pons. A recent large meta-analysis implicated damage to anteromedial basilar artery perforators after sudden descending herniation [88] as the main cause. Outcome in the setting of Duret hemorrhage is poor and often fatal.

9.3 Ischemia and Infarction

Post-traumatic ischemia is another secondary effect of trauma that leads to poorer clinical outcomes. MRI is most sensitive to detect secondary ischemic injury as areas of increased signal intensity on T2-weighted images with corresponding restricted diffusion [89]. The most common post-traumatic ischemic injury is inflicted on the ipsilateral posterior cerebral artery territory due to supratentorial mass effect. Causes can be extra-axial or intracranial hemorrhage resulting in mass effect and downward transtentorial herniation. Buildup of supratentorial pressure and mass effect may ultimately lead to impingement of the posterior cerebral artery between the free edge of the tentorium and the herniating brain. Anterior cerebral artery impingement can occur along the free edge of the falx in the setting of subfalcine herniation. Frank compression of the middle cerebral artery is less common [89, 90]. More distal vessel compromise can also occur relating to vasospasm in the setting of acute subarachnoid hemorrhage.

9.4 Infections

Penetrating head trauma (Figs. 7.17 and 7.18) involving contaminated foreign objects or the introduction of non-sterile portions of the patient’s own anatomy (paranasal sinuses, skin, etc.), which then penetrate the intracranial compartment can introduce bacteria and other infectious agents. The spectrum of post-traumatic infection ranges from local wound/scalp infection and cellulitis to more hazardous intracranial infections such as meningitis, ventriculitis, cerebritis, and abscess [91]. Imaging findings may show abnormal enhancement of the leptomeninges, ventricles, or a rim enhancing collection, respectively, on contrast-enhanced studies, with MRI having greater sensitivity. Classically, areas of pyogenic infection will carry signature restricted diffusion.

Fig. 7.17
A 3-D C T image of the skull and 3 medical scans of the brain. The 3-D and the non-contrasted C T scans highlight the fracture in the bilateral parietal bones. The bottom left and right scans highlight the less dense region near the hyperintense and hypointense region at the left parietal lobe.

Gunshot wound to the left parietal lobe by a stray bullet in a young child, initial non-contrast CT scan. The 3D volume rendered reconstructed CT scan through the skull and the sagittal CT scan reconstructed images demonstrate a complex elevated comminuted fracture through the bilateral parietal bones (top left and right images, arrows). Axial non-contrast CT scan images demonstrate the bullet fragments lodged within the left parietal lobe associated with multiple foci of intracranial air and microhemorrhage (bottom left and right images, arrows). The non-contrast CT scan also shows diffuse sulcal effacement and ventricular compression compatible with diffuse cerebral edema and raised ICP

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Fig. 7.18
4 medical scans of the brain. Top left. A less dense region at the left parietal lobe is highlighted. Top right. An arrow and an arrowhead point to hypodense and dark regions, respectively. The bottom left and right scans indicate a large hypodense region in the left parietal lobe.

Gunshot wound to the left parietal lobe by a stray bullet in a young child, follow-up MRI scan. Extensive edema and hemorrhage are present within the left parietal lobe along the bullet track (top left image, arrow). The diffusion-weighted images demonstrate a large left parietal contusion/infarction (top right image, arrow). Note the bilateral paramedial occipital lobe infarction from herniation and compression of the posterior cerebral arteries (top right image, arrowheads). T2-weighted FLAIR (bottom left image) and SWI (bottom right image) show the related edema and hemorrhage in the left parietal lobe

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10 Post-traumatic Sequelae

10.1 Post-traumatic Encephalomalacia

In the later phases after serious head trauma, many chronic changes can occur to the brain. Post-traumatic encephalomalacia is the long-term result of brain tissue loss and death. After the initial insult, the damaged brain tissue undergoes gliosis or scarring often with surrounding cystic cavitation commonly called encephalomalacia [92]. The most common areas of post-traumatic encephalomalacia are the anterior and basal portions of the temporal lobes as these are often injured from contusions from the impact against the skull base [93]. CT imaging reveals atrophic hypodense regions, and MRI demonstrates gliotic T2 hyperintense and/or cystic regions that correlate to the post-traumatic contusions and/or infarctions. Long-term clinical symptoms from encephalomalacia depend on the extent and location of the injury, as well as individual factors such as age and plasticity of the brain at the time of injury. Deficits may vary but can include chronic focal neurological deficits, behavioral changes, and seizures, and may result in life-long disability [93].

10.2 Traumatic CSF Leak

Cerebral spinal fluid (CSF) leak is another complication seen in up to 2% after head trauma, with 12–30% reported in cases involving skull base fractures [94]. Leaks may also occur at the cribriform plate and along the walls of the frontal sinuses often associated with fractures that involve communications between the paranasal sinuses and intracranial compartment [95]. CSF leaks can be difficult to detect but signs of pneumocephalus can help point to areas of potential leak. Persistent sinus opacification adjacent to a fracture can be another important clue. If CSF leak is suspected into the paranasal sinuses, nasopharynx, or nasal passages, sampling of nasal fluid and testing for beta-2 transferrin can be done for confirmation. Chronic CSF leaks may present with intracranial hypotension and its concomitant imaging findings or recurrent meningitis. Both CT and MR, contrast-enhanced cisternography,and/or myelography can be useful to try to localize leaks.

10.3 Growing Skull Fracture

Growing fractures are rare though may occur in pediatric patients [96]. Incidence is reported as about <0.05–1.6% of cases. Findings include a fracture line which continues to widen due to increased extra-axial brain herniation from the skull defect. These cases may be associated with meningoceles and/or encephalomalacia as the herniated brain parenchyma begins to infarct [97].

10.4 Diabetes Insipidus (DI)

Trauma to the pituitary infundibulum can result in central diabetes insipidus (DI). Evaluation of the pituitary gland is typically done with dedicated MRI. Healthy patients typically have T1 hyperintensity in the posterior pituitary gland. Lack of this bright spot may be seen in DI though the finding is nonspecific [98]. Findings of an ectopic posterior pituitary can be seen congenitally; however, in the setting of a history of significant head trauma and acute onset DI, can indicate a proximal stump from a transected infundibulum or a retracted stalk.

11 Concluding Remarks

Cross-sectional imaging for patients who sustain craniocerebral trauma is an essential tool for prognosis and management. Both CT and MRI have revolutionized our ability to detect the sequelae of acute head trauma inside the cranial vault and determine the potential effects on the brain. Unenhanced CT is a critical tool for initial diagnosis of severity and extent of injury as well as to appropriately triage patients that need close monitoring and/or immediate neurosurgical intervention. CT is the primary imaging modality because of its speed, availability, lack of contraindications, and high sensitivity for hemorrhage and fractures. MRI is useful in many circumstances and provides unparalleled tissue contrast without ionizing radiation. MRI is used in situations such as assessing complications, working up patients with clinical and CT discordance, and as a more sensitive tool to detect intracranial injury. Overall, given the high incidence of TBI-related injuries globally especially in elderly and young populations, imaging continues to be crucial for diagnosis and understanding patterns of injury to provide optimal management for these patients.

Take-Home Messages

  • Traumatic brain injury is common and can affect individuals of all ages.

  • Neuroimaging is critical for assessment and triage of patients who have sustained head trauma.

  • CT and MRI are complementary: CT is widely available in emergency settings and MRI is sensitive to more subtle injuries.