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

General Imaging Characteristics of Hemorrhage

The appearance of ICH on a CT scan 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 a CT scan in patients with normal hemoglobin levels (approximately 15 g/dL) and typically appears as a hyperattenuating mass. This appearance is typical because, immediately after extravasation, clot formation occurs with a progressive increase in attenuation over 72 hours as a result of increased hemoglobin concentration and separation of low-density serum. On the other hand, in anemic patients with a hemoglobin level less than 10 g/dL, acute hemorrhage can appear isoattenuating to the brain and can make detection difficult. Subsequently, after 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 an unretracted clot that appears to be hypoattenuating and resembles a whirlpool; this sign may indicate active bleeding and typically occurs in a posttraumatic setting. It is important to recognize this sign, because 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.

Use of an intravenous contrast agent usually is not necessary for CT detection of ICH. If a contrast agent is used, an intraaxial 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 extraaxial hematomas also can demonstrate peripheral enhancement, usually because of reactive changes and formation of granulation tissue. Unexpected areas of enhancement should raise concern, because active bleeding can appear as contrast pooling. Refer to the section on aneurysms and vascular malformations in this chapter for a discussion of CT angiography in the setting of acute ICH.

MRI has greatly revolutionized the evaluation of ICH. The evolution of hemorrhage from the hyperacute to the chronic stage will have corresponding signal changes on T1-weighted images (T1WIs), T2-weighted images (T2WIs), 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. Although it is beyond the scope of this chapter, a description of the physics of the signal characteristics of blood products on MRI 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 hemorrhages evolve are summarized in Table 1-1 .

Epidural Hemorrhage

Epidural hematoma is the term generally applied to a hemorrhage that forms between the inner table of the calvarium and the outer layer of the dura because of its masslike behavior. More than 90% of epidural hematomas 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. An epidural hematoma typically has a hyperdense, biconvex appearance. It may cross the midline but generally does not cross sutures (because the dura has its attachment at the sutures), although this might not hold true if a fracture disrupts the suture. Epidural hematomas usually have an arterial source, commonly a tear of the middle meningeal artery, and much less commonly (in less than 10% of cases) a 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, because 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 the patient’s condition, but generally the first follow-up CT scan may be obtained after 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 a 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 (e.g., motor vehicle collisions [MVCs], assaults, and falls, with the latter especially occurring in the elderly population). An SDH causes a 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. SDHs have a high association with subarachnoid hemorrhage. Acute SDHs thicker than 2 cm that occur with other parenchymal injuries are associated with greater than 50% mortality. As the SDH evolves to the subacute stage (within 5 days to 3 weeks) and then to the chronic stage (after more than 3 weeks), it decreases in attenuation, becoming isodense to the brain and finally to CSF. A subacute SDH can have a layered appearance as a result of separation of formed elements from serum. Subacute hemorrhages may be relatively inconspicuous when they are 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 because findings are symmetric. One should beware of bilateral isoattenuating SDHs, particularly in elderly patients who do not have generous sulci and ventricles. At this stage, the SDH should be conspicuous on MRI, especially on FLAIR sequences. A subacute SDH also may be very conspicuous on T1WIs because of 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, such as in a patient prone to repeated falls who is brought in because of a change in mental status. On both CT and MRI, these collections typically have a crescentic shape and may demonstrate enhancing septations and membranes surrounding the collection after administration of a contrast agent. Calcification of chronic SDH can occur and may be quite extensive ( Fig. 1-5 ). Areas of hyperdensity within a larger hypodense SDH may indicate an acute component due to recurrent bleeding, termed an “acute on chronic subdural hematoma.” Mixed density collections also may be acute as a result of active bleeding or CSF accumulation as a result of tearing of the arachnoid membrane. A chronic SDH is usually isointense to CSF on both T1WIs and T2WIs, 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 as a result of hyperintensity based on protein content. Hemosiderin within the hematoma will cause a signal void because of the susceptibility effect, and “blooming” (i.e., the hematoma appears to be larger than its true size) will be noted on a gradient-echo sequence.

A subdural hygroma is another type of collection that is commonly thought to be synonymous with a chronic subdural hematoma. 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 persons still use this term interchangeably with chronic subdural hematoma. CT demonstrates a fluid collection isodense to CSF in the subdural space. MRI can be useful in differentiating CSF from a chronic hematoma based on the imaging characteristics of the fluid on all sequences. Occasionally hygromas are difficult to differentiate from the prominence of the extraaxial CSF space associated with cerebral atrophy. The position of the cortical veins can be a helpful clue. In the presence of 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. SAH can be due to a variety of causes, including trauma, a ruptured aneurysm, hypertension, arteriovenous malformation, occult spinal vascular malformation, and hemorrhagic transformation of an ischemic infarction. SAH is often associated with overlying traumatic SDH. SAHs generally do not cause mass effect or focal regions of edema. However, in patients presenting with ominous signs on clinical grading scales, such as stupor or coma, diffuse cerebral edema may be evident. On CT, hyperdensity is seen within the sulci and/or basilar cisterns ( Figs. 1-6 and 1-7 ).

Although MRI may be as sensitive as CT for the detection of acute parenchymal hemorrhage and SAH, CT generally remains the modality of choice (and the imaging gold standard). The sensitivity of CT for the 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 the hemoglobin concentration and the size and location of the hemorrhage. CT is widely available, can be performed rapidly, and is relatively inexpensive. In several small studies, MRI has demonstrated sensitivity equivalent to CT for detection of acute parenchymal hemorrhage and SAH. In some cases of “CT-negative” (subacute) hemorrhage, MRI has shown greater sensitivity. However, results may be confounded by artifacts from CSF pulsations, an elevated level of protein (meningitis), or oxygen concentration (i.e., a high fraction of inspired oxygen) in CSF on FLAIR images and the presence of blood products from previous microhemorrhages on gradient-echo images.

Intraventricular Hemorrhage

In the adult population, intraventricular hemorrhage (IVH) is typically caused by trauma. It can result from extension of a parenchymal hemorrhage into the ventricles or from redistribution of SAH. Primary IVH is uncommon and is usually caused by a ruptured aneurysm, an intraventricular tumor, vascular malformation, or coagulopathy ( Fig. 1-8 ). Large IVHs are quite conspicuous on CT or MRI. 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 dependent densities within the atria and occipital horns of the lateral ventricles. Normal choroid plexus calcifications in the atria of lateral ventricles, in the fourth ventricle, and extending through the foramina of Luschka should not be mistaken for acute IVH.

Another less common type of extracerebral ICH that may present acutely is a pituitary hemorrhage, which 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 (e.g., macroadenoma and germinoma) and, less commonly, trauma.

Contusion

Parenchymal contusions result from blunt trauma and can occur in the cortex or white matter. Their locations are typically at the site of greatest impact of brain on bone, including the anterior/inferior frontal lobes and the temporal lobes. They can be considered coup (occurring at the site of impact) or contrecoup (opposite the site of impact) types. On CT, a contusion typically appears as an area of hyperdensity with a surrounding rim of hypodense edema. A parenchymal contusion can initially appear as a focal area of subtle hypodensity and may blossom on follow-up examination at 12 to 24 hours with development of an obvious central area of hyperdensity and a larger surrounding zone of hypodense edema ( Fig. 1-9 ). On MRI, signal characteristics reflect the hemorrhagic and edematous components. Over time, the density and signal characteristics of the hemorrhage will evolve in a fashion similar to a spontaneous hemorrhage. Parenchymal hemorrhage due to penetrating trauma, such as from a gunshot wound or impalement, will follow the same general pattern of evolution.

Diffuse Axonal Injury

Diffuse axonal injury (DAI) is another type of traumatic brain injury that may present with parenchymal hemorrhages and is distinct from a parenchymal contusion. DAI is an injury to the axons caused by acceleration/deceleration injury with a rotational component (usually from an MVC or other blunt trauma to the head). Complete transection of axons may occur with injury to the associated capillaries, or partial disruption of the axons may occur. DAI lesions typically occur at the interfaces of gray and white matter in the cerebral hemispheres, the body and splenium of the corpus callosum, the midbrain, and the upper pons. Lesions also may be seen in the basal ganglia. Patients sustaining DAI typically lose consciousness at the moment of impact. DAI may be suspected when the clinical examination is worse than expected based on the findings of an initial CT scan. Usually, the greater the number of lesions, the worse the prognosis. Persons 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 complete transection of the axons and associated capillaries has occurred ( Fig. 1-10 ). MRI is more sensitive than CT for detection of DAI. Approximately 30% of persons with negative CT findings will demonstrate abnormal findings on MRI. These findings include FLAIR and T2WI 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 DAI lesions 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 MRI 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 is well suited to the evaluation of white matter tracts and has been shown to be more sensitive than conventional MRI for detection of DAI and correlates more closely with clinical outcomes. Diffusion tensor imaging may be helpful for long-term diagnostic evaluation of patients with mild traumatic brain injury more so than in the initial emergency setting.

Subfalcine Herniation

Subfalcine herniation occurs as a result of displacement and impingement of the cingulate gyrus underneath the falx. It is usually caused by mass effect on the frontal lobe and is associated with ipsilateral lateral ventricle compression and obstruction of the foramen of Monro with dilatation of the contralateral ventricle (“trapped ventricle”). The degree of midline shift (not synonymous with subfalcine herniation) can be estimated by drawing a line between the anterior and posterior attachments of the falx and measuring the shift of the septum pellucidum relative to this line (see Fig. 1-3 ). Anterior cerebral artery territory infarct(s) may result from this type of herniation.

Transtentorial Herniation

Transtentorial herniations include two major types: descending transtentorial herniation (DTH) and ascending transtentorial herniation (ATH). An early DTH is known as uncal herniation , in which the uncus (i.e., the anterior portion of the parahippocampal gyrus) is displaced medially and occupies the ipsilateral suprasellar cistern. A later-stage DTH is caused by continued mass effect with displacement of the remainder of the medial temporal lobe through the tentorial 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, the brainstem shifts in the same direction. Occasionally, when marked mass effect is present, 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—that is, hemorrhages of the midbrain and pons caused by stretching and tearing of the arterial perforators. In cases of bilateral mass effect, displacement of both temporal lobes and midbrain can occur 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, compression of the oculomotor nerve (cranial nerve [CN] III) can occur with an associated palsy. ATH is less common and is caused by superior displacement of the cerebellum and brainstem through the incisura. ATH is usually due to mass effect in the posterior fossa (as from hemorrhage, tumor, or infarct), and imaging shows compression on the posterolateral midbrain with associated effacement of the ambient and quadrigeminal plate cisterns. Hydrocephalus is usually present as a result of obstruction at the level of the cerebral aqueduct of Sylvius.

Tonsillar Herniation

Tonsillar herniation is caused by downward displacement of the cerebellar tonsils through the foramen magnum into the spinal canal (generally by more than 5 mm). Imaging shows a peg-like configuration to the tonsils with obliteration of the CSF space in the foramen magnum ( Fig. 1-12 ). Complications include obstructive hydrocephalus from compression of the fourth ventricle. Mild tonsillar ectopia, Chiari I malformations, and sagging tonsils due to intracranial hypotension should not be mistaken for acute tonsillar herniation, but it should be considered seriously when downward mass effect is expected based on brain edema, mass, or hemorrhage.

Extracranial Herniation

An extracranial herniation is the displacement of brain parenchyma through a cranial and dural defect that is usually caused by trauma or a craniectomy (usually performed to prevent downward herniation from acute cerebral edema). Complications may include infarction of the herniated brain tissue.

Transalar Herniation

Transalar herniation is uncommon and, by itself, does not cause symptoms. It is usually associated with subfalcine and transtentorial herniations. This type of herniation is caused by displacement of the temporal lobe anteriorly or of the frontal lobe posteriorly across the sphenoid wing. One should look for anterior or posterior displacement of the middle cerebral artery to identify this type of herniation.

In the setting of severe head trauma, many of these different types of injuries may coexist. The mechanism of injury should correspond with the degree of injury. In cases when the reported mechanism is mild, nonaccidental trauma (e.g., “Trauma X” and “shaken-baby syndrome”) should be considered. Infants, children, persons with mental or physical disabilities, and elderly persons are particularly at risk. Skull fractures, SAH, SDH, contusions, shear injuries, infarcts, vertebral compression fractures, and retinal hemorrhages constitute the usual neuroradiologic spectrum of abnormalities. Injuries of different ages, metaphyseal and rib fractures, and visceral injuries are other common findings of child abuse.

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 causes. (Refer to the section on aneurysms and vascular malformations in this chapter for a discussion of CT angiography in the setting of acute ICH.) Hemorrhages resulting from use of illicit drugs and vascular malformations are commonly found in young adults ( Fig. 1-14 ). Sickle cell disease and venous infarcts also may present with parenchymal hemorrhage. A ruptured intracranial aneurysm occasionally may cause a parenchymal hemorrhage in association with SAH. Hypertensive hemorrhages most commonly occur in the basal ganglia and thalamus but also may primarily arise within the cerebral hemispheres, brainstem, or cerebellum. Cerebral amyloid angiopathy (CAA) is another common cause of ICH in patients older than 65 years. CAA can be found in patients with mild cognitive impairment, Alzheimer-type dementia, and Down syndrome with extracellular deposition of β-amyloid occurring in the cortex and subcortical white matter. CAA can be hereditary (autosomal dominant, Dutch type), sporadic (with the presence of the Apoε4 allele), or acquired (as from hemodialysis). The lobar hemorrhages of CAA typically occur in the frontal and parietal regions. MRI is sensitive for the detection of hemosiderin deposition resulting from multiple microhemorrhages over the course of time that appear 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 cause 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 the “acute stroke” window and level settings (see Fig. 1-15 ). A very narrow window width of 8 Hounsfield units (HUs) and a level of 32 HUs (compared with 80 and 40 HUs, 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). This medication is currently approved by the Food and Drug Administration for use within 3 hours of onset based on guidelines from the National Institute of Neurologic Disorders and Stroke rt-PA trial. Since 2013, its use within 4.5 hours of stroke onset in selected patients has been endorsed in a joint clinical policy statement of the American College of Emergency Physicians, American Academy of Neurology, and Neurocritical Care Society. Beyond this time, the risk of ICH 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 commonly been applied in stroke trials. The Alberta Stroke Program early CT score, a 10-point topographic scoring system, was 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 and is one piece of data that may be considered in determining patient management.

Magnetic Resonance: Diffusion-Weighted Imaging

MRI 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). Energy depletion will trigger a cascade that alters the internal cellular milieu, such as the glutamate excitotoxic pathway, in which reduced energy-dependent glutamate reuptake within the synaptic clefts results in the 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 approach minimizes the effects of patient motion, which is especially important when the clinical presentation includes alteration of mental status. The apparent diffusion coefficient (ADC) value is a quantitative measure that may be calculated from the diffusion-weighted images. Because diffusion-weighted images rely on both diffusion and T2 effects, it is wise to confirm that the ADC values are indeed reduced before diagnosing an acute infarct. This confirmation will reduce the number of false-positive results due to the “T2 shine-through” effect from old infarcts (gliosis) or other T2 hyperintense processes such as vasogenic edema.

Acute ischemic infarcts appear as hyperintense regions on DWI (see Fig. 1-15 ) 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 examination prompted by persistent symptoms. It is also possible that a region of ischemia (prior to a completed infarction) may not be detected on an initial imaging study, thus providing a false-negative result. False-positive results on DWI can be due to processes that mimic stroke and also cause diffusion restriction, such as certain neoplasms, multifocal metastatic disease, and abscesses. The presence or absence of associated findings on conventional MRI sequences—such as loss of gray–white matter differentiation on T1WIs and hyperintense edema on FLAIR and T2WIs—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 are presumed to be due to occlusion of small perforating branches as a result of embolic, atheromatous, or thrombotic lesions. Lacunar infarcts occur most commonly in the basal ganglia, internal and external capsules, immediate periventricular white matter (corona radiata), and, less frequently, in 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 ). Although MRI 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 also may assist in selecting the most appropriate pathway for patients with central embolic sources of infarcts based on the detection of infarcts in different vascular territories.

MRI 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 MRI 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 ADC pseudonormalization usually taking place during the next few weeks. Final ADC values will vary based on the degree of gliosis or cavitation of the infarct. It should be noted that infarct development depends on the magnitude and duration of ischemia and the metabolic demands of the affected tissue. Although 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.