DOI: 10.1148/rg.272065155
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.
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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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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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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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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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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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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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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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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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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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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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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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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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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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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.
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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.
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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.
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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.
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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.
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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 (*).
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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).
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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.
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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.
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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.
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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).
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.)
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Copyright © 2007 by the Radiological Society of North America.
