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Patterns Contrast Enhancement

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Patterns Contrast Enhancement

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Department of Radiology and Radiological Sciences Uniformed Services University of the Health Sciences 4301 Jones Bridge Road Bethesda, Maryland 20814 301-295-3145

Ring Enhancing Lesions


James G. Smirniotopoulos, M.D. Professor of Radiology and Neurology Chairman, Department of Radiology and Nuclear Medicine Uniformed Services University of the Health Sciences 4301 Jones Bridge Road Bethesda, MD 20814 Voice: 301-295-3145 FAX: 301-295-3893 Email: jsmirnio@usuhs.mil Visit us on the WEB at: http://rad.usuhs.edu

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DISCLAIMER: The opinions expressed herein are those of the author(s), and are not necessarily representative of the Uniformed Services University of the Health Sciences (USUHS), the Department of Defense (DOD); or the World Health Organization (WHO). Medicine is a constantly changing field, and medical information is subject to frequent correction and revision. Therefore the reader is entirely responsible for verifying the accuracy and relevance of the information contained herein. Portions copyright 1997-2000 James G. Smirniotopoulos, M.D.

Contrast enhancement occurs primarily because of a relative increase i blood volume or blood flow and/or from an abnormal increase in permeability due to an absence of the blood-brain-barrier (BBB). Ring enhancing lesions represent a special subset of contrast enhancing abnormalities.

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Patterns Contrast Enhancement

http://rad.usuhs.edu/rad/handouts/jsmirnio/ring...

CONTRAST ENHANCEMENT Vascularity Permeability The popular mnemonic for ring-enhancing lesions is: M - Metastasis, MS A - Abscess (also cerebritis) G - Glioblastoma, Granuloma I -Infarct (esp. Basal ganglia) C - Contusion (rare) A - AIDS (Toxo, etc.) L - Lymphoma (in aids) D - Demyelination (active) R - Resolving hematoma, Radiation change (necrosis)

The primary characteristic of ring-enhancing lesions is that the center i composed of avascular tissue (dead or dying neoplastic tissue), old blo infected and necrotic brain (abscess and cerebritis), tumor secreted flu normal tissue adjacent to bands or rings of abnormal tissue. Therefore or more of the following is usually present:

Necrotic (dead) tissue (neoplasm, radiation necrosis, old infarction) Hemorrhage (blood old or new) Cyst fluid (craniopharyngioma, pilocytic astrocytoma, hemangioblastoma Pus (abscess) Normal tissue (reparative phase of demyelination)
Demyelinating Disease

One of the more complex causes of a ring-enhancing lesion is demyelinating disease. The most common and therefore classic example is multiple sclerosis The underlying lesion in MS is a perivascular inflammatory process associated w destruction and removal of pre-existing normal myelin. During the active phas inflammation, there is a transient disruption of the blood-brain-barrier. Howev since this occurs in the white matter, which is relatively sparsely vascularized (compared to gray matter) the extravasation of contrast is relatively limited an usually not accompanied by perilesional edema. Usually, for a self-limited perio 4-8 weeks, there is limited contrast enhancement in a ring pattern. The ring enhancing area is the advancing zone of inflammation; the center is a region of demyelination with reinstatement of the integrity of the BBB; and on the outsid normal brain not yet affected the process. Because the process is perivascular, of the characteristic lesions of MS (that usually doesn't enhance) is the periven inflammation around the small veins that run perpendicular to the lateral marg the lateral ventricles - these are the "Dawson fingers" of demyelination.
Abscess and Cerebritis

Acute pyogenic infections of the CNS first cause cerebritis (the brain's version o cellulitis) that then proceeds to an organized abscess. First the infection goes unchecked. Then, the blood-brain-barrier is disrupted, allowing inflammatory c (polymorphonuclear leukocytes) and proteins (antibiodies) to leave the bloodst and cross into the brain. As the infection and the immune reaction lead to necr there is a proliferation of capillaries and fibroblasts that will begin to form a wa separate the infection and dead brain from the normal tissue. The reactive pro usually creates, both pathologically and radiologically, a uniform rim of hypervascular connective tissue (granulation tissue) that has a relative uniform smooth inner and outer margin. The abscess wall is usually of almost uniform thickness, although the white matter side of the abscess is usually thinner than gray matter side. An abscess wall is invariably less than 10 mm in maximal

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thickness.

http://rad.usuhs.edu/rad/handouts/jsmirnio/ring...

CONTRAST ENHANCEMENT Ring Lesion Features For Infection ORGANIZED ABSCESS thin and uniform wall (3-7 mm.) smooth inner margin does not "fill in" on CT, MR? CEREBRITIS (infection w/o organization): variable wall (may be smooth) smooth/variable inner margin has "fill-in" on DDD (w/o fluid level)

CONTRAST ENHANCEMENT Abscess 2 - 4 wks. for ORGANIZED WALL 2 LAYERS MESENCHYMAL (capillaries, fibroblasts, collagen) ASTROGLIAL (reactive astrocytes) WALL facing GM is well formed 3-7 mm WALL FACING WM IS THINNER/WEAKER Daughter Abscess Ventricular Spill ("pyocephalus")

Neoplastic Ring Enhancing Lesions

Neoplastic ring lesions can occur with both benign 'cystic' tumors as well as wit aggressive malignant masses. Highly aggressive malignant tumors are often complicated by necrosis - usually central necrosis. Necrosis is usually a progre irregular haphazard and heterogeneous process. Malignant rings are usually unilocular or multilocular heterogeneous enhancing masses with rims that vary considerable from thin to thick and typically have a very shaggy inner margin. Usually, these features allow necrotic malignant tumors (e.g. glioblastoma multiforme) to be distinguished from more benign inflammatory lesions like an abscess. Unfortunately, benign fluid producing tumors can also become ring-enhancing masses. It may be difficult to distinguish these benign tumors malignant ones by imaging alone. However, adding in location and patient age be very helpful. Pilocytic astrocytoma, pleomorphic xanthoastrocytoma, and ganglioglioma usually present in childhood. Pilocytic astrocytoma usually prese the cerebellum. Pleomorphic xanthoastrocytoma usually occurs in very young children and is usually very superficial. Ganglioglioma also present in young pa (children and adult) in the temporal lobe. Hemangioblastoma usually presents cerebellum. CONTRAST ENHANCEMENT Ring Lesion Features For Neoplasm NECROTIC NEOPLASM: thick and irregular wall shaggy inner margin (usually) may "fill in" heterogeneously on delayed images these are usually aggressive and malignant tumors CYSTIC NEOPLASM: thin wall +/- MURAL NODULE PART OF WALL MAY NOT ENHANCE smooth inner margin uniform fluid enhancement or FLUID LEVEL these are often benign and/or low-grade tumors

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Ring enhancing infarct

Ring enhancement in an infarct is very rare. However, when an infarct involves deep gray matter - like the basal ganglia - the shape of the enhancing gray ma will create a ring lesion. CONTRAST ENHANCEMENT Hematoma EARLY: Hyperdense, round/oval Homogeneous mass of RBC's Proportional mass effect for volume Edema "Halo", not spreading LATER: Iso-/Hypodense, smaller Reactive capillaries form outside Uniform rim of enhancement May see "vasogenic" edema

Post Operative Ring Enhancement

CONTRAST ENHANCEMENT Post-Operative RESIDUAL TUMOR (left behind) RECURRENT TUMOR (grew back) INFECTION NORMAL POSTOPERATIVE CHANGE (surgical trauma, healing) RADIATION Tx.?

References

1. Aoki S, Sasaki Y, Machida T, and Tanioka H. Contrast-Enhanced Images in Patients with Meningioma: Importance of Enhancemen the Dura Adjacent to the Tumor. AJNR 1990;11935-938.

2. Bourekas EC, Lewin JS, and Lanzieri CF. Case Report: Postcontr Meningeal MR Enhancement Secondary to Intracranial Hypotensi Caused by Lumbar Puncture. J Comput Assist Tomogr 1995;19(2):299-301.

3. Cairncross JG, Pexman JHW, Rathbone MP, and DelMaestro RF. Postoperative Contrast Enhancement in Patients with Brain Tumo Ann Neurol 1985;17570-572.

4. Caellas AR, Lpez MC, Isern EG, and Gaern XM. Postcontras Dural MR Enhancement and Acute CSF Intracranial Hypotension. J Comput Assist Tomogr 1995;19(6):1008-1009.

5. Chamberlain MC, Sandy AD, Press GA. Leptomeningeal metasta comparison of gadolinium-enhanced MR and contrast-enhanced C the brain. Neurology 1990;40:435-8.

6. DeLaPaz RL. Advances in brain tumor diagnostic imaging. Curr Neurol 1995;8:430-6.

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7. Gado M, Phelps M, Coleman R. An extravascular component of contrast enhancement in cranial computed tomography. Radiolog 1975;177:589-3.

8. Gupta S, Gupta RK, Banerjee D, Gujral RB. Problems with the d tail sign. Neuroradiology 1993;35:541-2. 9. Kramer R, Janetos G, Perlstein G. An approach to contrast enhancement in computed tomography of the brain. Radiol 1975;16:641-7.

10. Laohaprasit V, Silbergeld DL, Ojemann GA, Eskridge JM, and W HR. Postoperative CT Contrast Enhancement Following Lobectom Epilepsy. J Neurosurg 1990;73392-395.

11. Latchaw RE, Gold LHA, and Torrije EJ. A protocol for the use o contrast enhancement in cranial computed tomography. Radiology 1978;126681-687.

12. Messina AV. Computed Tomography: Contrast Enhancement in Resolving Intracerebral Hemorrhage. Am J Roentgenol 1976;1271050-1052.

13. Mittl Jr. RL and Yousem DM. Frequency of Unexplained Menin Enhancement in the Brain after Lumbar Puncture. AJNR Am J Neuroradiol 1994;15633-638.

14. Nagele T, Petersen D, Klose U, Grodd W, Opitz H, Voigt K. The tail adjacent to meningiomas studied by dynamic contrast-enhan MRI: a comparison with histopathology. Neuroradiology 1994;36:303-7.

15. Paakko E, Patronal N, Schellinger D. Meningeal Gd-DTPA enhancement in patients with malignances. J of computer assiste tomography 1990;14:542-6.

16. Phillips M, Ryals T, Kambhu S, Yuh W. Neoplastic vs inflamma meningeal enhancement with Gd-DTPA. J of computer assisted tomography 1990;24:536-41.

17. Pullicino P and Kendall BE. Contrast Enhancement in Ischaem Lesions. Neuroradiol 1980;19235-239. 18. Senegor M. Prominent meningeal tail sign in a patient with a metastatic tumor. Neurosurg 1991;29:294-6.

19. Steinhoff H, Aviles C. Contrast enhancement response of intracranial neoplasms: its validity for the differential diagnosis o tumors in CT, in Lanksch, W, Kazner E. (eds): Cranial conputerize tomography. New york, springre-Verlag 1976;151-61.

20. Tien RD, Yang PJ, Chu PK. Dural tail sign: a specific MR sign fo meningioma? J Comput Assist Tomogr 1991;15:64-6.

21. Tokumaru A, O'uchi T, Eguchi T, Kawamoto S, Kokubo T, Suzu and Kameda T. Prominent Meningeal Enhancement Adjacent to Meingioma on Gd-DTPA-enhanced MR Images: Histopathologic Correlation. Radiology 1990;175431-433.

22. Tokumaru A, O'uchi T, Eguchi T, Kawmoto S, Kokubo T, Suzuk Kameda T. Prominent meningeal enhancement adjacent to meningioma on go-DTPA-enhanced MR Images. Histopathologic Correlation. Radiology 1990;175:431-3.

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23. Wilms G, Lammens M, Marchal G, Demaerel P, Verplancke J, V Calenbergh J, Goffin J, Plets C, and Baert AL. Prominent Dural Enhancement Adjacent to Nonmeningiomatous Malignant Lesions Contrast Enhanced MR Images. AJNR Am J Neuroradiol 1991;12761-764.

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