Traumatic and Nontraumatic Emergencies of the Brain, Head, and Neck

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CHAPTER 1 Traumatic and Nontraumatic Emergencies of the Brain, Head, and Neck

Glenn D. Barest, Asim Z. Mian, Rohini N. Nadgir, Osamu Sakai

Create a list of the disorders of the brain, head, and neck that might commonly be expected to present to an emergency department (ED) and describe the typical imaging features. At first, this challenge seems straightforward enough. However, when put to the task, it soon becomes clear that almost every disorder within the realm of neuroradiology/head and neck radiology might at one time or another present as an acute emergency. Certain diagnoses like stroke, fractures, and epiglottitis are musts. Others such as oligodendroglioma, perhaps a slowly growing lesion, might seem less clear-cut. But realize that a wide variety of processes will result in an alteration in mental status leading to an ED visit with imaging playing a key role in diagnosis and appropriate management. On admission, inpatient workups now occur on a 24/7 basis with many complex exams completed during the night shift. On-call radiologists (often residents or fellows) are expected to provide wet readings or complete interpretations for complex cases covering the full spectrum of medicine, pediatrics, surgery, and related subspecialties. It was not that many years ago that the radiologist was faced with a seemingly never-ending stack of plain films from the ED, inpatient wards, and intensive care units in need of rapid interpretations. This work was interrupted by an occasional computed tomography (CT) scan. In this new millennium, the radiologist must maintain a rapid pace to review thousands of cross-sectional CT and magnetic resonance (MR) images with two-dimensional (2D) and three-dimensional (3D) reformats during a typical shift. For this reason, the majority of the discussion and examples in this chapter are based on these modalities and latest techniques. The last realization for authors is that the most daunting part of the task is to boil down all of the disorders and details to a set of requisites. Division of this chapter into sections is not quite as neat as one might think. It is not possible to separate the vascular system from discussion of the brain, head and neck, or spine. The imaging methods applied to the extracranial vessels in the setting of stroke are similar to those for blunt or penetrating trauma to the neck. One may, therefore, notice mention of similar techniques and findings in several places with examples appropriate to the context. All would do well to study the other volumes in the Requisites series (especially Neuroradiology, Musculoskeletal Imaging, and Pediatric Radiology), which cover this material in great detail. In this first attempt at condensing so much material into one useful volume, important topics have inevitably been neglected. It is hoped that this section can serve as a starting point for further study and become a valuable reference to on-call radiologists, emergency room physicians, and residents of both specialties.

INTRACRANIAL HEMORRHAGE AND TRAUMATIC BRAIN INJURY

Whether in the setting of head trauma or spontaneous development of headache or alteration of mental status, the ability to diagnose intracranial hemorrhage is of primary importance for all practitioners. These are some of the most common indications for brain imaging in the emergency setting. Almost invariably, the requisition will read, “Rule out bleed.” An understanding of traumatic and nontraumatic causes of intracranial hemorrhage, the usual workup, and their recognition is, therefore, important and seems like a natural starting point. Discussion of the important types of mass effect resulting from intracranial hemorrhages and traumatic brain injury is also included in this section. An understanding of hemorrhage and herniation syndromes is central to the discussion of other topics that follow, such as stroke and neoplasms.

The word hemorrhage has Greek origins: the prefix haima-, meaning “blood,” and the suffix rrhage, meaning “to gush or burst forth.” Intracranial hemorrhage (ICH) affects 15 per 100,000 individuals, with 350 hypertensive hemorrhages per 100,000 elderly patients. ICH is typically more common in the African American and Asian populations. Bleeding may take place within the substance of the brain (intra-ax.) or along the surface of the brain (extra-axial). Intra-axial hemorrhage implies parenchymal hemorrhage located in the cerebrum, cerebellum, or brainstem. Extra-axial hemorrhages include epidural, subdural, and subarachnoid hemorrhages, and intraventricular hemorrhage can be considered in this group as well. Hemorrhages can lead to different types of brain herniation, from direct mass effect and associated edema to development of hydrocephalus, causing significant morbidity and mortality.

General Imaging Characteristics of Hemorrhage

The appearance of ICH by CT can vary depending on the age of the hemorrhage and the hemoglobin level. The attenuation of blood is typically based on the protein content of which hemoglobin contributes a major portion. Therefore, the appearance of hyperacute/acute blood is easily detected on CT in patients with normal hemoglobin levels (approximately 15 g/dL) and typically appears as a hyperattenuating mass. This is because, immediately following extravasation, clot formation occurs with a progressive increase in attenuation over 72 hours due to increased hemoglobin concentration and separation of low-density serum. On the other hand, in anemic patients with hemoglobin less than 10 g/dL, acute hemorrhage can appear isoattenuating to the brain and can make detection difficult. Subsequently, following breakdown and hemolysis, the attenuation of the clot decreases until it becomes nearly isoattenuating to cerebrospinal fluid (CSF) by approximately 2 months. In the emergency setting, one should be aware of the “swirl” sign with unretracted clot appearing hypoattenuating and resembling a whirlpool; this may indicate active bleeding and typically occurs in a post-traumatic setting. It is important to recognize this sign, as prompt surgical evacuation may be required. The amount of mass effect on nearby tissues will depend on the size and location of the hemorrhage as well as the amount of secondary vasogenic edema that develops.

Administration of intravenous contrast material is usually not necessary for CT evaluation of ICH. If contrast is given, intra-axial hemorrhage can demonstrate an enhancing ring that is usually due to reactive changes and formation of a vascularized capsule, which typically occurs 5 to 7 days after the event and can last up to 6 months. Subacute and chronic extra-axial hematomas can also demonstrate peripheral enhancement usually due to reactive changes and granulation tissue formation. Unexpected areas of enhancement should raise concern, as active bleeding can appear as contrast pooling.

MR imaging has greatly revolutionized the evaluation of intracranial hemorrhage. The evolution of hemorrhage from the hyperacute to the chronic stage will have corresponding signal changes on T1-weighted images (T1WI), T2-weighted images (T2WI), fluid attenuated inversion recovery (FLAIR) images, and gradient-echo sequences. These properties can assist in detection and understanding of the time course of the injury. While beyond the scope of this chapter, description of the physics of the signal characteristics of blood products on MR is generally based on the paramagnetic effects of iron and the diamagnetic effects of protein in the hemoglobin molecule. The usual signal characteristics of hemorrhage and the general time course over which they evolve is summarized in Table 1-1.

EXTRA-AXIAL HEMORRHAGE

Extra-axial hemorrhage occurs within the cranial vault but outside of brain tissue. Hemorrhage can collect in the epidural, subdural, or subarachnoid spaces and may be traumatic or spontaneous. It is important to recognize these entities because of their potential for significant morbidity and mortality. Poor clinical outcomes are usually the result of mass effect from the hemorrhage, which can lead to herniation, increased intracranial pressure, and ischemia. Intraventricular hemorrhage will be considered with these other types of extracerebral hemorrhage.

Epidural Hemorrhage

Epidural hematoma is the term generally applied to hemorrhage that forms between the inner table of the calvarium and the outer layer of the dura due to its masslike behavior. More than 90% are associated with fractures in the temporoparietal, frontal, and parieto-occipital regions. CT is usually the most efficient method for evaluation of this type of hemorrhage. Epidural hematoma typically has a hyperdense, biconvex, or lens-shaped appearance. It may cross the midline but does not cross sutures (since the dura has its attachment at the sutures). This might not hold true if a fracture disrupts the suture. There is usually an arterial source, commonly due to tear of the middle meningeal artery and much less commonly (less than 10%) due to tear of the middle meningeal vein, diploic vein, or venous sinus (Figs. 1-1 and 1-2). The classic clinical presentation describes a patient with a “lucid” interval, although the incidence of this finding varies from 5% to 50% in the literature. Prompt identification of an epidural hematoma is critical, as evacuation or early reevaluation may be required. Management is based on clinical status, and therefore alert and oriented patients with small hematomas may be safely observed. The timing of follow-up CT depends on patient condition, but, generally, the first CT scan may be obtained in 6 to 8 hours and, if the patient is stable, follow-up may be extended to 24 hours or more afterward.

Subdural Collections

Subdural hematoma (SDH) is the term generally applied to hemorrhage that collects in the potential space between the inner layer of the dura and the arachnoid membrane. It is typically the result of trauma (motor vehicle collision, assaults, and falls, the latter especially in the elderly population), causing tear of the bridging vein(s), and has a hyperattenuating, crescentic appearance overlying the cerebral hemisphere (Fig. 1-3). These hemorrhages can cross sutures and may track along the falx and tentorium but do not cross the midline. Inward displacement of the cortical vessels may be noted on a contrast-enhanced scan. There is a high association with subarachnoid hemorrhage. Acute SDHs thicker than 2 cm, seen with other parenchymal injuries, are associated with greater than 50% mortality. As the SDH evolves to the subacute (5 days to 3 weeks) and then chronic (more than 3 weeks) stage, it decreases in attenuation, becoming isodense to the brain and finally to CSF. Subacute SDH can have a layered appearance due to separation of formed elements from serum. Subacute hemorrhages may be relatively inconspicuous when isodense, and therefore it is especially important to recognize signs of mass effect, such as sulcal effacement, asymmetry of lateral ventricles, and shift of midline structures, as well as sulci that do not extend to the skull (Fig. 1-4). Bilateral isoattenuating SDHs can be especially challenging since findings are symmetric. Beware of this, particularly in the elderly patient who does not have generous sulci and ventricles. At this stage, the SDH should be conspicuous on MR imaging, especially on FLAIR sequences. A subacute SDH may also be very conspicuous on T1-weighted images due to the hyperintensity of methemoglobin.

Chronic subdural hematomas are collections that have been present for more than 3 weeks. Even a chronic hematoma may present in the emergency setting; for example, in a patient prone to repeated falls, brought in because of a change in mental status. On both CT and MR, these collections typically have a crescentic shape and may demonstrate enhancing septations and membranes surrounding the collection after contrast administration. Calcification of chronic SDH can occur and be quite extensive (Fig. 1-5). Areas of hyperdensity within a larger hypodense SDH may indicate an acute component due to recurrent bleeding, an “acute on chronic subdural hemorrhage.” Mixed density collections may also be acute, due to active bleeding or CSF accumulation due to tear of the arachnoid membrane. Chronic SDH is usually isointense to CSF on both T1WI and T2WI, but the appearance can be variable depending on any recurrent bleeding within the collection. The FLAIR sequence is typically very sensitive for detection of chronic SDH due to hyperintensity based on protein content. Hemosiderin within the hematoma will cause a signal void due to susceptibility effect, and “blooming” (appears to be larger than its true size) will be noted on gradient-echo sequence.

Subdural hygroma is another type of collection and is commonly thought to be synonymous with chronic subdural hemorrhage. The actual definition of a hygroma is an accumulation of fluid due to a tear in the arachnoid membrane, usually by some type of trauma or from rapid ventricular decompression with associated accumulation of CSF within the subdural space. Many still use this term interchangeably with chronic subdural hematoma. CT demonstrates a fluid collection isodense to CSF in the subdural space. MR can be useful in differentiating CSF from chronic hematoma based on the imaging characteristics of the fluid on all sequences. Occasionally hygromas are difficult to differentiate from the prominence of the extra-axial CSF space associated with cerebral atrophy. Position of the cortical veins can be a helpful clue. In atrophy, the cortical veins are visible traversing the subarachnoid space, whereas with a hygroma they are displaced inward along with the arachnoid membrane by the fluid in the subdural space.

Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) fills the space between the pia and the arachnoid membrane, outlining the sulci and basilar cisterns. This can be due to a variety of causes, including trauma, ruptured aneurysm, hypertension, arteriovenous malformation, occult spinal vascular malformation, and hemorrhagic transformation of ischemic infarction. SAH is often associated with overlying traumatic subdural hematoma. Subarachnoid hemorrhages generally do not cause mass effect or edema. On CT, hyperdensity is seen within the sulci and/or basilar cisterns (Figs. 1-6 and 1-7).

Although MR imaging may be as sensitive for the detection of acute intraparenchymal and subarachnoid hemorrhage, CT generally remains the modality of choice (and imaging gold standard). Sensitivity of CT for detection of SAH compared with CSF analysis can vary from up to 98% to 100% within 12 hours to approximately 85% to 90% after 24 hours of symptom onset. Other factors affecting sensitivity are hemoglobin concentration, size, and location of the hemorrhage. CT is widely available, rapid, and relatively inexpensive. In several small studies, MR has demonstrated sensitivity equivalent to CT for detection of acute parenchymal hemorrhage and SAH. In some cases of “CT-negative” (subacute) hemorrhage, MR has shown greater sensitivity. However, results may be confounded by artifacts from CSF pulsations, elevated protein (meningitis), or oxygen concentration (high fraction of inspired oxygen) in CSF on FLAIR images and presence of blood products from previous microhemorrhages on gradient-echo images.

Intraventricular Hemorrhage

Intraventricular hemorrhage (IVH) is typically caused by trauma in the adult population. It can result from extension of parenchymal hemorrhage into the ventricles or redistribution of subarachnoid hemorrhage. Primary intraventricular hemorrhage is uncommon and usually caused by a ruptured aneurysm, intraventricular tumor, vascular malformation, or coagulopathy (Fig. 1-8). Large IVHs are quite conspicuous on CT or MR. They may occupy a majority of the ventricle(s) and may result in hydrocephalus and increased intracranial pressure. Small amounts of IVH may be difficult to detect; one must check carefully for layering hemorrhage within the atria and occipital horns of the lateral ventricles. Normal choroid plexus calcifications in the atria of lateral ventricles, the fourth ventricle, and extending through the foramina of Luschka should not be mistaken for acute IVH.

Another less common type of extracerebral intracranial hemorrhage that may present acutely is pituitary hemorrhage. It is usually associated with pituitary apoplexy due to pituitary necrosis that may become hemorrhagic. Presenting symptoms may include headache, visual loss, ophthalmoplegia, nausea, and vomiting. Other causes of pituitary hemorrhage include tumors (macroadenoma, germinoma) and, less commonly, trauma.

INTRA-AXIAL HEMORRHAGE

The cause of intra-axial (parenchymal) hemorrhages can generally be categorized as spontaneous or traumatic. Traumatic causes include blunt injury from motor vehicle collision (MVC) assault, and penetrating injuries such as gunshot wounds. There are many spontaneous causes, and these are discussed in the section on hemorrhagic stroke.

Diffuse Axonal Injury

Diffuse axonal injury (DAI) is another type of traumatic brain injury that may present with parenchymal hemorrhages and is distinct from parenchymal contusion. DAI is an injury to the axons caused by acceleration/deceleration injury with a rotational component (usually from motor vehicle collision or other blunt trauma to the head). There may be complete transection of axons with injury to the associated capillaries, or partial disruption of the axons. The lesions of DAI typically occur at the inter-faces of gray and white matter in the cerebral hemispheres, the body and splenium of the corpus callosum, midbrain, and upper pons. Lesions may also be seen in the basal ganglia. Patients sustaining DAI typically lose consciousness at the moment of impact. DAI may be suspected when the clinical exam is worse than expected based on the findings on initial CT scan. Usually, the greater the number of lesions, the worse the prognosis. Individuals who recover usually demonstrate lingering effects such as headaches and cognitive deficits. Initial CT scans in more than half of patients with DAI may be negative. CT findings include hypodense foci due to edema in areas of incomplete axonal disruption and hyperdense foci due to petechial hemorrhage where there is complete transection of the axons and associated capillaries (Fig. 1-10). MR is more sensitive than CT for detection of DAI. Approximately 30% of those negative by CT will demonstrate abnormal findings on MR. These findings include FLAIR and T2 hyperintensities (edema) and gradient-echo hypointensities (hemorrhages) (Fig. 1-11). Lesions may appear hyperintense on diffusion-weighted images. It is estimated that more than 80% of the lesions of DAI are nonhemorrhagic. Generally, if imaging is repeated within 3 to 5 days, more lesions will become apparent as the process evolves. A staging system for DAI based on locations of lesions on histopathology may be applied to MR findings. Stage 1 is based on subcortical lesions in the frontal and temporal lobes. Stage 2 will also show lesions in the corpus callosum and lobar white matter, and stage 3 will have lesions in the midbrain and pons. Diffusion tensor imaging, particularly helpful in evaluation of white matter tracts, has been shown to be more sensitive than conventional MR for detection of diffuse axonal injury and correlates more closely with clinical outcomes.

BRAIN HERNIATIONS

Brain herniation is a potentially devastating complication of increased intracranial pressure. The most common causes include intracranial hemorrhages, brain tumors, and cerebral edema from stroke or anoxic injury. To explain this concept, a common example from the literature describes the brain as being separated into multiple compartments within a rigid container. Any shift of the brain from one compartment to another is considered herniation. With shift of the brain, there can be mass effect on adjacent and contralateral parenchyma, the brainstem, major intracranial vessels, and cranial nerves. As a result, the feared complications of herniations include ischemic infarcts due to compression of the major intracranial vessels (commonly, the anterior and posterior cerebral arteries), cranial nerve palsies, and “brain death” due to compression and ischemia of the brainstem. The major types of intracranial herniations include subfalcine, transtentorial, tonsillar herniation through the foramen magnum, extracranial (through a defect in the skull), and, less commonly, transalar herniation. Once the complications of herniation have developed, it is often too late to intervene. Therefore, it is best to recognize the signs of impending herniation, when prompt neurosurgical intervention may avert disaster.

Transtentorial Herniation

Transtentorial herniations include two major types, which are the descending transtentorial herniation (DTH) and the ascending transtentorial herniation (ATH). An early DTH is known as uncal herniation, in which the uncus is displaced medially and occupies the ipsilateral suprasellar cistern. A later-stage DTH is caused by continued mass effect with displacement of the medial temporal lobe through the incisura, which completely occupies the suprasellar cistern (along with the uncus) and causes enlargement of the ipsilateral and effacement of the contralateral ambient cisterns. This phenomenon occurs because, as there is marked shifting of brain in the supratentorial compartment, there is also shift of the brainstem in the same direction. There is also compression of the ipsilateral cerebral peduncle. Occasionally, when there is marked mass effect, there can be compression of the contralateral cerebral peduncle against the tentorium, or “Kernohan’s notch,” which leads to ipsilateral motor weakness (this phenomenon may be a false localizing sign). Other imaging findings include a “trapped” temporal horn of the lateral ventricle contralateral to the side of the mass and Duret hemorrhages—hemorrhages of the midbrain and pons caused by stretching and tearing of the arterial perforators. In cases of bilateral mass effect, there can be displacement of both temporal lobes and midbrain through the incisura leading to effacement of the basilar cisterns bilaterally. Complications of this type of herniation include compression of the posterior cerebral artery and penetrating basal arteries with associated infarcts in these vascular distributions (see Fig. 1-2). In addition, there can be compression of the oculomotor nerve (CN III) with an associated palsy. ATH is less common and is caused by superior displacement of the cerebellum and brainstem through the incisura. It is usually due to mass effect in the posterior fossa (as from hemorrhage, tumor, or infarct), and on imaging there is compression on the posterolateral midbrain bilaterally with associated effacement of the ambient and quadrigeminal plate cisterns. There is usually hydrocephalus due to obstruction at the level of the cerebral aqueduct of Sylvius.

ACUTE CEREBROVASCULAR DISORDERS

Although usually not due to trauma, acute cerebrovascular disorders are treated with the same urgency as traumatic injuries or spontaneous intracranial hemorrhage. In the United States approximately 700,000 strokes occur each year. Almost 30% are recurrent, and 75% occur in patients over the age of 65. The 20% mortality rate is surpassed only by cardiac disease and cancer. Stroke is the leading cause of severe, long-term disability and long-term care. Estimates of annual cost exceed $50 billion. One clinical definition of stroke is a neurologic deficit caused by inadequate supply of oxygen to a region of the brain. Stroke can be due to a low flow state or rupture of a vessel and therefore may be divided into ischemic and hemorrhagic varieties. The definition of stroke used for current clinical trials requires symptoms lasting more than 24 hours or imaging of an acute clinically relevant brain lesion in a patient with rapidly vanishing symptoms. A transient ischemic attack (TIA) used to imply resolution of the deficit within a 24-hour time period. The proposed new definition of TIA is a brief episode of neurologic dysfunction caused by a focal disturbance of brain or retinal ischemia, with clinical symptoms typically lasting less than 1 hour, and without evidence of infarction. Estimates of the annual incidence of TIA in the United States vary from 200,000 to 500,000. Evidence of acute infarction may be identified by MR imaging in up to 50% of patients who meet the clinical criteria for a TIA. Semantics can be unclear when an abnormality is detected on imaging in the absence of symptoms.

Hemorrhagic Stroke: Spontaneous Parenchymal Hemorrhage

Approximately 10% to 15% of strokes present with an acute parenchymal hemorrhage. The most common cause is hypertension (Fig. 1-13). Coagulopathies, hematologic disorders including hypercoagulable states, amyloid angiopathy, drugs, vascular malformations and aneurysms, vasculitides, and tumors round out the usual list of etiologies. Hemorrhages resulting from illicit drug use and vascular malformations are commonly found in young adults (Fig. 1-14). Sickle cell disease and venous infarcts may also present with parenchymal hemorrhage. A ruptured intracranial aneurysm may occasionally cause a parenchymal hemorrhage in association with subarachnoid hemorrhage. Hypertensive hemorrhages most commonly occur in the basal ganglia and thalami but may also primarily arise within the cerebral hemispheres, brainstem, or cerebellum. Cerebral amyloid angiopathy (CAA) is another common cause of intracranial hemorrhages in patients over 65 years of age. CAA can be found in patients with mild cognitive impairment, dementia of Alzheimer type, and Down syndrome with extracellular deposition of beta amyloid occurring in the cortex and subcortical white matter. CAA can be hereditary (autosomal dominant, Dutch type), sporadic (presence of Apoε4 allele), or acquired (as from hemodialysis). The lobar hemorrhages of CAA typically occur in the frontal and parietal regions. MR is sensitive for the detection of hemosiderin deposition resulting from multiple microhemorrhages over the course of time appearing as small hypointense foci on gradient-echo sequences.

Imaging of Acute Ischemic Stroke

Computed Tomography

The role of imaging in acute stroke diagnosis and management continues to evolve. Since the mid-1970s, unenhanced CT has been the first-line modality to determine the etiology of acute neurologic deficits. CT can offer the chance to detect an ischemic infarct, generally in the middle cerebral artery territory, within 3 hours in up to one third of cases based on findings of subtle parenchymal hypodensity, loss of gray–white matter differentiation (including loss of the insular ribbon or margins of basal ganglia; Fig. 1-15), and effacement of sulci. A hyperdense vessel sign may indicate the presence of an acute thrombus and support the diagnosis. The sensitivity for detection of acute stroke has been shown to increase with the use of an “acute stroke” window and level settings (see Fig. 1-15). A very narrow window width of 8 Hounsfield units (HU) and a level of 32 HU (compared with 80 and 20 HU, respectively) may increase the sensitivity of CT to approximately 70% without a loss of specificity. CT is currently used to screen patients who may be considered for treatment with intravenous recombinant tissue plasminogen activator (rt-PA) within 3 hours of onset based on guidelines from the National Institute of Neurologic Disorders and Stroke (NINDS) rt-PA trial. Beyond 3 hours, the risk of intracranial hemorrhage due to intravenous thrombolysis was shown to outweigh potential benefits. An association between larger stroke volumes (greater than one third of the middle cerebral artery territory) and reperfusion hemorrhage was initially reported. This criterion for the use of 100 mL estimated infarct volume has been commonly applied in stroke trials. The Alberta Stroke Program early CT score (ASPECTS), a 10-point topographic scoring system, was later developed to try to more easily quantify initial stroke volumes. This score has been shown to correlate with the initial National Institutes of Health stroke score (NIHSS).

Magnetic Resonance: Diffusion-weighted Imaging

MR, with diffusion-weighted imaging (DWI), which became widely available in routine clinical practice in the late 1990s, offers significantly greater sensitivity and specificity for the detection of acute stroke (greater than 90% compared with approximately 60% for CT). To put it very simply, energy depletion will trigger a cascade that will alter the internal cellular milieu and result in development of cytotoxic edema. The restriction of water molecule diffusion appears as hyperintensity on diffusion-weighted images. The diffusion “experiment” can be performed with a variety of rapid imaging techniques, such as echo planar imaging, and can acquire images of the entire brain in half a minute. This minimizes the effects of patient motion, especially important when the clinical presentation includes alteration of mental status. The apparent diffusion coefficient value is a quantitative measure that may be calculated from the diffusion-weighted images. Since diffusion-weighted images rely on both diffusion and T2 effects, it is wise to confirm that the apparent diffusion coefficient values are indeed reduced before diagnosing an acute infarct. This will reduce the number of false positives due to “T2 shine-through” effect from old infarcts (gliosis) or other T2 hyperintense processes such as vasogenic edema.

Acute ischemic infarcts may appear as hyperintense regions on DWI (see Fig. 1-15), and this can occur as quickly as 30 minutes after onset. Up to 100% sensitivity has been demonstrated in clinical studies. However, in routine practice, small lesions in the brainstem may not be perceived initially, only to be detected on a follow-up exam prompted by persistent symptoms. It is also possible that a region of ischemia (prior to completed infarction) may go undetected on an initial imaging study, resulting in a false negative result. False positives on DWI can be due to processes that mimic stroke and also cause diffusion restriction, such as certain neoplasms, multifocal metastatic disease, and abscesses. Presence or absence of associated findings on conventional MR sequences—such as loss of gray–white matter differentiation on T1WI, and hyperintense edema on FLAIR and T2WI—may help with diagnosis, although these signs may be inconspicuous for 6 to 12 hours after stroke onset. Blooming on gradient-echo sequences due to intravascular thrombus and loss of expected vascular flow voids are other useful clues.

Lacunar infarcts are generally less than 1 cm in diameter and presumed to be due to occlusion of small perforating branches due to embolic, atheromatous, or thrombotic lesions. They occur most commonly in the basal ganglia, internal and external capsules, immediate periventricular white matter (corona radiata), and, less frequently, the centrum semiovale. Occlusion of basilar artery perforators will result in lacunes in the brainstem. Diffusion imaging offers the ability to identify very small, acute infarcts even in the background of chronic white matter disease and remote lacunes (Fig. 1-16). While MR is still considered a relatively expensive technique, it has the potential to reduce the number of unnecessary hospital admissions for recurrent small vessel infarcts in many patients. It may also help to select the most appropriate pathway for patients with central embolic sources of infarcts based on detection of infarcts in different vascular territories.

MR is also valuable in the setting of neonatal hypoxic ischemic encephalopathy. Cranial ultrasonography and CT may be used to evaluate germinal matrix hemorrhages, periventricular leukomalacia, and hydrocephalus. Diffusion-weighted MR is most sensitive for evaluating the different patterns of injury. In preterm infants subjected to mild hypotension, the periventricular regions are most often affected. With more severe hypotension, the basal ganglia, brainstem, and cerebellum may be involved. In full-term infants with mild hypotension, infarcts in the border zones between anterior and middle cerebral arteries or between middle and posterior cerebral arteries may result. Severe hypotension may result in infarcts of basal ganglia, hippocampi, corticospinal tracts, and sensorimotor cortex.

Diffusion-weighted hyperintensity generally begins to decline after a few days, with the process of apparent diffusion coefficient (ADC) pseudonormalization usually taking place over the next few weeks. Final ADC values will vary based on degree of gliosis or cavitation of the infarct. It should be noted that infarction development depends on the magnitude and duration of ischemia and the metabolic demands of the affected tissue. While diffusion restriction due to ischemia almost always results in infarction, rare cases of spontaneous reversible diffusion abnormalities have been reported, as well as those occurring in the setting of thrombolytic therapy.

Magnetic Resonance Angiography

Noninvasive imaging of the vessels of the head and neck with MR angiography (MRA) based upon time-of-flight or phase-contrast MRA techniques can be used to locate stenoses and occlusions in the extracranial and intracranial arterial systems (see Fig. 1-15). Gadolinium-enhanced MRA has become the standard of care at some institutions; this requires consideration of renal function. Complete brain MR and head and neck MRA examinations can be acquired in less than 30 minutes and have become the routine standard of care, often performed immediately or soon after completion of CT. It must be stressed that patient safety is a primary concern and therefore careful attention to screening for potential contraindications prior to MR scanning is a requisite at all times.

Magnetic Resonance: Perfusion Imaging

It became clear from imaging-based stroke trials that final infarct volumes were often larger than those identified by imaging at the time of admission. Advances in rapid scanning techniques soon led to the ability to obtain functional images of brain perfusion. By demonstrating an ischemic zone at the periphery of an acute infarct, salvageable tissue (the so-called penumbra) could be targeted with novel therapies. Dynamic gadolinium-enhanced T2∗ perfusion-weighted imaging (PWI) is a commercially available technique that is based on the decrease in tissue signal intensity as a function of time during passage of a bolus of contrast. Functional “maps” of different perfusion parameters in the entire brain may be calculated from the time-signal intensity curves obtained during a minute-long acquisition. Cerebral blood volume (CBV) and tissue mean transit time (MTT) can be estimated using different methods, most commonly with deconvolution analysis. One limitation of MR-based techniques is that the blood volume estimate is a relative value. Cerebral blood flow (CBF) can be estimated by dividing CBV by MTT. A penumbra will be identified when a region of decreased CBF or prolonged MTT is larger than the infarct detected by DWI—a perfusion mismatch. Based on the extent of the mismatch, aggressive therapies may be pursued in order to limit the final infarct volume.

In some cases, the perfusion abnormality may exactly match the diffusion abnormality, and thus there is no penumbra. The final infarct volume is not expected to increase further. In other cases, where prompt reperfusion has occurred, such as from early vessel recanalization, the perfusion abnormality may be smaller than the abnormality. In both of these situations, the risk of aggressive treatment is probably not warranted. The potential of improved clinical outcomes from therapeutic strategies based on perfusion imaging may result from either salvage of tissue at risk or reduction of complications.

Thus, the paradigm of acute stroke imaging is shifting based on therapeutic trials such as Desmoteplase in Acute Ischemic Stoke (DIAS) and Dose Escalation of Desmoteplase for Acute Ischemic Stroke (DEDAS). These were imaging-based trials of a novel drug derived from bat saliva that catalyzes the conversion of plasminogen to plasmin, which breaks down fibrin to dissolve intravascular blood clots. Eligibility was based on clinical symptoms and demonstration of a perfusion mismatch within 3 to 9 hours of onset. Results were promising and demonstrated the value of advanced imaging compared with unenhanced CT and a strict time limit alone.

Computed Tomography: Perfusion Imaging

The advent and wide availability of helical and, more recently, of multidetector CT (MDCT) scanners has led to the use of CT angiography (CTA) and CT perfusion (CTP) imaging in the workup of suspected acute ischemic stroke. The ability to acquire a large 3D volume of data rapidly during bolus contrast administration combined with submillimeter spatial resolution results in CT angiographic images that in many instances approach the diagnostic quality of more invasive digital subtraction angiograms. Large detector arrays and cine or shuttle modes of scanner operation allow for generous coverage of the brain during perfusion studies. Detector arrays from 4 to 64 rows wide are available now and newer models with 256 and more are in development. Analogous to PWI, CT perfusion is based on measurement of tissue density as a function of time during a first pass of intravenous contrast and commonly uses deconvolution analysis. In contrast to PWI, as a result of the proportionate increase in tissue attenuation due to iodine concentration, quantitative (rather than relative) estimation of CBV (and therefore CBF) can be obtained by CTP.

CTP applied in the setting of acute stroke has been validated with clinical outcomes and follow-up imaging and also by comparison with diffusion-weighted imaging. Wintermark and colleagues have proposed that regions with CBV less than 2.5 mL/100 g be considered the “core infarct” and regions with CBF reduction of more than 34% be defined as the penumbra. These values are based on correspondence with initial DWI abnormality and final infarct size. Schaefer and colleagues have proposed other absolute values and the use of normalized CBV and CBF ratios to help distinguish ischemic tissue likely to infarct from that likely to survive following intra-arterial recanalization therapy. Perfusion maps can be visually compared to determine if a penumbra is present but may underestimate or overestimate the extent of tissue at risk (Fig. 1-17). Software packages are available that can automatically segment the processed perfusion maps into core infarct, penumbra, and normal regions based on thresholding techniques.

The ongoing MR RESCUE (MR and recanalization of stroke clots using embolectomy) trial is employing a similar, automated analysis of PWI data to determine eligibility for inclusion. Patients presenting with intracranial arterial occlusions within 8 hours of symptom onset and having a suitable penumbra are randomized to embolectomy with the Merci Retriever device (Fig. 1-18).

Data from the recently completed DIAS 2 trial, a phase III study that used either DWI/PWI/MRA or CT/CTP/CTA as eligibility criteria, are still being analyzed. However, initial reports suggest that the results were not as favorable as those of previous trials. It is hoped that analysis of outcomes with respect to imaging features may help to identify a subset of patients who might achieve therapeutic benefits with a reduced risk of symptomatic hemorrhage.

Hemorrhagic Transformation

Hemorrhagic transformation of an ischemic infarct, thought to result from reperfusion injury, can be a dreaded complication of therapy or may happen spontaneously within hours or after a period of several weeks (Fig. 1-19). If a large hematoma is present at the time of initial imaging, it may not be possible to distinguish a primary parenchymal hemorrhage from hemorrhagic transformation. The blood products generally cause substantial artifacts on DWI. However, if the hemorrhage is confined within a larger zone of restricted diffusion, the etiology may be clear. Petechial hemorrhage occurs very commonly within an ischemic infarct, is best detected by gradient-echo imaging, and does not usually lead to increased morbidity.

Cortical Laminar Necrosis

A pattern of gyriform T1 hyperintensity developing a week or two after an ischemic infarct may be attributed to cortical laminar necrosis (Fig. 1-20). It seems that gray matter is more vulnerable to ischemic necrosis than white matter (especially the third layer of the six cortical layers), and, although the signal changes may lead one to diagnose hemorrhage or calcification, in one histologic study neither was detected. The exact cause of the T1 shortening is uncertain, but it may be due to high concentrations of proteins and macromolecules.

Cerebral Venous Infarction and Sinus Thrombosis

An uncommon (annual incidence estimates of less than 1 case per 100,000 population) but important cause of hemorrhage is cerebral venous thrombosis (Fig. 1-21). This may affect cortical veins and other portions of the superficial and deep venous drainage systems. Hypercoagulable states due to pregnancy and the postpartum period, or from oral contraceptive use, dehydration, regional infections, and trauma, are relatively common causes. Common presenting symptoms include headache, seizure, and focal neurologic deficits. Fluctuating symptoms and intracranial hypertension are common as well. Bilateral parenchymal hemorrhages or infarcts that do not obey usual arterial territorial borders can be clues to diagnosis. A working knowledge of the normal anatomy of the major venous structures and the common variants is necessary to avoid diagnostic pitfalls, especially false positives. On unenhanced CT, normal venous structures may appear denser than usual due to dehydration or elevated hematocrit, whereas thrombosis should appear hyperdense relative to arteries. A filling defect or occlusion may be detected on contrast-enhanced CT. CT venography can be performed with thin-section, volumetric technique allowing for creation of 2D and 3D reconstructions. Normal and thrombosed venous sinuses take on many different appearances on MR depending on scan parameters, flow velocity, and turbulence. Unexpected hyperintensity, loss of usual flow voids, and blooming on gradient-echo sequence are clues that flow-sensitive MR venography (MRV) should be performed. Time-of-flight MRV may be less sensitive than phase contrast technique due to shine-through of methemoglobin in a thrombosed sinus simulating flow in the vessel. Contrast-enhanced MRV may be more sensitive, although enhancement of chronic thrombus can be misleading. Associated findings of edema, hemorrhage, or ischemic infarct may help toward arriving at the correct diagnosis, but brain swelling without signal changes has been reported in up to approximately 40% of patients. Cavernous sinus thrombosis is discussed in relation to complex sinus and orbit infections in the section on head and neck imaging. Prompt diagnosis of cerebral thrombosis is critical, as many of the parenchymal changes may be reversible. Systemic anticoagulation and local catheter-based thrombolytic, mechanical, or rheolytic clot dissolution are treatment considerations. Intracranial hypertension and collateral formation leading to dural arteriovenous malformations are possible long-term sequelae.

ANEURYSMS, VASCULAR MALFORMATIONS, AND VASCULAR INJURIES

Aneurysms and cerebral vascular malformations present in various ways in the emergency setting. Subarachnoid hemorrhage resulting from a ruptured aneurysm and parenchymal hemorrhage related to an arteriovenous malformation are dramatic examples of problems that may present with headache as the chief complaint. Presenting symptoms of nausea and vomiting are common with hemorrhages arising in the posterior fossa. On routine noncontrast CT, large unruptured aneurysms may simulate other mass lesions and displace or compress adjacent structures. Arteriovenous malformations may also be conspicuous on routine CT based on abnormally enlarged feeding arteries and draining veins or internal calcifications (Fig. 1-22).

The traditional gold standard for diagnostic evaluation of vascular lesions, both spontaneous and traumatic, is digital subtraction angiography (DSA). The risk of major complication from this invasive procedure is low in experienced hands and treatment (complete or partial) with endovascular techniques is possible for many types of aneurysms and other vascular lesions. That being said, the constantly improving technology and clinical experience with CT angiography have led to a substantial decrease in the number of diagnostic angiograms (at some institutions). CTA is commonly applied in the setting of spine, facial, and skull base fractures. One study of CTA in 2004 in the setting of acute SAH reported a sensitivity of 89% and specificity of 100% for detection of aneurysms. Many centers have adopted immediate CTA in their protocol for the workup of spontaneous SAH (Fig. 1-23

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