DOI: 10.1148/rg.272065155
RadioGraphics 2007;27:525-551
From the Archives of the AFIP
Patterns of Contrast Enhancement in the Brain and Meninges1
James G. Smirniotopoulos, MD,
Frances M. Murphy, MD, MPH,
Elizabeth J. Rushing, MD,
John H. Rees, MD and
Jason W. Schroeder, LT, MC, USNR
1 From the Departments of Radiology and Radiological Sciences (J.G.S., J.H.R.); Neurology (J.G.S., F.M.M.), Biomedical Informatics (J.G.S.), and Pathology (E.J.R.), Uniformed Services University, 4301 Jones Bridge Rd, Bethesda, MD 20813; Departments of Radiologic Pathology (J.G.S.) and Neuropathology and Ophthalmic Pathology (E.J.R.), Armed Forces Institute of Pathology, Washington, DC; Department of Veterans Affairs, Veterans Health Administration, Washington, DC (F.M.M.); Department of Radiology, Georgetown University Medical Center, Washington, DC (J.H.R.); and Department of Radiology, National Naval Medical Center, Bethesda, Md (J.W.S.). Received August 21, 2006; revision requested September 20 and received November 21; accepted December 5. All authors have no financial relationships to disclose.
Address correspondence to J.G.S. (e-mail: james-smirnio{at}usuhs.mil ).
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Abstract
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Contrast material enhancement for cross-sectional imaging has been used since the mid 1970s for computed tomography and the mid 1980s for magnetic resonance imaging. Knowledge of the patterns and mechanisms of contrast enhancement facilitate radiologic differential diagnosis. Brain and spinal cord enhancement is related to both intravascular and extravascular contrast material. Extraaxial enhancing lesions include primary neoplasms (meningioma), granulomatous disease (sarcoid), and metastases (which often manifest as mass lesions). Linear pachymeningeal (dura-arachnoid) enhancement occurs after surgery and with spontaneous intracranial hypotension. Leptomeningeal (pia-arachnoid) enhancement is present in meningitis and meningoencephalitis. Superficial gyral enhancement is seen after reperfusion in cerebral ischemia, during the healing phase of cerebral infarction, and with encephalitis. Nodular subcortical lesions are typical for hematogenous dissemination and may be neoplastic (metastases) or infectious (septic emboli). Deeper lesions may form rings or affect the ventricular margins. Ring enhancement that is smooth and thin is typical of an organizing abscess, whereas thick irregular rings suggest a necrotic neoplasm. Some low-grade neoplasms are "fluid-secreting," and they may form heterogeneously enhancing lesions with an incomplete ring sign as well as the classic "cyst-with-nodule" morphology. Demyelinating lesions, including both classic multiple sclerosis and tumefactive demyelination, may also create an open ring or incomplete ring sign. Thick and irregular periventricular enhancement is typical for primary central nervous system lymphoma. Thin enhancement of the ventricular margin occurs with infectious ependymitis. Understanding the classic patterns of lesion enhancement—and the radiologic-pathologic mechanisms that produce them—can improve image assessment and differential diagnosis.
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LEARNING OBJECTIVES FOR TEST 6
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After reading this article and taking the test, the reader will be able to:- Define contrast enhancement as it applies to CT and MR imaging of the brain and meninges.
- Explain the role of the blood-brain barrier and vascularity in contrast enhancement in the central nervous system.
- Use the patterns of enhancement to distinguish different pathologic processes in the brain and meninges.
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Introduction
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Enhancement with contrast material has been used for cross-sectional neuroimaging since the early days of computed tomography (CT). Initially, both urographic and angiographic iodine-based contrast agents (which had already been approved for parenteral injection) were used for contrast material–enhanced CT studies. These agents have largely been supplanted by low- and iso-osmolar contrast agents that have a lower frequency of side effects and a higher safety margin. Between 1988 and 2004, five gadolinium-based contrast agents were approved by the U.S. Food and Drug Administration for intravascular injection for contrast-enhanced magnetic resonance (MR) imaging. There are many tools for analyzing MR or CT images to produce a differential diagnosis. Contemporary imaging includes not only the acquisition of static anatomic images but also dynamic, physiologic, and chemical imaging—all of which can be used to focus a differential diagnosis. This article highlights the use of contrast material as one of these tools, with discussions of the appearance and location of the common patterns of lesion enhancement seen on MR and CT images.
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Mechanisms of Contrast Material Enhancement
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Contrast material enhancement in the central nervous system (CNS) is a combination of two primary processes: intravascular (vascular) enhancement and interstitial (extravascular) enhancement (1,2). Intravascular enhancement may reflect neovascularity, vasodilatation or hyperemia, and shortened transit time or shunting. The brain, spinal cord, and nerves create a selectively permeable capillary membrane to protect themselves from plasma proteins and inflammatory cells: the blood-brain barrier. This barrier is primarily a result of endothelial cell specialization, but it requires a close relationship of the foot process of the perivascular astrocytes in the brain and spinal cord. The neural capillaries have a continuous basement membrane, narrow intercellular gaps, junctional complexes, and a paucity of pinocytotic vesicles. The semipermeable blood-brain barrier blocks lipophobic compounds and creates a unique interstitial fluid environment for the neural tissues. In contrast, lipophilic compounds (measured by octanol/water partition fraction), as well as certain chemicals that are actively transported, may cross the blood-brain barrier with ease. Certain cells that possess the correct surface marker proteins may pass unimpeded through the blood-brain barrier, whereas most other cells are excluded.
After a bolus injection of contrast material into a large peripheral vein, the blood level of the agent rises rapidly, creating a gradient across the capillary endothelial membrane, since the extravascular interstitial fluid does not have the compound. In regions with relatively free capillary permeability, the contrast agent will leak across the vessel wall and begin to accumulate in the perivascular interstitial fluid. In the brain, spinal cord, and proximal cranial and spinal nerves, the intact blood-brain barrier will prevent leakage of contrast material. Interstitial enhancement is related to alterations in the permeability of the blood-brain-barrier, whereas intravascular enhancement is proportional to increases in blood flow or blood volume. At CT, intravascular and interstitial enhancement may be seen simultaneously. When rapid dynamic CT images are obtained, as in CT angiography, most of the observed enhancement is intravascular. When CT imaging is delayed for 10–15 minutes after a bolus infusion, most of the observed enhancement is interstitial. At intermediate times, or with a continuous drip infusion of contrast material, enhancement is a composite variable mixture of both intravascular and interstitial compartments.
Several features of the MR imaging protocols alter the observations of contrast material enhancement. Most pulse sequences are subject to the "flow void phenomena," whereby rapidly flowing fluids have low signal intensity (3). As a result, vascular shunt lesions, such as vein of Galen malformation and arteriovenous malformation, appear dark on MR images. In addition, interstitial enhancement on MR images requires both free water protons and gadolinium. If a tissue is "dry" (ie, without water or free water), gadolinium enhancement will not be observed on routine T1-weighted MR images. For example, the skull and dura mater usually show vivid enhancement of the falx and tentorium on contrast-enhanced CT images, but they do not routinely demonstrate similar enhancement on MR images. Normal dura mater, which is extraaxial nonneural connective tissue, does not have a blood-brain barrier, but it lacks sufficient water to show the T1 shortening required for enhancement on MR images.
Various physiologic and pathologic conditions (which may either be unrelated or secondary to the primary lesions under investigation) produce abnormal contrast enhancement. New blood vessels (angiogenesis), active inflammation (infectious and noninfectious), cerebral ischemia, and pressure overload (ecclampsia and hypertension) are all associated with alterations in permeability of the blood-brain barrier. In addition, reactive hyperemia and neovascularity often have increased blood volume and blood flow (compared with that in normal brain tissue) and typically will show a shortened mean transit time. These features of abnormally increased capillary permeability and altered blood volume and flow result in abnormal contrast enhancement on static gadolinium-enhanced MR images, static iodine-enhanced CT scans, and conventional angiograms. Similarly, results of perfusion and flow studies will be abnormal, regardless of whether flow is measured at MR imaging, CT, or angiography. CT and MR imaging can help measure relative cerebral blood flow (rCBF), relative blood volume (rCBV), and mean transit time (MTT). Angiographic signs of rCBV include dilated veins, early opacification reflects rCBF, and early draining veins indicate a shortened MTT.
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Extraaxial Enhancement
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Extraaxial enhancement in the CNS may be classified as either pachymeningeal or leptomeningeal. The pachymeninges (thick meninges) are the dura mater, which comprises two fused membranes derived from the embryonic meninx primativa: the periosteum of the inner table of the skull and a meningeal layer. Pachymeningeal enhancement may be manifested up against the bone, or it may involve the dural reflections of the falx cerebri, tentorium cerebelli, falx cerebelli, and cavernous sinus. The leptomeninges (skinny meninges) are the pia and arachnoid. Leptomeningeal enhancement may occur on the surface of the brain or in the subarachnoid space. Because the normal, thin arachnoid membrane is attached to the inner surface of the dura mater, the pachymeningeal pattern of enhancement is also described as dura-arachnoid enhancement. In comparison, enhancement on the surface of the brain is called pial or pia-arachnoid enhancement. The enhancement follows along the pial surface of the brain and fills the subarachnoid spaces of the sulci and cisterns. This pattern is often referred to as leptomeningeal enhancement and is usually described as having a "gyriform" or "serpentine" appearance.
Pachymeningeal or Dura-Arachnoid Enhancement
The vessels within the dura mater do not produce a blood-brain barrier. Endogenous and exogenous compounds, such as serum albumin, fibrinogen, and hemosiderin, readily leak into (and out of) the normal dura mater. Normal dural enhancement is well seen on CT scans in the dural reflections of the falx cerebri, tentorium cerebelli, and falx cerebelli. However, enhancement of the dura mater against the cortical bone of the inner table of the skull is usually inconspicuous and not recognized because it appears "white on white." On T1-weighted MR images, the normal dura mater and inner table bone are uniformly hypointense. After the administration of gadolinium-based contrast material, the normal dura mater shows only thin, linear, and discontinuous enhancement (4).
Extraaxial pachymeningeal enhancement may arise from various benign or malignant processes, including transient postoperative changes, intracranial hypotension, neoplasms such as meningiomas, metastatic disease (from breast and prostate cancer), secondary CNS lymphoma, and granulomatous disease.
Postoperative meningeal enhancement occurs in a majority of patients and may be dura-arachnoid or pia-arachnoid (5). In patients who have not undergone surgery, other causes of this enhancement pattern should be considered. Although such enhancement has been reported after uncomplicated lumbar puncture, this observation is rare, occurring in less than 5% of patients (6).
Intracranial hypotension is a benign cause of pachymeningeal enhancement that may be localized or diffuse and can be seen on MR images in patients after surgery or with idiopathic loss of cerebrospinal fluid pressure (Figs 1, 2). When the cerebrospinal fluid pressure drops, there may be secondary fluid shifts that increase the volume of capacitance veins in the subarachnoid space. Prolonged intracranial hypotension may lead to vasocongestion and interstitial edema in the dura mater, findings similar to those seen in the dural tail of a meningioma. Intracranial hypotension may be caused by a skull fracture with leakage of cerebrospinal fluid. More often, it may follow an uncomplicated lumbar puncture; however, in many cases it is idiopathic. MR imaging is relatively sensitive and specific in the detection of benign or spontaneous intracranial hypotension. The classic findings and imaging features include headache that is orthostatic (postural) and worse when upright, thick linear enhancement of the pachymeninges, no enhancement of the sulci or brain surface, enhancement above and below the tentorium, enlargement of the pituitary gland, descent of the brain (low cerebellar tonsils, downward displacement of the iter of the third ventricle below the incisural line), and subdural effusions or hemorrhage in some patients (4,7,8). Pia-arachnoid (leptomeningeal) enhancement is not typical of benign intracranial hypotension, but it may be seen in postoperative patients.
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Figure 1a. Dura-arachnoid pachymeningeal enhancement. (a) Diagram illustrates dura-arachnoid enhancement, which occurs adjacent to the inner table of the skull; in the falx within the interhemispheric fissure; and also in the tentorium between the cerebellum, vermis, and occipital lobes. Pure dural enhancement, without pial or subarachnoid involvement, will not fill in the sulci or basilar cisterns. (b) Postoperative coronal gadolinium-enhanced T1-weighted MR image of a patient in whom a shunt catheter had been placed in the high right parietal region (arrow) demonstrates diffuse and relatively thin dura-arachnoid enhancement along the inner table of the skull and in the dural reflections of the falx and tentorium (arrowheads). There are bilateral subdural fluid collections, larger on the right (*).
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Figure 1b. Dura-arachnoid pachymeningeal enhancement. (a) Diagram illustrates dura-arachnoid enhancement, which occurs adjacent to the inner table of the skull; in the falx within the interhemispheric fissure; and also in the tentorium between the cerebellum, vermis, and occipital lobes. Pure dural enhancement, without pial or subarachnoid involvement, will not fill in the sulci or basilar cisterns. (b) Postoperative coronal gadolinium-enhanced T1-weighted MR image of a patient in whom a shunt catheter had been placed in the high right parietal region (arrow) demonstrates diffuse and relatively thin dura-arachnoid enhancement along the inner table of the skull and in the dural reflections of the falx and tentorium (arrowheads). There are bilateral subdural fluid collections, larger on the right (*).
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Figure 2. Dura-arachnoid pachymeningeal enhancement in a patient with intracranial hypotension. Sagittal gadolinium-enhanced T1-weighted MR image shows diffuse enhancement of the dura-arachnoid including the falx cerebri. Intracranial hypotension causes not only enhancement but also diffuse thickening of the pachymeninges. This abnormal thickening is especially prominent in the dura mater along the clivus (arrows) and tentorium (arrowheads). (Courtesy of Lazslo Mechtler, MD, Dent Neurological Institute, Buffalo, NY.)
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Extraaxial neoplasms may produce pachymeningeal enhancement. The most common primary dural neoplasm is meningioma, a benign tumor of meningothelial cells (Figs 3, 4). Meningiomas are slowly growing, well-localized, WHO (World Health Organization) grade 1 lesions that are usually resectable for cure (9–11). They typically manifest in patients in the 4th–6th decades of life, and they are roughly twice as common in women as in men. The typical meningioma is a localized lesion with a broad base of dural attachment (Fig 3b). This neoplasm actually arises from the arachnoid membrane that is attached to the inner layer of the dura mater. Even in the early days of CT, the accuracy of cross-sectional imaging in the detection and characterization of meningioma was very good (12). Contrast-enhanced MR imaging demonstrates a new finding (one not observed at CT): the dural tail or "dural flair." The dural tail is a curvilinear region of dural enhancement adjacent to the bulky hemispheric tumor (13–15) (Fig 4). The finding was originally thought to represent dural infiltration by tumor, and resection of all enhancing dura mater was thought to be appropriate (16). However, later studies helped confirm that most of the linear dural enhancement, especially when it was more than a centimeter away from the tumor bulk, was probably caused by a reactive process (17). This reactive process includes both vasocongestion and accumulation of interstitial edema, both of which increase the thickness of the dura mater (Fig 5). Because the dural capillaries are "nonneural," they do not form a blood-brain barrier, and, with accumulation of water within the dura mater, contrast material enhancement occurs.
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Figure 3a. Dural tail enhancement with meningioma. (3a) Diagram illustrates the thin, relatively curvilinear enhancement that extends from the edge of a meningioma. Most of this enhancement is caused by vasocongestion and edema, rather than neoplastic infiltration. The bulk of the neoplastic tissue is in the hemispheric extraaxial mass; nonetheless, the dural tail must be carefully evaluated at surgery to avoid leaving neoplastic tissue behind. (3b) Photograph of a resected meningioma shows the dense, "meaty," well-vascularized neoplastic tissue. At the margin of the lesion, there is a "claw" of neoplastic tissue (arrowhead) overlying the dura mater (arrows) that is not directly involved with tumor.
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Figure 3b. Dural tail enhancement with meningioma. (3a) Diagram illustrates the thin, relatively curvilinear enhancement that extends from the edge of a meningioma. Most of this enhancement is caused by vasocongestion and edema, rather than neoplastic infiltration. The bulk of the neoplastic tissue is in the hemispheric extraaxial mass; nonetheless, the dural tail must be carefully evaluated at surgery to avoid leaving neoplastic tissue behind. (3b) Photograph of a resected meningioma shows the dense, "meaty," well-vascularized neoplastic tissue. At the margin of the lesion, there is a "claw" of neoplastic tissue (arrowhead) overlying the dura mater (arrows) that is not directly involved with tumor.
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Figure 4. Dural tail enhancement with meningioma. Sagittal gadolinium-enhanced T1-weighted MR image reveals a large extraaxial enhancing mass. The dural tail (arrows) extends several centimeters from the smooth edge of the densely enhancing hemispheric mass. Most of this dural tail enhancement is caused by reactive changes in the dura mater.
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Figure 5. Dural tail tissue adjacent to meningioma. Lower portion of the photomicrograph (original magnification, x250; hematoxylin-eosin [H-E] stain) shows normal dura mater that is largely collagen. The upper region shows reactive changes characterized by vascular congestion and loosening of the connective tissue. Slow flow within these vessels and accumulation of edema in the dura mater allow enhancement to be visualized on gadolinium-enhanced T1-weighted MR images.
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Metastatic disease involving the dura mater most often arises from breast carcinoma in women and prostate cancer in men. Secondary CNS lymphoma is usually extraaxial and may be epidural, dural, subdural, subarachnoid, and combinations of these (Figs 6, 7).
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Figure 6a. Mixed pachymeningeal and leptomeningeal enhancement in dural lymphoma. Axial gadolinium-enhanced MR images obtained with FLAIR (a) and T1-weighted (b) pulse sequences show superficial extraaxial enhancement adjacent to the right parietal and occipital lobes. The enhancement is both pia-arachnoid, which extends into the subarachnoid spaces of the sulci (arrowheads in b), and dura-arachnoid, which runs along the inner margin of the skull.
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Figure 6b. Mixed pachymeningeal and leptomeningeal enhancement in dural lymphoma. Axial gadolinium-enhanced MR images obtained with FLAIR (a) and T1-weighted (b) pulse sequences show superficial extraaxial enhancement adjacent to the right parietal and occipital lobes. The enhancement is both pia-arachnoid, which extends into the subarachnoid spaces of the sulci (arrowheads in b), and dura-arachnoid, which runs along the inner margin of the skull.
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Figure 7. Dural (subdural) lymphoma. Operative photograph shows the dura mater (arrows). Under this tough connective tissue membrane is a soft cream-colored mass of lymphoma cells. The next membrane layer is the arachnoid, and much of the lymphoma is above it. Note, however, the few small areas with milky or cloudy discoloration, which can be seen through the arachnoid (arrowheads): These areas are subarachnoid lymphoma. Extraaxial lymphoma, such as this case, is almost invariably metastatic to the CNS, whereas primary lymphoma is typically intraaxial within the brain.
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Granulomatous disease, including sarcoid, tuberculosis, Wegener granulomatous, luetic gummas, rheumatoid nodules, and fungal disease, may each produce dural masses and may produce pachymeningeal enhancement. These granulomatous processes typically affect the basilar meninges, rather than involving the convexities of the cerebral hemispheres.
Leptomeningeal or Pia-Arachnoid Enhancement
Enhancement of the pia mater or enhancement that extends into the subarachnoid spaces of the sulci and cisterns is leptomeningeal enhancement (Fig 8a). Leptomeningeal enhancement is usually associated with meningitis, which may be bacterial, viral, or fungal. The primary mechanism of this enhancement is breakdown of the blood-brain barrier without angiogenesis. Glycoproteins released by bacteria cause breakdown of the blood-brain barrier and allow contrast material to leak from vessels into the cerebrospinal fluid. Bacterial and viral meningitis exhibit enhancement that is typically thin and linear (Fig 9). The subarachnoid space is infiltrated with inflammatory cells, and the permeability in the meninges may increase because of bacterial glycoproteins released into the subarachnoid space (18) (Figs 9, 10). Fungal meningitis, however, may produce thicker, lumpy, or nodular enhancement in the subarachnoid space (1).
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Figure 8a. Pia-arachnoid leptomeningeal enhancement. (a) Diagram illustrates the enhancement pattern, which follows the pial surface of the brain and fills the subarachnoid spaces of the sulci and cisterns. (b, c) Axial contrast-enhanced CT scan (b) and gadolinium-enhanced T1-weighted MR image (c) in a case of carcinomatous meningitis show pia-arachnoid enhancement along the surface of the brain and extending into the subarachnoid spaces between the cerebellar folia.
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Figure 8b. Pia-arachnoid leptomeningeal enhancement. (a) Diagram illustrates the enhancement pattern, which follows the pial surface of the brain and fills the subarachnoid spaces of the sulci and cisterns. (b, c) Axial contrast-enhanced CT scan (b) and gadolinium-enhanced T1-weighted MR image (c) in a case of carcinomatous meningitis show pia-arachnoid enhancement along the surface of the brain and extending into the subarachnoid spaces between the cerebellar folia.
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Figure 8c. Pia-arachnoid leptomeningeal enhancement. (a) Diagram illustrates the enhancement pattern, which follows the pial surface of the brain and fills the subarachnoid spaces of the sulci and cisterns. (b, c) Axial contrast-enhanced CT scan (b) and gadolinium-enhanced T1-weighted MR image (c) in a case of carcinomatous meningitis show pia-arachnoid enhancement along the surface of the brain and extending into the subarachnoid spaces between the cerebellar folia.
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Figure 9. Pia-arachnoid leptomeningeal enhancement. Axial gadolinium-enhanced T1-weighted MR image shows relatively diffuse linear pial enhancement on the surface of the midbrain and subarachnoid space enhancement, which extends into multiple sulci (arrowheads).
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Figure 10. Pia-arachnoid leptomeningeal pattern in bacterial (Streptococcus pneumoniae) meningitis. Photomicrograph (original magnification, x400; H-E stain) shows a dense inflammatory infiltrate along the surface of the brain that fills the subarachnoid space (center and top).
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Neoplasms may spread into the subarachnoid space and produce enhancement of the brain surface and subarachnoid space, a pathologic process that is often called "carcinomatous meningitis" (Fig 8b, 8c). Both primary tumors (medulloblastoma, ependymoma, glioblastoma, and oligodendroglioma) and secondary tumors (eg, lymphoma and breast cancer) may spread through the subarachnoid space. Neoplastic disease in the subarachnoid space may produce thicker, lumpy, or nodular enhancement, similar to that of fungal disease (1). Despite the logic of these distinctions, carcinomatous meningitis can appear surprisingly thin and linear, as illustrated in our example (Fig 8b, 8c).
The patient’s clinical presentation provides clues for the differential diagnosis, when fever or other signs of infection exist. Lumbar puncture may reveal a pleocytosis, and cerebrospinal fluid cultures may demonstrate the organism. Some cases of viral meningitis will be reported as "culture negative" or "sterile." Viral encephalitis (as well as sarcoidosis) may also produce enhancement along the cranial nerves, in addition to the brain surface. Normal cranial nerves never enhance within the subarachnoid space, and such enhancement is always abnormal. Primary nerve sheath tumors such as schwannoma may enhance in the subarachnoid space but are usually recognized as a lump or mass along the nerve.
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Intraaxial Enhancement
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Gyral Enhancement
Superficial enhancement of the brain parenchyma is usually caused by vascular or inflammatory processes and is only rarely neoplastic (Fig 11). Vascular causes of serpentine (gyral) enhancement include vasodilatation after reperfusion of ischemic brain, the vasodilatation phase of migraine headache, posterior reversible encephalopathy syndrome (PRES), and vasodilatation with seizures (19–21). Serpentine enhancement from breakdown of the blood-brain barrier is most often seen in acutely reperfused cerebral infarction, subacute cerebral infarction, PRES, meningitis, and encephalitis. The primary distinction between vascular and inflammatory causes of the serpentine pattern of enhancement relies on correlation with clinical history and the region of enhancement. An abrupt onset of symptoms suggests a vascular cause, whereas a more indolent history and nonspecific headache or lethargy suggests inflammation or infection. Gyral lesions affecting a single artery territory are often vascular, whereas inflammatory lesions may affect multiple territories. The most common vascular processes affect the middle cerebral artery territory (up to 60% of cases). However, PRES lesions usually localize in the posterior cerebral artery territory (21–27).
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Figure 11a. Cortical gyral enhancement. (a) Diagram illustrates gyral enhancement that is localized to the superficial gray matter of the cerebral cortex. There is no enhancement of the arachnoid, and none in the subarachnoid space or sulci. (b) Coronal gadolinium-enhanced T1-weighted MR image in a case of herpes encephalitis shows multifocal, intraaxial, curvilinear, cortical gyri-form enhancement that involves both temporal lobes. The enhancement is most prominent on the right but is also seen in the left insular region (arrows) as well as in the medial frontal lobes and cingulate gyrus (arrowhead).
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Figure 11b. Cortical gyral enhancement. (a) Diagram illustrates gyral enhancement that is localized to the superficial gray matter of the cerebral cortex. There is no enhancement of the arachnoid, and none in the subarachnoid space or sulci. (b) Coronal gadolinium-enhanced T1-weighted MR image in a case of herpes encephalitis shows multifocal, intraaxial, curvilinear, cortical gyri-form enhancement that involves both temporal lobes. The enhancement is most prominent on the right but is also seen in the left insular region (arrows) as well as in the medial frontal lobes and cingulate gyrus (arrowhead).
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Herpes virus encephalitis produces superficial gray matter disease, changing signal intensity, and a breakdown of the blood-brain barrier to produce contrast enhancement in a cortical gyral pattern. Herpes encephalitis most often begins in the medial temporal lobes (uncus) and in the cingulate gyrus of the medial frontal and parietal lobes (Fig 11) (22–24,28). Pathologic specimens often show petechial hemorrhage and inflammation in these same locations (Fig 12). The lesion distribution is consistent with the hypothesis that herpes virus infection follows the olfactory pathways from the nasal cavity into the brain. The corticalgyral enhancement in herpes encephalitis may lag behind the onset of signs and symptoms and may be suppressed by steroid medications; thus, the absence of enhancement does not exclude encephalitis.
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Figure 12. Herpes encephalitis. Photograph of a coronally sectioned gross specimen shows multiple petechial hemorrhages (arrowheads) and some granular atrophy of the insular cortex and the undersurface and medial temporal lobe. Scale is in centimeters.
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Vascular gyral enhancement results from various mechanisms with variable time courses. The earliest enhancement can be caused by reversible blood-brain barrier changes when ischemia lasts for only several hours before reperfusion occurs (25,29–31). Early reperfusion may also produce vasodilatation, with increased blood volume and shortened mean transit time. These features were first observed at conventional angiography; they were described as dynamic changes and were called "luxury perfusion" because of the increased blood flow (32). The increased blood flow is caused by autoregulation mechanisms, which are "tricked" by the increased tissue PCO2 that accumulates before reperfusion occurs. Ischemia or infarction may demonstrate gyral enhancement on both CT and MR images within minutes (with early reperfusion) (Fig 13). In the healing phases of cerebral infarction, from several days (5–7 days) to several weeks after the event, there will be vascular proliferation or hypertrophy (Fig 14). Contrast enhancement usually fades away between 4 weeks and 4 months after the stroke, and enhancement is usually replaced by brain volume loss (33). The vascular changes facilitate the breakdown and removal of the dead brain tissue and lead to the encephalomalacia and atrophy characteristic of old "healed" infarction. The imaging appearance of postictal states may mimic the findings of cerebral infarction in several features, including gyral swelling, increased signal intensity on T2-weighted images and decreased signal intensity on T1-weighted images, sulcal effacement, and gyral enhancement (21). Reperfusion, whether acute (eg, after thrombolysis) or subacute to chronic ("healing" infarction), is required to deliver contrast material to produce enhancement.
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Figure 13a. Cortical gyral enhancement in embolic cerebral infarction in a 65-year-old woman. (a) On an axial nonenhanced CT scan, the sulci in the right hemisphere are normally prominent; on the left, the parietal sulci are effaced within a wedge-shaped region of abnormal hypoattenuation. The gyral surface is actually slightly hyperattenuating due to reperfusion injury with secondary petechial hemorrhage in the infarcted cortex. (b) Axial contrast-enhanced CT scan shows cortical gyral enhancement. The same endothelial damage that allows red cells to extravasate also permits contrast material to escape the vascular lumen and enter the brain parenchyma.
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Figure 13b. Cortical gyral enhancement in embolic cerebral infarction in a 65-year-old woman. (a) On an axial nonenhanced CT scan, the sulci in the right hemisphere are normally prominent; on the left, the parietal sulci are effaced within a wedge-shaped region of abnormal hypoattenuation. The gyral surface is actually slightly hyperattenuating due to reperfusion injury with secondary petechial hemorrhage in the infarcted cortex. (b) Axial contrast-enhanced CT scan shows cortical gyral enhancement. The same endothelial damage that allows red cells to extravasate also permits contrast material to escape the vascular lumen and enter the brain parenchyma.
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Figure 14a. Cortical gyral enhancement in subacute thrombotic cerebral infarction. (a) Axial contrast-enhanced CT scan shows enhancement that is limited to the opercular surfaces, insula, and caudate nucleus head (all of which are gray matter). (b) Photograph of an axially sectioned gross specimen shows green staining, which is caused by bilirubin bound to serum albumin, and which outlines areas of the brain where the blood-brain-barrier is no longer intact. Note how the green stain is almost exclusively in the gray matter of the cortex (arrowheads), basal ganglia (*), caudate nucleus, and claustrum. In these areas, the healing process would have removed the infarcted tissue, resulting in encephalomalacia and atrophy, if the patient had not died (the jaundiced patient died 2 weeks after left internal carotid thrombosis caused infarction of the anterior and middle cerebral artery territories).
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Figure 14b. Cortical gyral enhancement in subacute thrombotic cerebral infarction. (a) Axial contrast-enhanced CT scan shows enhancement that is limited to the opercular surfaces, insula, and caudate nucleus head (all of which are gray matter). (b) Photograph of an axially sectioned gross specimen shows green staining, which is caused by bilirubin bound to serum albumin, and which outlines areas of the brain where the blood-brain-barrier is no longer intact. Note how the green stain is almost exclusively in the gray matter of the cortex (arrowheads), basal ganglia (*), caudate nucleus, and claustrum. In these areas, the healing process would have removed the infarcted tissue, resulting in encephalomalacia and atrophy, if the patient had not died (the jaundiced patient died 2 weeks after left internal carotid thrombosis caused infarction of the anterior and middle cerebral artery territories).
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Nodular Cortical and Subcortical Enhancement
A pattern of nodular enhancing lesions in subcortical and cortical parenchyma is typical for hematogenous dissemination of metastatic neoplasms and clot emboli. These lesions usually appear as small (<2-cm) circumscribed lesions near the gray matter–white matter junction (Figs 15, 16). Metastatic disease usually travels into the brain through the arteries and less commonly via the venous system. CNS metastases are distributed by blood flow, and the majority are supratentorial in the cerebral hemispheres, most often in the territory of the middle cerebral artery (34). Metastatic disease that follows venous pathways into the CNS usually arises from a primary pelvic malignancy and travels through the prevertebral veins of the Batson venous plexus. This venous route into the retroclival venous plexus partially accounts for the preferential distribution of some pelvic metastases into the posterior fossa (cerebellum and brainstem).
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Figure 15. Subcortical nodular enhancement. Diagram illustrates nodular lesions near the gray matter–white matter junction and one near the deep gray matter. This pattern is typical for metastatic cancer and clot emboli. Because of their typical subcortical location, metastases often manifest with cortical symptoms or seizures while the lesions are small (often <1 cm in diameter).
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Figure 16a. Subcortical nodular enhancement in metastatic melanoma. (a) Axial nonenhanced CT scan demonstrates multiple nodular lesions that are hyperattenuating because of microscopic hemorrhages. (b) Photograph of an axially sectioned gross specimen shows black discoloration of these secondary (metastatic) melanoma nodules. The melanin pigment in these lesions makes them easy to see. The hematogenously disseminated lesions are all in or near the cortex, the gray matter–white matter junction, or deep gray matter of the basal ganglia; the greatest filtration of intravascular particulate material occurs in these areas.
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Figure 16b. Subcortical nodular enhancement in metastatic melanoma. (a) Axial nonenhanced CT scan demonstrates multiple nodular lesions that are hyperattenuating because of microscopic hemorrhages. (b) Photograph of an axially sectioned gross specimen shows black discoloration of these secondary (metastatic) melanoma nodules. The melanin pigment in these lesions makes them easy to see. The hematogenously disseminated lesions are all in or near the cortex, the gray matter–white matter junction, or deep gray matter of the basal ganglia; the greatest filtration of intravascular particulate material occurs in these areas.
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Metastatic lesions are typically subcortical, occurring in or near the gray matter–white matter (corticomedullary) junction, whereas primary tumors are usually deeper (35). The subcortical gray matter–white matter pattern of nodule distribution reflects the filtration of intravascular particulate material in the region, where vessels branch and taper at the transition from the abundant vessels in the cortical gray matter into the relatively sparse vasculature of the white matter. Tumor emboli must do more than disseminate through the vessel: The tumor must take hold and grow. Metastases usually are well demarcated, with a distinct "pushing margin" in gross pathologic specimens and on images (Fig 16). Angiogenesis allows the metastases to grow larger than 5 mm but also produces blood-brain barrier abnormality, which results in contrast enhancement and considerable perilesional vasogenic edema. Because of their typical location, cortical and subcortical metastases, even as small lesions, are likely to cause noticeable neurologic symptoms, including seizures. This characteristic is one of the reasons why metastases are typically first identified while they are solid nodular lesions, often 0.5–2.5 cm in diameter (Figs 15, 16). In contrast, primary glial tumors, such as low-grade and high-grade astrocytomas, arise away from the cortex and deep in the white matter, and they are usually much larger (2.5–5.0 cm in diameter) when they produce symptoms.
In approximately 40%–60% of cases of metastatic disease, routine contrast-enhanced CT and MR images will demonstrate a solitary metastatic lesion, although increasing the dose of contrast agent and using delayed imaging protocols may reveal additional metastatic lesions.
Deep and Periventricular Enhancement
Lesions near the gray matter–white matter junction are typical of hematogenous spread, as discussed in the previous section. Lesions that manifest deeper within the cerebral hemispheres usually have other causes. These deeper subcortical lesions may involve the white matter, the deep gray nuclei (eg, basal ganglia, thalamus), or both white and gray matter. Metabolic diseases and toxins may preferentially damage the deep gray matter. Various diseases that affect myelin production or repair primarily damage the white matter. Most leukoencephalopathies become destructive during their natural evolution and lead to a decreased volume of affected white matter. These changes may produce alterations of increased water signal intensity on MR images and decreased attenuation on CT images. Many pathologic processes will produce enhancement with localization similar to the signal change pattern. We look for these clear-cut distinctions between deep white matter lesions and deep gray matter lesions as a guide to differential diagnosis. However, many diseases affect both the gray matter and the white matter in the deep periventricular region, and some of these are more common in immunocompromised patients, such as those with toxoplasmosis and primary CNS lymphoma.
Deep Ring-enhancing Lesions
Ring-enhancing lesions may be superficial, but they are usually subcortical or deep. Schwartz et al (36) reviewed 221 ring-enhancing lesions seen on MR images and reported that 40% were gliomas; 30%, metastases; 8%, abscesses; and 6%, demyelinating disease. In their series, 45% of metastases and 77% of gliomas were single lesions, whereas abscesses and multiple sclerosis lesions were multiple in 75% and 85% of patients, respectively (36). Both necrotic metastases and hematogenous abscesses typically manifest as cortical or subcortical lesions with cavitation. Metastatic deposits are often solid nodular lesions that may become ring-enhancing because of necrosis (eg, after chemotherapy or irradiation) (Fig 17). Multiple cortical or subcortical ring-enhancing lesions have an infectious etiology (ie, they represent brain abscesses) in patients with subacute bacterial endocarditis, indwelling catheters, or other implanted devices such as cardiac valves. Deep white matter ring-enhancing lesions, especially those with mass effect and surrounding vasogenic edema, are most often either primary neoplasms (eg, glioblastoma multiforme) or abscesses (Fig 18).
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Figure 17. Subcortical nodular enhancement in metastatic breast cancer. Axial gadolinium-enhanced T1-weighted MR image shows multiple ring-enhancing lesions from necrosis of the metastases. The majority of these lesions are near the cortex or deep gray matter, with most being at the gray matter–white matter junction. This appearance is similar to those of septic emboli and abscesses, which indicates the need for good clinical correlation.
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Figure 18. Smooth ring-enhancing pattern in late cerebritis and subsequent cerebral abscess. Diagram illustrates a thin (<10 mm) rim of enhancement, which is usually very smooth along the inner margin; this pattern is characteristic of an abscess. The lesion is surrounded by a crown of vasogenic edema spreading into the white matter.
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Cerebritis and Abscess
Pyogenic infections of the CNS usually arise from septic emboli transmitted hematogenously. Less frequently, transdural spread may occur from adjacent sinus infections (sphenoid, ethmoid, frontal, and mastoid air cells). After an initial unorganized inflammation or cerebritis, the successful immune response will include angiogenic neovascularity and collagen deposition (ie, a capsule of granulation tissue) and formation of an abscess. A layer of astrogliosis surrounds the granulation tissue (37,38). Ring enhancement in an abscess reflects the granulation tissue in its wall that has both increased vascularity and abnormally permeable capillaries. Collagen in the wall reinforces it to localize and confine the infected brain and pus. Preceding this organized abscess stage is cerebritis. Cerebritis is an acute inflammatory reaction with altered permeability of the native vessels but without angiogenesis or neovascularity. Before angiogenesis, the signal intensity and attenuation changes are directly caused by the inflammatory process, and perilesional vasogenic edema is variable and may be minimal. In the immunocompetent patient, cerebritis progresses to form an organized abscess. An intermediate stage of transition from cerebritis to an organized abscess may be suspected when the lesion does not have a sharp margin or a wall that is less discrete (Fig 19). On initial CT and MR images, cerebritis will appear as a ring-enhancing lesion (Fig 19a–19c). In cerebritis without a collagen capsule, images obtained over 20–40 minutes may show "fill-in" of the ring center (39). This "filling-in" does not occur in a well-organized abscess and suggests cerebritis (39). Cerebritis is often treated nonsurgically with high-dose antibiotics.
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Figure 19a. Smooth ring-enhancing pattern in late cerebritis and subsequent cerebral abscess. (a) Axial T2-weighted MR image shows a circular mass with extensive perilesional vasogenic edema that surrounds a dark rim (the abscess wall). Mild mass effect on the mid-line structures is seen. (b) On an axial gadolinium-enhanced T1-weighted MR image, the inner wall of the ring-enhancing lesion is smoother than the slightly irregular outer wall. This appearance reflects an earlier stage in the organization of the infection, as it makes the transition from cerebritis to abscess, since a more organized abscess will appear smoother. (c) Axial CT scan shows a sharply marginated, ringed lesion with surrounding perilesional vasogenic edema. (d) On an axial diffusion-weighted MR image, the lesion has markedly restricted diffusion (hyperintensity) due to the viscous pus and necrotic brain tissue in the abscess core.
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Figure 19b. Smooth ring-enhancing pattern in late cerebritis and subsequent cerebral abscess. (a) Axial T2-weighted MR image shows a circular mass with extensive perilesional vasogenic edema that surrounds a dark rim (the abscess wall). Mild mass effect on the mid-line structures is seen. (b) On an axial gadolinium-enhanced T1-weighted MR image, the inner wall of the ring-enhancing lesion is smoother than the slightly irregular outer wall. This appearance reflects an earlier stage in the organization of the infection, as it makes the transition from cerebritis to abscess, since a more organized abscess will appear smoother. (c) Axial CT scan shows a sharply marginated, ringed lesion with surrounding perilesional vasogenic edema. (d) On an axial diffusion-weighted MR image, the lesion has markedly restricted diffusion (hyperintensity) due to the viscous pus and necrotic brain tissue in the abscess core.
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Figure 19c. Smooth ring-enhancing pattern in late cerebritis and subsequent cerebral abscess. (a) Axial T2-weighted MR image shows a circular mass with extensive perilesional vasogenic edema that surrounds a dark rim (the abscess wall). Mild mass effect on the mid-line structures is seen. (b) On an axial gadolinium-enhanced T1-weighted MR image, the inner wall of the ring-enhancing lesion is smoother than the slightly irregular outer wall. This appearance reflects an earlier stage in the organization of the infection, as it makes the transition from cerebritis to abscess, since a more organized abscess will appear smoother. (c) Axial CT scan shows a sharply marginated, ringed lesion with surrounding perilesional vasogenic edema. (d) On an axial diffusion-weighted MR image, the lesion has markedly restricted diffusion (hyperintensity) due to the viscous pus and necrotic brain tissue in the abscess core.
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Figure 19d. Smooth ring-enhancing pattern in late cerebritis and subsequent cerebral abscess. (a) Axial T2-weighted MR image shows a circular mass with extensive perilesional vasogenic edema that surrounds a dark rim (the abscess wall). Mild mass effect on the mid-line structures is seen. (b) On an axial gadolinium-enhanced T1-weighted MR image, the inner wall of the ring-enhancing lesion is smoother than the slightly irregular outer wall. This appearance reflects an earlier stage in the organization of the infection, as it makes the transition from cerebritis to abscess, since a more organized abscess will appear smoother. (c) Axial CT scan shows a sharply marginated, ringed lesion with surrounding perilesional vasogenic edema. (d) On an axial diffusion-weighted MR image, the lesion has markedly restricted diffusion (hyperintensity) due to the viscous pus and necrotic brain tissue in the abscess core.
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An abscess is the result of organization and partial neutralization of an infection. In the brain, an abscess may develop a well-formed capsule in 2–4 weeks. The organizing infection forms concentric zones or layers (37–39) (Fig 20): (a) necrotic brain in the innermost layer, (b) reactive white cells (macrophages, monocytes) and fibroblasts, (c) capillary vascular proliferation and collagen capsule formation, (d) neovascularity and active cerebritis, and (e) reactive astrogliosis and vasogenic edema in the outer margin.
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Figure 20. Brain abscess. Photomicrograph (original magnification, x250; H-E stain) shows the microscopic layers from top to bottom: reactive gliosis and the brain margin, vascular proliferation with collagen formation (granulation tissue), migrating white blood cells (monocytes), and pus. polys = polymorphonuclear leukocytes (Courtesy of Joseph Parisi, MD, Mayo Clinic, Rochester, Minn.)
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The rim of reactive tissue is usually thin (2–7 mm), uniformly convex, and smooth on both the outer and inner aspects (Fig 21).
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Figure 21. Cerebral abscess in a patient with AIDS who died of multiple brain abscesses from Toxoplasma gondii. Photograph of an axially sectioned gross specimen shows an abscess in the thalamus with three macroscopic zones: a reddish region of neovascularity (arrowheads), a white region of extravascular white cells and pus (*), and an inner zone of liquefaction necrosis (N). Liquefaction necrosis occurs in lipid-rich organs (such as the brain), when an exuberant leukocytic reaction brings lytic enzymes into the infected region. Scale is in centimeters.
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The ring-enhancing lesion of a cerebral abscess is classically described as having a smooth inner margin and a smooth outer margin. However, in some examples, especially during the transition from cerebritis to abscess, the outer rim of enhancement may resemble the corona of a solar eclipse (Fig 18b). An abscess rim is typically hypointense on T2-weighted MR images, and a variety of explanations have been proposed, including dense collagen, blood products (hemosiderin), and paramagnetic free radicals (eg, atomic oxygen produced by leukocytes that are attacking the bacteria) (40). Almost 90% of abscesses demonstrate a hypointense rim, and 75% form a continuous hypointense rim (36). The abscess wall often appears thicker on the gray matter or "oxygen side" of the ring and thinner along the white matter or ventricular side. The thinner margin of the deep or medial aspect of the lesion is predisposed to daughter abscess formation and deep rupture of the abscess into the ventricle (which leads to pyocephalus and high mortality).
Occasionally, the outer perimeter of the abscess wall can appear irregular. The enhancement is both interstitial (from increased capillary permeability) and intravascular (from increased perfusion in the granulation tissue). The interstitial contrast material usually does not migrate into the center of an abscess cavity, even on delayed images, because of the viscosity of the pus and liquefaction necrosis. The viscosity of the necrotic center also explains its high signal intensity on diffusion-weighted images (Fig 19d) and corresponding reduced diffusion coefficient and therefore low signal intensity on the apparent diffusion coefficient maps.
Necrotic High-grade Primary Neoplasms
Necrotic neoplasms are usually, but not exclusively, malignant, and they may be primary or metastatic. Imaging features of a necrotic neoplasm include a thick irregular ring with a shaggy inner margin, multilocular and complex ring patterns, and a wall that is thicker than 10 mm (at least in some areas) (Fig 22). Deep lesions with this pattern—especially when they are located in the corpus callosum and thalamus—are usually primary astrocytic glial neoplasms. In adults, such lesions are usually diffusely infiltrating astrocytomas, with 60% being higher grade (ie, WHO grade 4 astrocytoma or glioblastoma multiforme).
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Figure 22a. Necrotic ring pattern of high-grade neoplasms. (a) Diagram illustrates a lesion with an enhanced rim that is very thick medially; the ring is thicker and more irregular than that seen in a typical abscess. The lesion is surrounded by a crown of vasogenic edema spreading into the white matter. (b, c) Glioblastoma multiforme. (b) Axial nonenhanced T2-weighted MR image shows a large heterogeneous mass that displaces the frontal horn of the lateral ventricle. (c) Axial gadolinium-enhanced T1-weighted MR image shows the irregular, heterogeneous ring-enhancing mass. The ring has a characteristically undulating or wavy margin, and its inner aspect is shaggy and irregular.
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Figure 22b. Necrotic ring pattern of high-grade neoplasms. (a) Diagram illustrates a lesion with an enhanced rim that is very thick medially; the ring is thicker and more irregular than that seen in a typical abscess. The lesion is surrounded by a crown of vasogenic edema spreading into the white matter. (b, c) Glioblastoma multiforme. (b) Axial nonenhanced T2-weighted MR image shows a large heterogeneous mass that displaces the frontal horn of the lateral ventricle. (c) Axial gadolinium-enhanced T1-weighted MR image shows the irregular, heterogeneous ring-enhancing mass. The ring has a characteristically undulating or wavy margin, and its inner aspect is shaggy and irregular.
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Figure 22c. Necrotic ring pattern of high-grade neoplasms. (a) Diagram illustrates a lesion with an enhanced rim that is very thick medially; the ring is thicker and more irregular than that seen in a typical abscess. The lesion is surrounded by a crown of vasogenic edema spreading into the white matter. (b, c) Glioblastoma multiforme. (b) Axial nonenhanced T2-weighted MR image shows a large heterogeneous mass that displaces the frontal horn of the lateral ventricle. (c) Axial gadolinium-enhanced T1-weighted MR image shows the irregular, heterogeneous ring-enhancing mass. The ring has a characteristically undulating or wavy margin, and its inner aspect is shaggy and irregular.
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High-grade primary tumors, exemplified by glioblastoma multiforme, 
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Abstract
LEARNING OBJECTIVES FOR TEST...
