Jeffrey A. Bennett
Christopher J. Krebs
David V. Smullen
Introduction
Appropriate care of the critically ill patient depends on rapid, accurate diagnosis. The tremendous advances in computed tomography (CT) and magnetic resonance imaging (MRI) technology enable sophisticated studies to be performed swiftly and help to achieve this goal in patients who are often unable to provide a history or remain immobile for long periods. Software allows thin-section axial CT images to be reformatted in any plane, enabling a more complete evaluation of fractures and soft tissue abnormalities. Three-dimensional reformations of contrast-enhanced CT angiograms provide outstanding images of cerebral aneurysms and other vascular abnormalities, which can be rotated to match what will be seen from a surgical approach. Anatomic imaging can also be supplemented with physiologic data obtained with CT, MRI, and nuclear medicine. This provides information about phenomena such as cerebral blood flow, cerebrospinal fluid (CSF) flow, or the rate and direction of diffusion of water in soft tissues. This type of data can clarify diagnoses such as brain infarction or abscesses, and can be used to investigate the effects of hydrocephalus, vasospasm, and brain herniation. The images also provide valuable prognostic information.
The process of neuroradiologic interpretation is complex. Excellent image quality is essential, and, to this end, the examination should be tailored to the clinical indication, with an appropriate selection of imaging parameters such as field of view and timing of intravenous contrast injection. The accurate interpretation of the images obtained then depends on a thorough knowledge of anatomy, normal anatomic variations, and pathophysiology. A basic knowledge of medical physics is also required to understand the imaging characteristics of both normal and abnormal tissues. Excellent communication between the radiologist and clinician is essential, as all radiologic studies must be interpreted in clinical context. It should be kept in mind that the hardest thing for the radiologist to do in real-time practice is to label a study as normal with great confidence. The consequences of incorrectly classifying a study normal could be, obviously, very grave. This chapter does not attempt to teach the process of ruling out pathology, but rather serves as an introduction to the use of both standard and advanced imaging techniques as applied to the critically ill, neurologically compromised patient. The focus is on classic imaging findings of the brain, head and neck, and spine in the acute setting.
Herniation Syndromes
A full description of any lesion includes location—for example, extra-axial, intra-axial, or intraventricular—size, density on CT or intensity on MRI with respect to normal tissue, the presence or absence of contrast enhancement, and the effect on surrounding structures. Many intracranial processes require immediate treatment to preserve brain function, and the urgency of any radiologic finding depends largely on the mass effect on normal neural tissue. This assessment must be made for all of the lesions subsequently described, and therefore is discussed first. The basic principle that allows this concept to be understood is that the brain and spinal cord are incompressible, and are contained in the confined space of the skull and spinal canal. Any abnormality, such as a hematoma, tumor, or edema, adds volume to this confined space and increases pressure, with the result that important normal structures are displaced. Initially, sulci in the region of the abnormality become compressed; with increasing mass effect, brain herniation occurs. Several distinct herniation syndromes have been described.
Subfalcine Herniation
This refers to brain that is shifted across the midline underneath the falx cerebri (Fig. 29.1). This tends to be more pronounced anteriorly, as the connections of the falx to the tentorium posteriorly are stronger and relatively immobile. There is compression of the ipsilateral lateral ventricle, and the contralateral temporal horn can become trapped and dilated as CSF continues to be produced there. This type of herniation can result in an anterior cerebral artery (ACA) territory infarct if the ACA is compressed against the dura. This is more likely to occur the more severe the midline shift, especially if greater than 1 cm.
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Figure 29.1. Postcontrast axial T1 magnetic resonance. A large left frontal mass results in subfalcine herniation with shift of the ventricles and septum pellucidum to the right across midline (black line). |
Transtentorial Herniation
This can occur in two separate directions, downward or upward, with respect to the incisura, which is an opening in the dura through which the brainstem passes. The plane of the incisura can be approximated on midline sagittal images by drawing a line from the dorsum sella to the junction of the vein of Galen and straight sinus (Fig. 29.2A). This line should normally bisect the interpeduncular fossa and tectum. The splenium of the corpus callosum should lie above this line. When there is downward transtentorial herniation from a supratentorial mass, the optic chiasm will be displaced toward the sella, the interpeduncular fossa will be compressed, the brainstem will appear buckled, and the splenium of the corpus callosum will lie below the plane of the incisura (Fig. 29.2B). When there is upward transtentorial herniation, usually from a cerebellar mass, the brainstem will be compressed against the clivus, the fourth ventricle will be compressed, and brainstem structures will become superiorly displaced with respect to the plane of the incisura.
On axial images, transtentorial herniation can be assessed by evaluating the circum mesencephalic cisterns. With downward transtentorial herniation, the ambient cisterns and suprasellar cistern will become effaced (Fig. 29.3). When there is upward transtentorial herniation, the quadrigeminal plate cistern becomes effaced (Fig. 29.4). Uncal herniation, a subtype of downward transtentorial herniation, usually occurs as a result of a middle cranial fossa mass, and is recognized by the mesial portion of the temporal lobe, the uncus, displaced into the suprasellar cistern, causing effacement of the crural cistern.
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Figure 29.2. A: Normal midline sagittal T1 magnetic resonance (MR). The plane of the incisura (white line) runs from the posterior sella to the junction of the vein of Galen and the straight sinus. B:Sagittal T1 weighted MR. A large tectal mass resulting in hydrocephalus and downward transtentorial herniation. Here, a line drawn along the plane of the incisura would intersect the splenium of the corpus callosum and pass above the interpeduncular fossa. |
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Figure 29.3. Axial computed tomography image in a patient with supratentorial mass effect resulting in downward transtentorial herniation. There is effacement of the suprasellar and ambient cisterns (white arrow) with preservation of the quadrigeminal plate cistern (black arrow). |
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Figure 29.4. Axial computed tomography image in a patient with posterior fossa mass effect resulting in upward transtentorial herniation. Notice the effacement of the quadrigeminal plate cistern (arrow). |
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Figure 29.5. Axial noncontrast computed tomography. There is diffuse brain edema with loss of normal gray–white differentiation, effacement of the sulci, and compression of the ventricles. |
Transtentorial herniation can cause vascular complications from compression of major arteries against the dura. Infarcts in both the anterior and posterior circulation can result. Postherniation hemorrhage can also occur when the mass effect resolves and the occluded vessel reperfuses. In the brainstem, these hemorrhages are referred to as Duret hemorrhages.
Tonsillar Herniation
This typically occurs as a result of a posterior fossa mass, and is recognized by the cerebellar tonsils being displaced through the foramen magnum. This can result in fourth ventricular outlet obstruction and hydrocephalus.
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Figure 29.6. Tc-99m diethylene triamine penta-acetate brain death study. Projection images demonstrate no evidence of intracranial blood flow. There is increased activity over the nasal region (the “hot nose” sign commonly seen in brain death due to persistent external carotid arterial flow). Images from over the abdomen indicate perfusion of both kidneys, important information in a potential organ donor. |
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Figure 29.7. Axial fluid-attenuated inversion recovery magnetic resonance. Subarachnoid blood is present as bright signal in the sylvian fissures and sulci. A small amount of intraventricular hemorrhage is seen layering dependently in the left lateral ventricle. |
Brain Edema
There are two types of brain edema, vasogenic and cytotoxic. Cytotoxic edema occurs with cell damage, as is seen with stroke. Cytotoxic edema is best detected with diffusion-weighted MR images. Vasogenic edema occurs with leakage of fluid into the extracellular space, and is a common finding associated with many lesions, including neoplasms and infection. Diffuse brain edema is recognized by loss of gray–white differentiation, effacement of sulci and cisterns, and slitlike ventricles (Fig. 29.5).
The intracranial vascular compartment, unlike the brain itself, is compressible, and so a mass within the confined space of the cranial vault that increases intracranial pressure will have a detrimental effect on the vascular compartment. Normally, there is a reserve volume and autoregulation ensures continued adequate blood flow to the brain despite increased intracranial pressure. However, this only works up to a point. Once intracranial pressure exceeds the capacity for blood to flow to the brain, brain death occurs. A nuclear medicine brain death study, often performed with Tc-99m diethylene triamine penta-acetate (DTPA), can be used to assess the presence of intracranial blood flow (Fig. 29.6).
Intracranial Hemorrhage
Noncontrast CT is the study of choice in the evaluation of acute intracranial hemorrhage, as it is a rapid, accessible test, which produces good contrast between the high-attenuating (bright) clot and the low-attenuating (dark) CSF. MRI is also very sensitive for the detection of blood products, and the appearance of the blood on different sequences can be used to date the hemorrhage. Fluid-attenuated inversion recovery (FLAIR) images provide good conspicuity of acute subarachnoid hemorrhage, as compared with conventional T1- and T2-weighted images. The FLAIR sequence is designed to suppress signal from the CSF so that it will appear dark. Subarachnoid hemorrhage appears bright on FLAIR images, and so becomes readily apparent (Fig. 29.7). The gradient recalled echo (GRE) sequence is also useful for the detection of blood products, as the hemoglobin affects the magnetic field in such a way as to decrease signal, the so-called susceptibility artifact. Thus, blood appears black on GRE images.
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Figure 29.8. Axial noncontrast computed tomography. Large right epidural hematoma with significant mass effect resulting in subfalcine herniation. Note the classic biconvex shape as the blood is confined by the frontoparietal suture anteriorly and the parieto-occipital suture posteriorly. There was an associated parietal bone fracture (not visualized on this image). |
As with all intracranial lesions, it is important to accurately localize hemorrhage on the imaging study, as this determines appropriate further workup and treatment. Moving from the outside in, this location can be extra-axial (i.e., epidural, subdural, or subarachnoid), intra-axial (i.e., involving the brain parenchyma itself), or intraventricular. The recognition of blood in each of these sites, and its implication, is discussed in this section.
Epidural Hematoma
An epidural hematoma occurs in the potential space between the inner table of the calvaria and the dura. It usually results from injury to a meningeal artery, although it can occur as a result of venous injury from trauma or surgery. The most common etiology is a skull fracture that crosses the middle meningeal artery, resulting in a temporal epidural hematoma. The arterial pressure is sufficient to separate the bone from the dura except at the sutures where the dura is very tightly adherent. This results in the classic biconvex shape of the hemorrhage, which is confined by suture lines (Fig. 29.8). An epidural hematoma can continue to expand and result in considerable mass effect, brain herniation, and death; it is, therefore, a surgical emergency.
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Figure 29.9. Axial noncontrast computed tomography. Bilateral subdural hematomas, left greater than right. There is a fluid–fluid level on the left secondary to settling out of the blood products as the patient was in a prolonged supine position. |
Subdural Hematoma
A subdural hematoma is located between the dura mater and the arachnoid, and usually results from tearing of bridging veins that course from the cortex to the dura. It is differentiated from an epidural hematoma in that it crosses sutures and has a crescent shape (Fig. 29.9). The etiology can be trauma, especially when there is rotational shear injury, but may also be secondary to a coagulopathy. Subdural hematomas are more common in elderly patients, where atrophy has resulted in a stretching of the bridging veins, predisposing them to injury.
Subarachnoid Hemorrhage
The “worst headache of my life” should bring to mind a subarachnoid hemorrhage (SAH). This type of hemorrhage is located between the arachnoid and pia mater, and therefore is detected on imaging studies as blood filling the sulci and basilar cisterns (Fig. 29.10). Small-volume or subacute SAH may not be detectable with CT, and therefore a lumbar puncture to look for xanthochromia may still be warranted, although MRI can also be used to detect subtle SAH. Once an SAH has been diagnosed, an investigation of its cause is necessary. The leading cause is aneurysmal rupture. Arterial venous malformation (AVM) is a less common etiology. The most appropriate initial imaging study to search for a vascular abnormality is CT angiography (CTA). This is a minimally invasive study that requires a rapid injection of intravenous contrast at 4 to 6 mL/sec, and thin-section helical CT imaging in the arterial phase. A volume of data is produced that can be reformatted in any plane or in three dimensions, thus facilitating a thorough search for the location, size, and orientation of an aneurysm (Fig. 29.11), or an analysis of an AVM including feeding arteries, draining veins, and any associated flow-related aneurysms. Twenty percent of patients with an aneurysm will have more than one. The location of the SAH, as well as an irregular shape of an aneurysm, can help identify which aneurysm has ruptured and which one must therefore be secured first. If an underlying etiology cannot be identified, a conventional angiogram is warranted. If this also is negative, the patient should be reimaged in 1 week to look for possible recanalization of a thrombosed aneurysm. This can be done with CTA or digital subtraction angiography; in 10% of the cases no underlying etiology will be identified.
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Figure 29.10. Axial noncontrast computed tomography. Diffuse subarachnoid blood products fill the anterior interhemispheric fissure and the basilar cisterns. This patient was found to have a ruptured anterior communicating artery aneurysm. |
Patients with SAH need to be monitored for vasospasm. This typically first appears at 48 hours, peaks around 72 hours, and then decreases over the following 4 days. While vasospasm can occur as far as 2 weeks following the sentinel event, this is less common. Vasospasm is detected on CTA as constriction of vessels, often with compensatory physiologic dilatation of the more distal vessels. Studies still need to be performed to determine the percentage narrowing of vessels that should be deemed significant. Conventional angiography is a dynamic study and is a useful tool to visualize slow blood flow through a constricted vessel and delayed filling of capillary vessels. CT perfusion imaging can provide similar information by repeatedly imaging the brain during a rapid intravenous infusion of contrast. An analysis can then be made of the time it takes for maximum contrast enhancement of different vascular territories, the volume of contrast reaching a vascular territory, and the perfusion rate. A patient with vasospasm and compensatory blood flow through collaterals often just needs to be followed or treated with triple-H therapy (hypervolemia, hypertension, and hemodilution). A patient with vasospasm and decreased perfusion may need endovascular intervention, which can be performed with an intra-arterial calcium channel blocker such as verapamil or by angioplasty (Fig. 29.12).
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Figure 29.11. Volume surface-shaded rendering from a computed tomography angiogram. There is a small aneurysm projecting anterosuperiorly at the origin of the middle cerebral artery on the right. |
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Figure 29.12. A: Axial computed tomography angiography image. Vasospasm affecting the left middle cerebral artery (MCA) and left posterior cerebral artery (PCA) following subarachnoid hemorrhage and aneurysm coiling. B: Frontal projection left internal carotid artery (ICA) angiogram also showing vasospasm in the left MCA. C: Frontal projection left ICA angiogram showing normal size of the left MCA following angioplasty for the vasospasm. |
Parenchymal Hemorrhage
Parenchymal hemorrhage has many etiologies and can be divided into traumatic versus nontraumatic causes. Traumatic causes include blunt and penetrating injuries resulting in a contusion, or rotational forces resulting in shear injury and diffuse axonal injury. Nontraumatic causes include hypertension (HTN), amyloid angiopathy, hemorrhagic stroke, hemorrhagic tumor, coagulopathy, and venous obstruction. In the setting of nontraumatic injury, the underlying etiology may not be evident on CT or MRI and correlation with the clinical history is vital.
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Figure 29.13. Axial noncontrast computed tomography. Hypertensive-related hemorrhage into the right basal ganglia. |
Parenchymal hemorrhage related to hypertension usually occurs with an acute elevation of blood pressure in the background of chronic hypertension. Chronic hypertension produces small-vessel disease that leads to lipohyalinosis. This affects the penetrating arteries such as the lenticulostriates and thalamoperforators, and explains why hypertensive hemorrhage most commonly occurs in the basal ganglia and thalamus (Fig. 29.13).
Amyloid angiopathy is deposition of β-amyloid in the media and adventitia of small- and midsized arteries of the leptomeninges and cortex. This leads to stenosis of the vessel lumen and weakening of the vessel wall, eventually resulting in the formation of microaneurysms. This predisposes patients to intraparenchymal—typically lobar—hemorrhages, which can be large and multiple. The most common locations are the frontal and parietal lobes.
Another nontraumatic source of intraparenchymal hemorrhage is venous obstruction. This has many causes, including hypercoagulable states, pregnancy, infection, malignancy, and birth control pills. The location of hemorrhage is dependent on the vascular territory of the occluded vein, and does not correspond to a typical arterial territory. Vascular congestion follows venous obstruction, which eventually leads to cell death and a venous infarct. This type of infarct tends to result in hemorrhage more frequently than arterial infarcts. The hemorrhage may also involve both cerebral hemispheres if there is occlusion of the superior sagittal sinus.
One important subset of patients with parenchymal hemorrhage is young patients with no history of trauma or other systemic disease. Special care should be given, and a careful search for an underlying vascular malformation such as AVM should be considered.
Intraventricular hemorrhage is usually secondary to extension from a parenchymal hemorrhage or has a traumatic etiology. Isolated intraventricular hemorrhage should raise the concern for an arterial venous malformation. Germinal matrix hemorrhage occurs in premature newborns and frequently extends into the ventricular system. Intraventricular hemorrhage is important to recognize because it can result in obstruction of CSF resorption and therefore hydrocephalus may ensue.
Parenchymal hemorrhage in the setting of trauma includes diffuse axonal injury (DAI) and contusion. DAI occurs secondary to rapid angular acceleration and deceleration, which results in disruption of axons and capillaries. The most common areas of involvement are the splenium of the corpus callosum, gray–white junction, and superior cerebellar peduncle. Only 20% of DAI cases are hemorrhagic, thus making MR more sensitive than CT. CT will show punctate areas of blood products surrounded by edema. MR demonstrates punctate areas of increased signal on FLAIR sequence and signal dropout on gradient echo sequence secondary to susceptibility artifact with hemorrhagic lesions. Nonhemorrhagic shear injury is detected by restricted diffusion on diffusion-weighted MR.
Brain contusion represents “bruising” of the brain cortex following multiple microhemorrhages. They can occur in a coup/contrecoup pattern. The underlying etiology is a combination of direct impact on the calvaria and the movement of the brain over bony ridges. The commonly involved areas are the frontal and temporal lobes. The temporal bones and roof of the orbit both have prominent bony ridges. The imaging hallmark of a brain contusion is a cortical hemorrhage with surrounding edema (Fig. 29.14).
Stroke
Stroke is the clinical term used to describe a permanent nontraumatic brain injury with resulting neurologic deficit. Strokes can be classified by their etiology as ischemic, secondary to hypoperfusion of an area of brain; hemorrhagic, rupture of a vascular structure leading to bleeding into the brain; or secondary to a substrate deficiency such as hypoglycemia. More than 75% of strokes are due to ischemia. A transient ischemic attack (TIA) is defined as transient neurologic symptoms or signs lasting less than 24 hours. An event that completely resolves after 24 hours is termed a reversible ischemic neurologic deficit (RIND).
Ischemic strokes can be thrombotic or embolic. In thrombotic strokes, clot forms locally on the wall of an artery, leading to decreased blood supply. In an embolic stroke, a clot becomes dislodged from the heart or an extracranial vessel, traveling to the brain and resulting in compromised blood supply. Both thrombotic and embolic strokes are secondary to blockage of arterial supply to an area of brain. However, in patients with a hypoperfusion state—hypotension, cardiac failure, dysrhythmia—decreased flow to the brain can result in damage to areas of brain with the least robust blood supply. This type of global hypoxic injury tends to occur first in the watershed areas of brain, for example, the anterior cerebral artery (ACA)–middle cerebral artery (MCA) or the MCA–posterior cerebral artery (PCA) watershed territories. Although far less common, stroke can also be the result of a venous occlusion. Predisposing factors include hypercoaguable states, pregnancy, meningitis, and sepsis. Blockage of venous outflow results in stasis of blood, which becomes deoxygenated, leading to subsequent neuronal death. Any venous structure can be involved, whether a cortical vein, a dural sinus, or the cavernous sinus. Venous infarcts should be considered in patients with ischemia affecting a nonarterial territory.
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Figure 29.14. Axial noncontrast computed tomography. Posttraumatic contusion (intraparenchymal hemorrhage) in the right frontal polar region with surrounding vasogenic edema. |
Noncontrast CT should be obtained as the initial imaging modality in patients with new neurologic deficits suspected of having a stroke. Noncontrast CT can rapidly identify patients with intracranial hemorrhage. Ischemic strokes will often show no discernible findings on noncontrasted study during the first 3 hours. Prior to 6 hours, only very subtle signs can be evident such as loss of gray–white matter distinction, haziness of the deep nuclei, or loss of the insular “ribbon” (Fig. 29.15). As time progresses, the patient will develop edema in the infarcted area, which can result in mass effect with shift of structures and potentially a herniation syndrome.
CT perfusion can often be rapidly obtained in evaluating patients for stroke. Perfusion CT produces color-coded maps of the brain at multiple levels showing differences in blood flow to areas of the brain. The color maps generated are mean transit time (MTT), cerebral blood flow (CBF), and cerebral blood volume (CBV) (Fig. 29.16). Mean transit time is the most sensitive measure to evaluate for any flow abnormality, but it is not specific. Flow will be prolonged in an area having a stroke, but also in areas with delayed flow for any reason, such as regions distal to a vascular stenosis. Decreased CBF is present in areas of the brain either at risk for or undergoing infarct. Cerebral blood volume is the most specific indicator of an area undergoing infarction. A low CBF with normal to increased CBV is an area at risk for ischemia but currently compensating for decreased flow by dilating vessels. Areas of brain with both decreased CBF and CBV are undergoing infarction. Limitations of perfusion CT include the need to administer intravenous contrast, long image acquisition times requiring often obtunded patients to hold completely still for 60 seconds, and the ability to only evaluate limited areas of the brain.
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Figure 29.15. Axial noncontrast computed tomography. Subtle loss of gray–white differentiation along the insular cortex on the left (arrows), the so-called “insular ribbon sign.” |
MRI with diffusion is currently the gold standard in acute stroke imaging. Once a hemorrhagic stroke has been excluded by CT, diffusion MR improves stroke detection to more than 95%. MR is much more sensitive for edema than CT. FLAIR sequences clearly demonstrate areas of edema not visible on CT (Fig. 29.17). Diffusion MR noninvasively detects ischemic changes within minutes of stroke onset. The technique sensitizes the images to detect microscopic—Brownian—motion of water molecules. The ability of water molecules to diffuse normally in an ischemic area rapidly decreases following onset of ischemia. Diffusion MR identifies areas of decreased water motion in regions of ischemia and displays them as bright areas (Fig. 29.17B). Since diffusion MR itself relies on T2-weighted sequences, some areas with high T2 signals that are not secondary to infarct-related edema can appear bright on diffusion imaging. Therefore, it is necessary to compare diffusion sequences with an apparent diffusion coefficient (ADC) map (Fig. 29.17C). Areas that are bright on diffusion and dark on ADC are consistent with acute infarct. Over time, the diffusion and ADC abnormalities will reverse as the stroke moves into a subacute phase. In evaluating for subacute stroke, contrast-enhanced T1-weighted MR can show enhancement of a subacute infarct as soon as 2 to 3 days following the event. Contrast enhancement can persist for 8 to 10 weeks. The “2-2-2” rule is usually followed: The enhancement begins at 2 days, peaks at 2 weeks, and resolves by 2 months. Contrast enhancement is also seen with CT imaging of subacute stroke (Fig. 29.18).
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Figure 29.16. Images from computed tomography perfusion exam. A: Mean transit time is delayed to the left middle cerebral artery (MCA) territory. B: Cerebral blood flow is decreased in the left MCA territory. C: Cerebral blood volume is also decreased to the left MCA territory consistent with infarcting tissue. |
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Figure 29.17. A: Axial fluid-attenuated inversion recovery magnetic resonance (MR). Cytotoxic edema is present as high signal in this patient with acute left middle cerebral artery (MCA) infarct. Axial diffusion-weighted MR (B) and axial apparent diffusion coefficient (ADC) map (C) showing high signal on the diffusion image and low signal on the ADC map in the left MCA territory consistent with diffusion restriction and acute infarct. |
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Figure 29.18. Pre- (A) and postcontrast (B) axial T1 magnetic resonance. Enhancing subacute infarct in the left posterior inferior cerebellar artery territory. |
Infection
Central nervous system (CNS) infections can progress rapidly, leading to stroke, hemorrhage, herniation, and death. Prompt recognition and initiation of therapy is therefore critical. Imaging can play an important role in evaluating for signs and complications of infection.
The discussion of CNS infection can take many different pathways, and may be divided into opportunistic and nonopportunistic infection, or specific pathogens can be studied individually. In the interest of simplicity, infection will be discussed anatomically. Noninfectious inflammatory disease will not be covered.
Leptomeningitis, commonly referred to as meningitis, is an inflammatory infiltration of the pia and arachnoid meninges that can be caused by bacterial, viral, or fungal agents. Most commonly, the infection occurs via hematogenous dissemination. It is important to initiate therapy quickly for patients suspected of having meningitis. Imaging is insensitive for early evidence of meningitis, as in early phases the brain most often appears normal. In fact, the most sensitive test for meningitis is a lumbar puncture, not an imaging exam. Imaging studies are more useful to evaluate for complications of meningitis. Noncontrast CT will often be relatively normal, but may show mild ventriculomegaly. Contrasted CT can show enhancing material within sulci and cisterns. CT angiography can show evidence of vasculitis, with multifocal areas of vessel irregularity.
MRI is a much more sensitive imaging modality for meningitis, though it, too, will often be unremarkable in the earliest stages of infection. FLAIR sequences can show high signal along the sulci from the proteinaceous material in the CSF (Fig. 29.19). Exudative material along the sulci will enhance in a serpiginous form on T1-weighted postcontrast images (Fig. 29.20). MRI is also useful to evaluate for complications of meningitis such as ventriculitis, abscess, and infarcts. Infarcts are common complications of advanced meningitis. A vasculitis is caused by meningeal irritation, which potentially can progress to hinder arterial flow to brain. Additionally, venous infarcts can be seen secondary to septic venous thrombosis (Fig. 29.21).
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Figure 29.19. Axial fluid-attenuated inversion recovery magnetic resonance. High signal in a serpiginous pattern along the sulci representing the high-protein inflammatory exudates in bacterial meningitis. |
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Figure 29.20. Postcontrast axial T1 magnetic resonance. Leptomeningeal enhancement in the characteristic serpiginous pattern along the sulci in a patient with bacterial meningitis. |
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Figure 29.21. Sagittal T1 magnetic resonance. High signal is seen within the superior sagittal sinus representing thrombus. |
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Figure 29.22. Postcontrast axial T1 magnetic resonance. Enhancement is present along the ependymal lining of the left lateral ventricle consistent with ventriculitis. |
Ventriculitis, also called ependymitis, is a complication of meningitis or ventricular shunting. Again, MR is much more sensitive than CT, and will demonstrate enhancement along the ventricular margins (Fig. 29.22). There will often be increased FLAIR signal surrounding the ventricles, and the ventricles may appear enlarged. Keep in mind that this imaging appearance is not specific to infection; for example, in an immunocompromised individual, this can be seen in lymphoma.
Pachymeningitis, an infiltration of the dura, can be differentiated from leptomeningitis by its thick nodular enhancement pattern that closely approximates the calvaria and does not extend into the sulci. Pachymeningitis can be seen with tuberculosis and fungal infections, but noninfectious etiologies such as sarcoid and carcinomatosis should be considered as well.
Focal pyogenic infections of brain parenchyma lead to cerebritis. Cerebritis is brain inflammation usually secondary to hematogenous dissemination of bacteria. Fungal and parasitic etiologies are also possible, but less common. The most common areas affected are the territories supplied by the middle cerebral artery, specifically the frontal and parietal lobes. In early cerebritis, only MR imaging will demonstrate an abnormality, with FLAIR sequences showing an area of increased signal intensity. Later imaging features include an unencapsulated, poorly defined mass with patchy contrast enhancement on CT and MR. Untreated, over time, this infectious, inflammatory mass will develop a capsule, become more organized, and eventually develop as a brain abscess. The capsule rim will enhance on postcontrast CT and MR (Fig. 29.23A). FLAIR and T2-weighted imaging will often show prominent vasogenic edema surrounding the abscesses (Fig. 29.23B). Often, the capsule will be thinnest on the ventricular side, which may help in distinguishing this ring-enhancing lesion from a malignancy. Additionally, brain abscesses will show restricted diffusion (Fig. 29.23C, D). The time course for the changes from cerebritis to abscess is approximately 2 weeks.
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Figure 29.23. A: Postcontrast axial T1 magnetic resonance: Multiple rim-enhancing lesions. B: Axial fluid-attenuated inversion recovery magnetic resonance. Prominent vasogenic edema surrounding the lesions. Axial diffusion (C) and axial apparent diffusion coefficient magnetic resonance images (D) showing that the lesions demonstrate restricted diffusion, consistent with multiple brain abscesses. Nocardia was the causative agent in this patient. |
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Figure 29.24. A, B: Axial fluid-attenuated inversion recovery magnetic resonance images. Bilateral asymmetric edema is present in the temporal lobes and insular cortex. This appearance should raise suspicion for herpes simplex virus encephalitis. |
Encephalitis is brain inflammation caused by a viral infection or a hypersensitivity reaction to a foreign protein; approximately 2,000 cases are reported each year. Sources include herpes simplex virus (HSV), mosquito-borne viruses, cytomegalovirus, and Epstein-Barr virus. Herpes encephalitis progresses rapidly and can result in death without prompt recognition and therapy. It is usually due to reactivation of latent HSV-1 virus in an immunocompetent patient, which ascends into the brain via the trigeminal and olfactory nerves. Although CT is insensitive to early features of this disease, MRI will show findings within 2 days of onset. Initially, edema is seen in the medial temporal, insula, and inferior frontal lobes (Fig. 29.24A, B). Occasionally this is unilateral, but more often, asymmetric bilateral disease is present. Postcontrast imaging will show patchy vague enhancement in initial phases, progressing to gyriform enhancement within 1 week.
An empyema is a loculated collection of pus that can develop intracranially in either the subdural or epidural space. These are commonly referred to as subdural or epidural abscesses. These infections are considered a neurosurgical emergency and must be drained expediently. Most of these are supratentorial and present as an extra-axial collection. This fluid collection is often isodense to CSF on CT imaging, making MRI superior to CT in evaluating the extent and nature of this collection. On T1-weighted MR, the fluid will be hyperintense to CSF because of proteinaceous material—pus—within it (Fig. 29.25). Often, prominent enhancement is present along the margins of the collection. Signal changes in adjacent brain parenchyma are also commonly seen secondary to cerebritis. An empyema can develop as a complication of meningitis in younger patients. In older individuals, contiguous spread from a paranasal sinus or ear infection is the most common etiology. Occasionally, it can be difficult to determine if an epidural fluid collection is an abscess or a hematoma, in which case follow-up CT exam may be useful.
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Figure 29.25. Axial postcontrast T1 magnetic resonance. Extra-axial fluid collection adjacent to right frontal lobe with enhancement along the dural margin, consistent with a subdural empyema. |
Subdural empyema, in its most basic form, is disruption of the arachnoid layer with a combination of both CSF and purulent material beneath the dura. The fluid collection can cover the convexities and tract within the interhemispheric fissure. A subdural empyema may present either acutely or chronically, and 10% of patients will go on to develop a brain abscess or venous thrombosis. MR is more sensitive than CT for its detection. The signal is low on T1-weighted images, and high on T2 and FLAIR images. A key imaging feature is that subdural empyemas demonstrate restricted diffusion and a subdural effusion does not. In the chronic setting, there is rim enhancement of the surrounding granulation tissue. An imaging pitfall is in differentiating a chronic subdural hematoma from a subdural empyema. Both look similar but should have a different clinical history.
Spine
The spine consists of both osseous and ligamentous components that transmit forces to allow movement while protecting the spinal cord and vertebral arteries. In terms of mechanical forces, the spine is divided into three columns. The anterior column includes the anterior longitudinal ligament and the anterior two thirds of the vertebral body and the annulus fibrosis. The middle column consists of the posterior third of the vertebral body, the posterior annulus, and the posterior longitudinal ligament. The facet joints, laminae, spinous processes, and interspinous ligaments comprise the posterior column. Interruption of two contiguous columns, including both osseous and ligamentous components, creates instability.
Following trauma, plain films or CT is initially obtained and evaluated for fracture and ligamentous injury. An initial assessment must be made of appropriate alignment in both coronal and sagittal planes. Spinal alignment is assessed in the sagittal plane with the use of the anterior vertebral body line, posterior vertebral body line, spinolaminar line, and dorsal surface articular pillar lines (Fig. 29.26). The atlantoaxial and craniocervical relationship are evaluated with various measurements, including the basion–dens interval of 12 mm or less, the Power's ratio, and the atlantoaxial distance of less than 2 mm in an adult. Abnormal alignment or a widened facet joint or intervertebral disc space raises suspicion for ligamentous injury, and should prompt additional imaging. Dynamic flexion and extension plain films or MR with STIR (short tau inversion recovery) sequences are helpful. Abnormal motion during flexion and extension or increased signal within the ligaments on STIR images is consistent with ligamentous injury (Fig. 29.27).
Spine fractures are classified according to the mechanism of injury as axial load, hyperflexion, hyperextension, lateral flexion, or rotational injuries. Variations of spine fractures are numerous and complex, and only the more common injuries are discussed in this section.
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Figure 29.26. Normal lateral view of the cervical spine with normal smooth curvature of the anterior vertebral body line, posterior vertebral body line, dorsal surface articular pillar line, and spinal laminar line. |
Axial load forces can produce a Jefferson fracture of C1 or a burst-type fracture. A Jefferson fracture is a C1 ring fracture where fractures are present in both the anterior and posterior rings and the lateral masses are dislocated laterally. Burst fractures are caused by severe axial compression leading to fractures of the anterior and posterior margins of the vertebral body with anterior and middle column involvement—an unstable injury, often with retropulsion of bony fragments into the canal.
Flexion injuries result in compression fractures, facet dislocations (unilateral or bilateral), or a flexion teardrop fracture. In contrast to a burst fracture, compression fractures only involve the anterior vertebral body (anterior column) and are stable as long as there is only anterior column involvement. A flexion teardrop injury is the most severe cervical spine injury. The “teardrop” is composed of a sheared fragment from the anteroinferior vertebral body, which is associated with bilateral facet subluxations, posterior subluxation of the vertebral body, and disruption of all major stabilizing ligaments. This injury often results in severe compromise of the spinal canal, cord compression, and neurologic impairment (Fig. 29.28).
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Figure 29.27. Sagittal short tau inversion recovery magnetic resonance. Focal disruption of the posterior longitudinal ligament at the C2 level (arrow). |
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Figure 29.28. Lateral plain film. Flexion teardrop fracture involving C7 with posterior subluxation of the C7 vertebral body. In this case, the teardrop was avulsed from the anterosuperior corner of the vertebral body, whereas an anteroinferior corner avulsion is more commonly seen. |
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Figure 29.29. Lateral plain film of the cervical spine. Extension teardrop fracture (arrow) with an avulsed bony fragment from the anteroinferior corner of C2. |
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Figure 29.30. Coronal cervical spine computed tomography reconstruction. Lateral flexion injury resulting in fracture of the left articular pillar of C7 (arrow). |
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Figure 29.31. Coronal reformation of computed tomography angiography. A focal defect is present in the left vertebral artery (arrow) immediately adjacent to transverse process fracture consistent with traumatic dissection. |
Extension injuries can result in a hangman's fracture, a pillar fracture, an extension teardrop fracture, or a hyperextension fracture–dislocation. A hangman's fracture is composed of bilateral pars or pedicle fractures of C2. This often results in widening of the canal, and there is usually no initial neurologic deficit; however, the injury is very unstable. Extension teardrop fractures commonly involve the upper cervical spine, most commonly at C2 where the anteroinferior corner avulses from the axis, tearing the anterior longitudinal ligament (Fig. 29.29). The unstable hyperextension fracture dislocation results from a severe hyperextension force. This causes a comminuted articular mass fracture with contralateral facet subluxation, mild anterior subluxation, and potential rupture of both the posterior and anterior longitudinal ligaments.
Injuries resulting in a lateral flexion force lead to transverse process fractures, lateral flexion dislocation of the dens, and lateral wedgelike compression fractures of a vertebral body (Fig. 29.30). Additionally, nerve root avulsions and damage to the brachial plexus are associated with a severe lateral flexion force.
Finally, rotational forces cause rotatory atlantoaxial subluxation, as well as injuries to the anterior and posterior longitudinal ligaments. Rotatory atlantoaxial subluxation can result in the patient holding the head in a persistently cocked orientation. In severe cases, rotatory atlantoaxial subluxation or fixation can compromise flow in the vertebral arteries. Radiographically, this presents as a persistent rotational abnormality in the alignment of C1 with C2.
Often, the direction of forces involved in a spinal injury is complex, and variations and combinations of the above-described injuries are seen. For example, dens fractures require a combination of flexion and extension as well as a shearing lateral force vector.
The vertebral arteries arise from the subclavian arteries and usually enter the cervical spine at C6. Should a fracture line cross the transverse foramen through which the vertebral artery runs, a CTA should be obtained to evaluate for traumatic injury. An intimal flap, focal narrowing, or even occlusion may be seen with vessel dissection (Fig. 29.31). Fractures that cross the carotid canal at the skull base may require similar evaluation with CTA.
When acute spinal cord compression symptoms present, an MR should be obtained to evaluate for a spinal epidural hematoma, acute disc herniation, or cord injury. Other than trauma, spinal epidural hematomas can be the result of anticoagulant therapy, vascular malformation, or systemic disease such as systemic lupus erythematosus. Even minor trauma can cause an epidural hematoma as the valveless venous plexus in the epidural space is prone to injury. MRI best demonstrates blood products in the epidural space (Fig. 29.32).
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Figure 29.32. Sagittal (A) and axial (B) T1 magnetic resonance of the lumbar spine in a patient with an L1 burst fracture. There is heterogeneous high signal intensity within the anterior epidural space extending from L1 through the upper sacrum representing epidural blood products (arrowheads). |
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Figure 29.33. A: Sagittal T2 magnetic resonance (MR). A two-level fracture in the midcervical spine narrows the canal diameter and results in cord contusion manifested by high T2 signal in the cord. B: Axial gradient MR. Areas of dark signal representing blood products are seen within the area of cord contusion (arrowheads). |
Spinal cord injury results in neurologic impairment. It can be caused by spinal cord compression from bony fragments, stretching injury, or impairment of the vascular supply (anterior spinal artery in the overwhelming majority of cases). Symptoms are related to the level and severity of injury. MR is the imaging modality of choice in evaluating for cord and nerve root injury. Increased T2 signal and enhancement are the hallmarks of injury (Fig. 29.33A). Cord contusions are often best visualized on gradient echo sequences, where the blood creates loss of signal and so appears black (Fig. 29.33B).
Suggested Readings
1. Gomori JM, Grossman RI. Mechanisms responsible for the MR appearance and evolution of intracranial hemorrhage. Radiographics. 1988;8:427.
2. Grossman RI, Yousem DM. Neuroradiology: The Requisites. 2nd ed. Philadelphia: Mosby; 2003.
3. Leach JL, Fortuna RB, Jones BV, et al. Imaging of cerebral venous thrombosis: current techniques, spectrum of findings, and diagnostic pitfalls. Radiographics. 2006;26:S19–S41.
4. Lell MM, Anders K, Uder M, et al. New techniques in CT angiography. Radiographics. 2006;26:S45–S62.
5. Lustrin ES, Karakas SP, Ortiz AO, et al. Pediatric cervical spine: normal anatomy, variants, and trauma. Radiographics. 2003;23:539.
6. Offiah CE, Turnbull IW. The imaging appearances of intracranial CNS infections in adult HIV and AIDS patients. Clin Radiol. 2006;61(5):393–401.
7. Srinivasan A, Goyal M, Azri FA, et al. State-of-the-art imaging of acute stroke. Radiographics. 2006;26:S75–S95.
