Extracerebral Hemorrhage, Etc.

Subject: radiology Topic: neurology 1 Lecturer Dr. Irene bandong 2t Shifting /sept 6 ‘08 Trans group: loa loa Girls EXTRACEREBRAL HEMORRHAGE 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.

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. SHEAR INJURIES

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

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

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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. IMAGING OF STROKE AND CEREBRAL ISCHEMIA CAUSES OF STROKE The five major causes of cerebral infarction are vascular thrombosis, cerebral embolism, hypotension, hypertensive hemorrhage, and 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. CT AND MR IMAGING Acute Infarcts CT and MR scans in patients with asymptomatic bruits or TIA's are usually negative, unless they disclose

abnormalities related to previous events. In patients with stroke, the earliest sign may be abnormal vascular density/signal. Acute thrombus or embolus is 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 on T1-weighted images. 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 graywhite contrast. It is often easier to appreciate the increased cortical signal on proton density-weighted images. The cortical swelling is more apparent on T1weighted 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. Subacute and Chronic Infarcts 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,

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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. Vascular Patterns 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.

Hemorrhagic Stroke The four major causes of hemorrhagic stroke are hypertension, hemorrhagic infarction, hypocoagulable state, and amyloid angiopathy. The criteria for hypertensive hemorrhage include a hypertensive 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

putamen; the thalamus in 25%; pons and brainstem, 10%; cerebellum, 10%, and cerebral hemispheres, 5%. 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. IMAGING OF CEREBRAL HEMORRHAGE MALFORMATIONS INTRACEREBRAL HEMORRHAGE CT Features

and AV

Together, hypertension, aneurysm, and vascular malformations account for 80% of intracerebral hemorrhages. All cerebral hematomas, whatever the cause, have a similar resolution pattern on CT. The rate of resolution depends on the size of the hematoma, usually within one to six weeks, and they resorb from the outside toward the center. Perihematoma 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. MR Appearance 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, the oxyhemoglobin is converted to deoxyhemoglobin within the 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

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high signal on T1-weighted images and remain high signal on the T2-weighted images. Another interesting phenomenon occurs around the periphery of hematomas. Macrophage activity results in degradation of the methemoglobin and conversion of the iron moiety to hemosiderin. Hemosiderin shortens T2 and produces a black ring around the hematoma on T2-weighted images. We have observed this ring as early as nine days after hemorrhage, and the ring becomes thicker over time. The amount of hemosiderin varies from one hematoma to another, and the specific physiologic and chemical factors that influence this are unknown. In small hematomas (less than 1 cm), we have noted low signal intensity from hemosiderin throughout the cavity. The length of time that the hemosiderin will remain in the area of a hematoma is also unknown, but we have observed hemosiderin at the site of a

VASCULAR MALFORMATIONS

Arteriovenous Malformation The arteriovenous (AV) malformation consists of a congenital abnormality of anomalous, dilated capillaries that result in shunting of blood from the arterial to venous side. AV malformations are by far the most common of the cerebrovascular malfor mations. One-half of patients present with seizures or a neurological deficit due to compression of normal brain or a steal phenomenon. The other half presents with hemorrhage. The hemorrhage is usually more benign than that due to a ruptured aneurysm. Ninety-five percent of AV malformations are in the supratentorial compartment, either in a lobar or deep location and 10% are in the infratentorial region. Dural supply is more commonly found with infra tentorial lesions although it is important to remember than any AV malformation adjacent to a dural surface can receive dural contributions.

previous hematoma as long as four years following the primary hemorrhage. From this discussion, it is apparent that the specific signal intensities of a hematoma on T1and T2-weighted images provide a clue as to the age of the hemorrhage. Hypertensive Hemorrhage The criteria for hypertensive hemorrhage include a hypertensive 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 putamen; the thalamus in 25%; pons and brainstem, 10%; cerebellum, 10%, and cerebral hemispheres, 5%.

CT features of an AV malformation on plain scan include a high- absorption irregular mass with large feeding arteries and draining veins, focal areas of calcification and no surrounding edema or mass effect. The contrast scan shows serpiginous enhancement with prominent arteries and veins. Due to the rapidly flowing blood from these lesions, a flow void is observed on MR scan. As a result, the characteristic feeding arteries and draining veins can be imaged without any injection of contrast material. One should suspect AV malformation as a cause of an intracerebral hemorrhage if the hemorrhage is lobar and away from the territory of the anterior communicating and middle cerebral arteries, and also in deep hemorrhages in younger, normotensive patients. It is important to remember that the hematoma may compress a small AV malformation. If the initial angiogram is negative, a follow-up study should be done one to two months later, after the hematoma and mass effect have resolved. AV malformations can thrombose either spontaneously or due to compression by the hematoma.

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Cavernous Angioma They are characterized by a honeycomb of endothelium-lined vascular spaces, separated by fibrous, collagenous bands with no intervening neural tissue. Most cavernous angiomas are asymptomatic and are noted incidentally on MR scans. They may cause seizures or a focal neurologic deficit, and on occasion they will be of sufficient size to produce symptoms by mass effect. The intralesional hemorrhages are usually small and occult clinically. Multiplicity is common. Cavernous angiomas invariably contain hemosiderin from chronic hemorrhage and are distinctly hypointense on T2-weighted MR images. Lesion margins are "fuzzy" due to the magnetic susceptibility effect of the hemosiderin, and a "blooming effect" occurs with gradient-echo sequences. Calcification is often present. Mild enhancement can be obscured by the hemosiderin. Larger cavernous angiomas have a more complex appearance from multiple hemorrhages of varying ages. Hemosiderin lines the perimeter of these lesions and also outlines the internal compartments that contain various components of hemorrhage. CT of Subarachnoid Hemorrhage The CT scan is important, first of all, to document the subarachnoid hemorrhage and to assess the amount of blood in the cisterns. Detection of subarachnoid blood is very dependent on how early the scan is obtained. Data in the literature vary from 60-90%. If the scan is obtained within four to five days, the detection rate is very high. Secondly, the CT helps localize the site of the aneurysm. This can be done by the distribution of blood within the cisterns and also with dynamic scanning following an IV bolus of contrast. Thirdly, the CT is important to evaluate complicating factors such as cerebral hematoma, ventricular rupture, hydrocephalus, cerebral infarction, impending uncal herniation and rebleed. Regarding CT patterns of ruptured aneurysm, an anterior communicating aneurysm is suggested by blood in the cisterna lamina terminalis, anterior pericallosal cistern, and interhemispheric fissure. Identification of clot within a cistern makes this sign more specific. There may be extension of blood into the septum pellucidum and lateral ventricle, and hematoma in the inferomedial frontal lobe. Localizing posterior communicating artery aneurysms is more difficult because the blood is usually diffuse within the cisterns. Intracerebral hematoma or ventricular rupture is unusual with posterior communicating aneurysms. Rupture of a middle cerebral aneurysm is characterized by blood in the sylvian fissure and a hematoma in the temporal lobe, which may also rupture into the adjacent temporal horn. Posterior fossa aneurysms often do not have good localizing findings on the CT scan.

It is not uncommon to find a small amount of blood in the ventricles in patients with subarachnoid hemorrhage. That does not necessarily mean that direct ventricular rupture has occurred because subarachnoid blood can enter the ventricular system in a retrograde manner. Ventricular rupture from a bleeding aneurysm is usually more dramatic, often showing a cast of blood or clot in a lateral ventricle. A subarachnoid hemorrhage with blood in the lateral ventricle is usually due to an anterior communicating aneurysm. Middle cerebral aneurysm is another possibility, but that should be associated with a temporal hematoma. Similarly, pericallosal aneurysms can rupture into the ventricle but then there should be hematoma in the corpus callosum as well. What is the role of a contrast scan in subarachnoid hemorrhage? The combination of clinical and plain scan findings is often fairly conclusive that a subarachnoid hemorrhage has occurred. If emergency arteriography is considered, contrast limitations need to be considered. We obtain the contrast scan if the diagnosis is in doubt, or if the plain scan shows a large intracerebral hematoma that needs emergency evacuation and there is no time for the angiogram. The detection rate of aneurysms with contrast scanning ranges from 40% for posterior communicating to 80% for anterior communicating, middle cerebral and basilar aneurysms. A common problem is that the subarachnoid blood obscures the enhancing aneurysm. Conventional MR sequences are very insensitive for detecting subarachnoid hemorrhage. Clots within cisterns can be detected, but in general, MR is not the procedure of choice in the work-up of patients with subarachnoid hemorrhage. Due to the flow void phenomenon, aneurysms about the circle of Willis can be identified on spin-echo MR images. With fluid-attenuated inversion recovery (FLAIR) sequences, the CSF is dark, so that subarachnoid hemorrhage can be seen more easily. These sequences may be helpful for detecting subarachnoid blood in the posterior fossa where CT has difficulty and in the sulci over the cerebral convexities. MULTIPLE SCLEROSIS On histologic examination, acute MS plaques show partial or complete destruction and loss of myelin with sparing of axon cylinders. They occur in a perivenular distribution and are associated with a neuroglial reaction and infiltration of mononuclear cells and lymphocytes. The perivascular demyelination gives the appearance of a finger pointing along the axis of the vessel. In the pathologic literature these elongated lesions have been named "Dawson's fingers." Active demyelination is accompanied by transient breakdown of the blood-brain barrier. Chronic lesions show predominantly gliosis. MS plaques are distributed throughout the white matter of the optic nerves, chiasm and tracts, the cerebrum, the brain stem, the cerebellum and the spinal cord.

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Imaging Features MS plaques are hyperintense on T2-weighted and FLAIR images and hypointense on T1-weighted scans. Specific signal intensities of MS lesions will vary depending on the magnetic field strength, the pulse sequence parameters, and partial volume effects. Occasionally, acute plaques may have a thin rim of relative T2 hypointensity or T1 hyperintensity. The T1 hyperintensity is attributed to free radicals, lipid-laden macrophages, and protein accumulations. MS plaques are usually discrete foci with well-defined margins. Most are small and irregular, but larger lesions can coalesce to form a confluent pattern. Multiple focal periventricular lesions can give a "lumpy-bumpy" appearance to the ventricular margins. As a result of their perivenular distribution, many periventricular plaques have an ovoid configuration, with their long axis oriented transversely on an axial scan. The ovoid lesion is the imaging correlate of "Dawson's finger." In general, MS plaques have a homogeneous texture without evidence of cystic or necrotic components. Hemorrhage is not a feature of MS lesions. Edema and mass effect are also uncommon. The periventricular white matter is a favorite site for MS plaques, particularly along the lateral aspects of the atria and occipital horns. The corpus callosum, corona radiata, internal capsule, visual pathways, and centrum semiovale are also commonly involved. When more than a few lesions are present, symmetric involvement of the cerebral hemispheres seems to be the rule. Any structures that contain myelin can harbor MS plaques, including the brain stem, spinal cord, subcortical Ufibers, and even within the gray matter of the cerebral cortex and basal ganglia. A distinctive site in the brain stem is the ventrolateral aspect of the pons at the fifth nerve root entry zone. Brain stem and cerebellar plaques are more prevalent in the adolescent age group. Lesions of the corpus callosum have been a special focus of study. On axial sections, plaques in the corpus callosum above the lateral ventricles have a transverse orientation along the course of the nerve fiber tracts and vessels. Sagittal FLAIR images are especially helpful to depict the small callosal lesions closely apposed to the superior ependymal surface of the lateral ventricles. Early edema and demyelination along subependymal veins produce a striated appearance. Atrophy of the corpus callosum is common in long-standing, chronic MS and is seen best on T1-weighted sagittal images. Involvement of the visual pathways, particularly the optic nerves, frequently occurs sometime during the course of disease. Patients may present with optic neuritis, although in about half of those cases, MRI will unveil other silent lesions in the brain. Imaging plaques in the optic nerves is a challenge even for MRI. Unenhanced spin-echo sequences are not very sensitive, and generally some type of fat suppression is required.

Probably the most sensitive method for detecting acute MS of the optic nerves is the combination of gadolinium enhancement and fat suppression. Gadolinium enhancement Since acute MS plaques are associated with transient breakdown of the blood-brain barrier, gadolinium contrast agents will produce enhancement of these lesions on T1-weighted images. Enhancement will be observed for 8 to 12 weeks following acute demyelination. Thus, Gd-enhanced MR can be used to assess lesion activity just like contrast-enhanced CT. Either nodular or ringlike enhancement may be seen early after contrast injection, but the central areas tend to fill in and become more homogeneous on delayed scans. Immediate postcontrast scans are most sensitive for detecting MS, and delayed scanning is not necessary. Contrast-enhanced MR can be used to follow the progression of disease and to assess the response to therapy. Occasionally, large plaques, also called tumefactive MS, may produce mass effect and simulate other mass lesions. However, compared with neoplastic or inflammatory processes, MS plaques have minimal surrounding edema and relatively less mass effect for the overall size of the white matter lesions. Balo's concentric sclerosis has a unique MR appearance. Like tumefactive MS, the plaques usually are quite large, but in addition, a concentric laminated pattern is seen on T2 and T1-weighted images. Similarly, post-contrast images often show rings of enhancement alternating with nonenhancing regions during the acute phase. Adrenoleukodystrophy Adrenoleukodystrophy is a peroxisomal disorder that results in abnormal accumulation of very long chain fatty acids. Several forms have been described, but xlinked adrenoleukodystrophy is the classic form that presents in males between the ages of 4 and 8. The neurologic findings of visual and behavioral problems, intellectual impairment and long tract signs can appear before or after adrenal gland insufficiency. Adrenoleukodystrophy is both a demyelinating and dysmyelinating disorder. Initially, it involves predominantly the parietal-occipital lobes and posterior visual pathways, but it extends forward into the frontal and temporal lobes as the disease progresses. Unlike the focal plaque-like character of multiple sclerosis, adrenoleukodystrophy tends to be contiguous within fiber tracts and often is confluent within the larger white matter bundles of the centrum semiovale. Both periventricular and subcortical white matter are affected, and in advanced disease the internal capsule, corpus callosum, corticospinal tracts and other white matter fiber tracts in the brain stem can be involved. The typical MR findings are large, symmetric, hyperintense lesions on T2-weighted images that are also

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clearly visible as hypointense areas on T1-weighted scans. The white matter abnormalities tend to be confluent and of homogeneous signal intensity. Sites of active demyelination along the advancing edges may be associated with blood-brain barrier disruption and enhance with paramagnetic contrast agents. Atypical features include frontal lobe involvement, unilateral involvement, calcifications and mass effect. INFECTIOUS AND INFLAMMATORY DISORDERS Inflammatory diseases of the brain include abscess, meningitis, encephalitis and vasculitis. The brain is protected from invading infectious agents by the calvarium, dura and blood- brain barrier. Moreover, the cerebral tissue itself is relatively resistant to infection. Most pyogenic infections are hematogenous and related to septicemia and endocarditis. Direct extension from an infected paranasal sinus or middle ear/mastoid is less common than in the pre-antibiotic era. Fungal infections are less common than bacterial infections, but are taking on more importance in AIDS patients and those immunocompromised by way of chemotherapy, neoplasia, or immunosuppressive therapy for organ transplantation. The most important viral infections of the central nervous system from an imaging point of view are aseptic meningitis, encephalitis, and progressive multifocal leukoencephalopathy (PML). Herpes simplex is responsible for a fulminant viral encephalitis, and both the human immunodeficiency virus (HIV) and cytomegalovirus (CMV) produce a white matter encephalitis associated with the AIDS epidemic.

ABSCESS Bacterial Brain abscesses may be related to infections of the paranasal sinuses, mastoids, middle ears as well as hematogenous seeding, but in 20% of cases a source is not discovered. Very rarely an abscess is secondary to meningitis. In children, more than 60% of cerebral abscesses are associated with congenital heart disease and right to left shunts. Presenting symptoms of a cerebral abscess include headache, drowsiness, confusion, seizures and focal neurologic deficits. Fever and leukocytosis are common during the invasive phase of a cerebral abscess but may resolve as the abscess becomes encapsulated. Organisms most frequently cultured from brain abscesses in otherwise immunocompetent individuals are staphylococcus and streptococcus. When the brain is inoculated with a pathogen, a local cerebritis develops. Pathologically, an area of cerebritis consists of vascular congestion, petechial hemorrhage and brain edema. The infection goes through a stage of cerebral softening, followed by

liquefaction and central cavitation. With time, the central necrotic areas become confluent and are encapsulated after one to two weeks. Edema, a prominent feature of cerebral abscess, may actually subside after the capsule forms. In the cerebritis stage, MR reveals high signal intensity on T2-weighted images, both centrally from inflammation and peripherally from edema. Areas of low signal are variably imaged on T1-weighted scans. As the progression to abscess ensues there is further prolongation of T1 and T2 centrally. The capsule becomes highlighted as a relatively isointense structure containing and surrounded by low signal on T1- weighted images, and high signal on T2-weighted images. Mottled areas of enhancement are seen with gadoliniumenhanced MR during the cerebritis stage, with an enhancing rim developing as the abscess matures. The enhancing rim may appear late in the cerebritis stage, prior to actual central necrosis. In some instances, the central area of necrosis has also enhanced on delayed scans, but not as commonly as is seen in necrotic tumors., Cysticercosis Neurocysticercosis is the most frequently encountered parasitic infestation of the CNS. Originally endemic in underdeveloped countries, predominantly Latin America, Africa, Asia and some portions of eastern Europe, it is becoming increasingly frequent in North America in immigrant populations. Humans become accidental hosts for the larval stage of Taenia Solium, the pork tapeworm, by ingesting contaminated material. The eggs hatch in the stomach and larvae burrow through the gut wall and become distributed by the circulatory system. There is a predilection for involvement of the brain. Patients most often present with seizures, elevated intracranial pressure, focal neurologic abnormalities and altered mental status. Asymptomatic infections are common. Four forms of neurocysticercosis are described: meningeal, parenchymal, ventricular and mixed. In all locations, death of the larva provokes a more intense inflammatory response, and in the case of an intraventricular lesion may lead to ependymitis. Parenchymal lesions consist of small cysts, large cysts and calcified lesions. Small (approximately 1.5 cm. in diameter) cysts may have a central area of relatively shorter T1 (isointense or hyperintense to cortex) and are uniformly hyperintense on T2-weighted images. Large (4-7 cm) cysts are usually multiloculated, adjacent to the subarachnoid space and may contain a mural nodule. The presence of a mural nodule or a T2-hypointense rim in encapsulated lesions may correlate with larval death. Visualization of calcified lesions has been variable with MR; overall there is an advantage for CT in this regard. Sometimes, calcified lesions are surrounded by edema, making them more conspicuous on MR. Basal cistern lesions can be difficult to identify but have been visualized as areas of intermediate signal intensity on

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T1-weighted images. Intraventricular cysticercosis results in deformable and mobile cysts that may cause intermittent hydrocephalus. MENINGITIS Bacterial Bacterial meningitis is an infection of the pia and arachnoid and adjacent cerebrospinal fluid. The outer arachnoid serves as a barrier to the spread of infection, but involvement of the subdural space can occur, resulting in a subdural empyema. This complication is more common in children than adults. The most common organisms involved are Hemophilus influenza, Neisseria meningitides (Meningococcus) and Streptococcus pneumoniae. Patients present with fever, headache, seizures, altered consciousness and neck stiffness. The overall mortality rate ranges from 5 to 15% for H. influenza and meningococcal meningitis to as high as 30% with streptococcal meningitis. In addition, persistent neurologic deficits are found in 10% of children after H. influenza meningitis and in 30% of patients with streptococcal meningitis. The ability of nonenhanced MR to image meningitis is extremely limited, and the majority of cases are normal or have mild hydrocephalus. In severe cases, the basal cisterns may be completely obliterated, with high signal intensity replacing the normal CSF signal on proton density images. Intermediate signal intensity may be seen in the basal cisterns on T1-weighted images in these cases. Meningeal enhancement often is not present, unless a chronic infection develops. Infection within the ventricles, either from direct extension from a shunt or abscess or progression of meningitis, may lead to ependymitis, resulting in hyperintensity outlining the ventricles on T2- weighted images and enhancement of the ependyma on T1weighted images with gadolinium. Subdural empyemas are better seen with MR than with CT, and the signal characteristics of the exudate in subdural empyema (higher signal than CSF) helps to differentiate it from benign extra-axial collections. Tuberculosis Tuberculous meningitis remains an important disease, becoming more common as an infectious agent in AIDS patients. As a rule, the evolution is less rapid than in pyogenic infections. Vasculitis and cerebral infarction, caused by inflammatory changes in the basal cisterns, are more

prevalent. The MR features of tuberculous meningitis are similar to the bacterial agents, but the chronic inflammation induces thick granulation tissue that produces a more striking enhancement pattern. Actual intracranial tuberculomas are rare in the United States. Mature tuberculomas are T2 hypointense. Central necrosis in some lesions results in a T2 bright core with a low signal intensity rim. ENCEPHALITIS Encephalitis refers to a diffuse parenchymal inflammation of the brain. Acute encephalitis of the nonherpetic type presents with signs and symptoms similar to meningitis but with the added features of any combination of convulsions, delirium, altered consciousness, aphasia, hemiparesis, ataxia, ocular palsies and facial weakness. The major causative agents are arthropod-borne arboviruses (Eastern and Western equine encephalitis, St. Louis encephalitis, California virus encephalitis). Eastern equine encephalitis is the most serious but fortunately also the least frequent of the arbovirus infections. The enteroviruses, such as coxsackie-virus and echoviruses, can produce a meningoencephalitis, but a more benign aseptic meningitis is more common with these organisms. MR reveals hyperintensity on T2-weighted scans within the cortical areas of involvement, associated with subcortical edema and mass effect. Herpes Simplex Herpes simplex is the commonest and gravest form of acute encephalitis with a 30-70% fatality rate and an equally high morbidity rate. It is almost always caused by Type 1 virus except in neonates where Type 2 predominates. Symptoms may reflect the propensity to involve the inferomedial frontal and temporal lobeshallucinations, seizures, personality changes and aphasia. MR has demonstrated positive findings in viral encephalitis as soon as 2 days after symptoms, more quickly and definitively than CT. Early involvement of the limbic system and temporal lobes is characteristic of herpes simplex encephalitis. The cortical abnormalities are first noted as ill-defined areas of high signal on T2weighted scans, usually beginning unilaterally but progressing to become bilateral. Edema, mass effect and gyral enhancement may also be present. Since MR is more sensitive than CT for detecting these early changes of encephalitis, hopefully it will improve the prognosis of this devastating disease. CONGENITAL INFECTIONS Congenital infections refer to maternally transmitted infections, which are most frequently caused by the group of TORCH pathogens, which include Toxoplasma, Others (Listeria, Treponema), Rubella, Cytomegalovirus, and Herpes simplex type 2. Nowadays, maybe another “H” should be added to emphasize the common occurrence of HIV in this subgroup of CNS

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infections. Congenital infections of the brain may produce diffuse, parenchymal inflammation with some unique characteristics, such as microcephaly, brain atrophy, hydrocephalus, neuronal migrational anomalies and cerebral calcifications. The degree of the destructive brain process and the resultant developmental abnormalities depend on the timing of the infection. The earlier in gestation the CNS involvement occurs, the more profound the brain destruction will be. In cases of congenital infections, where the prerequisite is involvement of the mother, even in a subclinical form, the causative agents may reach the fetus, either during the gestation via a hematogenous - transplacental route, or during the birth as the fetus passes through the infected birth canal. Toxoplasmosis Toxoplasmosis is caused by the parasite Toxoplasma gondii, which is typically passed hematogenously through the placenta to the fetus. There is a large percentage of the population, approaching 50%, which has been infected by the parasite sometime in their life, but congenital toxoplasmosis occurs only when the mother becomes infected during pregnancy. Infected fetuses have a high incidence (almost 50%) of CNS involvement. Early infection before 20 weeks of pregnancy is associated with severe, persistent neurologic abnormalities, whereas late infection after 30 weeks is rarely associated with deficits. Neuroimaging of congenital toxoplasmosis may reveal a whole spectrum of findings such as intracranial calcifications, hydrocephalus, brain atrophy, microcephaly and neuronal migrational anomalies. Cytomegalovirus Cytomegalovirus (CMV) is a member of the herpesvirus family, which subclinically infects nearly all the population at some time in their life and is the most frequent cause of a congenital viral infection. Congenital infection occurs after primary or secondary (reactivation) maternal infection, and the virus reaches the fetus via the transplacental route. CNS involvement is a very important manifestation of the disease, and as with toxoplasmosis, earlier infection results in poorer outcome with more severe and persistent neurologic sequelae. CMV produces a diffuse encephalitic infectious process, which results in multifocal destructive changes in the brain that lead to calcifications and microcephaly. The immature cells in the germinal matrix region are the first involved areas in the brain. Necrosis and calcifications of those areas explain the predilection for thick or nodular calcifications in the periventricular area. Intracranial calcifications may also be found in the cortical and subcortical region, as well as in the basal ganglia, so differentiation between congenital infection

from CMV or toxoplasmosis is not certain based on imaging criteria alone. Herpes Simplex Virus Herpes simplex virus (HSV) is a DNA virus and a member of the herpesvirus family, which has two different serotypes, herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2). They produce the most important acute viral encephalitis in the neonate. In over 80% of cases of herpes simplex encephalitis, HSV-2 is the causative agent. The infection is most commonly acquired during delivery through an infected birth canal, although hematogenous transmission through the placenta does occur. An explanation for the observed rarity of early transplacental infection is that it causes severe destruction in the fetus, resulting in spontaneous abortions rather than maldevelopment of the CNS. However, if infants survive the early hematogenous infection, the devastating effect of the panencephalitis results in findings similar to those of other placentally transmitted infections, such as microcephaly, cerebral atrophy and necrosis, and intracranial calcifications, but to a greater degree and with more severe neurological sequelae. An important and unique imaging finding in HSV-2 encephalitis is a linear, gyriform cortical pattern of increased attenuation on CT and hyperintensity on T1weighted images, overlying abnormal edematous and/or necrotic white matter. The cortical imaging features have been attributed to the presence of microcalcifications or to changes in local vascularity. SUPRATENTORIAL BRAIN TUMORS In the diagnostic work-up of intracranial tumors, the primary goals of the imaging studies are to detect the abnormality, localize and determine its extent, characterize the lesion, and provide a list of differential diagnoses or, if possible, the specific diagnosis. Correlative studies have proved that MR is more sensitive than CT for detecting intracranial masses. Moreover, the multiplanar capability of MR is very helpful to determine the anatomic site of origin of lesions and to demarcate extension into adjacent compartments and brain structures. The superior contrast resolution of MR displays the different components of lesions more clearly. MR can assess the vascularity of lesions without contrast infusion. On the other hand, CT detects calcification far better than MR, a useful finding for differential diagnosis. Gradient-echo techniques improve MR detection of calcification by accentuating the diamagnetic susceptibility properties of calcium salts, but the observed low signal on T2-weighted images is nonspecific, in that any accompanying paramagnetic ions would produce the same effect. Contrast enhancement with gadolinium increases both the sensitivity and specificity of MR. Gadolinium is a blood-brain barrier (BBB) contrast agent like iodinated agents for CT. It does not cross the intact BBB, but when the BBB is absent or deficient, gadolinium

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enters the interstitial space to produce enhancement (increased signal) on T1-weighted images. All the collective knowledge learned from contrast-enhanced CT can be applied directly to the gadolinium-enhanced MR images. Although the enhancement patterns are not tumor specific, the additional information is often helpful for diagnosis. Lesions can be classified as homogeneous or heterogeneous, and necrotic and cystic components are seen more clearly. The margins of enhancement provide a gross measure of tumor extension. Contrast MR is particularly valuable for extra-axial tumors because they tend to be isointense to the brain on plain scan.

The common signal characteristics of intra-axial tumors include high signal intensity on T2-weighted images and low signal on T1-weighted images, unless fat or hemorrhage is present. Fat and subacute hemorrhage (methemoglobin) exhibit high signal on T1-weighted images, and acute hemorrhage (deoxyhemoglobin) and chronic hemorrhage (hemosiderin/ferritin) show low signal intensity on T2-weighted scans. Gliomas have poorly defined margins on plain MR. They infiltrate along white matter fiber tracts, and the deeper lesions have a propensity to extend across the corpus callosum into the opposite hemisphere. They are often quite large by the time of clinical presentation.

CEREBRAL GLIOMAS

The higher grade gliomas, particularly glioblastomas, appear heterogeneous due to central necrosis with cellular debris, fluid, and hemorrhage. Peritumoral edema and mass effect are common features. Following injection of gadolinium, T1-weighted images show irregular ring enhancement, with nodularity and nonenhancing necrotic foci. As mentioned above, gliomas are infiltrative lesions, and microscopic fingers of tumor usually extend beyond the margin of enhancement. Enhanced scans are particularly helpful to outline subependymal spread of tumor along a ventricular surface, as well as leptomeningeal involvement. Although highly malignant, anaplastic astrocytomas may or may not exhibit breakdown of the blood-brain barrier. In general, the presence or lack of enhancement alone is not helpful in grading astrocytomas.

Gliomas are malignant tumors of the glial cells of the brain and account for 30-40% of all primary intracranial tumors. They occur predominantly in the cerebral hemispheres, but the brain stem and cerebellum are frequent locations in children, and they are also found in the spinal cord. The peak incidence is during middle adult life, when patients present with seizures or symptoms related to the location of the gliomas and the brain structures involved. Astrocytomas are graded according to their histologic appearance. Grade 1 astrocytomas have welldifferentiated astrocytes and well-defined margins. The clinical course often proceeds over many years and complete cures are possible. The pilocytic variant is a low-grade tumor with a distinct capsule that is commonly found in children. The giant cell astrocytoma is a specialized tumor that develops from pre-existing hamartomas in patients with tuberous sclerosis. Grade 2 astrocytomas are well-differentiated but diffusely infiltrating tumors. The fibrillary type is most common, and although initially benign, they may evolve into a higher grade tumor over time. This changing character of gliomas makes histological classification difficult from sample biopsies, because different parts of the tumor often exhibit varying degrees of malignancy. The higher grade astrocytomas are very cellular and pleomorphic. Anaplastic astrocytomas (Grade 3) are very aggressive tumors, readily infiltrate adjacent brain structures, and have a uniformly poor prognosis. Glioblastoma multiforme (Grade 4) has the added histologic features of endothelial proliferation and necrosis. Multicentric foci of tumor may be seen in 4 to 6% of glioblastomas. Gliomatosis cerebri is an unusual condition with diffuse contiguous involvement of multiple lobes of the brain. Oligodendrogliomas are the most benign of the gliomas. Calcification is common, and they occur predominantly in the frontal lobes. The mixed neuronal and glial tumors are found mostly in children and young adults. They are slow-growing and are found predominantly in the temporal lobes and around the third ventricle. Intratumoral cysts and calcification are common.

The lower grade astrocytomas tend to be more homogeneous without central necrosis. Large cystic components may be present. The cysts have smooth walls, and the fluid is of uniform signal, to distinguish them from necrosis. Enhancement is variable, depending on the integrity of the blood-brain barrier.

LYMPHOMA Primary malignant lymphoma is a non-Hodgkin's lymphoma that occurs in the brain in the absence of systemic involvement. These tumors are highly cellular and grow rapidly. Favorite sites include the deeper parts of the frontal and parietal lobes, basal ganglia, and hypothalamus. Most occur in patients who are immunocompromised secondary to chemotherapy or acquired immunodeficiency syndrome (AIDS) or in organ transplant recipients who are on immunosuppressant drugs. Cerebral lymphomas are very radiosensitive and respond dramatically to steroid therapy. Lymphomas typically appear as homogeneous, slightly high signal to isointense masses deep within the brain on T2-weighted images. The observed mild T2

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prolongation is probably related to dense cell packing within these tumors, leaving relatively little interstitial space for accumulation of water. They are frequently found in close proximity to the corpus callosum and have a propensity to extend across the corpus callosum into the opposite hemisphere, a feature that mimics glioblastoma. Multiple lesions are present in as many as 50%. Despite their rapid growth, central necrosis is uncommon. They are associated with only a mild or moderate amount of peritumoral edema. By time of presentation they can be quite large and yet produce relatively little mass effect, a feature that sets lymphoma apart from glioblastoma and metastases. Intratumoral cysts and hemorrhage are unusual. Most lymphomas show bright homogeneous contrast enhancement. The pattern is modified somewhat in AIDS patients. Multiplicity seems to be more common. Moreover, lymphomas exhibit more aggressive behavior and readily outgrow their blood supply. As a result, central necrosis and ring enhancement are often seen in lymphomatous masses in AIDS patients. On MR spectroscopy, lymphomas exhibit elevated choline little or no NAA. METASTATIC DISEASE Metastases to the brain occur by hematogenous spread, and multiple lesions are found in 70% of cases. The most common primaries are lung, breast, and melanoma, in that order of frequency. Other potential sources include the gastrointestinal tract, kidney, and thyroid. Metastases from other locations are uncommon. Clinical symptoms are nonspecific and no different from primary brain tumors. If a parenchymal lesion breaks through the cortex, tumor can extend and seed along the leptomeninges. Metastatic lesions can be found anywhere in the brain but a favorite site is near the brain surface at the corticomedullary junction of both the cerebrum and cerebellum. They are hyperintense on plain T2-weighted images. Areas of necrosis are prevalent in the larger lesions, accounting for their heterogeneous internal texture. Peritumoral edema is a prominent feature, but multiplicity is the most helpful sign to suggest metastatic disease as the likely diagnosis. Correlative studies have shown MR to be more sensitive than CT for detecting metastases, particularly lesions near the base of the brain and in the posterior fossa. One limitation of plain MR is the frequency of periventricular white matter hyperintensities found in the same older age group at risk for metastatic disease. Gadolinium enhanced MR has resulted in improved delineation of metastatic disease compared with nonenhanced scans. Moderate to marked enhancement is the rule, nodular for the smaller lesions and ringlike with central nonenhancing areas for the larger ones. Controlled clinical trials have also shown

that contrast-enhanced MR is more sensitive than both plain MR and contrast-enhanced CT for detecting cerebral metastases. In patients with a known primary, T1-weighted enhanced MR is probably sufficient to screen the brain for metastatic disease. Hemorrhage is present in 3 to 14% of brain metastases, mainly in melanoma, choriocarcinoma, renal cell carcinoma, bronchogenic carcinoma, and thyroid carcinoma. The presence of nonhemorrhagic tissue and pronounced surrounding vasogenic edema are clues to the underlying neoplasm. Metastatic melanoma has been a topic of special interest in the MR literature because of the presence of paramagnetic, stable free radicals within melanin. The MR appearance is variable depending on the histology of the melanoma and the components of hemoglobin. Most are hyperintense to white matter on T1-weighted scans and hypointense on T2-weighted scans. Atlas and coworkers observed three distinct signal intensity patterns. Nonhemorrhagic melanotic melanoma was markedly hyperintense on T1-weighted images and isointense or mildly hypointense on T2-weighted images. Nonhemorrhagic amelanotic melanoma appeared isointense or slightly hypointense on T1-weighted scans and isointense or slightly hyperintense on T2-weighted scans. The signal pattern for hemorrhagic melanoma was variable depending on the components of hemoglobin. Some uncertainty remains as to whether the predominant effect on signal intensity within melanomas is due to stable free radicals, chelated metal ions, or hemoglobin. INTRAVENTRICULAR TUMORS The intraventricular location is unique in that many of the tumor types are more commonly associated with extra-axial locations. Patients often present with obstructive hydrocephalus. Most intraventricular tumors are relatively benign and have well-defined margins. As they grow, the tumors expand the ventricle of origin. With malignant degeneration, extension into the brain parenchymal occurs. The primary blood supply to intraventricular lesions is derived from the choroidal arteries. MENINGIOMA Meningiomas account for 15% of all intracranial tumors and are the most common extra-axial tumor. They originate from the dura or arachnoid and occur in middle-aged adults. Women are affected twice as often as men. Meningiomas are well-differentiated, benign, and encapsulated lesions that indent the brain as they enlarge. They grow slowly and may be present for many years before producing symptoms. The histologic picture shows cells of uniform size that tend to form whorls or psammoma bodies. The parasagittal region is the most frequent site for meningiomas, followed by the sphenoid wings,

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parasellar region, olfactory groove, cerebello-pontine angle, and rarely the intraventricular region. Meningiomas often induce an osteoblastic reaction in the adjacent bone, resulting in a characteristic focal hyperostosis. They are also hypervascular, receiving their blood supply predominantly from dural vessels. Most meningiomas are isointense with cortex on T1- and T2-weighted images. A heterogeneous internal texture is found in all but the smallest meningiomas. The mottled pattern is likely due to a combination of flow void from vascularity, focal calcification, small cystic foci, and entrapped CSF spaces. Hemorrhage is not a common feature. An interface between the brain and lesion is often present, representing a CSF cleft, a vascular rim, or a dural margin. MR has special advantages over CT in assessing venous sinus involvement and arterial encasement. Occasionally, a densely calcified meningioma is encountered that is distinctly hypointense on all pulse sequences. Meningiomas show intense enhancement with gadolinium and are sharply circumscribed. They have a characteristic broad base of attachment against a dural surface. Associated hyperostosis may result in thickening of low signal bone as well as diminished signal from the diploic spaces. Although meningiomas are not invasive, vasogenic edema is present in the adjacent brain in 30% of cases. Contrast scans are especially helpful for imaging the en plaque meningiomas that occur at the skull base. MR spectroscopy shows elevated alanine and glutamates, no NAA, and markedly decreased creatine. BRAIN STEM AND POSTERIOR FOSSA CRANIAL NERVES ANATOMY The cranial nerve nuclei are located in the tegmentum of the brainstem, just ventral to the cerebral aqueduct and 4th ventricle. The 3rd nerves (oculomotor) pick up parasympathetic fibers from the Edinger-Westfall nucleus and course ventrally through the substance of the midbrain to exit in the interpeduncular cistern. The cisternal segments continue ventrally between the posterior cerebral and superior cerebellar arteries and enter the cavernous sinuses. The 4th nerves (trochlear) are the only cranial nerves to cross the midline. They course dorsally and cross behind the aqueduct, exit the dorsal midbrain, and travel forward in the ambient cisterns to reach the cavernous sinuses. Other major structures within the midbrain include the pyramidal (corticospinal and corticobulbar) tracts within the cerebral peduncles, the substantia nigra, the red nuclei, the decussation of the superior cerebellar peduncles, and the superior and inferior colliculi of the quadrigeminal plate. The pons contains the nuclei for the 5th (trigeminal), 6th (abducens), 7th (facial), and the 8th (acoustic) cranial nerves. The 5th nerve enters the midportion of the pons ventrolaterally. The spinal tract and

nucleus of the 5th nerve extends from the upper pons all the way down into the upper spinal cord. The 6th exists ventrally at the pontomedullary junction. Both the 5th and 6th nerves course through the cavernous sinus. The 7th nerve loops posteriorly around the 6th nerve nucleus and indents the floor of the 4th ventricle (facial colliculus). The 7th and 8th nerves exist the inferior pons inferiolaterally, traverse the cerebellopontine cistern and enter the internal auditory canal. The anterior pons (basis pontis) contains a large number of transverse fibers from the middle cerebellar peduncles and longitudinal, dispersed bundles of the pyramidal tracts. The medulla contains the remaining cranial nerves. Nerves 9 (glossopharyngeal), 10 (vagus), and 11 (spinal accessory) exist laterally just posterior to the olivary nucleus and course toward the jugular foramen. The 12th cranial nerve (hypoglossal) exists the medulla ventral to the olive and courses ventrally to the hypoglossal canal. The medulla also contains the decussation of the pyramids (corticospinal tracts) ventrally and the inferior cerebellar peduncles posteriorly. Two other important fiber tracts are the medial longitudinal fasciculus (MLF) and the medial lemniscus. The MLF, which connects the 3rd, 4th, and 6th cranial nerve nuclei, lies in a paramedian position just ventral to the aqueduct and 4th ventricle. The medial lemniscus, the major sensory tract, ascends through the brainstem just ventral to the MLF. Pathology Nerve sheath tumors Tumors of schwann cell origin include schwannoma and neurofibroma. Schwannomas are more common and most arise from the 8th cranial nerve. Neurofibromas are usually associated with neurofibromatosis. Acoustic neuromas originate on the vestibular division of the eighth cranial nerve just within the internal auditory canal. Bilateral lesions are common with NF 2. They usually present in middle-aged adults with a sensorineural hearing loss, but other symptoms include headache, vertigo, tinnitus, unsteady gait, and facial weakness. Large tumors may fill the cerebellopontine angle cistern and compress adjacent brain structures, producing additional symptoms. Most schwannomas are isointense to the brain on MR images, but some are distinctly hyperintense with T2-weighted sequences. Occasionally, a schwannoma will be hyperintense on T1-weighted images owing to foci of hemorrhage. They may be heterogeneous on T2weighted images as well, particularly the larger ones, due to necrosis, hemorrhagic components, and occasional calcification. With small intracanalicular tumors, partial voluming effects may result in uneven signal intensity.

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Gadolinium causes approximately 50% shortening of the T1 relaxation time of schwannomas, making them appear very bright on T1-weighted images. Those lesions that are heterogeneous on plain scan will likely exhibit heterogeneous enhancement as well. Meningioma Meningiomas originate from the dura or arachnoid and occur in middle-aged adults. In the posterior fossa, most meningiomas are found in the cerebellopontine angle. Women are affected twice as often as men. Meningiomas are well-differentiated, benign, and encapsulated lesions that indent the brain as they enlarge. They grow slowly and may be present for many years before producing symptoms. The histologic picture shows cells of uniform size that tend to form whorls or psammoma bodies. They are hypervascular, receiving their blood supply predominantly from dural vessels. Most meningiomas are isointense with cortex on T1- and T2-weighted images. A heterogeneous internal texture is found in all but the smallest meningiomas. The mottled pattern is likely due to a combination of flow void from vascularity, focal calcification, small cystic foci, and entrapped CSF spaces. Hemorrhage is not a common feature. An interface between the brain and the lesion is often present, representing a CSF cleft, a vascular rim, or a dural margin. MR has special advantages over CT in assessing venous sinus involvement and arterial encasement. Occasionally, a densely calcified meningioma is encountered that is distinctly hypointense on all pulse sequences. Meningiomas show intense enhancement with gadolinium and are sharply circumscribed. They have a characteristic broad base of attachment against a dural surface. Contrast scans are especially helpful for imaging the en plaque meningiomas that occur at the skull base. Arachnoid Cyst Arachnoid cysts are benign but slowly grow as they accumulate fluid, compressing normal brain structures. Most are smoothly marginated and homogeneous. They are not calcified and do not enhance. The cyst fluid is usually isointense with CSF on all pulse sequences. The cysts may appear higher signal than CSF on intermediate T2-weighted images due to dampening of the CSF pulsations that normally results in signal loss in the ventricles and cisterns. This effect will be less apparent with pulse sequences that incorporate flow compensation techniques. INTRAAXIAL TUMORS Except for hemangioblastoma and metastatic disease, the majority of intra-axial posterior fossa

tumors occur in children. Cerebellar astrocytoma accounts for 33% of these childhood tumors, medulloblastoma 26%, brain stem glioma 21%, ependymoma 14% and choroid plexus papilloma, only 2%. Brain Stem Glioma Most brain stem gliomas are relatively benign initially but frequently evolve to a higher grade. They usually present with a cranial nerve palsy, most often involving the 6th or 7th nerves. The pons is the common location, but they also occur in the medulla and midbrain. These tumors infiltrate the brain stem and induce surrounding vasogenic edema in the brain parenchyma. Since both the tumor and edema are hyperintense on T2-weighted images, tumor margins tend to be indistinct and poorly defined. Brain stem gliomas are relatively homogeneous masses without much cystic change, necrosis, vascularity or calcification. About 50% of cases will show mild enhancement. As the gliomas grow, they enlarge the brain stem, producing effacement of the basal cisterns, anterior displacement of the basilar artery against the clivus, and compression and posterior bowing of the fourth ventricle. Hydrocephalus is often present. Exophytic growth is a well-known feature of these tumors. Cerebellar Astrocytoma Cerebellar astrocytoma is the most common CNS tumor in children. They tend to be lower grade than the supratentorial variety found in adults and are often quite large by time of presentation. The majority are hemispheric in location, a helpful but not absolute criterion to distinguish them from medulloblastoma. More than 50% of cerebellar astrocytomas are cystic, and the cyst contents often have elevated protein, making them slightly higher signal than CSF but lower signal than brain on T1-weighted images. The solid components are hyperintense to brain on proton densityweighted images. Both solid tumor and cyst are bright on T2-weighted scans. Calcification is occasionally present. Peritumoral edema is not pronounced, and in general, their margins are defined better than in supratentorial gliomas. Cerebellar astrocytomas exhibit nodular or ringlike enhancement. Since these tumors are frequently large, mass effect is a prominent feature. Anterior and lateral displacement of the fourth ventricle is common. Upward herniation of the superior vermis and downward herniation of the cerebellar tonsils can also occur. Medulloblastoma (and PNET) The majority of medulloblastomas occur in children between four and eight years old, and males

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outnumber females three to one. Primitive neuroectodermal tumors (PNET) may present at birth or early infancy. Medulloblastomas and PNETS arise from remnants of primitive neuro-ectoderm in the roof of the fourth ventricle. These tumors are very malignant and exhibit an aggressive biologic behavior, commonly invading the adjacent brain stem and leptomeninges. Widespread dissemination through the ventricular system and distant seeding to other areas of the neuraxis occurs in as high as 30%.

The classic MR appearance of hemangioblastoma is a cystic mass with a brightly enhancing nodule. About 60% are cystic, so solid lesions are not uncommon. Calcification is rare. Hemangioblastomas are sharply marginated and induce minimal surrounding parenchymal reaction. The tumor nodules are hypervascular and the vascular pedicle often produces a characteristic flow void on MR.

Medulloblastomas are primarily midline vermian lesions, but hemispheric locations are also possible. Since they arise close to the fourth ventricle, growth predominantly into the ventricle may make them simulate an intraventricular mass. Necrosis, hemorrhage and cavitation are common features, giving these tumors a heterogeneous appearance on MR, but not to the same degree as seen with ependymomas. Calcification is rare in medulloblastomas. They are hypervascular lesions and show moderate contrast enhancement.

Metastases to the brain occur by hematogenous spread, and multiple lesions are found in 70% of cases. The most common primaries are lung, breast, and melanoma, in that order of frequency. Other potential sources include the gastrointestinal tract, kidney, and thyroid. Metastases from other locations are uncommon. Clinical symptoms are nonspecific and no different from primary brain tumors. If a parenchymal lesion breaks through the cortex, tumor can extend and seed along the leptomeninges.

Ependymoma About 70% of ependymomas are found in the fourth ventricle. The atria of the lateral ventricles are another common site. Males are affected twice as often as females. They originate from the ependyma of the ventricles but may grow either into the ventricle or into the brain substance. Ependymomas are slow-growing, but malignant, tumors and grow by expansion and infiltration. Ventricular and subarachnoid seeding are not infrequent. Most ependymomas arise in the floor of the fourth ventricle. They have a propensity to extend through the foramina of Luschka and Magendie into the basal cisterns. They tend to be well defined, particularly if they are marginated by CSF within a ventricle or cistern. Calcification is present in 50%, cysts and necrotic areas are common, and most are moderately vascular. These properties account for their heterogeneous internal texture on both plain and contrast scans.

Hemangioblastoma Hemangioblastoma is a benign tumor of middle age. In fact, it is the most common primary intra-axial tumor of the posterior fossa in adults. About 20% are associated with Hippel-Lindau disease, and hereditary factors have been implicated in another 20%. The cerebellum and vermis are the common sites, but hemangioblastomas can also be found in the medulla and spinal cord. Multiplicity is a well-known feature but is present in only about 10% of cases. Histologic examination reveals a meshwork of capillaries and small vessels.

Metastatic disease

Metastatic lesions can be found anywhere in the brain but a favorite site is near the brain surface at the corticomedullary junction of both the cerebrum and cerebellum. They are hyperintense on plain T2-weighted images. Areas of necrosis are prevalent in the larger lesions, accounting for their heterogeneous internal texture. Peritumoral edema is a prominent feature, but multiplicity is the most helpful sign to suggest metastatic disease as the likely diagnosis. Hemorrhage is present in 3 to 14% of brain metastases, mainly in melanoma, choriocarcinoma, renal cell carcinoma, bronchogenic carcinoma, and thyroid carcinoma. The presence of nonhemorrhagic tissue and pronounced surrounding vasogenic edema are clues to the underlying neoplasm. Gadolinium enhanced MR results in improved delineation of metastatic disease compared with nonenhanced scans. Moderate to marked enhancement is the rule, nodular for the smaller lesions and ringlike with central nonenhancing areas for the larger ones. Correlative studies have shown MR to be more sensitive than CT for detecting metastases, particularly lesions near the base of the brain and in the posterior fossa.

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