7.5.1. Epidural Hematoma

Epidural hematoma (EDH) is an extracerebral collection of blood between the inner table of the skull and the dura, essentially underlying a bare bone surface. EDH occurs in <1% of patients with head injuries [13]. EDH is typically found on the “coup” injury side, and is commonly associated with a skull fracture and laceration of the underlying blood vessel(s), notably the dural vasculature [14]. The recommended imaging method is CT, which depicts both the fracture and resulting hemorrhage. EDHs are commonly biconvex in appearance and typically do not cross suture lines but may cross the tentorium or falx; their mass effect is mostly caused by the size of extracerebral collection [14]. In the early stage, an epidural hematoma may appear heterogeneous on CT with hyperdense areas of clotted blood and hypodense whirls of non-coagulated blood that in time becomes more homogeneous [14]. This “swirl sign” is an ominous feature, and should be carefully noted and communicated to the treating physicians, as it represents active hemorrhage into the collection [15]. Rapid progression has been noted.

EDH may be arterial or venous in origin (Table 7.2). Arterial EDH is caused by injury of a meningeal artery, commonly the middle meningeal artery. The typical location is the temporoparietal region, with 75% of EDH occurring adjacent to the temporal bone (Fig. 7.4). When the blood vessel is lacerated, arterial bleeding results in a rapidly expanding hematoma that exerts mass effect on the brain, focal deformity of the brain and an increase in intracranial pressure (ICP). The size of the EDH may continue to increase until the arterial perfusion pressure is equilibrated with the elevated ICP. Emergency decompressive surgery is indicated to remove the EDH, stop hemorrhage, and reduce compression on the brain.

Table 7.2

Epidural versus subdural hematoma

Fig. 7.4

(a, b) Acute left arterial epidural hematoma. Non-contrast CT-scan upon admission. The left-sided hematoma is biconvex, and is limited by the coronal suture anteriorly and by the lambdoid suture posteriorly. The mass effect causes a shift of the midline (more...)

Venous EDH results from rupture/laceration of a dural venous sinus, or bleeding from diploic veins, again often associated with a skull fracture [16]. Venous EDH is usually located near the anterior wall of the middle cranial fossa (injury of sphenoparietal sinus and/or fracture of the greater wing of the sphenoid bone), the vertex (injury of the superior sagittal sinus and/or fracture of the frontal or parietal bone), or against the occiput near the tentorium (injury of the transverse sinus and/or occipital fracture) [8] (Fig. 7.5).

Fig. 7.5

(a, b) Venous epidural hematomas, shown in two different patients. Venous epidural hematomas typically are found (a) anteriorly in the middle cranial fossa adjacent to the sphenoparietal sinus and greater wing of the sphenoid bone, or (b) adjacent to (more...)

Few EDH patients will not undergo craniotomy and evacuation, often on an emergent basis. One unusual and typically indolent EDH is known; anterior temporal EDH is often a low-pressure hemorrhage and typically do not expand. There is no usual requirement for surgical intervention [16]. Conversely, posterior fossa EDH may urgently require surgical evacuation because of early brainstem compression [16].

7.5.2. Subdural Hematoma

A subdural hematoma (SDH) represents an extracerebral collection of blood in the potential space between the dura mater and the arachnoid membrane, or “epiarachnoid.” SDHs are relatively common and occur in about 30% cases of severe head trauma [13]. They are more commonly found on the contre-coup injury side and are not as strongly associated with fractures as EDH [14]. The origin is almost invariably venous, caused by injury of superficial bridging cortical veins. They do cross sutures and may be holohemispheric, and are typically limited by the falx and tentorium [14].

On CT, an acute SDH is seen as crescentic hyperdense structure between brain and the inner border of skull (Fig. 7.6). On modern CT scanners, the arachnoid space may be seen adjacent to the brain opposing the SDH. SDHs do not penetrate into sulci. Over time, the density decreases and they may become isodense to the adjacent brain. Therefore, MRI may be a preferred imaging method in later stages.

Fig. 7.6

(a–c) Acute left subdural hematoma. The CT-scan shows hyperdense areas of clotted blood and some hypodense components indicating active bleeding. There is mass effect on the left cerebral hemisphere, with transtentorial herniation. The high-density (more...)

Subacute SDH occurs as hyperintense lesion on T1 and T2-weighed images due to extracellular methemoglobin [17] (Fig. 7.7). Chronic subdural hematoma is also well evaluated by MRI, which can clearly distinguish the size and extent of the collection as well as the development of the enhancing, capillary-rich membrane associated with resorbing SDH [17]. Chronic subdural hematomas are variable in signal but may retain T1 or FLAIR hyperintensity (Fig. 7.8).

Fig. 7.7

(a, b) Subacute left subdural hematoma. MRI examination performed with (a) sagittal SE T1-weighted image and (b) axial TSE T2-weighted image. The MR images show the typical appearance of a crescent-shaped left subdural hematoma. There are multiple internal (more...)

Fig. 7.8

(a, b) Chronic left subdural hematoma. MRI examination, including (a) axial TSE T2-weighted image and (b) axial turbo-FLAIR image with fat saturation. On the T2-weighted scan, the chronic subdural hematoma overlying the left cerebral hemisphere is hyperintense, (more...)

The development of the vascular membranes, that are common in chronic SDH, is an important feature in the subsequent development of rehemorrhage into these collections, representing the “acute on chronic” form of SDH. These collections may appear quite complex in nature, with mixed and layered signal intensities, and are difficult to manage [18].

Finally, the occasional occurrence of an acute low-density subdural collection in the trauma patient is a known phenomenon. A tear in the arachnoid may allow CSF to enter the potential subdural space and produce an enlarging fluid collection known as a subdural hygroma. These may spontaneously resolve but also are monitored for mass effect.

7.5.3. Traumatic Subarachnoid Hemorrhage

Traumatic subarachnoid hemorrhage (SAH) is common and often focal. It can be due to superficial cerebral abrasions, direct leptomeningeal vascular injury, or intraventricular hemorrhage with subarachnoid reflux [8]. The estimated incidence rates for SAH are 10–25 per 100,000 per year [19]. Acute SAH is easy recognizable on non-contrast CT as gyriform high attenuation in the subarachnoid space. It will penetrate sulci. The attenuation of blood on CT decreases as the hemoglobin concentration decreases [20]. The combination of SWI and FLAIR yields a distinctly higher detection rate for SAH due to their complementary detection capabilities [21]. FLAIR is sensitive for superficial/convexity SAH, while SWI adds value for the centrally located SAH, e.g., the interhemispheric fissure, interpeduncular fossa, supracerebellar cistern, and intraventricular subarachnoid blood [21]. The recognition of subtle SAH is important in the trauma setting, as this finding alone will typically result in an extended in-hospital evaluation of the patient.

7.5.4. Traumatic Intraventricular Hemorrhage

Traumatic intraventricular hemorrhage (IVH) occurs as a result of the tearing of subependymal or choroidal veins or reflux of SAH into the ventricular system. It may also be seen in association with diffuse axonal injury of the corpus callosum. The incidence of IVH in nonpenetrating head injury is 1.5–3% and 10–25% of patients with severe head injury [22].

On CT IVH may appear as a hyperdense collection in the ventricular system. MRI is more sensitive to IVH and DWI and FLAIR are the preferred sequences for identifying IVH (Fig. 7.9). During the first 48 h IVH appears hyperintense on FLAIR, but subsequently the signal intensity may be variable [23]. Pulsatile flow artifacts in the third and fourth ventricle may compromise the usefulness of the FLAIR technique [8]. 3D-FLAIR techniques are more useful in this regard. SWI is extremely sensitive in detecting intraventricular hemorrhage. IVH appears as a typical hypointense area of susceptibility [24].

Fig. 7.9

(a, b) Posttraumatic intraventricular and subarachnoid hemorrhage. MRI examination, including (a) axial turbo-FLAIR image with fat saturation and (b) axial diffusion-weighted trace image (b = 1000). In the left occipital horn, there is (more...)

7.6.1. Cerebral Contusion, Hemorrhagic Vs Non-hemorrhagic, Coup Versus Contre-Coup

Cerebral contusions are focal injuries of the brain surface due to direct impact with the skull and are most common at sides of bony protuberances or overlying irregular areas of the floor of the anterior or middle fossa. They are, in essence, to be considered as “a bruise of the brain.” The consequent lesions are hemorrhagic or edematous and may progress to necrosis [25].

All contusions are hemorrhagic, but the extent of edema versus hemorrhage in an individual contusion will determine its appearance on CT. MR will consistently depict hemorrhage, notably on SWI or GRE sequences. Hemorrhagic contusions are superficial and have either a “salt-and-pepper” appearance or may appear more solid [26]. When a traumatic brain injury results in a cerebral contusion, they may progress during the first several hours and can be associated with SAH [27]. Predominantly affected areas are located in the supratentorial region—anterior frontal and temporal lobes and the gyri around the Sylvian fissure.

On CT, hemorrhagic contusions appear as heterogeneous, hyperdense cortical lesions surrounded by an irregularly marginated hypodense (edematous) component. In the acute stage, CT may be more sensitive than MRI, as acute hemorrhage can be nearly indistinguishable from brain parenchyma on MRI. Subsequent CT performed between 24 and 48 h after traumatic brain injury often demonstrates previously undetected contusions or more extensive hemorrhage and increased edema. MRI is more sensitive than CT to depict cerebral contusions after the first 24 h because of the visualization of “non-hemorrhagic” contusion, or contusions with predominant edema. This is particularly true of FLAIR [8, 25]. The ability of MRI to detect hemorrhagic brain lesions increases proportionally to the evolution of blood products in these lesions. Hemosiderin and also deoxyhemoglobin have increased magnetic susceptibility that make SWI or T2∗ gradient-echo sequences very sensitive for detecting hemorrhagic lesions [28, 29]. Four to six months after injury the lesions become cystic and lose volume and therefore hypodense on CT [30], although MR findings of hemorrhage persist.

Table 7.3 provides an overview of sequential signal intensity changes of intracranial hemorrhage on MRI.

Table 7.3

Sequential signal intensity changes of intracranial hemorrhage on MRI (1,5 T)

Contusions may be bihemispheric and occur along the vector of the force applied to the skull on the site of impact and the opposite region of brain. These injuries are referred to as “coup” (side of injury) or “contre-coup” (opposite the injury). In closed-head injury, for example, after an abrupt stop, the force translation can result in this pattern [30]. The coup-injury is on the side of primary impact, often identified by scalp lesions or skull fracture. “Contre-coup” lesions are the mechanical consequence of an acceleration/deceleration trauma and occur on the opposite side of impact. They are often larger and more extensive than the coup lesions, perhaps because of the initial displacement of the brain toward the contre-coup location [8, 30, 31].

7.6.2. Diffuse Axonal Injury (DAI)

Diffuse axonal injury is a common type of primary neuronal injury in patients with severe head trauma with an incidence up to 50% of trauma victims [30, 32]. DAI occurs when the brain is exposed to shear-strain forces that leads to lesions at interfaces between two adjacent tissues with different densities or rigidities, such as gray and white matter [33] or areas where the brain is relatively anchored to an adjacent structure, such as the cerebral or cerebellar peduncles or corpus callosum. Predominantly affected areas in decreasing order of frequency are: gray-white matter junction, corpus callosum, basal ganglia, brainstem, and mesencephalon. The severity of the lesions increases towards the cerebellum, whereas axonal injury in the brainstem is considered to be an indicator for degeneration to coma in DAI [8, 33].

Its’ important clinical relevance and various clinical manifestations have contributed to the development of radiological imaging techniques for detection of DAI. As mentioned, DAI is a common primary injury in brain trauma and CT examination is still the mode of choice in severe trauma patients in the acute phase because of its great value in detecting petechial hemorrhagic lesions, fractures and because of its rapid and convenient acquisition. Unfortunately, CT significantly underestimates the extent and number of DAI lesions, especially of non-hemorrhagic lesions [34] (Fig. 7.10). Therefore, whenever there is a discrepancy between the clinical status of the patient and the CT findings, MRI can provide very important information. In the early stage, diffusion-weighted images are of great importance to detect DAI. In addition, FLAIR sequences are useful for the detection of areas of gliosis. Gradient-echo sequences (GRE) and more recently susceptibility-weighted imaging (SWI) are also superior to CT in subacute or chronic hemorrhagic head injuries because of paramagnetic blood degradation products [33, 34].

Fig. 7.10

(a–f) Diffuse axonal injuries in a 14-year-old boy, 4 days after a motor vehicle accident: (a) axial non-contrast CT-scan; (b) axial turbo-FLAIR image; (c) axial TSE T2-weighted image; (d) axial gradient-echo FLASH T2∗-weighted (more...)

New advanced MRI techniques like diffusion tensor imaging (DTI) offer more sensitive detection and differentiation of DAI. In DTI, the specific water diffusion direction in the white matter is used to detect microstructural conditions that result in restriction in the diffusion of the molecules and alter the values seen on FA (fractional anisotropy) maps [35, 36]. A recent study showed that DTI is a very qualitative and useful way for clinical evaluation of DAI. The authors found decreased anisotropy in the corpus callosum even in patients with normal results on FLAIR and GRE [37]. Multiple additional studies demonstrate the utility of DTI, but application to individual patients remains challenging because of a wide number of variables [38]. DTI and the derived FA values remain an important research tool, and are being widely investigated to determine what value they may provide in the individual patient. For the present time, these remain largely research tools.

7.7.1. Carotid Artery-Cavernous Sinus Fistula (CCF)

In the traumatic carotid artery-cavernous sinus fistula (CCF), there occurs a direct communication between the cavernous segment of the internal carotid artery (ICA) and the cavernous sinus. The underlying cause is often a laceration of the ICA due to blunt or penetration head trauma. The fistula leads to engorgement and dilatation of the cavernous sinus with successive congestion of the superior ophthalmic vein (SOV) and inferior petrosal sinus [28].

Specific imaging signs of CCF are enlargement of the cavernous sinus or ipsilateral SOV on CT or MR and multiple flow-voids on MRI. MRA may demonstrate arterialized flow in the cavernous sinus or SOV.

7.7.2. Traumatic Aneurysms

Traumatic intracranial aneurysms are rare and represent <1% of all aneurysms. They are most common in children [39]. Predominant locations are the cavernous and infraclinoid segment of ICA, as well as along the anterior cerebral artery.

The gold-standard in imaging of traumatic aneurysms is cerebral angiography, but CT angiography (CTA) is widely used because of its speed and ease of acquisition [40].

7.7.3. Traumatic Vascular Dissection

Traumatic vascular dissections are unusual complications of significant head injury. The injury is caused by a tear in the intimal layer of an artery, resulting in several potential findings, notably diversion of blood flow into a potential “false” lumen within the media. Dissection occurs as a consequence of contiguous bony injury (fractures), rotational forces and torsion of the vessel in blunt head trauma or less frequently with penetrating trauma [41]. The incidence in blunt trauma victims is 0.86% for ICA and 0.53% for traumatic vertebral artery dissections. A common indication for vascular imaging in this setting is fractures of the skull base extending through the carotid canal.

Again, different techniques may provide a diagnosis of vessel dissection. Conventional angiography remains a useful examination. Although the intramural hematoma cannot be visualized, the “string-sign” and a “flame-shaped tapering” are common radiological features [42]. Ultrasound examinations, especially B-mode and Color-flow Doppler, are also increasingly used in detection of traumatic dissections. To detect subtle luminal abnormalities or wall abnormalities in dissection, both CT and MRI, as well as CTA and MRA are superior to catheter angiography.

7.8.1. Definition

Secondary brain damage results from the posttraumatic pathophysiologic cascade that follows the initial injury and contributes to delayed tissue injury and neuronal loss.

7.8.2. Intracranial Hypertension

Intracranial hypertension may occur after severe cerebral injury and can be a significant finding, resulting in progressive neural dysfunction. After traumatic brain injury, intracranial hypertension may be caused by cumulative edema, hemorrhage, or swelling after contusion. The presence of any of these signs is suspicious: loss of gray-white junction indicating cerebral edema, midline shift, a significant hematoma, herniation, or change in ventricular shape or size [28].

7.8.2.1. Brain Herniation (Table 7.4)

Cerebral herniation is the most common and dangerous secondary effect of increased ICP [8]. Cerebral herniation is the most common secondary effect of an expanding intracranial mass. Due to the herniation the subarachnoid spaces and basal cisterns become obliterated, hydrocephalus develops, vascular compression may result in brain ischemia, and compression on vital brain tissue may cause profound neurological deficits.

Table 7.4

Cerebral herniation types

7.8.3. Ischemic Lesions and Infarction

Posttraumatic ischemic lesions are common craniocerebral trauma complications with poor clinical outcome. MRI plays an important role in diagnosing this condition by demonstrating multiple areas of abnormal signal intensity on T2-weighted and FLAIR images [8]. On diffusion-weighted scans, these lesions are seen in the acute phase as hyperintense signal with corresponding hypointense signal on ADC [44]. Of all posttraumatic ischemic lesions, the classic lesion is an ipsilateral posterior cerebral artery infarction in the setting of significant supratentorial mass effect, secondary to any traumatic lesion with mass effect. The causative lesion may be an extra-axial hemorrhage or intracranial hemorrhage associated with edema and mass effect. The posterior cerebral artery may be compressed and transiently occluded between the brain and the free edge of the tentorium. Other intracranial arteries may be occluded or compromised secondary to herniation, including the middle and anterior cerebral arteries [45].

7.8.4. Infections

The risk of local wound infections, meningitis, ventriculitis, or cerebral abscess are particularly high among penetrating head trauma because of the presence of contaminated foreign objects, skin, hair, and bone fragments driven into the brain tissue along the projectile track [46].

7.9.1. Posttraumatic Encephalomalacia

The term “posttraumatic encephalomalacia” refers to loss of brain tissue after craniocerebral trauma. Gross pathology shows weakening or cystic cavitation of brain tissue, with blurred cortical margins and surrounded by gliotic scar tissue. The basal part of the temporal lobes and anterior pole of the temporal lobes are most frequently affected. CT scans show hypodense areas of tissue loss, particularly in these parts of the brain. On MRI, encephalomalacia is identified as (multi-)cystic areas of tissue loss, surrounded by an irregular rim of gliosis, best seen on FLAIR images as a hyperintense rim (Fig. 7.11). Posttraumatic encephalomalacia is a very serious condition, resulting in life-long disability, neurological dysfunction, epilepsy, or even death in some cases. Another common form of posttraumatic encephalomalacia involves the olfactory nerve, which is frequently injured in shear injury.

Fig. 7.11

(a, b) Posttraumatic encephalomalacia and gliosis. Axial (a) and coronal (b) turbo-FLAIR images with spectral fat saturation. MRI performed 4 years after severe head injury. There are areas of posttraumatic tissue loss in the basal part of the (more...)

7.9.2. Growing Skull Fracture

A growing skull fracture is a rare but well-known complication of pediatric head trauma [47]. Its incidence ranges from <0.05% to 1.6% [48]. CT and MRI findings include a diastatic fracture and brain herniation through the skull defect; it can also be accompanied by cystic lesions (meningocele) within the fracture and encephalomalacia [48].

7.9.3. Traumatic CSF Leaks

Traumatic cerebrospinal leakage is a complication seen in 2% of all head-injured patients and in 12–30% of cases of basilar skull fractures [49]. The most common locations are the cribriform plate (forming the roof of the ethmoid) and the walls of the frontal sinus [50]. Intracranial air may be an important sign. Careful evaluation of fractures that are contiguous to sinuses is key to making a correct diagnosis. Persistent opacification of sinuses contiguous to a fracture are of particular suspicion. Suggesting the presence of a CSF leak will usually result in testing of fluid in the contiguous sinus for the presence of beta-2 transferrin, a dependable marker of CSF.

7.9.4. Diabetes Insipidus

The prevalence of central diabetes insipidus (DI) after TBI is 1.7–26%, often resulting from injury or transection of the infundibulum. MRI is the technique of choice for pituitary imaging. A sagittal T1-weighted image demonstrates a posterior pituitary “bright spot” in healthy individuals. The absence of this “bright spot” in diabetes insipidus is a nonspecific sign of DI [51]. In addition to the absence of this sign, an ectopic “bright spot” in the proximal stump of the transected, retracted proximal stalk or hypothalamus may be identified. If there is clinical suspicion of trauma-related DI, a dedicated pituitary examination is the appropriate examination.

7.10.1. Diffusion Weighted Imaging (DWI) with ADC Maps

Diffusion-weighted imaging measures the motion of water molecules and thus helps visualize the physiologic state in the brain [8]. There are physiologic phase-shifts or signal loss due to this normal semi-random motion of water molecules. In distinction, areas with abnormal diffusion reflect alterations in the normal water diffusion and appear bright on DWI [29]. The apparent diffusion coefficient (ADC) values indicate the decrease in the diffusion with corresponding hypointense signal on ADC maps [29]. DWI has become an important tool in diagnosing TBI, acute stroke, and white matter diseases [8].

7.10.2. Diffusion Tensor Imaging (DTI), Diffusion Kurtosis Imaging (DKI)

Diffusion tensor Imaging (DTI) is derived from specialized DWI with multiple directions, and can measure not only the degree, but also the direction of water diffusion [52]. It allows in–vivo visualization of the integrity of white matter tracts. The main application is in diffuse axonal injury.

Diffusion kurtosis Imaging (DKI) is an extended technique, derived from DTI, and allows diffusional kurtosis to be evaluated using diffusion-weighted imaging techniques [53]. With DKI, both gray and white matter can be evaluated.

7.10.3. Outcome Prediction with Imaging Parameters

Imaging is a very important clinical tool for diagnosis, prognosis, and visualizing therapy outcomes following TBI. Although structural imaging techniques such as CT or MRI offer a rapid evaluation of the brain status and may help predict survival, more information is necessary. Detailed information of cerebral perfusion has also proven useful in management and in assessing outcomes [29].

Several imaging techniques are available to visualize the brain physiology: CT perfusion, MR perfusion, SPECT, fMRI (functional MRI), PET, and MRS (MR Spectroscopy). While obviously important research tools, these techniques are occasionally finding their way into clinical imaging to answer clinical questions.

MRI sequences like DTI, FLAIR, GRE/SWI, and DWI are increasingly used in many research models predicting outcome [54].