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From the Archives of the AFIP

Patterns of Contrast Enhancement in the Brain and Meninges¹

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 ).

	Abstract

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Mechanisms of Contrast Material... Extraaxial Enhancement Intraaxial Enhancement References

 
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.

	LEARNING OBJECTIVES FOR TEST 6

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Mechanisms of Contrast Material... Extraaxial Enhancement Intraaxial Enhancement References

 
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.
  

	Introduction

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Mechanisms of Contrast Material... Extraaxial Enhancement Intraaxial Enhancement References

 
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.

	Mechanisms of Contrast Material Enhancement

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Mechanisms of Contrast Material... Extraaxial Enhancement Intraaxial Enhancement References

 
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.

	Extraaxial Enhancement

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Mechanisms of Contrast Material... Extraaxial Enhancement Intraaxial Enhancement References

 
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.

View larger version (60K): [in this window] [in a new window] [Download PPT slide]   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 (*).

View larger version (142K): [in this window] [in a new window] [Download PPT slide]   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 (*).

View larger version (169K): [in this window] [in a new window] [Download PPT slide]   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.)

View larger version (69K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (116K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (143K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (170K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (118K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (116K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (157K): [in this window] [in a new window] [Download PPT slide]   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.

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).

View larger version (70K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (117K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (122K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (145K): [in this window] [in a new window] [Download PPT slide]   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).

View larger version (164K): [in this window] [in a new window] [Download PPT slide]   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).

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.

	Intraaxial Enhancement

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Mechanisms of Contrast Material... Extraaxial Enhancement Intraaxial Enhancement References

 
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).

View larger version (64K): [in this window] [in a new window] [Download PPT slide]   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).

View larger version (137K): [in this window] [in a new window] [Download PPT slide]   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).

View larger version (130K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (110K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (148K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (127K): [in this window] [in a new window] [Download PPT slide]   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).

View larger version (141K): [in this window] [in a new window] [Download PPT slide]   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).

View larger version (79K): [in this window] [in a new window] [Download PPT slide]   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).

View larger version (155K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (126K): [in this window] [in a new window] [Download PPT slide]   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.

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).

View larger version (160K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (75K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (176K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (154K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (146K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (106K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (173K): [in this window] [in a new window] [Download PPT slide]   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.)

View larger version (112K): [in this window] [in a new window] [Download PPT slide]   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.

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).

View larger version (74K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (144K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (151K): [in this window] [in a new window] [Download PPT slide]   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.

View larger version (206K): [in this window] [in a new window] [Download PPT slide]   Figure 23.  Glioblastoma multiforme. Photomicrograph (original magnification, x250; H-E stain) shows vascular proliferation with thick-walled capillaries, which are called glomeruloid vessels (G) because they resemble the tuft of vessels in the renal glomeruli.

View larger version (157K): [in this window] [in a new window] [Download PPT slide]   Figure 24a.  Glioblastoma multiforme. (a) Axial contrast-enhanced CT scan shows a mass with a complex appearance. The outer cortical region of the tumor (*) has a thick irregular rim with a shaggy inner margin (an appearance that is more typical of a glioblastoma multiforme). The relatively smooth and thin deep inner margin mimics the thin reactive rim of an abscess wall. (b) Lateral angiogram, obtained after an internal carotid injection, shows a large, hypervascular mass with irregular vascularity, pooling of contrast material, and early draining veins (arrows). Early draining veins are the angiographic sign of a short mean transit time (MTT). Modern MR perfusion imaging would also demonstrate increased perfusion (elevated rCBV and rCBF) and a shortened MTT. (c) Photograph of a coronally sectioned gross specimen shows the outer cortical region of the tumor with the more typical, thick irregular rim (*) and shaggy inner margin and the relatively smooth, thin, deep inner margin (arrows). Within the neoplasm is a region of hemorrhagic necrosis. Scale is in centimeters.

View larger version (168K): [in this window] [in a new window] [Download PPT slide]   Figure 24b.  Glioblastoma multiforme. (a) Axial contrast-enhanced CT scan shows a mass with a complex appearance. The outer cortical region of the tumor (*) has a thick irregular rim with a shaggy inner margin (an appearance that is more typical of a glioblastoma multiforme). The relatively smooth and thin deep inner margin mimics the thin reactive rim of an abscess wall. (b) Lateral angiogram, obtained after an internal carotid injection, shows a large, hypervascular mass with irregular vascularity, pooling of contrast material, and early draining veins (arrows). Early draining veins are the angiographic sign of a short mean transit time (MTT). Modern MR perfusion imaging would also demonstrate increased perfusion (elevated rCBV and rCBF) and a shortened MTT. (c) Photograph of a coronally sectioned gross specimen shows the outer cortical region of the tumor with the more typical, thick irregular rim (*) and shaggy inner margin and the relatively smooth, thin, deep inner margin (arrows). Within the neoplasm is a region of hemorrhagic necrosis. Scale is in centimeters.

View larger version (114K): [in this window] [in a new window] [Download PPT slide]   Figure 24c.  Glioblastoma multiforme. (a) Axial contrast-enhanced CT scan shows a mass with a complex appearance. The outer cortical region of the tumor (*) has a thick irregular rim with a shaggy inner margin (an appearance that is more typical of a glioblastoma multiforme). The relatively smooth and thin deep inner margin mimics the thin reactive rim of an abscess wall. (b) Lateral angiogram, obtained after an internal carotid injection, shows a large, hypervascular mass with irregular vascularity, pooling of contrast material, and early draining veins (arrows). Early draining veins are the angiographic sign of a short mean transit time (MTT). Modern MR perfusion imaging would also demonstrate increased perfusion (elevated rCBV and rCBF) and a shortened MTT. (c) Photograph of a coronally sectioned gross specimen shows the outer cortical region of the tumor with the more typical, thick irregular rim (*) and shaggy inner margin and the relatively smooth, thin, deep inner margin (arrows). Within the neoplasm is a region of hemorrhagic necrosis. Scale is in centimeters.

View larger version (78K): [in this window] [in a new window] [Download PPT slide]   Figure 25.  Fluid-secreting neoplasm (cyst with mural nodule pattern). Diagram illustrates a "cystic" mass with a "mural nodule," which is the classic description for a pilocytic astrocytoma. This pattern is seen in a variety of fluid-secreting neoplasms, including hemangioblastoma, ganglioglioma, and pleomorphic xanthoastrocytoma.

View larger version (177K): [in this window] [in a new window] [Download PPT slide]   Figure 26.  Pilocytic astrocytoma. Photomicrograph (original magnification, x400; H-E stain) shows the typical biphasic pattern of alternating dense regions (arrows) and loose areas with microcysts (*).

View larger version (117K): [in this window] [in a new window] [Download PPT slide]   Figure 27.  Pilocytic astrocytoma. Photograph of an axially sectioned gross specimen of the cerebellum clearly shows the tumor fluid cavity (C) with a surrounding thin (<2-mm) region of nonneoplastic reactive gliosis (arrowheads).

View larger version (120K): [in this window] [in a new window] [Download PPT slide]   Figure 28a.  Pilocytic astrocytoma. (a) Axial nonenhanced T1-weighted MR image shows a smooth-margined mass in the cerebellum surrounded by a cyst with fluid that is higher intensity than the cerebrospinal fluid in the fourth ventricle. (b) Axial gadolinium-enhanced T1-weighted MR image shows intense enhancement of the mural nodule, but the rim surrounding the fluid secreted by the tumor does not enhance. A cystic mass with a mural nodule in the cerebellum is classic for a pilocytic astrocytoma. Note that this example has three fluid collections and that one of them (arrow) is actually inside the tumor nodule.

View larger version (123K): [in this window] [in a new window] [Download PPT slide]   Figure 28b.  Pilocytic astrocytoma. (a) Axial nonenhanced T1-weighted MR image shows a smooth-margined mass in the cerebellum surrounded by a cyst with fluid that is higher intensity than the cerebrospinal fluid in the fourth ventricle. (b) Axial gadolinium-enhanced T1-weighted MR image shows intense enhancement of the mural nodule, but the rim surrounding the fluid secreted by the tumor does not enhance. A cystic mass with a mural nodule in the cerebellum is classic for a pilocytic astrocytoma. Note that this example has three fluid collections and that one of them (arrow) is actually inside the tumor nodule.

View larger version (177K): [in this window] [in a new window] [Download PPT slide]   Figure 29.  Demyelination (multiple sclerosis). Photomicrograph (original magnification, x400; H-E stain) shows a perivascular infiltrate of inflammatory cells in the upper right corner but no angiogenesis.

View larger version (71K): [in this window] [in a new window] [Download PPT slide]   Figure 30.  Open ring pattern. Diagram illustrates a lesion with an incomplete rim (only part of the rim enhances). This appearance may be seen in multiple sclerosis (without mass effect as in this drawing), tumefactive demyelination (with mass effect), and fluid-secreting neoplasms (with associated mass effect and occasionally with surrounding vasogenic edema).

View larger version (118K): [in this window] [in a new window] [Download PPT slide]   Figure 31a.  Demyelination. (a) Axial gadolinium-enhanced T1-weighted MR image shows two rimmed lesions; neither has a completely circumferential rim of enhancement (arrows). The left frontal lesion has a more conspicuous open ring sign. Note the absence of surrounding vasogenic edema—another potential differential feature to distinguish demyelination from both abscess and neoplasm. (b) Axial T2-weighted MR image shows the two homogeneous, hyperintense lesions and the conspicuous absence of vasogenic edema.

View larger version (130K): [in this window] [in a new window] [Download PPT slide]   Figure 31b.  Demyelination. (a) Axial gadolinium-enhanced T1-weighted MR image shows two rimmed lesions; neither has a completely circumferential rim of enhancement (arrows). The left frontal lesion has a more conspicuous open ring sign. Note the absence of surrounding vasogenic edema—another potential differential feature to distinguish demyelination from both abscess and neoplasm. (b) Axial T2-weighted MR image shows the two homogeneous, hyperintense lesions and the conspicuous absence of vasogenic edema.

View larger version (58K): [in this window] [in a new window] [Download PPT slide]   Figure 32.  Periventricular pattern. Diagram illustrates thick periventricular enhancement, as shown around the right lateral ventricle. This enhancement pattern is usually neoplastic and is most commonly seen in a high-grade astrocytoma or primary CNS lymphoma. Thin periventricular enhancement, as shown around the left lateral ventricle, is usually infectious.

View larger version (114K): [in this window] [in a new window] [Download PPT slide]   Figure 33a.  Thick periventricular enhancement in primary CNS lymphoma in an adult patient with AIDS. (a) Axial nonenhanced CT scan shows a thick rind of periventricular hyperattenuation, with surrounding vasogenic edema. (b) Axial contrast-enhanced CT scan shows abnormal enhancement around both lateral ventricles. This "rind" is much thicker around the right lateral ventricle and involves the same areas that were hyperattenuating before contrast material administration. (c) Photograph of a coronally sectioned gross specimen shows periventricular discoloration around the frontal horns, due to neoplastic lymphocyte infiltration. (d) Photomicrograph (original magnification, x250; H-E stain) shows infiltration of small, round, blue cells in the periventricular region, adjacent to the frontal horn of the lateral ventricle.

View larger version (126K): [in this window] [in a new window] [Download PPT slide]   Figure 33b.  Thick periventricular enhancement in primary CNS lymphoma in an adult patient with AIDS. (a) Axial nonenhanced CT scan shows a thick rind of periventricular hyperattenuation, with surrounding vasogenic edema. (b) Axial contrast-enhanced CT scan shows abnormal enhancement around both lateral ventricles. This "rind" is much thicker around the right lateral ventricle and involves the same areas that were hyperattenuating before contrast material administration. (c) Photograph of a coronally sectioned gross specimen shows periventricular discoloration around the frontal horns, due to neoplastic lymphocyte infiltration. (d) Photomicrograph (original magnification, x250; H-E stain) shows infiltration of small, round, blue cells in the periventricular region, adjacent to the frontal horn of the lateral ventricle.

View larger version (127K): [in this window] [in a new window] [Download PPT slide]   Figure 33c.  Thick periventricular enhancement in primary CNS lymphoma in an adult patient with AIDS. (a) Axial nonenhanced CT scan shows a thick rind of periventricular hyperattenuation, with surrounding vasogenic edema. (b) Axial contrast-enhanced CT scan shows abnormal enhancement around both lateral ventricles. This "rind" is much thicker around the right lateral ventricle and involves the same areas that were hyperattenuating before contrast material administration. (c) Photograph of a coronally sectioned gross specimen shows periventricular discoloration around the frontal horns, due to neoplastic lymphocyte infiltration. (d) Photomicrograph (original magnification, x250; H-E stain) shows infiltration of small, round, blue cells in the periventricular region, adjacent to the frontal horn of the lateral ventricle.

View larger version (146K): [in this window] [in a new window] [Download PPT slide]   Figure 33d.  Thick periventricular enhancement in primary CNS lymphoma in an adult patient with AIDS. (a) Axial nonenhanced CT scan shows a thick rind of periventricular hyperattenuation, with surrounding vasogenic edema. (b) Axial contrast-enhanced CT scan shows abnormal enhancement around both lateral ventricles. This "rind" is much thicker around the right lateral ventricle and involves the same areas that were hyperattenuating before contrast material administration. (c) Photograph of a coronally sectioned gross specimen shows periventricular discoloration around the frontal horns, due to neoplastic lymphocyte infiltration. (d) Photomicrograph (original magnification, x250; H-E stain) shows infiltration of small, round, blue cells in the periventricular region, adjacent to the frontal horn of the lateral ventricle.

View larger version (145K): [in this window] [in a new window] [Download PPT slide]   Figure 34.  Thin periventricular enhancement in cytomegalovirus ependymitis. Two axial gadolinium-enhanced T1-weighted MR images show abnormal enhancement completely surrounding both lateral ventricles. The enhancement is thin and very uniform. Cytomegalovirus causes an inflammation of the ventricular lining and produces ependymitis. (Courtesy of Vince Mathews, MD, University of Indiana, Indianapolis, Ind.)

	Footnotes

 

Abbreviations: CNS = central nervous system, H-E = hematoxylin-eosin, WHO = World Health Organization

The opinions and assertions contained herein are the private views of the authors and are not be construed as official nor as reflecting the views of the Uniformed Services University or the Departments of Defense or Veterans Affairs.

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