Paul & Juhl’s Essentials of Radiologic Imaging
7th Edition

Chapter 11
Intracranial Diseases
W. Douglas Brown
Charles M. Strother
Patrick A. Turski
Lindell R. Gentry
W. D. Brown and L. R. Gentry: Department of Radiology, University of Wisconsin Hospital and Clinics, Madison, Wisconsin 53792-3252.
C. M. Strother and P. A. Turski: Department of Radiology, University of Wisconsin Clinical Science Center, Madison, Wisconsin 53792-3252.
Successful radiologic evaluation of the brain and other cranial contents requires detailed knowledge of anatomy, pathology, and the technologies available. Although this chapter largely follows the usual descriptive format of a radiology text, the reader should always be cognizant that many cases seen in actual practice will not precisely match the classic textbook images and descriptions. Only critical thinking, with a solid foundation in neuroanatomy and neuropathology, will yield optimal diagnoses in difficult cases.
Unlike most organs of the body, the brain is not made up of one or a few tissue types. The brain consists of countless tissues, each with different functional significance and susceptibility to various pathologies. A thorough understanding of the three meningeal layers is also clinically important. Until a few years ago, this detailed anatomy was visible in living humans only to the neurosurgeon. The situation began to change with the advent of CT. With the maturation of high-resolution MRI, the radiologist is constantly faced with tomographic images that present greater anatomic detail than has ever before been visible in the living patient. Many medical schools still do not teach detailed sectional neuroanatomy, so the imager who is beginning to train in neuroradiology must typically learn or relearn a great deal of anatomy. This information is clearly beyond the scope of this chapter, and the reader is referred to other sources.21,22,25,70 An understanding of neuropathology that exceeds that taught in most medical schools is likewise of great importance. Most radiologists spend little time in the pathology literature. However, familiarity with the basics of neuropathology,113 knowledge of major reference texts,62,133 attendance at brain autopsies, and positive interaction with local neuropathologists will make one a better neuroradiologist.
DIAGNOSTIC TECHNIQUES
Knowledge of the technologies for neuroimaging is important in three major respects. A clinical radiologist is often faced with choosing the best or first imaging procedure for evaluation of a patient with certain history, signs, and symptoms. The radiologist must tailor any examination for best demonstration of the pathology. And the radiologist must know the strengths and weaknesses and especially the artifacts of each technology in order to correctly interpret the findings. Given the large and rapidly evolving array and complexity of technologies—ultrasound, CT, angiographic, radionuclide, and especially new MR techniques—consultation with an expert in neuroradiology is often very valuable.
Magnetic Resonance Imaging and Computed Tomography
Exceptional contrast resolution, multiplanar capability, the ability to tailor the exam to emphasize different tissue characteristics, and the lack of known harmful effects combine to make MRI the preferred technique for the diagnostic evaluation of most patients with neurologic disease. Important exceptions where CT remains the technique of choice for initial examination are (a) evaluation of patients after acute trauma; (b) evaluation of patients suspected of having an acute intracranial hemorrhage; (c) evaluation of patients with diseases affecting primarily the skull base or calvaria; and (d) for patients with contraindications to MRI. Because of its speed, availability, and high resolution, CT remains an important and extremely useful diagnostic tool.
The array of MRI techniques presently available is too large and complex for discussion in this chapter. However, to maximize information obtained from a particular examination, one must have not only an understanding of the changes occurring with various disease states but also some understanding of how images obtained from these altered tissues are imaged by various MRI pulse sequences.162 In general, the use of a short-TR/short-TE sequence and long-TR/short-
P.374

and long-TE pulse sequences (spin echo or fast spin echo) provides a set of images that provide an overview of the T1, proton density, and T2 characteristics of the tissue being imaged (Fig. 11-1); this is usually the minimum group of images for a diagnostic examination. Other sequences and sometimes intravenous contrast are added according to the suspected pathology. One must also tailor the choice of imaging planes. In almost all circumstances the imaging protocol should contain images in at least two planes; the optimal planes will depend on the nature and location of the lesions.
FIG. 11-1 Normal MRI. (A) Short-TR/TE (T1-weighted) sequence. (B) Long-TR/short-TE (proton-density-weighted) sequence. (C) Long-TR/long-TE (T2-weighted) sequence. These images illustrate well the differences in signal intensities of cerebrospinal fluid, gray matter, and white matter as seen on these commonly used pulse sequences.
There are also many different ways to perform a CT scan, and, as with MRI, each scan should be tailored to optimize clinical information in a particular case. Parameters to be varied include slice thickness, plane of imaging, radiographic technique (tube current and slice time), reconstruction filter, the use of contrast, the use of spiral imaging, and the windows used for printing the images. Good clinical information and careful decisions are needed to plan imaging for optimal patient care.
The primary reason for the use of intravenous contrast in brain imaging is different from that in the remainder of the body. The agents used (iodinated contrast media for CT, paramagnetic media usually containing gadolinium for MRI) do not cross the blood-brain barrier (BBB). Because many lesions cause disruption of this barrier, intravenous contrast will localize in the brain tissue specifically at sites of these pathologies; this may add to both the sensitivity and specificity of the examination. For CT the administration of intravenous contrast also allows improved definition of both vascular and dural structures (Fig. 11-2). The situation is more complex for MRI, where vascular enhancement depends greatly on the velocity of blood flow and the specific MRI sequence used (Fig. 11-3); therefore, contrast is less often needed for vascular evaluations with MRI.
FIG. 11-2. Normal CT scan performed (A and B) following the intravenous administration of iodinated contrast medium. Arterial and venous structures at the base of the brain are prominent in these images. There is also enhancement of the falx cerebri and choroid plexus of the lateral ventricles.
FIG. 11-3. Normal MR scan (T1-weighted) A, B, C, D, E, F intravenous contrast medium. (A, B, C without contrast, D, E, F, with contrast.) (continued)
FIG. 11-3. Continued.
Although many lesions are seen better following infusion of intravenous contrast medium, the added information is often trivial compared with the added cost and increased time of the examination, and not clinically important. In general, intravenous contrast media need not be used for CT or MRI scans performed for evaluation of most congenital malformations, dementia, trauma, hydrocephalus, suspected stroke or hemorrhage, or in cases of chronic epilepsy. Contrast administration is indicated in the CT evaluation of many but not all patients with vascular abnormalities as well as for CT and MRI studies performed for suspected neoplastic, infectious, or inflammatory disorders. The routine use of a
P.375

nonenhanced CT scan before an enhanced scan is of limited usefulness and is recommended only for the evaluation of lesions thought to have hemorrhagic or calcified components.
The usual dosage for intravenous contrast medium results in the administration of 30 to 45 g of iodine, which can be given as an intravenous (IV) drip or as an IV bolus depending on the clinical situation.71 For MRI, the dose of gadolinium agents is 0.1 to 0.3 mmol/kg.
Intrathecal contrast media can also be occasionally used to advantage in cranial CT scanning. Scans performed shortly after the injection of low doses of water-soluble contrast medium (in the range of 1 g of iodine) into the lumbar subarachnoid space provide excellent depiction of the cisternal spaces about the brain. This technique may be indicated in certain circumstances when an MR examination cannot be performed or when information about cerebrospinal fluid (CSF) leaks or the presence of communication between various CSF-containing spaces is required37 (Fig. 11-4). Small volumes of subarachnoid air may also be used effectively as a contrast medium for CT scans,122 but with very few exceptions, the natural contrast provided by the CSF on MRI examinations has eliminated the need for CT scans with subarachnoid contrast medium.
FIG. 11-4. (A) Axial computed tomogram at level of the foramen magnum. Water-soluble contrast medium in the subarachnoid space outlines the margins of the vertebral arteries, cerebellar tonsils, and the medulla. (B) Axial computed tomogram at midbrain level. Water-soluble contrast medium opacifies the subarachnoid space and allows clear definition of the midbrain and adjacent structures.
Ultrasound
The use of ultrasound for evaluation of intracranial structures is limited by the thick calvaria in the adult. However, there are specific situations in which this modality is very valuable. Brain imaging in neonates and infants is excellent with high-frequency ultrasound thanks to the fontanels, which are still open. Ultrasound is usually the imaging modality of choice for sick patients in this age range. Transcranial Doppler probes are optimized for evaluation of intracranial blood flow in adults through the relatively thin squamous portion of the lateral skull. These examinations may be very useful in the setting of possible vasospasm and during certain angiographic procedures. Extracranially, Doppler ultrasound is an important means for the noninvasive evaluation of the carotid arteries.
Skull Films
Skull radiography no longer has any meaningful role in the diagnostic evaluation of patients suspected of having neurologic disease. The technique is insensitive, nonspecific, and redundant because even when abnormalities are seen on skull radiographs, it is rare that the findings provide sufficient information on which to base patient management.152 Similarly, plain film evaluation of the sella turcica is very limited in its usefulness155,156; skull films have been replaced by MRI for diagnosis of pituitary lesions. Even though skull radiography no longer plays a significant role in clinical practice, knowledge of skull anatomy is essential for proper interpretation of CT and magnetic resonance scans of the head. This knowledge may be facilitated through the study of multiple projections of skull radiographs, which provide a means for correlating the spatial relationships of structures seen on cross-sectional images. For a discussion of the changes that occur in the skull as a result of intracranial disease, see Yock165 and Newton and Potts.111
Angiography
Catheter arteriography remains an important tool in neuroradiology. However, as has been the case with plain skull films and more recently with CT, many of the indications
P.376

for cerebral angiography have been eliminated by the information provided by MRI and MR angiography. Over the last two decades cerebral angiography has evolved from a technique used largely to detect the presence of structural lesions to one that is performed primarily to add specificity to ambiguous CT, Doppler ultrasound, or MRA findings or to assist in the planning of neurosurgical or interventional radiologic procedures for vascular disease. In the future, these indications will be further reduced through the increasing capabilities of MR angiography. In its current state, MR angiography is quite suitable in many instances as a screening and diagnostic examination for both intracranial and extracranial diseases that involve primarily the large vessels of the neck, skull base, or dural coverings (Fig. 11-5).119
FIG. 11-5. Magnetic resonance angiography. (A) Normal MR arteriogram (two-dimensional time-of-flight), axial slab, through the circle of Willis. (B) Magnetic resonance arteriogram from another patient at the same level, demonstrating markedly diminished left middle cerebral artery flow as a result of internal carotid occlusion. (C) Normal MR venogram (two-dimensional phase contrast), median sagittal slab. (D) Magnetic resonance venogram of another patient at the same location, demonstrating lack of flow in the superior sagittal and straight sinuses because of dural sinus thromboses.
The primary indication for cerebral angiography is for the evaluation of patients with vascular disease (atherosclerosis, aneurysms, arteriovenous malformations and fistulas, arteritis, and posttraumatic vascular lesions), either intra- or extracranial. Angiography is uncommonly required as part of the diagnostic assessment of neoplasms or other neurologic diseases.
Conventional film-screen angiography is performed by rapidly injecting an iodine-containing contrast medium into one of the arteries supplying the brain or its coverings and
P.377

then obtaining a series of roentgenograms in rapid sequence. The site of injection, the volume of contrast medium used, and the filming sequence employed all depend on the specific problem under evaluation. Almost all conventional cerebral angiography is now performed with the Seldinger technique, in which a catheter is inserted percutaneously into one of the femoral arteries and guided fluoroscopically to the appropriate site. Direct carotid puncture or brachial artery injections are rarely required or indicated. The risks of conventional angiography conducted by experienced personnel are small but significant in that they include stroke and damage to the site of arterial puncture. The age and general medical condition of the patient are important factors that influence the magnitude of these risks.
The application of digital electronic techniques to angiographic equipment has eliminated much of the need for film-screen techniques in neuroangiography. Digital subtraction techniques allow one to perform angiography following either an intravenous or an intraarterial injection of contrast medium at a smaller volume and concentration than would be possible if film-screen techniques were employed. Intraarterial digital subtraction angiography allows procedures to be carried out in less time and at less expense than with conventional methods with, in most cases, an insignificant loss of spatial resolution.
APPROACH TO THE NEURORADIOLOGIC STUDY
As with any type of radiologic study (or history and physical examination, for that matter) the most reliable means to ensure that relevant information is gathered and reported is to have a habitual pattern for assessing the images and reporting the results. This pattern should be individually tailored and well thought through, so that the interpreter of the images has the highest possible likelihood of finding all significant abnormalities. Thus, the student of neuroradiology should take pains to develop explicit search patterns for viewing brain images that take advantage of his or her knowledge of neuroanatomy and neuropathology in general, the particular technology used, and the specific clinical information available for the current patient. In reporting the findings the neuroimager should always strive to be as precise as possible. For instance, one should never use the term “meningeal enhancement.” Dural enhancement and pial enhancement have clearly different appearances and wholly different clinical significance. Similarly, vague localizations such as “frontoparietal” can often be markedly improved by simply noting the location of the lesion with respect to the central sulcus. The radiologist should also avoid unnecessary equivocation. For instance, subarachnoid hemorrhage has a pathognomonic appearance; its reporting need not begin with a description of “high-attenuation material surrounding the brain.” The following sections deal with the general neuroimaging issues of calcium and edema.
Intracranial Calcification and Ossification
Certain structures within the skull normally calcify, whereas other calcifications seen on CT or other images are of pathologic significance. An outline listing the major
P.378

causes of normal and abnormal intracranial calcification is found in Table 11-1. A few areas of normal calcification deserve brief discussion.
TABLE 11-1. Causes of intracranial calcification and mineralization
In adults there is almost always pineal calcification and usually calcification of the immediately adjacent habenular commissures. However, visualization of calcification in the pineal body on CT scans is rare in individuals younger than 6 years of age. Pineal calcification is usually in the form of a cluster of amorphous, irregular densities or may be solitary. The normal calcified pineal ranges up to 10 or 12 mm in greatest diameter but is usually between 3 and 5 mm. When calcifications greater than 1 cm in diameter are observed, the question of an abnormality such as a pineocytoma or arteriovenous malformation should be raised.
Calcification of portions of the choroid plexus sufficient to allow visualization on CT scans occurs in almost all adults and is frequently present in children. Calcification is most frequently seen at the glomera (in the atria of the lateral ventricles) but may be present at any site. One should note that the choroid plexus of the fourth ventricle extends through the lateral ventricular foramina (of Luschka) and may therefore be seen as a calcified or enhancing “mass” in the cerebellopontine angle.
Plaquelike areas of calcification and ossification are common
P.379

P.380

in the dura, particularly in the falx and along both the free and attached edges of the tentorium. The free edges of the tentorium posterior to the sella (the so-called petroclinoid ligaments) are particularly prone to dense calcification. Heavy calcification of the falx, and less frequently of the tentorium, is reported as a component of the basal cell nevus syndrome; otherwise, these calcified plaques are of no clinical significance.
Hyperostosis frontalis interna is an overgrowth of the inner table of the frontal bone with a very characteristic appearance; it is usually symmetric and is found chiefly in older women. The diploic space and external table are not affected. It is important to distinguish hyperostosis frontalis interna from the bony hypertrophy that results from meningioma or fibrous dysplasia; but except for the rare en plaque meningioma, there is little problem in making this distinction.
Edema
An increase in water in the brain tissues (edema) is a sign of many pathologic states. In general, this increased fluid is primarily intracellular (because of some insult to the cell) or extracellular (generally related to loss of the blood-brain barrier and resultant shifts of protein and water from the intravascular space into the intercellular tissue spaces). Thus, the former has been called cytotoxic edema and is seen in strokes, hypoxemic injuries such as near-drowning, viral cerebritis, and cortical edema resulting from status epilepticus. The latter has been termed vasogenic edema and is most often associated with metastatic or primary neoplasms and infection. These types of edema in their pure forms are easily recognizable. Cytotoxic edema is seen primarily in the neuronal cell bodies (hence, the gray matter). On CT this leads to a diminished density of gray matter and therefore to blurring or loss of visible distinction between gray matter and white matter. On MRI there is diminished signal on T1-weighted images and increased signal on T2-weighted images, as with other pathologies that have higher water content than normal brain. In contrast, vasogenic edema is primarily a white matter phenomenon because the intercellular spaces are larger in the white matter. A notable exception is the corpus callosum, which is so tightly bundled that there is little extracellular space, and therefore vasogenic edema does not spread through it readily.
Significant edema in a significant volume of brain may also cause serious problems because of the resulting increase in brain volume versus the fixed volumes of the intracranial compartments. A localized area of increased volume as a result of a primary pathology or the edema it incites may cause brain tissue to be deformed or to herniate from one compartment into another. Brain herniation involves direct physical deformation of the brain parenchyma, injury of the brain along the edges of dural reflections across which it is squeezed, pressure on other portions of the brain (especially the midbrain and medulla), and often compromise of its vascular supply. It may also compromise other structures such as cranial nerves, as in the classic blown pupil caused by transtentorial herniation of the uncus and parahippocampal gyrus of the medial temporal lobe. Brain herniations may lead to death, particularly in the cases of downward brainstem herniation or cerebellar tonsillar herniation, which compromise the medulla. Increased brain volume within the fixed volume of the calvaria may also cause death through
P.381

an overall pressure effect. The brain becomes ischemic and dies when intracranial pressure approaches and exceeds arterial perfusion pressure; no blood for the brain is able to enter the cranium. For these reasons, evaluation of brain volume and other sources of mass effect is an important part of the neuroradiologic assessment of patients with a large variety of primary pathologies.
SPECIFIC DISEASE STATES
Neoplasms
Intracranial neoplasms have been classified by a variety of methods, their anatomic locations and cells of origin being the bases of the most common classifications. Precise anatomic localization of an intracranial neoplasm is of fundamental importance in that this information gives one the best hope of being specific about the diagnosis and prognosis of the lesion.
The wide availability, increased contrast sensitivity, and multiplanar capabilities of MRI have made this technique the procedure of choice for the initial evaluation of patients suspected of having an intracranial tumor. There is no routine MR method that optimizes the capabilities of the technology for detection of all tumors. Most protocols include T1-weighted, proton density, and T2-weighted images plus T1-weighted images with contrast enhancement; these examinations are best performed both with and without intravenous contrast. If properly used, MR is quite sensitive and can detect the great majority of these lesions. Magnetic resonance imaging can also provide information that in many instances allows accurate identification of the tumor’s site of origin and more precise localization of its anatomic extent.
Some tumors of the central nervous system (CNS) tend to have a predilection for certain anatomic sites, whereas others occur throughout the intracranial space. It is thus useful to identify a lesion’s location and to define whether it is within (intraaxial) or outside (extraaxial) the brain. Nearly 70% of tumors in adults are supratentorial, but the reverse is the case in children. The most common primary tumors of the adult are astrocytomas and glioblastomas; in children, at least half of all such lesions are astrocytomas of the cerebellum or brainstem. In general, an extraaxial location of a neoplasm implies a more favorable prognosis than does an intraparenchymal location.133 The incidence of various intracranial tumors as listed by Potts125 is as follows: gliomas, 43%; meningiomas, 15%; pituitary adenomas, 13%; acoustic neuromas, 6.5%; congenital tumors, 4%; blood vessel tumors, 3%; and miscellaneous, 9%. These figures vary somewhat depending on the source (i.e., surgical versus autopsy series).24
Supratentorial Tumors
Gliomas
Gliomas are graded histologically on a numerical scale, from 1 through 4, a higher number indicating a more malignant tumor histology. Grade 4 tumors are called glioblastoma multiforme; grade 3 tumors are anaplastic astrocytomas; and grades 1 and 2 are the more benign astrocytomas.85 It is important to realize that in many instances variations of grades occur throughout any particular tumor; therefore, biopsy samples are subject to considerable error. Classification of these tumors can also be based on cell morphology (fibrillary or pilocytic) and on site of origin (supra- or infratentorial). These data provide additional information regarding their biological behavior and eventual prognosis. As is the case with the numerical grading scale, these classifications are not without fault; gliomas are seldom of a pure histologic type. Except for the juvenile pilocytic astrocytoma, which almost uniformly has an excellent prognosis, it is difficult to offer guidelines about the biological behavior of these tumors based on imaging studies.113
Glioblastoma Multiforme and Anaplastic Astrocytoma
Glioblastoma multiforme is an invasive, malignant tumor of astrocytic origin; it is the most common of the gliomas occurring above the tentorium, forming about 40% of all such tumors. The tumor occurs most frequently between the ages of 40 and 60 years. The duration of symptoms usually is short, with the time between onset and the initial examination averaging about 6 months. Glioblastoma may occur anywhere in the brain; it is characterized by its infiltrative nature and its ability to spread rapidly. Involvement of both cerebral hemispheres via spread across the corpus callosum is common. The tumor also may spread through the ventricular system or subarachnoid space. True multicentric tumors of this nature are rare.
Unenhanced MR scans classically show the tumor margin to be low signal intensity on T1-weighted images and of much higher signal intensity than the surrounding brain on T2-weighted images; the increased signal intensity is related to vasogenic edema. The great majority of these tumors show marked enhancement following administration of intravenous contrast medium. This enhancement occurs because of the tumor’s neovascularity and the resulting increased permeability of the blood-brain barrier. On gadolinium-enhanced scans, the margins of the tumor are usually irregular and the pattern of the enhancement is heterogeneous. Evidence of mass effect is usually present. Some displacement of the ventricular system away from the lesion is typical; often there is gross distortion of the ventricle on the side of the lesion. When the tumor involves the frontal or parietal lobes, it is prone to extend across the midline through the corpus callosum so that deformity of the opposite ventricle may also be seen. The central areas of these tumors are often necrotic. Gross cysts sometimes occur but are relatively rare in untreated tumors (Fig. 11-6).160
FIG. 11-6. Glioblastoma multiforme. (A and B) Axial contrast-enhanced T1-weighted MR images demonstrate a large necrotic mass in the right posterior temporal region extending into the right parietal lobe (arrows). There is dilation of the right temporal horn; the distal portion of the temporal horn is trapped as a result of compression of the atrium. (C and D) Axial T1-weighted images with contrast at a higher level reveal extension of the neoplasm into the splenium of the corpus callosum (arrow); (E and F) Axial T2-weighted images demonstrate high signal intensity associated with the neoplasm and the adjacent vasogenic edema. The heterogeneous areas of lower signal intensity centrally indicate regions of microhemorrhage and calcification (arrow)
Magnetic resonance scans of glioblastomas more closely reflect the pathologic changes of hypercellularity, hemorrhage, necrosis, and hypervascularity than do CT scans. Thus, on these examinations, areas of cystic change, hemorrhage,
P.382

P.383

and neovascularity are more commonly demonstrated than on CT scans. The MRI also allows more precise recognition of the tumor mass than does CT. It has been shown to be impossible, however, to accurately differentiate the infiltrating margin of these tumors from adjacent normal brain tissue.
The angiographic findings in glioblastomas vary somewhat, but typically the tumor is very vascular, and a bizarre pattern of neovascularity with irregularly dilated arteries and early filling of dilated veins is seen. On angiography these tumors may appear to be well circumscribed, and the extent of neovascularity may vary greatly from one area to another. Avascular areas within a glioblastoma are usually the result of necrosis or cyst formation. Vascular displacements away from the area of the lesion with stretching and straightening of branches are a common observation. In some cases a diffuse stain or blush is seen during the late arterial or capillary phase. Angiography is now seldom required for either the diagnosis or management of tumors of this type.
Anaplastic astrocytomas are the second most common glioma occurring above the tentorium. This grade represents approximately 32% of all such tumors (Fig. 11-7).
FIG. 11-7. Anaplastic astrocytoma. (A and B) Axial contrast-enhanced T1-weighted images reveal a large right frontal mass resulting in compression of the corpus callosum and subfalcine herniation. (C and D) The axial T2-weighted images reveal high signal intensity within the neoplasm with a small amount of surrounding edema. Analysis of the surgical specimen revealed a spectrum of histologic features. Portions of the tumor were characteristic of anaplastic astrocytoma, and other portions of the tumor were more indicative of a lower-grade astrocytoma.
P.384

Low-Grade Astrocytoma
The duration of symptoms at the time of diagnosis averages 3 years for low-grade astrocytomas. These tumors may involve any part of the brain; depending on their topography and biological behavior, the radiographic features of these tumors are quite diverse. This section discusses astrocytomas occurring above the tentorium; others are discussed subsequently. Large cysts commonly form in astrocytomas, particularly in those of pilocytic type, and the cystic element may predominate in both the pathologic and radiographic appearance of the lesion. Calcification occurs in the minority of these tumors. The degree of contrast enhancement varies, depending on both the aggressiveness and the cellular makeup of the tumor. It is important to recognize that in these tumors as well as in other neoplasms of the CNS, the degree of enhancement tends to be more intense and more extensive in malignant than in benign tumors, although this feature does not reliably predict the malignancy of a particular tumor.127
Depending on the size of the lesion, enhanced CT scans may be normal or show only mass effect, with displacement, distortion, or compression of the ventricular system. In some small or low-grade lesions, there is very little mass effect, and the tumor may be difficult or impossible to detect on CT scans (Fig. 11-8). Because of its increased tissue contrast, MRI is more accurate than CT in demonstrating the gross borders of these tumors. Most astrocytomas are slightly hypointense on T1 and hyperintense on T2 images. The degree of homogeneity varies, with the more benign lesions tending to be homogeneous and the more malignant ones heterogeneous. The degree of adjacent edema also varies, with more malignant tumors being associated with considerable edema. Most show no enhancement.
FIG. 11-8. Low-grade astrocytoma. The patient presented with new onset of seizures (A). The contrast-enhanced axial CT scan fails to demonstrate the medial left temporal lobe neoplasm. A small amount of mass effect associated with the uncus of the hippocampus can be appreciated (arrow). (B and C) The axial T2-weighted images clearly indicate a high-signal-intensity neoplasm extending along the parahippocampal gyrus (arrows)
The juvenile pilocytic astrocytoma, a variety of tumor that occurs predominantly in children, has features that usually allow accurate diagnosis by MRI. The great majority of these tumors occur either in or adjacent to the visual pathways or posterior fossa; they are well defined; and they enhance markedly on both CT and MRI. Cyst formation is common. Regardless of their location, these tumors are low grade and only occasionally recur after complete resection.92 They are discussed further in the sections on juxtasellar tumors and posterior fossa tumors.
The angiographic features of astrocytomas depend on the histologic nature of the tumor; lesions with predominant malignant features show abnormalities quite similar to those described for glioblastomas; tumors with mixed benign and malignant features show intermediate changes; lesions of a benign nature show only evidence of avascular mass effect or no changes at all. In the capillary phase of the arteriogram, a tumor stain may be present, at times either in a nodular component of the lesion or, if the entire mass is solid, throughout the tumor. Only rarely is angiography required for either the diagnosis or management of these tumors.
Oligodendroglioma
Oligodendrogliomas make up about 7% of supratentorial gliomas. Most of them are found in adults, the average age at the time of diagnosis being 45 years. Oligodendrogliomas usually grow slowly, and the duration of symptoms before diagnosis averages 11 years. These tumors occur almost exclusively in the cerebral hemispheres, and there is a definite predilection for the frontal lobes. Because of its slow growth, calcification within the tumor occurs very frequently; the calcium usually is distributed in the form of coarse, irregular strands. As in astrocytoma, other types of calcification may also occur, and the pattern of calcification does not allow one to make a specific histologic diagnosis.91
The findings on MR scans are similar to those seen in other glial neoplasms such as astrocytomas. Because of a lack of neovascularity and minimal disruption of the BBB, the enhancement following administration of intravenous contrast medium is usually only slight. The presence of heavy calcification may provide a clue about the nature of the lesion but, as already mentioned, is a nonspecific sign. The calcifications in these tumors are seen on spin-echo sequences as areas of low signal intensity that may be confused with the signal void of abnormal vessels.93 Cystic or necrotic changes are rare unless the lesion has undergone malignant degeneration (Fig. 11-9).160
FIG. 11-9. Anaplastic oligodendroglioma. (A and B) The axial T1-weighted images reveal minimal heterogeneous contrast enhancement. The central areas of low signal intensity indicate necrosis (arrow); (C and D) The spin density images better delineate the extent of the vasogenic edema and the vascular structures within and adjacent to the neoplasm (arrows); (E and F) The axial T2-weighted images demonstrate that large portions of the left temporal lobe are involved by the neoplastic process.
Arteriography shows displacement of vessels away from the mass, with stretching of small adjacent branches. Seldom is there significant neovascularity; the interior of the tumor usually does not develop a tumor stain during the capillary phase of the angiogram.
Miscellaneous Primary Supratentorial Tumors
Gangliogliomas are low-grade neoplasms presenting in children and young adults. Frequently the lesion is detected as a result of the new onset of seizures. The lesions often contain cysts (Fig. 11-10) and may be predominantly cystic with a mural nodule. The cyst is well delineated, and the nodule may contain calcification. Common locations include the temporal and frontal lobes35,65,121.
FIG. 11-10. Exophytic temporal lobe ganglioglioma. (A and B) Axial T1-weighted images with intravenous contrast enhancement identify a large mass originating from the medial aspect of the left temporal lobe. The lesion has both solid and cystic components. A large exophytic component extends through the tentorial incisura into the superior cerebellar cistern. The tumor has also compressed the atrium of the left lateral ventricle.
Dysembryoplastic neuroepithelial tumors (DNETs) are benign lesions that are frequently associated with cortical dysplasia and have an appearance on MRI similar to that of a low-grade astrocytoma. The lesion is cortically based and shows low signal intensity on T1-weighted images and increased signal on T2-weighted images (Fig. 11-11).90,116
FIG. 11-11. Dysembryoplastic neuroepithelial tumor. The T1-weighted images indicate a well-circumscribed neoplasm originating in the cortical region (arrows) The inner table of the skull has been remodeled in response to the mass, suggesting a slow-growing neoplasm.
Pleomorphic xanthoastrocytoma is an unusual distinct subtype of astrocytoma. This slow-growing tumor is generally considered benign and presents with slow progression of symptoms related to increasing mass effect. An enhancing nodule with a surrounding tumor cyst is the most typical appearance.95,120
P.385

P.386

P.387

Ependymoma
Ependymomas comprise about 5% of all supratentorial gliomas. The duration of symptoms at the time of diagnosis is usually relatively short, being less than 1 year in many cases. The average age at the time of diagnosis in supratentorial ependymomas is reported to be 30 years. Infratentorial ependymomas occur most frequently in children and adolescents and are much more common than are the supratentorial variety.
Many supratentorial ependymomas probably arise from ependymal cell nests situated about the margins of the lateral ventricles; they frequently occur near the atrium of the lateral ventricle. Ependymomas often contain scattered small or punctate calcium deposits, which may be visible on unenhanced CT scans. On these scans, ependymomas most often are isodense or slightly hyperdense as compared with the adjacent normal brain. Cystic changes frequently occur, and at times the lesion may appear to be almost entirely cystic. Most ependymomas are enhanced to some degree following administration of intravenous contrast medium. These neoplasms show no specific signal characteristics on MRI, but the multiplanar capabilities of MRI are advantageous in demonstrating the location and pathway of spread of these tumors.143
Meningiomas
Meningiomas are extraaxial tumors that arise from the arachnoid; the great majority of them are benign. Common locations of meningiomas include sites along the superior sagittal sinus, particularly in the posterior frontal and parietal areas and overlying the convexities of the cerebral hemispheres a short distance away from the midline. Other frequent sites for development of these tumors are in the region of the tuberculum sellae or just anterior to the tuberculum along the olfactory groove; along the edges of the sphenoidal ridge; and somewhat less frequently along the margins of the falx cerebri and the tentorium. Grossly, meningiomas vary in shape from a globular configuration to a flat type of growth, the so-called meningioma en plaque.
P.388

Meningiomas usually receive a major portion of their blood supply from the arteries that supply the normal dura at the site from which they arise. Aggressive or malignant types of this tumor may also parasitize the vasculature of the adjacent brain. Meningiomas that arise from or adjacent to the dural sinuses may invade and obstruct these structures. Most meningiomas that arise near bone incite some type of osseous response,58 most often hyperostosis (hypertrophy). They may invade the bone and occasionally will extend through it to form a hyperostotic density along the outer table of the skull. In other instances, extensive bone destruction is apparent; rarely, the bone overlying a meningioma is completely destroyed, with a soft-tissue mass bulging externally.
Tumors that cause a pure hyperostotic type of bone reaction tend to recur infrequently, whereas those that cause a destructive or mixed bone reaction recur much more often. In 60% to 65% of patients with meningiomas, changes seen on plain films of the skull will strongly suggest both the diagnosis and location of the tumor; nevertheless, these studies are not indicated because they do not allow assessment of the tumor’s size and thus are not of value in deciding on management. Likewise, angiography provides typical findings but is now rarely used for diagnostic purposes. Depending on the size, location, and likely vascularity of the tumor, angiography may be indicated to decide whether removal will be facilitated by preoperative embolization. Initial assessment of all these features is best performed by MRI,28,57 which allows more precise assessment of the extent, location, and vascularity of these tumors than does CT.
Calcification within meningiomas is found in 15% to 20% of cases. The calcium deposits typically are in the form of small punctate densities that are rather uniformly distributed throughout the tumor mass.138 These sandlike deposits are known as psammoma bodies and are in part responsible for the homogeneous increase in attenuation that is typical of the unenhanced CT appearance of these lesions. Some very slow-growing meningiomas form densely calcified masses, which may have little if any soft-tissue component.11
On unenhanced CT scans, most meningiomas are homogeneous and show slightly increased attenuation. The degree of edema surrounding them varies greatly; some lesions cause marked edema of the adjacent brain, and others do not. This feature depends in part on their rate of growth. Scans usually show a relationship of the tumor to the dura. Following intravenous contrast administration, the typical meningioma is enhanced in a homogeneous manner, has very well-defined margins (Fig. 11-12), and frequently manifests an adjacent dural tail. Slow-growing, heavily calcified lesions may not show any enhancement; aggressive or malignant lesions often show heterogeneous enhancement.110,134
FIG. 11-12. Convexity meningioma. (A) The T2-weighted images show a relatively isointense tumor compared to normal brain tissue. The central low-signal-intensity structures (arrow) are hypertrophied meningeal vessels supplying the meningioma. (B) The axial T1-weighted images with contrast reveal a homogeneously enhancing dural-based neoplasm. Note the thickened dura adjacent to the meningioma; an enhancing dural tail is commonly observed associated with meningiomas (arrow)
On MRI studies, meningiomas are typically isointense to
P.389

slightly hypointense with respect to gray matter on T1-weighted images and isointense to hyperintense on proton density and T2-weighted images.168 Most of these tumors have sharply defined margins and homogeneous signal intensities.33 The ability to perform brain imaging in multiple projections without the presence of artifact created by the bone of the calvaria greatly improves the ability to define the full extent of these lesions, especially when they involve the skull base (Fig. 11-13).157 Most meningiomas enhance significantly following administration of paramagnetic contrast
P.390

medium.23 Enhancement of the dura adjacent to the bulk of the tumor mass is a useful diagnostic sign (Figs. 11-14 and 11-15).
FIG. 11-13. Planum sphenoidale meningioma. The sagittal T1-weighted images with intravenous contrast enhancement reveal a dural-based neoplasm arising from the planum sphenoidale. The lesion extends posteriorly into the suprasellar region, resulting in the compression of the optic chiasm. Note the dural tail extending from the anterior margin of the meningioma.
FIG. 11-14. Tentorial meningioma. (A) The T1-weighted image with intravenous contrast enhancement indicates a large, dural-based, homogeneously enhancing meningioma. The right transverse sinus also enhances, suggesting that flow may be altered within the dural sinus (arrows). (B) Lateral view of the left external carotid arteriogram indicates hypertrophy of the posterior branch of the middle artery (arrow). Note the starburst pattern of increased vascularity related to the arterial supply to the meningioma.
FIG. 11-15. Parasagittal meningioma with invasion of the sagittal sinus. The coronal T1-weighted image with intravenous contrast material reveals an en plaque meningioma extending along the right parietal convexity, obliterating the sagittal sinus and extending along the superior aspect of the parietal lobe. Note the lack of flow void in the region of the sagittal sinus.
The angiographic findings of the typical meningioma are quite characteristic: the major arterial supply is from dural arteries; tumor vessels are usually uniform so that opacification is relatively constant throughout the tumor; the arterial branches surround the tumor in an arclike manner, sending small tributaries toward the center of the mass; and parenchymal staining is dense. Nonetheless, angiography is not required in the diagnostic evaluation of meningiomas unless there is concern about the ability at surgery to control the arterial supply because of the location of the lesion. In these instances, a preoperative embolization procedure may be required (Fig. 11-16).
FIG. 11-16. Convexity meningioma arising from the pterion. (A) The axial T1-weighted image with intravenous contrast material indicates a large dural-based homogeneously enhancing mass. There are multiple central flow voids indicating hypertrophied vascular structures (arrow). (B) The axial spin-density-weighted image indicates extensive edema involving the right basal ganglia structures and white matter of the right temporal lobe. (C and D) The right common carotid arteriogram indicates a hyper vascular mass supplied by branches of the right middle meningeal artery (arrowhead). Note the intense tumor stain (arrows).
Juxtasellar Tumors
Pituitary Adenoma
The classification of pituitary adenomas divides these lesions into two major groups, those that are hormonally active and those that are hormonally inactive. The active ones are then further divided according to the hormones they secrete. Depending on their size, pituitary adenomas are designated as either macroadenomas (>1 cm) or microadenomas (< 1 cm). Macroadenomas are the majority of hormonally inactive tumors and typically become clinically manifest as a result of their size, causing compression of adjacent neural structures, especially the optic chiasm. Patients with microadenomas usually seek medical attention because of abnormal hormone secretion. Specific types of pituitary adenomas include prolactin-, growth-hormone-, and ACTH-secreting adenomas. Prolactinomas in women are associated with galactorrhea and amenorrhea; in men, they most often cause hypogonadism. Growth-hormone-secreting adenomas that occur before bone growth has ceased cause gigantism, whereas those that occur later result in acromegaly. ACTH-secreting tumors are associated with Cushing’s disease. Most pituitary adenomas occur in adults.8
Magnetic resonance imaging is the technique of choice for evaluation of the juxtasellar area.36,40 On T1-weighted MR scans performed immediately following administration of intravenous gadolinium contrast medium, most pituitary microadenomas are seen as an area of reduced signal intensity within the enhancing pituitary gland.137 This pattern is variable, however, with exceptions occurring as a result of hemorrhage, with differences in the tumor histology, and as a function of the time elapsed between administration of the contrast and performance of the scan. Other MR findings seen with microadenomas are an increase in the height of the gland (normally < 10 mm), alteration in the contour of the upper margin of the gland from concave or straight to convex, erosion of the floor of the sella turcica adjacent to an area of hypointensity, and displacement of the normally midline pituitary stalk away from an area of diminished enhancement in the gland (Fig. 11-17). Considerable variation occurs in the size and configuration of the normal pituitary gland, especially in women of childbearing age; great care must be exercised in the diagnosis of pituitary microadenomas on the basis of MR scans performed without associated evidence of a hormonal abnormality.131,147
FIG. 11-17. Prolactin-secreting pituitary microadenoma. The T1-weighted image with intravenous contrast enhancement reveals the low-signal-intensity lesion in the left lobe of the pituitary gland. There is an upward convex margin of the left lobe of the gland, indicating focal expansion (arrow).
Depending on their size and pattern of growth, pituitary macroadenomas have a variable appearance on MR scans. Most of them are hypointense or isointense on unenhanced T1-weighted MR scans; following administration of intravenous gadolinium contrast medium, marked homogeneous enhancement is typical (Fig. 11-18). Cystic or necrotic areas occur frequently in very large pituitary adenomas; on MR scans these appear as areas of reduced signal on T1-weighted images. Many macroadenomas have areas of high signal intensity on the T1-weighted images; this reflects the presence of prior hemorrhage (Fig. 11-19).
FIG. 11-18. The coronal T1-weighted image with intravenous contrast enhancement reveals a large intrasellar mass. The lesion measures greater than 1 cm in diameter, indicating a pituitary macroadenoma. Note the expansion of the tumor into the sphenoid sinus. There is also extension into the suprasellar cistern with partial compression of the optic chiasm (arrows).
FIG. 11-19. Hemorrhagic pituitary macroadenoma. The sagittal T1-weighted images without intravenous contrast material indicate a high-signal-intensity intrasellar mass. Close inspection indicates a fluid level within this lesion (arrow). The pituitary fossa has been expanded, and there is suprasellar extension. Transsphenoidal surgery revealed hemorrhagic fluid within a pituitary macroadenoma.
Macroadenomas are best imaged with MRI because this technique provides the best means for visualizing the relationship of these tumors to adjacent neural and vascular structures. The extent of a suprasellar tumor is easily demonstrated in both coronal and sagittal images. It is more difficult to be sure about lateral extension of these tumors. Displacement
P.391

P.392

of the cavernous segments of the internal carotid arteries may occur without tumor invasion of the cavernous sinus (Fig. 11-20). Abnormal signal intensity lateral to this segment of the artery, however, usually indicates extension of the tumor into the cavernous sinus.
FIG. 11-20. Growth-hormone-secreting pituitary macroadenoma with invasion of the left cavernous sinus. The coronal T1-weighted images without contrast indicate a convex outward margin of the left cavernous sinus (arrow). The left internal carotid artery is elevated, and the patient presented with cranial nerve dysfunction on the left.
Pituitary macroadenomas must be distinguished from other mass lesions that occur in the juxtasellar area, such as meningiomas (Fig. 11-21), giant carotid aneurysms (Fig. 11-22), and optic gliomas (Fig. 11-23).73,80 In most instances, the use of sagittal and coronal scans and intravenous contrast medium allows this to be determined without difficulty because the relationship of the mass to adjacent structures as well as the presence or absence of any associated
P.393

P.394

bony abnormality can be well assessed. Only occasionally is angiography required as part of the diagnostic evaluation of a suspected pituitary macroadenoma.
FIG. 11-21. Juxtasellar meningioma. (A and B) The homogeneously enhancing lesion has encased the supraclinoid carotid artery and extends along the dura of the right cavernous sinus. Encasement of the carotid artery and dural extension are common findings associated with juxtasellar meningiomas.
FIG. 11-22. Giant aneurysm extending into the suprasellar region (A). The sagittal T1-weighted images indicate a heterogeneous mass resulting in upward compression of the floor of the third ventricle (arrow). (B) The coronal T1-weighted image reveals a large flow void (arrow) within the lesion, indicating a partially thrombosed giant suprasellar aneurysm.
FIG. 11-23. Optic nerve glioma in a patient with neurofibromatosis type 1. Note the marked expansion of the right optic nerve as a result of the diffuse pilocytic astrocytoma.
Optic Glioma
Gliomas that involve the optic pathways are slow-growing tumors that occur most often in children with neurofibromatosis type 1. They may involve one or both optic nerves, the chiasm, optic tracts, or optic radiations. Because of their early occurrence and slow rate of growth, optic gliomas frequently are associated with enlargement of the optic foramina and alteration in the configuration of the pituitary fossa. It is often impossible to distinguish these tumors either by their behavior or by their location from a primary glioma of the hypothalamus.135
Magnetic resonance imaging is the technique of choice for evaluation of the patient suspected of having an optic glioma. These tumors are usually isointense on T1-weighted images and hyperintense on T2-weighted scans. They occasionally enhance following intravenous contrast medium administration.175
Craniopharyngioma
This congenital tumor arises from remnants of Rathke’s pouch. Craniopharyngioma is largely a tumor of childhood and adolescence; however, occurrence in older adults is by no means rare. In younger children the presenting complaint is often related to increased intracranial pressure; in older children and adults, symptoms are most often of a visual or endocrine nature. Delayed growth is the most common endocrine-related symptom associated with craniopharyngioma.77
Calcification occurs in as many as 80% of children with this tumor; it is much less common in adults. Most craniopharyngiomas are suprasellar in location, but at least 10% to 15% are confined solely to the pituitary fossa. Cystic changes of either a unilocular or a multilocular nature occur very frequently. The CT scan appearance of these tumors is variable depending on the amount of calcification and cystic change present with the tumor.46 Tumors that have extensive cystic change most often appear as well-defined areas of decreased attenuation with areas of calcification about their periphery (Fig. 11-24). Tumors that are mostly solid are usually of increased attenuation on noncontrast scans.
FIG. 11-24. Suprasellar craniopharyngioma (A). The axial CT images were obtained without intravenous contrast enhancement. There is dense calcification within the wall of the neoplasm (arrows). Note the dilation of the temporal horn secondary to obstructive hydrocephalus. (B) The sagittal T1-weighted image indicates a large suprasellar neoplasm expanding the pituitary fossa and compressing the third ventricle. The lesion is relatively homogeneous in signal intensity. (C) The axial T1-weighted image with intravenous contrast enhancement indicates enhancement of the cyst wall. There is a small amount of enhancement involving the adjacent floor of the third ventricle. Temporal horn dilation secondary to obstructive hydrocephalus is again noted.
As is the case in evaluation of pituitary adenomas, MRI is the technique of choice for the evaluation of craniopharyngiomas. Thin-section coronal and sagittal T1-weighted images are particularly helpful. Craniopharyngiomas have a variable appearance on MRI, depending on their degree of calcification as well as the extent of cystic changes in the tumor. Solid portions of craniopharyngiomas are usually heterogeneous, with calcifications appearing as low intensity on both T1- and T2-weighted images, while noncalcified portions are isointense or hypointense on T1 images and hyperintense on T2 images. Cystic portions of this tumor are often filled with a lipid-type fluid or old hemorrhage that is of high signal intensity on both T1- and T2-weighted images (Fig. 11-25).1 Following intravenous contrast medium administration, the capsule of cystic tumors shows enhancement on both CT and MRI. Solid portions of these tumors often enhance in a homogeneous manner.
FIG. 11-25. Craniopharyngioma. The sagittal T1-weighted image without contrast material reveals a large suprasellar neoplasm with two regions of high signal intensity (arrows). Craniopharyngiomas frequently contain regions of high signal intensity on T1-weighted images secondary to lipid material within the tumor cyst. Portions of the lesion may also show high signal intensity secondary to blood breakdown products from prior intratumoral hemorrhage.
Other Supratentorial Tumors
Tumors of the Pineal Gland
Tumors of the pineal gland are rare, contributing approximately 0.5% to 1% of all intracranial tumors; they are usually manifested during the first three decades of life. Pineal region neoplasms originate from pineal parenchymal cells (pineoblastoma and pineocytoma), germ cells (germinomas, teratomas, embryonal carcinoma, choriocarcinoma), or glial cells. This is also a common site for lipomas. Germ-cell tumors are the most common type and occur much more often in men than in women. Synchronous germinomas can arise in the pineal region and from the infundibulum (Fig. 11-26).146 Tumors arising from the pineal parenchymal cells occur in equal numbers in men and women. A variety of glial tumors also occur in the pineal region. Because many of these tumors tend to infiltrate diffusely, it is often impossible to determine from imaging studies whether a lesion has its origin within the pineal gland or the adjacent neural parenchyma (especially the midbrain tectal plate).
FIG. 11-26. Synchronous germinomas involving the floor of the third ventricle and pineal region. (A and B) The sagittal T1-weighted images with intravenous contrast demonstrate abnormal enhancement involving the pineal region (arrowheads). There is also enhancement involving the optic and infundibular recesses of the third ventricle with involvement of the optic chiasm (arrowheads). (C and D) The coronal T1-weighted images with intravenous contrast material confirm the presence of optic chiasm involvement. The chiasm is enlarged and enhances diffusely (arrowheads). The patient presented with diabetes insipidus.
Teratomas and most pineal parenchymal tumors (pineocytomas and pineoblastomas) show some degree of calcification. The observation of calcification in the region of the pineal gland in a child under the age of 7 years is thus somewhat suggestive of a neoplasm because the normal pineal gland usually does not calcify at this age.169 In one study,
P.395

P.396

fewer than 11% of children between the ages of 11 and 14 had pineal calcification present on CT scans.170
The ability of MRI to provide high-quality coronal and sagittal images has made it superior to CT for evaluating patients with pineal region tumors.167 Multiplanar images greatly assist in the location of the apparent center of a mass and, therefore, are useful in judging the nature of its origin. However, the various types of pineal and pineal region tumors cannot be distinguished accurately on the basis of MR scan findings alone, except for teratomas, which are almost always partially cystic and are markedly heterogeneous in signal intensity because of the presence of hair, bone, and especially teeth.141 Germinomas and pineoblastomas often are isointense with gray matter on both T1- and T2-weighted images. All may have calcifications, and most show significant enhancement following the administration of intravenous contrast medium.56 The pattern of enhancement varies; some are homogeneous, but others are not; some have well-defined margins, but the margins of others are indistinct. Edema of the brain adjacent to a pineal tumor is unusual. Because of their relationship to the aqueduct of Sylvius, many of these tumors are associated with hydrocephalus.49
Colloid Cyst
Colloid cysts develop in the anterior portion of the third ventricle, usually arising from the roof. Because of its location, the lesion may block either one or, as is more often the case, both of the interventricular foramina, thereby causing hydrocephalus. In some instances obstruction is intermittent. This tumor shows no predilection for either sex and usually becomes manifest during adult life.88
As seen on unenhanced CT scans, a colloid cyst characteristically appears as a well-demarcated, symmetric midline mass of increased density located at the level of the interventricular foramina. An occasional colloid cyst that is isodense with the adjacent brain has been reported. On contrast scans, the outer margin of the mass may enhance slightly (Fig. 11-27).48 Because the diagnosis of a colloid cyst depends primarily on the recognition of its location and the ability to discern that the adjacent brain is normal, the multiplanar nature of MRI alone makes it the technique of choice for evaluation of these lesions. The contents of colloid cysts are variable; therefore, their signal characteristics on MRI are not specific.151
FIG. 11-27. Colloid cyst of the anterior third ventricle. The coronal T1-weighted image without contrast material reveals a high-signal-intensity lesion adjacent to the foramen of Monro. The well-circumscribed margins of the lesion and location support the diagnosis of colloid cyst.
Because colloid cysts are benign lesions that cause symptoms only as a result of the hydrocephalus they produce, it is important that they be recognized so that appropriate treatment may be attempted. Treatment may be either removal of the cyst or decompression of the hydrocephalus without cyst removal.161
Astrocytomas that originate from the tissue around the interventricular foramen can usually be distinguished from colloid cysts because they typically are poorly defined, have indistinct margins, and are either isodense or hypodense on unenhanced CT scans.
Epidermoid Tumor
Epidermoids are congenital lesions derived from ectoderm. They are found more frequently as intradiploic lesions in the bones of the skull than as intracranial lesions; both are uncommon. There is no age or sex predilection. Desquamation of cholesterol-containing debris from the lining of this tumor accounts for its slow growth. Symptoms usually occur as the result of compression of adjacent neural structures. The most common location for an epidermoid is the cerebellopontine angle cistern.50 Other sites of occurrence are the juxtasellar area or in one of the lateral ventricles or the fourth ventricle.150
The CT density of an epidermoid is the same as or slightly lower than that of cerebrospinal fluid. Calcification of the tumor’s margins is uncommon, but when it occurs, it is one feature that helps in distinguishing epidermoids from arachnoid cysts on CT scans. Characteristically, the surface of an epidermoid is rough and nodular, and some are cauliflower-like with deep clefts; arachnoid cysts are smooth. This difference has been used to make a definitive diagnosis using intrathecal contrast. Epidermoids do not enhance after administration of intravenous contrast medium. On MRI, epidermoids tend to have signal intensities that are similar to that of CSF on all pulse sequences; occasionally heterogeneous internal signal intensity can be observed.
P.397

Dermoid Tumor
Dermoids are rare congenital tumors derived from ectoderm and mesoderm. Almost all dermoids occur in the midline, and, like epidermoids, most of these tumors cause symptoms because of compression of adjacent neural structures. Occasionally, a dermoid may rupture spontaneously into either the ventricular system or the subarachnoid cisterns, causing an intense chemical ventriculitis or meningitis. The lining of these lesions contains hair follicles and glandular elements as well as squamous epithelium. On CT scan the density of dermoids is variable but typically is similar to that of fat. Dense calcification representing partially formed dental elements is seen within some dermoids, and calcification of a portion of the outer margin is commonly observed.100
The characteristic fatlike signal intensities from the secretions of these tumors often allow an accurate diagnosis to be made with MRI. On both CT and MRI, fat-fluid levels are sometimes seen within some dermoids; their presence within the ventricular system indicates rupture.32 Dermoids do not enhance following administration of intravenous contrast medium (Fig. 11-28).
FIG. 11-28. Suprasellar dermoid. (A) The sagittal T1-weighted image without intravenous contrast material reveals a high-signal-intensity suprasellar mass extending along the planum sphenoidale. (B) Following the administration of intravenous contrast material and fat saturation, there is a small amount of enhancement along the peripheral aspects of the lesion (arrow). The majority of the mass suppresses with fat saturation. A dermoid was encountered at surgery.
Lipoma
Lipomas, lesions derived from mesoderm, occur infrequently. Like dermoids, they usually occur in the midline, the most common locations being the corpus callosum, the vermis, and the quadrigeminal cistern. The majority of lipomas are incidental findings. When they occur in the corpus callosum, they are often associated with callosal dysgenesis. The fat density or signal of these lesions gives them a characteristic appearance on both CT scans and MRI. Calcification is frequent in their periphery, especially in lipomas that occur in the corpus callosum.
P.398

Infratentorial Tumors
Astrocytoma
Astrocytoma is the most common primary infratentorial tumor. Astrocytomas of the brainstem and cerebellum account for as many as 50% of childhood tumors in some series. These tumors range in their biological behavior from very slow-growing nodules to diffusely infiltrating lesions. Their radiographic appearance depends primarily on their histologic nature but also is influenced by their location.64
Astrocytomas of the brainstem occur most frequently in children but are not unusual in adults. They account for about one-third of all infratentorial tumors. They may originate at any level of the brainstem but are most common in the pons. Rapidly growing, diffusely infiltrating tumors (fibrillary astrocytomas) are more common than the slow-growing varieties.44 Because of diffuse infiltration of these tumors, large segments of the brainstem are often found to be abnormal. At the time of diagnosis, the clinical signs and symptoms produced by brainstem astrocytomas are often mild in relation to the large size of the tumor. It is not uncommon to observe a low-grade astrocytoma involving the entire brainstem and even extending into both the cervical portion of the spinal cord and the cerebellum. Astrocytomas commonly form exophytic extensions along the surface of the brainstem and occasionally can simulate an extraaxial mass lesion. In very low-grade lesions, the only indication of the presence of an abnormality may be distortion of the shape and increase in the size of the involved brainstem segment (Fig. 11-29).145 Calcification in brainstem astrocytomas is not observed as frequently as in the case of similar supratentorial tumors. Following the administration of intravenous gadolinium contrast medium, there is a variable pattern; higher-grade or malignant tumors tend to enhance intensely while those that are less aggressive enhance slightly or not at all.9
FIG. 11-29. Brainstem glioma. (A) The axial T1-weighted image without intravenous contrast enhancement reveals marked expansion of the pons. The basilar artery has been enveloped by the neoplasm. There is a small amount of hemorrhage along the left lateral aspect of the neoplasm (arrow). The fourth ventricle is also compressed by the lesion. (B) The axial T2-weighted image confirms the marked expansion of the brainstem. There is low signal intensity in the region of the hemorrhage, indicating intracellular methemoglobin.
MRI is more sensitive than CT for detection of both the presence and the extent of these tumors. On T1-weighted images, most of these lesions are hypointense: on T2 images they are hyperintense. Small cystic changes are not uncommon.
P.399

Astrocytomas arising in the cerebellum are a common CNS tumor of childhood. Two major types of cerebellar astrocytoma exist. The most frequent is the pilocytic variety, which is well demarcated, benign, and often cystic. Less common is the diffusely infiltrative (fibrillary) variety that is poorly defined and often malignant. Calcification is unusual in either the solid or the cystic variety of this tumor.108 Most of the lesions of either type arise in the cerebellar hemispheres.69
On MRI the cystic pilocytic astrocytoma is seen as a well-circumscribed mass with signal characteristics that are similar to those of cerebrospinal fluid. Often there is a mural nodule; the nodule and rim of the cyst enhance after administration of intravenous contrast medium. Solid varieties of these tumors are hypointense on T1-weighted images and hyperintense on T2-weighted scans (Fig. 11-30).5
FIG. 11-30. Pilocytic astrocytoma. (A and B) The axial T1-weighted images with intravenous contrast enhancement reveal an irregularly shaped nodule along the posterior aspect of the tumor cyst (arrow). (C and D) The axial T2-weighted images confirm the presence of a large tumor cyst producing compression of the fourth ventricle. The nodule connects to several septations within the cystic portions of the neoplasm.
The infiltrating variety of cerebellar astrocytoma (fibrillary astrocytoma) has an appearance on MRI that is similar to that of its brainstem counterpart.
Hemangioblastoma
These benign tumors, found mostly in adults, occur most often in the cerebellum. They also occur regularly, however, in the brainstem and spinal cord; supratentorial occurrences are rare. These neoplasms are sometimes associated with the von Hippel-Lindau disease; in this setting the chance of their being multiple increases significantly (Fig. 11-31). As many as half of all hemangioblastomas are mostly cystic; the remainder are divided between those that are partially cystic and solid and those that are entirely solid. Regardless of whether they are cystic or solid, hemangioblastomas have extensive vascularity (Fig. 11-32).75 The cystic variety typically has a well-defined mural nodule that receives its blood supply from adjacent pial vessels. At times the vascularity of these tumors is so extensive that the masses may simulate arteriovenous malformations. Calcification is usually not seen.10
FIG. 11-31. Multiple hemangioblastomas in a patient with von Hippel-Lindau disease. The axial T1-weighted image reveals multiple hemangioblastomas (arrows). There is a large cyst associated with the right cerebellar hemangioblastoma.
FIG. 11-32. Solitary hemangioblastoma. (A) There is a solitary enhancing lesion located in the posterior left cerebellar hemisphere. (B) The left vertebral arteriogram indicates a hypervascular lesion with arteriovenous shunting. Note the early filling vein (arrow) indicative of a hemangioblastoma.
These tumors vary in appearance depending primarily on whether they are cystic or solid. On noncontrast CT, lesions that are largely cystic appear as well-defined masses with attenuation similar to CSF; careful observation will usually reveal an isodense mural nodule. Solid hemangioblastomas are most often isodense. Likewise, on MRI, the cystic portion of a hemangioblastoma typically has signal characteristics that are the same as those of CSF. Solid portions of these tumors are usually hypointense to adjacent brain on T1-weighted scans and hyperintense on T2-weighted images. Following administration of intravenous contrast medium, the solid portion of a hemangioblastoma enhances intensely both on CT and T1-weighted MR scans. On the basis of MR findings alone, it may be difficult to distinguish a cystic cerebellar hemangioblastoma from a cystic cerebellar astrocytoma. Angiography usually allows this differential
P.400

to be made because the mural nodule of a cystic hemangioblastoma typically has enlarged feeding arteries and draining veins, a feature not common in astrocytomas of this nature.144
Primitive Neuroectodermal Tumors (Medulloblastoma)
These malignant tumors, traditionally called medulloblastomas when they originate in the cerebellum, are the most common posterior fossa tumors of childhood and are unusual in adults.87 They spread both by direct extension and by dissemination of tumor cells throughout the subarachnoid space.129 The great majority of childhood medulloblastomas occur in the vermis along the roof of the fourth ventricle. Most medulloblastomas in adults originate more laterally in one of the cerebellar hemispheres. It is unusual for a medulloblastoma to have a significant cystic component, the majority of them being composed of densely cellular tissue; likewise, calcification within these tumors is not prominent. With increasing length of survival of patients with these as well as some other malignant tumors of the CNS, there are increasing reports of extraneural metastases, particularly to lymph nodes and bone. Osseous metastases from medulloblastomas occur chiefly in the axial skeleton and may be osteolytic, osteoblastic, or of mixed type.118 Because most medulloblastomas originate in the cerebellar vermis and grow into the fourth ventricle, obstructive hydrocephalus is common and is frequently the cause of the initial complaint.132
On MR scans the most typical appearance of a medulloblastoma
P.401

is a midline vermian mass. As with other posterior fossa tumors, MRI is superior to CT for depicting the origin and full extent of these lesions.97 Probably because of their dense cellularity and scant cytoplasm, most medulloblastomas are of somewhat lower signal intensity on T2-weighted images than are most other primary brain tumors.105 Both the primary lesion and its parenchymal and subarachnoid metastases enhance markedly after administration of paramagnetic contrast medium (Fig. 11-33). Except for their location, tumors that originate in the cerebellar hemispheres have a similar appearance. On enhanced CT scans medulloblastomas show an intense increase in their density and are seen to have sharply defined margins. Both the subarachnoid and subependymal metastases of these tumors enhance following administration of intravenous contrast medium.108,173
FIG. 11-33. Medulloblastoma with leptomeningeal dissemination. (A) The axial T1-weighted images with intravenous contrast material reveal residual medulloblastoma involving the posterior fourth ventricle. (B) A higher section indicates metastatic disease producing leptomeningeal enhancement (arrows). There are also large metastatic deposits within the suprasellar cistern and within the ventricular system. (C) Slightly higher section confirms the presence of extensive disease involving the lateral ventricles.
Ependymoma
From 60% to 75% of ependymomas occur in the posterior fossa and usually have their origin along the floor of the fourth ventricle. Except for location, they are similar in appearance to supratentorial ependymomas, which have already been described. Their tendency to spread along the outlets of the fourth ventricle and into the upper cervical spinal canal, along with the frequent occurrence of prominent calcifications, helps to differentiate some cases from medulloblastomas (Fig. 11-34). As an additional differential point, the enhancement seen in these tumors tends to be less intense and more heterogeneous than that which occurs in medulloblastomas.115
FIG. 11-34. Extraventricular extension of fourth ventricular ependymoma. The sagittal T1-weighted images without intravenous contrast enhancement reveal a large neoplasm encasing the basilar artery and extending caudally along the premedullary cistern into the upper cervical subarachnoid space. The extension of the tumor out of forth ventricle and through the foramen magnum is characteristic of an ependymoma.
P.402

Schwannoma
Schwannomas are benign tumors that occur along the course of cranial, spinal, and peripheral nerves. The previous designation of these tumors as neuromas or neurilemmomas is misleading and should not be used. The discussion that follows is limited to those tumors that involve the cranial nerves.102
Schwannomas are primarily tumors of adults and occur considerably more often in women than in men, a 2:1 ratio being reported in some series. The eighth cranial nerve is most frequently involved; most of the other tumors occur on the fifth nerve. There is no explanation for the tendency of these tumors to occur in sensory nerves almost exclusively. Of those schwannomas that originate from the eighth cranial nerve, approximately 75% involve the vestibular division, usually its intracanalicular portion. Because of their location, eighth-nerve schwannomas often produce signs and symptoms when they are quite small. These include a characteristic hearing loss, tinnitus, and less often vertigo or dizziness.107 Large eighth-nerve lesions may also cause dysfunction of the fifth and seventh cranial nerves. Schwannomas
P.403

account for the great majority of tumors that occur in the cerebellopontine angle.
The appearance of an eighth cranial nerve schwannoma on an unenhanced CT scan depends primarily on its size. Large lesions are visible because of obliteration of the ipsilateral cerebellopontine angle cistern, displacement of the brainstem and fourth ventricle, and widening of the contralateral cerebellopontine angle cistern. Small lesions may be occult or may manifest themselves only by enlargement of the ipsilateral internal auditory canal. Following administration of intravenous contrast medium, schwannomas enhance significantly. Very small tumors that are confined to the internal auditory canal may not, however, be visualized on even the best routine CT scans. Magnetic resonance imaging is, therefore, recommended over CT as the technique of choice for the evaluation of patients suspected of having a cerebellopontine angle lesion.96
Most schwannomas are well seen on thin-section (3 mm) T1-weighted scans performed in either an axial or coronal projection (Fig. 11-35). On T2-weighted images, these tumors have reduced signal intensity compared to cerebrospinal fluid and may thus be visualized on thin-section T2-weighted images. Because of almost constant, intense enhancement after administration of a gadolinium contrast medium, this technique allows visualization of very small tumors within both the cerebellopontine angle cistern and the internal auditory canal itself.
FIG. 11-35. Left eighth nerve schwannoma. The axial T1-weighted images with intravenous contrast enhancement reveal a left cerebellopontine angle mass in the left internal auditory canal. The internal auditory canal is expanded secondary to the neoplasm.
Except for location, schwannomas of the other cranial nerves appear similar on MRI and CT scan to those of the eighth nerve. The MRI is also the technique of choice for evaluation of these lesions.
Other Intracranial Tumors
Choroid Plexus Papilloma
This rare, benign tumor, which usually occurs in children, may originate anywhere that choroid plexus occurs but is most often found within either the fourth ventricle or one of the lateral ventricles. It is often pedunculated, giving it some mobility. It is frequently associated with hydrocephalus, the cause of which may be both obstruction of cerebrospinal fluid circulation and overproduction of cerebrospinal fluid. Because these tumors are within the choroid plexus and thus outside the BBB, contrast enhancement is marked.171
Choroid plexus papillomas typically have multiple areas of calcification and cystic changes. Their vascularity is usually prominent, and areas of hemorrhage are common. The MRI appearance of these lesions reflects these characteristics
P.404

so that these tumors typically have heterogeneous signal intensities on both T1- and T2-weighted images. In many instances, prominent areas of hypointensity caused by either calcification or vascularity are present. Contrast enhancement is prominent. Angiography is sometimes indicated before surgical removal of these tumors to outline their extensive blood supply, which is derived from the choroidal arteries (Fig. 11-36).30
FIG. 11-36. Choroid plexus papilloma. (A and B) The axial T1-weighted images with intravenous contrast enhancement reveal a large, irregularly lobulated mass within the right lateral ventricle. The ventricular system is enlarged, possibly secondary to overproduction of CSF.
Chordoma
Chordomas are benign but locally invasive tumors that arise from intraosseous remnants of the notochord. Their most common locations are at either end of the spinal column—the body of the sphenoid bone and clivus and the sacrococcygeal area. They grow slowly but cause extensive local bone destruction. Neurologic signs and symptoms are produced as the result of the compression of local neural structures. On unenhanced CT scans, chordomas of the clivus and sphenoid bone appear as areas of bone destruction associated with an irregular soft tissue mass, which may extend into both the basilar cisterns and the nasopharynx. Calcification is usually present within the soft-tissue component of the tumor. Most chordomas are somewhat enhanced following administration of intravenous contrast medium. On occasion these tumors may invaginate the adjacent brainstem and, on the basis of axial CT scan findings alone, may be difficult to distinguish from an intraaxial mass. They may sometimes resemble a clivus meningioma.
Although MRI is inferior to CT for demonstrating the bone destruction associated with these tumors, it is superior in defining the extent of the lesion and usually allows an accurate diagnosis to be made. Typically these lesions are hypointense on T1 images and are hyperintense on T2-weighted scans.
Metastatic Tumors
Metastasis of a remote primary tumor to the brain, its coverings, and the skull is common. Most metastatic tumors arise as the result of hematogenous spread; the initial tumor implants thus tend to occur in the distribution of end arteries, that is, at the gray-white matter junction and in the distribution of deep perforating arteries. Common primary sources are melanoma and tumors of the lung, breast, colon, and kidney. Carcinomas of the breast and lung account for over half of all metastatic brain tumors. There is wide variability in the CT and MR appearance of metastatic brain tumors. Among factors that influence this variation are the primary source of the tumor (i.e., its cellularity); vascularity and biological
P.405

behavior; the number and location of the tumor(s) within the brain; and whether previous treatment has been directed to the area of the tumor.
On unenhanced CT scans, metastatic tumors most often are seen as multiple (solitary metastases also occur commonly, up to 40%) fairly discrete areas of isodensity or slight hyperdensity surrounded by low-density edema that extends along and through the white matter; in the majority of metastatic tumors the edema is substantial. For reasons that are not clear, however, some metastases produce almost no edema; when isodense with the adjacent brain, these may be occult on scans performed without intravenous contrast. Except for metastases from primary osseous tumors (especially osteogenic sarcomas), calcification is unusual in untreated metastatic brain tumors. Some metastatic tumors show a tendency to hemorrhage spontaneously; these include melanoma, renal cell carcinoma, and choriocarcinoma.
As is the case in unenhanced CT scans, the appearance of metastatic brain tumors on scans performed following the use of intravenous contrast medium varies. Most metastases will be enhanced to some degree, but the pattern that they exhibit shows great variability; enhancement may be ringlike or diffuse (either homogeneous or heterogeneous). Tumors in individuals being treated with corticosteroids may not enhance as intensely because of the medication’s stabilizing effect on the BBB. Metastases to the brain may involve the subarachnoid space because of pial involvement (Fig. 11-37).139 This may occur either as an isolated phenomenon or may be seen in association with parenchymal tumors. These pial implants appear on contrast-enhanced CT as either areas of nodular high density or as generalized enhancement occurring along the subarachnoid cisterns, fissures, and sulci.148,149 Melanoma is one tumor that is particularly prone to this type of involvement.126
FIG. 11-37. Leptomeningeal carcinomatosis from metastatic breast carcinoma. (A and B) The axial T1-weighted images with intravenous contrast enhancement reveal marked leptomeningeal enhancement. Note the enhancement of the pial surface of the midbrain and the enhancement of the fifth cranial nerve (arrowheads). Lumbar puncture confirmed the diagnosis of leptomeningeal carcinomatosis.
Magnetic resonance imaging is more sensitive than CT for the detection of CNS metastatic tumors and is thus the technique of choice for evaluating patients suspected of having such disease.166 While many metastatic tumors can be recognized on noncontrast-enhanced scans, the use of intravenous contrast medium increases detection of small and peripheral tumor deposits.72 As is the case on CT scans, the appearance of metastatic tumors on MRI is variable. Typically, however, the tumor is seen as an area of hypointensity on T1-weighted images and heterogeneous hyperintensity on T2-weighted images. Surrounding most metastatic tumors is edema, which has less signal variation (i.e., it is more homogeneous than the tumor itself). Hemorrhage, cystic change, and necrosis are all common in metastatic tumors and account for the variable signal intensities of these lesions. Most metastases enhance following administration of
P.406

intravenous contrast medium; as with CT, the pattern of enhancement is variable.
On the basis of CT or MRI scan findings alone, it is impossible to predict with accuracy the primary source of a metastatic tumor. Likewise, a solitary metastasis cannot reliably be distinguished from a primary neoplasm of the brain (Fig. 11-38).
FIG. 11-38. Solitary metastasis to the left occipital lobe secondary to breast carcinoma. Note the relatively well-circumscribed enhancement and surrounding vasogenic edema. The lesion is located at the gray-white junction, a common location for metastatic disease.
Lymphoma
In the absence of clinical or radiologic evidence of systemic disease, involvement of the CNS by non-Hodgkin’s lymphoma is designated primary CNS lymphoma. This previously unusual lesion, representing fewer than 2% of all brain tumors, is now occurring with increasing frequency because of the AIDS epidemic. Patients who are immunocompromised are at increased risk for the occurrence of both systemic and primary CNS lymphoma. A significant number of these tumors are multicentric at the time of their diagnosis. Although some primary CNS lymphomas are responsive to treatment, the overall prognosis is worse than for tumors with similar histology occurring outside the CNS.18
Non-Hodgkin’s lymphoma that occurs in the CNS as the result of spread of systemic disease is also uncommon. This type of involvement occurs most often with tumors of diffuse histology and in patients with advanced disease. Hodgkin’s disease rarely involves either the brain or the meninges but is more frequent in the latter site.81
All types of lymphoma are found most frequently in the cerebral hemispheres, with the basal ganglia, corpus callosum, and periventricular white matter being the areas that are especially likely to be involved.130 On CT scans performed without contrast medium, these tumors are isodense to hyperdense. Following the administration of intravenous contrast medium, they typically are enhanced significantly (Fig. 11-39). The pattern of enhancement varies but is generally marked and (except in patients with AIDS) usually homogeneous. On CT scan some primary lymphomas may closely mimic a meningioma.29,104
FIG. 11-39. Primary intracranial lymphoma. (A) The axial CT image without contrast material indicates expansion of the splenium of the corpus callosum. The lesion is hyperdense on the noncontrast exam. (B) Following contrast enhancement, there is very intense enhancement of the lesion with edema extending into the adjacent white matter.
On MRI, lymphomas tend to show hypointensity on T1-weighted images and to be hyperintense on T2-weighted scans. Almost all lymphomas enhance following administration of intravenous paramagnetic contrast medium. There are no specific signs that allow differentiation of CNS lymphomas from other neoplasms of the brain by MRI.31
Leukemia
With increasing survival of patients with many types of leukemia, CNS complications are of increasing incidence and significance. The major CNS complications of leukemia are infections, hemorrhages, parenchymal or subarachnoid leukemic infiltrations, and abnormalities related to therapy. Mild hydrocephalus is common. Computed tomographic scans are effective in demonstrating most of these, and the technique plays an important role in the management of such patients.67,117 However, MRI is superior to CT for demonstration of parenchymal or subarachnoid infiltrations; it is less efficient in detection of small recent hemorrhages.
Arachnoid Cysts
Intracranial arachnoid cysts are found in various locations, with the most common being within the middle cranial fossa and sylvian fissure. Other sites of involvement are the cerebellopontine angle cisterns, the suprasellar region and choroidal fissures, the pericollicular area, and the interhemispheric fissure. The majority of arachnoid cysts are congenital. The symptoms they produce depend on both their size and location; it is by compression of the adjacent neural structures that they cause neurologic dysfunction. On CT scan they appear as well-demarcated, thin-walled masses with attenuation values the same as those of cerebrospinal fluid. They do not contain calcium or fat, and their margins are not enhanced following administration of intravenous contrast medium. Large arachnoid cysts may cause deformity of the adjacent calvaria. Some arachnoid cysts communicate freely with the subarachnoid space and ventricular system, whereas others are at least partially isolated. Computed tomographic scans performed with low doses of water-soluble contrast medium in the intracranial subarachnoid
P.407

space are valuable in determining the cerebrospinal fluid dynamics associated with these lesions.52,94 Largely because of their multiplanar nature, arachnoid cysts are demonstrated more clearly on MRI than on CT; their signal characteristics match those of CSF on all pulse sequences (Fig. 11-40).
FIG. 11-40. (A) Sagittal T1-, (B) axial proton density, and (C) axial T2-weighted images from a patient with a quadrigeminal cistern arachnoid cyst. The signal characteristics of the lesion follow those of cerebrospinal fluid. Signal from adjacent vascular and dural structures accounts for the low-signal intensity areas seen around the anterior margin of the lesion on the axial images.
Dementia
Alzheimer’s Disease
Alzheimer’s disease is the most common cause of both presenile (onset before the age of 60) and senile dementia. Clinically, it is characterized by the gradual and relentless progression of cognitive impairment; by the terminal phase of the disease patients are totally dependent. Histologically, the differences between the findings in dementia of the Alzheimer type and those that occur with normal aging are quantitatively different but qualitatively the same (neurofibrillary tangles and senile plaques).
Both CT and MRI scans of patients with Alzheimer’s disease are often normal, or they may show enlargement of the lateral and third ventricles and prominence of cortical sulci. The severity of these changes varies greatly, and they overlap with those that occur with aging. Recent studies indicate that structural (i.e., atrophic) changes in the temporal lobe, particularly the hippocampus, occur in Alzheimer’s disease; high-resolution coronal MRI allows one to make hippocampal volume measurements. Perfusion and metabolic imaging with PET and SPECT show a characteristic pattern of early involvement of the temporal-parietal association cortices with later severe involvement of the prefrontal areas27,89; in the earlier stages there are no anatomic correlates to the physiological deficits.
Ischemic Dementia
Atherosclerotic cerebrovascular disease, particularly when associated with chronic hypertension, is a common etiologic factor in dementia. Loss of intellectual capacity is frequently noted in patients who suffer large bilateral infarcts; cognitive decline is often stepwise as discrete infarcts accrue. Diffuse subcortical ischemic damage without large cortical strokes may also cause a slowly progressive dementing illness, which has been termed Binswanger’s disease,98 and these may occur together.19 On CT and MR scans, patients with ischemic dementia have abnormal density or signal in large areas of the cerebral hemispheres. In multi-infarct dementia, these areas of infarction may involve the
P.408

cortex, white matter, and basal ganglia. In classic Binswanger’s disease the areas of ischemic damage are confined to perforating vessel territories (i.e., the basal ganglia and deep white matter with sparing of the immediate subcortical tissue). Physiological imaging of patients with ischemic dementia tends to show a patchy pattern that corresponds to the multitude of ischemic lesions.55,89
Other Causes of Dementia
It should be emphasized that there is marked overlap in findings seen on imaging studies of many patients with Alzheimer’s disease, multi-infarct dementia, and Binswanger’s disease. The pathologic processes often coexist in older persons, and many cases of dementia are apparently of mixed cause. It is seldom that an accurate diagnosis can be made on the basis of anatomic imaging studies alone.14
There are many other causes of acute or chronic loss of memory and cognitive function. Some, such as Huntington’s disease (with severe caudate nucleus atrophy), Pick’s disease (with extreme atrophy of the prefrontal and anterior temporal areas), occasional large frontal lobe neoplasms, and subdural hematomas and other traumatic injuries result in changes in the brain that are recognizable on routine CT and MRI scans. Other causes of dementia such as Parkinson’s disease or chronic viral illnesses, or the dementia or delirium caused by a large variety of metabolic disorders, may produce no anatomic findings at all or only nonspecific volume loss. The pseudodementia of depression is also without findings on routine neuroimaging.
White Matter Disease
Multiple Sclerosis
Multiple sclerosis (MS) is the most common demyelinating disease. The age of clinical onset of symptoms is most often after the age of 20 and before the age of 50; women are more often affected than are men. The disease is characterized clinically by exacerbations and remissions, and pathologically by multiple plaques representing areas of demyelination
P.409

and varying inflammatory activity. Although the distribution of demyelination seen in multiple sclerosis is somewhat random, there is a tendency toward involvement of the periventricular white matter, the corpus callosum, and the visual system from optic nerves to the occipital lobes. The spinal cord is also frequently a site of involvement. Symptomatic cord involvement may occur with asymptomatic brain lesions, so that brain imaging in suspected MS is generally indicated. The lesions of MS have some tendency to be symmetric.
Older imaging techniques had little place in the diagnostic evaluation of patients suspected to have MS, but MRI has proved to be sensitive for demonstrating multiple sclerosis plaques as an aid to diagnosis and is also useful for follow-up of patients receiving experimental therapies for this disease. The MS plaques are well seen as high-signal lesions on long-TR images (Fig. 11-41) and are especially well demonstrated by flair sequences. Acute plaques (areas of active demyelination) often enhance following administration of intravenous contrast medium. The number and distribution of areas of demyelination do not accurately correlate with the clinical severity of the disease. On occasion, solitary plaques of multiple sclerosis may present as a large mass lesion. It is emphasized that there are no specific MRI findings
P.410

of multiple sclerosis, and numerous other white-matter diseases may simulate this condition.51
FIG. 11-41. Multiple sclerosis. (A) Midline sagittal image using a flair sequence. MS plaques are visible in the genu and splenium of the corpus callosum. (B) Sagittal flair image through the lateral ventricle shows the typical pattern of plaques radiating outward from the ventricular surface. (C) Proton density fast spin echo image just above the ventricles, showing plaques in their typical axial appearance.
Necrotizing Leukoencephalopathy
Necrotizing leukoencephalopathy is a disease that occurs primarily in children who have leukemia. It is seen most often in those who have been treated with a combination of cranial radiation and methotrexate. The outcome of the disease is variable. On CT scan necrotizing leukoencephalopathy is characterized by diffuse areas of hypodensity in the white matter; as the disease progresses, white-matter calcifications become common. During the active phase of the disease, contrast enhancement is typical, but the pattern is variable.67,84 As is true for other white-matter diseases, MRI is more sensitive than CT for detection of necrotizing leukoencephalopathy; early lesions have increased signal on T2-weighted images.
Toxic/Metabolic Demyelination
Various toxic and metabolic abnormalities, especially large electrolyte shifts, can cause damage to myelin sheaths in the CNS. The best-known example is central pontine myelinolysis (CPM), which was originally a disease of treated alcoholics with massive sodium shifts76 and has been seen in more recent years in liver transplant patients. Extrapontine myelinolysis is also seen in similar circumstances.76,86
Other White-Matter Diseases
Many other diseases involve the white matter either by destruction of normal myelin (myelinoclastic or demyelinating diseases) or because of inadequate myelin formation or maintenance (dysmyelinating diseases). The white-matter lesions of progressive multifocal leukoencephalopathy (PML) and AIDS are discussed in the section on brain infections; dysmyelinating diseases are touched on in the section on congenital diseases. A full discussion of white-matter diseases is beyond the scope of an introductory text; their radiographic manifestations are discussed in detail elsewhere.38,39,114,158,163
Trauma
Until recently, CT had supplanted all other radiographic techniques as a method for the diagnostic evaluation of patients with head trauma, whether acute or chronic. However, MRI is now gradually supplanting this role. In spite of the demonstrated superiority of MRI over CT for detection of posttraumatic injuries, CT remains the technique of choice for the initial assessment of patients with severe head injury. This is true both because a CT examination is faster than an MR scan and because it also allows accurate recognition of those patients who require acute neurosurgical intervention (i.e., hematoma evacuation). Following stabilization, patients who have had significant head injuries or who have unexplained neurologic deficits may benefit from an MRI examination because this technique has been shown to depict the full extent of injury to the brain more effectively than CT.53
It is now possible to clearly visualize both the direct and the indirect effects of trauma on the brain with currently available CT and MRI techniques. Subarachnoid, intraparenchymal, and extraaxial (subdural and epidural) hemorrhages can occur as the result of both closed-head injury and penetrating trauma. These types of injuries are usually best evaluated with CT scanning. Contusions, diffuse axonal shearing injuries, and diffuse swelling of the brain also commonly occur after significant trauma. These types of injuries are often more clearly demonstrated with MRI than with CT scans.
Traumatic parenchymal hematomas appear as clearly defined areas of increased density on CT scans. In the acute stage, their margins are usually irregular but very distinct, and there usually is little surrounding edema. Acute hematomas are typically very homogeneous in character unless there is impairment of the clotting mechanism. Traumatic intraparenchymal hematomas occur most frequently in the inferior aspects of the frontal and temporal lobes and in the basal ganglia. Significant head injuries may be associated with the development of extraventricular obstructive hydrocephalus because of the associated arachnoid scarring, which causes blockage of the cerebrospinal fluid absorptive pathways.
Shearing injuries are the result of severe stresses placed on the axons by rotational acceleration/deceleration of the brain.172 Both axons and small penetrating vessels are susceptible to shearing injury as the brain is suddenly rotated during high-velocity trauma. The result of this type of injury is multiple, small, well-defined areas of edema and petecchial hemorrhages. The areas of the brain that are susceptible to injury tend to occur in the corticomedullary junctions, corpus callosum, and upper brainstem. Shearing injuries often reflect severe and extensive damage to the brain and are frequently associated with severe neurologic deficits (Fig. 11-42).
FIG. 11-42. (A) Axial noncontrast computed tomogram of a patient with severe head trauma. A hemorrhagic contusion is present in the left frontal lobe adjacent to the orbital roof. Two small hematomas are present in the left temporal lobe; there is blood in the posterior portions of both lateral ventricles. (B) Computed tomographic section at a higher level shows multiple white matter hemorrhages.
Contusions of the brain are often noted in those patients who have experienced significant head trauma. These lesions may not be visualized with CT scans performed shortly after an injury unless the contusions are very large or are associated with significant hemorrhage. After 1 to 2 hours, they become more apparent, appearing as areas of mixed low and high density because of the presence of small hemorrhages with surrounding edema. These injuries tend to be superficial and occur adjacent to bony prominences. They are especially frequent in the portions of the frontal and temporal lobes that lie next to the calvaria (Fig. 11-42). Enlargement of a hematoma in an area of contusion occurring 24 to 72 hours following an initial injury is one of the complications associated with closed-head trauma.
P.411

Computed tomography allows excellent detection and evaluation of intracranial foreign bodies and depressed skull fractures, making other radiographic techniques seldom needed in these conditions.
Subdural Hematoma
Bleeding into the subdural space is a frequent complication of head injury, resulting in the formation of a subdural hematoma. These lesions are most common over the convexity of the cerebral hemisphere but may develop at any site over the surface of the brain. They occur infrequently, however, in the posterior fossa. Bilateral subdural hematomas are not uncommon, occurring in approximately 20% of patients. The early use of CT scanning in those patients suffering from acute head trauma has significantly reduced the previously high mortality rate associated with acute subdural hematomas.
The appearance of a subdural hematoma on CT depends on several important factors: the age of the blood, whether repeated episodes of bleeding have occurred, whether the lesion is unilateral or bilateral, and the level of the patient’s hematocrit at the time of the injury. It is most useful to divide subdural hematomas into those that are hyperdense, isodense, and hypodense in relation to the adjacent area of the brain.61 Blood within the subdural space is hyperdense in its early stage (1–10 days). Over a period of one to three weeks, the subdural blood becomes isodense. After one month, it appears as hypodense to brain tissue. There is extensive variation of this sequence of events due to occasional rebleeding into a subdural hematoma. The hematoma may also show differences in the attenuation values of blood caused by the hematocrit effect.
Using CT scan criteria it is sometimes difficult to accurately classify subdural hematomas as acute, subacute, or chronic. In the majority of instances, however, hyperdense subdural collections have occurred recently, isodense lesions will have been present for at least several days, and hypodense lesions are likely to be of a chronic nature.
With the exception of those instances in which the patient has a very low hematocrit, subdural hematomas studied with CT soon after their occurrence appear as hyperdense collections having a crescentic configuration. The degree of mass effect present in association with these lesions is almost always greater than that which can be accounted for on the basis of the size of the hematoma, a reflection of the underlying brain swelling and injury that accompanies these injuries. The medial margin of very large lesions may sometimes be straight or even convex, thus somewhat simulating an epidural collection. If scans are performed soon after the injury or if there are disorders of the coagulation system, the subdural collection may be heterogeneous, a phenomenon thought to be due to the presence of incomplete clotting within the hematoma (Fig. 11-43).
FIG. 11-43. Axial noncontrast computed tomogram shows a large subdural hematoma extending over the entire lateral surface of the left cerebral hemisphere. A sedimentation level is seen in this acute subdural hematoma of a patient whose clotting function was impaired.
Although they are encountered infrequently, it is important to be aware of the existence of isodense subdural hematomas because they may be occult, even on high quality CT scans. Unilateral effacement of cortical sulci, asymmetries in the gray-white matter junction, ventricular asymmetries, and unilateral mass effect are all signs that serve to alert one to the presence of a unilateral, isodense, subdural hematoma (Fig. 11-44).60 Bilateral lesions of this nature may be more
P.412

difficult to recognize. In older adults, the presence of a supernormal-appearing scan (i.e., one in which the cortical sulci and ventricular system appear like those of a much younger person) is one clue that such lesions may be present. The administration of intravenous contrast medium is valuable in that it results in opacification of the cortical vessels, thereby allowing good definition of the margins of the brain. The MRI is now the study of choice for evaluation of suspected isodense subdural hematomas.
FIG. 11-44. (A) Axial noncontrast computed tomogram shows inward displacement of the gray white matter junction of the left cerebral hemisphere. Although most of this chronic subdural hematoma is isodense, a small sedimentation level is apparent in its posterior portion. (B) Computed tomographic section at the same level as A performed after administration of intravenous contrast medium. There is now good visualization of the lateral margin of the left cerebral hemisphere, which is marked by opacified cortical veins.
Chronic subdural hematomas usually appear on CT scans as well-defined crescentic collections. These lesions are hypodense as compared with those of the adjacent brain. As is the case with acute lesions, a very large chronic subdural hematoma may have a straight or even concave medial margin. In particular, certain scar-encapsulated subdural hematomas swell from osmotic forces as the blood breaks down, leading to a biconvex collection of the same shape as an epidural hematoma, though of water density. Compartmentalization and heterogeneous density or signal within the hematoma may indicate episodes of rebleeding. Occasionally, sedimentation levels are seen in dependent portions of such lesions. Calcification of the margins of these lesions frequently occurs.
On MRI, subdural hematomas that appear hypodense on CT will have a high signal intensity on T1-weighted images because of the methemoglobin that they contain. Because of its sensitivity in detecting blood degradation products of different ages, MRI is more sensitive than CT for identification
P.413

of subdural hematomas that have undergone multiple episodes of bleeding. These lesions are seen as having multiple foci of different signal intensities characteristic of hemoglobin breakdown products of different ages. The membranes separating these areas have low signal intensities on images made with all pulse sequences.
Subdural Hygroma
A subdural hygroma represents the accumulation of clear fluid in the subdural space. It is observed in up to 10% of patients following head trauma. It may be hard to separate from a chronic subdural hematoma on CT. These lesions are much easier to evaluate with MRI. The etiology is thought to be from traumatic tearing of the arachnoid membrane, which allows accumulation of cerebrospinal fluid in the subdural space. The mechanisms causing those that are noted in the absence of trauma are poorly understood but may include birth injury, congenital lesion, or minimal unrecognized trauma. Subdural hygromas are usually not symptomatic, and with time they resolve spontaneously. Except for their size, subdural hygromas appear similar on CT scan to the description given for chronic subdural hematomas. These lesions should not be confused with atrophic changes because the CT scan appearance of the two conditions is quite different (Fig. 11-45). Atrophy produces widening of the cortical sulci, and the involved gyri are not significantly displaced away from the margin of the calvaria. Subdural hygromas can occasionally cause mass effect, displace the brain away from the skull margin, and obliterate the adjacent sulci.
FIG. 11-45. Axial noncontrast computed tomogram shows a small, low-density, extra axial collection over the right frontal lobe. There is slight mass effect and the adjacent sulci are compressed.
Epidural Hematoma
Epidural hematomas occur as a result of injury to meningeal vessels and are most often the result of arterial rather than venous disruptions. The most common location of an epidural hematoma is over the lateral surface of the cerebral hemispheres, but, like subdural hematomas, they may occur in other places as well.
In the first hour after injury a CT scan may show portions of the blood to be low in density on CT, denoting that the hematoma has not yet clotted or is still bleeding (hyperacute hematoma) (Fig. 11-46). This finding indicates a neurosurgical emergency. After 1 to 2 hours an epidural hematoma is mostly hyperdense (acute hematoma) on CT scans. Acute epidural hematomas can rarely be hypodense on CT scans in patients with severe anemia or disseminated intravascular coagulation. Because they occur between the dura and the calvaria, epidural hematomas are more constrained than subdural collections. This is the explanation for their typical biconvex configuration. It also accounts for the observation that they sometimes cross the midline because they can cross external to the reflection of the falx. Epidural hematomas do not usually cross sutures unless the meningeal artery is injured at another site. Angiography is no longer performed
P.414

in the evaluation of patients with either subdural or epidural hematomas.
FIG. 11-46. Axial noncontrast computed tomogram shows an acute epidural hematoma over the lateral surface of the right cerebral hemisphere. The nonhomogeneous attenuation levels within it are the result of incomplete clotting.
Carotid Cavernous Fistula
The internal carotid artery is situated so that a fracture of the walls of the carotid canal can easily result in laceration of the intracavernous internal carotid artery. This allows the high-pressure arterial blood to be shunted into the low-pressure cavernous sinus, creating an internal carotid artery-cavernous sinus fistula (carotid-cavernous fistula). Patients presenting with carotid-cavernous fistulas have usually suffered severe head trauma. Abnormal communications may also occur between the meningeal branches of the external carotid arteries and the cavernous sinus; these fistulae are, however, usually unrelated to trauma and are usually lower in pressure. Fistulae between the internal carotid artery and the cavernous sinus are usually high-flow lesions that produce striking ocular signs and symptoms.34 Endovascular techniques are the treatment of choice for treating carotid cavernous sinus fistula (Fig. 11-47).
FIG. 11-47. (A) Left internal carotid lateral digital subtraction arteriogram shows rapid opacification of the cavernous sinus and both the superior and inferior ophthalmic veins (arrows). There is a tear in the cavernous segment of the internal carotid artery. (B) Left internal carotid lateral digital subtraction arteriogram performed following detachment of a balloon within the cavernous sinus. The fistula is occluded and the internal carotid artery now appears normal. The margins of the balloon are faintly seen (arrows).
The CT and MRI findings of a high-flow internal carotid artery-cavernous sinus fistula include enlargement of the cavernous sinus and the ipsilateral superior ophthalmic vein; proptosis may also be present. Depending on their size, dural or indirect fistulas may show similar findings or may be occult on both CT and MRI scans. Angiography provides the definitive diagnosis in both of these conditions.
Child Abuse
Nonaccidental trauma in the young child can take many forms. One of the most specific neuroradiologic findings is subdural hemorrhage, especially interhemispheric in location, in the absence of severe explanatory trauma such as a motor vehicle accident (Fig. 11-48). Injuries caused by choking, squeezing, and throwing are often associated. The radiologist must be careful to identify the additional resulting brain lesions, often ischemic, because these have a major impact on prognosis.
FIG. 11-48. Shaken baby. Axial nonenhanced CT shows a large amount of acute subdural hemorrhage, both between the hemispheres and over the convexities. There is also diminished density and loss of gray-white differentiation in the left hemisphere because of associated hypoxic-ischemic injury.
Infectious Diseases
The major classes of infection are well known to the physician: pyogenic, atypical bacterial, fungal, viral, parasitic. All of these affect the brain and its surroundings, as do the prion (previously called slow virus) diseases. The latter do not cause specific radiologic findings and are not discussed further in this chapter. In utero and perinatal infections are discussed in the section on congenital diseases. Because the imaging manifestations of CNS infection are limited in number, the information provided by diagnostic neuroimaging can be optimized only in the clinical setting in which an infectious illness occurs and is known. The role of imaging techniques in the diagnosis and management of patients with CNS infections is discussed elsewhere.7,41,74,114,164
Meningitis, as the term is usually applied, refers to infection
P.415

in the subarachnoid space; it therefore involves primarily the leptomeninges. The brain parenchyma, dura, and the subdural and epidural spaces may be secondarily involved. Depending on the virulence of a particular infection, the imaging findings are highly variable. At the most severe extreme there may be striking pial and ependymal enhancement, abnormal signal or density in the CSF caused by high protein content or frank pus, secondary brain edema, or strokes from the vasospasm caused by the CSF infection (Fig. 11-49). Chronic fungal meningitis such as cryptococcus, at the other extreme, may cause no imaging findings or merely minimal ventricular enlargement. Findings caused by specific infectious agents are discussed below.
FIG. 11-49. Pyogenic meningitis. (A and B) Postcontrast axial CT images. Though this extreme case looks superficially like subarachnoid hemorrhage, the high-attenuation appearance of the pial surfaces and filling the subarachnoid spaces is abnormal enhancement caused by the meningitis; it was not present on noncontrast images. Patchy diminished density in the brain parenchyma may represent encephalitis or ischemic lesions from vasospasm caused by the subarachnoid infection.
Subdural and Epidural Empyema
Although suppurative infections in the subdural or epidural space are uncommon, it is important that they be recognized because, untreated, they are associated with high mortality. Infections of this nature may occur in association with osteomyelitis of the skull, sinusitis, meningitis, or penetrating trauma. In general, on CT and MR scans, these lesions appear as extraaxial fluid collections; in the subdural space they may extend into the interhemispheric fissure or along the margins of the tentorium. Following administration of intravenous contrast medium, variable enhancement is seen about the margins of both subdural and epidural empyemas. Abnormal signal or density is often present within the adjacent brain.99,174 Subdural empyemas, like subdural hematomas, are limited by the attachments of the dura; this may be the only way to distinguish an epidural from a subdural suppurative process.
Cerebritis and Brain Abscess
Primary cerebritis or (more generally) encephalitis is also seen in infections with various pathogens, or combined meningoencephalitis may be present at the time of imaging. Depending on the infectious agent, there may be primary involvement of white matter or gray matter; either a great or small amount of edema; and the presence or absence of enhancement or necrosis. Several specific examples are discussed below.
Brain abscesses occur most frequently because of hematogenous dissemination of infectious agents, often from the lungs. They may also result from the direct spread of an infection from a location such as a paranasal sinus or the middle ear. Abscesses that develop from the hematogenous spread of microorganisms occur most frequently in the cerebral hemispheres, along the corticomedullary junction, and in the basal ganglia. A wide variety of organisms has been associated with brain abscesses; none of these produce totally characteristic radiographic findings. Immunosuppression, cyanotic heart disease, and pulmonary arteriovenous fistulas predispose patients to the development of brain abscess. The ability to define the extent and characteristics of a brain abscess with CT, MRI, and ultrasound, and the use of these methods as guides for the surgical treatment of abscesses, have greatly reduced the high morbidity and mortality previously associated with these lesions.
During the course of its development, a brain abscess evolves through a number of stages.15 Initially, it is a poorly defined area consisting of small, scattered foci of cerebritis; when mature, it is a well-demarcated, encapsulated lesion, the central portion of which consists of suppurative material and tissue debris. The appearance of a brain abscess on CT, MRI, or ultrasound depends primarily on the stage in its development during which the study is performed.42
On CT scans, early infection may be seen only as areas of hypodensity, with little, if any, enhancement occurring after administration of intravenous contrast medium. Over time, as neovascularity and a collagen capsule develop, a pattern of ring enhancement will become apparent. The margin of an incompletely encapsulated abscess becomes thicker and shows increased intensity of enhancement on scans performed 30 to 45 minutes following intravenous contrast administration. The margin of a mature abscess does not show this temporal pattern and often may even decrease in intensity on delayed scans. Except in individuals who are taking corticosteroids, studies done before the onset of treatment
P.416

usually show extensive vasogenic edema surrounding the area of a brain abscess (Fig. 11-50). Except in the immunocompromised patient, multiple abscesses are unusual.
FIG. 11-50. (A) Axial noncontrast computed tomogram shows marked mass effect in the left frontal lobe. Ringlike areas of isodense tissue are surrounded by low-density edema. (B) Axial computed tomographic section at the same level performed after administration of intravenous contrast medium shows enhancement of the periphery of a multiloculated abscess cavity. The patient had a right-to-left cardiac shunt.
Magnetic resonance imaging is superior to CT for evaluation of patients with brain abscesses because of its increased contrast sensitivity (i.e., better detection of edema and characterization of the various elements of an abscess) and its superior ability to detect a subtle mass effect.66 The abscess capsule is its hallmark, and this is best characterized on either contrast-enhanced or T2-weighted MRI scans. The thin, relatively smooth capsule has a tendency to be slightly thicker on its peripheral side and enhances uniformly. On T2-weighted scans the capsule is often hypointense compared to gray matter. Often, adjacent, smaller satellite capsules are present, particularly along the margin of an abscess that faces one of the lateral ventricles. Healing of an abscess is indicated by a decrease in its size. It is important to emphasize that both CT and MR enhancement of the capsule may persist for some time despite adequate treatment.
Atypical Bacteria, Fungi, and Parasites
As elsewhere in the body, mycobacteria may infect the brain and its surroundings in a variety of patterns. Most common is a granulomatous meningitis; this causes nodular pial enhancement, especially in the cisterns at the base of the brain, that is indistinguishable from sarcoidosis or other granulomatous meningitides. Mycobacteria may also cause encephalitis or a gross abscess in the brain parenchyma or in an extraaxial location, which may calcify when healed.
Various fungi have widely differing pathologic patterns and, therefore, radiologic appearances. The microscopic abscesses of disseminated candidiasis are generally radiologically occult. Cryptococcal meningitis is also usually unremarkable radiologically, though rarely perivascular space gelatinous pseudocysts may be seen. Paranasal sinus mucormycosis is well known as a grossly destructive lesion, usually in diabetic patients, that may invade the cranial cavity locally. While Aspergillus is usually present in the sinuses as a saprophyte, when it is invasive it can behave in a locally destructive manner like mucormycosis. Aspergillus in the sinuses has a characteristically low signal on T2-weighted images because of its tendency to accumulate iron. Angioinvasive Aspergillus of the lung is associated with systemic embolization of the organism. Although this may cause cerebritis or brain abscess, the angioinvasive character of the organism predisposes it to invade vessel walls and present
P.417

as strokes or primary hemorrhages that are not obviously infectious in etiology (Fig. 11-51).20
FIG. 11-51. Aspergillus. Bilateral infarction and hemorrhage in the territories of the lenticulostriate perforating arteries caused by cerebrovascular involvement by angioinvasive Aspergillus, which has spread hematogenously from the lungs.
Of the parasitic infections, three that are seen with some frequency in this country have characteristic appearances that are mentioned here. The most commonly seen brain parasite at present is Toxoplasma gondii. A very high percentage of the adult population is seropositive for Toxoplasma; the dormant intracellular parasite becomes aggressively active under a compromised immune system, particularly in AIDS. The infection rapidly causes an area of necrosis with a surrounding rim of enhancement and a great deal of vasogenic edema, giving the appearance of an abscess. Because pyogenic infections are not a primary feature of AIDS, Toxoplasma recrudescence and lymphoma are the primary diagnostic considerations when an HIV-positive patient presents with a ring-enhancing brain mass. In utero, Toxoplasma is one of the TORCH agents that causes brain destruction and calcification, as discussed in the section on congenital diseases. Two other parasites that classically infect the brain are the tapeworms Echinococcus and Taenia solium. Echinococcal infection (hydatid disease) affects the brain in a minority of cases, but the cystic, ring-enhancing larva (usually solitary) is characteristic in appearance. Tissue infection by Taenia solium is the cause of the state called cysticercosis. The small larvae (usually multiple) that reach the brain may remain asymptomatic as long as they are living; but when the encysted larvae die, there is an inflammatory reaction that may lead to seizures and ring-enhancing brain lesions. Eventual punctate calcifications are the end stage radiologically.
Viral Infections
Mild nonspecific viral meningitides are common, but certain viruses may be listed that have particularly severe or characteristic involvement of the meninges and/or brain. Progressive multifocal leukoencephalopathy (PML) is a relentless demyelinating disease that occurs in patients who are immunocompromised. Originally seen in patients treated for leukemia and lymphoma, then in patients immunosuppressed for organ transplants, it is now most commonly seen in patients with AIDS. The myelin destruction results from infection of oligodendroglia by papovaviruses, usually the JC virus. On CT and MR scans the lesions of PML are seen as areas of hypodensity or abnormal signal in the immediately subcortical white matter, with a tendency toward symmetry. Beginning as multiple discrete lesions, they grow to become a confluent abnormality with a scalloped peripheral border that simply represents extension into the white matter of the gyri. Mass effect is often absent, and enhancement is uncommon.26,39,101
P.418

Human Immunodeficiency Virus
Neuroimaging in AIDS has recently been extensively reviewed.123,124 HIV directly infects the brain; this causes global volume loss and often a diffuse hazy high signal in the cerebral white matter on T2-weighted images, without enhancement or edema. The clinical correlate is the AIDS dementia complex (ADC). Clinically manifest neurologic involvement occurs in well over 50% of individuals infected by HIV; CNS abnormalities are even more commonly present on postmortem examination. A large variety of secondary infectious processes are commonly seen intracranially in individuals with AIDS; in many instances, multiple infectious processes and neoplastic diseases may exist simultaneously. Cryptococcal meningitis, Toxoplasma infection, and PML have already been discussed. Patients with AIDS or immune compromise for other reasons are also prone to cytomegalovirus (CMV) infection, which especially affects the retina, meninges, and ependyma. This infection is often radiologically occult or may cause brain volume loss indistinguishable from that caused by HIV directly. In some instances there may be a diffuse though usually mild enhancement of the ependyma or pia to signal the presence of CMV ventriculitis or meningitis. Many other secondary infections are increased in patients with AIDS, but these generally yield few or no specific radiologic findings.
The immune system also plays a role in preventing and controlling neoplasms; two neoplasm that are common in AIDS are Kaposi’s sarcoma and lymphoma. The former rarely affects the cranial contents. Lymphomas in AIDS may be either systemic or primary to the CNS. The CNS lymphoma in AIDS behaves somewhat differently than in patients without AIDS, possibly because of the lack of immune system control of its growth. It usually shows central necrosis (rarely seen in brain lymphoma outside of AIDS) and tends to incite a very large amount of edema. Thus, this lesion has an appearance essentially identical to that of the other common mass lesion in AIDS, Toxoplasma.
Herpes Simplex
Herpes simplex virus type 1 usually causes a severe necrotizing encephalitis that can occur at any age but is most often seen in adults. Herpes encephalitis has a characteristic perisylvian anatomic distribution involving the temporal lobes, orbital surfaces of the frontal lobes, and insular cortex while sparing the basal nuclei. If untreated it is often fatal; those persons who survive are frequently left with severe neurologic deficits. Institution of antiviral therapy is therefore indicated as soon as this entity is clinically suspected, though brain biopsy may be required for definitive diagnosis. Most adults in the general population have antibodies to the herpes simplex type 1 virus. This organism is known to exist in a latent form within the trigeminal ganglia of many asymptomatic people; spread from this site has been proposed as an explanation for the typical anatomic pattern of this infection.41
Computed tomography is insensitive at initial presentation; MRI is somewhat better.74,82 Small areas of hemorrhage are typical slightly later in the course. Within a short time edema in the infected tissue leads to density and signal abnormalities and local mass effect. Early in the infection, enhancement is minimal if present; later, it often becomes striking. A gyral configuration of the abnormal enhancement is said to be characteristic,43,63 though this is a nonspecific healing response in damaged cortex, as is seen commonly after strokes.
Herpes simplex type 2 encephalitis is most commonly seen in neonates as part of a systemic infection, frequently from maternal type 2 genital infection. This type of herpes encephalitis affects the brain globally, without the typical geographic distribution of type 1 herpes infection. It is one of the TORCH agents discussed under congenital destructive lesions.
The immune system response to an infection may play a significant role in the disease it causes. The fact that herpes encephalitis may be indolent in immune-compromised persons rather than taking its usual necrotizing course indicates the role of the immune system in the destructive nature of that infection. A classic example of a parainfectious disease (one that follows a viral syndrome but is not caused directly by viral infection of the CNS) is acute disseminated encephalomyelitis (ADEM). In this entity multiple lesions of the brain and spinal cord usually appear 1 to 3 weeks after a viral infection or occasionally after vaccination. These lesions may affect gray matter and white matter, are variably
P.419

edematous in the acute phase, and sometimes show enhancement. ADEM is usually self-limited, though uncommonly it may recur in a patient. In many cases there is remarkable radiologic as well as clinical recovery, but more severe cases may lead to death.
Early Infection
In utero or perinatal infection may cause severe damage to the brain. Of particular interest are the so-called TORCH agents; the name is an acronym for Toxoplasma, rubella, CMV, and herpes. These infections have been grouped together because in past years they have been common causes for severe global brain damage in early life and because they share such radiologic features as severe white matter loss and calcification. The reader is referred to Chapter 16 in Osborn114 for further discussion and radiologic distinctions among these infections.
Congenital Malformations
Congenital abnormalities of the brain and its surrounding structures may be genetic in etiology or may occur as a result of discrete or presumed insults to the antenatal brain at various times in its development, commonly infection. The major brain malformations were described and named for their gross appearances before the mechanisms for disordered brain formation were understood. Though some remain idiopathic, recent research has significantly increased our understanding of genetic deficiencies, insults, and mechanisms that play a role in these disorders,7,14,154 and this trend will certainly continue. The student of these diseases should therefore make an effort to understand brain formation and the known mechanisms for some of the major malformations. One should also understand that insults to the developing brain have different results depending on the amount of brain affected and on the time of the insult during development. It is a truism that congenital abnormalities are associated with other congenital abnormalities. Nowhere is this more evident than in the brain, and many of these associations can be traced to the time at which an insult occurred. It should also be noted that several malformations are associated with a block of CSF egress through the cerebral aqueduct or fourth ventricle and therefore cause congenital hydrocephalus.
Migration Anomalies
In the developing brain the primary site of cerebral neuronal cell origin is the periventricular germinal matrix. Glial cells form radiating pathways along which the neurons then migrate to the brain surface. This migration occurs in waves, which are associated with the development of the laminated cerebral cortex.7,103 Further cell division within the developing cortex contributes to a massive expansion of its size (surface area) and therefore to the infolding that leads to the final pattern of gyri and sulci. This pattern of migration, cortical expansion, and formation of gyri can be interrupted globally or focally by an insult that acts at one moment or over an extended period; these factors lead to a wide variety of brain malformations.
Severe generalized failure of neuron migration results in a very thick, disordered cortex that cannot form normal gyri. This thickened cortex is more easily seen by a variety of MRI sequences than by CT. In almost all of these cases the sylvian fissure is primitive in appearance: a broad groove with absent or poorly formed opercula. Depending on the severity and surface features, this malformation is descriptively termed pachygyria (gyri present but few and large), agyria (no gyri present), or polymicrogyria (clusters of neurons form tiny irregularities on a brain surface that may be rather featureless grossly). These often occur together. The term lissencephaly (“smooth brain”) is also used, usually as a general term to include the gyral abnormalities discussed above. The small surface features of polymicrogyria are too small to be routinely seen radiologically; this entity may be present when the radiologic appearance is one of lissencephaly or schizencephaly (see below). However, very thin MR slices may show characteristic cortical irregularities.7 Thus, these abnormalities are not fundamentally discrete diseases but different gross features of an underlying migrational disturbance that may result from genetic, infectious, or other causes.
Two other migration anomalies have characteristic imaging appearances. A late wave of neuronal migration may be halted after the cortex is fairly well populated. In this circumstance, the cortex may form reasonably normal gyri and sulci, but there remains a stripe of neurons that are subcortical in location. This is called a band heterotopia. Or a group of neurons may fail to migrate at all from the germinal matrix area. These are focal, often multiple, and are termed nodular heterotopia; in these patients the cortex is generally well formed grossly. Because the clinical features of seizures and mental retardation (or lesser diminution of IQ) are related to the degree of cortical disorganization, they range from very severe in lissencephaly patients to sometimes very mild or absent in patients with small amounts of nodular heterotopia.
Schizencephaly
Focal destructive lesions early in brain development, before major neuronal migrations, may result in a cleft in the brain that is lined by gray matter. This gray matter lining is abnormal, often showing the polymicrogyria pattern seen in focal cortical dysplasia.7 This condition is termed schizencephaly and has been descriptively divided into open-lip and closed-lip varieties, depending on whether the cleft remains widely patent or the growing edges come into contact. The former, being the result of involvement of a greater brain volume, generally has a worse neurologic prognosis. Because the brain destruction extends from the ependyma through the cortex, closed-lip schizencephaly is associated with an underlying dimple in the ependymal surface. The cortex lining the cleft is not continuous at the ependymal end of the cleft. One should take care not to confuse the cortex-lined schizencephaly with the primitive sylvian fissure seen in some brain malformations; the latter
P.420

will have continuous (abnormally thick) cortex beneath the prominent cleft, seen best by MR.
Hypoxic-Ischemic Injury
Occlusion of both internal carotid arteries is believed to lead to the condition called hydranencephaly, in which the brainstem and thalami are present and the head is fully formed but the cerebral hemispheres are absent. Focal destructive lesions that occur in utero, because the immature brain does not respond to injury with a gliotic response, may form thin-walled cystic cavities that often communicate with the ventricular system; such a cavity is classically termed porencephaly.
In the second and early third trimesters the deep cerebral white matter and the involuting germinal matrix are particularly susceptible to hypoxic-ischemic insult.7,83 Premature infants at this stage of development also have immature, pressure-passive cerebral vasculature, and they often undergo extreme cardiorespiratory stresses. When there is germinal matrix ischemic damage, this often results in the intracranial hemorrhage (ICH) characteristic of premature infants. The neurologic prognosis of these infants correlates well with the radiologic grading114,136,159 of ICH:
Table. No caption available.
Hypoxic-ischemic damage of the white matter surrounding the bodies and atria of the lateral ventricles in the immature brain is not as prone to hemorrhage. Such injury, termed periventricular leukomalacia (PVL),153 appears in the acute phase as white matter that is hyperechoic on ultrasound. This area of infarction evolves through a partially cystic phase to total liquefaction. The end stage appears on CT and MRI scans as a local widening and irregularity of the atrium and surrounding parts of the lateral ventricles, symmetric or asymmetric and variable in severity. Because the affected white matter includes portions of the corticospinal tracts, the clinical correlate is the classic cerebral palsy findings of spastic diparesis or quadriparesis, usually more severe in the upper extremities.
Holoprosencephaly
Major forebrain anomalies include the holoprosencephaly spectrum and abnormalities of the corpus callosum. The holoprosencephalies are midline malformations in which there is failure to induce the development of the most rostral part of the brain.7 This leads to a variably severe failure of separation and development of the cerebral hemispheres and diencephalic structures. The holoprosencephaly spectrum is classically divided by severity into regimes termed lobar (hemispheres almost separated, and the corpus callosum only slightly abnormal) to semi-lobar to alobar (no hemispheric separation or corpus callosum, and the thalami completely fused). In the last case the forebrain is very severely malformed, often consisting of a flattened tissue mass without any normal structure; most of the intracranial volume may be taken up by the associated dorsal cyst. The holoprosencephalies are associated with varying degrees of hypogenesis or absence of olfactory and optic structures. One type of septo-optic dysplasia (SOD), which as the name implies consists of optic nerve atrophy and absence of the septum pellucidum, may be a disorder at the mild end of the holoprosencephaly spectrum. Other cases of SOD appear to be locally destructive in etiology.4,7,16
Callosal Dysgenesis
Agenesis of the corpus callosum may occur as an isolated abnormality or may be seen in association with a host of other congenital abnormalities of the brain. The formation of the corpus callosum is well worked out in timing and mechanism.3,128,140 This structure develops over a significant period beginning in the seventh week of gestation and follows a well-defined progression: from midgenu through body, then posterior body and anterior genu at about the same time, then splenium followed closely by the final elaboration of the rostrum.6 Therefore, depending on the time of the arrest in its development, there may be no corpus callosum (agenesis); or the rostrum, rostrum and posterior segments, or all but the upper genu may be absent (hypogenesis or partial hypogenesis) (Fig. 11-52). The formation of the cingulate gyrus is linked to callosal development. Therefore, the cingulate gyrus and sulcus may be wholly or partially absent in callosal dysgenesis, allowing the medial hemispheric sulci to radiate all the way down to the third ventricle. The normal cingulum is replaced by the abnormal white matter bundles of Probst. This causes a characteristic straightening (on axial images) and bull’s horn appearance (on coronal images) of the frontal horns of the lateral ventricles. Because of the lack of splenium and the white matter connecting the occipital lobes, the atria and occipital horns of the ventricles are enlarged, a condition termed colpocephaly. There is often upward expansion of the third ventricle. The anterior commissure may be enlarged.
FIG. 11-52. Incomplete genesis of the corpus callosum. This midline sagittal T1-weighted image shows only a truncated genu and bulbous anterior body of the corpus callosum; the posterior body, splenium, and rostrum are absent. Note that the cingulate sulcus is absent and the medial hemispheric sulci radiate all the way down to the third ventricle posteriorly, where the corpus callosum has not formed.
Dandy-Walker Malformation
Major hindbrain malformation complexes include the Dandy-Walker malformation and its variants, and the various Chiari malformations. The classic Dandy-Walker malformation consists of agenesis of the vermis and ballooning of a fourth ventricular cyst, which enlarges the posterior fossa. The tentorium and its dural sinuses are elevated, and the occipital squamosa is enlarged. The term “Dandy-Walker variant” refers to partial dysgenesis of the vermis (the inferior portion being affected) with less severe distortion of the fourth ventricle and
P.421

posterior fossa. This lesion should be differentiated from an arachnoid cyst of the posterior fossa.
Neural Tube Closure and Chiari Malformations
Maternal folate deficiency has been shown to increase the incidence of neural tube closure defects. The most common and extreme form of congenital brain malformation caused by failure of neural tube closure is anencephaly; this abnormality consists of the absence of the scalp, calvaria, and most of the brain. Of the less severe neural tube closure abnormalities seen in clinical practice, the most important are the Chiari malformations.
Of the four hindbrain malformations originally described by Chiari, the first three designations remain in common use. The rare Chiari III malformation consists of a cervical encephalocele. The Chiari II malformation (Fig. 11-53) occurs in patients with spina bifida from failure of closure at both ends of the neural tube. The primary feature of the brain malformation is marked downward displacement of the medulla and cerebellum and, therefore, the fourth ventricle, causing an enlarged foramen magnum and often a characteristic kinking of the cervicomedullary junction. The posterior fossa is very small with posterior concavity of the petrous bones, and the dural reflections are deficient. The crowding and high position (with respect to the midbrain) of the superior cerebellar vermis give it a heart-shaped appearance where it surrounds the beaked tectum of the midbrain. The deficient falx is associated with interdigitation of cerebral hemisphere gyri across the midline. Fourth ventricular compression and hydrocephalus are present, and syringomyelia is common. These features have been discussed in detail by Naidich and associates in a series of articles on this subject.109
FIG. 11-53. Chiari II malformation. (A and B) Midline and paramedian sagittal T1-weighted images show the very low position of the medulla, cerebellum, and fourth ventricle. Note also the very low position of the transverse sinus (the flow void visible just above foramen magnum) and the beaked appearance of the midbrain tectum. (C) An axial T2-weighted image shows the inferior cerebellar hemispheres surrounding the upper medulla at the level of foramen magnum. (D) Axial CT shows mild interdigitation of sulci anteriorly and the ventriculoperitoneal shunt catheter necessitated by this patient’s congenital hydrocephalus.
In contrast, the Chiari I malformation is defined by low position of the cerebellar tonsils (at least 5 mm below the plane of foramen magnum) and sometimes the cerebellar vermis, with normal position of the brainstem and fourth ventricle (Fig. 11-54). This abnormality may have several pathophysiological types.7 In its more severe forms it causes cervicomedullary compression and hydrocephalus; it is also associated with an increased incidence of spinal cord cysts. Milder forms are generally asymptomatic and are found quite frequently on sagittal MRI imaging.
FIG. 11-54. Sagittal T1-weighted MR image from a patient with a Chiari I malformation. The cerebellar tonsils are displaced caudally through the foramen magnum. The fourth ventricle has a normal position.
Leukodystrophies and Other Metabolic Disorders
The number of identified genetic brain diseases is large and increasing rapidly. Many of these result in a handful of nonspecific imaging findings such as a small brain, relative paucity of white matter, or modest delay in myelination. Others cause gross abnormalities of the white matter and/or gray matter that present at birth, in infancy, or later in life. These include the leukodystrophies, mucopolysaccharidoses, mitochondrial diseases, and other groups of diseases. The reader is referred to several texts for discussions of these entities.7,39,114
The best known dysmyelinating disease that presents later in life is adrenoleukodystrophy (ALD), an X-linked disease that usually presents in boys during late childhood or adolescence with progressive visual and behavioral disturbances, leading to quadriparesis, seizures, and death. The radiologic correlate is symmetric demyelination, which proceeds in a characteristic posterior-to-anterior pattern. There may be enhancement along the leading (anterior) edge of the demyelination. This genetic disease may also be seen in milder forms presenting in adult men or carrier women, usually in families with known ALD patients. In this form the brain is usually unaffected, but there is involvement of the spinal cord and peripheral nerves; the clinical disease is therefore referred to as adrenomyeloneuropathy.
Neurocutaneous Syndromes
There is another particularly important category of genetic diseases with which the neuroimager should be familiar: the phakomatoses, or neurocutaneous syndromes. Only a brief survey of the more common of these diseases is presented here; the reader is referred to other texts for further information.7,114,142
The primary cephalic manifestations of von Hippel-Lindau disease are retinal and cerebellar hemangioblastomas. The latter are described in the section on brain neoplasms. The major components of Sturge-Weber syndrome (encephalotrigeminal angiomatosis) are a facial port wine nevus and a similar leptomeningeal vascular malformation over part of the cerebral surface. The name is misleading because the facial vascular malformation has no real connection with the trigeminal nerve or its branches. The pial vascular malformation leads to chronic ischemic damage to the underlying brain and a characteristic dystrophic calcification of that abnormal cortex described as tramtrack calcification. The pial
P.422

P.423

vascular malformation also enhances strongly on MRI with intravenous contrast.
Tuberous Sclerosis
Tuberous sclerosis is a disease of hamartomas throughout the body; two types of hamartomas are seen in the brain. There are large ill-formed surface masses (cortical only as the term is applied loosely) with a somewhat spherical appearance, which are referred to as cortical tubers and have given the disease its name. These hamartomas have high signal on T2-weighted images and, of course, lack a normal cortical architecture on high-resolution imaging. There are also small hamartomatous subependymal nodules, which typically calcify and are therefore quite characteristic in their CT appearance (Fig. 11-55). These patients generally have severe mental retardation and seizures (though some persons with mild forms are found) and are therefore diagnosed early in life. The primary reason for later imaging is that these patients are prone to the development of a very characteristic neoplasm, the subependymal giant cell astrocytoma, which is identified as a large or enlarging, enhancing ependymal mass generally near the interventricular foramina (of Monro).
FIG. 11-55. Tuberous sclerosis. (A) Noncontrast axial CT slice at the level of the top of the ventricles shows low attenuation near the cortex in the right hemisphere; these are cortical tubers. (B) A lower CT slice shows several calcified subependymal nodules. (C and D) Coronal flair images show the cortical tubers well, plus abnormal signal radiating out from the periventricular tissue to the surface, indicating the associated migration abnormality.
Neurofibromatosis
The neurofibromatoses (NF) are a category of phakomatoses whose characterization has undergone significant change in recent years. The best known are type I (von Recklinghausen’s disease) and type II. The skull and brain manifestations of NF type I are protean and highly variable in penetrance. Classic skull malformations include hypoplasia of the sphenoid bone leading to a poorly separated orbit and middle cranial fossa and to sutural defects (Fig. 11-56). Optic gliomas (described in the section on neoplasms) are common, as are other low-grade gliomas and hamartomas in the white matter and basal ganglia. Neurofibromatosis type II is characterized by bilateral eighth cranial nerve schwannomas as well as schwannomas of other cranial nerves and multiple meningiomas.
FIG. 11-56. Neurofibromatosis type I. Both CT scout image (A) and axial slices (B-D) show severe right sphenoid bone dysplasia in a patient with von Recklinghausen disease.
Developmental and Senile Volume Changes
During rapid head growth in the young child, especially from approximately 6 to 18 months of age, there may be periods when the ventricles and the subarachnoid spaces become quite prominent. Such patients are usually studied because the pediatrician notes rapid increase in head circumference in an otherwise healthy child. The radiologist should, of course, search for evidence of abnormalities that may be associated with early hydrocephalus. But this finding is almost always a benign normal variant; the neurologically normal child with this finding should simply be followed clinically. If repeat imaging is performed (which is not generally indicated), by 2 years of age the enlargement of the CSF spaces will have resolved.
At the other extreme of life, loss of brain substance is a normal function of aging. With aging there is both an increase in size of the ventricular system and an increase in the prominence of the cortical sulci54; these alterations, however, do not correlate either with changes in the metabolism of the brain as measured with positron emission tomography (PET) techniques or with the presence or absence of cognitive impairment. This finding is best described as brain parenchymal volume loss rather than atrophy because (cortical) atrophy is a pathologic description, and its presence cannot be diagnosed accurately by imaging techniques.
Hydrocephalus
The term hydrocephalus generally refers to those conditions that produce an imbalance between the rate of production and absorption of the cerebrospinal fluid. Hydrocephalus normally occurs as the result of obstruction to the flow and absorption of cerebrospinal fluid (CSF); overproduction of CSF is very rare. Implied is the presence of increased intraventricular pressure; usually there is also an increased volume of CSF within the ventricular system. Hydrocephalus may be either congenital or acquired.
Hydrocephalus may occur if CSF flow is blocked at any site along the normal route from the choroid plexus, through the ventricular system, to the arachnoid granulations, which are primarily in the superior sagittal sinus. It is known that alternate, though much less efficient, routes of cerebrospinal fluid absorption exist by way of both the ventricular ependyma and the arachnoid membrane.
The term communicating hydrocephalus has been used to refer to instances in which there is a block to CSF flow outside the ventricular system; noncommunicating hydrocephalus correspondingly refers to the presence of an occlusion within the ventricular system. Hydrocephalus ex vacuo
P.424

has sometimes been used to refer to increased CSF volume simply caused by the loss of brain tissue volume. All of these terms are incomplete and are potentially confusing. Because essentially all forms of hydrocephalus are related to obstruction of cerebrospinal fluid flow, the use of these terms should be replaced with descriptions that indicate the location of the obstruction. This classification system has been discussed in detail by Harwood-Nash and Fitz and more recently by Floodmark.47,68 The development of hydrocephalus in children is usually associated with an increase in head size. This is unusual in adults.45
Acquired Hydrocephalus
Many pathologic conditions, including inflammatory, infectious, traumatic, and neoplastic disorders, can cause hydrocephalus. The presence of increased intraventricular or intracranial pressure can rarely be diagnosed accurately using imaging techniques. In instances of suspected hydrocephalus, it is the goal of the imaging evaluation to identify any abnormality of the ventricular
P.425

or subarachnoid space morphology and, if otherwise unexplained ventriculomegaly is present, to demonstrate the site and nature of any impediment to the flow of CSF that may be present. Magnetic resonance imaging is the best available imaging method with which to achieve this goal.
Most patients with hydrocephalus have enlargement of the part(s) of their ventricular system proximal to the level of obstruction. Even in the face of increased intraventricular pressure, however, all portions of the involved ventricular system may not dilate equally. For example, in response to an obstruction of the basal cisterns, the temporal and occipital horns of the lateral ventricles dilate earlier and to a greater degree than the third and fourth ventricles.
When there is significant obstruction of the circulation of cerebrospinal fluid, its passage through the ependymal lining of the ventricles into the adjacent white matter of the cerebral
P.426

hemispheres occurs and may correct the imbalance between the rates of production and absorption. On CT scan this is manifested by periventricular hypodensity, which is often more pronounced in the parietal and occipital regions; it appears as a symmetric and smooth periventricular band of increased signal intensity on T2-weighted images.
In children with patent anterior fontanels, ultrasound is an ideal way to assess ventricular size. Alternatively, MRI allows visualization of CSF movement as well as evaluation of the ventricles and sulci; on T2-weighted images, the low signal intensity of flowing CSF in the cerebral aqueduct stands out in contrast to the higher signal intensity of the adjacent tectum of the mesencephalon, a useful sign of aqueductal patency.12
Normal-Pressure Hydrocephalus
The term “normal-pressure hydrocephalus” (NPH) was originally used to describe the syndrome of dementia, gait disturbances, and urinary incontinence occurring in patients with ventricular enlargement and normal cerebrospinal fluid pressure. The diagnosis subsequently has been applied with such indiscretion that there is now great confusion in the literature about the pathogenesis, pathophysiology, and treatment of the condition. Although a full discussion of this subject is beyond the scope of this text, a few general comments are warranted.
The finding of large ventricles and normal or small cortical sulci in the presence of normal CSF pressure has been called NPH by some. This does not reflect the original use of the term, and its use should be discouraged because these observations may be seen in a host of clinical settings, including normal variation and clinically unimportant leptomeningeal fibrosis.
The success of surgical treatment of NPH (i.e., shunting) varies greatly among reported series. Improvement is most likely when treatment is reserved for those patients who show evidence of progression of mild dementia, ataxia, and urinary incontinence, and who are shown to have lateral ventricular enlargement and small or obliterated cortical sulci.78 Recent MRI studies suggest that improvement is most likely to occur in those patients with the appropriate clinical findings (i.e., recent and slowly progressive dementia), gait ataxia, and urinary incontinence as well as evidence of rapid CSF flow in their fourth ventricle and cerebral aqueduct, seen as accentuated signal loss on heavily T2-weighted images.
Vascular Disease
Extracranial Occlusive Disease
In 1914, Ramsey Hunt first suggested that stenosis of a carotid artery in the neck could cause a stroke. Since that time, a clear relationship between thromboembolic stroke and vascular disease of the carotid and vertebral arteries has been established. Current evidence suggests that at least as many ischemic episodes are caused by embolization of platelet debris from atherosclerotic lesions within these arteries as those that result in impairment of blood flow by hemodynamically significant stenosis. Ischemia of the brain may therefore result either from diminished blood flow occurring as the result of a significant stenosis or because of arterial blockage occurring as a sequel to embolization.
Although the incidence and type of atherosclerotic lesions present in the extracranial arteries of asymptomatic persons are unknown, it is established that advanced lesions of this nature are sometimes present in the cervical arteries of neurologically asymptomatic people. This observation in part explains the controversy and lack of guidelines for diagnostic evaluation and management of patients with asymptomatic atherosclerotic disease. It seems prudent to regard these abnormalities as only part of a more generalized vasculopathy affecting arteries throughout the body and to direct therapy at the underlying cause of the disorder rather than to marshal all efforts toward correction of morphologic abnormalities found in isolated arterial segments.
The diagnostic evaluation and management of those patients with symptomatic vascular disease is less controversial. Optimal application of established guidelines, however, depends on an accurate assessment of the type of arterial lesion that is present as well as precise characterization of the type of neurologic dysfunction. Once it has occurred, the course of an ischemic stroke is largely refractory to therapy, and the end result is persistent neurologic dysfunction or death in a majority of patients. An effective therapy must therefore be prophylactic, a restriction requiring recognition of the population at risk before they suffer neurologic damage. Risks known to be important in this regard are the presence of all degrees of arterial hypertension, smoking, and a history of intermittent episodes of neurologic dysfunction (i.e., transient ischemic attacks).
Asymptomatic Vascular Disease
Many patients with asymptomatic vascular disease, for a variety of reasons, have a carotid bruit. Although there is an increased incidence of stroke associated with an asymptomatic bruit, the risk is not confined to the arterial territory from which the bruit originates. Results of the Asymptomatic Carotid Atherosclerosis (ACAS) Study Group have shown benefit of endarterectomy in all patients with 60% or greater stenosis of the internal carotid artery.2
Both duplex ultrasonography and magnetic resonance angiography offer means for the accurate noninvasive screening of patients in this category. When properly used either alone or in combination, these techniques allow recognition of hemodynamically significant lesions (reduction of arterial lumen by at least 80%) in the cervical portion of the carotid arteries about 95% of the time. In the unusual instances when these techniques are inconclusive or results are in disagreement, further evaluation may then be carried out using arteriographic techniques described in the following section.
P.427

Symptomatic Vascular Disease
Guidelines for the diagnostic evaluation of patients with specific symptoms of extracranial vascular disease, such as carotid artery territory transient ischemic attacks or an evolving or completed stroke, are reasonably well defined. Guidelines for the care of patients with nonspecific symptoms are much more ambiguous and are beyond the scope of this text.
It has been established through a carefully performed multicenter randomized trial that carotid endarterectomy is highly beneficial in patients who have a carotid artery transient ischemic attack and an ipsilateral internal carotid artery stenosis of 70% or greater.112 There is also general agreement that this procedure is acceptable but unproved therapy in patients with other combinations of symptoms and internal carotid artery stenosis. For a discussion of these guidelines, the interested reader is referred to the AHA consensus statement.106 One requirement for the optimal application of this therapy is precise characterization of the morphologic status of both the intracranial and extracranial arteries. Recent improvements in duplex ultrasonography and magnetic resonance angiography (MRA) now make it possible in most situations to modify previous guidelines stating that all symptomatic patients be evaluated with standard catheter arteriography. Today, MRA can be used in combination with duplex ultrasonography as the primary modalities for the diagnostic evaluation of most patients with symptomatic as well as with asymptomatic extracranial vascular disease (Fig. 11-57). The combination of velocity measurement and visualization of the artery in question with color or power Doppler provides the best method to assure accuracy when performing an ultrasound evaluation. Peak systolic velocities (PSVs) over 120 m/sec indicate the presence of a stenosis of 60% or greater, whereas the presence of PSVs over 150 m/sec indicate the presence of a stenosis of at least 70%. Cardiac arrhythmias, aortic insufficiency and a variety of other vascular abnormalities, either upstream or downstream from the carotid bifurcation, may cause inaccuracies in velocity measurements. Also, differentiation between an occluded artery and one that is nearly occluded, i.e., 99% stenosis, remains difficult using ultrasound techniques. Ultrasound techniques have not yet been proven to provide adequate information regarding the status of the intracranial vasculature. Such information is important in an evaluation that is aimed at deriving a recommendation regarding the benefit of endarterectomy. For this reason, the use of MRA using some combination of two- and three-dimensional techniques is recommended. In this way, it is now possible to accurately characterize in a noninvasive manner the significant features of the extracranial and intracranial vasculature in the majority of instances. Only in those circumstances where there is disagreement between an ultrasound and an MRA evaluation is the use of standard catheter angiography usually needed.
FIG. 11-57. Carotid stenosis by three angiographic modalities: (A) digital subtraction catheter arteriography; (B) two-dimensional time-of-flight MR angiography; and (C) three-dimensional time-of-flight MR angiography.
Arteriography, when required, is best carried out using digital subtraction techniques. There is now little need for and little place for film-screen techniques or intravenous digital subtraction techniques.
Atherosclerotic vascular lesions occur most often at regions of hemodynamic stress, particularly at points of major arterial bifurcations. The principal sites of atherosclerotic lesions of the extracranial cervical vasculature are the origins of the brachiocephalic vessels, the carotid bifurcations, and the origins of the vertebral arteries. Stenosis produced by an atherosclerotic plaque tends to narrow the lumen of the involved artery in an eccentric fashion (Fig. 11-58). Small discrete areas of calcification often can be seen adjacent to and within a plaque extending into a narrowed artery. The angiographic diagnosis of arterial occlusion is usually not difficult, the abnormality being characterized by a sudden termination of the arterial lumen. The configuration of an arterial occlusion varies with the artery, sometimes being rounded and at other times being quite angular. Arterial ulceration cannot be detected accurately using any currently available imaging technique other than those that employ radioactive platelets. Arterial ulceration may even go undetected on direct inspection of the involved vessel. Radiographic assessment of arteries involved by atherosclerosis should be limited to description of the vessel as smooth or irregular and to the degree of narrowing that may be present. The two methods most widely used to define the percentage diameter stenosis of the internal carotid artery require biplanar views of the artery. One method, the “N” or NASCET
P.428

(North American Symptomatic Carotid Endarterectomy Trial) method, defines the residual lumen as a percentage of the normal distal internal artery. The other, the “E” or ECST (European Carotid Surgery Trial) approach, defines the residual lumen as a percentage of the diameter of the internal carotid artery bulb. In general, the “N” method is best used for reports of angiographic examinations, whereas the “E” method lends itself to reports of ultrasound examinations.
FIG. 11-58. Lateral selective common carotid arteriogram. There is an irregular stenosis of the internal carotid artery. From this study, one cannot be sure whether ulceration is present.
Brain Infarction
Brain infarction may occur as the end result of a large number of pathologic processes, by far the most common of which is atherosclerosis. Approximately 60% of ischemic brain infarcts are etiologically related to atherosclerotic disease of the extracranial segment of the internal carotid artery. A significant percentage of all embolic brain infarctions also result from emboli that originate within the heart. Other causes of brain infarction, besides atherosclerotic vascular disease, include other primary arterial diseases such as fibromuscular hyperplasia, arterial dissections, and arteritis; venous occlusive disease and a host of more unusual diseases such as septic and tumor embolizations may also be associated with infarction of the brain.
Although CT continues to be the most commonly employed imaging technique for evaluation of patients with suspected strokes, MRI has been shown to be a superior method both in permitting earlier detection of ischemic changes and in allowing identification of infarcts not visible on CT scans. Nonetheless, with the availability of effective acute therapy, i.e., thrombolysis, for some individuals with an acute stroke, CT is the recommended imaging modality for initial evaluation of patients suspected of having a stroke. The reason for this is that in order to obtain rapid and appropriate stratification of individuals with ischemic stoke into therapeutic protocols, it is imperative that individuals with hemorrhagic lesions be accurately and quickly identified. Currently CT allows this to be done much faster and with more accuracy than does MRI. For evaluation of individuals in the subacute or chronic phase of a stroke, MRI does offer considerable advantages over CT. These advantages arise from the superior contrast and spatial resolution of MRI as well as from its freedom from artifact caused by the bone and air at the skull base. Current experience indicates that with the use of perfusion and diffusion imaging, MRI allows identification of areas of reversible ischemia (the penumbra) as well as of tissue that has been irreversibly injured. These techniques are rapidly becoming available in clinical practice and hold great promise for being useful in management of this common disease. Most symptomatic infarctions can be recognized with conventional MRI within 12 to 24 hours of their occurrence. The MRI is especially useful in demonstrating ischemic changes that involve the brainstem or cerebellum. In most instances, the use of intravenous contrast medium is not required for the diagnosis of infarction, either with CT scanning or with MRI. The suggestive evidence that the use of contrast-enhanced CT scans in evaluation of cerebral infarcts is associated with increased damage to neural structures provides added incentive to avoid contrast administration when possible.
The CT scan findings seen following an infarct depend on the size of the abnormality, whether the infarct is associated with significant hemorrhage, the amount of time that has elapsed between the occurrence of the infarct and the CT scan, and, to a lesser degree, the location of the infarct within the brain. Computed tomographic scans performed in the initial 24 hours following a nonhemorrhagic infarct may be normal, especially if the lesion is small or if it is located in the brainstem or cerebellum. A significant number of large infarcts involving one of the cerebral hemispheres will, however, be evident on CT scanning, even in the first several hours following their onset. Signs that may indicate an acute infarct are loss of the distinction between gray and white matter and subtle obliteration of cortical sulci. In typical examples, scans performed after an interval of more than 24 hours show an area of reduced density that can be related to a single vascular distribution. The character of the infarct evolves from an area of poorly defined heterogeneous reduced density, which causes mass effect, to one with no mass effect, sharp margins, and homogeneous attenuation values that may approach those of cerebrospinal fluid (Fig. 11-59). The subarachnoid space and ventricle adjacent to
P.429

an old infarct are usually dilated. These changes have a variable time course; however, it is highly unusual for an infarct to have significant mass effect after it has been present for 2 weeks, and within 3 weeks its margins should be clearly defined. If intravenous contrast medium is given, a variable pattern of enhancement may be seen from 4 to 5 days following occurrence of the infarct for as long as 2 to 3 months after its origin. Although the configuration of abnormal enhancement in a brain infarct often assumes a gyral pattern, this is not specific and may be seen in numerous other pathologic conditions. The distribution of abnormal enhancement does not correlate with the amount of brain parenchyma that will ultimately be destroyed.
FIG. 11-59. Stroke. Noncontrast CT slice at the level of the lateral ventricles shows infarction of the right middle cerebral artery territory, including the lateral lenticulostriate perforators to the caudate and putamen. Note the sharp boundaries, loss of gray-white differentiation, and edema causing shift of the midline.
Magnetic resonance imaging provides a means for demonstrating ischemic changes in the brain earlier than any other imaging technique: abnormalities have been shown with some techniques within minutes following experimental arterial occlusion. On conventional T1-weighted images, areas of infarction are seen as an area of decreased signal intensity with a loss of the normal signal differences between gray and white matter. On T2-weighted images areas of infarction appear as high signal intensity (Fig. 11-60). In pathologic studies of infarcted brain tissue, small areas of hemorrhage into infarcts are very common; these small hemorrhages are often not apparent on high-resolution CT scans but are frequently seen on MRI studies. Depending on the stage of evolution of the hemorrhage, their signal intensities are variable, ranging from predominantly low signal intensities on both T1- and T2-weighted images in the acute stage to high signal intensities on T1- and T2-weighted images in subacute lesions and then again to low signal intensities in long-standing infarcts. For details of the evolution of the pattern of
P.430

MRI signal intensities in parenchymal hemorrhages, see the following section.
FIG. 11-60. (A) Axial T1- and (B) T2-weighted images from a patient with acute and old infarcts. The acute infarct is in the right basal ganglia. On the T1-weighted image it is seen only as an area of vague mass effect. Contrast this with the old infarct in the left basal ganglia, which, because of the changes of encephalomalacia, is clearly seen as an area of low signal intensity. The old infarct has no mass effect.
Occlusion of dural sinuses, and particularly associated occlusion of surface veins, causes venous hypertension and slowed flow and may lead to venous infarction. Because of the association with midline dural sinus thromboses, these infarcts are often bilateral and more or less symmetric. Because arterial pressure to the infarcting tissues is preserved, significant hemorrhage is typical. Evidence of thrombosis or other abnormalities of the dural sinuses should be sought in patients with bilateral hemorrhagic infarction. Predisposing factors include dehydration (especially in small children), cancer with paraneoplastic hypercoagulation, and other clotting abnormalities.
Nontraumatic Intracranial Hemorrhage
Most intracranial hemorrhages are the result of trauma and have been discussed in a previous section. Nontraumatic causes of intracranial hemorrhage include hypertension, aneurysms, and vascular malformations. Careful analysis of the CT scan and MRI findings often allows determination of the likely cause of a nontraumatic hemorrhage. In addition to the causes discussed in detail below, hemorrhage into a metastatic lesion is relatively frequent, most commonly into metastases from melanoma and renal cell primaries. In older adults with otherwise unexplained peripheral hemorrhage in the cerebral hemispheres, especially if recurrent, amyloid (congophilic) angiopathy is a likely cause.
Hypertensive Hemorrhages
Hypertension is an important etiologic factor in intracranial hemorrhages. If chronic, it results in the presence of structural arterial changes that in themselves predispose to the development of hemorrhages. The presence of elevated blood pressure is also thought to increase the risk of hemorrhage from other unrelated vascular abnormalities such as aneurysms and arteriovenous malformations.
Hypertensive hemorrhages occur most often in the external capsule. This location is followed in frequency by the thalamus, the internal capsule, the cerebellum and pons, and the lobar white matter of the cerebral hemispheres (Fig. 11-61). Hematomas of this nature frequently rupture into the ventricular system but rarely are seen in association with subarachnoid hemorrhage. This feature helps in distinguishing these lesions from traumatic hematomas in which the opposite combination is the case. Although the use of contrast-enhanced CT scans is usually not indicated in evaluation of these lesions, it should be noted that as they resolve, hematomas of any nature may be enhanced to simulate closely other mass lesions (i.e., neoplasms and inflammatory abnormalities).
FIG. 11-61. Axial noncontrast computed tomogram showing a large hematoma in the left basal ganglia that has ruptured into the lateral ventricle and is causing marked subfascial herniation.
As is the case for hematomas of any etiology, hypertensive hemorrhages appear on CT scans as areas of high density with sharply defined borders. Unless there is still active bleeding or impairment of coagulation, the density of a hematoma is homogeneous. Acutely, on CT scans, edema is not seen in association with a hypertensive hematoma. Over a period of several days following the initial hemorrhage, however, edema develops, and low density is commonly seen peripheral to the margin of a hypertensive hematoma. Over a period of several weeks, the density of a hematoma changes from high density to isodense and finally to hypodense, the end stage being an area of encephalomalacia having attenuation values similar to those of CSF.
The MRI appearance of a hematoma is variable, depending on a large number of interrelated factors. These include, among others, the age of the hemorrhage and, thus, the stage of degradation of both its cellular (erythrocytes) and noncellular (hemoglobin) elements; its location (i.e., parenchymal, subarachnoid, subdural, or epidural); the presence or absence of an associated abnormality (i.e., an arteriovenous malformation or neoplasm); and the magnetic field
P.431

strength and pulse sequence used to obtain the image. A complete description of these variables and their effects on the MR image is beyond the scope of this text. For a further discussion, see Bradley.13
In spite of the complexities and variations associated with the MRI appearance of hemorrhages, however, several relatively consistent observations are noteworthy. On MR scans performed within several hours of the onset of a hemorrhage, a hematoma not associated with an underlying lesion appears similar to most other brain lesions (i.e., slightly hypointense on T1-weighted images and hyperintense on T2-weighted images). During the first 24 hours, this appearance changes so that the hematoma is of definite low signal intensity on both T1- and T2-weighted images. Unlike on CT scans, surrounding edema (high signal intensity on T2-weighted sequences) may often be visualized on MR images obtained during this stage of a hematoma’s evolution. During the first week after its occurrence, a hematoma becomes of predominant high signal intensity on both T1- and T2-weighted images. This change in signal intensity from low to high follows the development of methemoglobin within the lesion and occurs gradually from the periphery of the hematoma to its center so that there is a steady replacement of low-signal areas by high-signal areas. The rim of a hematoma at this stage of evolution is seen as a sharply defined zone of very low signal intensity; this is the result of accumulation of hemosiderin, the end product of hemoglobin degradation. After several weeks or even months, a hematoma loses its mass effect and assumes signal intensities similar to those of the adjacent brain and CSF. Small areas of both high and low signal intensity may persist, however, almost indefinitely.
Intracranial Aneurysms
An aneurysm is a dilation of an artery. Most aneurysms that arise from the arteries of the brain are acquired as the result of hemodynamic stresses and are classified pathologically as saccular or berry aneurysms. Other types of aneurysms also occur in the CNS vasculature, but they are much less common. These include atherosclerotic, mycotic (infectious), and posttraumatic aneurysms. Saccular aneurysms most often become symptomatic during adult life because of rupture that results in subarachnoid and/or intraparenchymal hemorrhage. It is important to recognize that saccular aneurysms are common, being present in as many as 5% to 9% of the adult population of North America. Most aneurysms never rupture. However, there are currently no reliable guidelines to predict the likelihood of rupture; once rupture occurs, over 60% of affected individuals will either die or have major neurologic dysfunction. Almost all berry aneurysms occur at points of major arterial branching, the three most common sites being the proximal segment of the middle cerebral artery, the anterior communicating artery, and the junction between the internal carotid artery and the posterior communicating artery. Aneurysms vary in size from those less than 1 mm in diameter to those that exceed 5 cm; those greater than 2.5 cm in diameter are designated giant aneurysms.
The first imaging study done on a patient with a suspected subarachnoid hemorrhage should be an unenhanced CT scan (Fig. 11-62). Although less sensitive than lumbar puncture, a CT scan not degraded by artifact and performed within 24 hours of hemorrhage will allow detection of blood within the subarachnoid space in about 85% of patients in whom an aneurysm has ruptured. Computed tomographic scanning also provides a good means for detection of other abnormalities that may be associated with the clinical presentation of a subarachnoid hemorrhage, e.g., arteriovenous malformation, neoplasm, and spontaneous intraparenchymal hemorrhage. In instances in which there is clinical suspicion of subarachnoid hemorrhage but the CT scan shows no evidence of subarachnoid blood, a lumbar puncture should be performed. Magnetic resonance imaging is not an adequate technique for the detection of acute subarachnoid hemorrhage.
FIG. 11-62. Subarachnoid hemorrhage. (A-D) Nonenhanced axial CT slices show massive subarachnoid hemorrhage in the basal cisterns and supracerebellar cistern and lesser amounts in the sylvian fissures bilaterally. There is reflux of blood into the ventricular system, and acute hydrocephalus.
Although there is no absolute correlation between the location of subarachnoid blood and that of a ruptured aneurysm, the accumulation of blood predominantly on one side of the cranial cavity or primarily above or below the tentorium provides some evidence as to where the lesion is most likely located. It is impossible to distinguish with adequate certainty a parenchymal hematoma that results from aneurysm rupture from one of another etiology; however, the presence of associated subarachnoid hemorrhage favors the diagnosis of an aneurysm. Intraventricular hemorrhage without associated parenchymal hemorrhage occurring as a result of an aneurysm rupture is most often from an anterior communicating artery aneurysm; less likely is hemorrhage from one of the posterior inferior cerebellar arteries.
In spite of the recent advances in MRA, standard catheter angiography is still the most sensitive technique for the detection of an intracranial aneurysm. Although the great majority of aneurysms larger than 5 mm in diameter can be well seen using MRA, the occurrence of slow and/or complex flow in some aneurysms can result in their not being visualized with MRA. Standard catheter angiography is also needed as a technique to allow planning of either endovascular or open surgical treatment of the lesion. Because of the occurrence of multiple aneurysms in as many as 30% of patients, the angiographic evaluation in suspected subarachnoid hemorrhage should include visualization of the entire intracranial circulation. Once an aneurysm is identified, special projections are often needed to define the relationship of the aneurysm to its parent artery and adjacent vascular structures (Fig. 11-63). Angiographic signs of aneurysm rupture include mass effect adjacent to the aneurysm, irregularity of the aneurysm surface, and the presence of focal vasospasm. In the presence of multiple aneurysms, the larger aneurysm will be the site of rupture more frequently than the smaller one. In as many as 15% of patients presenting with subarachnoid hemorrhage, no abnormality is seen on the initial angiographic study. With few exceptions, under
P.432

P.433

these circumstances the study should be repeated after an interval of 7 to 10 days.
FIG. 11-63. (A) Anteroposterior projection of a right internal carotid angiogram. Although an aneurysm of the right middle cerebral artery is seen (arrow), the relationship of its neck to the adjacent branches cannot be appreciated fully. (B) An oblique projection allows visualization of the neck of the aneurysm.
There are two major complications caused by major subarachnoid hemorrhage in the patients who survive the initial events. Acute and/or chronic hydrocephalus can result from intraventricular clots or from occlusion of the arachnoid granulations; this may be effectively treated with a ventriculostomy and eventual ventriculoperitoneal shunt. The second major complication is vasospasm caused by the irritating effects of the blood on the surface arteries of the brain. This spasm is sometimes treatable using intravascular techniques but often results in infarcts.
Vascular Malformations
Vascular malformations are developmental anomalies that have been classified in a variety of ways. McCormick’s widely used classification separates these lesions into four principal types: (a) arteriovenous malformation, (b) telangiectasis, (c) cavernous malformation (cavernoma), and (d) venous malformation (venous angioma/developmental venous anomaly). Cavernous malformations and venous malformations are recognized frequently on CT and MRI examinations. Transitional types of vascular malformations also occur. Although much less common than cavernomas or venous angiomas, arteriovenous malformations are more familiar. They often become symptomatic because of their tendency to hemorrhage and to produce venous hypertension or a steal effect.
Venous Angiomas (Developmental Venous Anomalies)
Most of these lesions are asymptomatic and are found as a result of an examination performed for other reasons. Currently there is considerable debate whether these lesions in fact represent a malformation at all, or whether they simply represent normal variants of the venous drainage. There are, however, instances in which venous angiomas are associated with hemorrhage as well as with more indirect symptoms such as headache or seizures. Venous angiomas are composed of abnormally dilated veins without any associated arterial or capillary abnormalities. The neural parenchyma in and around a venous malformation is histologically normal. There are no guidelines as to how to determine if a particular venous malformation is likely to become symptomatic or is more or less likely to hemorrhage.
Venous angiomas are most frequently found in the white matter of the cerebral hemispheres but also occur regularly in the white matter of the cerebellum. On CT scans performed without the use of intravenous contrast medium, they may not be apparent or may be seen as small, well-defined areas of increased density. Contrast-enhanced scans show them as tubular areas of increased density extending from the deep white matter of the cerebral hemispheres or cerebellum to reach veins of either the subependymal or cortical drainage system (Fig. 11-64). The reliable CT diagnosis of a venous malformation requires that one be able to trace the lesion from its nidus to either the ventricular or subarachnoid surface of the involved portion of the brain.
FIG. 11-64. Venous angiomas. (A and B) Postcontrast CT images show two tubular enhancing structures that extend from the ventricular margin to the brain surface through normal brain tissue. Superficially these became continuous with surface veins, which drained into the superior sagittal sinus.
P.434

Angiography reveals venous malformations as a cluster of enlarged deep medullary veins draining through one or more veins, emptying into a cortical or subependymal vein (Fig. 11-65). The draining veins of these lesions are enlarged, but neither they nor the nidus of the malformation causes mass effect. Some have compared the angiographic appearance of venous malformations to that of a caput medusae. Venous malformations are best seen in the late venous phase of an angiogram; no abnormality is present in the arterial phase of such a study.
FIG. 11-65. Venous phase of an internal carotid arteriogram. The venous angioma in the left frontal lobe resembles a caput medusae.
P.435

Arteriovenous Malformations
Arteriovenous malformations are anomalous collections of histologically abnormal arteries and veins that may occur in any part of the CNS. They are most common within the distribution of the middle cerebral artery but are by no means unusual in other parts of the brain; most of them occur above the tentorium. These lesions may rupture and produce intracranial hemorrhages; they are also frequently a cause of headache, and at times they may produce neurologic signs and symptoms as the result of either a vascular steal effect or venous hypertension. Arteriovenous malformations have been classified according to the source of their arterial supply into pial, mixed pial and dural, and dural types. Of these, the pure pial malformations are the most common. There is frequently calcification in and around the vessels of an arteriovenous malformation; the adjacent area of the brain is often atrophic.
Computed tomographic scans often provide clear evidence of the presence of an arteriovenous malformation. Lesions that have not caused hemorrhage have a variable appearance and may be seen on noncontrast scans as areas of either low density or mottled high and low density. Small or superficial malformations may not be apparent on noncontrast scans. Following administration of intravenous contrast medium, arteriovenous malformations show striking enhancement, the classic pattern being an irregular central area of increased density from which extend multiple, well-defined serpentine structures of various sizes (Fig. 11-66). These structures represent the dilated feeding arteries and draining veins of the malformation. The enhancement of an arteriovenous malformation is the result of both the increased blood pool within the lesion and impairment of the BBB of the adjacent neural parenchyma. The CT scan appearance of an arteriovenous malformation that has hemorrhaged is often less characteristic because the resulting hematoma masks the features of the vascular malformation. The presence of vascular calcification and prominent calvarial vascular grooves and foramina, in association with an intracranial hematoma, suggests the diagnosis of an arteriovenous malformation. This diagnosis should also be suspected when intracranial hematomas are found in young normotensive patients who have no other historic feature (e.g., trauma) to explain the etiology of their hemorrhage.
FIG. 11-66. (A) Axial noncontrast computed tomogram shows areas of calcification and increased density in the left temporal lobe. There is a slight mass effect. The left temporal horn is dilated. (B) Axial computed tomogram at the same level performed after administration of intravenous contrast medium. There is enhancement of the large feeding arteries, nidus, and draining veins of this temporal lobe arteriovenous malformation.
Magnetic resonance imaging is superior to CT both for the diagnosis of arteriovenous malformations and for determining their exact relationship to adjacent neural structures. The feeding arteries, nidus, and draining veins appear in most instances as areas of signal void on both T1- and T2-weighted sequences. The high signal intensity sometimes caused by slow or turbulent blood flow and the frequent occurrence of calcification in these lesions often result in heterogeneous signal intensities, however, and make it difficult to determine with MRI whether there is either recent or old hemorrhage in the malformation.
Although the diagnosis of an arteriovenous malformation can usually be made on the basis of CT or MRI scan findings alone, angiography is required to make a decision regarding the treatment of the lesion. Proper angiography requires the selective study of all arteries that may supply tissue in the area where the malformation is located. Because of the
P.436

prominent arteriovenous shunting that occurs in these malformations, rapid sequence filming is essential to allow definition of the exact morphology of the abnormality. The typical angiographic appearance of an arteriovenous malformation is that of several dilated tortuous arteries supplying a tangle of abnormal vessels, from which emerge one or more enlarged draining veins (Fig. 11-67). Arteriovenous malformations do not produce mass effect unless there has been a recent hemorrhage or there is an associated venous varix formation.
FIG. 11-67. (A) Towne projection of a left vertebral arteriogram. There is an arteriovenous malformation in the medial surface of the left temporal lobe. The enlarged feeder, the nidus, and the dilated draining vein are all seen on this film. (B) This lateral projection of a left vertebral arteriogram provides better visualization of the relationship of the draining veins to the nidus of the malformation seen in A.
Vein of Galen Malformations (Aneurysms)
This is a particular subtype of arteriovenous malformation that derives its name from the fact that the vein of Galen serves as the venous outflow of the lesion. The term “vein of Galen aneurysm” used in the older literature is misleading because the aneurysmal enlargement of the vein of Galen is only a secondary manifestation of the arteriovenous malformation. This lesion usually manifests during childhood. Large lesions with high flow cause high-output cardiac failure in newborns; less severe lesions typically are noted because of the occurrence of hydrocephalus. The arterial component of vein of Galen malformations is usually derived from the choroidal arteries and the anterior cerebral arteries (Fig. 11-68). With current embolization techniques, many of these lesions can be treated effectively.
FIG. 11-68. Lateral projection of an internal carotid arteriogram. Enlarged anterior cerebral and posterior choroidal arteries are seen entering the nidus of a vein of Galen malformation. There is also opacification of the dilated vein of Galen.
Dural Arteriovenous Fistulas/Malformations
Pure dural fistulas/malformations result either from the persistence of a normal embryonic dural arteriovenous fistula or from the creation of this fistula during the recanalization
P.437

of a thrombosed dural sinus. The arterial supply of this type of lesion is derived from dural branches of the internal and external carotid artery and the vertebral artery; the venous drainage is in common with the brain. These abnormalities are associated with a wide variety of clinical presentations; some are incidental findings, others cause only a bruit, and still others are associated with severe symptoms because of intracranial hemorrhage, venous hypertension, or steal phenomenon. Dural arteriovenous fistula cannot be consistently diagnosed using either CT or MR scanning. Angiography is required both for diagnostic purposes and as a means to allow planning of optimal treatment. Interventional techniques (i.e., embolization) play an important role in the management of many of these lesions (Fig. 11-69).
FIG. 11-69. (A) Lateral projection of left external carotid arteriogram. There is early opacification of the sigmoid sinus and adjacent veins. The arterial supply to this dural arteriovenous fistula comprises the posterior branch of the middle meningeal artery and the transmastoid branch of the occipital artery. (B) Lateral projection of a left common carotid arteriogram done following embolization of the dural arteriovenous fistula shown in A. The arteriovenous shunts have been obliterated, and the proximal segments of the feeding arteries have been preserved.
Epilepsy
There are a limited number of functional reactions of the brain to injury. There may be local or global dysfunction, which takes a variety of forms. Or there may be abnormally increased firing of cerebral neurons, sometimes local, often primarily or secondarily global, that is manifest as seizures. Because it is a nonspecific reaction to cerebral cortical injury or chemical abnormality, a new seizure in an adult is commonly caused by (clinical or subclinical) ischemic disease or by metastatic or primary cerebral neoplasm, toxins and drugs, infection, trauma, or other insults. Chronic epilepsy that begins in childhood may also have a discrete cause such as a global or focal brain malformation (including small areas of cortical dysplasia), slow-growing neoplasms such as ganglioglioma, or lesions such as cavernous angiomata or trauma. Often there is no grossly visible lesion. When the temporal lobes are involved, there is sometimes damage to the hippocampus that further potentiates or incites seizures. Temporal lobe epilepsy is generally difficult to control medically, and these patients are often imaged on multiple occasions over several years before eventual surgical therapy. Radiologically, lesional epilepsy (caused by a grossly identifiable malformation, neoplasm, or injury) is as straightforward as other situations in which a mass or brain injury is sought. However, specialized MRI techniques and very careful image analysis are required for evaluation of many epilepsy cases in which the radiologic findings may be extremely subtle, consisting of small areas of thickened cortex (dysplasia) or modest atrophy of the hippocampal formation (which correlates with the pathologic finding of hippocampal or mesial temporal sclerosis), which may be without significant signal abnormality. Specifically, a coronal section oriented obliquely so that it is perpendicular to the axis of the temporal lobe is generally the most valuable imaging plane. Three-dimensional imaging with very thin slices and good gray-white differentiation (such as a spoiled gradient-echo technique) is excellent for anatomic definition of the hippocampal formations and the neocortex (Fig. 11-70). Flair images are very sensitive for subtle abnormalities of signal in the hippocampus.
FIG. 11-70. Hippocampal atrophy. A coronal SPGR image through the central brainstem and bodies of the hippocampi shows significant left hippocampal atrophy in a patient with chronic temporal lobe epilepsy. No other lesion was identified.
P.438

REFERENCES
1. Ahmadi J, Destian S, Apuzzo MLJ, et al: Cystic fluid in craniopharyngiomas: MR imaging and quantitative analysis. Radiology 182:783–785, 1992.
2. Asymptomatic Carotid Atherosclerosis (ACAS) Study Group: Endarterectomy for asymptomatic carotid artery stenosis. JAMA 273:1421–1428, 1995
3. Barkovich AJ, Norman D: Anomalies of the corpus callosum: correlation with further anomalies of the brain. Am J Neuroradiol 9:493–501, 1988
4. Barkovich AJ, Fram EK, Norman D: Septo-optic dysplasia: MR imaging. Radiology 171:189–192, 1989
5. Barkovich AJ. Pediatric brain tumors. Semin US CT MR 13:412-448, 1992
6. Barkovich AJ, Lyon G, Evrard P: Formation, maturation, and disorders of white matter. Am J Neuroradiol 13:447–461, 1992
7. Barkovich AJ: Pediatric Neuroimaging, 2nd ed, pp 9–19, 55–128, 177–320, 569–618. New York, Raven Press, 1995
8. Bartuska DG, Kleinman DS, Kodroff KS, Piatok DJ: The sellar/parasellar endocrinopathies: a brief clinical overview. Semin US CT MR 14:178–181, 1993
9. Bilaniuk LT, Zimmer RA, Littman P, et al: Computed tomography of brainstem gliomas in children. Radiology 134:89, 1980
10. Bilaniuk LT: Adult infratentorial tumors. Semin Roentgenol 25:155–173, 1990
11. Black PMcL: Meningiomas. Neurosurgery 32:643–657, 1993
12. Bradley WG, Kortman KE, Burgoyne B: Flowing cerebrospinal fluid in normal and hydrocephalic states: Appearance on MR images. Radiology 159:611, 1986
13. Bradley WG: Hemorrhage and vascular abnormalities. In MRI Atlas of the Brain. New York, Raven Press, 1990
14. Braffman BH, Trojanowski JO, Atlas SW: The aging brain and neurodegenerative disorders. In Magnetic Resonance of the Brain and Spinal Cord. New York, Raven Press, 1991
15. Britt RH, Enzmann DR, Yeager AS: Neuropathological and computerized tomographic findings in experimental brain abscess. J Neurosurg 55:590, 1981
16. Brodsky MC, Glasier CM: Optic nerve hypoplasia: clinical significance of associated central nervous system abnormalities on magnetic resonance imaging. Arch Ophthalmol 111:66–74, 1993
17. Bronen RA, Cheung G, Charles JT, et al: Imaging findings in hippocampal sclerosis; correlation with pathology. Am J Neuroradiol 12:933–940, 1991
18. Brown JH, Stallmeyer MJB, Lustrin ES, et al: Primary cerebral lymphoma. Am J Roentgenol 165:626, 1995
19. Brown WD, Frackowiak RSJ: Cerebral blood flow and metabolism studies in multi-infarct dementia. Alzheimer Dis Assoc Dis 5:131–143, 1991
20. Brown WD, Miles JM, Knechtle SJ: Patterns of hematogenous cerebral aspergillosis in organ transplantation and other causes of immunocompromise. Abstract Book for the 31st Annual Meeting of the American Society of Neuroradiology, pp 167–168, 1993
21. Brown WD: Brain: Supratentorial cortical anatomy. Neuroimag Clin North Am 8(1), 1998
22. Brown WD: Brain: Supratentorial central nuclei and tracts. Neuroimag Clin North Am 8(1), 1998
23. Buetow MP, Burton PC, Smirniotopoulos JG: Typical atypical, and misleading features in meningioma. RadioGraphics 11:1087–1100, 1991
24. Burger PC, Scheithauer BW, Vogel FS: Brain tumors. In Surgical Pathology of the Nervous System and Its Coverings, 3rd ed, pp 193–437. New York, Churchill Livingston, 1991
25. Carpenter MB: Core Text of Neuroanatomy, 4th ed. Baltimore, Williams & Wilkins, 1991
26. Carroll BA, Lane B, Norman D, et al: Diagnosis of progressive multifocal leukoencephalopathy by computed tomography. Radiology 122:137, 1977
27. Chase TN, Foster NL, Fedio P, Brooks R, Mansi L, Di Chiro G: Regional cortical dysfunction in Alzheimer’s disease as determined by positron emission tomography. Ann Neurol 15(Suppl):S170–S174, 1984
28. Claveria LE, Sutton D, Tress B: The radiological diagnosis of meningiomas, the impact of EMI scanning. Br J Radiol 50:15, 1977
29. Clifford RJ, Reese DF, Scheithauer BW: Radiographic findings in 32 cases of primary CNS lymphoma. Am J Roentgenol 146:271, 1986
30. Coates TL, Hinshaw DB Jr, Peekman N, et al: Pediatric choroid plexus neoplasms: MR and CT and pathologic correlation. Radiology 173:81–88, 1989
31. Cordoliani Y-S, Derosier C, Pharaboz C, et al: Primary cerebral lymphoma in patients with AIDS: MR findings: 17 cases. Am J Roentgenol 159:841–847, 1992
32. Cornell SH, Graf CJ, Dolan KD: Fat-fluid levels in intracranial epidermoid cysts. Am J Roentgenol 128:502, 1977
33. Daemerel P, Wilms G, Lammeus M, et al: Intracranial meningiomas: correlation between MR imaging and histology in fifty patients. J Comput Assist Tomogr 15:45–51, 1991
34. Debrun G: Treatment of carotid cavernous and vertebral fistulas. In Fein JM, Flamm ES (eds): Cerebrovascular Surgery, Vol 4. New York, Springer-Verlag, 1985
35. Diepholder HM, Schwechheimer K, Mohadjer M, et al: A clinicopathologic and immunomorphologic study of 13 cases of ganglioglioma. Cancer 68:2192–2201, 1991
36. Donovan JL, Nesbit GM: Distinction of masses involving the sella and suprasellar space; specificity of imaging features. Am J Roentgenol 167:597, 1996
37. Drayer BP, Rosenbaum AE, Kennerdell JS, et al: Computed tomographic diagnosis of suprasellar masses by intrathecal enhancement. Radiology 123:339, 1977
38. Edwards MK, Bonnin JM: White matter disease. In Magnetic Resonance Imaging of the Brain and Spine. New York, Raven Press, 1991
39. Edwards-Brown MK, Bonnin JM: White matter diseases. In Atlas SW (ed): Magnetic Resonance Imaging of the Brain and Spine, 2nd ed, pp 649–706. New York, Lippincott-Raven, 1996
40. Elster AD: Modern imaging of the pituitary. Radiology 187:1–14, 1993
41. Enzmann DR: Imaging of infections and inflammations of the central nervous system. In: Computed Tomography, Ultrasound and Nuclear Magnetic Resonance. New York, Raven Press, 1984
42. Enzmann DR, Britt RH, Placone R: Staging of human brain abscess by computed tomography. Radiology 146:703, 1983
43. Enzmann DR, Ransom B, Norman D, et al: Computed tomography of herpes simplex encephalitis. Radiology 129:419, 1978
44. Epstein FJ, Farmer J-P: Brain stem glioma growth patterns. J Neurosurg 78:408–412, 1993
45. Fishman RA: Cerebrospinal Fluid in Diseases of the Nervous System. Philadelphia, WB Saunders, 1980
46. Fitz CR, Wortzman G, Harwood-Nash DC, et al: Computed tomography in craniopharyngioma. Radiology 127:687, 1978
P.439

47. Floodmark O: Hydrocephalus. In Putnam CE, Ravin C (eds): Textbook of Diagnostic Imaging. Philadelphia, WB Saunders, 1986
48. Ganti SP, Antones JL, Louis KM, et al: Computed tomography in the diagnosis of colloid cyst of the third ventricle. Radiology 128:385, 1981
49. Ganti SR, Hilal SK, Stein BM, et al: CT of pineal region tumors. Am J Neuroradiol 7:97, 1986
50. Gao P-Y, Osborn AG, Smirniotopoulos JG, Harris CP: Epidermoid tumor of the cerebellopontine angle. Am J Neuroradiol 13:863–872, 1992
51. Gebarski S, Gabrielsen TO, et al: The initial diagnosis of multiple sclerosis: Clinical impact of magnetic resonance imaging. Ann Neurol 17:469, 1985
52. Gentry LR, Menezes AH, Turski PA: Suprasellar arachnoid cyst; 2. Evaluation of CSF dynamics. Am J Neuroradiol 7:87, 1986
53. Gentry LR: Primary neuronal injuries. In Current Concepts in Imaging of Craniofacial Trauma: Neuroimaging Clinics of North America. Philadelphia, WB Saunders, 1991
54. George AE, De Leon MJ: Computed tomography and positron emission tomography in aging and dementia. In Latchaw RE: Computed Tomography of the Head, Neck and Spine. Chicago, Year Book Medical Publishers, 1985
55. Gibbs JM, Frackowiak RSJ, Legg NJ: Regional cerebral blood flow and oxygen metabolism in dementia due to vascular disease. Gerontology 32(Suppl 1):84–88, 1986
56. Ginier BL, Kim R, Lane B: Synchronous primary brain tumors. Acad Radiol 2:926, 1995
57. Goldberg HI: Extraaxial brain tumors. In Magnetic Resonance Imaging of the Brain and Spine. New York, Raven Press, 1991
58. Goldsher D, Litt AW, Pinto RS, et al: Dural “tail” associated with meningiomas on Gd-DTPA-enhanced MR images: characteristics, differential diagnostic value, and possible implications of treatment. Radiology 176:447–450, 1990
59. Gould SJ, Howard S, Hope PL, Reynold EOR: Periventricular intraparenchymal cerebral hemorrhage in preterm infants: the role of venous infarction. J Pathol 151:197–202, 1987
60. George AE, Russell EJ, Kricheff II: White matter buckling: CT sign of extra-axial intracranial mass. Am J Neuroradiol 1:425, 1980
61. Graeb D: Intracranial trauma. In Putnam C, Ravin C (eds): Textbook of Diagnostic Imaging. Philadelphia, WB Saunders, 1986
62. Graham DI, Lantos PL (eds): Greenfield’s Neuropathology, 6th ed. New York, Arnold, 1997
63. Greenberg SB, Taber L, Setimus E, et al: Computerized tomography in brain biopsy proven herpes simplex encephalitis. Arch Neurol 38:58, 1981
64. Gusnard DA. Cerebellar neoplasms in children: Semin Roentgenol 25:263–278, 1990
65. Haddad SF, Moore SA, Menezes AH, VanGilder JCX: Ganglioglioma: 13 years of experience. Neurosurgery 31:171–178, 1992
66. Haimes AB, Zimmerman JRD, Morgello S, et al: MR imaging of brain abscesses. Am J Neuroradiol 10:279, 1989
67. Hara T, Kishikawa T, Miyazaki S, et al: Central nervous system complications in childhood leukemia. Correlation between clinical and computed tomographic findings. Am J Pediatr Hematol Oncol 6:129, 1984
68. Harwood-Nash DC, Fitz CR: Neuroradiology in Infants and Children. St Louis, CV Mosby, 1976
69. Harwood-Nash DC: Primary neoplasms of the central nervous system in children. Cancer 67:1223–1228, 1991
70. Hayman LA, Hinck VC: Clinical Brain Imaging: Normal Structure and Functional Anatomy. St Louis, Mosby Year Book, 1992.
71. Hayman LA, Hinck VC: Water soluble iodinated contrast media. In Latchaw RE (ed): Computed Tomography of the Head, Neck and Spine. Chicago, Year Book Medical Publishers, 1985
72. Healy ME, Hesselink JR, Press GA, Middleton MS: Increased detection of intracranial metastases with intravenous Gd-DTPA. Radiology 165:619, 1987
73. Hershey BL: Suprasellar masses: diagnosis and differential diagnosis. Semin US CT MR 14:215–23, 1993
74. Hesselink JR: Infectious and inflammatory diseases. In Neuroimaging Clinics of North America. Philadelphia, WB Saunders, 1991
75. Ho VB, Smirniotopoulos JG, Murphy FM, Rushing EJ: Radiologic-pathologic correlation: hemangioblastoma. Am J Neuroradiol 13:1343–1352, 1992
76. Ho VB, Fitz CR, Yoder CC, Geyer CA: Resolving MR features in resolving myelinolysis (central pontine and extrapontine myelinolysis). Am J Neuroradiol 14:163–167, 1993
77. Hoffman HJ, de Silva M, Humphries RP, et al: Aggressive surgical management of craniopharyngiomas in children. J Neurosurg 76:47–52, 1992
78. Huckman MS: Normal pressure hydrocephalus: Evaluation of the diagnostic and prognostic tests. Am J Neuroradiol 2:385, 1981
79. Jack CR Jr, Sharbrough FW, Twomey CK, et al: Temporal lobe seizures: Lateralization with MR volume measurements of the hippocampal formation. Radiology 175:423–429, 1990
80. Johnsen DE, Woodruff WW, Allen IS, et al: MR imaging of the sellar and juxtasellar regions. RadioGraphics 11:727–758, 1991
81. Johnson BA, Fram EK, Johnson PC, et al: Variable MR appearance of primary lymphoma of the central nervous system: comparison with histopathologic features. Am J Neuroradiol 18:563, 1997
82. Jordan J, Enzmann DR: Encephalitis. In Neuroimaging Clinics of North America. Philadelphia, WB Saunders, 1991
83. Keeney SE, Adcock EW, McArdle CB: Prospective observations of 100 high-risk neonates by high-field (1.5 Tesla) magnetic resonance imaging of the central nervous system: II. Lesions associated with hypoxic-ischemic encephalopathy. Pediatrics 87:431–438, 1991
84. Kingsley DPE, Kendall BE: Cranial computed tomography in leukemia. Neuroradiology 16:543, 1978
85. Kleihues P, Burger PC, Scheithauer BW: The new WHO classification of brain tumors. Brain Pathol 3:255–268, 1993
86. Koci TM, Chiang F, Chow P, et al: Thalamic extrapontine lesions in central pontine myelinolysis. Am J Neuroradiol 11:1229–1233, 1990
87. Koci TM, Chiang F, Mehringer CM, et al: Adult cerebellar medulloblastoma: imaging features with emphasis on MR. Am J Neuroradiol 14:929–939, 1993
88. Konovalov AN, Gorelyshev SK: Surgical treatment of anterior third ventricular tumors. Acta Neurochir (Wien) 118:33–39, 1992
89. Kuhl DE, Metter EJ, Riege WH: Patterns of cerebral glucose utilization in depression, multiple infarct dementia and Alzheimer’s disease. Res Publ Assoc Res Nerv Ment Dis 63:211–226, 1985
90. Kuroiwa T, Bergey GK, Rothman MI, et al: Radiologic appearance of the dysembryoplastic neuroepithelial tumor. Radiology 197:233, 1995
91. Kyritsis AP, Yung WKA, Bruner J, et al: The treatment of anaplastic oligodendrogliomas and mixed gliomas. Neurosurgery 32:365–371, 1993
92. Lee Y, Tassel P, Bruner J, Moser R, Share J: Juvenile pilocytic astrocytomas: CT and MR characteristics. Am J Neuroradiol 10:363, 1989
93. Lee Y, Tassel PV: Intracranial oligodendrogliomas: Imaging findings in 35 untreated cases. Am J Neuroradiol 10:119, 1989
94. Leo JS, Pinto RS, Hulvat GF, et al: Computed tomography of arachnoid cyst. Radiology 130:675, 1979
95. Levy RA, Allen R, McKeever P: Pleomorphic xanthoastrocytoma presenting with massive intracranial hemorrhage. Am J Neuroradiol 17:154, 1996
96. Lhuillier FM, Doyon DL, Halimi PhM, et al: Magnetic resonance imaging of acoustic neuromas: pitfalls and differential diagnosis. Neuroradiol 34:144–149, 1992
97. Lizak PF, Woodruff WW: Posterior fossa neoplasms: multiplanar imaging. Semin US CT MR 3:182–206, 1992
98. Louizou LA, Kendall BE, Marshall J: Subcortical arteriosclerotic encephalopathy: A clinical and radiological investigation. J Neurol Neurosurg Psychiatry 44:294, 1981
99. Luken MG, Whelan MA: Recent diagnostic experience with subdural empyema. J Neurosurg 52:764, 1980
100. Lunardi P, Missori P: Supratentorial dermoid cysts. J Neurosurg 75:262–266, 1991
101. Mark AS, Atlas SW: Progressive multifocal leukoencephalopathy in patients with AIDS: appearance on MR images. Radiology 173:517–521, 1989
102. Mark AS, Seltzer S, Harnsberger HR: Sensorineural hearing loss: more than meets the eye? Am J Neuroradiol 14:37–45, 1993
103. McConnell S, Kaznowski C: Cell cycle dependence of laminar determination in the developing cerebral cortex. Science 254:282–285, 1991
104. Mendenhall NP, Thar TL, Agee OF, et al: Primary lymphoma of the central nervous system: Computerized tomography scan characteristics and treatment results for 12 cases. Cancer 52:1993, 1983
P.440

105. Meyers SP, Kemp SS, Tarr RW: MR imaging features of medulloblastomas. Am J Roentgenol 158:865–895, 1992
106. Moore WS, Barnett HJ, Beebe HG, et al: Guidelines for carotid endarterectomy. A multidisciplinary consensus statement from the ad hoc committee, American Heart Association. Stroke 26:188–201, 1995
107. Mulkens TH, Parizel PM, Martin J-J, et al: Acoustic schwannoma: MR findings in 84 tumors. Am J Roentgenol 160:395–398, 1993
108. Naidich TP, Lin JP, Leeds NE, et al: Primary tumors and other masses of the cerebellum and fourth ventricle: Differential diagnosis by computed tomography. Neuroradiology 14:153, 1977
109. Naidich TP, Pudlowski RM, Naidich JB: Computed tomographic signs of Chiari II malformations: I. Skull and dural partitions. II. Midbrain and cerebellum. III. Ventricles and cisterns. Radiology 134:65, 391, 657, 1980
110. New PFJ, Aronov S, Hesselink JR: National Cancer Institute study: Evaluation of computed tomography in diagnosis of intracranial neoplasms. IV. Meningiomas. Radiology 136:665, 1980
111. Newton TH, Potts DG: Radiology of the skull and brain, 4 vols. St Louis, CV Mosby, 1978
112. North American symptomatic carotid endarterectomy trial collaborators: Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 325;445, 1991
113. Okazaki H: Neoplastic and related conditions. Fundamentals of Neuropathology, 2nd ed, pp 203–274. Tokyo, Igaku-Shoin, 1989
114. Osborn A: Diagnostic Neuroradiology, pp 1–116, 173–174, 401, 784. St Louis, CV Mosby, 1994
115. Oser AB, Moran CJ, Kaufman BA, Park TS: Intracranial tumor in children: MR imaging findings within 24 hours of craniotomy. Radiology 205:807, 1997
116. Ostertun B, Wolf HK, Campos MG, et al: Dysembryoplastic neuroepithelial tumors. Am J Neuroradiol 17:419, 1996
117. Pagani JJ, Libshitz HI, Wallace S, et al: Central nervous system leukemia and lymphoma: Computed tomographic manifestations. Am J Roentgenol 137:1195, 1981
118. Park TS, Hoffman HJ, Hendrick EB, et al: Medulloblastoma: Clinical presentation and management; experience at the Hospital for Sick Children, Toronto, 1950–1980. J Neurosurg 58:543, 1983
119. Perl J II, Turski PA, Masaryk TJ: MR angiography: Techniques and clinical applications. In Atlas SW (ed): Magnetic Resonance Imaging of the Brain and Spine, 2nd ed, pp 1547–1618. New York, Lippincott-Raven, 1996
120. Petropoulou K, Whiteman MLH, Altman NR, et al: CT and MRI of pleomorphic xanthoastrocytoma; unusual biologic behavior. J Comput Assist Tomogr 19:860, 1995
121. Pilcher WH, Silbergeld DL, Berger MS, Ojemann GA: Intraoperative electrocorticography during tumor resection: impact on seizure outcome in patients with gangliogliomas. J Neurosurg 78:891–902, 1993
122. Pinto RS, Kricheff II, Bergeron RT, et al: Small acoustic neuromas: Detection by high resolution gas CT cisternography. Am J Neuroradiol 139:129, 1982
123. Post MJD (ed): Neuroimaging of AIDS I. Neuroimag Clin North Am 7:1–408, 1997
124. Post MJD (ed): Neuroimaging of AIDS II. Neuroimag Clin North Am 7:409–657, 1997
125. Potts DG: Brain tumors: Radiologic localization and diagnosis. Radiol Clin North Am 3:511, 1965
126. Potts DG, Abbott GF, Von Sneidern JV: National Cancer Institute study: Evaluation of computed tomography in the diagnosis of intracranial neoplasms. III. Metastatic tumors. Radiology 136:657, 1980
127. Pronin IN, Holoday AI, Petraikin AV: MRI of high-grade glial tumors; correlation between the degree of contrast enhancement and the volume of surrounding edema. Neuroradiology 39:348, 1997
128. Rakic P, Yakovlev PI: Development of the corpus callosum and cavum septae in man. J Comp Neurol 132:45–72, 1968
129. Robles HA, Smirniotopoulos JG, Figueroa RE: Understanding the radiology of intracranial primitive neuroectodermal tumors from a pathological perspective: a review. Semin US CT MR 13:170–181, 1992
130. Roman-Goldstein SM, Goldman DL, Howieson J, et al: MR in primary CNS lymphoma in immunologically normal patients. Am J Neuroradiol 13:1207–1213, 1992
131. Roppolo HM, Latchaw RE, Meyer JD, et al: Normal pituitary gland: 1. Macroscopic anatomy, CT correlation. Am J Neuroradiol 4:927, 1983
132. Rorke LB, Gilles FH, Davis RL, et al: Revision of the World Health Organization classification of brain tumors for childhood brain tumors. Cancer 56:1869–1886, 1985
133. Russell DS, Rubinstein LJ: Pathology of Tumors of the Nervous System, 5th ed. Baltimore, Williams & Wilkins, 1989
134. Russell EJ, Kircheff II, Budzilovich GN, et al: Atypical computed tomographic features of intracranial meningioma: Radiological-pathologic correlation in a series of 130 consecutive cases. Radiology 135:673, 1980
135. Savoiardo M, Harwood-Nash D, Tadmor R, et al: Gliomas of the intracranial anterior optic pathways in children. Radiology 138:601, 1981
136. Schellinger D, Grant EG, Manz HJ, Patronas NJ: Intraparenchymal hemorrhage in preterm neonates: a broadening spectrum. Am J Neuroradiol 9:327–333, 1988
137. Schwartzberg DG: Imaging of pituitary tumors. Semin US CT MR 13:207–223, 1992
138. Sheporaitis L, Osborn AG, Smirniotopoulos JG, Clunie DA, Howieson J, D’Agostino AN: Radiologic-pathologic correlation intracranial meningioma. Am J Neuroradiol 13:29–37, 1992
139. Shirai H, Imai S, Kajihara Y, et al: MRI in carcinomatous encephalitis. Neuroradiology 39:437, 1997
140. Silver J, Lorenz SE, Wahlstein D, Coughlin J: Axonal guidance during development of the great cerebral commissures: descriptive and experimental studies, in vivo, on the role of preformed glial pathways. J Comp Neurol 210:10–29, 1982
141. Smirniotopoulos JG, Rushing EJ, Mena H: Pineal region masses: differential diagnosis. RadioGraphics 12:577–596, 1992
142. Smirniotopoulos JG, Murphy FM: Central nervous system manifestations of the phakomatoses and other inherited syndromes. In Atlas SW (ed): Magnetic Resonance Imaging of the Brain and Spine, 2nd ed, pp 773–802. New York, Lippincott-Raven, 1996
143. Spoto G, Press G, Hesselink J, Solomon M: Intracranial ependymoma and subependymoma: MR manifestations. Am J Neuroradiol 11:83, 1990
144. Seeger JF, Burke BP, Knake JE, et al: Computed tomographic and angiographic evaluation of hemangioblastomas. Radiology 138:65, 1981
145. Stroink AR, Hoffman JH, Hendrick EB, Humphreys RP: Diagnosis and management of pediatric brainstem gliomas. J Neurosurg 65:745–750, 1986
146. Sugiyama K, Uozumi T, Kiya K, et al: Intracranial germ-cell tumor with synchronous lesions in the pineal and suprasellar regions: report of six cases and review of the literature. Surg Neurol 38:114–120, 1993
147. Swartz JD, Russell KB, Basile BA, et al: High resolution computed tomographic appearance of the intrasellar contents in women of childbearing age. Radiology 147:115, 1983
148. Sze G, Soletsky S, Bronen R, Krol G: MR imaging of the cranial meninges with emphasis on contrast enhancement and meningeal carcinomatosis. Am J Neuroradiol 153:965–975, 1989
149. Sze G: Diseases of the intracranial meninges: MR imaging features. Am J Roentgenol 160:727–733, 1993
150. Tampieri D, Melanson D, Ethier R: MR imaging of epidermoid cysts. Am J Neuroradiol 10:351–356, 1989
151. Tien RD: Intraventricular mass lesions of the brain: CT and MR findings. Am J Roentgenol 157:1283–1290, 1991
152. Tress BM: The need for skull radiography in patients presenting for CT. Radiology 146:87, 1983
153. Truwit CL, Barkovich AJ, Koch TK, Ferriero DM: Cerebral palsy: MR findings in 40 patients. Am J Neuroradiol 13:67–78, 1992
154. Truwit CL, Barkovich AJ: Disorders of brain development. In Atlas SW (ed): Magnetic Resonance Imaging of the Brain and Spine, 2nd ed, pp 179–264. New York, Lippincott-Raven, 1996
155. Turski PA, Newton TH, Horton B: Anatomic correlation with complex motion tomography in 100 sphenoid specimens. Am J Neuroradiol 2:331, 1981
156. Turski PA, Newton TH, Horton B: Sellar contour: Anatomic polytomographic correlation. Am J Roentgenol 137:213, 1981
157. Vagner-Capodano AM, Grisoli F, Gambarelli D, et al: Correlation between cytogenetic and histopathological findings in 75 human meningiomas. Neurosurgery 32:892–900, 1993
P.441

158. Valk J, van der Knaap MS: Magnetic Resonance of Myelin, Myelination, and Myelin Disorders. New York, Springer Verlag, 1989
159. Volpe JJ: Neurology of the newborn. Philadelphia: WB Saunders, 1987
160. Vonofakos D, Barcu H, Hacker H: Oligodendrogliomas: CT patterns and emphasis on features indicating malignancy. J Comput Assist Tomogr 3:783, 1979
161. Waggenspack GA, Guinto FC Jr: MR and CT of passes of the anterosuperior third ventricle. Am J Neuroradiol 10:105–110, 1989
162. Wehrli FW, McGowan JC: The basis of MR contrast. In Atlas SW (ed): Magnetic Resonance Imaging of the Brain and Spine, 2nd ed, pp 29–48. New York, Lippincott-Raven, 1996
163. Weinstein MA, Modic MT, Keyser CK: Diseases of the white matter. In Latchaw RE (ed): Computed Tomography of the Head, Neck and Spine. Chicago, Year Book Medical Publishers, 1985
164. Whiteman MLH, Bowen BC, Post MJD, Bell MD: Intracranial Infection. In Atlas SW (ed): Magnetic Resonance Imaging of the Brain and Spine, 2nd ed, pp 707–772. New York, Lippincott-Raven, 1996
165. Yock DH: Techniques in imaging of the brain. Part 1: The skull. In Rosenberg RN (ed): The Clinical Neurosciences, Vol 4. New York, Churchill Livingstone, 1984
166. Yuh WTC, Engelken JD, Muhonen MG, et al: Experience with high-dose gadolinium MR imaging in the evaluation of brain metastases. Am J Neuroradiol 13:335–345, 1992
167. Zee C-S, Segall H, Apuzzo M, et al: MR imaging of pineal region neoplasms. J Comput Assist Tomogr 15:56–63, 1991
168. Zee CS, Chin T, Segall HD, et al: Magnetic resonance imaging of meningiomas. Semin US CT MR 13:154–169, 1992
169. Zimmerman RA, Bilaniuk LT: Age-related incidence of pineal calcification detected by computed tomography. Radiology 142:659, 1982
170. Zimmerman RA, Bilaniuk LT: Computed tomography in pediatric head trauma. J Neuroradiol 8:157, 1981
171. Zimmerman RA, Bilaniuk LT: Computed tomography of choroid plexus lesions. J Comput Assist Tomogr 3:93, 1979
172. Zimmerman RA, Bilaniuk LT, Genneralli T: Computed tomography of shearing injuries of the cerebral white matter. Radiology 127:393, 1978
173. Zimmerman RA, Bilaniuk LT, Pahlajani H: Spectrum of medulloblastomas demonstrated by computed tomography. Radiology 126:137, 1978
174. Zimmerman RD, Leeds NE, Danziger A: Subdural empyema: CT findings. Radiology 150:417, 1984
175. Zimmerman RA: Imaging of intrasellar, suprasellar and parasellar tumors. Semin Roentgenol 25:174–197, 1990