Acute epidural hematomas are often associated with skull fractures and lacerations of the dural vessels, most often meningeal arteries and veins but occasionally a dural sinus. Two-thirds of epidural hematomas are in the temporo-parietal region and they usually have a biconvex or lentiform configuration. Epidurals are limited by the firmer attachment of the dura at the suture margins, but they may cross the midline, especially with superior sagittal sinus lacerations, and they also can bridge the supra- and infratentorial compartments with tears along the torcula and transverse sinuses.

Subdural hematomas, both acute and chronic, are most often caused by bleeding from torn bridging dural veins. Subdural hematomas are less frequently associated with skull fractures, but more frequently associated with parenchymal brain damage. The subdural space is a more freely communicating space and the hematomas form a crescentic shaped layer over the brain surface. Subdural hematomas readily cross suture lines but do not cross the midline. Instead, they extend along the dura of the falx into the interhemispheric fissure and onto the tentorium, which epidurals cannot do. Both epidural and subdural hemorrhages occur within the confined space of the bony calvarium and compress the adjacent brain, often requiring emergency evacuation.

Chronic subdural hematomas are usually related to a slower venous bleed without accompanying cerebral parenchymal injury. A thick,vascular dural membrane forms that can be a source for repeated episodes of hemorrhage. These collections are more often biconvex, rather than the crescentic shape of acute subdural hematomas. The injury leading to a chronic subdural can be relatively minor and may have occurred weeks before presentation. Patients often present with disturbances of mentation and consciousness rather than focal or lateralizing signs. An iatrogenic cause is overshunting or too rapid decompression of chronic hydrocephalus.

Multiple studies have demonstrated improved visualization of extra-axial hemorrhage with MR compared to CT, largely related to the high conspicuity of hyperintense subacute hemorrhage (methemoglobin) on T1-weighted images and the multiplanar capabilities of MR. Coronal images are very helpful for identifying subtemporal collections and hemorrhage adjacent to the tentorium cerebelli. Chronic subdural hematomas are

often isointense with gray matter on T1-weighted images, probably due to dilution and partial resorption or breakdown of free methemoglobin. High T1 signal within what otherwise appears to be a chronic subdural hematoma suggests rebleeding. Hemosiderin is rarely seen in subdural hematomas without repeated episodes of bleeding, due to either low macrophage activity or removal of hemosiderin that has formed. The presence of membranous strands coursing through an extra-axial collection is additional evidence for a chronic subdural hematoma. The thick subdural membranes will also enhance following contrast infusion.

Severe head injuries are often associated with rotational forces that produce shear stresses on the brain parenchyma. The brain itself has very little rigidity and is extremely incompressible. Brain volume can be decreased only by exerting great pressure. On the other hand, the brain is soft and malleable. Relatively little effort is required to distort the shape of the brain. The parenchyma is of relatively uniform density, except for differences between the CSF of the ventricles and surrounding brain tissue. Slight differences in density also exist between gray and white matter.

When the skull is rapidly rotated, it carries along the superficial brain parenchyma but the deeper structures lag behind, causing axial stretching, separation and disruption of nerve fiber tracts. Shear stresses are most marked at junctions between tissues of differing densities. As a result, shear injuries commonly occur at gray/white matter junctions, but they are also found in the deeper white matter of the corpus callosum, centrum semiovale, brain stem (mostly the midbrain and rostral pons) and cerebellum. Lesions in the basal ganglionic regions are usually found along the borders between the ganglia and the internal or external capsules, in other words, the deep gray-white matter junctions of the cerebral hemispheres. The thalamic and basal ganglia injuries are hemorrhagic in slightly more than 50% of cases. On the other hand, shear injuries of the corpus callosum and centrum semiovale are more often nonhemorrhagic.

Attempts to correlate CT findings with acute and chronic sequelae of closed head trauma have been discouraging, largely related to the insensitivity of CT to many cerebral injuries. Chiefly among these, poorly seen by CT and well seen by MR, are the diffuse axonal injuries or white matter shear injuries. These injuries constitute the most frequent

MARY YVETTE ALLAIN TINA RALPH SHERYL BART HEINRICH PIPOY TLE JAM CECILLE DENESSE VINCE HOOPS CES XTIAN LAINEY RIZ KIX EZRA GOLDIE BUFF MONA AM MAAN ADI KC
PENG KARLA ALPHE AARON KYTH ANNE EISA KRING CANDY ISAY MARCO JOSHUA FARS RAIN JASSIE MIKA SHAR ERIKA MACKY VIKI JOAN PREI KATE BAM AMS HANNAH MEMAY PAU
RACHE ESTHER JOEL GLENN TONI

findings on MR in head trauma, comprising as high as 40% of all lesions. Shear injuries are most often multiple, ovoid and parallel to white matter fiber bundles. They are hyperintense on T2 and hypointense of T1-weighted scans, unless hemorrhagic components are present, in which case more complex patterns are observed. During transition phases of hematoma evolution, combinations of methemoglobin, hemosiderin rings and peripheral edema can result in layers of differing signal intensity and a target-like appearance. The axial plane is the primary plane of imaging for both cortical contusions and shear injuries, but supplemental coronal views are helpful to assess injuries to the body of the corpus callosum and the inferior frontal and temporal lobes. Fast scan techniques or gradient-echo images have lower resolution but are useful in uncooperative patients. Contrast enhancement has little role in the evaluation of brain contusions.

The five major causes of cerebral infarction are vascular thrombosis, cerebral embolism, hypotension, hypertensive

anoxia/hypoxia. Thrombotic strokes may occur abruptly but the clinical picture often shows gradual worsening over the first few hours. Primary causes of arterial thrombosis include atherosclerosis, hypercoagulable states, arteritis, and dissection. Secondary compromise of vascular structures can result from traumatic injury, intracranial mass effect, neoplastic encasement, meningeal processes, and vasospasm.

Embolic strokes characteristically have a very abrupt onset. After a number of hours, there may be sudden improvement in symptoms as the embolus lyses and travels more distally. The source of the embolus is usually either the heart (patients with atrial fibrillation or previous myocardial infarction) or ulcerated plaques at the carotid bifurcation in the neck.

Hypotension can be cardiac in origin or result from blood volume loss or septic shock. Hypertension can cause a primary intracerebral hemorrhage, or the elevated arterial pressure can overwhelm the brain's autoregulatory mechanism, resulting in breakthrough of the blood-brain barrier and brain edema. The latter phenomenon of hypertensive encephalopathy is a potential complication of eclampsia, but is usually transient and reversible. Anoxia/hypoxia events are usually related to respiratory compromise from severe lung disease, perinatal problems, near drowning, high altitude, carbon monoxide inhalation, or CNS mediated effects.

abnormalities related to previous events. In patients with stroke, the earliest sign may be abnormal vascular density/signal.

hyperdense on CT. Acute clot may be difficult to detect on MR, but the occluded artery should be apparent by the absence of a normal flow void. The absent flow void is easiest to see in the larger arteries at the base of the brain on T2-weighted images. It is not possible to conclusively distinguish a complete occlusion from a critical stenosis with markedly reduced flow. Subacute clot is hyperintense and is easiest to visualize in the basilar and middle cerebral arteries on T1-weighted images. One must be careful not to mistake in-flow enhancement with intraluminal clot. This phenomenon is most often observed in the end slices of a multislice set in arteries with slow flow entering the imaging volume.

Another valuable sign of acute stroke is arterial enhancement. With slow arterial flow, the spin-echo is able to capture the intravascular signal, and the T1 shortening effect of the gadolinium renders the arteries hyperintense

Arterial enhancement is more apparent in the smaller distal branches. It will be present in up to 45% of patients during the first week.

The first parenchymal changes observed on CT and MR reflect the cytotoxic edema affecting primarily the gray matter. It is important to remember that the CT scan may be negative for the first 24-36 hours. Massive infarctions may be visible as early as 6 hours. The MR scan is usually positive within three to four hours following a stroke. One of the earlier signs on CT is loss of the normal gray-white contrast as the edematous cortex becomes isodense to the underlying white matter. A similar phenomenon is not observed on MR because the increased water in the gray matter renders the cortex higher signal on T2-weighted images and lower signal on T1-weighted images, thereby increasing gray- white contrast. It is often easier to appreciate the increased cortical signal on proton density-weighted images. The cortical swelling is more apparent on T1- weighted scans. Cortical edema produces effacement of the sulci on both CT and MR.

After 6-8 hours the accompanying vasogenic edema highlights the areas of brain infarction. These fluid shifts are more profound and are responsible for effacement of the ventricles and midline shifts. The mass effect increases over the first few days and becomes maximal at about five days.

The subacute stage begins during the second week with capillary proliferation in the area of infarcted brain tissue. This neovascularity is devoid of any blood-brain barrier and intravascular contrast freely diffuses into the interstitial spaces. The serpiginous character of the gyral enhancement is quite distinctive of cerebral infarction. A focal cerebritis or encephalitis can mimic this pattern,

but usually the clinical picture sets apart these entities. Following contrast infusion, infarcts will typically enhanced between 2 and 8 weeks, but the enhancement can persist for up to three months.

As an infarct evolves, it becomes progressively lower in density on CT (higher in signal on T2-weighted images) and more well defined over the next few weeks, eventually approaching the density of CSF. As the mass effect resolves and the infarcted tissue is resorbed, the adjacent sulci and ventricle will enlarge. The end result is a chronic infarct with focal areas of cystic encephalomalacia and some surrounding parenchymal change due to gliosis.

Since most infarcts result from occlusion of vessels, the CT or MR pattern of abnormality should follow one of the major vascular territories, such as the anterior cerebral, middle cerebral or posterior cerebral arteries. Infarcts can usually be distinguished from inflammatory and neoplastic disease because unlike the white matter pattern of edema found with tumors and abscesses, infarcts involve the cortex as well and, therefore, the abnormal density or signal intensity should extend peripherally to involve the cortex. As mentioned above, the enhancement pattern of infarcts is also fairly characteristic, having a gyral pattern of enhancement along the cortex. If a stroke is due to systemic hypotension or hypoxia, the area of infarction is commonly found in watershed areas between the major vascular territories.

Lacunar infarction results from occlusion of the small penetrating arteries at the base of the brain, including the lenticulostriate and thalamoperforating arteries. They are smaller infarcts (less than 1 cm) and are found in the basal ganglia, thalamus and brainstem. MR is far more sensitive than CT for detecting small lacunar infarcts, particularly in the brainstem where CT scans are often degraded by artifacts from the bone at the skull base.

The four major causes of hemorrhagic stroke are hypertension, hemorrhagic infarction, hypocoagulable state, and amyloid angiopathy. The criteria for

patient, 60 years of age or older, and a basal ganglia or thalamic location of the hemorrhage. A CT scan is the procedure of choice for evaluating these patients. Arteriography is necessary only if one of these criteria is missing. Hypertensive hemorrhages are often large and devastating. Since they are deep hemorrhages and near ventricular surfaces, ventricular rupture is common. One-half of hypertensive hemorrhages occur in the

In stroke patients, despite the fact that the CT is often negative for the first 24-48 hours, it is often obtained on the day of admission to exclude an intracerebral hemorrhage before the patient is placed on anticoagulant therapy. Hemorrhage into an infarct can occur during the first week, usually between the third and fifth days. Hemorrhagic infarction is a hallmark of embolic infarction. This occurs after the embolus breaks up, resulting in reperfusion of the infarcted area. As mentioned above, hemorrhage is also common with venous infarction.

MALFORMATIONS
INTRACEREBRAL HEMORRHAGE
CT Features

Together, hypertension, aneurysm, and vascular malformations account for 80% of intracerebral hemorrhages. All cerebral hematomas, whatever the cause, have a similar

depends on the size of the hematoma,

usually within one to six weeks,

the outside toward the center.

low density appears in 24-48 hours. Rim

enhancement appears in one week and persists for six weeks. The end result of a hematoma is decreased parenchymal density, focal atrophy and local ventricular dilatation.

Intracerebral hematomas have a very dynamic appearance on MR, changing in signal intensity over time. Acute blood, in the form the oxyhemogloblin, is isointense with the brain parenchyma. Within a few hours,

hematoma. Deoxyhemoglobin has a predominant effect of shortening T2, resulting in low signal on T2-weighted images. After three to four days, the deoxyhemoglobin is progressively converted to methemoglobin, which is a paramagnetic substance. Although methemoglobin shortens both T1 and T2, the predominant effect is T1 shortening. As a result, at this stage, hematomas are high signal in both T1-and T2-weighted images. Over the next few months, the methemoglobin is slowly broken down into hemichromes which produce only mild T1 shortening. Hematomas at this end stage are slightly