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Contributors
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- By Mitchell Aboulafia, Frederick Adams, Marilyn McCord Adams, Robert M. Adams, Laird Addis, James W. Allard, David Allison, William P. Alston, Karl Ameriks, C. Anthony Anderson, David Leech Anderson, Lanier Anderson, Roger Ariew, David Armstrong, Denis G. Arnold, E. J. Ashworth, Margaret Atherton, Robin Attfield, Bruce Aune, Edward Wilson Averill, Jody Azzouni, Kent Bach, Andrew Bailey, Lynne Rudder Baker, Thomas R. Baldwin, Jon Barwise, George Bealer, William Bechtel, Lawrence C. Becker, Mark A. Bedau, Ernst Behler, José A. Benardete, Ermanno Bencivenga, Jan Berg, Michael Bergmann, Robert L. Bernasconi, Sven Bernecker, Bernard Berofsky, Rod Bertolet, Charles J. Beyer, Christian Beyer, Joseph Bien, Joseph Bien, Peg Birmingham, Ivan Boh, James Bohman, Daniel Bonevac, Laurence BonJour, William J. Bouwsma, Raymond D. Bradley, Myles Brand, Richard B. Brandt, Michael E. Bratman, Stephen E. Braude, Daniel Breazeale, Angela Breitenbach, Jason Bridges, David O. Brink, Gordon G. Brittan, Justin Broackes, Dan W. Brock, Aaron Bronfman, Jeffrey E. Brower, Bartosz Brozek, Anthony Brueckner, Jeffrey Bub, Lara Buchak, Otavio Bueno, Ann E. Bumpus, Robert W. Burch, John Burgess, Arthur W. Burks, Panayot Butchvarov, Robert E. Butts, Marina Bykova, Patrick Byrne, David Carr, Noël Carroll, Edward S. Casey, Victor Caston, Victor Caston, Albert Casullo, Robert L. Causey, Alan K. L. Chan, Ruth Chang, Deen K. Chatterjee, Andrew Chignell, Roderick M. Chisholm, Kelly J. Clark, E. J. Coffman, Robin Collins, Brian P. Copenhaver, John Corcoran, John Cottingham, Roger Crisp, Frederick J. Crosson, Antonio S. Cua, Phillip D. Cummins, Martin Curd, Adam Cureton, Andrew Cutrofello, Stephen Darwall, Paul Sheldon Davies, Wayne A. Davis, Timothy Joseph Day, Claudio de Almeida, Mario De Caro, Mario De Caro, John Deigh, C. F. Delaney, Daniel C. Dennett, Michael R. DePaul, Michael Detlefsen, Daniel Trent Devereux, Philip E. Devine, John M. Dillon, Martin C. Dillon, Robert DiSalle, Mary Domski, Alan Donagan, Paul Draper, Fred Dretske, Mircea Dumitru, Wilhelm Dupré, Gerald Dworkin, John Earman, Ellery Eells, Catherine Z. Elgin, Berent Enç, Ronald P. Endicott, Edward Erwin, John Etchemendy, C. Stephen Evans, Susan L. Feagin, Solomon Feferman, Richard Feldman, Arthur Fine, Maurice A. Finocchiaro, William FitzPatrick, Richard E. Flathman, Gvozden Flego, Richard Foley, Graeme Forbes, Rainer Forst, Malcolm R. Forster, Daniel Fouke, Patrick Francken, Samuel Freeman, Elizabeth Fricker, Miranda Fricker, Michael Friedman, Michael Fuerstein, Richard A. Fumerton, Alan Gabbey, Pieranna Garavaso, Daniel Garber, Jorge L. A. Garcia, Robert K. Garcia, Don Garrett, Philip Gasper, Gerald Gaus, Berys Gaut, Bernard Gert, Roger F. Gibson, Cody Gilmore, Carl Ginet, Alan H. Goldman, Alvin I. Goldman, Alfonso Gömez-Lobo, Lenn E. Goodman, Robert M. Gordon, Stefan Gosepath, Jorge J. E. Gracia, Daniel W. Graham, George A. Graham, Peter J. Graham, Richard E. Grandy, I. Grattan-Guinness, John Greco, Philip T. Grier, Nicholas Griffin, Nicholas Griffin, David A. Griffiths, Paul J. Griffiths, Stephen R. Grimm, Charles L. Griswold, Charles B. Guignon, Pete A. Y. Gunter, Dimitri Gutas, Gary Gutting, Paul Guyer, Kwame Gyekye, Oscar A. Haac, Raul Hakli, Raul Hakli, Michael Hallett, Edward C. Halper, Jean Hampton, R. James Hankinson, K. R. Hanley, Russell Hardin, Robert M. Harnish, William Harper, David Harrah, Kevin Hart, Ali Hasan, William Hasker, John Haugeland, Roger Hausheer, William Heald, Peter Heath, Richard Heck, John F. Heil, Vincent F. Hendricks, Stephen Hetherington, Francis Heylighen, Kathleen Marie Higgins, Risto Hilpinen, Harold T. Hodes, Joshua Hoffman, Alan Holland, Robert L. Holmes, Richard Holton, Brad W. Hooker, Terence E. Horgan, Tamara Horowitz, Paul Horwich, Vittorio Hösle, Paul Hoβfeld, Daniel Howard-Snyder, Frances Howard-Snyder, Anne Hudson, Deal W. Hudson, Carl A. Huffman, David L. Hull, Patricia Huntington, Thomas Hurka, Paul Hurley, Rosalind Hursthouse, Guillermo Hurtado, Ronald E. Hustwit, Sarah Hutton, Jonathan Jenkins Ichikawa, Harry A. Ide, David Ingram, Philip J. Ivanhoe, Alfred L. Ivry, Frank Jackson, Dale Jacquette, Joseph Jedwab, Richard Jeffrey, David Alan Johnson, Edward Johnson, Mark D. Jordan, Richard Joyce, Hwa Yol Jung, Robert Hillary Kane, Tomis Kapitan, Jacquelyn Ann K. Kegley, James A. Keller, Ralph Kennedy, Sergei Khoruzhii, Jaegwon Kim, Yersu Kim, Nathan L. King, Patricia Kitcher, Peter D. Klein, E. D. Klemke, Virginia Klenk, George L. Kline, Christian Klotz, Simo Knuuttila, Joseph J. Kockelmans, Konstantin Kolenda, Sebastian Tomasz Kołodziejczyk, Isaac Kramnick, Richard Kraut, Fred Kroon, Manfred Kuehn, Steven T. Kuhn, Henry E. Kyburg, John Lachs, Jennifer Lackey, Stephen E. Lahey, Andrea Lavazza, Thomas H. Leahey, Joo Heung Lee, Keith Lehrer, Dorothy Leland, Noah M. Lemos, Ernest LePore, Sarah-Jane Leslie, Isaac Levi, Andrew Levine, Alan E. Lewis, Daniel E. Little, Shu-hsien Liu, Shu-hsien Liu, Alan K. L. Chan, Brian Loar, Lawrence B. Lombard, John Longeway, Dominic McIver Lopes, Michael J. Loux, E. J. Lowe, Steven Luper, Eugene C. Luschei, William G. Lycan, David Lyons, David Macarthur, Danielle Macbeth, Scott MacDonald, Jacob L. Mackey, Louis H. Mackey, Penelope Mackie, Edward H. Madden, Penelope Maddy, G. B. Madison, Bernd Magnus, Pekka Mäkelä, Rudolf A. Makkreel, David Manley, William E. Mann (W.E.M.), Vladimir Marchenkov, Peter Markie, Jean-Pierre Marquis, Ausonio Marras, Mike W. Martin, A. P. Martinich, William L. McBride, David McCabe, Storrs McCall, Hugh J. McCann, Robert N. McCauley, John J. McDermott, Sarah McGrath, Ralph McInerny, Daniel J. McKaughan, Thomas McKay, Michael McKinsey, Brian P. McLaughlin, Ernan McMullin, Anthonie Meijers, Jack W. Meiland, William Jason Melanson, Alfred R. Mele, Joseph R. Mendola, Christopher Menzel, Michael J. Meyer, Christian B. Miller, David W. Miller, Peter Millican, Robert N. Minor, Phillip Mitsis, James A. Montmarquet, Michael S. Moore, Tim Moore, Benjamin Morison, Donald R. Morrison, Stephen J. Morse, Paul K. Moser, Alexander P. D. Mourelatos, Ian Mueller, James Bernard Murphy, Mark C. Murphy, Steven Nadler, Jan Narveson, Alan Nelson, Jerome Neu, Samuel Newlands, Kai Nielsen, Ilkka Niiniluoto, Carlos G. Noreña, Calvin G. Normore, David Fate Norton, Nikolaj Nottelmann, Donald Nute, David S. Oderberg, Steve Odin, Michael O’Rourke, Willard G. Oxtoby, Heinz Paetzold, George S. Pappas, Anthony J. Parel, Lydia Patton, R. P. Peerenboom, Francis Jeffry Pelletier, Adriaan T. Peperzak, Derk Pereboom, Jaroslav Peregrin, Glen Pettigrove, Philip Pettit, Edmund L. Pincoffs, Andrew Pinsent, Robert B. Pippin, Alvin Plantinga, Louis P. Pojman, Richard H. Popkin, John F. Post, Carl J. Posy, William J. Prior, Richard Purtill, Michael Quante, Philip L. Quinn, Philip L. Quinn, Elizabeth S. Radcliffe, Diana Raffman, Gerard Raulet, Stephen L. Read, Andrews Reath, Andrew Reisner, Nicholas Rescher, Henry S. Richardson, Robert C. Richardson, Thomas Ricketts, Wayne D. Riggs, Mark Roberts, Robert C. Roberts, Luke Robinson, Alexander Rosenberg, Gary Rosenkranz, Bernice Glatzer Rosenthal, Adina L. Roskies, William L. Rowe, T. M. Rudavsky, Michael Ruse, Bruce Russell, Lilly-Marlene Russow, Dan Ryder, R. M. Sainsbury, Joseph Salerno, Nathan Salmon, Wesley C. Salmon, Constantine Sandis, David H. Sanford, Marco Santambrogio, David Sapire, Ruth A. Saunders, Geoffrey Sayre-McCord, Charles Sayward, James P. Scanlan, Richard Schacht, Tamar Schapiro, Frederick F. Schmitt, Jerome B. Schneewind, Calvin O. Schrag, Alan D. Schrift, George F. Schumm, Jean-Loup Seban, David N. Sedley, Kenneth Seeskin, Krister Segerberg, Charlene Haddock Seigfried, Dennis M. Senchuk, James F. Sennett, William Lad Sessions, Stewart Shapiro, Tommie Shelby, Donald W. Sherburne, Christopher Shields, Roger A. Shiner, Sydney Shoemaker, Robert K. Shope, Kwong-loi Shun, Wilfried Sieg, A. John Simmons, Robert L. Simon, Marcus G. Singer, Georgette Sinkler, Walter Sinnott-Armstrong, Matti T. Sintonen, Lawrence Sklar, Brian Skyrms, Robert C. Sleigh, Michael Anthony Slote, Hans Sluga, Barry Smith, Michael Smith, Robin Smith, Robert Sokolowski, Robert C. Solomon, Marta Soniewicka, Philip Soper, Ernest Sosa, Nicholas Southwood, Paul Vincent Spade, T. L. S. Sprigge, Eric O. Springsted, George J. Stack, Rebecca Stangl, Jason Stanley, Florian Steinberger, Sören Stenlund, Christopher Stephens, James P. Sterba, Josef Stern, Matthias Steup, M. A. Stewart, Leopold Stubenberg, Edith Dudley Sulla, Frederick Suppe, Jere Paul Surber, David George Sussman, Sigrún Svavarsdóttir, Zeno G. Swijtink, Richard Swinburne, Charles C. Taliaferro, Robert B. Talisse, John Tasioulas, Paul Teller, Larry S. Temkin, Mark Textor, H. S. Thayer, Peter Thielke, Alan Thomas, Amie L. Thomasson, Katherine Thomson-Jones, Joshua C. Thurow, Vzalerie Tiberius, Terrence N. Tice, Paul Tidman, Mark C. Timmons, William Tolhurst, James E. Tomberlin, Rosemarie Tong, Lawrence Torcello, Kelly Trogdon, J. D. Trout, Robert E. Tully, Raimo Tuomela, John Turri, Martin M. Tweedale, Thomas Uebel, Jennifer Uleman, James Van Cleve, Harry van der Linden, Peter van Inwagen, Bryan W. Van Norden, René van Woudenberg, Donald Phillip Verene, Samantha Vice, Thomas Vinci, Donald Wayne Viney, Barbara Von Eckardt, Peter B. M. Vranas, Steven J. Wagner, William J. Wainwright, Paul E. Walker, Robert E. Wall, Craig Walton, Douglas Walton, Eric Watkins, Richard A. Watson, Michael V. Wedin, Rudolph H. Weingartner, Paul Weirich, Paul J. Weithman, Carl Wellman, Howard Wettstein, Samuel C. Wheeler, Stephen A. White, Jennifer Whiting, Edward R. Wierenga, Michael Williams, Fred Wilson, W. Kent Wilson, Kenneth P. Winkler, John F. Wippel, Jan Woleński, Allan B. Wolter, Nicholas P. Wolterstorff, Rega Wood, W. Jay Wood, Paul Woodruff, Alison Wylie, Gideon Yaffe, Takashi Yagisawa, Yutaka Yamamoto, Keith E. Yandell, Xiaomei Yang, Dean Zimmerman, Günter Zoller, Catherine Zuckert, Michael Zuckert, Jack A. Zupko (J.A.Z.)
- Edited by Robert Audi, University of Notre Dame, Indiana
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- The Cambridge Dictionary of Philosophy
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- 05 August 2015
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- 27 April 2015, pp ix-xxx
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Contributors
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- By Timothy Beach, Steven Bozarth, Palma J. Buttles, Christopher Carr, Dana Cavallaro, James Doyle, Jonathan Flood, Lee Florea, Thomas G. Garrison, Liwy Grazioso Sierra, Robert E. Griffin, Angela Hood, Stephen Houston, Gerald Islebe, John G. Jones, Brian Lane, Zachary Larsen, Sheryl Luzzadder-Beach, Kevin Magee, Timothy Murtha, Carmen E. Ramos, Edwin Román, Payson Sheets, Kenneth B. Tankersley, Richard E. Terry, Kim M. Thompson, Fred Valdez, Eric Weaver, David Webster
- Edited by David L. Lentz, University of Cincinnati, Nicholas P. Dunning, University of Cincinnati, Vernon L. Scarborough, University of Cincinnati
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- Tikal
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- 05 February 2015
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- 23 February 2015, pp xiii-xvi
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Case 3 - Missed intracranial hemorrhage
- from Neuroradiology: extra–axial and vascular
- Edited by Martin L. Gunn
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- Pearls and Pitfalls in Emergency Radiology
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- 05 March 2013
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- 02 May 2013, pp 8-10
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Summary
Imaging description
Traumatic head injuries may result in intraparenchymal, intraventricular, subarachnoid, subdural, or epidural hemorrhage. Acute hemorrhage is characterized by hyperattenuation on CT, and the classic appearances of the various types of hemorrhage are well known. However, certain types of hemorrhage may be overlooked, especially subdural and subarachnoid hemorrhages.
Images from a head CT are routinely reviewed in the axial plane. However, important findings may be missed on axial images alone. In particular, hemorrhages oriented in a horizontal plane are prone to volume-averaging effects which may result in false-negative results. This is especially true of hemorrhages which occur adjacent to bone, such as the floor of the anterior and middle cranial fossae, where volume-averaging with adjacent bone leads to decreased detection (Figure 3.1). This issue is compounded by the fact that hemorrhages have a tendency to occur adjacent to bony structures in certain mechanisms of injury [1].
The addition of coronal and sagittal reformations may improve the diagnostic accuracy by reducing both false-negative and false-positive results (Figure 3.2). A study of 109 patients with intracranial hemorrhage found that the addition of coronal reformations resulted in a change in interpretation in approximately 25% of cases, compared with axial images alone [2].
Another cause of missed hemorrhage involves the use of inappropriate window and level values (Figure 3.3). If the window is too narrow, a small subdural hemorrhage may be difficult to distinguish from the adjacent bone. Optimal values for the window and level will vary among scanners, but a reasonable starting point may be a window of 200 and a level of 50.
Case 17 - Dilated superior ophthalmic vein
- from Neuroradiology: head and neck
- Edited by Martin L. Gunn
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- Pearls and Pitfalls in Emergency Radiology
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- 05 March 2013
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Summary
Imaging description
The superior ophthalmic vein (SOV) is formed by the confluence of the angular, supraorbital, and supratrochlear veins. Anteriorly, it is located medially near the trochlea. As it passes posteriorly, it courses beneath the superior rectus muscle and curves laterally. It passes outside the muscular annulus and enters the cavernous sinus [1, 2]. The vein is valveless throughout its course.
The diameter of the normal SOV ranges from 1 to 2.9 mm as measured on coronal MR images, with a mean diameter of approximately 2 mm [3]. When evaluating an SOV that appears enlarged it is important to assess for symmetry and enhancement characteristics. However, note that mild asymmetry can be normal.
Enlargement of the SOV has been described in several conditions. In the acute setting, enlargement may be caused by a cavernous-carotid fistula (CCF) or increased intracranial pressure (ICP).
A CCF may develop from trauma, surgery, or spontaneously. Fistulas can be described according to the Barrow classification, forming via a direct connection from the internal carotid artery or indirectly via the internal and/or external carotid arteries [4]. Radiologic findings include enlargement of the ipsilateral SOV, often with arterialized enhancement and signal characteristics on CT angiography (CTA) and MR angiography (MRA). The globe is often proptotic (Figure 17.1). Evaluation with conventional angiography is usually required to delineate the sites of fistula formation and for treatment [5].
Case 22 - Pseudosubluxation of C2–C3
- from Section 2 - Spine
- Edited by Martin L. Gunn
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- Pearls and Pitfalls in Emergency Radiology
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- 05 March 2013
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Summary
Imaging description
Pseudosubluxation refers to physiologic anterior spondylolisthesis of C2 on C3, caused by ligamentous laxity and a more horizontal position of the facet joints compared with adults. It is seen in children less than 16 years of age, with most patients less than eight years of age. Rarely, it may be seen in an adult patient [1].
Lateral radiographs will reveal anterior displacement of the C2 vertebral body relative to C3. Displacement is most conspicuous during flexion, and may resolve during extension. A posterior cervical line may be drawn between the anterior cortex of the C1 and C3 posterior arches. This line, referred to as Swischuk’s line, should pass within 2 mm of the anterior cortex of the C2 posterior arch (Figure 22.1) [2]. If it does not, injury should be suspected [3].
CT will reveal similar findings to those seen on radiography. However, one may more confidently exclude a fracture of the axis in the setting of malalignment. If there is concern for ligamentous injury, MRI should be obtained. The absence of ligamentous edema is reassuring, and further suggestive of the normal variant of C2–C3 pseudosubluxation (Figure 22.2).
An important discriminator is the age of the patient. Pseudosubluxation of C2–C3 is much more common in children less than eight years of age. As the age increases beyond eight, this variant becomes much less common. Therefore, if malalignment at C2–C3 is identified in an older child or adult, it should be viewed with a much higher suspicion of injury.
Case 14 - Diffuse axonal injury
- from Neuroradiology: intra-axial
- Edited by Martin L. Gunn
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- Pearls and Pitfalls in Emergency Radiology
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Summary
Imaging description
Diffuse axonal injury (DAI) is caused by shearing forces that occur during rapid acceleration or deceleration of the brain. This results in tearing of the axons. Most lesions are small and multiple. Characteristic locations include the gray–white matter junctions (Figure 14.1), splenium of the corpus callosum, basal ganglia, internal capsules, and dorsolateral brainstem [1, 2].
It has been previously reported that most DAI lesions are non-hemorrhagic. However, both pathologic literature and imaging studies with improved techniques suggest that more lesions are hemorrhagic than previously thought [3]. Lesions may be seen on CT if there is sufficient hemorrhage or edema to produce discernible hyperattenuation or hypoattenuation, respectively. However, CT is very insensitive to the detection of DAI, and this limitation should be realized when imaging a patient with traumatic brain injury.
MRI is more sensitive for the detection of DAI, and will detect many lesions which are not visible on CT [4]. FLAIR and T2-weighted images will depict DAI lesions as foci of increased signal. However, these sequences are also relatively insensitive. Since most blood products are paramagnetic (including deoxyhemoglobin, intracellular methemoglobin, and hemosiderin), they produce susceptibility effect on gradient-recalled echo (GRE) images. GRE images are therefore sensitive to the identification of microhemorrhages and detect more foci of DAI than conventional MRI sequences (Figure 14.2). Susceptibility-weighted imaging (SWI) has been shown to detect even more lesions than GRE images [5].
Case 10 - Pineal cyst
- from Neuroradiology: extra–axial and vascular
- Edited by Martin L. Gunn
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- Pearls and Pitfalls in Emergency Radiology
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- 05 March 2013
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Summary
Imaging description
Pineal cysts are common incidental findings detected on CT and MRI. They are round or oval in shape, and may be unilocular or multilocular. On CT, the cyst will demonstrate hypoattenuation compared with brain parenchyma, and there may be pineal calcifications adjacent to the cyst periphery. Most cysts are 2–15 mm in diameter. Thin-section images and sagittal reformatted images are often helpful in their evaluation (Figures 10.1 and 10.2).
Sometimes it is difficult to confirm the benign nature of a cystic pineal lesion on a routine head CT, so a MRI is obtained. Features of a benign pineal cyst include thin walls and lack of a solid internal component. The cyst walls will normally enhance, but the enhancement should be smooth and linear. The cyst contents will often differ in signal from cerebrospinal fluid (CSF), and FLAIR images often show non-suppression of signal.
High-resolution MR sequences, such as balanced steady state free precession (SSFP) and constructive interference steady state (CISS) sequences, may demonstrate internal architecture such as thin internal septations and smaller internal cysts. These findings should not be viewed as suspicious for malignancy [1].
A cyst may enlarge over time due to hemorrhage or accumulation of fluid. This may result in local mass effect. Compression of the superior colliculus may result in upward gaze palsy (Parinaud syndrome), and effacement of the cerebral aqueduct may lead to obstructive hydrocephalus (Figure 10.3). Thus, it is important to assess the relationship of the cyst to adjacent structures, specifically the tectal plate and cerebral aqueduct.
Case 2 - Non-aneurysmal perimesencephalic subarachnoid hemorrhage
- from Neuroradiology: extra–axial and vascular
- Edited by Martin L. Gunn
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- Pearls and Pitfalls in Emergency Radiology
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Summary
Imaging description
Most cases of non-traumatic subarachnoid hemorrhage (SAH) are caused by aneurysm rupture. However, approximately 15% of patients will have no identifiable cause on CT angiography (CTA). In these patients, it is important to assess the pattern of SAH.
A subset of patients with CTA-negative SAH will have a pattern known as non-aneurysmal perimesencephalic subarachnoid hemorrhage (NAPH) (Figure 2.1). Criteria have been established for this, and include the following [1, 2]:
Subarachnoid hemorrhage within the perimesencephalic cisterns, centered anterior to the midbrain.
Possible extension into the posterior aspect of the anterior interhemispheric fissure, but not completely filling the anterior interhemispheric fissure.
Possible extension into the medial aspects of the Sylvian fissures, but no extension laterally within the fissures (Figure 2.2).
Possible small amounts of layering intraventricular hemorrhage sedimentation, but no frank intraventricular hemorrhage.
No intraparenchymal hemorrhage.
Case 7 - Blunt cerebrovascular injury
- from Neuroradiology: extra–axial and vascular
- Edited by Martin L. Gunn
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Case 18 - Orbital fractures
- from Neuroradiology: head and neck
- Edited by Martin L. Gunn
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Summary
Imaging description
Blunt trauma to the orbit often results in an orbital wall fracture. The predominant fracture patterns are different between adults and pediatric patients. In adults, the medial orbital wall and the orbital floor are the most common sites of fracture (Figure 18.1). In children, especially those less than seven years of age, the most common orbital fracture involves the orbital roof. This is explained by the prominence of the frontal bone relative to the size of the face in children. Also, the frontal sinus does not develop until the age of seven years; thus, there is lack of the normal cushioning effect from the sinus, and frontal bone fractures tend to extend into the orbital roof [1].
A trapdoor fracture may occur in children and young adults (Figure 18.2). In this type of injury a linear orbital floor fracture results in inferior bony displacement. However, due to the elasticity of the floor, the bone fragment swings back to the normal position in a hinge-like manner. These types of fractures may be subtle, but they are associated with a high rate of tissue entrapment [2]. If there is any evidence of orbital fat inferior to the orbital floor, a fracture must be presumed present. Another useful finding is hemorrhage within the maxillary sinus, which is often but not always associated with an orbital floor fracture (Figure 18.3).
Case 16 - Globe injuries
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- Edited by Martin L. Gunn
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- Pearls and Pitfalls in Emergency Radiology
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Summary
Imaging description
Globe injuries often present with subtle or confusing appearances on CT. A systematic approach is useful, paying particular attention to the anterior chamber, the lens, the vitreous body, the shape of the globe, and the presence of foreign objects.
The anterior chamber should be scrutinized with respect to size and attenuation. Decreased depth of the anterior chamber may be caused by a full-thickness corneal laceration or by anterior dislocation of the lens (Figure 16.1). Increased depth of the anterior chamber may be seen with a posterior globe rupture [1]. The change in depth may be subtle, and it is most helpful to compare with the contralateral globe. Increased attenuation within the anterior chamber indicates the presence of hemorrhage, known as a hyphema (Figures 16.2 and 16.3).
Injury to the zonular attachments of the lens may result in posterior (more common) or anterior lens dislocation, and dislocations may be partial. Trauma to the lens capsule may result in the influx of fluid, leading to hypoattenuation of the lens; this is known as a traumatic cataract (Figure 16.4).
The posterior chamber may rupture, producing deformity along the posterior margin of the globe. There may also be detachment of the vitreous, choroid, or retina (Figure 16.5). Each type of detachment demonstrates a different morphology. Vitreous detachment usually begins posteriorly and crosses the optic disk. Choroid detachment extends anteriorly to the margin of the lens, and diverges posteriorly as it approaches the optic disk (Figure 16.6). Retinal detachment extends anteriorly to the ora serrata, and converges posteriorly on the optic disk (Figure 16.7).
Case 4 - Pseudo-subarachnoid hemorrhage
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- Edited by Martin L. Gunn
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- Pearls and Pitfalls in Emergency Radiology
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Summary
Imaging description
Pseudo-subarachnoid hemorrhage (pseudo-SAH) refers to increased attenuation within the basal cisterns and subarachnoid spaces that mimics subarachnoid hemorrhage (SAH), but has a different etiology. The causes of pseudo-SAH include diffuse cerebral edema, meningitis, and intrathecal contrast [1].
Diffuse cerebral edema is the most common cause of pseudo-SAH. Cerebral edema leads to decreased attenuation of the brain parenchyma. There is also compression of the dural venous sinuses, which may lead to venous congestion and engorgement of the superficial veins. The combination of decreased brain attenuation and venous engorgement is postulated to be the etiology of pseudo-SAH in the setting of cerebral edema (Figure 4.1) [2].
The measured attenuation of the subarachnoid spaces will be lower than that seen with true SAH. Venous engorgement will demonstrate attenuation coefficients of 30–42HU. SAH will demonstrate higher attenuation. Therefore, if accurate measurements can be made, the distinction of pseudo-SAH from true SAH can be made in the setting of cerebral edema [3]. When cerebral edema is caused by a hypoxic event, there may be loss of the gray–white matter differentiation, especially involving the basal ganglia (Figure 4.2).
Exudative meningitis leads to increased protein content within the subarachnoid space. This may rarely produce a pattern of pseudo-SAH [4]. Similar findings may be seen along the pachymeninges (Figure 4.3).
Case 6 - Ventricular enlargement
- from Neuroradiology: extra–axial and vascular
- Edited by Martin L. Gunn
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- Pearls and Pitfalls in Emergency Radiology
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Summary
Imaging description
Enlarged ventricles can be caused by hydrocephalus or parenchymal loss. Hydrocephalus is classified as non-communicating (obstructive) or communicating. It is important to try and distinguish among these different patterns, as this will direct further workup and management.
Non-communicating hydrocephalus results from obstruction of the ventricular outflow of cerebrospinal fluid (CSF). Frequent causes include neoplasms, aqueductal stenosis, and intraventricular hemorrhage. The site of obstruction can be implied by which ventricles are enlarged.
Communicating hydrocephalus usually results from obstruction of CSF resorption at the arachnoid granulations. Less common causes include overproduction of CSF and compromised venous outflow. Normal-pressure hydrocephalus (NPH) is a specific form of communicating hydrocephalus which is associated with the clinical triad of dementia, ataxia, and urinary incontinence.
Hydrocephalus may lead to transpendymal edema, caused by transpendymal resorption of CSF. This will produce a rim of decreased attenuation (CT) or high T2/FLAIR signal (MRI) around the lateral ventricles (Figure 6.1). This usually indicates an acute enlargement of the ventricles [1].
Some apparent cases of communicating hydrocephalus are caused by fourth ventricular outflow obstruction. An apparent obstructive lesion may not be evident; CT and conventional MRI may miss small webs which obstruct outflow at the foramina of Luschka and Magendie. The addition of 3D constructive interference in the steady state (CISS) images may allow for improved detection of small membranes at the suspected site of obstruction (Figure 6.2) [2].
Case 5 - Arachnoid granulations
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- Edited by Martin L. Gunn
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- Pearls and Pitfalls in Emergency Radiology
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Imaging description
Arachnoid villi represent the normal sites of cerebrospinal fluid (CSF) resorption from the subarachnoid space into the venous sinuses. The villi are not visible radiologically, but they may enlarge over time due to distension with CSF. This causes progressive penetration of the arachnoid membrane into the dura, beneath the vascular endothelium of the venous sinus. The result is formation of an arachnoid granulation. These granulations tend to increase in size and number with age.
Arachnoid granulations are most commonly located within the transverse sinuses, superior sagittal sinus, and parasagittal venous lacunae [1]. They usually range in size from 2 to 8 mm [2], though may be larger than 10 mm at which time they are referred to as “giant” arachnoid granulations.
Contrast-enhanced CT demonstrates a round or oval filling defect within a dural venous sinus. An arachnoid granulation typically occurs where a superficial vein drains into the venous sinus, which is thought to induce a focal weakness in the sinus wall. There may be a smooth corticated erosion of the adjacent calvarium. A granulation will never demonstrate hyperattenuation on non-enhanced CT, unlike dural venous sinus thrombosis, which commonly demonstrates increased attenuation (Figures 5.1 and 5.2).
Usually, an arachnoid granulation will follow CSF signal on all MR sequences (Figure 5.3) [3]. However, several studies have demonstrated that this rule does not always hold true, especially with giant granulations. For instance, the signal may be higher than CSF on both T1- and T2-weighted images, and suppression on FLAIR images may be incomplete. In these cases, the characteristic shape, location, and lack of solid enhancement are helpful clues to the correct diagnosis [4].
Case 19 - Variants of the upper cervical spine
- from Section 2 - Spine
- Edited by Martin L. Gunn
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- Book:
- Pearls and Pitfalls in Emergency Radiology
- Published online:
- 05 March 2013
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- 02 May 2013, pp 69-71
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Summary
Imaging description
There are several skeletal variants of the C1 and C2 vertebrae which may be confused with injury. Knowledge of the normal development of these vertebrae is essential for distinguishing anatomic variants from pathology.
The atlas typically develops from three primary ossification centers: one anterior arch and two neural arches. Two neurocentral synchondroses separate the anterior arch from the neural arches (Figure 19.1). A single posterior synchondrosis separates the neural arches. The atlas is normally fused by eight years of age [1].
The axis typically develops from five primary ossification centers: two odontoid centers, two neural arches, and one centrum. The odontoid centers usually fuse prior to birth (Figure 19.2). The remaining primary centers are usually fused by six years of age. A secondary center of ossification, known as the os terminale, forms at the odontoid tip and usually fuses by 12 years of age [2].
Incomplete fusion of the atlas may result in a cleft, usually at the site of a synchondrosis. The cleft will usually demonstrate a smooth margin at a characteristic location, and should not be mistaken for a fracture (Figure 19.3). If there is non-development of the anterior arch, the neural arches may overgrow and attempt to fuse anteriorly, resulting in an anterior midline cleft (Figure 19.4).
Case 15 - Orbital infection
- from Neuroradiology: head and neck
- Edited by Martin L. Gunn
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- Book:
- Pearls and Pitfalls in Emergency Radiology
- Published online:
- 05 March 2013
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- 02 May 2013, pp 56-59
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Summary
Imaging description
The evaluation of an orbital infection should seek to define the extent of infection, the source of infection, and the presence of complications.
An imperative distinction is preseptal (periorbital) versus postseptal (orbital) cellulitis. The orbital septum is a thin fibrous layer of the eyelids that blends with the periosteum of the bony orbit. The septum cannot be specifically delineated on conventional imaging, but its position can be inferred. Inflammatory changes posterior to the septum, such as fat stranding, muscle enlargement, and abscess formation, imply the presence of orbital cellulitis (Figures 15.1 and 15.2). Inflammatory changes entirely anterior to the septum are classified as periorbital cellulitis [1].
The most common cause of an orbital infection is sinusitis, especially of the ethmoid sinus. Therefore, the sinuses should be scrutinized for signs of inflammation (Figure 15.1). Infection spreads through the bony walls via perivascular routes [2]. Other sources of infection include orbital foreign objects, adjacent dermal infection, and septicemia. An uncommon source is odontogenic infection (Figures 15.3 and 15.4), which usually arises from the maxillary dentition and spreads through the paranasal sinuses, premaxillary tissues, or infratemporal fossa. The most common signs of dental infection include periapical lucency, indistinctness of the lamina dura, and widening of the periodontal ligament space [3].
Contributors
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- By Phillip L. Ackerman, Soon Ang, Susan M. Barnett, G. David Batty, Anna S. Beninger, Jillian Brass, Meghan M. Burke, Nancy Cantor, Priyanka B. Carr, David R. Caruso, Stephen J. Ceci, Lillia Cherkasskiy, Joanna Christodoulou, Andrew R. A. Conway, Christine E. Daley, Janet E. Davidson, Jim Davies, Katie Davis, Ian J. Deary, Colin G. DeYoung, Ron Dumont, Carol S. Dweck, Linn Van Dyne, Pascale M. J. Engel de Abreu, Joseph F. Fagan, David Henry Feldman, Kurt W. Fischer, Marisa H. Fisher, James R. Flynn, Liane Gabora, Howard Gardner, Glenn Geher, Sarah J. Getz, Judith Glück, Ashok K. Goel, Megan M. Griffin, Elena L. Grigorenko, Richard J. Haier, Diane F. Halpern, Christopher Hertzog, Robert M. Hodapp, Earl Hunt, Alan S. Kaufman, James C. Kaufman, Scott Barry Kaufman, Iris A. Kemp, John F. Kihlstrom, Joni M. Lakin, Christina S. Lee, David F. Lohman, N. J. Mackintosh, Brooke Macnamara, Samuel D. Mandelman, John D. Mayer, Richard E. Mayer, Martha J. Morelock, Ted Nettelbeck, Raymond S. Nickerson, Weihua Niu, Anthony J. Onwuegbuzie, Jonathan A. Plucker, Sally M. Reis, Joseph S. Renzulli, Heiner Rindermann, L. Todd Rose, Anne Russon, Peter Salovey, Scott Seider, Ellen L. Short, Keith E. Stanovich, Ursula M. Staudinger, Robert J. Sternberg, Carli A. Straight, Lisa A. Suzuki, Mei Ling Tan, Maggie E. Toplak, Susana Urbina, Richard K. Wagner, Richard F. West, Wendy M. Williams, John O. Willis, Thomas R. Zentall
- Edited by Robert J. Sternberg, Oklahoma State University, Scott Barry Kaufman, New York University
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- Book:
- The Cambridge Handbook of Intelligence
- Published online:
- 05 June 2012
- Print publication:
- 30 May 2011, pp xi-xiv
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