2005 Proceedings - ASNR

2005 Proceedings - ASNR

2005 Proceedings - ASNR


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<strong>2005</strong><br />


43 rd Annual Meeting<br />

May 23-27, <strong>2005</strong><br />

Metro Toronto Convention Centre<br />

Toronto, Ontario, Canada<br />

American Society<br />

of Neuroradiology<br />

<strong>2005</strong> <strong>Proceedings</strong> includes<br />

Interactive CD-ROM

<strong>ASNR</strong><br />

American Society of Neuroradiology<br />

Dear Colleagues,<br />

The <strong>ASNR</strong> 43nd Annual Meeting and NER Symposium <strong>2005</strong> breaks new ground in attendance and programming.<br />

Patricia A. Hudgins, M.D., President-Elect/Program Chair, has collected topical and important educational and<br />

scientific sessions. Thje meeting covers the clinical and technological developments important for our practice and<br />

the Symposium provides an excellent review of head and neck imaging in cancer.<br />

The Annual Meeting has over 40 Focus Sessions developed in cooperation with the American Society of Functional<br />

Neuroradiology (ASFNR), American Society of Head and Neck Radiology (ASHNR), American Society of Pediatric<br />

Neuroradiology (ASPNR), American Society of Interventional and Therapeutic Neuroradiology (ASITN) and the<br />

American Society of Spine Radiology (ASSR), covering a wide range of topics of interest for both the sub-specialist<br />

in neuroradiology as well as the general neuroradiologist. I wish to extend a special thanks to the following<br />

Co-Chairs for their efforts in organizing the programming for the following specialty areas:<br />

American Society of Functional Neuroradiology (ASFNR) ..............................................Andrei I Holodny, M.D.<br />

American Society of Head and Neck Radiology (ASHNR)..............................................Roy A. Holliday, M.D.<br />

American Society of Interventional and Therapeutic Neuroradiology (ASITN) ............John D. Barr, M.D.<br />

American Society of Pediatric Neuroradiology (ASPNR) .................................................Marvin D. Nelson, M.D.<br />

American Society of Spine Radiology (ASSR) ...................................................................Gordon K. Sze, M.D.<br />

Other program highlights include the Advanced Imaging Seminars providing an in-depth look at advanced imaging<br />

techniques (perfusion, diffusion, spectroscopy, parallel and high field imaging), a Research Grant Writing Seminar,<br />

Expanded ELC Workshop and Lectures, National Library of Medicine (NLM) workshops, the successful breakfast,<br />

lunch and reception, How-To Sessions and new this year the <strong>ASNR</strong> Business Center sessions. Don’t miss the<br />

Wednesday morning Special Session: Surviving Change: Neuroradiology Practice.<br />

The annual meeting provides a unique opportunity to gain a better understanding of how the <strong>ASNR</strong> functions<br />

to assist the practice of neuroradiology during a time of rapid change.<br />

The meeting also provides excellent opportunities to renew old friendships and make new ones, join the Welcome<br />

Reception with Technical Exhibitors on Monday evening and see a portrait of neuroradiology as seen by the<br />

performing artists of the Second City Toronto Comedy Troupe.<br />

See Toronto, join a dinner tour and sample the optional tour programs during your stay.<br />

On behalf of the entire Executive Committee, welcome to Toronto, Ontario, Canada for the NER Foundation<br />

Symposium <strong>2005</strong> and <strong>ASNR</strong> 43rd Annual Meeting where advanced technology, clinical imaging and interventional<br />

neuroradiological excellence come together.<br />

Sincerely,<br />

Victor M. Haughton, M.D.<br />

<strong>ASNR</strong> President<br />


<strong>ASNR</strong> <strong>2005</strong>

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How to use your <strong>Proceedings</strong> CD-Rom (continued)<br />

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Table of Contents Addendum NeuroNews<br />

II..................................................................................2004 - <strong>2005</strong> <strong>ASNR</strong> Executive Committee<br />

II – III............................................2004 - <strong>2005</strong> <strong>ASNR</strong> Annual Meeting Arrangements Committees<br />

IV ....................................................................................................................<strong>ASNR</strong>/AJNR Staff<br />

V – VI ......................................................................<strong>ASNR</strong> 43rd Annual Meeting Invited Speakers<br />

VII....................................................................................................................All About Toronto<br />

VII ..........................................................................................................Walking Map of Toronto<br />

VIII – XI ..................................................................Metro Toronto Convention Centre Floor Plans<br />

XIII – XIV ............................................Scientific Posters and Scientific Exhibits (Printed and Electronic)<br />

XV – XVII ........................................................................................................Technical Exhibits<br />

XVIII – XX ....................................................................................................General Information<br />

XXI..........................................................................................Social Program and Optional Tours<br />

XXII ..................................................................................................................Guest Hospitality<br />

XXIII ........................................................................................................Future <strong>ASNR</strong> Meetings<br />

XXIII ....................................................................................<strong>ASNR</strong> Past Presidents and Founders<br />

XXIV – XXV ........................................................................................Past Meetings of the <strong>ASNR</strong><br />

XXVI ..............................................................................<strong>2005</strong> <strong>ASNR</strong> Gold Medal Award Recipient<br />

XXVII ............................................................................Past <strong>ASNR</strong> Gold Medal Award Recipients<br />

XXVII ............................................................................................<strong>2005</strong> <strong>ASNR</strong> Honorary Member<br />

XXVIII ............................................................................Past <strong>ASNR</strong> Honorary Member Recipients<br />

XXVIII ....................................................................2004 <strong>ASNR</strong> Outstanding Presentation Awards<br />

XXIX ............................................................................2004 Regional Society Best Paper Awards<br />

XXIX ........<strong>2005</strong> NER Foundation Award for Outstanding Contributions in Research Award Recipient<br />

XXIX ..........Past NER Foundation Award for Outstanding Contributions in Research Award Recipient<br />

XXX......................<strong>2005</strong>-2006 Berlex/NER Foundation Fellowship in Basic Science Research Award<br />

XXX – XXXI ......Past Berlex/NER Foundation Fellowship in Basic Science Research Award Recipients<br />

XXXII ..................................NER Foundation Scholar Award in Neuroradiology Research Recipients<br />

XXXII............................................Past NER Foundation Scholar Award in Neuroradiology Research<br />

XXXII ........<strong>2005</strong> NER Foundation/Boston Scientific Fellowship in Cerebrovascular Disease Research<br />

XXXIII ......................NER Foundation Outcomes Research Grant Related to Neuroradiology Imaging<br />

XXXIII ............................................................................<strong>2005</strong> Cornelius G. Dyke Memorial Award<br />

XXXIII – XXXIV ........................................Past <strong>ASNR</strong> Cornelius G. Dyke Memorial Award Recipients<br />

XXXV – XXXVI................................................<strong>ASNR</strong> 43rd Annual Meeting Accreditation Statement,<br />

Educational Objectives, and Target Audience<br />

XXXVI – XXXVIII ............................Electronic Learning Center (ELC) <strong>2005</strong> Workshops and Lectures<br />

XXXIX ....................................................................National Library of Medicine (NLM) Workshops<br />

XXXIX ......................................................................................................<strong>ASNR</strong> Business Center<br />

XXXIX..........................................................................................Research Grant Writing Seminar<br />

XL ....................................................................................................................How-To Sessions<br />

XLI – XLVI ........................................................................................Scientific Program Overview<br />

Page 1..............................................................................................................Monday Sessions<br />

Page 67............................................................................................................Tuesday Sessions<br />

Page 139 ....................................................................................................Wednesday Sessions<br />

Page 183 ........................................................................................................Thursday Sessions<br />

Page 255 ............................................................................................................Friday Sessions<br />

Page 285 ........................................................................................................Scientific Posters<br />

Page 385 ..........................................................................................Scientific Exhibits (Printed)<br />

Page 427................................................................................Electronic Scientific Exhibits (eSE)<br />

Page 447........................................................................................Index of Program Participants<br />

I<br />

Toronto, Canada Canada

May 21-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

II<br />


2004-<strong>2005</strong> <strong>ASNR</strong> Executive Committee<br />

Victor M. Haughton, MD<br />

President<br />

Patricia A. Hudgins, MD<br />

President-Elect/Program Chair<br />

Robert I. Grossman, MD<br />

Vice President<br />

M. Judith Donovan Post, MD, FACR<br />

Treasurer<br />

John R. Hesselink, MD, FACR<br />

Secretary<br />

James M. Provenzale, MD<br />

Member-at-Large<br />

Howard A. Rowley, MD<br />

Research Committee Chair<br />

Andrei I. Holodny, MD<br />

Functional Representative<br />

Vijay M. Rao, MD<br />

Head and Neck Representative<br />

Gary R. Duckwiler, MD<br />

Interventional Representative<br />

Marvin D. Nelson, MD<br />

Pediatric Representative<br />

Gordon K. Sze, MD<br />

Spine Representative<br />

Charles M. Strother, MD<br />

First Past-President<br />

Patrick A. Turski, MD<br />

Second Past-President<br />

William P. Dillon, MD<br />

Third Past-President<br />

J. Arliss Pollock, MD<br />

Clinical Practice Committee Chair<br />

James G. Smirniotopoulos, MD<br />

Education Committee Chair<br />

Charlotte H. Rydberg, MD<br />

Rules Committee Chair<br />

Mauricio Castillo, MD<br />

Publications Committee Chair<br />

Andrew W. Litt, MD<br />

AMA Delegate<br />

Kelly K. Koeller, MD<br />

ACR Representative<br />

Robert R. Lukin, MD<br />

ABR Representative<br />

Glenn S. Forbes, MD, FACR<br />

ABR Representative<br />

William G. Bradley, MD<br />

ACR Neuro/MRI Commission Liaison<br />

James B. Gantenberg, CHE<br />

<strong>ASNR</strong> Executive Director/CEO,<br />

Commercial Relations Committee Chair<br />

2004-<strong>2005</strong> Meeting Arrangements Committees<br />

Scientific Program Committee<br />

Scientific Program Committee<br />

Patricia A. Hudgins, MD<br />

President-Elect/Program Chair<br />

Roy A. Holliday, MD<br />

Head and Neck Representative<br />

John D. Barr, MD<br />

Interventional Representative<br />

Andrei I. Holodny, MD<br />

Functional Representative<br />

Marvin D. Nelson, MD<br />

Pediatric Representative<br />

Gordon K. Sze, MD<br />

Spine Representative<br />

Michael Brant-Zawadzki, MD<br />

Hugh D. Curtin, MD<br />

Nancy I. Fischbein, MD<br />

Lawrence E. Ginsberg, MD<br />

R. Gilberto Gonzalez, MD, PhD<br />

Robert I. Grossman, MD<br />

Victor M. Haughton, MD<br />

John R. Hesselink, MD, FACR<br />

Emanuel Kanal, MD<br />

Edward E. Kassel, MD<br />

Gregory L. Katzman, MD<br />

Walter Kucharczyk, MD, FRCPC<br />

Laurie A. Loevner, MD<br />

Carolyn Cidis Meltzer, MD<br />

David J. Mikulis, MD<br />

Suresh K. Mukherji, MD<br />

Jay J. Pillai, MD<br />

J. Arliss Pollock, MD<br />

Robert M. Quencer, MD<br />

Timothy P.L. Roberts, PhD<br />

Howard A. Rowley, MD<br />

David Saloner, PhD<br />

Hervey D. Segall, MD<br />

James G. Smirniotopoulos, MD<br />

A. Gregory Sorensen, MD<br />

Richard H. Wiggins, III, MD<br />

Robert D. Zimmerman, MD


2004-<strong>2005</strong> Meeting Arrangements Committees (continued)<br />

Audio Visual Committee<br />

Erin M. Simon, MD<br />

Chair<br />

Edward A. Michals, MD<br />

Consultant<br />

Robert M. Barr, MD<br />

Alexander B. Baxter, MD<br />

Jacqueline A. Bello, MD<br />

Richard M. Berger, MD<br />

Brian C. Bowen, PhD, MD<br />

Orest B. Boyko, MD, PhD<br />

Phillip W. Chao, MD<br />

Dale A. Charletta, MD<br />

Dianna Chooljian, MD<br />

Raquel Del Carpio-O’Donovan, MD<br />

Colin P. Derdeyn, MD<br />

David B. Granato, MD<br />

Rose Marie Holt, MD, PhD<br />

Anil Khosla, MD<br />

Kelly K. Koeller, MD<br />

Robert A. Koenigsberg, DO, FACR<br />

Warren W. Lam, MD<br />

John I. Lane, MD<br />

Joel R. Meyer, MD<br />

Pratik Mukherjee, MD, PhD<br />

Walter L. Olsen, MD, PhD<br />

Tina Young Poussaint, MD<br />

Joshua S. Shimony, MD, PhD<br />

Harish N. Shownkeen, MD<br />

Murray A. Solomon, MD<br />

Jeffrey A. Stone, MD<br />

Vance E. Watson, MD<br />

Richard H. Wiggins, III, MD<br />

Electronic Learning Center (ELC) Committee<br />

Gregory L. Katzman, MD<br />

Chair<br />

Richard H. Wiggins, III, MD<br />

Vice Chair, Syllabus Editor<br />

Richard M. Berger, MD<br />

Vice Chair, Moderator and Technical Coordination<br />

Hervey D. Segall, MD<br />

Chair Emeritus<br />

Scientific Exhibits Committee<br />

Linda A. Heier, MD<br />

Chair<br />

Stephen Gebarski, MD<br />

Consultant<br />

Richard M. Berger, MD<br />

Nancy J. Fischbein, MD<br />

Jill V. Hunter, MD<br />

Prabhakar P. Kesava, MD<br />

Leena M. Ketonen, MD<br />

Bernadette L. Koch, MD<br />

Kelly K. Koeller, MD<br />

Jonathan S. Lewin, MD<br />

Gary M. Nesbit, MD<br />

Susan Palasis, MD<br />

Gregory W. Petermann, MD<br />

Jay J. Pillai, MD<br />

Erin M. Simon, MD<br />

Evelyn M. Sklar, MD<br />

David M. Yousem, MD, MBA<br />

Technical Exhibits Committee<br />

Lawrence N. Tanenbaum, MD<br />

Chair<br />

Alan L. Williams, MD, FACR, MBA<br />

Vice Chair<br />

Walter S. Bartynski, MD<br />

Brian C. Bowen, PhD, MD<br />

Ray A. Brinker, MD<br />

Thomas S. Dina, MD<br />

Glen K. Geremia, MD<br />

Andrei I. Holodny, MD<br />

John M. Mathis, MD, MSc<br />

John Perl, II, MD<br />

C. Douglas Phillips, MD<br />

Donald S. Willig, MD<br />

Gregg H. Zoarski, MD<br />

Local Arrangements Committee<br />

Victor M. Haughton, MD<br />

President<br />

Patricia A. Hudgins, MD<br />

President-Elect/Program Chair<br />

Susan I. Blaser, MD<br />

Sylvester Chuang, MD<br />

Lyne N. DeTilly, MD<br />

Allan J. Fox, MD, FRCPC, FACR<br />

Edward E. Kassel, MD<br />

Walter Kucharczyk, MD FRCPC<br />

Timothy P.L. Roberts, PhD<br />

Karel G. TerBrugge, MD<br />

Robert Willinsky, MD<br />

III<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

IV<br />

<strong>ASNR</strong> Staff<br />

<strong>ASNR</strong> STAFF<br />

American Society of Neuroradiology<br />

Headquarters Office<br />

2210 Midwest Road, Suite 207<br />

Oak Brook, IL 60523-8205<br />

Telephone: 630-574-0220<br />

Fax: 630-574-0661/630-574-1740<br />

Internet: http://www.asnr.org<br />

James B. Gantenberg, CHE<br />

Executive Director/CEO<br />

Ext. 224, jgantenberg@asnr.org<br />

Arthur An<br />

Educational Technologist<br />

Ext. 243, aan@asnr.org<br />

Angelo Artemakis<br />

Director of Communications and Media Management<br />

Ext. 227, aartemakis@asnr.org<br />

Ken Cammarata<br />

Director of Specialty Societies and Member Services<br />

Ext. 226, kcammarata@asnr.org<br />

Tina Cheng, CPA<br />

Director of Finance and Information Systems<br />

Ext. 225, tcheng@asnr.org<br />

Maurine Dennis, MPH, MBA<br />

Director of Clinical Practice Services<br />

Ext. 233, mdennis@asnr.org<br />

AJNR Staff<br />


American Journal of Neuroradiology<br />

Headquarters Office<br />

2210 Midwest Road, Suite 205<br />

Oak Brook, IL 60523-8205<br />

Telephone: 630-574-1487<br />

Fax: 630-574-0326<br />

Internet: http://www.ajnr.org<br />

Bridget Donohue, MA<br />

Managing Editor<br />

Ext. 2, bdonohue@asnr.org<br />

Mary Harder<br />

Editorial Assistant<br />

Ext. 3, mharder@asnr.org<br />

Derrick J. Leaks, MA<br />

Editorial Assistant<br />

Ext. 4, dleaks@asnr.org<br />

Hayley Whittington<br />

Publications Assistant<br />

Ext. 1, hwhittington@asnr.org<br />

Pat Galle-Bingham<br />

Staff Accountant<br />

Ext. 222, pgalle-bingham@asnr.org<br />

Valerie Geisendorfer, CMP<br />

Meetings Coordinator<br />

Ext. 231, vgeisendorfer@asnr.org<br />

Bonnie Mack<br />

Membership/Society Coordinator<br />

Ext. 234, bmack@asnr.org<br />

Karen Mansfield<br />

Office Manager/Executive Assistant<br />

Ext. 221, kmansfield@asnr.org<br />

Catherine Neis, MTA<br />

Senior Logistics and Programming Specialist<br />

Ext. 232, cneis@asnr.org<br />

Barbara Schell, CAE<br />

Manager of Scientific Meetings<br />

Ext. 228, bschell@asnr.org<br />

Debbie Seitz<br />

CPC Administrative Assistant<br />

Ext. 236, dseitz@asnr.org<br />

Lora J. Tannehill, CMP<br />

Director of Scientific Meetings<br />

Ext. 229, ltannehill@asnr.org<br />

Additional Email Addresses<br />

Executive<br />

executive@asnr.org<br />

Clinical Practice<br />

cpc@asnr.org<br />

Communications<br />

communications@asnr.org<br />

Finance<br />

finance@asnr.org<br />

Meetings<br />

meetings@asnr.org<br />

Membership<br />



43rd Annual Meeting Invited Speakers<br />

James J. Abrahams, MD<br />

Yale University School of Medicine<br />

Walter H. Backes, PhD<br />

Maastricht University Hospital, The Netherlands<br />

Roland Bammer, PhD<br />

Stanford University<br />

John D. Barr, MD<br />

Mid South Imaging and Therapeutics,<br />

Memphis, TN<br />

Susan I. Blaser, MD<br />

The Hospital for Sick Children<br />

Toronto, ON, Canada<br />

Brian C. Bowen, MD, PhD<br />

University of Miami School of Medicine<br />

William G. Bradley, MD, PhD, FACR<br />

University of California San Diego Healthcare<br />

Allan L. Brook, MD<br />

Montefiore Medical Center, Bronx, NY<br />

R. Nick Bryan, MD, PhD<br />

University of Pennsylvania Health System<br />

Patricia E. Burrows, MD<br />

Children’s Hospital, Boston, MA<br />

Mauricio Castillo, MD<br />

University of North Carolina School of Medicine<br />

John J. Connors, III, MD<br />

Miami Cardiac and Vascular Institute<br />

H. Christian Davidson, MD<br />

University of Utah<br />

Colin P. Derdeyn, MD<br />

Washington University, School of Medicine,<br />

St. Louis, MO<br />

William P. Dillon, MD<br />

University of California Medical Center,<br />

San Francisco<br />

Gary R. Duckwiler, MD<br />

University of California Los Angeles,<br />

School of Medicine<br />

William K. Erly, MD<br />

University of Arizona<br />

Aaron S. Field, MD, PhD<br />

University of Wisconsin Hospital and Clinics<br />

Alisa D. Gean, MD<br />

University of California Medical Center,<br />

San Francisco<br />

Bassem A. Georgy, MD<br />

Valley Radiology Consultants, Escondido, CA<br />

Floyd H. Gilles, MD<br />

Children’s Hospital, Los Angeles<br />

J. Rob Gimbel, MD, FACC<br />

East Tennessee Heart Consultants, Knoxville, TN<br />

Lawrence E. Ginsberg, MD<br />

MD Anderson Cancer Center, Houston, TX<br />

Charles M. Glasier, MD<br />

Arkansas Children’s Hospital, Little Rock, AK<br />

Xavier Golay, PhD<br />

National Neuroscience Institute, Singapore<br />

R. Gilberto Gonzalez, MD, PhD<br />

Massachusetts General Hospital<br />

P. Ellen Grant, MD<br />

Massachusetts General Hospital<br />

Robert I. Grossman, MD<br />

New York University Medical Center<br />

Patrick Gullane, MB, FRCSC, FACS<br />

University Health Network, Toronto, ON, Canada<br />

H. Ric Harnsberger, MD<br />

University of Utah<br />

Anton N. Hasso, MD FACR<br />

University of California Irvine Medical Center<br />

Gary Lee Hedlund, DO<br />

Primary Children’s Medical Center, Salt Lake City, UT<br />

Eric C. Holland, MD<br />

Memorial Sloan-Kettering Cancer Center<br />

Andrei I. Holodny, MD<br />

Memorial Sloan-Kettering Cancer Center<br />

Jill V. Hunter, MD<br />

Texas Children’s Hospital, Houston, TX<br />

Blake A. Johnson, MD<br />

Center for Diagnostic Imaging, St. Louis, MO<br />

Michele H. Johnson, MD<br />

Yale University School of Medicine<br />

Blaise V. Jones, MD<br />

Children’s Hospital Medical Center, Cinncinnati, OH<br />

Emanuel Kanal, MD<br />

University of Pittsburgh Medical Center<br />

Sasan Karimi, MD<br />

Memorial Sloan-Kettering Cancer Center<br />

Edward E. Kassel, MD<br />

Mount Sinai Hospital, Toronto, ON, Canada<br />

V<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

VI<br />


43rd Annual Meeting Invited Speakers (continued)<br />

Spyros Kollias, MD<br />

Institute of Neuroradiology, University Hospital,<br />

Zurich, Switzerland<br />

Andrew Ku, MD<br />

Allegheny General Hospital, Pittsburgh, PA<br />

Christiane Kuhl, PhD<br />

University of Bonn, Germany<br />

Alan Leviton, MD, MS<br />

The Children’s Hospital, Boston, MA<br />

Lisa H. Lowe, MD<br />

Children’s Mercy Hospital, Kansas City, MO<br />

Helmi Lutsep, MD<br />

Oregon Health and Sciences University<br />

Joseph A. Maldjian, MD<br />

Wake Forest University School of Medicine<br />

Michael P. Marks, MD<br />

Stanford University Medical Center<br />

Gary M. Nesbit, MD<br />

Oregon Health and Science University<br />

Brian O’Sullivan, MD, FRCPI<br />

Princess Margaret Hospital,<br />

Toronto, ON, Canada<br />

Ashok Panigrahy, MD<br />

The Children’s Hospital, Los Angeles, CA<br />

Jeffrey R. Petrella, MD<br />

Duke University Medical Center<br />

Jay J. Pillai, MD<br />

Medical College of Georgia<br />

J. Arliss Pollock, MD<br />

Radiological Associates, Sacramento, CA<br />

James M. Provenzale, MD<br />

Duke University Medical Center<br />

Klaas P. Pruessmann, PhD<br />

University and ETH Zurich, Switzerland<br />

Janet S. Rasey, PhD<br />

University of Washington<br />

Deborah L. Reede, MD<br />

The Long Island College Hospital<br />

Timothy P.L. Roberts, PhD<br />

University of Toronto, ON, Canada<br />

Caroline D. Robson, MB, ChB<br />

The Children’s Hospital, Boston, MA<br />

Brian D. Ross, MD<br />

University of Michigan<br />

Jeffrey S. Ross, MD<br />

Cleveland Clinic Foundation<br />

Howard A. Rowley, MD<br />

University of Wisconsin Hospital and Clinics<br />

Eric J. Russell, MD, FACR<br />

Northwestern University, Chicago, IL<br />

James T. Rutka, MD, PhD<br />

The Hospital for Sick Children, Toronto, ON, Canada<br />

Yutakes Sato, MD<br />

University of Iowa Hospitals and Clinics, Iowa City, IA<br />

Pamela W. Schaefer, MD<br />

Massachusetts General Hospital<br />

Kurt P. Schellhas, MD<br />

Center for Diagnostic Imaging, St. Louis, MO<br />

Eric D. Schwartz, MD<br />

Hospital of the University of Pennsylvania<br />

Deborah R. Shatzkes, MD<br />

New York University Medical Center<br />

Erin M. Simon, MD<br />

The Children’s Hospital of Philadelphia<br />

James Smirniotopoulos, MD<br />

Uniformed Services University, Bethesda, MD<br />

Wendy R.K. Smoker, MD, FACR<br />

University of Iowa College of Medicine<br />

O. Carter Snead, III, MD<br />

The Hospital for Sick Children, Toronto, ON, Canada<br />

A. Gregory Sorensen, MD<br />

Massachusetts General Hospital<br />

Philip E. Stieg, MD<br />

Cornell University<br />

Jeffrey L. Sunshine, MD, PhD<br />

University Hospitals of Cleveland<br />

Marshall S. Sussman, PhD<br />

University of Toronto, ON, Canada<br />

Gordon K. Sze, MD<br />

Yale University<br />

J. Michael Tyszka, PhD<br />

California Institute of Technology<br />

John L. Ulmer, MD<br />

Medical College of Wisconsin<br />

Alyssa T. Watanabe, MD<br />

Long Beach Memorial Medical Center<br />

Bruce M. Wenig, MD<br />

Beth Israel Medical Center, New York, NY<br />

Richard H. Wiggins, III, MD<br />

University of Utah<br />

Edward D. Wirth, III, MD, PhD<br />

Geron Corporation<br />

Wade H.M. Wong, DO<br />

University of California, San Diego<br />

Wayne F. Yakes, MD<br />

Vascular Malformation Center, Engelwood, CO<br />

David M. Yousem, MD, MBA<br />

The John Hopkins Medical Institute<br />

Robert A. Zimmerman, MD<br />

The Children’s Hospital of Philadelphia<br />

Robert D. Zimmerman, MD<br />

New York Presbyterian Hospital


About Toronto, Ontario, Canada<br />

Toronto, the seat of government for the Province of<br />

Ontario, is also the cultural, entertainment, and<br />

financial capital of Canada. Toronto is a great city for<br />

visitors. It boasts a thriving arts community, reliable<br />

services and one of the safest urban environments in<br />

the world.<br />

The personality of Toronto, reflected in its slogan,<br />

“The World Within a City,” ® is represented by a<br />

mosaic of colorful cultures from around the world.<br />

Individuals often retain their cultural identities<br />

complete with traditions, languages and customs.<br />

You’ll see these personalities in the vibrant, quirky<br />

neighborhoods and experience it in the diversity of<br />

the arts, theatres, and dining.<br />

Walking Map of Toronto, Ontario, Canada<br />

Toronto offers <strong>ASNR</strong> 43rd Annual Meeting attendees<br />

an endless choice of activities. It boasts world-class<br />

museums such as the Royal Ontario Museum,<br />

fascinating and historic architecture including the CN<br />

Tower, Old and New City Hall, and lovely public spaces<br />

like Queen’s Park and Nathan Phillips Square. Music,<br />

film, theatre, dance and cultural events are<br />

everywhere. Adding to Toronto’s landscape are 150<br />

pieces of public art and monuments in addition to the<br />

over 2,000 moveable works of fine art on display in<br />

public buildings such as City Hall. Many of the city’s<br />

cultural attractions, ethnic and trendy neighborhoods,<br />

shopping areas such as the Eaton Centre, and<br />

Toronto’s waterfront are just a short walk or taxi ride<br />

away from the Fairmont Royal York Hotel, the <strong>ASNR</strong><br />

headquarters hotel.<br />

<strong>ASNR</strong> would like to thank NORTHSTAR Travel Media, LLC for the use of their Toronto, ON, Canada downtown area map.<br />

VII<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

VIII<br />

Level 100<br />

(As of 3/24/05)<br />

F<br />

101<br />

Headquarters<br />

Office<br />


Theatre<br />

102<br />

Breakout Session<br />

Room 1<br />

FOYER<br />


Directory<br />

Theatre<br />

Entrance<br />

Electronic103<br />

B<br />

Learning<br />

Center<br />

and NLM<br />

Workshops103<br />

A<br />

WR<br />

COATS<br />


WR<br />

Front Street<br />


Reception Hall 10<br />

A B C<br />

CME<br />

Pavilion<br />

WR<br />

y<br />

d<br />

a<br />

e<br />

R<br />

r<br />

e<br />

k<br />

a<br />

e<br />

p<br />

S<br />

m<br />

o<br />

o<br />

R<br />

Ov<br />

Sea<br />

Food<br />



eception Hall 104<br />

B C D<br />

WR<br />

y<br />

d<br />

a<br />

e<br />

R<br />

r<br />

e<br />

k<br />

a<br />

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p<br />

S<br />

m<br />

o<br />

o<br />

R<br />

Overflow<br />

Seating for<br />

Food Service<br />



Directory Directory<br />

Breakout Session<br />

Room 2<br />

Constitution Hall<br />


MTCC<br />

108<br />



105 106 107<br />

10 9 8<br />

7<br />

P<br />

M<br />

A<br />

R<br />

6 5 4 3 2<br />

Breakout Session<br />

Room 3<br />

D<br />

R<br />

A<br />

O<br />

B<br />

D<br />

Level 100<br />

(As of 3/24/05)<br />

WR WR<br />


Toronto, Canada Canada<br />



May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

X<br />

Level 200<br />

(Entrance Level)<br />

(As of 3/24/05)<br />

Elevator<br />

Express Onsite Self<br />

Registration<br />

AJNR<br />

Meeting and<br />

Announcements<br />

M ESSA GE<br />

BOARD<br />

NER<br />


BOARD<br />

Internal Street<br />

2<br />

201 A 201 C 201 E<br />

202 A<br />

202 C<br />

Reg<br />

Office<br />

203 A 203 C<br />

Elevator<br />

Committee Committee Committee Committee Committee Committee<br />

Room Room Room Food Service Room Room<br />

Research Session/<br />

<strong>ASNR</strong> Business<br />

Center<br />

Committee<br />

Room<br />

Committee Committee Committee<br />

Room Food Service Room<br />

Committee<br />

Room<br />

Executive<br />

Committee<br />

Office<br />

201 B 201 D 201 F<br />

202 B 202 D<br />

203 B<br />

203 D<br />

204<br />

Summit<br />

Room<br />

Express Onsite Self<br />

Registration<br />

AJNR<br />

205<br />

Breakout<br />

Session 4<br />

M 2<br />

Meeting and<br />

Announcements<br />

M ESSA GE<br />

BOARD<br />

NER<br />


BOARD<br />

M ESSAG E<br />

BOARD<br />

Directory<br />

Directory<br />

Restau rant<br />

Th eatre<br />

Entra nce<br />

Front Street



12'h drape<br />

8'h drape<br />




F.H.C.<br />


Entrance<br />


F.H.C<br />

Entrance<br />

F.H.C.<br />

F.H.C.<br />

F.H.C.<br />

F.H.C.<br />

F.H.C.<br />


OPEN<br />

OPEN<br />

Technical<br />

8'h drape<br />

8'h drape<br />

F.H.C.<br />

100<br />

Micrus<br />

F.H.C.<br />

Scientific Exhibits<br />

101<br />

Bracco<br />

Diagnos.<br />

103<br />

4-D<br />

Neuro.<br />

200<br />

201<br />

401 301<br />

Kyphon<br />

Inc.<br />

GE<br />

Healthcare<br />

Philips<br />

Medical<br />

Systems<br />

Cardinal<br />

Health<br />


104<br />

Shelley<br />

Med. Tech.<br />

106<br />

Cook Inc.<br />

107<br />

MicroVention<br />

110<br />

111<br />

407 406 307 306 207<br />

VSM<br />

Night- Lippincott<br />

Springer Integra<br />

MedTech<br />

Hawk Williams<br />

Spinal<br />

409<br />

Kopp<br />

Develop.<br />

411<br />

311<br />

8'h drape<br />

SE66 SE82<br />

SE67 SE83<br />

SE65 SE81<br />

SE68 SE84<br />

SE64 SE80<br />

SE69 SE85<br />

SE63 SE79<br />

SE70 SE86<br />

SE61 SE78<br />

SE71 SE87<br />

SE60 SE77<br />

SE72 SE88<br />

SE59 SE76<br />

SE73 SE89<br />

SE58 SE75 SE91<br />

SE90<br />

SE49<br />

SE50<br />

SE48<br />

SE51<br />

SE47<br />

SE52<br />

SE46<br />

SE53<br />

SE45<br />

SE54<br />

SE44<br />

SE55<br />

SE43<br />

SE56<br />

SE42<br />

SE57<br />

SE16 SE33<br />

SE17 SE34<br />

SE15 SE32<br />

SE18 SE35<br />

SE14 SE31<br />

SE19 SE36<br />

SE13 SE30<br />

SE20 SE37<br />

SE12 SE29<br />

SE21 SE38<br />

SE11 SE27<br />

SE22 SE39<br />

SE10 SE26<br />

SE23 SE40<br />

SE9<br />

SE25<br />

SE24 SE41<br />

SE1<br />

SE2<br />

SE3<br />

SE4<br />

SE5<br />

SE6<br />

Food Service<br />

TeraRecon<br />

Siemen<br />

Medical<br />

Hitachi<br />

Medical<br />

Vital<br />

Images,<br />

Inc.<br />

SE7<br />

SE8<br />

217<br />

Electronic<br />

Scientific Exhibits<br />

(eSE)<br />

117 116<br />

Virtual<br />

Berlex<br />

Rad.<br />

Imaging<br />

118<br />

Elsevier<br />

120<br />

Amirsys<br />

Boston<br />

Scientific<br />

417 317<br />

Arthrocare<br />

Stryker<br />

419<br />

421<br />

P001 P028 P029 P056 P057 P084 P085 P112 P113 P141 P142 P169 P170<br />

P002 P027 P030 P055 P058 P083 P086 P111 P114 P140 P143 P168 P171 P184<br />

P003 P026 P031 P054 P059 P082 P087 P110 P115 P139 P144 P167 P172 P183<br />

P004 P025 P032 P053 P060 P081 P088 P109 P116 P138 P145 P166 P173 P182<br />

P005 P024 P033 P052 P061 P080 P089<br />

P108 P117 P137 P146 P165 P174 P181<br />

P006 P023 P034 P051 P062 P079 P090 P107 P118 P136 P147 P164 P175 P180<br />

P007 P022 P035 P050 P063 P078 P091 P106 P119 P135 P148 P163 P176 P179<br />

P008 P021 P036 P049 P064 P077 P092 P105 P120 P134 P149 P162 P177 P178<br />

P009 P020 P037 P048 P065 P076 P093 P104 P121 P133 P150 P161<br />

P010 P019 P038<br />

P047 P066 P075 P094 P103 P123 P132 P151 P160<br />

P011 P018 P039 P046 P067 P074 P095 P102 P125 P131 P152 P159<br />

P012 P017<br />

P045<br />

P040<br />

P068 P073 P096 P101 P126 P130 P153 P158<br />

P013 P016 P041 P044 P069 P072 P097 P100 P127 P129 P154 P157<br />

P014 P015 P042 P043 P070 P071 P098 P099<br />

P128 P155 P156<br />

8'h drape<br />

T.F.H.C.<br />

222 123<br />

National Advanced<br />

Library Imaging<br />

322 223<br />

Advanced Invivo<br />

Bio<br />

324 225<br />

<strong>ASNR</strong> SNR<br />

T.F.H.C.<br />

8'h drape<br />

8'h drape<br />


RAMP<br />

Sc<br />

Posters<br />

8'h drape<br />



LEAD<br />

Food Service<br />

F.H.C.<br />

F.H.C.<br />


F.H.C.<br />

F.H.C.<br />

F.H.C.<br />

F.H.C.<br />


F.H.C.<br />

F.H.C.<br />




Level 300<br />

(As of 3/24/05)<br />

XI<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XII<br />

Exhibit Hall B — Level 300<br />

(As of 3/24/05)<br />

SE1<br />

SE2<br />

SE3<br />

SE4<br />

SE5<br />

SE6<br />

SE7<br />

SE8<br />

P001<br />

P002<br />

P003<br />

P004<br />

P005<br />

P006<br />

P007<br />

P008<br />

P009<br />

P010<br />

P011<br />

P012<br />

P013<br />

P014<br />

P028<br />

P027<br />

P026<br />

P025<br />

P024<br />

P023<br />

P022<br />

P021<br />

P020<br />

P019<br />

P018<br />

P017<br />

P016<br />

P015<br />

Scientific Posters, Scientific Exhibits<br />

and Electronic Scientific Exhibits (eSE)<br />

SE16<br />

SE14<br />

SE16A<br />

SE15<br />

SE17<br />

SE18<br />

SE13<br />

SE20<br />

SE12<br />

SE21<br />

SE11<br />

SE22<br />

SE10<br />

SE9<br />

Note: A missing number indicates an abstract has been withdrawn.<br />

SE23<br />

SE24<br />

P029<br />

P030<br />

P031<br />

P032<br />

P033<br />

P034<br />

P035<br />

P036<br />

P037<br />

P038<br />

P039<br />

P040<br />

P041<br />

P042<br />

P056<br />

P055<br />

P054<br />

P053<br />

P052<br />

P051<br />

P050<br />

P049<br />

SE33<br />

SE34<br />

SE32<br />

SE35<br />

SE31<br />

SE36<br />

SE30<br />

SE37<br />

SE29<br />

SE38<br />

SE27<br />

SE39<br />

SE26<br />

SE40<br />

SE25<br />

P048<br />

P047<br />

P046<br />

P044<br />

P043<br />

SE41<br />

P057<br />

P058<br />

P059<br />

P060<br />

P061<br />

P062<br />

P063<br />

P064<br />

P065<br />

P066<br />

P067<br />

P068<br />

P069<br />

P070<br />

P084<br />

P083<br />

P082<br />

P081<br />

P080<br />

P079<br />

P078<br />

P077<br />

P076<br />

P075<br />

P074<br />

P073<br />

P072<br />

P071<br />

SE49<br />

SE50<br />

SE48<br />

SE51<br />

SE47<br />

SE52<br />

SE46<br />

SE53<br />

SE45<br />

SE54<br />

SE44<br />

SE55<br />

SE43<br />

SE56<br />

SE42<br />

SE57<br />

P085<br />

P086<br />

P087<br />

P088<br />

P089<br />

P090<br />

P091<br />

P092<br />

P093<br />

P094<br />

P095<br />

P096<br />

P097<br />

P098<br />

P112<br />

P111<br />

P110<br />

P109<br />

P108<br />

P107<br />

P106<br />

P105<br />

P104<br />

P103<br />

P102<br />

P101<br />

P100<br />

P099<br />

SE64<br />

SE65<br />

SE63<br />

SE66<br />

SE62<br />

SE67<br />

SE61<br />

SE68<br />

SE60<br />

SE69<br />

SE59<br />

SE70<br />

SE58A<br />

SE71<br />

SE58<br />

P113<br />

P114<br />

P115<br />

P116<br />

P117<br />

P118<br />

P119<br />

P120<br />

P121<br />

P123<br />

P125<br />

P126<br />

P127<br />

SE72<br />

P141<br />

P140<br />

P139<br />

P138<br />

P137<br />

P136<br />

P135<br />

P134<br />

P133<br />

P132<br />

P131<br />

P130<br />

P129<br />

P128<br />

SE80<br />

SE81<br />

SE79<br />

SE81A<br />

SE78<br />

SE82<br />

SE77<br />

SE83<br />

SE76<br />

SE84<br />

SE75<br />

SE85<br />

SE74<br />

SE86<br />

SE73<br />

P143<br />

P144<br />

P145<br />

P146<br />

P147<br />

P148<br />

P149<br />

P150<br />

P151<br />

P152<br />

P153<br />

P154<br />

P155<br />

SE87<br />

P169<br />

P168<br />

P167<br />

P166<br />

P165<br />

P164<br />

P163<br />

P162<br />

P161<br />

P160<br />

P159<br />

P158<br />

P157<br />

P156<br />

SE91<br />

SE90<br />

SE89<br />

SE88<br />

Stand Alone eSE Exhibits Shared eSE Exhibits<br />

eSE Presentations 1-31 can be accessed from any shared eSE computer.<br />

eSE Presentations 32-41 can be accessed on assigned computer only. See sign in eSE area for details.<br />

P170<br />

P171<br />

P172<br />

P173<br />

P174<br />

P175<br />

P176<br />

P177<br />

P184<br />

P183<br />

P182<br />

P181<br />

P180<br />

P179<br />


Printed and Electronic Scientific Exhibits (eSE)<br />

Note: A missing number indicates an abstract has been withdrawn.<br />


Adult Brain ................1-39<br />

Functional................40-43<br />

Head and Neck ........44-70<br />

Interventional ..........71-73<br />

Pediatrics ................75-81<br />

Socioeconomic ..............82<br />

Spine ......................83-91<br />

SE1<br />

SE2<br />

SE3<br />

SE4<br />

SE5<br />

SE6<br />

SE7<br />

SE8<br />

SE16<br />

SE15<br />

SE17<br />

SE14<br />

SE16A<br />

SE18<br />

SE13<br />

SE20<br />

SE12<br />

SE21<br />

SE11<br />

SE22<br />

SE10<br />

SE9<br />

SE23<br />

SE24<br />


SE33<br />

SE34<br />

SE32<br />

SE35<br />

SE31<br />

SE36<br />

SE30<br />

SE37<br />

SE29<br />

SE38<br />

SE27<br />

SE39<br />

SE26<br />

SE40<br />

SE25<br />

SE41<br />

Shared/(Stand Alone)<br />

Adult Brain ................1-10<br />

Functional ....................11<br />

(32, 35)<br />

Head and Neck ........12-25 (36-37)<br />

Interventional ................26 (38)<br />

Pediatrics ................27-29<br />

Spine ......................30-31<br />

(39-41)<br />

SE49<br />

SE50<br />

SE48<br />

SE51<br />

SE47<br />

SE52<br />

SE46<br />

SE53<br />

SE45<br />

SE54<br />

SE44<br />

SE55<br />

SE43<br />

SE56<br />

SE42<br />

SE57<br />

SE64<br />

SE65<br />

SE63<br />

SE66<br />

SE62<br />

SE67<br />

SE61<br />

SE68<br />

SE60<br />

SE69<br />

SE59<br />

SE70<br />

SE58A<br />

SE71<br />

SE58<br />

SE72<br />

Exhibit Hall B — Level 300<br />

SE80<br />

SE81<br />

SE79<br />

SE81A<br />

SE78<br />

SE82<br />

SE77<br />

SE83<br />

SE76<br />

SE84<br />

SE75<br />

SE85<br />

SE74<br />

SE86<br />

SE73<br />

SE87<br />

SE91<br />

SE90<br />

SE89<br />

SE88<br />

(As of 3/24/05)<br />

Stand Alone eSE Exhibits Shared eSE Exhibits<br />

eSE Presentations 1-31 can be accessed from any shared eSE<br />

computer. eSE Presentations 32-41 can be accessed on assigned<br />

computer only. Refer to sign in eSE area for further details.<br />

XIII<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XIV<br />

Exhibit Hall B — Level 300<br />

(As of 3/24/05) SCIENTIFIC POSTERS<br />

P001<br />

P002<br />

P003<br />

P004<br />

P005<br />

P006<br />

P007<br />

P008<br />

P009<br />

P010<br />

P011<br />

P012<br />

P013<br />

P014<br />

P028<br />

P027<br />

P026<br />

P025<br />

P024<br />

P023<br />

P022<br />

P021<br />

P020<br />

P019<br />

P018<br />

P017<br />

P016<br />

P015<br />

P029<br />

P030<br />

P031<br />

P032<br />

P033<br />

P034<br />

P035<br />

P036<br />

P037<br />

P038<br />

P039<br />

P040<br />

P041<br />

P042<br />

Scientific Posters Exhibits<br />

P056<br />

P055<br />

P054<br />

P053<br />

P052<br />

P051<br />

P050<br />

P049<br />

P048<br />

P047<br />

P046<br />

P044<br />

P043<br />

P057<br />

P058<br />

P059<br />

P060<br />

P061<br />

P062<br />

P063<br />

P064<br />

P065<br />

P066<br />

P067<br />

P068<br />

P069<br />

P070<br />

Note: A missing number indicates an abstract has been withdrawn.<br />

P084<br />

P083<br />

P082<br />

P081<br />

P080<br />

P079<br />

P078<br />

P077<br />

P076<br />

P075<br />

P074<br />

P073<br />

P072<br />

P071<br />

P085<br />

P086<br />

P087<br />

P088<br />

P089<br />

P090<br />

P091<br />

P092<br />

P093<br />

P094<br />

P095<br />

P096<br />

P097<br />

P098<br />

P112<br />

P111<br />

P110<br />

P109<br />

P108<br />

P107<br />

P106<br />

P105<br />

P104<br />

P103<br />

P102<br />

P101<br />

P100<br />

P099<br />

P113<br />

P114<br />

P115<br />

P116<br />

P117<br />

P118<br />

P119<br />

P120<br />

P121<br />

P123<br />

P125<br />

P126<br />

P127<br />

P130<br />

P129<br />

P128<br />

Adult Brain ................1-81<br />

Functional..............82-102<br />

Head and Neck ....103-120<br />

Interventional ......121-148<br />

Pediatrics ............149-172<br />

Socioeconomic ............173<br />

Spine ..................174-184<br />

P141<br />

P140<br />

P139<br />

P138<br />

P137<br />

P136<br />

P135<br />

P134<br />

P133<br />

P132<br />

P131<br />

P143<br />

P144<br />

P145<br />

P146<br />

P147<br />

P148<br />

P149<br />

P150<br />

P151<br />

P152<br />

P153<br />

P154<br />

P155<br />

P169<br />

P168<br />

P167<br />

P166<br />

P165<br />

P164<br />

P163<br />

P162<br />

P161<br />

P160<br />

P159<br />

P158<br />

P157<br />

P156<br />

P170<br />

P171<br />

P172<br />

P173<br />

P174<br />

P175<br />

P176<br />

P177<br />

P184<br />

P183<br />

P182<br />

P181<br />

P180<br />

P179<br />


401 301<br />

Cardinal<br />

Health<br />

407 406 307 306<br />

VSM<br />

MedTech<br />

409<br />

Kopp<br />

Develop.<br />

411<br />

Vital<br />

Images,<br />

Inc.<br />

417 317<br />

Arthrocare<br />

419<br />

421<br />

Night-<br />

Hawk<br />

Technical Exhibits<br />

Philips<br />

Medical<br />

Systems<br />

Hitachi<br />

Medical<br />

Stryker<br />

Lippincott<br />

Williams<br />

311<br />

GE<br />

Healthcare<br />

201<br />

207<br />

Springer Integra<br />

Spinal<br />

Food Service<br />

Boston<br />

Scientific<br />

322<br />

Advanced<br />

Bio<br />

324<br />

<strong>ASNR</strong><br />

223<br />

Invivo<br />

225<br />

SNR<br />

217<br />

Exhibit Hall A — Level 300<br />

(As of 3/24/05)<br />

200<br />

Kyphon<br />

Inc.<br />

101<br />

Bracco<br />

Diagnos.<br />

103<br />

4-D<br />

Neuro.<br />

107<br />

MicroVention<br />

111<br />

222 123<br />

National<br />

Library<br />

Siemens<br />

Medical<br />

Berlex<br />

Imaging<br />

100<br />

Micrus<br />

104<br />

Shelley<br />

Med. Tech.<br />

106<br />

Cook Inc.<br />

110<br />

TeraRecon<br />

117 116<br />

Advanced<br />

Imaging<br />

Virtual<br />

Rad.<br />

118<br />

Elsevier<br />

120<br />

Amirsys<br />

XV<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XVI<br />

Technical TECHNICAL Exhibits (As of 3/24/05) EXHIBITS<br />

Metro Toronto Convention Centre — Exhibit Hall A<br />

Monday, May 23 — Welcome Reception ........................................................6:00 pm – 7:30 pm<br />

Tuesday, May 24 through Thursday, May 26 ..................................................9:30 am – 4:00 pm<br />

Wednesday, May 25 — Evening of Comedy & Cuisine......................Reception 6:15 pm – 7:30 pm<br />

Performance 8:00 pm - 9:00 pm<br />

4-D Neuroimaging ......................................Booth 103<br />

9727 Pacific Heights Boulevard<br />

San Diego, CA 92121<br />

Advanced Biomaterial Systems, Inc. ..........Booth 322<br />

100 Passaic Avenue<br />

Chatham, NJ 07928<br />

Advanced Imaging Research ......................Booth 123<br />

4700 Lakeside Avenue, Suite 400<br />

Cleveland, OH 44114<br />

Amirsys, Inc...............................................Booth 120<br />

25092 Morro Court<br />

Laguna Hills, CA 92653<br />

ArthroCare Spine........................................Booth 417<br />

680 Vaqueros Avenue<br />

Sunnyvale, CA 94085<br />

<strong>ASNR</strong>/NER Foundation ................................Booth 324<br />

2210 Midwest Road, Suite 207<br />

Oak Brook, IL 60523-8205<br />

Berlex Imaging ..........................................Booth 117<br />

P.O. Box 100<br />

Montville, NJ 07045<br />

Boston Scientific........................................Booth 217<br />

47900 Bayside Parkway<br />

Fremont, CA 94538<br />

Bracco Diagnostics, Inc. ............................Booth 101<br />

107 College Road East<br />

Princeton, NJ 08543<br />

Cardinal Health, Special Procedures ..........Booth 401<br />

1500 Waukegan Road<br />

McGaw Park, IL 60085<br />

Cook Incorporated......................................Booth 106<br />

750 Daniels Way, P.O. Box 489<br />

Bloomington, IN 47402-0489<br />

Elsevier ....................................................Booth 118<br />

1 Goldthorne Avenue<br />

Toronto, ON M8Z 5S7, Canada<br />

GE Healthcare............................................Booth 201<br />

3000 N. Grandview Boulevard, W-402<br />

Waukesha, WI 53188<br />

Hitachi Medical Systems America, Inc. ......Booth 311<br />

1959 Summit Commerce Park<br />

Twinsburg, OH 44087<br />

Integra Spinal Specialties ..........................Booth 207<br />

12001 Network Blvd., Building F<br />

San Antonio, TX 78249<br />

Invivo ........................................................Booth 223<br />

N27 W23676 Paul Road<br />

Pewaukee, WI 53072


Technical Exhibits (As of 3/24/05)<br />

Kopp Development Inc. ..............................Booth 409<br />

785 NE Dixie Highway<br />

Jensen Beach, FL 34957<br />

Kyphon Inc. ..............................................Booth 200<br />

1221 Crossman Avenue<br />

Sunnyvale, CA 94089<br />

Lippincott, Williams & Wilkins ..................Booth 307<br />

21 Ripley Crescent<br />

Brampton, ON L6Y 4S8, Canada<br />

MicroVention, Inc.......................................Booth 107<br />

75 Columbia, Suite A<br />

Aliso Viejo, CA 92656<br />

Micrus Corporation ....................................Booth 100<br />

610 Palomar Avenue<br />

Sunnyvale, CA 94085<br />

National Library of Medicine (NLM)..................Booth 222<br />

University of Washington, Box 357155<br />

Seattle, WA 98195<br />

NightHawk Radiology Services ..................Booth 406<br />

250 Northwest Boulevard, Suite 202<br />

Coeur d’Alene, ID 83814<br />

Philips Medical Systems ............................Booth 301<br />

3000 Minuteman Road<br />

Andover, MA 01810<br />

Shelley Medical Imaging Technologies ......Booth 104<br />

157 Ashley Crescent<br />

London, ON N6E 3P9, Canada<br />

Siemens Medical Solutions ........................Booth 111<br />

1230 Shorebird Way<br />

Mountain View, CA 94043<br />

Springer ....................................................Booth 306<br />

175 Fifth Avenue<br />

New York, NY 10010-7858<br />

Stryker ......................................................Booth 317<br />

4100 East Milham<br />

Kalamazoo, MI 49001<br />

TeraRecon, Inc...........................................Booth 110<br />

2955 Campus Drive #325<br />

San Mateo, CA 94403<br />

Virtual Radiologic Consultants ....................Booth 116<br />

5995 Opus Parkway, Suite 200<br />

Minneapolis, MN 55343-9058<br />

Vital Images, Inc. ......................................Booth 411<br />

3300 Fernbrook Lane North, Suite 200<br />

Plymouth, MN 55447<br />

VSM MedTech Ltd. ....................................Booth 407<br />

9 Burbridge Street<br />

Coquillam, BC V3K 7B2, Canada<br />

World Federation of Neuroradiological<br />

Societies (WFNRS) ....................................Booth 225<br />

Meeting Dates:<br />

Adelaide, Australia – March 19-24, 2006<br />

XVII<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XVIII<br />

General GENERAL Information INFORMATION<br />


Registration will take place in the North Building<br />

Lobby (Level 200) of the Metro Toronto Convention<br />

Centre. The registration desk will be open during<br />

the following hours:<br />

Friday, May 20 ......................5:00 pm - 8:00 pm<br />

Saturday, May 21 ..................8:00 am - 6:00 pm<br />

Sunday, May 22 ....................6:30 am - 6:00 pm<br />

Monday, May 23 ....................6:30 am - 6:00 pm<br />

Tuesday, May 24 ....................6:30 am - 6:00 pm<br />

Wednesday, May 25 ................6:30 am - 6:00 pm<br />

Thursday, May 26 ..................6:30 am - 6:00 pm<br />

Friday, May 27 ....................6:30 am - 11:45 am<br />


Metro Toronto Convention Centre<br />

— Room 104B (Level 100)<br />

Friday, May 20........................5:00 pm - 8:00 pm<br />

Saturday, May 21 ....................8:00 am - 6:00 pm<br />

Sunday, May 22 through<br />

Thursday, May 26 ................6:00 am - 6:00 pm<br />

Friday, May 27 ....................6:00 am - 11:45 am<br />


Please wear name badges at all times while you are<br />

attending the scientific sessions, social programs,<br />

and technical exhibits. Badge colors are identified<br />

as follows:<br />

<strong>ASNR</strong>, ASFNR, ASHNR, ASITN, ASPNR,<br />

or ASSR Member ......................................Blue<br />

Non-Member ..............................................Green<br />

Fellow/Trainee ................................................Tan<br />

Other Professional ......................................Yellow<br />

Guest ........................................................Peach<br />

Exhibitor ......................................................Gold<br />

Staff ........................................................Purple<br />


Metro Toronto Convention Centre<br />

— Room 104A (Level 100)<br />

Saturday, May 21 ..................1:00 pm - 9:00 pm<br />

Sunday, May 22 through<br />

Thursday, May 26 ................6:30 am - 9:00 pm<br />

Friday, May 27 ......................6:30 am - 1:00 pm<br />


Please refer to the Daily Postings on the Meetings &<br />

Announcements Board located in the Metro Toronto<br />

Convention Centre North Building Lobby (Level 200).<br />


The Meetings & Announcements Board is located in<br />

the North Building Lobby (Level 200) of the Metro<br />

Toronto Convention Centre. Please refer to the Daily<br />

Postings on the Meetings & Announcements Board for<br />

information on committee meetings.<br />


The Message Center is located on Level 300 near the<br />

escalators in Hall B. They will have computer terminals<br />

available to registered attendees that can be used to<br />

access/send external email and to leave internal<br />

messages for other attendees and/or exhibitors.<br />


Metro Toronto Convention Centre<br />

255 Front Street West<br />

Toronto, ON M5V 2W6, Canada<br />

Phone: 416-585-8000

General GENERAL Information INFORMATION<br />


Within the Metro Toronto Convention Centre:<br />

In the event of a medical emergency, please contact<br />

Security Control immediately. Attendees may contact<br />

Security Control by dialing extension 8160 from any<br />

house phone located in the facility. Emergency personnel<br />

will be dispatched immediately to your location.<br />

The caller should provide the following:<br />

1. Determine name of specific meeting room<br />

or exhibit hall where the situation has occurred.<br />

2. Identify yourself as an <strong>ASNR</strong> attendee, reference<br />

your exact location, and provide details on the<br />

nature of the emergency situation.<br />

3. Provide a brief but concise description of the<br />

problem, be prepared to answer any questions<br />

that the operator may ask you, and remain on<br />

the line.<br />

Contacting Security Control will greatly minimize<br />

response time in the event an emergency medical<br />

unit needs to report to the Convention Centre.<br />

Security personnel can quickly assess the situation<br />

and bring emergency personnel directly to the<br />

scene, saving precious minutes. For this reason, the<br />

Metro Toronto Convention Centre management<br />

requests that attendees not contact 911 directly.<br />


St. Michael’s Hospital<br />

30 Bond Street<br />

Toronto, ON M5B 1WB, Canada<br />

Phone: 416-360-4000<br />


Shoppers Drugmart - Royal Bank Plaza<br />

(Underground - near the Fairmont Royal York)<br />

200 Bay Street<br />

Toronto, ON, M5J 2J3 Canada<br />

Phone: 416-865-0001<br />

Hours: Monday - Friday, 7:00 am - 6:30 pm<br />

Saturday, 10:00 am - 4:30 pm<br />

Sunday, CLOSED<br />


Shoppers Drugmart at Bay & Gerrard<br />

700 Bay Street<br />

Toronto, ON, M5G 1Z6, Canada<br />

Phone: 416-979-2424<br />


The Fairmont Royal York Hotel<br />

100 Front Street West<br />

Toronto, ON M5J 1E3 Canada<br />

Phone: 416-368-2511<br />

Fax: 416-368-9040<br />



The Xerox Centre at The Fairmont Royal York provides<br />

business travelers with the best printing technology<br />

available. It also offers an “office away from the<br />

office” for guests of The Fairmont Royal York. The<br />

quiet, efficient facility will let you be more productive<br />

during your stay.<br />

Hours: Mon. - Fri. 7:00 am - 10:00 pm<br />

Sat. and Sun. 10:00 am - 6:00 pm<br />


The Printing House (TPH)<br />

123 Front Street West<br />

Toronto, ON Canada<br />

Phone: 416-865-1660<br />

Fax: 416-865-9997<br />

Hours: Mon. - Fri. 8:00 am - 6:00 pm<br />

Sat. and Sun. 10:00 am - 4 pm<br />

XIX<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XX<br />


General Information (continued)<br />


<strong>ASNR</strong> Food Service will be served in Exhibit Hall A during<br />

technical exhibition hours or in Room 105/106 Foyer.<br />

Continental Breakfasts, Morning and Afternoon Coffee<br />

Service and Box Lunches are provided complimentary<br />

throughout the week. Please refer to the schedule below.<br />

Continental Breakfast<br />

Sunday, May 22 through<br />

Friday, May 27 ..................Room 105/106 Foyer<br />

(Level 100)<br />

Additional seating in Room 104D<br />

How-To Session Breakfasts<br />

Sunday, May 22 through<br />

Thursday, May 26..............Room 105/106 Foyer<br />

(Level 100)<br />

Morning Breaks<br />

Sunday, May 22 ............Theatre Foyer (Level 100)<br />

Monday, May 23 ....Room 105/106 Foyer (Level 100)<br />

and Theatre Foyer (Level 100)<br />

Tuesday, May 24 through<br />

Thursday, May 26 ....................................Hall A<br />

Friday, May 27 ....................Room 105/106 Foyer<br />

(Level 100)<br />

Box Lunches<br />

Sunday, May 22 through<br />

Monday, May 23..................Room 105/106 Foyer<br />

(Level 100)<br />

Tuesday, May 24 through<br />

Thursday, May 26 ....................................Hall A<br />

For Breaks and Lunches, use Room 104D for additional seating Saturday<br />

through Monday & Friday when Technical Exhibition is closed.<br />

How-To Session Lunches<br />

Sunday, May 22 through<br />

Wednesday, May 25 ..........Room 105/106 Foyer<br />

(Level 100)<br />

Afternoon Breaks<br />

Saturday, May 21 through<br />

Sunday, May 22..........Theatre Foyer (Level 100)<br />

Monday, May 23....Room 105/106 Foyer (Level 100)<br />

Theatre Foyer (Level 100)<br />

Tuesday, May 24 through<br />

Thursday, May 26 ....................................Hall A<br />

How-To Session Receptions<br />

Sunday, May 22<br />

(5:30 pm - 7:00 pm)............Room 105/106 Foyer<br />

(Level 100)<br />

Tuesday, May 24<br />

(6:00 pm - 7:30 pm)............Room 105/106 Foyer<br />

(Level 100)<br />

MEETING LOCATION: Metro Toronto Convention Centre<br />

NOTE: All scientific sessions and exhibits are<br />

located at the Metro Toronto Convention Centre.<br />

Registration<br />

North Building Lobby (Level 200)<br />

CME Pavilion Terminals<br />

Room 104A (Level 100)<br />

E-Access/Messaging Center<br />

Level 300 (outside Hall B)<br />

How-To Breakfast/Lunch/Reception Sessions<br />

Room 105/106<br />

Focus/Scientific Paper Sessions<br />

Room 105/106, Theatre, Room 107 and Room 205<br />


Workshops<br />

Room 103 (Level 100)<br />

Lectures<br />

Room 205 (Level 200)<br />


Workshops<br />

Room 103 (Level 100)<br />


Scientific Exhibits, Electronic Scientific Exhibits,<br />

Scientific Posters<br />

Hall B (Level 300)<br />

Technical Exhibits<br />

Hall A (Level 300)<br />


Past-Presidents’ and Executive Committee Office<br />

Room 203D (Level 200)<br />

Headquarters Office<br />

Room 101 (Level 100)<br />

Meetings & Announcements Board<br />

North Building Lobby (Level 200)<br />

Coat Check<br />

Level 100 by escalators<br />

Hours of Operation:<br />

Saturday, May 21 ................12:00 pm - 6:00 pm<br />

Sunday, May 22 through<br />

Thursday, May 26 ................6:30 am - 6:30 pm<br />

Friday, May 27 ......................6:30 am - 1:00 pm


Optional Tour Desk Hours<br />

The Fairmont Royal York Hotel – Tudor 8 (Main Mezzanine Level)<br />

Saturday, May 21 ..............................................................................................12:00 pm – 4:00 pm<br />

Sunday, May 22 through Thursday, May 26............................................................8:00 am – 2:00 pm<br />


Social Program<br />

An exciting social program has been planned for registrants and their registered guests during the<br />

<strong>ASNR</strong> 43rd Annual Meeting.<br />

Welcome Reception with<br />

Evening of Comedy and Cuisine<br />

Technical Exhibitors<br />

Wednesday, May 25<br />

Monday, May 23<br />

6:15 pm - 7:30 pm - Reception - Hall A (Level 300)<br />

6:00 pm – 7:30 pm<br />

8:00 pm – 9:00 pm - Second City Performance<br />

Hall A (Level 300)<br />

Theater (Level 100)<br />

Metro Toronto Convention Centre<br />

Metro Toronto Convention Centre<br />

The Welcome Reception with Technical Exhibitors offers<br />

the perfect opportunity for a preview of this year’s<br />

Technical Exhibit, the <strong>ASNR</strong>’s annual showcase for the<br />

newest products and services for the field of<br />

neuroradiology. Enjoy complimentary pre-dinner hors<br />

d’oeuvres and beverages while you learn about the newest<br />

technology. Connect with old friends, make new ones and<br />

meet representatives from the companies participating in<br />

this year’s technical exhibition.<br />

This casual social setting allows plenty of time for informal<br />

discussion with the company representatives. So bring your<br />

product and service challenges and come in search of<br />

solutions to the place where advanced technology and<br />

diagnostic and interventional neuroradiological excellence<br />

come together.<br />

The Scientific Exhibit (poster, scientific and electronic<br />

scientific exhibits) will also be available for viewing<br />

throughout the evening’s reception.<br />

Ticket required for admission: A ticket to the Welcome<br />

Reception with Technical Exhibitors is included in the fee for<br />

registration categories that include Monday, May 23 and in<br />

the Guest Hospitality fee.<br />

Combine the cuisine of Toronto’s many ethnic cultures, the<br />

comedy of the world-renowned Second City Toronto and the<br />

camaraderie of fellow neuroradiologists from all over the<br />

world and what do you get? A spectacular evening of fun,<br />

food and frivolity! During a pre-performance reception, enjoy<br />

an appetizer buffet highlighting the tastes and cuisines<br />

representing the many cultures from around the world that<br />

have found a home in Toronto. Then settle in for a laughterfilled<br />

performance provided by the Second City Toronto<br />

comedy troupe. This internationally famous institution noted<br />

for improvisation has been the launching pad for many of the<br />

comedy world’s best and brightest. Second City Toronto<br />

alumni include Dan Aykroyd, Gilda Radner, John Candy,<br />

Catherine O’Hara, Mike Myers and Martin Short, to name<br />

just a few. Skilled at finding humor in the absurdity of<br />

everyday life, their satire can be appreciated by everyone.<br />

This evening’s show will feature “The Best of Second City”<br />

sketches, a look at the field of neuroradiology through the<br />

eyes of these talented comedians, and a chance for audience<br />

interaction as they create sketches from ideas shouted from<br />

the audience.<br />

Ticket required for admission: A ticket to the Evening of<br />

Comedy and Cuisine is included in the fee for registration<br />

categories that include Wednesday, May 25 and in the Guest<br />

Hospitality fee.<br />

XXI<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XXII<br />


Guest Hospitality<br />


The Fairmont Royal York Hotel<br />

Tudor 8 (Main Mezzanine Level)<br />

The Guest Hospitality area, available to <strong>ASNR</strong> registered<br />

guests, provides complimentary food service, visitor<br />

information and special presentations. Teens and<br />

younger individuals who are with registered guests, but<br />

are not themselves registered, may also visit the<br />

hospitality room. Afternoon snacks and beverages will<br />

be offered on Saturday, May 21. Continental breakfast,<br />

afternoon snacks and beverages will be available from<br />

Saturday, May 21 - Thursday, May 26 and continental<br />

breakfast only on Friday, May 27.<br />

Guest Hospitality is a great place to start your<br />

mornings and plan the remainder of your day. It’s<br />

an ideal location to see old friends and meet<br />

new acquaintances.<br />

A representative from the Toronto area will be<br />

available to acquaint you with suggestions on what to<br />

see and do while in Toronto. Be sure to stop by to<br />

pick up visitor information and brochures available in<br />

Guest Hospitality on citywide attractions, downtown<br />

maps, and shopping and restaurant guides to assist<br />

you in planning your week.<br />


The Fairmont Royal York Hotel<br />

Tudor 8 (Main Mezzanine Level)<br />

Saturday, May 21 ................12:00 pm – 4:00 pm<br />

Sunday, May 22 through<br />

Thursday, May 26................8:00 am – 2:00 pm<br />

Friday, May 27 ....................8:00 am – 11:30 am<br />


A highlight of the Guest Hospitality program is a<br />

schedule of complimentary entertaining presentations<br />

on a variety of interesting topics. Presentations will take<br />

place in Tudor 7 at the The Fairmont Royal York Hotel.<br />

“Welcome to Toronto” Orientation<br />

Toronto offers a theatre scene that rivals London and New<br />

York, shopping with an international flair, miles of<br />

waterfront, beaches and walking trails, over 20 ethnically<br />

diverse neighborhoods and many fun attractions. So much to<br />

see and do, but so little time.<br />

This session will help participants make the most of their<br />

stay in Toronto. The presentation will provide tips on how to<br />

get those sought after theatre tickets, the hottest dining<br />

spots, current exhibits at Toronto’s world class museums,<br />

those unique and out of the way boutiques and how to get<br />

from “here to there.”<br />

Presentation given by: Tourism Toronto<br />

This program will be offered twice.<br />

Sunday, May 22 10:00 am – 11:00 am<br />

Tuesday, May 24 10:00 am – 11:00 am<br />

Lights, Camera, Action!<br />

Are you a film buff? Have you ever wondered what goes on<br />

behind the scenes when filming a movie? What happens<br />

when a film crew uses your home? How do they film those<br />

chase scenes? How pampered are those movie stars? Now is<br />

your chance to find out! Toronto is becoming known as<br />

Hollywood North because of the many feature films that have<br />

been made there including My Big Fat Greek Wedding and,<br />

more recently, Confessions of a Teenage Drama Queen.<br />

Rhonda Silverstone, Film Commissioner, Toronto Film and<br />

Television Office, and Donna Zuchlinski, Provincial Film<br />

Commissioner, Ontario, will give you an insider’s view of what<br />

it takes to get from concept to the big screen. During their<br />

presentation, they will share stories of the challenges, the<br />

strangest requests and funniest moments they’ve experienced<br />

as the mavens of Toronto’s Hollywood North.<br />

Monday, May 23 10:00 am – 11:00 am<br />

Picasso and Ceramics<br />

The Gardiner Museum of Ceramic Art is the only museum in<br />

Canada entirely devoted to ceramics. Situated in the heart of<br />

downtown Toronto, across from the Royal Ontario Museum, the<br />

Gardiner is one of Toronto's outstanding cultural destinations.<br />

Although the museum will be closed for renovation during the<br />

<strong>ASNR</strong> meeting, <strong>ASNR</strong> Guest Hospitality participants can still<br />

have an experience from this “jewel box” of ceramic treasurers.<br />

Sue Jeffries, Gardiner Museum Curator of Contemporary<br />

Ceramics, will present “Picasso and Ceramics”, highlights from<br />

the Museum’s most recent exhibition.<br />

Pablo Picasso was the most influential artist of the 20th<br />

century. His universally recognized name connotes energy,<br />

daring and originality. Although seldom described as a ceramic<br />

artist, Picasso devoted considerable energy to the medium over<br />

a period of twenty years at the height of his fame, producing an<br />

estimated 4,500 ceramic works. Ms. Jeffries’ presentation will<br />

highlight his appropriation of historic ceramic traditions and<br />

his major innovations when he took these forms and reinvigorated<br />

them in his own inimitable way.<br />

Thursday, May 26 10:00 am – 11:00 am


Future <strong>ASNR</strong> Annual Meetings<br />

2006<br />

44th Annual Meeting<br />

April 29 – May 5<br />

San Diego Convention Center<br />

San Diego, California<br />

2007<br />

45th Annual Meeting<br />

June 9 – 15<br />

Hyatt Regency Chicago Hotel<br />

Chicago, Illinois<br />

2008<br />

46th Annual Meeting<br />

May 31 – June 6<br />

Morial Convention Center<br />

New Orleans, Louisiana<br />

2009<br />

47th Annual Meeting<br />

May 16 – 22<br />

Vancouver Convention &<br />

Exhibition Centre<br />

Vancouver, British Columbia,<br />

Canada<br />

<strong>ASNR</strong> Past Presidents and Founders<br />


1962-64 Juan M. Taveras, MD*<br />

1964-65 Mannie M. Schechter, MD*<br />

1965-66 Donald L. McRae, MD*<br />

1966-67 Ernest H. Wood, MD*<br />

1967-68 Harold O. Peterson, MD*<br />

1968-69 Colin B. Holman, MD<br />

1969-70 Giovanni Di Chiro, MD*<br />

1970-71 D. Gordon Potts, MD<br />

1971-72 Norman E. Chase, MD<br />

1972-73 Fred J. Hodges, III, MD<br />

1973-74 T. Hans Newton, MD<br />

1974-75 Hillier L. Baker, Jr., MD<br />

1975-76 Irvin I. Kricheff, MD<br />

1976-77 Norman E. Leeds, MD<br />

1977-78 Sadek K. Hilal, MD*<br />

1978-79 Stephen A. Kieffer, MD<br />

1979-80 David O. Davis, MD<br />

1980-81 George Wortzman, MD<br />

1981-82 Gabriel H. Wilson, MD<br />

1982-83 Arthur E. Rosenbaum, MD<br />

1983-84 O. Wayne Houser, MD<br />

1984-85 Samuel M. Wolpert, MD<br />

1985-86 R. Thomas Bergeron, MD<br />

1986-87 Derek C. Harwood-Nash, MD*<br />

1987-88 Michael S. Huckman, MD<br />

1988-89 Anne G. Osborn, MD<br />

1989-90 Joseph F. Sackett, MD<br />

1990-91 Anton N. Hasso, MD, FACR<br />

1991-92 R. Nick Bryan, MD, PhD<br />

1992-93 David Norman, MD<br />

2010<br />

48th Annual Meeting<br />

May 15 – 21<br />

Hynes Convention Center<br />

Boston, Massachusetts<br />

1993-94 Glenn Forbes, MD<br />

1994-95 Robert M. Quencer, MD<br />

1995-96 Robert R. Lukin, MD<br />

1996-97 Burton P. Drayer, MD<br />

1997-98 Richard E. Latchaw, MD<br />

1998-99 A. James Barkovich, MD<br />

1999-00 Eric J. Russell, MD, FACR<br />

2000-01 William S. Ball, Jr., MD<br />

2001-02 William P. Dillon, MD<br />

2002-03 Patrick A. Turski, MD<br />

2003-04 Charles M. Strother, MD<br />


Norman E. Chase, MD<br />

Giovanni Di Chiro, MD*<br />

William N. Hanafee, MD<br />

Fred J. Hodges, III, MD<br />

Colin B. Holman, MD<br />

Norman E. Leeds, MD<br />

Eugene V. Leslie, MD<br />

Donald L. McRae, MD*<br />

Thomas H. Newton, MD<br />

Harold O. Peterson, MD*<br />

D. Gordon Potts, MD<br />

Mannie M. Schechter, MD*<br />

Juan M. Taveras, MD*<br />

Ernest H. Wood, MD*<br />

*deceased<br />

XXIII<br />

Toronto, Canada Canada

May 21-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XXIV<br />


Past <strong>ASNR</strong> Annual Meetings<br />

Organizational Meeting<br />

May 19, 1962<br />

Keene’s English Chophouse<br />

New York<br />

Second Business Meeting<br />

October 5, 1962<br />

Shoreham Hotel<br />

Washington, DC<br />

First Annual Meeting<br />

October 7, 1963<br />

Queen Elizabeth Hotel<br />

Montreal<br />

Second Annual Meeting<br />

September 23, 1964<br />

Waldorf Astoria<br />

New York<br />

Third Annual Meeting<br />

June 11, 1965<br />

Dennis Hotel<br />

Atlantic City<br />

Fourth Annual Meeting<br />

June 15-16, 1966<br />

Sheraton-Park Hotel<br />

Washington, DC<br />

Fifth Annual Meeting<br />

May 15, 1967<br />

Columbia University<br />

New York<br />

Sixth Annual Meeting<br />

September 27-28, 1968<br />

Jung Hotel<br />

New Orleans<br />

Seventh Annual Meeting<br />

May 13-19, 1969<br />

Joint Meeting with American Association<br />

of Neurological Surgeons<br />

Sheraton-Cleveland Hotel<br />

Cleveland<br />

Eighth Annual Meeting<br />

February 12-13, 1970<br />

Washington Hilton<br />

Washington<br />

Ninth Annual Meeting<br />

May 27-29, 1971<br />

Fairmont Hotel<br />

San Francisco<br />

Tenth Annual Meeting<br />

February 21-24, 1972<br />

Maria-lsabel Sheraton<br />

Mexico City<br />

Eleventh Annual Meeting<br />

May 26-28, 1973<br />

Statler Hilton<br />

Boston<br />

Twelfth Annual Meeting<br />

March 14, 1974<br />

(In conjunction with X Symposium<br />

Neuroradiologicum)<br />

Convention Center<br />

Punta del Este, Uruguay<br />

Thirteenth Annual Meeting<br />

June 3-7, 1975<br />

Bayshore Inn<br />

Vancouver<br />

Fourteenth Annual Meeting<br />

May 18-22, 1976<br />

Peachtree Plaza<br />

Atlanta<br />

Fifteenth Annual Meeting<br />

March 27-31, 1977<br />

Hamilton Princess Hotel<br />

Bermuda<br />

Sixteenth Annual Meeting<br />

February 26-March 2, 1978<br />

Hyatt Regency<br />

New Orleans<br />

Seventeenth Annual Meeting<br />

May 20-24, 1979<br />

Hotel Toronto<br />

Toronto<br />

Eighteenth Annual Meeting<br />

March 16-21, 1980<br />

Century Plaza<br />

Los Angeles<br />

Nineteenth Annual Meeting<br />

May 5-9, 1981<br />

Marriott Hotel<br />

Chicago<br />

Twentieth Annual Meeting<br />

October 10-16, 1982<br />

(In conjunction with XII Symposium<br />

Neuroradiologicum)<br />

Washington Hilton<br />

Washington, DC<br />

Twenty-First Annual Meeting<br />

June 5-9, 1983<br />

St. Francis Hotel<br />

San Francisco

Past <strong>ASNR</strong> PAST Annual Meetings MEETINGS<br />

(continued)<br />

Twenty-Second Annual Meeting<br />

June 2-7, 1984<br />

Westin Copley Place Hotel<br />

Boston<br />

Twenty-Third Annual Meeting<br />

February 18-23, 1985<br />

Marriott Hotel<br />

New Orleans<br />

Twenty-Fourth Annual Meeting<br />

January 19-23, 1986<br />

Sheraton Harbor Island Hotel<br />

San Diego<br />

Twenty-Fifth Annual Meeting<br />

(Silver Anniversary)<br />

May 10-15, 1987<br />

New York Hilton<br />

New York<br />

Twenty-Sixth Annual Meeting<br />

May 15-20, 1988<br />

Chicago Hilton & Towers<br />

Chicago<br />

Twenty-Seventh Annual Meeting<br />

March 19-24, 1989<br />

The Peabody Orlando<br />

Orlando<br />

Twenty-Eighth Annual Meeting<br />

March 19-23, 1990<br />

Century Plaza Hotel & Tower<br />

Los Angeles<br />

Twenty-Ninth Annual Meeting<br />

June 9-14, 1991<br />

The Washington Hilton and Towers<br />

Washington, DC<br />

Thirtieth Annual Meeting<br />

May 31-June 5, 1992<br />

Adam’s Mark<br />

St. Louis<br />

Thirty-First Annual Meeting<br />

May 17-20, 1993<br />

Vancouver Trade and Convention Centre<br />

Vancouver<br />

Thirty-Second Annual Meeting<br />

May 3-7, 1994<br />

Opryland Hotel and Conference Center<br />

Nashville<br />

Thirty-Third Annual Meeting<br />

May 23-27, 1995<br />

Sheraton Chicago Hotel and Towers<br />

Chicago<br />

Thirty-Fourth Annual Meeting<br />

June 23-27, 1996<br />

Washington State Convention and Trade Center<br />

Seattle<br />

Thirty-Fifth Annual Meeting<br />

May 18-22, 1997<br />

Metro Toronto Convention Centre<br />

Toronto<br />

Thirty-Sixth Annual Meeting<br />

May 17-21, 1998<br />

(In conjunction with XVI Symposium<br />

Neuroradiologicum)<br />

Pennsylvania Convention Center<br />

Philadelphia<br />

Thirty-Seventh Annual Meeting<br />

May 23-28, 1999<br />

San Diego Convention Center<br />

San Diego<br />

Thirty-Eighth Annual Meeting<br />

April 4-8, 2000<br />

Hyatt Regency Atlanta<br />

Atlanta<br />

Thirty-Ninth Annual Meeting<br />

April 23-27, 2001<br />

Hynes Convention Center<br />

Boston<br />

Fortieth Annual Meeting<br />

May 13-17, 2002<br />

Vancouver Convention & Exhibition Centre<br />

Vancouver<br />

Forty-First Annual Meeting<br />

April 28 – May 2, 2003<br />

Marriott Wardman Park Hotel<br />

Washington, DC<br />

Forty-Second Annual Meeting<br />

June 7 – June 11, 2004<br />

Washington State Convention and Trade Center<br />

Seattle<br />

XXV<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XXVI<br />


Awards and Honors<br />

<strong>2005</strong> <strong>ASNR</strong> Gold Medal Award<br />

The Gold Medal fosters the highest standards of the American Society of Neuroradiology,<br />

based on exceptional quality, service, and excellence, and not necessarily on fame. It<br />

emphasizes both professional and personal attributes… individuals who are superb<br />

neuroradiologists, clinicians, or scientists, and truly outstanding. The recipients are<br />

individuals who have extended themselves beyond furthering their own careers through<br />

contributions at all levels of professional strata, with an accent on consistency and duration<br />

of these outstanding contributions.<br />

Samuel M. Wolpert, MD<br />

In 1976, Dr. Wolpert published “Angiography of Posterior Fossa<br />

Dr. Samuel (Muli) Wolpert was Tumors.” The timing of the publication was unfortunate, since<br />

born in Johannesburg, South computerized axial tomography had recently been discovered;<br />

Africa in 1930, educated in and at the time, many thought that there would be no future<br />

public schools and went to the need for posterior fossa angiography. In 1977, he became<br />

University of the Witwatersrand Treasurer of the <strong>ASNR</strong> and during his tenure presented the idea<br />

Medical School, where he of an <strong>ASNR</strong> journal to the President of the <strong>ASNR</strong>, Dr. Sadek<br />

graduated in 1953. In South Hilal, and his Executive Committee. Dr. Wolpert and Dr. Leeds<br />

Africa, after completing his chaired the search committee for an editor-in-chief and,<br />

internship, he spent time as a eventually, Dr. Juan Taveras was chosen as Editor of the AJNR.<br />

resident in Internal Medicine, He invited Dr. Wolpert to be the first Associate Editor, and the<br />

Orthopaedic Surgery and finally initial issue of the AJNR appeared at the beginning of 1980.<br />

Radiology. After traveling to London, he trained at Guy's The history of neuroradiology has been one of Muli's interests,<br />

Hospital and St. Mary's Hospital, and received a D.M.R.D. and recently he edited a series of papers on Neuroradiologic<br />

(Diploma in Medical Radiodiagnosis) in 1960. He then returned Classics which appeared in the AJNR. He became President of<br />

to radiological hospital practice in South Africa.<br />

the <strong>ASNR</strong> in 1984.<br />

In 1963-1964, Dr. Mannie Schechter, Senior Neuroradiologist In 1992, Dr. Wolpert was the lead neuroradiological investigator<br />

at the Albert Einstein College of Medicine (AECOM) in New York in one of the first studies on the value of intravenous<br />

and a major influence on Dr. Wolpert's career, visited his home recombinant tissue plasminogen activator in the treatment of<br />

country of South Africa. Mannie offered Dr. Wolpert a two-year acute stroke. The Boston Floating Hospital, a pediatric hospital,<br />

NIH fellowship in Neuroradiology. Through this fortunate visit of is part of NEMC, and many of Dr. Wolpert's publications were on<br />

Dr. Schechter to South Africa, Muli emigrated to the United pediatric neuroradiology. This interest culminated in the<br />

States in December 1964, and commenced a two-year publication of “MRI in Pediatric Neuroradiology,” by Dr. Wolpert<br />

fellowship at AECOM in January 1965.<br />

and Dr. Patrick Barnes of Children's Hospital in 1992. Dr.<br />

Wolpert is a charter member of the Board of Directors of the<br />

Dr. Wolpert did not initially intend to specialize in<br />

American Society of Pediatric Neuroradiology (ASPNR). In June<br />

neuroradiology, but impressed by the quality of the<br />

2004, because of his interest in and publications on pediatric<br />

neurologists, neurosurgeons and neuropathologists at the<br />

neuroradiology, Dr. Wolpert received a Special Recognition Award<br />

AECOM, as well as by the charisma and competence of Mannie<br />

from the ASPNR. He has published 3 books, 114 papers and 24<br />

Schechter, he decided that this was going to be his ultimate<br />

chapters. He has had multiple speaking engagements, in the<br />

career choice. In 1967, Drs. Alice Ettinger and Robert Paul of<br />

United States and overseas, and was Vice-President of the New<br />

the New England Medical Center Hospitals (NEMC) in Boston<br />

England Roentgen Ray Society, as well as a member of numerous<br />

recruited Dr. Wolpert as a neuroradiologist. He stayed at NEMC<br />

radiological societies. He has been an examiner for the American<br />

for the next 30 years.<br />

Board of Radiology and a CAQ examiner in neuroradiology.<br />

He climbed the academic ladder at Tufts University School of<br />

Now living in Santa Fe and retired after a part-time<br />

Medicine, becoming a full professor of Radiology in 1974, and<br />

neuroradiology stint at the University of New Mexico Health<br />

of Neurology in 1979. He initiated a fellowship training<br />

Medical Center, Dr. Wolpert is devoting his time<br />

program, training 36 fellows between 1971 and 1997, and also<br />

(unsuccessfully) to reducing his golf handicap, oil painting (also<br />

started the Boston Neuroradiology Club. With Dr. Bennett<br />

unsuccessfully) and opera. (He has been a backstage docent at<br />

Stein's encouragement, Muli commenced embolizing AVMs<br />

the Santa Fe Opera for the last 5 years). Dr. Wolpert and his<br />

utilizing silastic emboli, which limited the hemorrhagic<br />

wife Cynthia have been married 48 years and have three<br />

complications that could ensue during surgical removal of the<br />

children, David (a physicist at NASA-Ames in California),<br />

AVMs. The two physicians were invited to discuss their<br />

Michelle (a bank officer in Houston), and Steven (a family<br />

experience at one of the national television morning shows. The<br />

practitioner in Phoenix).<br />

show was advertised as “Sam's balls cure stroke.”


Awards and Honors<br />

Past <strong>ASNR</strong> Gold Medal Award Recipients<br />

1995<br />

Juan M. Taveras, MD*<br />

T. Hans Newton, MD<br />

1996<br />

Sadek K. Hilal, MD*<br />

Giovanni Di Chiro, MD*<br />

1997<br />

Derek C. Harwood-Nash, MB, ChB.,<br />


<strong>2005</strong> <strong>ASNR</strong> Honorary Member<br />

Professor Luc Picard<br />

1998<br />

Irvin I. Kricheff, MD<br />

D. Gordon Potts, MD<br />

1999<br />

Grant B. Hieshima, MD<br />

Michael S. Huckman, MD<br />

2000<br />

Hillier L. “Bud” Baker, Jr., MD<br />

2001<br />

O. Wayne Houser, MD<br />

J. Arliss Pollock, MD<br />

Dr. Luc Picard, a neuroradiologist<br />

and a neurologist, graduated<br />

from the University of Nancy,<br />

France. He was initially trained in<br />

neurology and worked in close<br />

cooperation with an interventional<br />

neuroradiology pioneer in Paris,<br />

Professor René Djindjian. Having<br />

been appointed Associate<br />

Professor of Radiology in 1970,<br />

he was in charge of all the<br />

neuroradiological investigations of the University Hospital.<br />

Thanks to his work, he created a full-fledged independent<br />

Department of Neuroradiology, of which he was appointed<br />

Director in 1977. He performed his first series of<br />

embolizations in 1968, and created a laboratory for<br />

experimental neuroradiology at Nancy. Having been<br />

appointed to the new Chair of Professor of Neuroradiology,<br />

he began his effort for the development of interventional<br />

neuroradiology. In 1982, he organized the annual meeting<br />

of the Working Group in Interventional Neuroradiology<br />

(WIN) at Val d'Isère-France. He is a founding member of the<br />

World Federation of Interventional and Therapeutic<br />

Neuroradiology, of which he was the President from 1993<br />

until 1995.<br />

With the expansion of his administrative responsibilities,<br />

he has dedicated himself to the development of<br />

neuroradiology as a specialty. He was founding member<br />

of the European Society of Neuroradiology (ESNR) and of<br />

the French Society of Neuroradiology (SFNR), of which<br />

he was appointed General Secretary before becoming<br />

President. Founding member of the Journal of<br />

Neuroradiology in 1974, he became its Chief Editor from<br />

1978 until 2002. He is also a founding Editorial Board<br />

member of Interventional Neuroradiology. As a tribute to<br />

his vast experience, he has given more than 300 guest<br />

2002<br />

R. Thomas Bergeron, MD<br />

David O. Davis, MD<br />

2003<br />

Norman E. Leeds, MD, FACR<br />

Anne G. Osborn, MD, FACR<br />

2004<br />

Ralph Heinz, MD, FACR<br />

Stephen A. Kieffer, MD, FACR<br />

*deceased<br />

lectures (United States, South America, Japan, China<br />

and India). His publications in diagnostic and<br />

therapeutic neuroradiology number over 400. He has<br />

organized many meetings, and particularly the XVIIth<br />

Symposium Neuroradiologicum in Paris in 2002. In<br />

1999, he was elected a member of the French National<br />

Academy of Surgery, and was awarded “Chevalier de la<br />

Légion d'Honneur” in 2002. At the present time, he<br />

serves as Vice-President of the World Federation of<br />

Neuroradiological Societies (WFNRS).<br />

Toronto, Canada<br />

Toronto, Canada<br />


May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XXVIII<br />


Awards and Honors<br />

Past <strong>ASNR</strong> Honorary Member Recipients<br />

Torsten Almen, MD<br />

James W. Bull, MD*<br />

Graeme M. Bydder, MD, ChB<br />

M. Paul Capp, MD<br />

Sten Cronqvist, MD*<br />

B. G. Ziedses des Plantes, MD*<br />

George du Boulay, MD*<br />

Richard R. Ernst, MD<br />

Torgny V. B. Greitz, MD<br />

Godfrey N. Hounsfield, PhD*<br />

Yun Peng Huang, MD<br />

Ian Isherwood, MD<br />

Pierre Lasjaunias, MD, PhD<br />

Awards and Honors<br />

<strong>ASNR</strong> 2004 Outstanding Presentation Awards<br />

<strong>ASNR</strong> is pleased to announce the winners of the Outstanding Presentation Awards given annually to the<br />

top paper or poster presentation from the prior Annual Meeting in general neuroradiology and the four<br />

neuroradiology specialties. A $1,000 award was given to each winner.<br />

General Neuroradiology<br />

“Evaluation of a Signal Intensity Mask in the<br />

Interpretation of Functional MR Imaging<br />

Activation Maps”<br />

Strigel, R. M., Haughton, V. M., Moritz, C., Field, A.<br />

S., Badie, B., Wood, D. A., Hartman, M., Rowley, H. A.<br />

University of Wisconsin at Madison<br />

Madison, WI<br />

Berlex Best Paper Award in General Neuroradiology<br />

“Assessment of Tissue Viability with Quantitative CT<br />

Perfusion in Acute Ischemic Stroke Patients Treated<br />

with Intraarterial Thrombolysis”<br />

Schaefer, P. W., Roccatagliata, L., Ledezma, C. J.,<br />

Gonzalez, R. G., Koroshetz, W. J., Lev, M. H.<br />

Massachusetts General Hospital<br />

Boston, MA<br />

Head and Neck Radiology<br />

“Physiologic Enhancement of the Labyrinth<br />

Demonstrated on Delayed FLAIR Imaging”<br />

Butman, J. A.<br />

Warren G. Magnuson Clinical Center,<br />

National Institutes of Health<br />

Bethesda, MD<br />

Paul C. Lauterbur, PhD<br />

Dennis LeBihan, MD, PhD<br />

Marco Leonardi, MD<br />

Erik Lindgren<br />

Claude H. Manelfe, MD<br />

Joseph Ransohoff, MD*<br />

Jesus Rodriguez-Carbajal, MD<br />

Lee F. Rogers, MD<br />

Prof. Lucy Balian Rorke<br />

Michael Radford Sage, MD,<br />


FRCPC (Ed), FHKCR (Hon)<br />

George Schuyler<br />

S. I. Seldinger, MD<br />

Fjodor Serbinenko, MD<br />

Mutsumasa Takahashi, MD<br />

Michel Ter Pogossian, MD*<br />

Galdino E. Valvassori, MD<br />

Marjo S. van der Knaap, MD<br />

Prof. Jacqueline Vignaud<br />

M. Gazi Yasargil, MD<br />

Ian R. Young, BSc, PhD<br />

*deceased<br />

Interventional Neuroradiology<br />

(The Michael Brothers Memorial Award)<br />

“Three-Dimensional Cerebral Angiography:<br />

Radiation Dose Comparison with Digital<br />

Subtraction Angiography”<br />

Schueler, B., Kallmes, D., Cloft, H. J.<br />

Mayo Clinic<br />

Rochester, MN<br />

Pediatric Neuroradiology<br />

(The Derek C. Harwood-Nash Award)<br />

“MR Imaging of the Fetal Cerebellar Vermis In Utero:<br />

Criteria for Abnormal Development, with Ultrasonographic<br />

and Clinicopathologic Correlation”<br />

Robinson, A. J. 1 , Blaser, S. 1 , Toi, A. 2 , Chitayat, D. 2 ,<br />

Ryan, G. 2 , Pantazi, S. 2 , Gundogan, M. 2 Laughlin, S. 1<br />

1Hospital for Sick Children, Toronto, ON, CANADA,<br />

2Mount Sinai Hospital, Toronto, ON, CANADA<br />

Spine Radiology<br />

“Can Real Time Video Fluoroscopy of the<br />

Cervical Spine Differentiate the Normal from<br />

the Abnormal Spine?”<br />

Rothman, S. L. G. 1 , Go, J. L. 1 , Irvine, B. 2 ,<br />

Kim, P. E. 1 , Zee, C. S. 1<br />

1University of Southern California, Los Angeles, CA<br />

2Private Practice, Redondo Beach, CA

AWARDS & Awards and Honors HONORS<br />

2004 Regional Society Awards<br />

The American Society of Neuroradiology is pleased to announce the recipients of the 2004 Regional Society<br />

Awards. These individuals were selected by the respective regional societies as having the best presentation at<br />

each society’s 2004 Annual Meeting.<br />

Eastern Neuroradiological Society (ENRS)<br />

(The Norman E. Leeds Award)<br />

“Characterization of Cerebral<br />

Aneurysms for Assessing Risk<br />

of Rupture Using Patient-<br />

Specific Computational<br />

Hemodynamic Models”<br />

Christopher M. Putman, MD<br />

Inova Fairfax Hospital<br />

Falls Church, VA<br />

Southeastern Neuroradiological Society<br />

(SENRS)<br />

“Are Protective Devices Necessary<br />

for Carotid Stenting?”<br />

Gregory J. Joseph, MD<br />

Presbyterian Hospital<br />

Charlotte, NC<br />

This award, created in 2004 in<br />

recognition of consistent excellence and<br />

lifelong accomplishment in basic or<br />

clinical neuroscience research, is given<br />

to an <strong>ASNR</strong> senior member over the age<br />

of 50 recognized in the neuroradiology<br />

field for distinguished long term achievement in<br />

basic or clinical research.<br />

The recipient of the award is:<br />

Dixon M. Moody, MD, FACR<br />

Wake Forest University, School of Medicine<br />

Winston-Salem, NC<br />

Dixon M. Moody, MD, FACR<br />

Dr. Moody is recognized worldwide for his contributions in<br />

radiologic-pathology correlation of brain microvascular<br />

anatomy and disease. A Charles A. Dana Foundation<br />

award recipient, he also has a long track record of NIH<br />

funding with the principal grant,<br />

originally (1984) a Jacob K.<br />

Javits Neuroscience Investigator<br />

Award, funded through 2008 –<br />

the 24th year of this project.<br />

Dr. Moody recently finished a 6year<br />

term on the Diagnostic<br />

Radiology Study Section of the<br />

National Institutes of Health<br />

(NIH). He served a 4-year term<br />

on the National Advisory Council<br />

of the National Institute of<br />

Neurological Diseases and Stroke (NINDS) of the NIH,<br />

which provides recommendations for the conduct and<br />

support of epidemiological and fundamental research on<br />

neurological diseases.<br />

Western Neuroradiological Society<br />

(WNRS) (The Gabriel H. Wilson Award)<br />

“Are There MR Imaging Features<br />

That Predict Regression of Lumbar<br />

Disk Herniation?”<br />

William K. Erly, MD<br />

University of Arizona<br />

Tucson, AZ<br />

The Neuroradiology Education and Research (NER) Foundation Award for<br />

Outstanding Contributions in Research<br />

In studies designed by Dr. Moody and funded by his<br />

grants, he and members of his team have been<br />

instrumental in furthering our understanding of the cause<br />

(lipid microemboli during cardiopulmonary bypass) of<br />

brain complications related to heart surgery and of<br />

strategies for its prevention. He published a<br />

comprehensive study of the normal human cerebral<br />

microvascular pattern. Contrary to prevailing opinion at<br />

the time, Moody demonstrated that germinal matrix<br />

hemorrhage in premature neonates results from rupture of<br />

veins rather than arterioles/capillaries; Charcôt-Bouchard<br />

microaneurysms are very rare and are not the etiology of<br />

most spontaneous brain hemorrhages; precapillary<br />

arteriolar-venular anastomoses (thoroughfare channels), a<br />

germinal matrix vascular rete, or intraparenchymal<br />

arteriole-to-arteriole shunts are not normally present in<br />

humans from the limits of viability in pre-term neonates to<br />

adults; the pathological substrate for the radiological<br />

finding of leukoaraiosis is apoptosis-induced<br />

oligodendrocyte cell death associated with capillary dropout<br />

and occasionally stenosis of the deep cerebral veins<br />

(periventricular venous collagenosis); string vessels,<br />

probably degenerating capillary/arterioles, are found in<br />

significantly increased numbers in subjects with<br />

Alzheimer’s disease – reinforcing the theory that a vascular<br />

component may contribute to this degenerative<br />

neurological disease.<br />

The 2004 Neuroradiology Education and Research<br />

(NER) Foundation Award for Outstanding Contributions<br />

in Research award recipient was:<br />

Robert I. Grossman, MD<br />

XXIX<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XXX<br />

AWARDS & Awards and Honors HONORS<br />

<strong>2005</strong>-2006 Berlex/NER Foundation Fellowship in Basic Science Research Award<br />

This fellowship, first awarded in 1986, was created by<br />

the <strong>ASNR</strong> with the support of Berlex Laboratories to<br />

stimulate the scientific development of promising<br />

young men and women, and to aid them in embarking<br />

on a career in academic radiology. It is specifically<br />

designed to provide educational opportunities for<br />

young radiologists who are not yet professionally<br />

established in the radiologic sciences to gain further<br />

insight into scientific investigation, and to develop<br />

competence in research. These fellowships are jointly<br />

sponsored by Berlex Laboratories, Inc. and the<br />

Neuroradiology Education and Research (NER)<br />

Foundation of the American Society of Neuroradiology.<br />

1986-87<br />

Jeremy B. Rubin, MD,<br />

Stanford University Medical Center<br />

“New Methods Using MRI to A se s Ventricular Shunt<br />

Function and Measure Intravenous Pre sure Non-invasively<br />

in Patients with Ventricular Shunt Catheters”<br />

1987-88<br />

No Award<br />

1988-89<br />

Apichai Jarenwattananon, MD,<br />

University of Wisconsin Medical Center<br />

“In-Vivo Sodium MRI (Na-MRI) in Canine<br />

Model of Status Epilepticus”<br />

Warren A. Stringer, MD,<br />

Loma Linda University Medical Center<br />

“Evaluation of the Relationships Between Cerebral<br />

Perfusion, Ventilation, and Intracranial Pressure by<br />

Xenon-enhanced Computed Tomography in Children<br />

with Cerebral Edema”<br />

1989-90<br />

Todd Lempert, MD,<br />

University of California at San Francisco<br />

“Evaluation of the Healing Response to Thrombogenic<br />

Coil Occlusion of Experimental Aneurysms”<br />

1990-91<br />

Lori L. Baker, MD,<br />

Stanford University Medical Center<br />

“Evaluation of MR Diffusion Imaging Versus Magnetic<br />

Susceptibility Enhanced Mapping of Perfusion Pool<br />

in Regional Cerebral Ischemia”<br />

The recipients of the <strong>2005</strong>-06 fellowships are:<br />

Srinivasan Mukundan, Jr., PhD, MD<br />

Duke University Medical Center<br />

“Toward the Development of a Nanoscale, Target-<br />

Specific Liposomal Platform Technology for Computed<br />

Tomography Based Molecular Imaging”<br />

Max Wintermark, MD<br />

University of California, San Francisco<br />

“Morphometric and Functional Characterization of<br />

Atherosclerotic Carotid Disease by Multidetector-Row<br />

CT-Angiography: A Comparative Study with Ex Vivo<br />

Histology and Imaging”<br />

Past Berlex/NER Foundation Fellowship in Basic Science Research Award<br />

1990-91 (continued)<br />

Lee H. Monsein, MD,<br />

The Johns Hopkins University School of Medicine<br />

“Primate Model of Reversible Regional<br />

Cerebral Ischemia”<br />

1991-92<br />

Steven N. Breiter, MD, The Johns Hopkins Hospital<br />

“Proton MRS in the Determination of Lactic Acid<br />

Concentration in Seizures, Both Human and Animal”<br />

Frank J. Lexa, VII, MD, University of Pennsylvania<br />

“MRI Demonstration of Axonal Transport<br />

in the Mammalian CNS”<br />

1992-93<br />

Michael A. Kraut, MD, PhD,<br />

The Johns Hopkins Hospital<br />

“Lactate Production and Metabolism<br />

in Cerebral Activation”<br />

Brian W. Chong, MD,<br />

University of California at San Diego<br />

“A Search for Hidden MRI Flow Patterns<br />

in Human Cranial Vessels”<br />

1993-94<br />

Thomas E. Conturo, MD, PhD,<br />

The Johns Hopkins Hospital and<br />

Johns Hopkins University<br />

“Mechanisms of the Phase Enhancement Effects of<br />

Bolus-Injected Paramagnetic Contrast Agents and<br />

Applications in Quantitative Cerebral Blood Volume<br />

and Flow Imaging”<br />

John P. Karis, MD, Barrow Neurological Institute<br />

“Epilepsy Localization: Advanced High Resolution<br />

MRI-PET FDG Correlation”

AWARDS & Awards and Honors HONORS<br />

Past Berlex/NER Foundation Fellowship in Basic Science Research Award (Continued)<br />

1994-95<br />

Jerry Burke, MD, Bowman Gray School of Medicine<br />

“Serial Positron Emission Tomography and Functional<br />

MR Imaging of Stroke”<br />

Robert Fulbright, MD,<br />

Yale University School of Medicine<br />

“Functional MR Imaging of the Spine”<br />

1995-96<br />

Norman J. Beauchamp, MD,<br />

The Johns Hopkins Hospital<br />

“The Natural History of ‘Areas of Risk of Infarction’ as<br />

Defined by Perfusion MRI and MR Spectroscopy”<br />

Anthony Masaryk, MD,<br />

University of Wisconsin-Madison<br />

“Analysis of Aneurysm Hemodynamics Using<br />

MRI/MRA Morphology and Flow Measurements<br />

Correlated with Hemodynamic Numerical Analysis<br />

and Simulation”<br />

1996-97<br />

Joseph T. Lurito, MD, PhD,<br />

The Johns Hopkins Hospital<br />

“Functional MRI and Electrophysiologic Correlates of<br />

Sub-modality Specific Somatosensory Activation”<br />

Jeffrey L. Sunshine, MD,<br />

University Hospitals of Cleveland<br />

“Early Identification of Ischemic Penumbra by Diffusion<br />

and Perfusion MR in Acute Stroke”<br />

1997-98<br />

Huy M. Do, MD,<br />

University of Virginia Health Sciences Center<br />

“The Neuroprotective Effect of Intraarterial<br />

Nerve Growth Factor (HGF) in a Rabbit Embolic<br />

Stroke Model”<br />

1998-99<br />

William F. Marx, MD, University of Virginia<br />

“Endovascular Treatment of Experimental Aneurysms<br />

Using Biologically Modified Embolic Coils:<br />

Promotion of Permanent Occlusion via<br />

Intra-aneurysmal Fibroblast Delivery”<br />

1999-00<br />

Kevin R. Moore, MD,<br />

University of Utah Center for Advanced Medical<br />

Technology<br />

“Meg-Constrained High-Resolution Surface-Coil MR<br />

Imaging and MR Spectroscopy for Evaluating<br />

Medically Refractory Epilepsy”<br />

John G. Short, MD, University of Virginia<br />

“Induction of Spinal Interbody Fusion Using Gene<br />

Therapy Tissue Engineering Techniques”<br />

2000-01<br />

John Port, MD, PhD,<br />

The Johns Hopkins Medical Institution<br />

“Imaging Selective Attention Mechanisms”<br />

Eric Schwartz, MD,<br />

Hospital of the University of Pennsylvania<br />

“Diffusion-based MR Imaging in a Rat Spinal Cord<br />

Following Injury and Transplantation”<br />

2001-02<br />

Pratik Mukherjee, MD, PhD,<br />

Mallinckrodt Institute of Radiology,<br />

Washington University School of Medicine<br />

“Comparison of Magnetic Resonance Imaging and<br />

Positron Emission Tomography in the Study of<br />

Cerebral Hemodynamics”<br />

2002-03<br />

John G. Dalle, DO,<br />

University of Utah School of Medicine<br />

“Polymer-Chelate Conjugates for Diagnostic<br />

Cancer Imaging”<br />

Christopher Lascola, MD, PhD,<br />

Duke University Medical Center<br />

“Magnetic Resonance Imaging of Spreading<br />

Depression-Induced Reactive Gliosis in Mice”<br />

2003-04<br />

Dheeraj Gandhi, MD,<br />

University of Michigan Health System<br />

“Can the Choline/Creatine Ratio Predict Early<br />

Treatment Response of Head and Neck Squamous<br />

Cell Carcinma Treated with Radiation Therapy in an<br />

Animal Model: A Prospective Study”<br />

Susan M. Kealey, MD,<br />

Duke University Medical Center<br />

“Correlation of MR Permeability Measurements<br />

with Histologic Markers of Angiogenesis in Rodent<br />

High-Grade Brain Tumors Before and After Treatment<br />

with Antiangiogenesis Agent PTK 787”<br />

2004-05<br />

Tuong Huu Le, MD, PhD<br />

University of California, San Francisco<br />

“Structural and Functional Correlates of Axonal<br />

Shearing in Traumatic Brain Injury: A Combined<br />

DTI, fMRI and MSI Study”<br />

Whitney B. Pope, MD, PhD<br />

David Geffen School of Medicine at University<br />

of California, Los Angeles<br />

“Identification of Unstable Atheroscelerotic Plaque at<br />

the Carotid Bisfurcation Using High-Resolution CT-<br />

PET Imaging: Correlation to Histopathology and<br />

Patient Symptoms”<br />

XXXI<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XXXII<br />


Awards and Honors<br />

Neuroradiology Education and Research (NER) Foundation Scholar Award in<br />

Neuroradiology Research*<br />

Since 1995, the NER Foundation has been in the<br />

process of raising funds to support neuroradiology<br />

research. This is one of the most important goals of<br />

the NER Foundation, and of the <strong>ASNR</strong> as the<br />

premier organization for neuroradiology. This award<br />

was created for young investigators in the early<br />

stages of their careers, to enhance their competency<br />

in areas important to the future of neuroradiology,<br />

including health services research, physiological<br />

imaging and interventional neuroradiology. It also<br />

affords the Foundation the opportunity to begin to<br />

develop leadership in these areas.<br />

1999<br />

L. Santiago Medina, MD, MPH<br />

Children’s Hospital Medical Center, Cincinnati, OH<br />

“The Role and Cost-Effectiveness of Imaging in<br />

Newborns with Suspected Occult Spinal Dysraphism”<br />

2000<br />

Melanie B. Fukui, MD<br />

University of Pittsburgh Medical Center, Pittsburgh, PA<br />

“Carotid Stenosis Evaluation: Cost-Effectiveness of<br />

Computed Tomographic Angiography vs. Magnetic<br />

Resonance Angiography”<br />

2001<br />

Soonmee Cha, MD<br />

New York University Medical Center, New York, NY<br />

“Dynamic Contrast Enhanced T2*-weighted MRI and<br />

Histopathological Assessment of Experimental Glioma”<br />

2002<br />

James D. Eastwood, MD<br />

Duke University Medical Center, Durham, NC<br />

“CT Perfusion Imaging in Subarachnoid<br />

Hemorrhage Related Vasospasm”<br />

<strong>2005</strong> NER Foundation/Boston Scientific Fellowship in Cerebrovascular Disease Research<br />

Established in 2002, this fellowship expanded<br />

eligibility to allow both neuroradiology fellows and<br />

all faculty at the Assistant Professor level to apply.<br />

It was created to provide an opportunity for a young<br />

neuroradiologist to pursue research in a topic that<br />

will advance the diagnosis and treatment of<br />

cerebrovascular disease, and is supported by<br />

Boston Scientific.<br />

The recipients of the <strong>2005</strong> scholar award are:<br />

Donna R. Roberts, MD<br />

University of California, San Francisco<br />

“The Assessment of Image-guided Transcranial<br />

Magnetic Stimulation as an Adjuvant to Extradural<br />

Cortical Stimulation for the Treatment of Chronic<br />

Facial Pain”<br />

Steven G. Imbesi, MD*<br />

University of California, San Diego Medical Center<br />

“Alteration of Intracranial Aneurysm Flow Dynamics:<br />

Development and Evaluation of Potential<br />

Neurointerventional Endovascular Treatment<br />

Regimens for Wide Necked Aneurysms”<br />

*recipient awarded second year of funding<br />

Past NER Foundation Scholar Award in Neuroradiology Research Recipients<br />

2003<br />

Steven G. Imbesi, MD<br />

University of California, San Diego Medical Center,<br />

San Diego, CA<br />

“Alteration of Intracranial Aneurysm Flow Dynamics:<br />

Development and Evaluation of Potential<br />

Neurointerventional Endovascular Treatment<br />

Regimens of Wide Necked Aneurysms”<br />

2004<br />

Pratik Mukherjee, MD, PhD<br />

University of California San Francisco,<br />

San Franciso, CA<br />

“Diffusion Tensor MR Imaging and Quantitative<br />

Tractography of Brain Development in<br />

Premature Newborns”<br />

The recipient of the <strong>2005</strong> fellowship is:<br />

Donna Hoghooghi, MD<br />

University of California, San Francisco<br />

“Extent and Effectiveness of Embolization and<br />

Determination of Vascular Supply of Meningiomas<br />

Using a Combined Interventional X-ray/MR<br />

Fluoroscopy Suite”


Awards and Honors<br />

Neuroradiology Education and Research (NER) Foundation Outcomes<br />

Research Grant Related to Neuroradiologic Imaging<br />

This newly created grant is targeted to the<br />

characterization of brain tumors and specifically, the<br />

differentiation of neoplastic from nonneoplastic<br />

condition, effect of MRS on need for biopsy or the<br />

election of a biopsy site, and evaluation of MRS in<br />

radiation necrosis.<br />

<strong>2005</strong> <strong>ASNR</strong> Cornelius G. Dyke Memorial Award<br />

No award is being given in <strong>2005</strong>.<br />

Past <strong>ASNR</strong> Cornelius G. Dyke Memorial Award Recipients<br />

1972<br />

George M. McCord, MD<br />

“The Venous Drainage to The Inferior Sagittal Sinus”<br />

1973<br />

Barton Lane, MD<br />

“Cerebrospinal Fluid Pulsations at Myelography:<br />

A Video-Densitometric Study”<br />

1974<br />

Jacques Theron, MD<br />

“Anatomical-Radiological Correlates of the Anterior<br />

Choroidal Artery”<br />

1975<br />

Thomas P. Naidich, MD<br />

“The Normal Anterior Inferior Cerebellar Artery”<br />

1976<br />

No Award<br />

1977<br />

Burton P. Drayer, MD<br />

“The Capacity for CT Diagnosis of Cerebral Infarction.<br />

An Experimental Study in the Non-Human Primate”<br />

The recipient of the <strong>2005</strong> grant is:<br />

William Hollingsworth, PhD<br />

University of Washington<br />

“Systematic Literature Review of Magnetic Resonance<br />

Spectroscopy (MRS) of the Characterization of<br />

Brain Tumors”<br />

1978<br />

Joseph A. Horton, MD<br />

“The Grain in the Stone: A Computer Search<br />

for Hidden CT Patterns”<br />

1979<br />

Dieter R. Enzmann, MD<br />

“Experimental Brain Abscess Evolution Studied with<br />

the CT Scan and Neuropathological Correlation”<br />

1980<br />

No Award<br />

1981<br />

A. Ronald Cowley, MD<br />

“The Influence of Fiber Tracts on the CT<br />

Appearance of Cerebral Edema: An<br />

Anatomical Pathological Correlation”<br />

1982<br />

B. Ludwig, MD<br />

“Postmortem CT and Autopsy in Perinatal<br />

Intracranial Hemorrhage”<br />

XXXIII<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XXXIV<br />

AWARDS & Awards and Honors HONORS<br />

Past <strong>ASNR</strong> Cornelius G. Dyke Memorial Award Recipients (continued)<br />

1983<br />

No Award<br />

1984<br />

Val M. Runge, MD<br />

“Contrast Enhanced Magnetic Resonance<br />

Evaluation of a Brain Abscess Model”<br />

1985<br />

No Award<br />

1986<br />

Jeremy B. Rubin, MD<br />

“Part 1 Imaging Spinal CSF Pulsation by<br />

2DFT Magnetic Resonance: Significance<br />

During Clinical Imaging”<br />

“Part 2 Harmonic Modulation of Proton MR<br />

Precessional Phase by Pulsatile Motion Origin<br />

of Spinal CSF Flow Phenomenon”<br />

1987<br />

No Award<br />

1988<br />

Vincent P. Mathews, MD<br />

“Gadolinium Enhanced MR Imaging of<br />

Experimental Bacterial Meningitis: Evaluation<br />

and Comparison of CT”<br />

1989<br />

Allen D. Elster, MD<br />

“Europium-DTPA: Development and Testing<br />

of a Gadolinium Analogue Traceable by<br />

Fluorescence Microscopy”<br />

1990<br />

Marvin D. Nelson, Jr., MD<br />

“The Search for Human Telencephalic<br />

Ventriculofungal Arteries”<br />

1991<br />

Udo P. Schmiedl, MD<br />

“Quantitation of Pathological Blood-Brain Barrier<br />

Permeability in an Astrocytic Glioma using Contrast<br />

Enhanced MR”<br />

1992<br />

R. Gilberto Gonzalez, MD<br />

“Quantitative In Vivo Human Brain Lithium Magnetic<br />

Resonance Spectroscopy”<br />

Frank J. Lexa, VII, MD<br />

“Wallerian Degeneration in the Feline Visual System:<br />

Characterization by Magnetization Transfer Rate<br />

with Histopathologic Correlation”<br />

1993<br />

Marc Jouandet, MD<br />

“Mapping the Human Cerebral Cortex<br />

with Brainprints”<br />

1994<br />

A. Gregory Sorensen, MD<br />

“Functional Magnetic Resonance Imaging of Brain<br />

Activity and Perfusion in Patients with Chronic<br />

Cortical Stroke A”<br />

1995<br />

John L. Ulmer, MD<br />

“Magnetization Transfer or Spin-Lock? An<br />

Investigation of Off-Resonance Saturation Pulse<br />

Imaging Using Varying Frequency Offsets”<br />

1996<br />

John C. Strainer, MD<br />

“fMRI of Primary Auditory Cortex: An Analysis of<br />

Pure Tone Activation and Tone Discrimination”<br />

1997<br />

Stephen G. Imbesi, MD<br />

“Why Do Ulcerated Atherosclerotic Caroid Artery<br />

Plaques Embolize? A Flow Dynamics Study”<br />

David F. Kallmes, MD<br />

“Guglielmi Detachable Coil Embolization for<br />

Unruptured Aneurysms in Neurosurgical<br />

Candidates: A Cost Effectiveness Exploration”<br />

1998<br />

No Award<br />

1999<br />

Aquilla S. Turk, DO<br />

“Definition of Aneurysm Ostium (Neck) and<br />

Morphology Using Intravascular Ultrasound:<br />

An Experimental Study in Canines”<br />

2000<br />

William F. Marx, MD<br />

“Endovascular Treatment of Experimental Aneurysms<br />

Using Biologically Modified Embolic Devices: Coil-<br />

Mediated Intra-Aneurysmal Delivery of Fibroblast<br />

Tissue Allografts”<br />

2001<br />

No Award<br />

2002<br />

Mehmet Kocak, MD<br />

“Functional MR Imaging of the Motor Homunculus:<br />

Towards Optimizing Paradigms for Clinical Scenarios”<br />

2003<br />

No Award<br />

2004<br />

Eric D. Schwartz, MD<br />

“Apparent Diffusion Coefficients Within Spinal Cord<br />

Transplants and Surrounding White Matter Correlate<br />

With Degree of Axonal Dieback Following Injury”

CME<br />


Continuing Medical Education (CME)<br />

The <strong>2005</strong> Continuing Medical Education (CME)<br />

Pavilion allows online recording of CME credits via the<br />

Internet. The improvements have created a faster and<br />

more user-friendly system for evaluating sessions and<br />

speakers and recording CME hours electronically.<br />

The CME Pavilion is easily accessible in Room 104A<br />

(Level 100). Please complete the evaluations for each<br />

session to assist in planning future meetings and to help<br />

us maintain accreditation of future programs.<br />


To access the CME evaluation program, run the<br />

“ExpoCard” included in your registration packet<br />

through the card reader at one of the terminals and<br />

follow the simple directions for selecting and<br />

evaluating the sessions you have attended. The<br />

CME credit hours awarded to a session will<br />

automatically be recorded in your record when the<br />

evaluation for a session is completed. Evaluations<br />

can be completed at the end of a session, during<br />

breaks, at the end of the day or the end of the week.<br />

You will be able to view a record of the sessions you<br />

have evaluated and the number of CME credit hours<br />

earned throughout the program. It will also be<br />

possible to print your certificate and transcript to<br />

take home with you.<br />

Please Note: To receive CME credit for sessions<br />

attended at the NER Foundation Symposium <strong>2005</strong><br />

and <strong>ASNR</strong> 43rd Annual Meeting, all evaluations must<br />

be entered by the end of the meeting. The CME<br />

Pavilion replaces the CME booklet of previous years<br />

and is the only method available for receiving your<br />

CME credit.<br />


Accreditation Statement<br />




An enhancement of the Continuing Medical Education<br />

online evaluation system allows for attendees to print<br />

out their official CME certificate for the number of<br />

hours claimed during the NER Foundation Symposium<br />

and <strong>ASNR</strong> 43rd Annual Meeting and take it with them<br />

when they leave. Go to any terminal in the CME<br />

Pavilion and follow the simple directions for printing<br />

out an official NER Foundation Symposium <strong>2005</strong> and<br />

<strong>ASNR</strong> 43rd Annual Meeting CME Certificate.<br />

Following the meeting, the <strong>ASNR</strong> <strong>2005</strong> CME<br />

Certificate site will be available online for 90 days for<br />

attendees to print out their CME certificates.<br />

Please Note: Due to the availability of CME Certificates<br />

online, certificates will not be mailed to attendees.<br />


If you wish to obtain a Letter of Attendance,<br />

please request one at the Registration Desk<br />

located in the North Building Lobby (Level 200)<br />

of the Metro Toronto Convention Centre.<br />

The American Society of Neuroradiology is accredited by the Accreditation Council for Continuing Medical<br />

Education (ACCME) to provide continuing medical education for physicians.<br />

The American Society of Neuroradiology designates this educational activity for a maximum of 34 category<br />

1 credits towards the American Medical Association Physician’s Recognition Award. Each physician should<br />

claim only those hours of credits that he/she spent in the educational activity.<br />

Target Audience<br />

The <strong>ASNR</strong> 43rd Annual Meeting is designed specifically for the practicing general neuroradiologist who wishes<br />

to integrate advanced imaging such as magnetic resonance spectroscopy, diffusion and perfusion imaging, and<br />

functional magnetic resonance imaging into his/her daily practice. Programming is also focused toward the<br />

neuroradiologist who seeks to better understand modern imaging techniques applied to a practice which includes<br />

adults or children, disorders of the spine, head and neck disease, and neurovascular intervention.<br />

XXXV<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XXXVI<br />


<strong>ASNR</strong> 43rd Annual Meeting Educational Objectives<br />

At the conclusion of this meeting, participants will be able to:<br />

General and Advanced Imaging Programming<br />

• Describe the current status of neuroradiological imaging of<br />

the head, neck, spine and interventional imaging in both<br />

adult and pediatric populations.<br />

• Apply state of the art techniques in diffusion imaging,<br />

perfusion imaging, MRS, parallel and high field MR in<br />

the treatment of both adult and pediatric populations.<br />

• Identify a rational imaging approach to stroke, central<br />

nervous system infection, and demyelinating disease.<br />

• Describe the differences between 1.5T and 3T MR<br />

imaging, with emphasis on image artifacts and how<br />

to improve signal-to-noise ratios.<br />

• Discuss MR safety issues, and re-evaluate the relative<br />

contraindications to MR imaging.<br />

Head and Neck Programming<br />

• Identify common imaging presentations of temporal bone<br />

lesions, including inflammatory processes involving the<br />

tympanic cavity, facial palsy, and tinnitus.<br />

• Identify on sectional imaging studies the major<br />

anatomic landmarks separating the superficial and<br />

deeper spaces of the face, and the course of major<br />

neural structures as they traverse the soft tissues<br />

of the neck and cervicothoracic junction.<br />

• Differentiate the imaging appearance of motor denervation<br />

from other pathologic processes involving the head and neck.<br />

• Interpret, in a systematic fashion, sectional-imaging studies<br />

performed on patients with proptosis, and discuss the<br />

evaluation of orbital lesions such as neoplasms and trauma.<br />

• List criteria by which a differential diagnosis of mandibular<br />

and major salivary gland lesions can be created.<br />

• Discuss the prognostic implications of differentiating highgrade<br />

from low-grade sarcomas, and list imaging findings<br />

that significantly impact the surgical and nonsurgical<br />

management of patients with sarcomas of head and neck.<br />

Interventional Programming<br />

• Describe the management strategies for treatment<br />

of cervical carotid artery stenosis.<br />

• Review characteristics and pathology associated with<br />

vascular and lymphatic malformations, and treatment<br />

options for both low-flow and hi-flow vascular malformations.<br />

• Describe the management strategies for treatment of<br />

patients with intracranial atherosclerotic stenosis.<br />

• Identify the processes which underlie reimbursement for<br />

both hospitals and physicians and the method and rationale<br />

of current reimbursement initiatives.<br />

• Examine the RUC survey process and its importance.<br />

• Review endovascular treatment, appropriate patient<br />

selection, relative benefits of each therapy and expected<br />

clinical outcomes for head and neck neoplasms.<br />

Functional Programming<br />

• Describe the use of pre-operative fMRI data in neurosurgical<br />

treatment planning.<br />

• Identify the common neurodegenerative disorders in the<br />

adult patient and review neuroradiologic imaging findings.<br />

• Review the role of angiogenesis in brain tumors.<br />

• Describe the advances in molecular imaging as they relate<br />

to neuroradiology.<br />

Pediatric Programming<br />

• Demonstrate how children with intractable seizure<br />

disorders are evaluated using advanced imaging<br />

techniques and monitoring.<br />

• Review and illustrate the various surgical methods currently<br />

being used to treat children with intractable seizures.<br />

• Discuss outcomes for the various procedures currently used<br />

to treat children with seizure disorders.<br />

• Using case-based methods, present imaging studies of both<br />

common and rare pediatric neurological abnormalities.<br />

• Review the history and pathology of focal white matter<br />

necrosis in children.<br />

• Review the studies of causation of pediatric lesions.<br />

• Describe the epidemiology of periventricular leukomalacia<br />

in premature and term infants.<br />

• Illustrate the appearance and distribution of pediatric lesions<br />

using advanced imaging techniques.<br />

Spine Programming<br />

• Evaluate the use of higher field strength and other advanced<br />

imaging techniques in the diagnosis of spinal problems<br />

in the adult population.<br />

• Discuss recent advances in multi-detector CT imaging<br />

of the spine.<br />

• Evaluate interventional procedures for use in management<br />

of the disorders and diseases in the adult spine, especially<br />

as they relate to pain management.<br />

• Review the imaging findings of common spinal diseases<br />

in an orderly concise manner.<br />

Electronic Learning Center (ELC) and National Library<br />

of Medicine (NLM) Programming<br />

• Demonstrate the basic knowledge of the use of the computer<br />

in the practice of neuroradiology with reference to hardware,<br />

operating system and peripherals for both the Macintosh<br />

and PC platforms.<br />

• Identify and demonstrate use of Internet resources<br />

including PubMed ® , MedlinePlus, other search engines,<br />

and literature search sites.

Electronic ELC Learning WORKSHOPS<br />

Center <strong>2005</strong> Workshops<br />

Gregory L. Katzman, MD, Chair, Program<br />

Hervey D. Segall, MD, Chair Emeritus<br />

ELC Workshops<br />

Electronic Learning Center (ELC) workshops provide the<br />

opportunity for participants to learn new electronic methods in<br />

an interactive small group environment. The workshop format<br />

allows for hands-on and experiential learning with computers,<br />

software, and knowledgeable assistants. Attendance is limited<br />

to 50 participants.<br />

NOTE: 2 participants per computer<br />

The <strong>2005</strong> ELC workshops and lectures will update<br />

attendees on the use of electronic methods useful for the<br />

practicing neuroradiologist and neuroradiologist-educator.<br />

This year’s program will build on the sessions offered at the<br />

2004 meeting.<br />

Workshop registrants will receive a copy of the ELC <strong>2005</strong><br />

Syllabus, an invaluable CD-ROM designed to complement the<br />

ELC program.<br />

The faculty and assisting moderators at the workshops include<br />

both PC and Mac users.<br />

PLEASE NOTE: There is an additional registration fee per<br />

workshop of $50 Member/Non member/Other Professional*;<br />

$10 Fellow/Trainee*.<br />

* Letter from Neuroradiology Fellowship Program Director<br />

confirming status is required. A letter from place of employment<br />

to confirm position is required for Other Professionals.<br />

NOTE: All ELC Workshops will be held in Room 103 (Level 100).<br />

All ELC ticket holders must be present in the room 5 minutes<br />

prior to the start of the session, or your ticket will be resold.<br />

ELC Workshop A: Introductory Powerpoint<br />

Monday, May 23 ■ 8:05am – 9:35am<br />

Tuesday, May 24 ■ 8:00am – 9:30am<br />

Wednesday, May 25 ■ 3:00pm – 4:30pm<br />

David S. Martin, MD (Tues/Wed)<br />

John L. Go, MD (Mon/Tues)<br />

The goal of this workshop is to instruct registrants in the creation<br />

of educational presentations by learning the core concepts of<br />

Microsoft PowerPoint software. Learn how lecture material can be<br />

developed for display using LCD projectors. Learning Objectives of<br />

this workshop include: creating a new presentation from scratch;<br />

using the Office and Presentation Assistants; copying, deleting,<br />

and modifying the sequence of slides; formatting and editing the<br />

text in slides; working with Clip Art, pictures, and other objects;<br />

preparing an entire presentation; saving a presentation in normal<br />

and HTML formats; and printing audience and speaker notes.<br />

ELC Workshop B: Advanced PowerPoint<br />

Monday, May 23 ■ 10:15am – 11:45am<br />

Tuesday, May 24 ■ 10:15am – 11:45am<br />

Wednesday, May 25 ■ 1:00pm – 2:30pm<br />

H. Christian Davidson, MD<br />

Richard H. Wiggins, III, MD<br />

This workshop will address the more advanced techniques of<br />

PowerPoint presentation construction, including insertion of<br />

graphs or tables, linking of objects, transitions, animations,<br />

Richard H. Wiggins, III, MD, Vice Chair, Syllabus Editor<br />

Richard M. Berger, MD, Vice Chair, Moderator & Technical Coordinator<br />

and adding sound or video clips. Learn how to create more<br />

dynamic presentations by making items appear and disappear<br />

on slides and inserting "hidden" controls in the slides. The<br />

lecturers will demonstrate how to link one PowerPoint<br />

presentation to another to control the flow of information and<br />

enable toggling between presentations. Lastly, comments will<br />

be made on the appropriate use of multimedia components for<br />

keeping a talk interesting yet avoiding audience distraction by<br />

too much flash.<br />

ELC Workshop C: Website Creation for the Novice<br />

Monday, May 23 ■ 1:00pm – 2:30pm<br />

Tuesday, May 24 ■ 3:00pm – 4:30pm<br />

Richard H. Wiggins, III, MD<br />

This course is geared toward anyone who is beginning to think<br />

about creating a website for work or personal use. Through a<br />

series of practical demonstrations and hands-on exercises, this<br />

workshop will help you acquire the skills necessary to build and<br />

maintain a basic website. Topics to be covered include: how a<br />

standard web editor works, how to create a basic web page<br />

using images and text, creating links between web pages,<br />

formatting text and paragraphs, creating and changing the<br />

layout of tables, and putting your pages on the web.<br />

ELC Workshop D: Adobe Photoshop and Elements<br />

Tuesday, May 24 ■ 1:00pm – 2:30pm<br />

Thursday, May 26 ■ 8:00am – 9:30am<br />

Richard M. Berger, MD<br />

This workshop will enable the attendee to become familiar<br />

with the more advanced graphics editing techniques and<br />

options available in Adobe "Photoshop" and its newer<br />

younger brother "Elements". This hands-on, interactive<br />

workshop will provide participants with the opportunity to<br />

learn how to edit images from any origin. Topics covered will<br />

include determining optimal image size and resolution for<br />

print, PowerPoint, and email graphics; adding text and arrow<br />

annotations; re-windowing and leveling; cropping and<br />

removing extraneous text and markings; and converting to<br />

gray-scale. Attendees will also use the more common<br />

graphics tools such as airbrush, blur, rubber stamp,<br />

eyedropper, magic wand, paint bucket, and others.<br />

ELC Workshop E: Advanced Website Production<br />

Thursday, May 26 ■ 10:15am – 11:45am<br />

Dale A. Charletta, MD<br />

This hands-on expert experience will cover the effective use of,<br />

and creating, advanced content for the internet. The session will<br />

cover various editors available for creating web pages in HTML<br />

(HyperText Markup Language) as well as how to insert XML<br />

(eXtensible Markup Language). Familiar tools, such as Microsoft<br />

Word and Netscape Communicator, will be discussed with a<br />

focus on the use of images, links, tables, and uploading content<br />

via FTP (file transfer protocol) to a web server. Advanced topics<br />

such as DHTML (dynamic HTML), CSS (cascading style sheets),<br />

Javascript, Java, Perl, and other languages used for web page<br />

creation will also be discussed.<br />

XXXVII<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />



Electronic Learning Center <strong>2005</strong> Lectures<br />

The ELC Lectures were introduced in 2001 in response to the<br />

overwhelming demand for computer education beyond what<br />

could be accommodated in small workshops. The ELC Lectures<br />

focus on topics that are of general interest and in which the<br />

hands-on experience is not as crucial to the learning process.<br />

• ELC lectures are held throughout the Annual Meeting<br />

in a large session room<br />

• ELC lectures are included in the Annual Meeting<br />

registration fee<br />

• No preregistration or ticket is required for admission<br />

ELC Lecture A: The Radiologist’s Computer:<br />

PC and Mac Perspectives<br />

Monday, May 23 ■ 8:05am – 9:05am<br />

Hervey D. Segall, MD | Gregory L. Katzman, MD<br />

Up-to-date basics of computer hardware and operating systems<br />

will be covered, including both the Macintosh and PC<br />

platforms. Components inside the computer (e.g. motherboard,<br />

processor, chipsets, drives, cards, etc.), peripherals (e.g.<br />

monitors, speakers, keyboards, etc.), and lastly connections<br />

will be discussed.<br />

ELC Lecture B: High Speed Connectivity Update<br />

Monday, May 23 ■ 1:00pm – 1:30pm<br />

Gerard J. Muro, MD<br />

Attendees will learn about the different types of highbandwidth<br />

internet access as well as the advantages and<br />

limitations of each. Basic principles in connecting a highbandwidth<br />

internet connection to a home LAN (Local Area<br />

Network) will also be presented, with a discussion of<br />

networking for both work and home.<br />

ELC Lecture C: Capturing and Using Image Files<br />

Monday, May 23 ■ 1:30pm – 2:30pm<br />

Barton F. Branstetter, VI, MD<br />

The audience will get an appreciation for some of the<br />

technical details of digital images, requirements for digital<br />

presentations, methods for obtaining digital images, and<br />

tricks for making PowerPoint lectures. Recommendations<br />

will also be made for image storage and organization.<br />

ELC Lecture D: Multimedia Conference Room <strong>2005</strong><br />

Tuesday, May 24 ■ 8:00am – 9:00am<br />

Venkata Natarajan, PhD<br />

This lecture will outline the creation of a modern digital<br />

multimedia conference room to facilitate more efficient<br />

presentation of radiology learning materials. Topics will<br />

include video requirements (projection devices, cameras,<br />

screens, and monitors) audio systems, teaching aids (laser<br />

pointers, lecterns, and interactive screens), presentation<br />

devices (computers, VCR/DVD players, slide projectors,<br />

overhead projectors, PACS and Workstations), network<br />

considerations (LAN and WAN), and overall ergonomics<br />

(lighting, soundproofing, seating, and room architecture).<br />

ELC Lecture E: Advanced Image Processing in MRI<br />

Tuesday, May 24 ■ 4:40pm – 5:40pm<br />

Todd B. Parrish, PhD<br />

Neuroradiology relies on sophisticated imaging equipment<br />

and software to generate images of the patient. The<br />

purpose of this talk is to start with the basics of imageprocessing<br />

and build an understanding as it relates to<br />

neuroimaging methods. The talk will cover issues such as<br />

image dimensionality, filtering, 3D imaging including surface<br />

rendering and maximum intensity projections, segmentation,<br />

normalization, and applications of image processing.<br />

Advanced topics such as diffusion tensor imaging and<br />

perfusion (DSC and ASL) processing will be covered.<br />

ELC Lecture F: fMRI Post-Processing<br />

Wednesday, May 25 ■ 4:40pm – 5:40pm<br />

Timothy P.L. Roberts, PhD<br />

This lecture will begin with an overview of the key processes of<br />

analysis for fMRI data. This includes re-alignment, modeling of<br />

hemodynamic response, hypothesis testing and statistical<br />

parametric mapping. We will discuss the characteristics of block<br />

vs. event-related designs. Lastly, comparison will be made of the<br />

commonly used data processing packages, including Stimulate,<br />

AFNI and SPM.<br />

ELC Lecture G: PDA’s and the Radiologist<br />

Wednesday, May 25 ■ 5:40pm – 6:10pm<br />

Richard H. Wiggins, III, MD<br />

Attendees will obtain the current understanding of PDA<br />

hardware features, expansion interfaces, and the differences<br />

between the various operating systems. The technological<br />

future for PDA’s will be discussed in light of the rapid evolution<br />

of these types of products.<br />

ELC Lecture H: Digital Teaching Files:<br />

An Overview of Techniques<br />

Thursday, May 26 ■ 8:00am – 9:00am<br />

Gregory L. Katzman, MD<br />

This lecture is directed at the novice, who may be considering<br />

constructing electronic digital teaching files on his or her<br />

desktop computer, either at work, on a laptop, or at home.<br />

Several simple methodologies will be presented, all of which<br />

are easily learned and inexpensive. Department-wide solutions<br />

and networks will not be discussed.


Business Center • Grant Writing Seminar<br />

NLM Workshops<br />

A showcase by the National Library of<br />

Medicine (NLM) will be offering handson-workshops<br />

focusing on PubMed ®<br />

and MedlinePlus throughout the <strong>ASNR</strong><br />

Annual Meeting. PubMed ® is the<br />

National Library of Medicine's webbased<br />

portal to the MEDLINE database.<br />

Searchable without charge, PubMed ® provides<br />

bibliographic access to the health literature, currently<br />

containing over 15 million citations to articles written over<br />

the past 50 years. NLM also produces MedlinePlus, a free<br />

consumer friendly source of up-to-date health information<br />

for patients. Visit and consult with expert librarians or testdrive<br />

these and other NLM resources.<br />

There is no registration fee for these workshops. To register<br />

for a workshop, please sign up at the ELC/NLM desk<br />

located outside Room 103 (Level 100).<br />


Room 103 (in cooperation with the Electric Learning Center<br />

(ELC) Committee).<br />

NLM Workshop: PubMed/MedlinePlus Advanced<br />

Tips and Tricks<br />

Monday, May 23 ■ 3:00pm – 4:00pm<br />

Wednesday, May 25 ■ 5:00pm – 6:00pm<br />

Linda Milgrom<br />

Learn to fine tune your PubMed searches and limit your<br />

retrieval to the most relevant articles. Have you used Cubby, an<br />

easy way to ask PubMed to send you periodic updates on topics<br />

of continuing interest? Try special features such as Clipboard,<br />

Clinical Queries, and History. Come to the demo and play<br />

Stump the Librarian. Any PubMed question is fair game.<br />

NLM Workshop: When PubMed Is Not the Answer…<br />

Tuesday, May 24 ■ 5:00pm – 6:00pm<br />

Thursday, May 26 ■ 1:00pm – 2:00pm<br />

Maryanne Blake<br />

PubMed may not always be the right tool for your information<br />

needs. At this session you will find out how to maximize the<br />

utility of your time on the Web and make your searches more<br />

effective and efficient. You’ll get helpful hints about using<br />

Web resources from a “search all the Web” site like Google to<br />

health-specific sites like Clinicaltrials.gov and MedlinePlus.<br />

<strong>ASNR</strong> GRANT WRITING SEMINAR (Possible Program Cancellation, if registration minimums are not met)<br />

Practical Tips on Getting Your Grant Funded, a two-part seminar on grant writing, will be presented by Janet S. Rasey,<br />

PhD., Director of the Research Funding Service at the University of Washington Medical Center in Seattle, Washington and<br />

a retired Professor of Radiation Oncology. This seminar is specifically designed for young investigators with an interest in<br />

writing funded research proposals.<br />

The workshop, presented over 2 days (4 hours each day), will focus on three major areas in the grant writing process,<br />

Before You Write, Writing the Grant, and The Review Process. Topics covered will include the elements of writing a<br />

competitive research grant with an emphasis on NIH R01 proposals and an explanation of grant review procedures and<br />

psychology. The seminar will take place on Monday, May 23 and Tuesday, May 24. Enrollment is limited to 25<br />

participants. Check at the <strong>ASNR</strong> registration desk, North Building Lobby (Level 100), for availability on-site.<br />

NEW<br />

<strong>ASNR</strong> BUSINESS CENTER<br />

Synopsis: The <strong>ASNR</strong> Business Center will offer executive lectures<br />

encompassing topics pertinent to management and<br />

administration for both private practice and academic<br />

departments. Business Center lectures will be given in two<br />

blocks, each of which is 90 minutes in duration. Within each<br />

block, three speakers are scheduled for 20-25 minute didactic<br />

lectures with 5-10 minutes of question and answer time.<br />

Goals: Topics will be presented spanning ability levels from<br />

basic review to specific financial principles. Experienced<br />

luminary neuroradiologist speakers with significant business<br />

experience will be recruited from within our own membership.<br />

Target Audience: Radiologists who make business decisions for<br />

their practices or any radiologist interested in learning more<br />

about the mechanisms by which a practice functions.<br />

Monday, May 23 1:00pm - 2:30pm<br />

“Welcome and Introduction to Business Issues in Radiology”<br />

Gregory L. Katzman, MD<br />

Chief, Department of Radiology<br />

VA Salt Lake City Health Care System<br />

“Net Present Value and Finance for Practicing Radiologists”<br />

Jonathan Breslau, MD<br />

Radiological Associates of Sacramento<br />

“Managerial Accounting Applications in Radiology”<br />

Frank J. Lexa, MD, MBA<br />

Professor, Wharton Graduate School of Business<br />

Tuesday, May 24 1:00pm - 2:30pm<br />

“Financial Perspectives and Concepts Useful in Radiology”<br />

Dieter Enzmann, MD, MBA<br />

Chairman, Radiology Department<br />

University of California, Los Angeles<br />

“Private Practice vs. Academic Management”<br />

Steven Stevens, MD<br />

Chairman, Radiology Department<br />

University of Utah<br />

“Offshore Teleradiology: Bane or Boon?”<br />

William G. Bradley, MD, PhD, FACR<br />

Chairman, Radiology Department<br />

University of California San Diego Healthcare<br />

Toronto, Canada Canada<br />


May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XL<br />


How-To Sessions (As of 3/24/05)<br />

In addition to the Technical Exhibition,<br />

the leadership of the <strong>ASNR</strong> is pleased to<br />

announce the ninth annual slate of<br />

instructional How-To forums. These<br />

sessions, presented in conjunction with<br />

major corporate contributors, deal with advances in imaging<br />

and procedures as well as principles in neuroradiology and<br />

image information management. How-To Luncheon Sessions<br />

are scheduled Sunday, May 21 through Wednesday, May 25.<br />

How-To Breakfast Sessions are scheduled Monday, May 23<br />

through Wednesday, May 25. Again in <strong>2005</strong>, How-To Session<br />

programming will be offered during specific breakfast, lunch<br />

and reception sessions.<br />

Monday, May 23..................6:50 am - 7:50 am<br />

“The New Breakthrough Data on Aneurysm Healing”<br />

John Perl, MD, Jacques Moret, MD,<br />

John C. Chaloupka<br />

Monday, May 23..............11:50 am - 12:50 pm<br />

“Theory and New Technology for Improving Interventional<br />

Therapy for Intracranial Atherosclerotic Disease:<br />

Full Results from Wingspan HDE Safety Study”<br />

Arani Bose, MD<br />

Wednesday, May 25 ............6:50 am - 7:50 am<br />

“CT Assessment of Perfusion in Stroke Patients”<br />

Lawrence N. Tanenbaum, MD<br />

“Multihance: How is it the Same, How is it Different?”<br />

Emanuel Kanal, MD<br />

Tuesday, May 24 ................6:00 pm - 7:30 pm<br />

Thursday, May 26 ................6:50 am - 7:50 am<br />

Sunday, May 22 ..................5:30 pm - 7:00 pm<br />

“HydroCoil Clinical Experience:<br />

Aneurysm Follow-Up and New Evaluation”<br />

John D. Barr, MD, John Thornton, MD,<br />

Karel G. TerBrugge, MD, Phil White, MD,<br />

Yasunari Niimi, MD<br />

The How-To Sessions offer a unique opportunity for<br />

neuroradiologists to discuss techniques, procedures, and<br />

products with their colleagues as well as with technical<br />

specialists from the imaging industry. Comments and<br />

suggestions from meeting registrants over the last eight years<br />

were integrated into this year’s format.<br />

The sessions vary and include both didactic presentations<br />

and demonstrations, all with a strong practical emphasis.<br />

A significant portion of each session is devoted to questions<br />

and answers. Indications, problems, and solutions relating<br />

to imaging techniques will be addressed including advances<br />

in helical CTA, CT perfusion, MDCT applications and MRI of<br />

the brain.<br />

Tuesday, May 24..................6:50 am - 7:50 am<br />

“Intraoperative MR-Guided Neurosurgery at 3T”<br />

Charles L. Truwit, MD<br />

Wednesday, May 25 ........11:50 am - 12:50 pm<br />

“MR Diffusion”<br />

Christopher G. Filippi, MD<br />

“Brain Perfusion”<br />

Max Wintermark, MD<br />

Sunday, May 22 ..............11:20 am - 12:20 pm<br />

“Advanced Interventional Neuro Imaging in the<br />

Angio Suite”<br />

Richard P. Klucznik, MD<br />

Tuesday, May 24 ............11:50 am - 12:50 pm<br />

“Advanced Neuro MRI with Tim”<br />

Edmond A. Knopp, MD<br />

Sunday, May 22 ..................6:50 am - 7:50 am<br />

PLEASE NOTE: Due to the direct financial support<br />

from these companies and the commercial content,<br />

CME credit will not be granted for these sessions.

Scientific PROGRAM Program Overview OVERVIEW<br />

(As of 3/24/05)<br />

Meals and Breaks: Breakfasts, Morning and Afternoon Coffee Service, and Box Lunches will be provided<br />

throughout the week. PLEASE NOTE: Annual Meeting food service locations vary throughout week based on<br />

Technical Exhibit hours and How-to Session programming.<br />

NOTE: Page numbers referenced throughout the program correspond to the page number within<br />

the Proceeding Book.<br />

<strong>ASNR</strong> 43RD ANNUAL MEETING<br />

Monday, May 23<br />

10:00am - 11:45am<br />


6:30am - 7:55am<br />

(A) INTERVENTIONAL: ENT Intervention<br />


and Miscellaneous (Page 4)<br />

(B) HEAD AND NECK: Temporal Bone,<br />

6:50am - 7:50am<br />

Sinonasal (Page 11)<br />


(C) INTERVENTIONAL: Aneurysms (Page 17)<br />

Sponsor: Boston Scientific<br />

(D) ADULT BRAIN: Vascular, Extracranial<br />

8:00am - 8:05am<br />

(Page 25)<br />


10:15am - 11:45am<br />

Victor M. Haughton, MD, <strong>ASNR</strong> President<br />


8:00am - 12:00pm<br />

Page 31<br />

(2) <strong>ASNR</strong> RESEARCH GRANT WRITING SEMINAR:<br />



Page 1<br />

8:05am- 9:05am<br />



Page 1<br />

8:05am - 9:35am<br />



Page 1<br />

8:05am- 9:35am<br />



Page 3<br />

8:05am- 9:35am<br />


Page 4<br />

9:35am - 9:55am<br />


11:45am - 12:50pm<br />


11:50am - 12:50pm<br />


Sponsor: Boston Scientific<br />

1:00pm - 1:30pm<br />



Page 32<br />

1:00pm - 2:30pm<br />



Page 32<br />

1:00pm - 2:30pm<br />



Page 34<br />

1:00pm - 2:30pm<br />


Page 36<br />

1:00pm - 2:30pm<br />

(13) <strong>ASNR</strong> BUSINESS CENTER - PART I<br />

Page 36<br />

XLI<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XLII<br />


Scientific Program Overview (continued) (As of 4/21/05)<br />

(Monday, May 23 continued)<br />

1:00pm - 2:30pm<br />



Page 36<br />

1:30pm - 2:00pm<br />



Page 36<br />

2:30pm - 2:55pm<br />


3:00pm - 4:00pm<br />




Page 36<br />

3:00pm - 4:30pm<br />


(A) HEAD AND NECK: Neck and Extracranial<br />

Carotid (Page 36)<br />

(B) INTERVENTIONAL: Arteriovenous<br />

Malformations/Fistulae (Page 43)<br />

(C) HEAD AND NECK: Neck, New<br />

Techniques, and Excerptas (Page 49)<br />

(D) ADULT BRAIN: Infarction and<br />

Vasospasm (Page 55)<br />

4:40pm - 6:10pm<br />


Page 62<br />

4:45pm - 6:15pm<br />


Page 63<br />

6:00pm - 7:30pm<br />


Tuesday, May 24<br />

6:30am - 7:55am<br />


6:50am - 7:50am<br />


Sponsor: Philips Medical Systems<br />

8:00am - 12:00pm<br />

(20) <strong>ASNR</strong> GRANT WRITING SEMINAR: PRACTICAL<br />


Page 67<br />

8:00am - 9:00am<br />


CONFERENCE ROOM <strong>2005</strong><br />

Page 67<br />

8:00am - 9:30am<br />



Page 67<br />

8:00am - 9:30am<br />


Page 69<br />

8:00am - 9:30am<br />




RESONANCE IMAGING? (General) (ARS)<br />

Page 72<br />

8:00am - 9:30am<br />


Page 72<br />

9:30am - 9:55am<br />


10:00am - 11:45am<br />


(A) INTERVENTIONAL: Intracranial<br />

Aneurysms (Page 73)<br />

(B) INTERVENTIONAL: Stroke Therapy<br />

and Stenting (Page 79)<br />

(C) INTERVENTIONAL: Angioplasty,<br />

Stenting, and New Techniques (Page 87)<br />

(D) ADULT BRAIN: Neoplasms and<br />

New Techniques (Page 94)

Scientific PROGRAM Program Overview OVERVIEW<br />

(continued) (As of 3/24/05)<br />

(Tuesday, May 24 continued)<br />

10:15am - 11:45am<br />


Page 101<br />

11:45am - 12:55pm<br />


11:50am - 12:50pm<br />


Sponsor: Siemens Medical Systems<br />

1:00pm - 2:30pm<br />


Page 101<br />

1:00pm - 2:30pm<br />




Page 102<br />

1:00pm - 2:45pm<br />


Page 103<br />

1:00pm - 2:30pm<br />

(31) <strong>ASNR</strong> BUSINESS CENTER - PART II<br />

Page 106<br />

1:00pm - 2:30pm<br />



Page 106<br />

2:30pm - 2:55pm<br />


3:00pm - 4:30pm<br />


(A) INTERVENTIONAL: Aneurysms and<br />

Spinal Vascular Malformations (Page 106)<br />

(B) ADULT BRAIN: Functional Imaging and<br />

Advanced Techniques (Page 112)<br />

(C) ADULT BRAIN: Functional and Advanced<br />

Imaging of Brain Neoplasms (Page 120)<br />

(D) ADULT BRAIN: Degenerative, Dementias<br />

and Destructive Lesions (Page 127)<br />

ARS = Audience Responce System<br />

3:00pm - 4:30pm<br />



Page 133<br />

4:40pm - 5:40pm<br />



Page 134<br />

4:40pm - 6:10pm<br />



Page 134<br />

4:40pm - 6:10pm<br />


Page 135<br />

4:45pm - 6:15pm<br />


Page 135<br />

5:00pm - 6:00pm<br />



Page 137<br />

6:00pm - 7:30pm<br />


Sponsor: GE Healthcare<br />

Wednesday, May 25<br />

6:30am - 7:55am<br />


6:50am - 7:50am<br />


Sponsor: Bracco Diagnostics Inc.<br />

8:00am - 9:30am<br />



Page 139<br />

8:00am - 9:30am<br />



Page 139<br />

9:30am - 9:55am<br />


XLIII<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XLIV<br />


Scientific Program Overview (continued) (As of 3/24/05)<br />

(Wednesday, May 25 continued)<br />

10:00am - 10:15am<br />

(42) <strong>ASNR</strong> PRESIDENTIAL ADDRESS<br />

Victor M. Haughton, MD, <strong>ASNR</strong> President<br />

10:15am - 11:05am<br />

(43) <strong>ASNR</strong> AWARDS PRESENTATION<br />

Presentation of <strong>2005</strong> <strong>ASNR</strong> Gold Medal Award<br />

Moderators: Victor M. Haughton, MD,<br />

<strong>ASNR</strong> President<br />

Michael Deck, MD, FACR,<br />

Chair, Gold Medal Award Committee<br />

Presentation of <strong>2005</strong> <strong>ASNR</strong> Honorary Member<br />

Moderator: Norman E. Leeds, MD,<br />

Chair, Honorary Member Committee<br />

Announcement of 2004 Outstanding<br />

Presentation Awards<br />

Moderator: James G. Smirniotopoulos, MD,<br />

Chair, Education Committee<br />

Presentation of the Neuroradiology Education and<br />

Research (NER) Foundation Award for Outstanding<br />

Contributions in Research<br />

Moderator: A. James Barkovich MD,<br />

Chair, Neuroradiology Education and<br />

Research (NER) Foundation<br />

Announcement of <strong>2005</strong> NER Foundation Scholar<br />

Award in Neuroradiology Research<br />

Moderator: A. James Barkovich MD,<br />

Chair Neuroradiology Education and<br />

Research (NER) Foundation<br />

Announcement of <strong>2005</strong> NER Foundation Outcome<br />

Research Grant in Neuroradiologic Imaging<br />

Announcement of <strong>2005</strong> NER Foundation/Boston<br />

Scientific Fellowship in Cerebrovascular<br />

Disease Research<br />

Announcement of <strong>2005</strong> Berlex/NER Foundation<br />

Fellowship in Basic Science Research Awards<br />

Moderator: Howard A. Rowley, MD,<br />

Chair, Research Committee<br />

11:05am - 11:10am<br />




Michael S. Huckman, MD, WFNRS President<br />

11:10am - 11:40am<br />


ANNUAL BUSINESS MEETING (Members only)<br />

11:40am - 12:55pm<br />


11:50am - 12:50pm<br />


Sponsor: Philips Medical Systems<br />

12:00pm - 12:55pm<br />



BUSINESS MEETING (Members only)<br />

1:00pm - 2:30pm<br />


Page 142<br />

1:00pm - 2:30pm<br />



Page 143<br />

1:00pm - 2:30pm<br />


Page 145<br />

1:00pm - 1:45pm<br />


Page 145<br />

1:00pm - 2:30pm<br />


Page 148<br />

2:30pm - 2:55pm<br />


3:00pm - 4:40pm<br />


(A) PEDIATRICS: Epilepsy and Non-Neoplastic<br />

Miscellaneous (Page 148)<br />

(B) ADULT BRAIN: Demyelinating and Miscellaneous<br />

Non-Neoplastic Lesions (Page 155)<br />

(C) SPINE: Functional and Degenerative<br />

(Page 163)<br />

(D) ADULT BRAIN: New Imaging and<br />

Post-Processing Techniques (Page 169)<br />

3:00pm - 4:30pm<br />

(52) ELC WORKSHOP A:<br />


Page 176


Scientific Program Overview (continued) (As of 3/24/05)<br />

(Wednesday, May 25 continued)<br />

4:40pm - 5:40pm<br />


Page 176<br />

4:40pm - 6:10pm<br />


(ASPNR) (ARS)<br />

Page 176<br />

4:40pm - 6:10pm<br />



Page 177<br />

4:45pm - 6:15pm<br />


Page 178<br />

5:00pm - 6:00pm<br />




Page 180<br />

5:40pm - 6:10pm<br />


Page 181<br />

6:15pm - 9:00pm<br />



Thursday, May 26<br />

6:30am - 7:55am<br />


Sponsor: GE Healthcare<br />

6:50am - 7:50am<br />


8:00am - 9:00am<br />



Page 183<br />

8:00am - 9:30am<br />

(60) UPDATES ON "PVL" (ASPNR)<br />

Page 183<br />

8:00am - 9:30am<br />

(61) CT VS. MR IN THE SPINE (ASSR)<br />

Page 185<br />

8:00am - 9:30am<br />


Page 187<br />

8:00am - 9:30am<br />



Page 188<br />

9:30am - 9:55am<br />


10:00am - 11:30am<br />



Functional and Advanced Imaging Techniques<br />

(Page 188)<br />

(B) ADULT BRAIN: Metabolic<br />

and Miscellaneous (Page 196)<br />

(C) ADULT BRAIN: Trauma and Vascular<br />

Lesions (Page 202)<br />

(D) Great Cases and Excerptas (Page 209)<br />

10:15am - 11:45am<br />



Page 220<br />

11:45am - 12:55pm<br />


12:00pm - 12:55pm<br />



(Members only)<br />

12:00pm - 12:55pm<br />



MEETING (Members only)<br />

1:00pm - 2:30pm<br />


Page 220<br />

XLV<br />

Toronto, Canada Canada

May 23-27, <strong>2005</strong><br />

May 23-27, <strong>2005</strong><br />

XLVI<br />

Scientific PROGRAM Program Overview (continued) OVERVIEW<br />

(As of 3/24/05)<br />

(Thursday, May 25 continued)<br />

Friday, May 27<br />

1:00pm - 2:30pm<br />


Page 221<br />

1:00pm - 2:30pm<br />


Page 223<br />

1:00pm - 2:00pm<br />



Page 224<br />

2:30pm - 2:55pm<br />


3:00pm - 4:30pm<br />


(A) ADULT BRAIN: Innovative Techniques<br />

and Miscellaneous (Page 224)<br />

(B) SPINE: Interventional and Innovative<br />

Techniques (Page 230)<br />

(C) PEDIATRICS: Vascular, Trauma and<br />

Tumors (Page 236)<br />

(D) PEDIATRICS: Vascular and<br />

Miscellaneous (Page 244)<br />

4:40pm - 6:10pm<br />



Page 251<br />

4:45pm - 6:15pm<br />


& HIGH FIELD<br />

Page 252<br />

6:30am - 7:55am<br />


8:00am - 9:30am<br />


(A) SPINE: Trauma, Degenerative and<br />

Interventional (Page 255)<br />

(B) PEDIATRICS: Miscellaneous (Page 262)<br />


Neoplasms (Page 269)<br />

(D) ADULT BRAIN: Miscellaneous (Page 275)<br />

9:30am - 9:55am<br />


10:00am - 11:30am<br />



Page 282<br />

10:00am - 11:30am<br />


Page 283<br />

11:30am - 11:45am<br />


Patricia A. Hudgins, MD, <strong>ASNR</strong> President



Monday Morning<br />

8:00 AM - 8:05 AM<br />

Theatre<br />

(1) Opening Remarks<br />

— Victor M. Haughton, MD, <strong>ASNR</strong> President<br />

Monday Morning<br />

8:00 AM - 12:00 PM<br />

Room 201<br />

(2) <strong>ASNR</strong> Research Grant Writing<br />

Seminar: Practical Tips on Getting<br />

Your Grant Funded - Part I<br />

Monday Morning<br />

8:05 AM - 9:05 AM<br />

Room 205<br />

— Janet S. Rasey, PhD<br />

(3) ELC Lecture A: The Radiologist's<br />

Computer: PC & Macintosh<br />

Perspectives<br />

— Hervey D. Segall, MD<br />

— Gregory L. Katzman, MD<br />

1<br />

NOTE ABOUT SCANNED IMAGES: Scanned images are included in the<br />

proceedings book. Some submitted images were reduced during the printing process, thereby<br />

decreasing clarity. The images as originally submitted can be viewed within the abstract on the<br />

<strong>ASNR</strong> website at www.asnr.org/<strong>2005</strong>.<br />

Monday Morning<br />

8:05 AM - 9:35 AM<br />

Theatre<br />

(4) Cervical Carotid Artery<br />

Atherosclerosis (ASITN)<br />

(5) Imaging the Cervical Carotid Artery<br />

— Jeffrey L. Sunshine, MD, PhD<br />

(6) Stroke Risk and Medical Treatment of Cervical<br />

Carotid Artery Stenosis<br />

— Helmi Lutsep, MD<br />

(7) Current Status of Carotid Artery Stenting<br />

— Gary R. Duckwiler, MD<br />

(8) Current Status of Endarterectomy<br />

— Philip E. Stieg, MD, PhD<br />

Case Management Discussion<br />

Moderator: Gary R. Duckwiler, MD<br />

Imaging the Cervical Carotid Artery<br />

Jeffrey L. Sunshine, MD, PhD<br />


Upon completion of this presentation, participants will be<br />

able to:<br />

1) Learn and review current tools to acquire and process<br />

images of the carotid arteries in the setting of potential<br />

neuro-intervention.<br />


We will discuss the conventional tools available to neuroradiologists<br />

with particular focus on CT and MR modalities.<br />

We will touch on any current issues in our gold standard of<br />

catheter angiography. In MR imaging we will review timeof-flight<br />

acquisitions with some attention to coil choices.<br />

Then we will look at the addition of contrast in MR imaging<br />

or CT to the acquisition. Postprocessing techniques will look<br />

at traditional newer methods of multiplanar interpretations.<br />


Monday<br />

Last we will look at the developing areas to evaluate plaque<br />

morphology and consequent risks for thromboembolic<br />

events. Endovascular imaging will be described at least in<br />

the model systems and trials now available.<br />

Stroke Risk and Medical Treatment of Cervical Carotid<br />

Artery Stenosis<br />

Helmi Lutsep, MD<br />

Dr. Lutsep is an Associate Professor in the Department of<br />

Neurology at Oregon Health & Science University. Dr.<br />

Lutsep completed her medical school and residency at the<br />

Mayo Clinic and completed a behavioral neurology fellowship<br />

at the University of California at Davis as well as a fellowship<br />

in cerebrovascular disease at Stanford University.<br />

She is a member of the stroke team and is the Associate<br />

Director of the Oregon Stroke Center. Dr. Lutsep’s research<br />

interests involve the development of therapies for stroke prevention,<br />

acute treatment and stroke recovery, with a focus on<br />

the use of devices in clinical stroke treatment. She also studies<br />

stroke imaging and the cognitive effects of focal brain<br />

lesions. Dr. Lutsep is the author of numerous publications<br />

and presentations. She serves on the executive board of the<br />

Western States Stroke Consortium and is a chief editor of the<br />

eMedicine online neurology textbook.<br />


Upon completion of this presentation, participants will be<br />

able to:<br />

1) Review the stroke risks in the medical compared to surgical<br />

groups of trials involving patients with symptomatic<br />

carotid artery stenosis.<br />

2) Compare the stroke risks in the medical compared to surgical<br />

groups of trials involving patients with asymptomatic<br />

carotid artery stenosis.<br />

3) Identify characteristics that increase stroke risk in patients<br />

with carotid artery stenosis.<br />


The risk of stroke due to cervical carotid artery stenosis is<br />

well elucidated from randomized trials of medical treatment<br />

versus endarterectomy in patients with either symptomatic<br />

or asymptomatic carotid stenosis. The North American<br />

Symptomatic Carotid Endarterectomy (NASCET) trial<br />

assessed risk in patients who had had symptoms ipsilateral to<br />

a carotid artery stenosis. In medically treated patients, a 70%<br />

or greater stenosis carried a stroke risk of 26% at 2 years<br />

(only 9% in the surgical group). In medically treated patients<br />

with near-occlusion and collateral formation, however, risks<br />

were lower. A 50-69% stenosis carried a stroke risk of 22%<br />

at 5 years (15.7% in the surgical group). In the 50-69%<br />

stenosis group, stroke risks in the medical treatment group<br />

were sufficiently lower in patients who presented with amaurosis<br />

instead of hemispheric symptoms, and in women compared<br />

to men, that there was no benefit to surgery compared<br />

to medical treatment. In all stenosis groups, stroke risks were<br />

higher in older patients compared to younger ones and benefits<br />

of surgery compared to medical treatment were greater<br />

in older patients. Two large trials, the North American<br />

Asymptomatic Carotid Atherosclerosis Study (ACAS) and<br />

the European Asymptomatic Carotid Surgery Trial (ACST),<br />

assessed stroke risks in asymptomatic vessels with approxi-<br />

2<br />

mately 60% or greater stenosis. In medically treated patients<br />

at 5 years, ACAS revealed an 11.0% rate of ipsilateral<br />

strokes and perioperative period events (5.1% with surgery),<br />

and ACST showed an 11.8% rate of strokes and perioperative<br />

period events (6.4% with surgery). Neither ACAS nor<br />

the larger ACST study suggested that stroke risk increased<br />

with increasing stenosis in asymptomatic patients. Since<br />

absolute risk reductions with surgery were lower than in<br />

symptomatic vessels, the 30-day surgical morbidity needed<br />

to be less than 3% for intervention to show benefit. The<br />

ACST trial did not show benefit of surgery for patients older<br />

than 74 years of age, but did show a modest benefit for<br />

women as well as stronger benefit for men. In these trials,<br />

medical treatment consisted of aspirin and risk factor control.<br />

Other antithrombotics have not been assessed in this<br />

population, although anticoagulation has been considered for<br />

symptomatic high-grade stenosis because of its high stroke<br />

risk.<br />

Current Status of Carotid Artery Stenting<br />

Gary R. Duckwiler, MD<br />


Upon completion of this presentation, participants will be<br />

able to:<br />

1) Know the current clinical indications for carotid artery<br />

stenting (CAS).<br />

2) Know the current approved devices for carotid artery<br />

stenting (CAS).<br />

3) Know the current or anticipated Medicare reimbursement<br />

guidelines for carotid artery stenting (CAS).<br />

4) Know the current clinical trials for carotid artery stenting<br />

(CAS).<br />


Carotid artery stenting (CAS) is now entering the mainstream<br />

of treatments for carotid atherosclerosis. With the<br />

FDA approval of devices, the demand for this procedure will<br />

increase. At the time of the conference, at least two devices<br />

will be on the market, with several more either approved or<br />

in process of approval. With the approval of the protection<br />

devices, they will likely be used as the standard of care.<br />

However, the payment guidelines are as of now uncertain.<br />

Although the Stenting and Angioplasty with Protection in<br />

Patients at HIgh Risk for Endarterectomy (Sapphire) study<br />

did indicate a better outcome in “high surgical risk” patients<br />

having a CAS versus a carotid endarterectomy (CEA), this<br />

pooled symptomatic and asymptomatic patients. (1) At the<br />

Food and Drug Administration (FDA) panel meeting regarding<br />

the Sapphire study, the issue of procedural risk in asymptomatic<br />

patients was a sore point of discussion. This issue is<br />

reflected in the recent Centers for Medicare & Medicaid<br />

Services (CMS) statement dated December 17th, 2004. (2)<br />

At this time, pending the comment period, CMS does not<br />

intend pay for CAS in asymptomatic patients outside of an<br />

ongoing study. Of course, the majority of patients in the<br />

United States having CEA or CAS are indeed asymptomatic.<br />

The CMS also has mandated a nationwide training and outcome<br />

analysis process, which is unprecedented and unspecified<br />

at present. It remains to be seen how this will affect the<br />

CAS practice. This issue will likely result in a study to<br />

resolve the status of CAS in asymptomatic patients. The

Carotid Revascularization Endarterectomy vs Stent Trial<br />

(CREST) study has applied and likely will begin to enroll<br />

asymptomatic patients in the randomization phase and help<br />

in clarifying this issue. At the conference, the latest detail of<br />

these issues will be discussed.<br />


1. Yadav JS, Wholey MH, Kuntz RE, et al. Stenting and angioplasty<br />

with protection in patients at high risk for<br />

endarterectomy investigators. N Engl J Med<br />

2004;351(15):1493-1501<br />

Current Status of Endarterectomy<br />

Philip E. Stieg, MD, PhD<br />

Dr. Philip E. Stieg is the Professor and Chairman of the<br />

Department of Neurological Surgery at Weill Medical<br />

College and Neurosurgeon-in-Chief at New York-<br />

Presbyterian Hospital. He received his BS degree in 1974<br />

from the University of Wisconsin at Madison, his PhD in<br />

Anatomy and Neuroscience from Albany Medical College of<br />

Union University in 1980, and his MD from the Medical<br />

College of Wisconsin in 1983. He completed his internship<br />

and residency at the University of Texas Southwestern<br />

Medical School and a fellowship in cell transplantation for<br />

restorative neurologic function at Karolinska Institute in<br />

Stockholm, Sweden. Dr. Stieg has developed an international<br />

reputation in the area of cerebrovascular disorders. He<br />

has been active in many international courses and been published<br />

broadly. He has contributed to groups such as the<br />

Joint Sections of Cerebrovascular Surgery of the American<br />

Association of Neurological Surgeons and Congress of<br />

Neurological Surgeons (AANS/CNS) where he now assists in<br />

the capacity as Secretary. In addition, he is President-Elect<br />

of the Society of University Neurosurgeons. A recipient of<br />

several awards and honors, including citations in “Who’s<br />

Who in Health and Medical Services” and “The Best<br />

Doctors in America,” Dr. Stieg has played a major role in<br />

developing and enhancing the neurosurgical programs at<br />

Harvard, Brigham and Women’s Hospital, and Children’s<br />

Hospital of Boston.<br />

Case Management Discussion<br />

3<br />

Monday Morning<br />

8:05 AM - 9:35 AM<br />

Room 105/106<br />

(5) Nonneoplastic Temporal Bone<br />

Imaging (ASHNR)<br />

(9) Middle Ear Disease<br />

Middle Ear Disease<br />

H. Ric Harnsberger, MD<br />

— H. Ric Harnsberger. MD<br />

(10) Tinnitus-Pulsatile and Not<br />

— Michele H Johnson, MD<br />

(11) Facial Palsy<br />

— Richard H. Wiggins, III, MD<br />

Moderators: H. Ric Harnsberger, MD<br />

Richard H. Wiggins, III, MD<br />


Upon completion of this presentation, participants will be<br />

able to:<br />

1) Review T-bone CT imaging anatomy of the middle ear<br />

and mastoid relative to congenital, inflammatory, and infectious<br />

diseases that occur in this area.<br />

2) Identify a rational imaging approach to non-neoplastic<br />

diseases of the middle ear and mastoid.<br />

3) Become familiar with the key facts, imaging findings, and<br />

differential diagnoses associated with congenital, inflammatory,<br />

and infectious diseases affecting the middle ear and<br />

mastoid.<br />


In this presentation middle ear-mastoid anatomy, imaging<br />

strategies and disease states will be reviewed. Complex temporal<br />

bone CT anatomy is simplified by focusing on anatomical<br />

structures of the middle ear-mastoid commonly affected<br />

by diseases of this area. Focusing on the normal structures<br />

that may be affected by cholesteatoma and otomastoiditis<br />

allows a practical anatomical review to be completed.<br />

Nonneoplastic diseases of the middle ear and mastoid fall<br />

into three major pathologic categories, congenital, inflammatory,<br />

and infectious. Chief among the lesions that may be<br />

encountered by the radiologist are congenital and acquired<br />

cholesteatoma, cholesterol granuloma, and otomastoiditis<br />

with extracranial or intracranial complications. Acquired<br />

cholesteatoma can be divided further into pars tensa, pars<br />

flaccida, and mural subtypes. Acute otomastoiditis causes a<br />


Monday<br />

range of extracranial and intracranial complications depending<br />

on direction of spread. In the case of lateral spread,<br />

postauricular abscess occurs. Cephalad spread through the<br />

tegmen tympani results in temporal lobe cerebritis or<br />

abscess. Medial spread across the sigmoid plate of the medial<br />

mastoid wall can cause sigmoid sinus thrombosis with or<br />

without vein of Labbe thrombosis with temporal lobe infarction.<br />

If the infection accesses the inner ear fluid spaces<br />

through the oval or round window, suppurative labyrinthitis<br />

may lead to meningitis of the IAC-CPA region. Finally,<br />

dehiscence of the inferior mastoid cortex may present as<br />

acute suppuration of the sternocleidomastoid muscle. Each<br />

of these infection-spread patterns with their associated complications<br />

will be highlighted in this talk.<br />


1. Penido Nde O, Borin A, Iha LC, et al. Intracranial complications<br />

of otitis media: 15 years of experience in 33 patients.<br />

Otolaryngol Head Neck Surg <strong>2005</strong>;132:37-42<br />

2. Vazquez E, Castellote A, Piqueras J, et al. Imaging of complications<br />

of acute mastoiditis in children. Radiographics<br />

2003;23:359-372<br />

3. Dobben GD, Raofi B, Mafee MF, et al. Otogenic intracranial<br />

inflammations: role of magnetic resonance imaging. Top<br />

Magn Reson Imaging 2000;11:76-86<br />

4. Swartz JD, Harnsberger HR, Mukherji SK. The temporal<br />

bone. Contemporary diagnostic dilemmas. Radiol Clin North<br />

Am 1998; 36:819-853<br />

Tinnitus-Pulsatile and Not<br />

Michele H Johnson, MD<br />

Facial Palsy<br />

Richard H. Wiggins, III, MD<br />


Upon completion of this presentation, participants will be<br />

able to:<br />

1) Understand the complicated anatomy of the facial nerve.<br />

2) Recognize the importance of the surrounding anatomical<br />

landscape of the intratemporal facial nerve course.<br />

3) Illustrate facial nerve pathology.<br />


It is imperative that the tortuous course of the facial nerve be<br />

taken into account when imaging the temporal bone. This is<br />

a mixed nerve, with branchial motor, visceral motor, general<br />

sensory, and special sensory functions. The accurate evaluation<br />

of these individual functions can greatly assist with the<br />

accurate localization of pathology along its entire course,<br />

from the nucleus of origin in the brain stem to the end organ<br />

(the tongue, facial expression muscles, and the lacrimal and<br />

salivary glands). Imaging of the facial nerve consists primarily<br />

of MR imaging and CT examinations. High resolution<br />

MR imaging is most useful for imaging the cisternal and<br />

canalicular segments of the nerve, while CT is most useful<br />

for evaluation of the osseous intratemporal nerve course.<br />

The pathology of the facial nerve is similar to other nervous<br />

structures of the head and neck, but the unique surrounding<br />

4<br />

anatomical landscape predicts and generates the imaging<br />

appearances seen.<br />


1. Harnsberger HR, Wiggins RH, et al. Diagnostic imaging:<br />

Head and neck. Amirsys 2004 pp I - 2 - 176-199<br />

2. Harnsberger HR, Wiggins RH, et al. Pocket radiologist top<br />

100 diagnoses: Temporal bone. Amirsys 2003<br />

Monday Morning<br />

8:00 AM - 9:35 AM<br />

Room 103<br />

(6) ELC Workshop A: Introductory<br />

PowerPoint<br />

Monday Morning<br />

10:00 AM - 11:30 AM<br />

Room 105/106<br />


Intervention and Miscellaneous<br />

(Scientific Papers 13 - 23)<br />

See also Parallel Sessions<br />

(7b) HEAD AND NECK: Temporal Bone, Sinonasal<br />

(7c) INTERVENTIONAL: Aneurysms<br />

(7d) ADULT BRAIN: Vascular, Extracranial<br />

Moderators: Gary M. Nesbit, MD<br />

Michael P. Marks, MD<br />

— John L. Go, MD<br />

Paper 13 Starting at 10:00 AM, Ending at 10:08 AM<br />

Intraarterial<br />

Carcinoma<br />

Tantivatana, J.<br />

Chemoinfusion of Nasopharyngeal<br />

Chulalongkorn University<br />

Bangkok, THAILAND<br />


Patients with advanced nasopharyngeal carcinoma who<br />

failed irradiation, surgery, or chemotherapy treatment suffer<br />

from locally recurrent symptoms. Few treatment options are<br />

available for palliation. We evaluate possible palliative inter-

vention with concept of transcatheter intraarterial delivery of<br />

chemotherapeutic agent directly to the involved vascular territory.<br />


Fifteen patients, 10 males and 5 females with locally recurrent<br />

nasopharyngeal carcinoma (NPC), including inoperable<br />

tumor, skull base invasion, failed irradiation or chemotherapy<br />

were treated with intraarterial chemoinfusion. Ninety mg<br />

of Paclitaxel was infused over a period of 2 hours via a<br />

microcatheter placed in corresponding branch of external<br />

carotid artery which supplied the tumor every 4-6 weeks for<br />

3 courses. Result of treatment was reviewed with follow-up<br />

period of 3 to 6 months.<br />


Nine patients had significantly decreased tumor volume.<br />

Three patients show no significant change of tumor volume.<br />

Two patients had progression of disease. One patient died of<br />

distant metastasis. One of five patients who had cranial<br />

nerve palsy improved. Three patients had transient alopecia.<br />

Four patients had transient hemifacial numbness. No hematologic<br />

or systemic side effect was found.<br />


Intraarterial chemoinfusion is a potential choice of local palliation<br />

in cases of recurrent or refractory tumor with poor<br />

response to radiation, iv chemotherapy, or surgery.<br />

KEY WORDS: Intraarterial chemotherapy, nasopharyngeal<br />

cancer, interventional radiology<br />

Paper 14 Starting at 10:08 AM, Ending at 10:16 AM<br />

Endovascular Treatment of Idiopathic Epistaxsis:<br />

Comparative Study of Unilateral versus Bilateral<br />

External Carotid Artery Embolization<br />

Myers, M. E. · Madison, M. T. · Goddard, J. · Myers, T.<br />

St. Paul Radiology<br />

St. Paul, MN<br />


Endovascular techniques for treating persistent idiopathic<br />

epistaxsis have become accepted medical practice. However,<br />

many varied approaches to treating this disease exist. We<br />

sought to determine whether embolizing branches of both<br />

external carotid arteries had any clinical advantage over unilateral<br />

embolization.<br />


All patients suffered from persistent unilateral epistaxsis<br />

despite agressive packing by ENT. A total of 150 patients<br />

were treated from 2000 to 2004 using endovascular techniques.<br />

Patients were randomized and treated either with<br />

bilateral internal maxillary and unilateral facial artery<br />

embolization (250 micron particles + gelfoam) or with unilateral<br />

internal maxillary artery embolization alone. Mean<br />

follow up was 24 months. Outcomes measured were recurrent<br />

epistaxsis, procedural complications, and facial pain.<br />


Seventy-five patients were entered into each treatment<br />

group. In the bilateral embolization group, there was 1<br />

rebleed requiring further treatment, 1 minor stroke, and 1<br />

5<br />

TIA. Facial pain requiring medication occurred in 15<br />

patients. In the unilateral embolization group, there were 2<br />

rebleeds requiring further treatment, no strokes or TIAs and<br />

2 patients with facial pain requiring medication.<br />


Endovascular embolization for treatment of idiopathic epistaxsis<br />

was safe and effective in both groups. The unilateral<br />

less invasive approach did not result an any significant<br />

increase in recurrent nosebleeds and had the added benefits<br />

of being less time consuming for the operator and considerably<br />

less postembolization facial pain for the patient.<br />

KEY WORDS: Epistaxsis<br />

Paper 15 Starting at 10:16 AM, Ending at 10:24 AM<br />

Ethanol Endovascular Repair of Ear Arteriovenous<br />

Malformations<br />

Yakes, W. F.<br />

Vascular Malformation Center<br />

Englewood, CO<br />


To determine the efficacy of ethanol endovascular repair of<br />

ear arteriovenous malformations (AVMs).<br />


Six patients (5 female, 1 male; age range 6-39 years; mean<br />

age: 22 years) with ear AVMs presented for therapy. Two<br />

patients had failed prior embolizations<br />

(PVA/coils/nBCA/steroids) and 2 patients had other therapies<br />

(laser/excisions/grafting). All presented with grossly<br />

enlarged painful ear with intermittent bleeding. All patients<br />

underwent transcatheter and direct puncture ethanol Rx (77<br />

procedures).<br />


All 6 patients were cured of the AVM at long-term follow up<br />

(mean follow up: 39 months). One patient had transient partial<br />

VII nerve palsy. Two patients had minor blisters.<br />


Ethanol endovascular repair of ear AVMs can effect cures in<br />

this vexing lesion.<br />

KEY WORDS: AVM, embolization, ethanol<br />

Paper 16 Starting at 10:24 AM, Ending at 10:32 AM<br />

Safety and Efficacy of Definitive Embolization of<br />

Meningiomas Trial: Rationale for Study and Study<br />

Design<br />

Bateman, B. T. · Berman, M. F. · Pile-Spellman, J.<br />

Columbia University<br />

New York, NY<br />


The purpose of this presentation is to discuss a new multicenter<br />

pilot study that is being initiated to determine the safety<br />

and efficacy of definitive embolization of meningiomas<br />

(SEDEM trial). In part one, outcomes from surgery and<br />


Monday<br />

radiosurgery will be discussed, providing a background on<br />

the currently accepted treatments for this disease. In part<br />

two, the literature on definitive meningioma embolization<br />

will be reviewed. In part three, the design of the SEDEM<br />

trial will be presented, as will any preliminary results from<br />

the trial that may be available.<br />


A systematic literature search was performed to identify all<br />

meningioma surgery series involving >100 patients published<br />

since 1980. Both short- and long-term outcomes were<br />

recorded. The radiosurgery literature also was reviewed, and<br />

the results of studies enrolling > 50 patients were recorded.<br />

The Nationwide Inpatient Sample, the largest discharge database<br />

available in the U.S. with approximately 8 million discharge<br />

records reported annually, was searched for all<br />

meningioma resections performed between1998-2002.<br />

Outcomes following resection were determined using this<br />

database. The literature available on definitive meningioma<br />

embolization also was reviewed and summarized. A multicenter<br />

study was designed to assess the safety and efficacy of<br />

treating meningiomas by definitive embolization.<br />


The review of the surgical literature showed a relatively high<br />

rate of morbidity and mortality following surgery, with mortality<br />

rates ranging from 1-9% and complication rates ranging<br />

from 10-29%. The search of the NIS database showed an<br />

overall in-hospital mortality rate of 1.9% following resection<br />

(but this rate climbed to 3% for patients 70-79 years old and<br />

7% for patients > 80). There is also a substantial risk of<br />

recurrence following surgery, with recurrence rates reported<br />

as high as 32% following gross total resection and 91% following<br />

subtotal resection. The review of the radiosurgery literature<br />

showed similar tumor control rates to surgery, with a<br />

slightly lower rate of complications (5-13%). But this<br />

modality is limited to tumors smaller than 3.5 cm. There is<br />

one case report of long-term control of a meningioma using<br />

embolization alone. There is also a series published of seven<br />

patients treated with embolization alone, with tumor control<br />

achieved in six of the patients. The trial which is being initiated,<br />

the SEDEM trial, is a multicenter study designed to<br />

provide estimates of the safety and efficacy of definitive<br />

embolization. Forty patients are to be enrolled, with each followed<br />

for at least 5 years after embolization with imaging<br />

and neurologic exams. Preliminary results from the SEDEM<br />

trial will be presented, if available.<br />


The review of outcomes from surgery and radiosurgery suggest<br />

that novel therapies that are safer and more effective<br />

need to be developed to treat meningiomas. The limited data<br />

on definitive embolization available from the literature suggest<br />

this is a promising approach, meriting further investigation.<br />

The SEDEM trial should do much to clarify the utility<br />

of definitive embolization as a therapeutic modality for<br />

meningiomas.<br />

KEY WORDS: Meningioma, embolization<br />

6<br />

Paper 17 Starting at 10:32 AM, Ending at 10:40 AM<br />

Quantification of Angiogenesis Using Angiography<br />

Gounis, M. J. 1 · Lieber, B. B. 1 · Webster, K. A. 2 · Bishopric,<br />

N. H. 2 · Spiga, M. G. 2 · Wakhloo, A. K. 2<br />

1 University of Miami, Coral Gables, FL, 2 University of<br />

Miami, Miami, FL<br />


Numerous methods of therapeutic angiogenesis, including<br />

different gene delivery vehicles as well as the route of<br />

administration of these vectors, have been studied using<br />

angiographic time-intensity data. Mathematical modeling of<br />

these data provides indices of the formation and function of<br />

new vessel growth in response to the treatment modality.<br />


The rabbit hindlimb model of ischemia was used for the in<br />

vivo study. Briefly, the external iliac artery was ligated and a<br />

segment of the left femoral artery was resected. High-speed<br />

angiographic images of the hindlimb vasculature were<br />

obtained prior to and after surgically induced ischemia and at<br />

various follow-up times (Siemens Angiostar Plus, Forchheim,<br />

Germany). Various treatments were studied, including intramuscular<br />

injections of adenoviral (Ad) and regulated adenoassociated<br />

(AAV) viral vectors expressing vascular endothelial<br />

growth factor (VEGF), as well as autologous bone marrow-<br />

derived stem cells that were transduced with these vectors<br />

ex vivo. Super selective intraarterial injections of these<br />

treatments under flow isolation were explored. All treatment<br />

groups were compared to control groups that had PBS injected.<br />

Using angiography, changes occurring within the visible<br />

arteries having a diameter greater than 250 µm and the<br />

microvasculature where arteries are too small to be resolved as<br />

individual vessels were quantified. The normalized, average<br />

inverted gray values (NAIGV) within were calculated. Timeintensity<br />

curves of the NAIGV throughout the observation<br />

period then were constructed and modeled. The model fit was<br />

optimized and the resulting parameters provide quantification<br />

new vessel formation as well as contrast trasport.<br />


In comparison with the control group, the group that<br />

received intramuscular injections of the Ad had significantly<br />

increased vessel growth and fluid transport through these<br />

vessels 1 week following treatment (p < 0.01). However, the<br />

functional angiogenesis dissipated at subsequent follow-up<br />

time points. Similar results were obtained in the angiographic<br />

quantification of the microvascular density, namely the 1<br />

week significant increase (p < 0.01) disappeared with time as<br />

compared to the control group. Histologic analyses indicated<br />

strong endothelial cell proliferation and angiogenesis during<br />

the first week of VEGF delivery that coincident closely with<br />

the transient surge of VEGF expression. Capillary density<br />

was enhanced during 1-3 weeks but returned to baseline after<br />

6 weeks. The latter decline of capillary density coincided<br />

with evidence of increased apoptosis. These results may help<br />

explain the absence of therapeutic benefit of single dose<br />

VEGF delivered by adenovirus. Current work using the regulated<br />

AAV indicates that sustained angiogenic benefit may<br />

be achieved. Superselective regulated AAV administration<br />

under flow arrest is being examined. The initial results indicate<br />

controlled neovascular formation, with organized vessel<br />

growth into the ischemic territory.


The described method of modeling dynamic angiographic<br />

data gives not only information on the geometry of new vessel<br />

growth, but has the ability to quantify the function of vessels<br />

that form in response to therapeutic angiogenesis. Our<br />

analysis suggests that a single dose of Ad to express VEGF<br />

does not produce sustained angiogenic vessels. New methods<br />

of therapeutic angiogenesis including the vector as well<br />

as the mode of administration are being studied.<br />

KEY WORDS: Angiogenesis, mathematical modeling,<br />

ischemia<br />

Paper 18 Starting at 10:40 AM, Ending at 10:48 AM<br />

Intraarterial Nicardipine for the Treatment of<br />

Subarachnoid Hemorrhage-Associated Vasospasm:<br />

Initial Clinical Experience with High-Dose Infusions<br />

Tejada, J. G. 1,2 · Chaloupka, J. C. 2 · Lee, S. K. 2,3 · Ugurel, M.<br />

S. 2 · Hayakawa, M. 2 · Taylor, R. A. 2<br />

1 2 Indiana University, Indianapolis, IN, University of<br />

Iowa, Iowa City, IA, 3University of Toronto, Toronto,<br />

ON, CANADA<br />


Delayed cerebral ischemia due to vasospasm is a major<br />

cause of morbidity and mortality following aneurysmal<br />

SAH. Although vasospasm refractory to medical therapy can<br />

be treated effectively by low-pressure balloon angioplasty,<br />

severe complications and limitations are associated with this<br />

technique. Alternatively, intraarterial infusion of papaverine<br />

has been shown to be at least transiently effective; however,<br />

several severe adverse effects also have been reported with<br />

this technique. Recently, alternative medications have been<br />

considered, such as amrinone and calcium-channel blockers.<br />

We report our initial experience with 11 patients treated with<br />

superselective IA nicardipine.<br />


Eleven consecutive patients with clinically significant and<br />

intractable vasospasm following aneurysmal SAH were<br />

treated with a high concentration (0.83 mg/mL) and high<br />

dose rate (0.415-0.83 mg/min) of nicardipine. Standard criteria<br />

for case selection/definition were used. After catheter<br />

angiographic confirmation of vasospasm, the affected arteries<br />

were targeted for superselective catheterization. Total<br />

dosages of 10 to 40 mg were infused. Control injections<br />

were obtained after 2-5 mg intervals to assess response.<br />


Eleven patients underwent a total of 20 procedures for<br />

intractable vasospasm over the past year. Most were higher<br />

Hunt-Hess grades {4/11 [36%] grade IV, 3/11 [27.2%] grade<br />

III. Neurologic deficits included depressed LOC [n = 11<br />

(100%)], paresis [n = 6 (54.5%)], aphasia [n = 1 (1%)], and<br />

facial nerve palsy [n = 1 (9%)]}. The angiographic results<br />

were very good with significant improvement in the diameter<br />

of the affected vessel seen in 18/20 (90%) of the procedures.<br />

In one procedure (10%) the result was excellent with<br />

complete restoration of the diameter of the vessel. Clinical<br />

improvement with resolution of the focal symptoms or overall<br />

improvement in GCS was demonstrated in 10/11<br />

(90.9%). One of 11(9%) died from complications related to<br />

the initial intracranial hemorrhage. The procedure was well<br />

7<br />

tolerated for all the patients. No complications were<br />

observed in 16/20(80%), while minor complications without<br />

sequelae were observed in 4/20 (20%). Ten of 11 (90.9%)<br />

patients finally were discharged from the hospital. Clinical<br />

follow up was possible in 9/11 (81.8%) patients, 2-8 months<br />

after hospital discharge.<br />


Rapid, high dose intraarterial nicardipine infusions for the<br />

treatment of SAH-associated vasospasm appear to be a safe<br />

and effective alternative intervention. Although retreatment<br />

was often necessary, such procedures seem to be well tolerated.<br />

Further clinical studies will be needed to confirm these<br />

results in a larger patient population.<br />

KEY WORDS: Vasospasm, nicardipine, intraarterial<br />

Paper 19 Starting at 10:48 AM, Ending at 10:56 AM<br />

Effects of Carotid or Vertebrobasilar Stent Placement on<br />

Cerebral Perfusion and Cognition<br />

Turk, A. S. · Niemann, D. · Moftakhar, R. · Rowley, H. ·<br />

Aagaard-Kientiz, B. · Turski, P.<br />

University of Wisconsin<br />

Madison, WI<br />


There are no well established physiologic or neuropsychological<br />

criteria for identifying which patients with stenosis of<br />

the cervicocerebral vessels are at high risk of stroke or cognitive<br />

impairment. Our purpose was to evaluate changes in<br />

cognitive performance and cerebral perfusion associated<br />

with endovascular stenting of the cervicocerebral vessels.<br />


A series of 28 patients, 30 to 88 years of age, who underwent<br />

31 stent procedures for arterial stenosis [14 extracranial<br />

carotid stents (ECS), 5 intracranial carotid stents (ICS) and<br />

12 extra or intracranial vertebrobasilar stents (VBS)] were<br />

reviewed retrospectively. All patients were evaluated with<br />

CT or MR perfusion studies before and after stent placement<br />

(Fig.). Cognitive response after stenting was evaluated with<br />

an informant questionnaire (informant questionnaire for cognitive<br />

decline in the elderly, IQ-CODE).<br />


In cases with anterior circulation stenoses (ECS and ICS<br />

group), 15 of 19 (79%) had a baseline perfusion abnormality<br />

and all patients showed improved perfusion after stenting.<br />

Six of 12 (50%) cases with posterior circulation stenoses<br />

(VBS group) had a baseline perfusion abnormality and 4 of<br />

the 6 patients showed improved perfusion after stenting.<br />

Degree of stenosis was the strongest predictor of the presence<br />

of a baseline perfusion abnormality (p = 0.03). Twentyfour<br />

of 31 (77%) of the cases showed improved cognitive<br />

scores after stent placement. Among patients with improvement<br />

in perfusion after stent placement, 16 of 19 (84%) had<br />

improved cognitive scores. Improved perfusion after stent<br />

placement was a significant predictor of cognitive improvement<br />

(p = 0.04). Patients who were stented on an elective<br />

basis demonstrated greater improvement in cognition as<br />

compared to patients stented urgently (p = 0.01).<br />


Monday<br />


Endovascular stenting of the cervicocerebral vessels can<br />

safely and effectively resolve cerebral perfusion abnormalities.<br />

Improvement in perfusion parameters is associated with<br />

cognitive improvement. Larger, blinded, prospective studies<br />

are warranted to confirm these preliminary observations.<br />

KEY WORDS: Stent, cerebral perfusion, cognition<br />

Paper 20 Starting at 10:56 AM, Ending at 11:04 AM<br />

Real-Time 3D Endovascular Navigation<br />

Pujol, S. 1 · Frerichs, K. 2 · Westin, C. 1 · Vosburgh, K. 1 ·<br />

Norbash, A. 3<br />

1 2 Harvard Medical School, Boston, MA, Brigham and<br />

Women’s Hospital, Boston, MA, 3Boston University School<br />

of Medicine, Boston, MA<br />


Endovascular therapy provides a minimally invasive solution<br />

for many vascular disorders. The procedure is monitored<br />

traditionally under fluoroscopic guidance, which intro-<br />

8<br />

duces a risk of radiation-induced morbidity. Multidetector<br />

CT angiography (CTA) can offer valuable anatomical information<br />

for the treatment of cerebral aneurysms. Our objective<br />

is to provide the neuroradiologist a computer-assisted<br />

navigation system to reduce the intraoperative X-ray exposure.<br />

The system displays — in real-time and without fluoroscopy<br />

— the position of the endovascular elements in a 3D<br />

model reconstructed from preoperative imaging.<br />


Our navigation system relies on the separation of the visualization<br />

of the patient’s anatomy, and the localization of the<br />

endovascular tools. During the preoperative phase, we<br />

reconstruct a 3D model of the brain vasculature from CTA<br />

exam (slice thickness of 2 mm - reconstruction interval of<br />

1.5 mm), using an implementation of the level-sets algorithm<br />

for contour detection. During the intraoperative phase, a<br />

magnetic localizer (MicroBird, Ascension Technology)<br />

tracks an endovascular guide whose tip is equipped with a<br />

miniaturized sensor. The navigation system registers in realtime<br />

the position of the tip of the guide inside the 3D CTA<br />

model of the vasculature. We have performed a first validation<br />

on a phantom of the head, made of a styrofoam skull and<br />

a plastic model of the cerebral vasculature. Four ECG electrodes<br />

were used as noninvasive fiducials, and seven control<br />

points were positioned along the vascular path. At the beginning<br />

of the procedure, the fiducials were palpated magnetically<br />

on the phantom, and the corresponding points were<br />

selected in CT images, in order to replace the CTA model in<br />

the reference frame of the magnetic localizer. The navigation<br />

system display was used to reach the control points with the<br />

endovascular guide. The accuracy was defined as the distance<br />

between the actual location of the guide, and its<br />

expected position measured for each control point in CT<br />

data. X-ray images of the guide validated the results of the<br />

navigation.<br />


The navigation system provides a real-time display of the<br />

endovascular guide within the 3D CTA model, using magnetic<br />

tracking. In our initial experiments, the overall system<br />

accuracy was 2.5 mm.<br />


We have developed a navigation system to assist neuroradiologists<br />

in the endovascular treatment of brain aneurysms.<br />

These phantom experiments demonstrated the potential to

provide real-time 3D navigation in cerebral arteries with<br />

clinically relevant accuracy, and thereby expect to reduce the<br />

use of fluoroscopy during neuroradiologic interventions.<br />

KEY WORDS: Computer-assisted navigation, interventional,<br />

aneurysm<br />

Paper 21 Starting at 11:04 AM, Ending at 11:12 AM<br />

Comparison of Image Quality and Feasibility of Clinical<br />

Use of Various Commercial Endoscopic Devices for<br />

Intraspinal Navigation<br />

Purdy, P. 1 · Fujimoto, T. 2 · Replogle, R. 1 · Giles, B. 1 ·<br />

Fujimoto, H. 3 · Miller, S. 1<br />

1 University of Texas Southwestern Medical Center, Dallas,<br />

TX, 2 Kobe University Medical School, Kobe, JAPAN,<br />

3 Okayama University Medical School, Okayama, JAPAN<br />


Percutaneous intraspinal navigation has been discussed as a<br />

potential technique for access to the CNS. The subarachnoid<br />

space is catheterized, usually via lumbar puncture, and the<br />

subarachnoid space is used as a conduit of transit. Fluoro and<br />

MR guidance has been described (1, 2). This purpose was to<br />

compare endoscopes for subarachnoid visualization.<br />


Using 3 unembalmed cadavers, devices were tested for visualization<br />

of the spinal cord, cranial nerves, and ventricles.<br />

These included a 1 mm diameter fiberscope introduced via<br />

an angiographic catheter, a 2.3 mm (7 F) fiberscope with a 1<br />

mm working lumen, a 2.8 mm fiberscope with a 1.2 mm<br />

working lumen, and a 3.8 mm videoscope (CCD chip on end<br />

of scope used for imaging). Each scope was introduced via<br />

an arterial sheath except for the videoscope, which required<br />

laminotomy. Images of the spinal cord, cranial nerves, and<br />

ventricular system were acquired. The 2.8 mm and 3.8 mm<br />

scopes were tested on the same cadaver. Comparisons of<br />

steerability, durability, field of view, and subjective image<br />

quality were performed with each device.<br />


Each device was introduced successfully into the lumbar<br />

subarachnoid space, and successful catheterization of the<br />

spinal canal, posterior fossa, and ventricular system was<br />

accomplished easily with each device. Steerability and durability<br />

of the fiberscope were limited and field of view was<br />

narrow. Anatomical identification was limited. Steerability<br />

and durability of the 2.3 mm and the 2.8 mm fiberscopes<br />

were better. Both had deflecting tips, improving control.<br />

Ventricular visualization was better than the 1 mm scope<br />

(Fig.). Image quality was slightly better using the 2.8 mm<br />

fiberscope. The videoscope was superior in image quality<br />

and durability, as well as field of view. Its steerability was<br />

similar to the others. Size may restrict it.<br />

9<br />


Prior studies have shown that spinal canal occlusion < 30%<br />

produces no spinal cord injury. In humans with a canal 1 cm<br />

diameter, either the 2.3 mm or 2.8 mm scope could be studied.<br />

Subarachnoid catheterization and visualization of spinal<br />

and cranial structures is feasible.<br />


1. Purdy PD, Replogle RE, Pride GL Jr, Adams C, Miller S,<br />

Samson D. Percutaneous intraspinal navigation (PIN): A<br />

feasibility study in cadavers of a new and minimally invasive<br />

approach to the spinal cord and brain. AJNR Am J<br />

Neuroradiol 2003;24:361-365<br />

2. Rappard G, Metzger GJ, Weatherall PT, Purdy PD.<br />

Interventional MR imaging with an endospinal imaging<br />

coil: Preliminary results with anatomic imaging of the<br />

canine and cadaver spinal cord. AJNR Am J Neuroradiol<br />

2004;25:835-839<br />

KEY WORDS: Endoscopes, percutaneous intraspinal navigation,<br />

subarachnoid<br />

Paper 22 Starting at 11:12 AM, Ending at 11:20 AM<br />

Endoscopic Visualization of the Spinal Cord via<br />

Intraspinal Navigation: A Comparison Study<br />

Giles, B. 1 · Fujimoto, T. 2 · Robert, R. 1 · Fujimoto, H. 3 · Miller,<br />

S. 1 · Purdy, P. 1<br />

1 University of Texas Southwestern Medical Center, Dallas,<br />

TX, 2 Kobe University Medical School, Kobe, JAPAN,<br />

3 Okayama University Medical School, Okayama, JAPAN<br />


Percutaneous intraspinal navigation (PIN) is a percutaneous<br />

approach to the cerebral subarachnoid space from a lumbar<br />

puncture (1). Development of procedures using this technique<br />

requires adequate instrumentation. The purpose of this<br />

study is to compare fiberscopic (imaging via optical fiber in<br />

scope) versus videoscopic (imaging via CCD chip at tip of<br />

scope) visualization of spinal cord structures. This approach<br />

may provide an alternative to traditional surgical approaches<br />

and may minimize the morbidity and mortality associated<br />

with open surgical exposure.<br />


An unembalmed male cadaver was obtained and transported<br />

to our research angiography suite and placed in the prone<br />

position. Access to the lumbar subarachnoid space was<br />


Monday<br />

achieved via lumbar puncture and a 2.8 mm outer diameter<br />

(OD) tip-deflecting fiberscope with a 1.2 mm working channel<br />

was introduced into the subarachnoid space through a 9<br />

French sheath. The endoscope was advanced cranially under<br />

endoscopic and X-ray fluoroscopic guidance. The fiberscope<br />

was removed and a 3.8 mm OD tip-deflecting videoscope<br />

with a 1.2 mm working channel then was introduced into the<br />

subarachnoid space via a partial second lumbar laminectomy<br />

secondary to the inability to place an adequately sized sheath<br />

percutaneously and advanced cranially. Endoscopic images<br />

were stored using a direct digital capture apparatus.<br />


Structures of the spinal cord were visualized readily with<br />

both scopes. Navigation from the lumbar entry to the foramen<br />

magnum was achieved easily and quickly with both<br />

scopes. The cauda equina was seen upon entering the subarachnoid<br />

space. As the endoscopes were advanced cranially<br />

the spinal cord was identified. Spinal nerve roots (Fig)<br />

were seen originating from the spinal cord and traversing laterally,<br />

exiting through the dura.<br />


Obtaining access to spinal cord structures via this intraspinal<br />

approach is technically feasible under endoscopic and fluoroscopic<br />

guidance. The videoscope provides a greater degree<br />

of detail of the surface anatomy and a higher degree of spatial<br />

resolution when compared to traditional fiberscopes.<br />

This approach may provide an alternative to traditional surgical<br />

approaches to the spinal cord. Reduction of the outer<br />

diameter of the videoscope should allow it to be placed percutaneously.<br />

The safety and efficacy of PIN should be<br />

explored.<br />


1. Purdy PD, Replogle RE, Pride GL Jr, Adams C, Miller S,<br />

Samson D. Percutaneous intraspinal navigation (PIN): A<br />

feasibility study in cadavers of a new and minimally invasive<br />

approach to the spinal cord and brain. AJNR Am J<br />

Neuroradiol 2003;24:361-365<br />

KEY WORDS: Spinal cord, endoscopy, percutaneous<br />

intraspinal navigation<br />

10<br />

Paper 23 Starting at 11:20 AM, Ending at 11:28 AM<br />

Endoscopic Visualization of Posterior Fossa Structures<br />

via Intraspinal Navigation: A Comparison Study<br />

Purdy, P. 1 · Giles, B. 1 · Fujimoto, T. 2 · Replogle, R. 1 ·<br />

Fujimoto, H. 3 · Miller, S. 1<br />

1 University of Texas Southwestern Medical Center, Dallas,<br />

TX, 2 Kobe University Medical School, Kobe, JAPAN,<br />

3 Okayama University Medical School, Okayama, JAPAN<br />


Multiple disorders, such as trigeminal neuralgia, acoustic<br />

neuromas, and basilar arteries aneurysms, effect posterior<br />

fossa structures and require open surgery for treatment. In an<br />

effort to reduce the morbidity and mortality associated with<br />

surgery, minimally invasive approaches are being explored.<br />

Percutaneous intraspinal navigation (PIN) (1), provides<br />

access to the cranial subarachnoid space via lumbar puncture.<br />

This study compares the ability to visualize posterior<br />

fossa structures between a fiberscope and a videoscope<br />

(endoscope with CCD video chip on its tip) via an intraspinal<br />

route and may provide an alternative minimally invasive<br />

approach to intracranial structures.<br />


An unembalmed male cadaver underwent access to the lumbar<br />

subarachnoid space via lumbar puncture and a 2.8 mm<br />

outer diameter (OD) tip-deflecting fiberscope with a 1.2 mm<br />

working channel was introduced into the subarachnoid space<br />

through a 9 French sheath. The scope was advanced cranially<br />

under visual and fluoroscopic guidance. The fiberscope<br />

was removed, and a 3.8 mm OD tip-deflecting videoscope<br />

with a 1.2 mm working channel then was introduced via a<br />

partial second lumbar laminectomy. Images were stored<br />

using a direct digital capture apparatus.<br />


Images of the posterior fossa structures were obtained using<br />

both scopes. Superior to the level of the cisterna magna the<br />

scope was directed anterolaterally. The seventh and eighth<br />

cranial nerves were identified and followed laterally. As the<br />

scopes were advanced cranially the fifth cranial nerve was<br />

identified. The scope was pulled back down to the level of<br />

the cisterna magna and directed cranially along the midline.<br />

The vertebral arteries were visualized and followed to the<br />

vertebrobasilar junction. The basilar artery was followed<br />

cranially and multiple pontine arteries were visualized. The<br />

third cranial nerve was identified and its relationship to the<br />

superior cerebellar and posterior cerebral arteries were readily<br />

appreciated (Fig).


Accessing the posterior fossa via an intraspinal approach is<br />

technically feasible under endoscopic and fluoroscopic guidance.<br />

The videoscope provides a greater degree of detail of<br />

the surface anatomy and a higher degree of spatial resolution<br />

than compared to traditional fiberscopes. This approach may<br />

provide an alternative to traditional skull-base surgical procedures.<br />

The safety and efficacy of PIN require further study.<br />


1. Purdy PD, Replogle RE, Pride GL Jr, Adams C, Miller S,<br />

Samson D. Percutaneous intraspinal navigation (PIN): A<br />

feasibility study in cadavers of a new and minimally invasive<br />

approach to the spinal cord and brain. AJNR Am J<br />

Neuroradiol 2003;24:361-365<br />

KEY WORDS: Percutaneous intraspinal navigation, endoscopy,<br />

posterior fossa<br />

Monday Morning<br />

10:00 AM - 11:33 AM<br />

Theatre<br />

(7b) HEAD AND NECK: Temporal<br />

Bone, Sinonasal<br />

(Scientific Papers 24 - 35)<br />

See also Parallel Sessions<br />

(7a) INTERVENTIONAL: ENT Intervention and<br />

Miscellaneous<br />

(7c) INTERVENTIONAL: Aneurysms<br />

(7d) ADULT BRAIN: Vascular, Extracranial<br />

Moderators: Mahmood F. Mafee, MD, FACR<br />

Alexander S. Mark, MD<br />

Paper 24 Starting at 10:00 AM, Ending at 10:08 AM<br />

Intralabyrinthine Schwannomas: Imaging Diagnosis and<br />

Classification<br />

Childs, A. M. 1 · Salzman, K. L. 1 · Harnsberger, H. R. 1 · Wiggins,<br />

R. H. 1 · Davidson, H. C. 1 · Kennedy, R. J. 2 · Shelton, C. 1<br />

1 2 University of Utah, Salt Lake City, UT, Private Practice<br />

Clinic, East Melbourne, AUSTRALIA<br />


Intralabyrinthine schwannomas are uncommon lesions seen<br />

both sporadically and in association with syndromes (NF2).<br />

They have characteristic features on MR imaging both in<br />

terms of location and signal characteristics. It is vital to identify<br />

these lesions in a timely manner, as prognosis and treatment<br />

hinge on their recognition. As a result, more standardized<br />

nomenclature would aid in the universal understanding<br />

of the anatomy of these lesions. The purpose of our study is<br />

11<br />

to characterize and name these rare lesions in a systematic<br />

and reproducible manner using anatomy as the basic tenet.<br />


A retrospective study of all patients with the diagnosis of<br />

vestibular schwannoma imaged between 1996 and 2004 was<br />

performed. Four hundred and two patients were reviewed,<br />

excluding those patients with known NF2. Patients with<br />

vestibular schwannoma whose tumors arose from the<br />

labyrinth (cochlea, vestibule, and semicircular canals) were<br />

included. Of these, 44 were included in the study. Patients<br />

were imaged with thin section, high-resolution T2 and contrast-enhanced<br />

imaging.<br />


There were 44 patients with a diagnosis of intralabyrinthine<br />

schwannoma. Thirty-five patients had complete histories<br />

available. There were 12 male and 23 female patients with an<br />

age range of 21 to 78 years with a mean of 53 years. The<br />

most common presenting symptom was progressive sensorineural<br />

hearing loss. Using thin section, high-resolution<br />

MR imaging on a 1.5 T magnet, lesions were characterized<br />

based on their anatomical location. These included intravestibular,<br />

intracochlear, vestibulocochlear, transmodiolar,<br />

transmacular, and transotic. In addition, signal characteristics<br />

and enhancement were described.<br />


Intralabyrinthine schwannomas are rare tumors which may<br />

represent a diagnostic dilemma. In this paper, we will characterize<br />

the MR appearance of these lesions using high-resolution<br />

techniques. In addition, we propose a classification<br />

system which will aid in identification as well as provide a<br />

reproducible method for diagnosis and a universal standard<br />

by which the surgical and radiologic communities can function.<br />

KEY WORDS: Intralabyrinthine, schwannoma<br />

Paper 25 Starting at 10:08 AM, Ending at 10:16 AM<br />

Two Measurements on Temporal Bone CT Increase<br />

Recognition of Inner Ear Malformation and Predict<br />

Sensorineural Hearing Loss<br />

Purcell, D. D. 1 · Fischbein, N. J. 2 · Johnson, J. 1 · Patel, A. 3 ·<br />

Lalwani, A. K. 4<br />

1University of California San Francisco Medical Center, San<br />

Francisco, CA, 2Stanford University Medical Center, Palo<br />

Alto, CA, 3University of California San Francisco School of<br />

Medicine, San Francisco, CA, 4New York University School<br />

of Medicine, New York, NY<br />


We previously have shown that two measurements of the<br />

cochlea and lateral semicircular canal (LSCC) on temporal<br />

bone CT scan can be used to detect malformations of the<br />

inner ear. In this prospective study, we sought to assess the<br />

reproducibility of the measurements of the cochlea and<br />

LSCC and determine if abnormal measurements predict sensorineural<br />

hearing loss (SNHL).<br />


Two readers independently measured the cochlear height on<br />

coronal section and the lateral semicircular canal (LSCC)<br />


Monday<br />

bony island width on axial section on 122 patients who<br />

underwent temporal bone CT. Each ear was interpreted and<br />

counted separately, and one reader read a subset of exams<br />

twice. Inter and intrareader variability was evaluated using<br />

intraclass correlation coefficients (ICC) based on random<br />

effects model. Hearing loss was determined by extracting<br />

pure tone audiometry data from medical records. We determined<br />

the positive and negative predictive values associated<br />

with each radiology finding.<br />


There was substantial inter and intraobserver agreement in<br />

the identification of abnormality on either measurement<br />

(ICCs of > 90%.). A measurement was considered abnormal<br />

if it fell outside two standard deviations from the average<br />

measurement. Identification of an abnormality on either<br />

measurement strongly predicted the presence of SNHL. If<br />

either cochlear hypoplasia or LSCC bony island dysplasia<br />

was identified, then the patient had SNHL (PPV 100%).<br />

Additionally, no patients without SNHL had abnormal measurements.<br />

Furthermore, review of the formal radiology<br />

reports demonstrated that both cochlear hypoplasia and<br />

LSSC dysplasia were overlooked in > 50% of patients with<br />

both abnormal measurements and SNHL.<br />


The measurement of coronal cochlear height and axial LSCC<br />

bony width on CT scan is both reproducible and highly predictive<br />

of SNHL. These measurements allow identification<br />

of cases of inner ear dysplasia missed by visual inspection<br />

alone. Therefore, the measurement of the cochlear height on<br />

coronal section and LSCC bony island width on axial section<br />

should be performed routinely on all temporal bone studies<br />

performed for hearing loss and/or suspected inner ear abnormality.<br />

KEY WORDS: Inner ear malformations, sensorineural hearing<br />

loss, standardized measurements<br />

12<br />

Paper 26 Starting at 10:16 AM, Ending at 10:24 AM<br />

Diagnostic Accuracy of Virtual Otoscopy and 3D<br />

Reconstructions in the Preoperative Assessment of the<br />

Ossicular Chain in Atticoantral Otitis Media: Work in<br />

Progress<br />

Panday, A. K. · Bapuraj, J. R. · Gupta, A. K. · Khandelwal,<br />

N. · Suri, S.<br />

Postgraduate Institute of Medical Education and Research<br />

Chandigarh, INDIA<br />


To assess the diagnostic accuracy of virtual otoscopy (VO)<br />

and 3D ossicular reconstructions in the preoperative assessment<br />

of the ossicular chain in atticoantral otitis media: work<br />

in progress.<br />


Forty patients of chronic suppurrative otits media with conductive<br />

deafness of > 35dB are to be included in this<br />

prospective study. Of these results of 33 patients are available<br />

for evaluation and presentation at the time of submission<br />

of this abstract. All patients underwent baseline axial<br />

HRCT on a multislice helical CT scanner (GE Lightspeed<br />

QXi, GE Medical Systems, Milwaukee, WI). The axial CT<br />

data set was utilized for (a) coronal and sagittal 2D reformations<br />

and (b) virtual otoscopy and 3D reconstructions. These<br />

were read independently by two neuroradiologists who were<br />

blinded to the clinical findings and to the findings of each<br />

other. The results were recorded with respect to identification<br />

of the bones and the integrity of the ossicular chain and<br />

articulations. A 3-point scoring system was used to assist in<br />

an objective assessment. All patients then underwent surgery<br />

and the preoperative findings were recorded by the surgeon<br />

using the same scoring system. The surgeon was blinded to<br />

the findings on imaging. The scores for the 2D, VO/3D and<br />

preoperative finding were compared using the chi square<br />

test. Accuracy of the 2D and 3D images were calculated with<br />

respect to the operative findings.<br />


Preliminary analyses indicate that there is significant correlation<br />

between 2D reformations, VO/3D reconstructions and<br />

operative findings for most parts of the ossicular chain. The<br />

accuracy of 2D reconstructions and VO for assessment of the<br />

larger ossicles (i.e., malleus and incus is comparable both<br />

being 100% accurate for evaluation of malleus, while the<br />

accuracy for the evaluation of the incus being 88.29% on<br />

VO/3D and 85.29% on 2D images). For evaluation of stapes<br />

superstructure, VO/3D images were more accurate (85.29%)<br />

than 2D images (76.47%). Evaluation for the type of ossicular<br />

destruction by both imaging modalities showed a high<br />

level of correlation (P < .001) with preoperative findings;<br />

however VO /3D images show a better correlation (R =<br />

0.8065) than HRCT /2D (R = .7273) images. For assessment<br />

of lenticular process of the incus both 2D and VO/3D image<br />

was unreliable (P > 0.1) Assessment of the incudostapedial<br />

joint by HRCT and 2D reformatted images is not reliable (P<br />

> 0.1); however significant correlation (P < 0.001) is present<br />

between VO/3D on preoperative findings.<br />


Three-dimensional/VO reconstructions are helpful in assessing<br />

the ossicles in cases of CSOM, which are more difficult

to observed on direct otoscopy. It is especially useful to<br />

demonstrate smaller structures such as the stapes superstructure<br />

which may influence decision regarding planning<br />

of ossiculoplasties in this condition.<br />

KEY WORDS: Temporal bone, multidetector CT, 3D reconstructions<br />

Dr. Bapuraj will present the paper.<br />

Paper 27 Starting at 10:24 AM, Ending at 10:32 AM<br />

Absent Semicircular Canals in CHARGE Syndrome:<br />

Radiologic Spectrum of Findings<br />

Morimoto, A. K. 1 · Wiggins, R. H. 1 · Mukherji, S. K. 2 ·<br />

Telian, S. A. 3 · Hudgins, P. A. 4 · Hedlund, G. L. 5 · Hamilton,<br />

B. 1 · Harnsberger, H. R. 1<br />

1 University of Utah, Salt Lake City, UT, 2 University of<br />

Michigan Health System, Ann Arbor, MI, 3 University of<br />

Michigan, Ann Arbor, MI, 4 Emory University, Atlanta, GA,<br />

5 Primary Children’s Hospital, Salt Lake City, UT<br />


This paper will describe the combination of CT and MR<br />

findings that characterize the middle and inner ear anomalies<br />

in CHARGE (Coloboma, heart defects, choanal atresia,<br />

mental retardation, genitourinary and ear anomalies) syndrome.<br />

The combined findings of abnormalities of the incus<br />

and stapes, oval window atresia, and abnormalities of components<br />

of the inner ear (dysplastic cochlea, hypoplastic or<br />

dysplastic vestibule, and absent semicircular canals) are<br />

characteristic of the CHARGE syndrome. Relative frequencies<br />

of each finding are described as well as discussion of the<br />

proposed embryogenesis.<br />


CT and MR imaging studies from 19 patients were studied<br />

retrospectively to categorize the various middle and inner ear<br />

anomalies associated with CHARGE syndrome. This sample<br />

of patients was gathered over several years from multiple<br />

institutions. The diagnosis of CHARGE was made by the<br />

referring team based on diagnostic criteria. Investigational<br />

review board approval was obtained under HIPAA regulations.<br />

CT and MR imaging studies were reviewed by two<br />

CAQ neuroradiologists to establish middle and inner ear<br />

anomalies. Criteria for evaluation were as follows: aplasia of<br />

the semicircular canals was noted when the canals were<br />

completely absent and an isolated vestibule was present.<br />

Cochlear anomalies were related to size of the basal and apical<br />

turns. Cochlear aperture size also was recorded as normal<br />

or abnormal (small aperture and/or bony bar presence or<br />

absence) and whether the cochlear nerve was intact. The criterion<br />

for large vestibular aqueduct was based on a diameter<br />

greater than 2 mm in the intraosseous portion. Atresia of the<br />

oval or round window was identified when they were<br />

obscured partly or completely by an osseous septum. The<br />

middle ear ossicles were evaluated for dysplasia and fusion.<br />

Dysplasia was noted if the ossicles demonstrated abnormal<br />

morphology or size. The criteria for fusion were based on<br />

ankylosis to the wall of the mesotympanum or interossicular<br />

fusion. Abnormal facial nerve segment positions also were<br />

recorded.<br />

13<br />


Each ear was evaluated separately with anomalies categorized<br />

as associated with right or left ears. Even with this<br />

association, no particular relevance to ear side was established.<br />

Thirty-two of 38 (84%) ears had some form of<br />

cochlear dysplasia. Sixteen of 38 (42%) ears had round window<br />

atresia or aplasia. Thirty-one of 38 (82%) ears had oval<br />

window atresia or aplasia. Nineteen of 38 (50%) ears had<br />

vestibular hypoplasia. Eleven of 38 (29%) ears had dysplasia<br />

of the vestibular aqueduct. All cases demonstrated absent<br />

semicircular canals. Regarding the facial nerve, all had normal<br />

labyrinthine segments. Thirty of 38 (79%) ears had posteriorly<br />

displaced first genu segments. Six of 38 (16%) ears<br />

had prolapsed or diagonal tympanic segments. Two of 38<br />

(0.05%) ears had diagonal mastoid segments. Other common<br />

findings included ossicular dysplasia and fusion, venous<br />

anomalies, and entrapped cochlea having a high association<br />

with cochlear nerve aplasia.<br />


CHARGE syndrome patients should be screened for conductive<br />

as well as sensorineural hearing loss. All patients in<br />

this review had absent semicircular canals and a majority<br />

had an abnormally positioned facial nerve involving the first<br />

genu and/or oval window atresia.<br />

KEY WORDS: Head and neck, absent semicircular canal,<br />

CHARGE<br />

Paper 28 Starting at 10:32 AM, Ending at 10:40 AM<br />

Cochlear-Carotid Interval: Anatomical Variation and<br />

Potential Clinical Implications<br />

Young, R. J. · Shatzkes, D. R. · Lalwani, A. K. · Babb, J. S.<br />

New York University Medical Center<br />

New York, NY<br />


A temporal bone CT study in a patient with intermittent tinnitus<br />

and hearing loss demonstrated absence of bone<br />

between the petrous internal carotid artery and the basal turn<br />

of the cochlea. Although the relationship between this<br />

patient’s symptomatology and this finding is uncertain, the<br />

potential implications with respect to increasingly popular<br />

cochlear implant surgery compelled us to analyze retrospectively<br />

a series of temporal bone CT scans in order to establish<br />

normative measurements for this region, which we<br />

termed the “cochlear-carotid interval” (CCI).<br />


Following IRB approval, two observers independently measured<br />

the bony interval between the cochlea and the petrous<br />

internal carotid artery on coronal images from 30 consecutive<br />

temporal bone CT studies. The 1 mm thick coronal<br />

images were acquired either directly or were reconstructed<br />

from an axial data set acquired at 0.75 or 0.6 mm slice thickness.<br />

All measurements were performed using electronic<br />

calipers on a Sienet MagicView VE 42 Siemens PACS station.<br />

Mixed model analysis of variance was used to evaluate<br />

differences between readers and sides with respect to the<br />

mean CCI while adjusting for age and accommodating the<br />

correlation among observations generated for the same subject.<br />


Monday<br />


The right CCI ranged from 0.2-3.8 mm (mean 1.2 ± 0.8 mm,<br />

median 0.9) and the left CCI ranged from 0.2-5.0 mm (mean<br />

1.1 ± 0.9 mm, median 0.8). The results indicate that the CCI<br />

did not exhibit a significant association with subject age (p =<br />

0.1336) and that there were no significant differences<br />

between readers (p = 0.824) or sides (p = 0.350) in terms of<br />

mean CCI.<br />

Fig. 1. Coronal CT images demonstrate the thickness of bone<br />

between the basal turn of the cochlea and petrous carotid<br />

canal (cochlea-carotid interval), (A) CCI = 0 in our index<br />

patient (single arrow) and (B) CCI = 1.2 mm in another<br />

patient (double arrow).<br />


The CCI varies widely between patients. Preoperative<br />

knowledge of thin or absent bone between the cochlea and<br />

petrous carotid may help prevent inadvertent penetration of<br />

the carotid canal during cochlear implant surgery. Analysis<br />

of larger data sets with clinical correlation may help determine<br />

any potential relationship of diminished CCI and tinnitus<br />

and/or hearing loss.<br />

KEY WORDS: Temporal bone, cochlea, carotid canal<br />

Paper 30 Starting at 10:48 AM, Ending at 10:56 AM<br />

Duplication of the Internal Auditory Canal<br />

Gasparini, F. F. · Papsin, B. C. · Shroff, M. · Friedberg, J. ·<br />

Padfield, N. · Blaser, S.<br />

Hospital for Sick Children<br />

Toronto, ON, CANADA<br />


To demonstrate a rare malformation which has significant<br />

implication in the surgical planning for cochlear implantation.<br />


Eight patients were identified retrospectively via a radiology<br />

report text search program. High-resolution petrous CT with<br />

direct axial and coronal views were evaluated. Parasagittal<br />

reconstruction and 3D reconstructions from the same data set<br />

were performed.<br />


Six patients had unilateral, and two patients had bilateral<br />

involvement. Sensorineural hearing loss was profound in<br />

each of the involved ears. In some patients the malformation<br />

showed a clearly separated internal auditory canal (IAC)<br />

from an isolated facial nerve canal (FNC) with each canal<br />

coursing in a different orientation. One of the canals led to<br />

the geniculate turn of the FNC and the other followed its nor-<br />

14<br />

mal course through the labyrinth. In other patients the IAC<br />

and the FNC were separated only by a transverse megacrest.<br />

All involved ears, except one, had a narrowed cochlear nerve<br />

canal (CNC). In three patients, the contralateral IAC and the<br />

CNC were normal. In the other three patients (one with bilateral<br />

involvement) the contralateral IAC was hypoplastic.<br />

One patient had bilateral transverse megacrest with normal<br />

size IAC. One patient had a medially displaced contralateral<br />

FNC, but normal size IAC. Both patients with bilateral<br />

involvement presented with dysplastic vestibules and horizontal<br />

semicircular canals.<br />


Duplication of the IAC is extremely rare and likely on the<br />

severe end of spectrum including transverse megacrest. IAC<br />

duplication in our patients was associated with profound sensorineural<br />

hearing loss, despite the variability in the size of<br />

the IAC. Severe hypoplasia of the cochlear nerve canal, a<br />

contraindication to cochlear implantation, was present in all<br />

patients with hypoplastic IAC, except one.<br />

KEY WORDS: Facial nerve canal, duplication, cochlear<br />

implantation<br />

Paper 31 Starting at 10:56 AM, Ending at 11:04 AM<br />

Optimization of Reconstruction Parameters for 64-Slice<br />

CT of the Temporal Bone<br />

Diehn, F. E. · Witte, R. J. · Lane, J. I. · Lindell, E. P. · Primak,<br />

A. N. · McCollough, C. H.<br />

Mayo Clinic<br />

Rochester, MN<br />


High-resolution, isotropic, spiral imaging of the temporal<br />

bone is now possible with 64-slice CT. The purpose of this<br />

study is to optimize the reconstruction parameters for 64slice<br />

CT evaluation of the temporal bone in the axial and<br />

coronal planes.<br />


All patients were scanned using the Somatom Sensation 64<br />

(Siemens Medical Solutions; Forchheim, Germany). Spiral<br />

data were acquired with the head in neutral position.<br />

Reconstruction parameters included slice thickness, reconstruction<br />

increment (overlap), field of view size, and kernel.<br />

Reconstructions were performed in the axial and coronal<br />

planes. All images were reviewed by three board-certified<br />

staff neuroradiologists. Subjective comparisons of anatomical<br />

detail were performed for various structures, including<br />

the scalar lamina and the anterior and posterior crura of the<br />

stapes in the axial plane, and the inferior wall of the facial<br />

nerve canal in the coronal plane.<br />


In all patients, the imaging consistently provided detailed<br />

visualization of the temporal bone. In the axial plane, optimal<br />

resolution of anatomical structures was seen with intermediate<br />

slice thickness (0.75 mm), 50% slice overlap, intermediate<br />

field of view (80 mm), and a sharp ultrahigh-resolution<br />

kernel. In the coronal plane, thinner slice thickness (0.49<br />

mm), smaller field of view (70 mm), and a sharp ultrahighresolution<br />

kernel resulted in optimal visualization of the<br />

anatomical structures.


Sixty-four-slice CT imaging provides fast, reliable, high-resolution<br />

examination of the temporal bone. Optimization of<br />

reconstruction parameters results in consistent visualization<br />

of previously difficult to image structures in both the axial<br />

and coronal plane.<br />

KEY WORDS: Temporal bone, 64-slice CT, postprocessing<br />

Paper 32 Starting at 11:04 AM, Ending at 11:12 AM<br />

Cerebrospinal Fluid Leaks: Correlation of High-<br />

Resolution Multiplanar Reformations with<br />

Intraoperative Findings<br />

La Fata, V. · McLean, N. · DelGaudio, J. · Hudgins, P. A.<br />

Emory University School of Medicine<br />

Atlanta, GA<br />


Cerebrospinal fluid (CSF) leaks from skull base defects are a<br />

debilitating problem, often resulting in significant morbidity.<br />

Preoperative evaluation of these patients is traditionally performed<br />

with thin-slice CT scan techniques and direct coronal<br />

acquisition. A cohort of patients with clinically suspected CSF<br />

leaks who underwent high-resolution axial CT scanning was<br />

reviewed retrospectively. Coronal and sagittal multiplanar reformations<br />

were performed for all examinations at a workstation.<br />

Surgical and/or endoscopic correlation was available for<br />

all patients. Both the site and the size of the bony skull base<br />

defects were correlated with the intraoperative findings.<br />


Sixteen patients with CSF leak underwent CT scanning, and<br />

these images were reviewed retrospectively. High-resolution<br />

CT scans were obtained using direct axial images at either<br />

0.625 mm or 1.25 mm increments, and multiplanar reformations<br />

were performed on a workstation. One patient underwent<br />

a screening sinus CT using 2.5 mm axial images. All<br />

CT scans were interpreted by two neuroradiologists who<br />

were blinded to the intraoperative findings. Determination of<br />

the site and size of the bony defects were arrived by consensus,<br />

using both the coronal and sagittal reformations. The<br />

size of the bony defect was measured using electronic<br />

calipers in the anterior-posterior and transverse dimensions.<br />

When available, MR scans were reviewed also to assess for<br />

the secondary signs of CSF leaks and skull base defects.<br />

Once the radiologic assessments were made, all cases were<br />

correlated with the intraoperative findings.<br />


There were 13 women, 3 men, age range 16 to 83 years<br />

(average age 47 years). Defects were presumed to be postsurgical<br />

(6/16), post-traumatic (2 /16), spontaneous (5/16),<br />

tumor-related (2/16) or congenital (1/16). Preoperative CT<br />

identified 19 osseous defects in 16 patients, and 16/19<br />

defects were confirmed at surgery. Most defects were less<br />

than 10 mm in maximal dimension. Defects were seen at the<br />

ethmoid roof (7/19), or at cribriform plate/ethmoid roof<br />

(12/19). Three osseous defects identified on CT were not<br />

confirmed at surgery; these included defects of the ethmoid<br />

roof (1/3), inferolateral right sphenoid (1/3) and posterior<br />

wall of the left frontal sinus (1/3). Surgeons reported a trend<br />

to CT over-estimating the size of the defect, when compared<br />

to direct observation.<br />

15<br />


Coronal and sagittal multiplanar reformations obtained from<br />

high-resolution CT using direct axial acquisitions performed<br />

remarkably well at preoperatively localizing skull base<br />

defects in patients who presented with CSF leaks. Skull base<br />

defects were most apparent on the coronal reformations.<br />

Although the bony defects that involved the posterior wall of<br />

the frontal sinus were not seen on the coronal images, these<br />

defects were well appreciated on sagittal reconstructions.<br />

When compared with intraoperative observation, CT overestimated<br />

the size of the bony defect in a significant portion of<br />

the cases, probably due to the fact that the skull base may be<br />

normally thin and even appear dehiscent without being associated<br />

with CSF leaks. We noted a trend of improved accuracy<br />

at estimating the size of the defect using the thinner<br />

slice acquisitions.<br />

KEY WORDS: Cerebrospinal, fluid, leak<br />

Paper 33 Starting at 11:12 AM, Ending at 11:20 AM<br />

Evaluating Tumors and Tumor-Like Lesions of the Nasal<br />

Cavity, the Paranasal Sinuses, and the Adjacent Skull<br />

Base with Diffusion-Weighted MR Imaging<br />

White, M. L. · Zhang, Y. · Robinson, R. A.<br />

University of Iowa Carver College of Medicine<br />

Iowa City, IA<br />


The purpose of this study was to evaluate the utility of diffusion-weighted<br />

MR imaging in depicting the cellularity of<br />

tumors in the nasal cavity, the paranasal sinuses, and the adjacent<br />

skull base. We hypothesized that the most cellular tumors<br />

would have the lowest apparent diffusion coefficient (ADC)<br />

values. This information could be useful in the differential<br />

diagnosis of malignant tumors and benign tumor-like lesions.<br />


Twenty-one consecutive patients (12 men and 9 women,<br />

ranging in age from 8 to 87 years) with histologically proven<br />

malignant tumors or benign tumor-like lesions in the nasal<br />

cavity, the paranasal sinuses, and the adjacent skull base<br />

were examined using a 1.5 T MR unit. The b-values were all<br />

1000 s/mm 2 . The 16 malignant tumors included rhabdomyosarcoma<br />

(2), squamous cell carcinoma (8), malignant<br />

melanoma (2), lymphoma (1), and neuroblastoma (3). The 5<br />

benign lesions were mesenchymal proliferative process, glomus<br />

tumor, polyp, mucocele, and neuroma and fibrosis.<br />

Apparent diffusion coefficient maps were generated off-line<br />

on an ADW 4.0 GE workstation using FuncTool. Regions of<br />

interests were drawn in representative areas of the tumors.<br />

Mean ADC values were compared with cellularity derived<br />

from resected or biopsy material.<br />


The mean ADC value in the malignant tumors was 10.06<br />

(range, 5.00 ~ 15.85) x 10 -4 mm 2 /s. By contrast, in the benign<br />

tumor-like lesions, the mean ADC value was 19.11 (range,<br />

12.27 ~25.20) x 10 -4 mm 2 /s. Despite having some overlap, the<br />

former was significantly lower than the latter (t-test, P <<br />

0.0005). In addition, ADC values were correlated inversely<br />

with the percentage of tumor cellularity. This relationship<br />

also was statistically significant. (Pearson correlation test, r<br />

= -0.623, P < 0.005).<br />


Monday<br />


Our study revealed that the ADC values may be predictive of<br />

tumor cellularity and may be useful in differentiating malignant<br />

tumors from benign lesions. This information is not<br />

obtained with conventional MR imaging, and diffusionweighted<br />

MR imaging may play an important role in the<br />

workup and treatment of tumors of the nasal cavity, the<br />

paranasal sinuses and adjacent skull base.<br />

KEY WORDS: Sinonasal tumor, diffusion-weighted imaging,<br />

ADC<br />

Paper 34 Starting at 11:20 AM, Ending at 11:28 AM<br />

Assessment of the Efficacy of Preoperative Embolization<br />

of Juvenile Angiofibromas with Respect to Blood Loss<br />

and Recurrence of Tumor<br />

Bapuraj, J. R. · Mitra, S. · Gupta, A. K. · Arya, V. ·<br />

Khandelwal, N. · Suri, S.<br />

Postgraduate Institute of Medical Education and Research<br />

Chandigarh, INDIA<br />


To assess the efficacy of preoperative embolization of juvenile<br />

nasopharyngeal angiofibroma (JNA) with respect to<br />

blood loss during surgery and recurrence of tumor.<br />


Twenty-four clinically and radiologically diagnosed cases of<br />

JNA were included in this randomized and prospective<br />

study. Twelve patients were randomly selected for preoperative<br />

embolization, 12 other were not embolized. CT scans<br />

were done preoperatively in all patients. A repeat scan was<br />

obtained at 6-month follow up to assess recurrence.<br />


Mean blood loss was 201.67 ml for embolized group while<br />

it was 788.75 ml for the nonembolized patients. This difference<br />

was found to be statistically significant (p < 0.01). The<br />

mean difference of Hb from preoperative to postoperative<br />

level was lower in the embolized group (0.9 gm/dl) than<br />

their nonembolized counterparts (2.1 gm/dl). The percentage<br />

rate of decrease of Hb from preoperative to postoperative<br />

level was lower in embolized patients (8.36) compared to the<br />

nonembolized ones (20.71). This difference was highly statistically<br />

significant (p < 0.01). Data were analyzed with<br />

respect to tumor grade. A significant difference was noted<br />

between the embolized and nonembolized patients with<br />

high-grade tumors but not between those with low-grade<br />

tumors. It is therefore, reasoned to infer that preoperative<br />

embolization of the branches of the external carotid artery<br />

appears to facilitate removal of high-grade tumors with minimal<br />

possible blood loss. The benefit of embolization in<br />

those with low-grade tumors is less obvious, probably due to<br />

less vascularity, and consequently, easier removal.<br />

Recurrence of tumor was defined as appearance of an<br />

enhancing mass in the review CT at 6 months in the sites of<br />

surgical exploration and removal. In the embolized group<br />

recurrence was present in 3 patients as compared to 5 patient<br />

in nonembolized group. However, reduction in the incidence<br />

of recurrences in the embolized group was statistically significant<br />

only when low-grade tumors were considered, not<br />

for high-grade tumors. Embolization and the technique of<br />

removal by endoscopy or open excision also were compared.<br />

16<br />

It was found that the blood loss following endoscopic<br />

removal averaged 229.37 ml, which is significantly less than<br />

that for open surgical excision (628.13 ml). This difference<br />

is statistically significant.<br />


Preoperative angio embolization is useful for reducing intraoperative<br />

blood loss and the risk of tumor recurrence. Hence<br />

this may be adopted as a standard preoperative adjunct in all<br />

advanced cases of nasopharyngeal angiofibroma, referred<br />

for surgery.<br />

KEY WORDS: Angiofibroma – nasopharynx, neoplasms,<br />

embolization therapy<br />

Paper 35 Starting at 11:28 AM, Ending at 11:33 AM<br />

Recurrent Aggressive Glomus Jugulare Tumor:<br />

Radiologic-Pathologic Correlation<br />

Johnson, M. H. · Moss, R. L. · Coehllo, D. · Martel, M. ·<br />

Barry, C. · Sasaki, C.<br />

Yale University School of Medicine<br />

New Haven, CT<br />


An aggressive recurrent glomus jugulare tumor is presented<br />

and correlated with the intraoperative appearance as well as<br />

the gross, histologic, and immunohistochemical patholologic<br />

findings, in order to emphasize the importance of compartmental<br />

analysis of recurrent tumors prior to treatment.<br />


A 25-year-old female presented with recurrence of a glomus<br />

jugulare tumor initially diagnosed, surgically excised, and<br />

treated with adjuvant radiation therapy in 1998. Analysis of<br />

outside MR imaging and in-house contrast-enhanced CT<br />

showed recurrent tumor within the parapharyngeal, and<br />

carotid spaces, as well as within the internal jugular vein. No<br />

significant intracranial recurrence was demonstrated.<br />

Preoperative angiography demonstrated near occlusion of<br />

the ipsilateral vertebral artery, which provided neovascular<br />

supply to the superior aspect of the tumor bed at the skull<br />

base. The posterior division of the ascending pharyngeal<br />

artery sent large feeding branches to a large pedunculated<br />

tumor mass within the internal jugular vein. Anterior division<br />

of the ascending pharyngeal artery supplied a medial<br />

tumor compartment within the parapharyngeal space.<br />

Following embolization of the superior and lateral compartments<br />

of the tumor, the patient was taken to surgery, and the<br />

jugular vein exposed. The jugular vein containing tumor was<br />

removed “en-bloc” and directly corresponded with the preoperative<br />

imaging. The medial/anterior compartment was<br />

excised in the same operation.<br />


Pathologic examination demonstrated paraganglioma (S-100<br />

negative) within the internal jugular vein, a 4 cm lateral neck<br />

tumor and a tumor infiltrated node within the parapharyngeal<br />

space.<br />


Learning objectives: 1. Compartmental analysis of crosssectional<br />

imaging in recurrent glomus jugulare may demonstrate<br />

operability of seemingly unresectable tumors.

2. Angiographic compartments and selective embolization of<br />

tumor compartments facilitates resection. 3. The compartmentalized<br />

imaging and angiographic mapping correlates<br />

directly with the surgical findings and gross pathology.<br />

KEY WORDS: Glomus jugulare, radiologic-pathologic correlation,<br />

interventional<br />

Monday Morning<br />

10:00 AM - 11:38 AM<br />

Room 107<br />

(7c) INTERVENTIONAL: Aneurysms<br />

(Scientific Papers 36 - 48)<br />

See also Parallel Sessions<br />

(7a) INTERVENTIONAL: ENT Intervention and<br />

Miscellaneous<br />

(7b) HEAD AND NECK: Temporal Bone, Sinonasal<br />

(7d) ADULT BRAIN: Vascular, Extracranial<br />

Moderators: Gary R. Duckwiler, MD<br />

Jacques G. Moret, MD<br />

Paper 36 Starting at 10:00 AM, Ending at 10:08 AM<br />

Characterization of Cerebral Aneurysms for Assessing<br />

Risk of Rupture Using Patient-Specific Computational<br />

Hemodynamics Models<br />

Cebral, J. R. · Castro, M. A. · Burgess, J. E. · Pergolizzi, R.<br />

M. · Putman, C. M.<br />

Inova Fairfax Hospital<br />

Falls Church, VA<br />


The purpose of our study was to demonstrate the feasibility<br />

of using patient-specific 3 D rotational angiography image<br />

data from clinical studies to construct corresponding realistic<br />

patient-specific computational fluid dynamics models of<br />

cerebral aneurysms. Then using these models, characterize<br />

intraaneurysmal flow patterns and explore their possible<br />

associations to the clinical history of aneurysmal rupture.<br />


Realistic patient-specific anatomical models of cerebral<br />

aneurysms were constructed from 3 D rotational angiography<br />

images of 28 patients. The pulsatile flow simulations<br />

were performed using an implicit finite element formulation<br />

using physiologic flow conditions derived from phase-contrast<br />

MR measurements on a different normal subject.<br />

Visualizations of wall shear stress, oscillatory shear stress,<br />

peak pressure, and the intraaneurysmal flow velocity were<br />

produced for each aneurysm. The aneurysms then were classified<br />

into different categories depending on the distribution<br />

of mean wall shear stress (WSS), peak pressure (PP), oscil-<br />

17<br />

latory shear stress (OSI), complexity of the flow pattern and<br />

size of the flow impingement region. These categories then<br />

were correlated with the clinical history of hemorrhage.<br />


Thirty-three aneurysms were studied in 28 patients ranging<br />

in age from 28 years to 85 years with a mean age of 49 years.<br />

Fourteen had documented subarchnoid hemorrhages that<br />

could be attributed to an intracranial aneurysm. These<br />

aneurysms consisted of 30 from the anterior circulation<br />

[internal carotid artery 17 (posterior communicating 3, cavernous<br />

3, paraclinoid 6, terminus 1, ophthalmic 2), anterior<br />

cerebral artery 2] and three from the posterior circulation<br />

aneurysms (basilar terminus 1, SCA 2). A total of 195<br />

anatomical and hemodynamic models were constructed and<br />

analyzed. No strong correlation with clinical history of rupture<br />

was observed for patterns of WSS, PP, or OSI.<br />

Unruptured aneurysms had large relative impingement zones<br />

in 88% and 92% of ruptured aneurysms had small relative<br />

impingement zones reaching a statistical significance using<br />

95% and 99% confidence intervals. The location of the<br />

inflow impingement showed a trend toward body and dome<br />

locations favoring unruptured aneurysms. Stable single vortex<br />

flow patterns were found in 75% of unruptured<br />

aneurysm, only reaching 90% confidence interval. Wall<br />

shear stress, PP, OSI, and impingement patterns were found<br />

to be independent of aneurysm size. Intraaneurysmal flow<br />

types show some positive correlation with size but all flow<br />

types were found in small and mid sized aneurysms.<br />


Patient-specific realistic anatomical and hemodynamic visualizations<br />

of cerebral aneurysms can be used to characterize<br />

aneurysm flow dynamics for clinical studies.<br />

Intraaneurysmal flow patterns are influenced strongly by<br />

patient-specific geometry but only loosely correlating to<br />

aneurysm size. Small relative size of the inflow jet impingement<br />

zone to the aneurysm size is associated with a clinical<br />

history of aneurysmal rupture.<br />

KEY WORDS: Aneurysm, cerebral, hemodynamic models<br />

This paper was selected by the Eastern Neuroradiology<br />

Society (ENRS) to receive the Norman E. Leeds Award for<br />

best scientific paper at its 16th Annual Meeting held August<br />

20-22, 2004. Dr. Putman will be the presenter.<br />

Paper 37 Starting at 10:08 AM, Ending at 10:16 AM<br />

Reconstruction of Normal Slipstream Flow in<br />

Intracranial Cerebral Arteries following Wide-Neck<br />

Aneurysm Embolization: Does Parent Vessel/Aneurysm<br />

Geometry Dictate Occlusion Device Choice?<br />

Imbesi, S. G. · Knox, K. · Kerber, C. W.<br />

University of California San Diego Medical Center<br />

San Diego, CA<br />


To evaluate and analyze the flow dynamics in intracranial<br />

parent vessel cerebral arteries following wide-neck<br />

aneurysm embolization with multiple iterations of parent<br />

vessel protection device placement.<br />


Monday<br />


We created multiple clear silicone elastic replicas of a sidewall<br />

and a bifurcation intracranial cerebral wide-neck<br />

aneurysm using the lost wax technique. The aneurysm dome<br />

measured 10 mm and the aneurysm neck measured 6 mm in<br />

both aneurysm types. The replicas were placed in a circuit of<br />

pulsatile non-Newtonian fluid and flows were adjusted to<br />

replicate human physiologic flow profiles, velocities, and<br />

volumes. Fluid slipstreams were opacified with isobaric dyes<br />

and images recorded using mini-DV digital video prior to<br />

aneurysm occlusion. Initially, coils were placed in the<br />

aneurysm sac without a parent vessel protection device.<br />

Then, coils were placed in identical copies of the aneurysm<br />

replica using nondetachable balloons, vascular stents, and<br />

new aneurysm neck bridge devices (Trispan) for parent vessel<br />

protection. Intravascular flow patterns then were evaluated<br />

again.<br />


Prior to treatment, analysis of flow in the cerebral arteries<br />

and adjacent aneurysm showed undisturbed slipstreams parallel<br />

to the vessel sidewall in the parent vessel proximal to<br />

the aneurysm sac. Flow then entered the distal aneurysm<br />

neck, formed a vortex pattern within the aneurysm sac, and<br />

exited the proximal aneurysm neck. As flow reentered the<br />

adjacent vessel, disturbed slipstreams were created within<br />

the distal portion of the parent vessel. Aneurysm embolization<br />

was not possible (coil migration into the parent vessel<br />

lumen) without parent vessel protection nor with nondetachable<br />

balloon placement in the parent vessel across the<br />

aneurysm neck given the extremely wide aneurysm neck.<br />

Aneurysm embolization was only possible using intravascular<br />

stents and Trispan for parent vessel protection in both<br />

aneurysm types; however, optimal configuration (i.e., not<br />

only coil retention within the aneurysm sac but, specifically,<br />

the recreation of undisturbed parallel slipstream flow in the<br />

distal parent vessel) could only be achieved with the<br />

intravascular stent across the sidewall aneurysm neck and<br />

with the Trispan across the bifurcation aneurysm neck, but<br />

not vice versa. While the stent could hold the coil mass within<br />

the aneurysm sac in the bifurcation aneurysm even though<br />

the aneurysm neck was not covered completely and undisturbed<br />

slipstream flow was attained within the stented distal<br />

parent vessel branch, slipstream flow through the jailed distal<br />

parent vessel branch showed a continued markedly disturbed<br />

flow pattern. With the Trispan positioned across the<br />

neck of the sidewall aneurysm, the stem and proximal portion<br />

of the device protruded into the parent vessel lumen,<br />

which resulted in a continued markedly disturbed slipstream<br />

flow pattern within the distal parent vessel segment.<br />

Choosing the appropriate device based on the aneurysm<br />

geometry and eliminating this disturbed flow should<br />

improve cerebral perfusion, reduce the incidence of distal<br />

emboli, and possibly even prevent aneurysm reformation.<br />


Use of clear silicone elastic replicas permits detailed analysis<br />

of individual intravascular flowing slipstreams.<br />

Knowledge of aneurysm flow dynamics and the recreation of<br />

normal parent vessel flow following aneurysm embolization<br />

should lead to a more efficacious and safer aneurysm obliteration.<br />

KEY WORDS: Vascular/intracranial, aneurysms, devices<br />

18<br />

Paper 38 Starting at 10:16 AM, Ending at 10:24 AM<br />

Small Aneurysms Do Rupture: A Single Center<br />

Experience with Small Intracranial Aneurysms<br />

Shownkeen, H. · Hall, M. J. · Origitano, T. · Anderson, D. ·<br />

Craig, E.<br />

Loyola University Medical Center<br />

Maywood, IL<br />


The 30-day mortality of aneurysmal subarachnoid hemorrhage<br />

(SAH) is approximately 45%. As a result of this high<br />

morbidity and mortality, preventing rupture is crucial and the<br />

basis of treating unruptured aneurysms. Determining the<br />

patient and aneurysm characteristics that result in increased<br />

SAH risk has been a topic of interest as the morbidity/mortality<br />

of treatment is not trivial. Prior studies, most notably<br />

the International Study of Unruptured Intracranial<br />

Aneurysms (ISUIA), have indicated a low rupture risk for<br />

small aneurysms. This review was compiled to highlight that<br />

small aneurysms do, however, rupture and in fact comprise a<br />

large percentage of aneurysms presenting with SAH at our<br />

institution.<br />


This is a retrospective review of patients with small<br />

aneurysms presenting at the author’s institution from 1997-<br />

2004. Aneurysms measuring less than or equal to 5 mm were<br />

defined as small. Medical records and radiologic studies and<br />

reports were assessed. Main areas of interest include the proportion<br />

of small aneurysms presenting with SAH, 30-day<br />

mortality, and the complications of intervention (both surgical<br />

and endovascular).<br />


This study comprises a total of 111 small aneurysms in 104<br />

patients. Seventy-eight of these patients presented with SAH<br />

(75%). In 15 patients, unruptured small aneurysms presented<br />

subsequent to evaluation of a larger ruptured or unruptured<br />

intracranial aneurysm. The remaining aneurysms were<br />

discovered on incidental imaging studies. Interestingly, all 8<br />

patients with small posterior circulation aneurysms and 89%<br />

of posterior communicating artery aneurysms presented with<br />

SAH. All of these aneurysms were treated. The 30-day mortality<br />

and the morbidity/mortality of treatment will be evaluated<br />

and discussed in detail.<br />


Results from prior studies have suggested the value of 7-10<br />

mm as the critical size for rupture. Data from the ISUIA suggests<br />

a very low risk of aneurysm rupture for UIAs less than<br />

10 mm. In a study evaluating patients with rupture of a previously<br />

unruptured aneurysm by Yasui, et al., however, a<br />

substantial number were less than 5 mm in size at initial<br />

diagnosis. A large proportion of aneurysms presenting at the<br />

author’s institution were less than or equal to 5 mm. Small<br />

aneurysms account for approximately 32% of all treated<br />

aneurysms at our institution. The majority of these<br />

aneurysms presented with SAH (especially when originating<br />

from the posterior communicating artery and posterior circulation).<br />

In fact of all 194 aneurysms presenting with SAH<br />

from 1997-2004, 78 were less than 5 mm (39.6%).<br />

Unfortunately, to date no small aneurysms have been followed<br />

prospectively at our institution and therefore the per-

centage of small aneurysms at risk of rupture cannot be<br />

determined. In light of the ISUIA study, which included a<br />

large amount of patients, this raises an interesting treatment<br />

dilemma. If small aneurysms tend to rupture at a low rate,<br />

why do these aneurysms constitute such a large proportion of<br />

aneurysms presenting with SAH at our institution and others?<br />

Additionally due to the historical risks of therapy, when<br />

is treatment of unruptured small aneurysms warranted? We<br />

will discuss our approach to treatment and the<br />

morbidity/mortality of small aneurysm therapy in detail.<br />

KEY WORDS: Aneurysm, small, intracranial<br />

Paper 39 Starting at 10:24 AM, Ending at 10:32 AM<br />

Correlation between Angiographic and Histologic<br />

Features after Coil Embolization in Elastase-Induced<br />

Aneurysm in Rabbits<br />

Ding, Y. · Dai, D. · Lewis, D. A. · Danielson, M. A. ·<br />

Kadirvel, R. · Cloft, H. J. · Kallmes, D. F.<br />

Mayo Clinic<br />

Rochester, MN<br />


To explore the relationship between angiographic and histologic<br />

features after coil embolization in elastase-induced rabbit<br />

aneurysms.<br />


One hundred six elastase-induced rabbit aneurysms<br />

embolized with various platinum coils were analyzed retrospectively.<br />

Digital subtraction angiography (DSA) was performed<br />

after embolization and before sacrifice. Aneurysms<br />

were harvested at 2 (n = 14), 4 (n = 33), 10 (n = 11), 16 (n =<br />

16), and 24 weeks (n = 32). H&E-stained slides were analyzed.<br />

Follow-up angiographic results (progressive occlusion,<br />

stable, recanalization, and coil compaction) were evaluated<br />

by comparing the aneurysm occlusion feature immediately<br />

after embolization and before sacrifice. Histologic features<br />

included the extent of thrombus organization (incomplete<br />

or complete thrombus organization) and shape of interface<br />

between aneurysm and parent artery (concave, flat, and<br />

convex). Concave interface was regarded as the sign of coil<br />

micro-compaction. Comparison between angiographic and<br />

histologic features was performed using Chi-Square test.<br />


Seventy-six (72%) of 106 aneurysms remained angiographically<br />

stable at follow up, in which incomplete thrombus<br />

organization and micro-compaction were found in 44 (58%)<br />

and 42 (55%) of these cases, respectively. Twenty-four<br />

(23%) of 106 aneurysms showed coil compaction/recanalization<br />

angiographically, in which incomplete thrombus<br />

organization and micro-compaction were found in 21 (88%)<br />

and 22 (92%) of these cases, respectively. Progressive occlusion<br />

was seen in six cases, half of which had incomplete<br />

organization and micro-compaction. More coil micro-compaction<br />

(49/68, 72%) was found in aneurysms with incomplete<br />

thrombus organization, compared with aneurysms with<br />

complete thrombus organization (18/38, 47%) (p < .05).<br />

Complete thrombus organization was found more frequently<br />

in angiographically stable or progressively occluded<br />

aneurysms as compared to aneurysms showing angiographic<br />

compaction (58% versus 12%, respectively, p < .01). Micro-<br />

19<br />

compaction was found more frequently in angiographically<br />

recanalized aneurysms, compared with aneurysms showing<br />

stable or progressive occlusion aneurysms (92% versus 55%,<br />

respectively, p < .001). Coil compaction seen histologically<br />

was more prevalent than that seen angiographically (63%<br />

versus 23%, respectively, p < .01).<br />

Fig. A. Embolized aneurysm before sacrifice intraarterial<br />

DSA right anterior oblique view, demonstrating complete<br />

aneurysm occlusion.<br />

Fig. B. Aneurysm as in A showing concave interface<br />

between aneurysm and parent artery, indicating coil microcompaction.<br />

(H&E stain, original magnification, x 1.4).<br />


In elastase-induced aneurysms, angiographically evident<br />

recanalization occurs in approximately one fourth of cases<br />

while histologic recanalization occurs in approximately two<br />

thirds of cases. Progressive occlusion is rare. Incomplete<br />

thrombus organization correlates with both angiographic and<br />

histologic compaction, suggesting that mechanical stabilization<br />

of aneurysms is important in healing.<br />

KEY WORDS: Aneurysm; embolization, histology; angiography,<br />

rabbit<br />

Paper 40 Starting at 10:32 AM, Ending at 10:40 AM<br />

Unusual Increased Cortical Density in Immediate<br />

Postembolization CT of Patients with Intracranial<br />

Aneurysms<br />

Ozturk, A. · Saatci, I. · Erdogan, C. · Akmangit, I. · Pamuk,<br />

A. G. · Cekirge, H. S.<br />

Hacettepe University Hospitals<br />

Ankara, TURKEY<br />


The purpose of this study is to evaluate the “focal cortical<br />

hyperdensity” finding observed in immediate postembolization<br />

CT of some patients with intracranial aneurysms after<br />

uneventful endovascular treatment.<br />


Monday<br />


This study consisted of 93 consecutive patients with 100<br />

intracranial aneurysms, ruptured or unruptured, in whom a<br />

cranial CT was obtained following the endosaccular<br />

aneurysm treatment. Simultaneous MR imaging as well as a<br />

repeat CT after 4-6 hours were obtained in the patients with<br />

abnormal finding in the initial CT. All patients had CT<br />

immediately before the treatment. The study group consisted<br />

of 74 aneurysms which were treated using balloon remodelling<br />

technique and 26 aneurysms treated with no balloon<br />

assistance. The patients who were treated with parent artery<br />

occlusion, intraextra cranial by-pass surgery associated with<br />

endovascular method or who had intraprocedural apparent<br />

aneurysm rupture, thrombus formation or distal emboli,<br />

major catheter induced vasospasm were excluded as well as<br />

the patients who had acute or subacute infarct in the relevant<br />

territory on preembolization CT.<br />


Cranial CT showed focal cortical hyperdensity (Fig. 1) in 40<br />

of 74 aneurysms (54%) which were treated with the aid of<br />

remodelling balloon, and 9 of 26 (34.6%), treated with no<br />

balloon assistance. Cortical hyperdensity was confined to the<br />

territory of the parent artery harboring the aneurysm and<br />

resolved in the repeated CT (Fig. 2). None of the patients<br />

were symptomatic. A statistically significant relationship<br />

was found between presence of this finding and increase in<br />

microcatheter time, increase in number of balloon inflation<br />

in patients who were treated with balloon assistance and also<br />

increase in total amount of contrast material in the entire<br />

group.<br />


Focal cortical hyperdensity may occur secondary to changes<br />

in blood-brain barrier secondary to hemodynamic effects of<br />

balloon inflation and temporary cesation of blood flow.<br />

Augmented contrast enhancement in the cortex is probably<br />

due to increase in blood-brain barrier permeability secondary<br />

to reperfusion. The awareness of this finding is crucial to differentiate<br />

this clinically insignificant finding from possible<br />

hemorrhage that will affect the patient’s immediate postprocedural<br />

medical management (i.e., anticoagulation and/or<br />

antiaggregan treatment).<br />

KEY WORDS: CT, intracranial aneurysms, endovascular<br />

treatment<br />

20<br />

Paper 41 Starting at 10:40 AM, Ending at 10:48 AM<br />

Long-Term Histopathologic and Immunohistochemical<br />

Comparison in Human, Rabbits, and Swine Aneurysms<br />

Embolized with Platinum Coils<br />

Dai, D. · Ding, Y. · Danielson, M. A. · Kadirvel, R. · Lewis,<br />

D. A. · Clot, H. J. · Kallmes, D. F.<br />

Mayo Clinic<br />

Rochester, MN<br />


To compare the histologic and immunohistochemical findings<br />

in experimental rabbit and swine aneurysms to that of a<br />

human aneurysm embolized with platinum coils, in order to<br />

clarify the cellular mechanisms of healing in these species.<br />


Elastase-induced aneurysms in rabbits (n = 6, harvested at 24<br />

weeks) and sidewall aneurysms in swine (n = 5, harvested at<br />

12 weeks) were created and embolized. A single human<br />

aneurysm that had been coiled 6 years prior to death was harvested<br />

following autopsy. Specimens were embedded in<br />

paraffin and stained with hematoxylin and eosin and Masson<br />

Trichrome staining. Immunohistochemical and immunofluorescence<br />

staining were performed for alpha smooth muscle<br />

actin (SMA), vimentin, and CD31.<br />


The human aneurysm was filled with homogeneous, faintly<br />

staining, hypocelluar, amorphous tissue. Vimentin and SMA<br />

double immunofluorescent staining showed scattered, sparse<br />

cells within dome positive for vimentin but negative SMA,<br />

indicating chronic inflammatory cells or fibrocytes (Fig.<br />

1A). A thin layer of hypocellular tissue traversing the entire<br />

neck was observed, lined with a single layer of flattened cells<br />

that were positive for CD31, indicating endothelial cells.<br />

Collagen deposition was absent within aneurysmal dome<br />

and along the neck. Five of six rabbits showed loose,<br />

hypocelluar tissue, with faintly stained, amorphous matrix<br />

within the dome. Vimentin and SMA double immunofluorescence<br />

staining within dome showed scattered, sparse cells<br />

within dome positive for vimentin but negative SMA (Fig.<br />

1B). A thin layer of hypocellular tissue across the neck was<br />

observed in these five aneurysms, which was lined with single<br />

layer of CD31-positive endothelial cells. Collagen deposition<br />

was absent within aneurysmal dome and along the<br />

neck in all six aneurysms. Swine aneurysm samples showed<br />

highly vascularized fibrous tissue within the dome, with<br />

abundant, dense collagen bundles. The cells within this<br />

fibrous matrix were positive for SMA and vimentin, indicating<br />

myofibroblastic lineage. Light microscopy showed thick,<br />

dense, hypercellular tissue across the entire neck, positive<br />

for vimentin and SMA, indicating a well developed neointima.

Photomicrographs of human brain aneurysm (A) and rabbit<br />

aneurysm (B) show scattered, sparse cells within the<br />

aneurysm dome, which are positive for vimentin and negative<br />

for SMA. (Immunofluorescence double staining with<br />

antibodies for SMA and vimentin.)<br />


The histopathologic reaction both in the dome and across the<br />

neck of rabbit, elastase-induced aneurysms treated with platinum<br />

coils is similar to that of human aneurysms. Swine<br />

aneurysms demonstrate dissimilar healing characteristics as<br />

compared to both rabbit and human aneurysms.<br />

KEY WORDS: Aneurysm; coil embolization, histopathology,<br />

immunohistochemistry<br />

Paper 42 Starting at 10:48 AM, Ending at 10:56 AM<br />

Immunophenotypic Evolution of Cells Involved in<br />

Healing of Rabbit Aneurysms Embolized with Platinum<br />

Coils<br />

Dai, D. · Ding, Y. · Kadirvel, R. · Lewis, D. A. · Cloft, H. J.<br />

· Kallmes, D. F.<br />

Mayo Clinic<br />

Rochester, MN<br />


To demonstrate the immuophenotypic evolution over time of<br />

cells involved in the healing process of experimental rabbit<br />

aneurysms embolized with platinum coils.<br />


Elastase-induced aneurysms were created and embolized<br />

with platinum coils in rabbits. Aneurysms were collected at<br />

2 weeks (n = 2), 4 weeks (n = 6), and 24 weeks (n = 6) following<br />

embolization. All specimens were embedded in<br />

paraffin and stained with hematoxylin and eosin and<br />

immunohistochemistry. Multiple antibodies, including alpha<br />

smooth muscle actin (SMA), myosin, desmin, vimentin, and<br />

CD31, were employed.<br />

21<br />


At two weeks, the majority of the aneurysmal lumen was filled<br />

with fresh thrombus. Scattered, sparse, spindled or satellitelike<br />

cells, distributed at the periphery of aneurysm lumen were<br />

noted, which were positive for SMA, myosin, and vimentin,<br />

indicating myofibroblastic differentiation. No CD31 positive<br />

cells were identified along the neck. Four weeks following<br />

embolization, most of the aneurysm lumens were filled with<br />

loose tissue, associated with small areas of poorly organized<br />

thrombus. All spindle cells within the loose tissue were strongly<br />

positive for SMA (Fig. 1A), with moderate reaction for<br />

myosin and vimentin, indicating myofibroblastic immuophenotype.<br />

Thin layers of fibrin mixed with scattered SMA-positive<br />

spindle cell were present along the aneurysm neck in five<br />

of six aneurysms. One of six aneurysms, with a very narrow<br />

neck, showed a thin layer of loose connective tissue lined with<br />

a single layer of CD31-positive endothelial. Twenty-four<br />

weeks following embolization, the aneurysm lumens were<br />

occupied completely with loose, mesh-like tissue. Most thinspindle<br />

cells within the loose tissue were negative for SMA<br />

(Fig. 1B), myosin and desmin, but positive for vimentin, indicating<br />

that SMA-positive myofibroblasts present at earlier time<br />

points had differentiated into fibrocytes. Thin layer of organized<br />

tissue lined with CD31 positive endothelial cells along the<br />

neck was found in five of six aneurysms.<br />

Photomicrographs of rabbit aneurysms embolized with platinum<br />

coils that shows spindled cells within the aneurysm<br />

dome at 4 weeks (A) are positive for SMA, but are negative<br />

for SMA at 24 weeks (B). Immunohistochemical staining<br />

with antibodies for SMA. (Original magnification x 100)<br />


Myofibroblasts, the key cellular component involved the healing<br />

of rabbits aneurysms embolized with platinum coils, gradually<br />

lose their contractile elements over time. The resultant<br />

tissue is comprised of fibrocytes within a loose, connective tissue<br />

matrix. These findings may allow more rational design of<br />

modified coils aimed at improving aneurysm healing.<br />

KEY WORDS: Aneurysm; coil embolization, cell<br />

immunophenotype, rabbit<br />

Acknowledgment: This project was supported by NIH grant<br />

NS42646.<br />


Monday<br />

Paper 43 Starting at 10:56 AM, Ending at 11:04 AM<br />

Histologic Comparison of HydroCoil Embolization<br />

System in Embolization of Aneurysms in Rabbits,<br />

Canines, and Humans<br />

Kallmes, D. F. 1 · Cloft, H. J. 1 · Cruise, G. 2<br />

1 2 Mayo Clinic, Rochester, MN, MicroVention, Inc., Aliso<br />

Viejo, CA<br />


To compare the histological features of experimental and<br />

clinical aneurysms embolized with HydroCoils.<br />


Rabbit elastase, canine bifurcation, and canine sidewall<br />

aneurysms were prepared according to the method of Altes<br />

(1), Graves (2), and German (3), respectively. The aneurysms<br />

were packed as densely as possible with HydroCoils. Followup<br />

evaluations ranged from 2 to 13 weeks. Human intracranial<br />

aneurysms were collected at autopsy, ranging from 2 to 4<br />

weeks postprocedure. All aneurysms were fixed in 10% neutral<br />

buffered formalin, embedded in methyl methacrylate, sectioned,<br />

and stained with hematoxylin and eosin. Outcome<br />

measures included: Durability [major compaction (0), minor<br />

compaction (1), stable (2), progressive occlusion (3)]; Sac<br />

organization [unorganized (0), mostly unorganized (1), mostly<br />

organized (2), organized (3)]; and Neck coverage [none (0),<br />

acellular (1), thin (2), thick (3)]. Total scores were obtained by<br />

summing the three component scores. Additionally, inflammation<br />

was compared between the experimental and human<br />

aneurysms.<br />


At 2 weeks, rabbit elastase (n = 9) aneurysms were scored 4.7<br />

± 0.7. Two-week data were not available in the canine bifurcation<br />

or sidewall models. At 4 weeks, rabbit elastase (n = 9),<br />

canine bifurcation (n = 8), and canine sidewall (n = 4)<br />

aneurysms were scored 7.7 ± 0.8, 8.1 ± 0.8, 8.5 ± 0.6, respectively.<br />

At 10-13 weeks, rabbit elastase (n = 9), canine bifurcation<br />

(n = 14), and canine sidewall (n = 4) aneurysms were<br />

scored 7.2 ± 0.4, 7.9 ± 1.1, 8.0 ± 0.0, respectively. Two human<br />

aneurysms were harvested at 2 weeks postprocedure. Both<br />

aneurysms were scored at 5. Two other human aneurysms<br />

were harvested at 4 weeks postprocedure. One of these was<br />

scored a 4 and the other scored a 5. Significant inflammation<br />

was not observed in any experimental or human aneurysm.<br />

Mild degrees of inflammation generally was observed at short<br />

follow ups and subsided at longer follow-up times.<br />

22<br />


In all three experimental aneurysm models, healing generally<br />

was completed at 4 weeks postprocedure, with stable or progressive<br />

occlusion, thin or thick neck coverings, and mostly<br />

organized to completely organized sacs. The tissue response did<br />

not change in the time course evaluated in this study, 10-13<br />

weeks. Rabbit and human aneurysms were similar at 2 weeks<br />

postprocedure. At 4 weeks, experimental aneurysms tended<br />

toward greater healing than the human aneurysms. Inflammation<br />

was equivalent, and minimal, in the experimental and human<br />

aneurysms. The development of experimental aneurysms that<br />

heal in a slower, more clinically relevant manner would improve<br />

the development of new aneurysm treatment therapies.<br />


1. AJR Am J Roentgenol 2000;174:349-354<br />

2. AJNR Am J Neuroradiol 1993;14:801-803<br />

3. N Engl J Med 1954;250:104-106<br />

KEY WORDS: Aneuysm, rabbit, hydrocoil<br />

Paper 44 Starting at 11:04 AM, Ending at 11:12 AM<br />

Vascular Remodeling in Healing of Swine Aneurysm<br />

Embolized with Platinum Coils<br />

Kadirvel, R. · Ding, Y. · Dai, D. · Danielson, M. A. · Lewis,<br />

D. A. · Kallmes, D. F.<br />

Mayo Clinic College of Medicine<br />

Rochester, MN<br />


Endovascular embolization using platinum coils has been<br />

widely used as a alternative therapy for the treatment of<br />

intracranial aneurysms. But the mechanism of aneurysm<br />

healing is poorly understood. The purpose of this study was<br />

to characterize the vascular remodeling in swine aneurysms<br />

after embolization with platinum coils.<br />


Five side-wall aneurysms were created microsurgically in common<br />

carotid arteries in swine. These aneurysms were embolized<br />

immediately after creation using platinum coils by endovascular<br />

means. Angiography was performed prior to and immediately<br />

after embolization and at the time of tissue harvest. After 12<br />

weeks of implantation, aneurysm samples were collected for histologic<br />

and biochemical analysis. Normal venous tissue was<br />

used as control tissue for protein expression studies.<br />


All five aneurysms were completely occluded angiographically<br />

at the time of embolization and at follow up. A fibrous<br />

membrane, on the order of 2000µ thick was seen at the neck<br />

of all five aneurysms. Three of five aneurysms showed highly<br />

vascularized fibrous tissue filled the aneurysms dome,<br />

with abundant, dense, disorganized collagen bundles. The<br />

cell bundles within fibrous matrix were positive for smooth<br />

muscle actin (SMA) and vimentin. Two of five aneurysms<br />

demonstrated dense chronic inflammatory tissue, primarily<br />

consisting of lymphocytes, histocytes, giant cells and thinwalled<br />

vessels within the dome. Thick, dense, hypercelluar<br />

tissue across the entire neck was observed in all aneurysms.<br />

Cells within this neointima were positive for SMA and<br />

vimentin. The expression of both MMP-2 (pro- and active<br />

forms) and MMP-9 (pro- and active forms) were found to be

high in aneurysms, whereas expression of their tissue<br />

inhibitors (TIMP-1 and - 2) was diminished significantly<br />

when compared with controls. VEGF and VCAM-1 expression<br />

were elevated in aneurysms. No significant changes in<br />

the expression of TGF -β and eNOS were observed.<br />


Even in healed aneurysms in this model, ongoing vessel<br />

remodeling may be present, as evidenced by over expression<br />

of metalloproteinases and diminished expression of their<br />

inhibitors. Angiogenesis or vasculogenesis as well as inflammation<br />

are prominent in healing aneurysms in swine.<br />

KEY WORDS: Aneurysm, embolization, vascular remodeling<br />

Paper 45 Starting at 11:12 AM, Ending at 11:20 AM<br />

Recanalization after Endovascular Treatment of<br />

Intracerebral Aneurysms<br />

Papanagiotou, P. · Grunwald, I. Q. · Roth, C. · Struffert, T. ·<br />

Gül, G. · Politi, M. · Reith, W.<br />

Clinic for Diagnostic and Interventional Neuroradiology<br />

Homburg, GERMANY<br />


The aim of his study was to evaluate the risks of endovascular<br />

therapy, aneurysm regrowth, recanalization, and the need<br />

for reembolization.<br />


A prospective analysis was performed on 200 endovascularly<br />

treated aneurysms from 2000 to 1/2004. Seventy-nine<br />

asymptomatic and 121 ruptured aneurysms were treated. The<br />

risk of endovascular therapy, aneurysm regrowth, recanalization,<br />

and the need for reembolization was evaluated.<br />


Mean observation time was 10 months. Complete occlusion<br />

(100%) in the initial intervention was achieved in 171 patients<br />

(85.5 %) an 80-95% occlusion rate in 21 aneurysms (10.5%).<br />

In 6 cases the occlusion rate was < 80% (4 %). One hundred<br />

and eighteen aneurysms were controlled after 10 months.<br />

Recanalization rate of all aneurysms in the first follow up was<br />

27/118 (22.8%). Eighty-three of 103 aneurysms (80.6%) with<br />

initial 100% occlusion rate remained completely occluded.<br />

Thirteen of 103 (12.6%) showed recanalization and 7/103<br />

(6.8%) a neck regrowth. In the group with 80-95% occlusion<br />

14 patients were reassessed: 1 showed spontaneous occlusion,<br />

in 7 cases (50%) the initial neck remained, in 6 cases (42.8%)<br />

recanalization increased. In one case the initial < 80% occlusion<br />

remained unchanged, in one case it increased. There was<br />

correlation between initial occlusion rate and recanalization.<br />

Bigger aneurysm size was associated with higher occurrence<br />

of recanalization. Aneurysm localization did not influence<br />

recanalization. Ten of 118 (8.4%) aneurysms were recoiled.<br />

From these one was the < 80% occluded aneurysm, 6 were<br />

from the 80-95% group, and the other 3 from the initially<br />

totally occluded group.<br />


One in four aneurysms will show a recurrence. Initial occlusion<br />

rate seems to have an influence on the recanalization rate.<br />

KEY WORDS: Aneurysms, endovascular, recanalization<br />

23<br />

Paper 46 Starting at 11:20 AM, Ending at 11:28 AM<br />

Efficacy of 3D Time-of-Flight MR Angiogram for a<br />

Follow Up of Embolized Cerebral Aneurysms<br />

Saguchi, T. · Murayama, Y. · Ishibashi, T. · Ebara, M. · Irie,<br />

K. · Takao, H. · Abe, T.<br />

Jikei University School of Medicine<br />

Tokyo, JAPAN<br />


A follow up of the embolized cerebral aneurysm with<br />

Guglielmi detachable coils (GDC) was performed mainly<br />

using craniograms and digital subtraction angiograms (DSA)<br />

so far. Recently, several authors have reported about an efficacy<br />

of the time-of-flight (TOF) MR angiogram (MRA) as a<br />

follow up after the embolized cerebral aneurysms. From the<br />

beginning of February 2004, we have been used 3D TOF<br />

MRA images for a less invasive and a useful follow up after<br />

GDC embolization. Then, they were compared with 3D DSA<br />

images that were obtained after GDC embolization on the<br />

3D workstation. We examined a usefulness of 3D TOF MRA<br />

as a follow up after GDC embolization.<br />


On the day after GDC embolization, 3D TOF MRA was performed<br />

for 50 patients. And as a follow up at our outpatient<br />

clinic, 3D TOF MRA was performed for 35 patients. We<br />

compared the 3D images between 3D TOF MRA and 3D<br />

DSA images after the embolized aneurysms.<br />


There was a close correlation about the postoperative findings<br />

between 3D TOF MRA images that performed on the day after<br />

the operation and 3D DSA images that performed right after<br />

the operation. It was revealed that a recanalization was seen on<br />

3D TOF MRA images for 4 patients among thirty-five cases<br />

of the follow-up patients. In some cases, partial defects of vascular<br />

images were seen on 3D MRA images that were caused<br />

by an artifact of embolized coils. Those findings were never<br />

seen on 3D DSA images. Those were thought to be a limitation<br />

of a diagnosis using 3D TOF MRA.<br />


Monday<br />


The findings of 3D images between 3D TOF MRA and 3D<br />

DSA that were reconstructed on the 3D workstation were<br />

closely correlated. Three-dimensional TOF MRA was very<br />

useful for a less invasive method of a diagnosis for a recanalization<br />

of the embolized aneurysms.<br />

KEY WORDS: 3D time of flight, MR angiography, aneurysm<br />

Paper 47 Starting at 11:28 AM, Ending at 11:33 AM<br />

Paraplegia after Acute Intracranial Subarachnoid<br />

Aneurysm Rupture: Extention of the Subarachnoid<br />

Hemorrhage into the Lumbosacral Region<br />

Lee, S. · Klurfan, P. · Willinsky, R. A. · Gunnarsson, T. ·<br />

terBrugge, K. G.<br />

The Toronto Western Hospital, University Health Network<br />

Toronto, ON, CANADA<br />


Extension of an intracranial subarachnoid hemorrhage into<br />

the lumbosacral region causing focal neurologic deficits is<br />

extremely rare. This report focuses on a patient with an<br />

acutely ruptured right posterior communicating artery<br />

aneurysm and extensive subarachnoid hemorrhage (Fischer<br />

grade IV) who presented with paraplegia.<br />


In addition to headache and a brief history of loss of consciousness,<br />

this 49-year-old female complained about acute<br />

onset of paraplegia (motor power; 0/5), hypoesthesia of both<br />

lower extremities and bilateral sciatica. There was no history<br />

of either lumbar puncture or trauma.<br />


Her aneurysm was treated successfully with endovascular<br />

techniques and subsequent spinal MR imaging revealed a<br />

significant amount of subarachnoid blood in the lumbosacral<br />

region. Her paraplegia has improved gradually with conservative<br />

treatment and her 3-month follow-up neurologic<br />

examination revealed normal motor power in the lower<br />

limbs and minimal paresthesia in her right lower leg. A 3month<br />

follow-up spinal MR imaging demonstrated complete<br />

resolution of the subarachnoid hemorrhage in the lumbosacral<br />

region.<br />


Although it is very rare, intracranial subarachnoid hemorrhage<br />

extension into the spinal canal in particular lumbosacral<br />

region should be included in the differential diagnosis<br />

of paraplegia after acute subarachnoid hemorrhage.<br />

KEY WORDS: Subarachnoid hemorrhage, paraplegia<br />

24<br />

Paper 48 Starting at 11:33 AM, Ending at 11:38 AM<br />

Differents Stages of Endovascular Reconstruction of<br />

Intracranial Aneurysms with Stents<br />

Lylyk, P. · Haas, L. J. · Miranda, C. · Ferrario, A. · Pabon, B.<br />

· Musacchio, A.<br />

ENERI<br />

Buenos Aires, ARGENTINA<br />


The technique of endovascular reconstruction has evolved in<br />

the last years and new devices are now available. After<br />

development of balloon expandible stents for coronary use,<br />

the techniques have evolved. We still need a device that can<br />

fullfill the ideal conditions for intracranial circulation so that<br />

the risks and complications of the technique can be diminished.<br />

Based on the experience in animal and in vitro laboratory<br />

and the clinical experience with balloon expandible<br />

and autoexpandible stents, the authors analyzed the features<br />

of the appropriate stent for intracranial circulation.<br />


Between June 1996 and June 2004, 232 consecutive patients<br />

with sacular, disecant or fusiform aneurysms, were selected<br />

for intracranial stenting. This work was divided into four<br />

steps: 1. Computation models; 2. In vitro study: To analyze<br />

the stents in laboratory with relation to their navigability and<br />

flexibility, radiopacity; 3. In vivo (animal) study: To analyze<br />

anatomy and stents adaptability, radiopacity, navigability,<br />

delivery system, in the external carotid artery in animal laboratory;<br />

4. Clinical: 232 patients with intracerebral aneurysm<br />

were treated in our institution. Mean age was 49 years (range<br />

11-72 years). They were divided into 2 groups. Group 1:<br />

Coronary stent experience: included patients with balloon<br />

expandible stents. Group 2: Autoexpandible stent intracranial:<br />

included patients with autoexpandible stents. All<br />

patients had CT or MR scan and DSA preprocedure. Balloon<br />

expandible stents were implanted in 135 patients and autoexpandible<br />

stents in 97. Aneurysms group: 78.5% received<br />

combined treatment (stent and coils). Twenty-one and onehalf<br />

percent of patients had a complete occlusion of the<br />

aneurysms only with stents.<br />


The patients were discharged under a rigid protocol with<br />

aspirin and clopidogrel treatment 72 hours before procedure<br />

and clopidogrel for an additional 90 days and aspirin continuously.<br />

The morbidity was 9.5% and mortality was 4.2%.<br />


This series indicates that treatment with stents is a factual,<br />

effective, and safe technique for endovascular reconstruction.<br />

The selection of the type of stent depends on each case<br />

in particular and on the aneurysm selected. Technical<br />

improvements on delivery systems are mandatory to obtain<br />

better results during deployment phase. Preprocedural regimen<br />

of antiplatelet agents 72 hours before procedure is<br />

important in all patients. More trials and long-term follow up<br />

are needed to define the precise indications and to determine<br />

permanent vessel patency and aneurysms occlusion rate.<br />

KEY WORDS: Aneurysms, endovascular reconstruction,<br />

intracranial stents

Monday Morning<br />

10:00 AM - 11:30 AM<br />

Room 205<br />

(7d) ADULT BRAIN: Vascular;<br />

Extracranial<br />

(Scientific Papers 49 - 59)<br />

See also Parallel Sessions<br />

(7a) INTERVENTIONAL: ENT Intervention and<br />

Miscellaneous<br />

(7b) HEAD AND NECK: Temporal Bone, Sinonasal<br />

(7c) INTERVENTIONAL: Aneurysms<br />

Moderators: J. Pablo Villablanca, MD<br />

Jeffrey L. Sunshine, MD, PhD<br />

Paper 49 Starting at 10:00 AM, Ending at 10:05 AM<br />

Bilateral Vertebral Artery Duplication Demonstrated by<br />

MR Angiography of the Neck: Its Embryologic Origins<br />

and Implications<br />

Omojola, M. F. · Ionete, C.<br />

Creighton University Medical Center<br />

Omaha, NE<br />


To report a case of bilateral duplication of the proximal vertebral<br />

artery and describe the embryologic origins and clinical<br />

implications.<br />


An 83-year-old male was referred to us for cranial MR imaging<br />

with MRA of the head and neck because of mild cognitive<br />

impairment. There was no other significant clinical<br />

abnormality or significant past medical history.<br />


His cranial MR images obtained on a 1.5 T system showed<br />

no significant abnormality other than incidental finding of a<br />

small right middle cranial fossa arachnoid cyst. Threedimensional<br />

time of flight cranial MRA is normal. The 2D<br />

time of flight neck MRA and 3D acquisition during intravenous<br />

gadolinium enhancement reveal bilateral proximal<br />

duplication of the vertebral arteries (Fig 1). A left proximal<br />

internal carotid artery with severe ulcerated stenosis also is<br />

present. On the right side, there are two separate origins of<br />

the vertebral artery from the right subclavian artery: one origin<br />

emanates proximally beyond the take off of the subclavian<br />

artery, makes a short loop and enters the carotid space<br />

staying in a medial relationship to the right common carotid<br />

artery while the second origin emanates from the subclavian<br />

artery adjacent to the origin of the right internal mammary<br />

artery, coursing straight and enters the foramen transver-<br />

25<br />

sarum at C7 vertebral level. Both vessels join in the foramen<br />

transversarum at C4-5 disk level to continue as the right vertebral<br />

artery. On the left side, there are two separate origins<br />

of the vertebral artery from the left subclavian artery: one<br />

emanates adjacent to the origin of the internal mammary<br />

artery, loops slightly forward and courses straight up behind<br />

the left common carotid artery while the other origin<br />

emanates from the subclavian artery just distal to the first<br />

and slightly larger enters the foramen transversarum at C7.<br />

Both vessels join in the foramen transversarum at C5-6 disk<br />

level to continue as the left vertebral artery.<br />


This is the only report of proximal bilateral vertebral artery<br />

duplication. They were discovered by serendipity and probably<br />

has no known neurologic consequence. It is due to persistence<br />

of the fifth and sixth intersegmental arteries bilaterally.<br />

KEY WORDS: Vertebral artery duplication, MR angiography<br />

Paper 50 Starting at 10:05 AM, Ending at 10:10 AM<br />

Pseudoaneurysm of the Anterior Spinal Artery in a<br />

Patient with Moyamoya: An Unusual Cause of<br />

Subarachnoid Hemorrhage<br />

Walz, D. M. · Woldenberg, R. · Setton, A.<br />

North Shore University Hospital<br />

Manhasset, NY<br />


To describe a pseudoaneurysm of the anterior spinal artery in<br />

a patient with moyamoya as the cause of recurrent subarachnoid<br />

hemorrhage and quadriplegia.<br />


A 58-year-old male presented with recurrent episodes of subarachnoid<br />

hemorrhage and subsequent quadriplegia. Initial<br />

diagnostic catheter angiogram of the intracranial circulation<br />

revealed diffuse occlusive vascular disease compatible with<br />

moyamoya and no definite associated aneurysm. As a result<br />

of progressively developing quadriplegia, MR imaging of<br />

the cervical region was obtained and revealed a vascular<br />

mass compressing the cervical cord with associated<br />

intraspinal hematoma. CT angiography confirmed a dense<br />

homogeneously enhancing vascular structure as the cause of<br />


Monday<br />

cord compression. Catheter angiography then was repeated<br />

with attention to the extracranial carotid and vertebral circulations.<br />

Findings included multivessel occlusion at the level<br />

of the skull base with extensive dural to pial collaterals.<br />

Occlusion of both vertebral arteries at the C1 level was<br />

noted. No intracranial aneurysms were identified. An<br />

enlarged anterior spinal artery was found off the left supreme<br />

intercostal artery that subsequently filled the basilar artery<br />

and both posterior cerebral artery territories. A 1.1 x 1.1 cm<br />

irregular bilobed pseudoaneurysm of the enlarged anterior<br />

spinal artery was noted with surrounding mass effect compatible<br />

with the above-mentioned hemorrhagic mass noted<br />

on the cross-sectional imaging studies (Fig. 1).<br />


Successful endovascular occlusion of the pseudoaneurysm<br />

was achieved.<br />


We present a highly unusual cause of subarachnoid hemorrhage<br />

in a patient with intra and extracranial occlusive vascular<br />

disease. Our case highlights the often rich and unique<br />

collateral networks that develop in association with occlusive<br />

disease as well as the need to evaluate the spinal axis<br />

and its vascular supply in cases of subarachnoid hemorrhage<br />

with a confounding clinical picture and without a definitive<br />

source of hemorrhage.<br />

KEY WORDS: Subarachnoid hemorrhage, moyamoya,<br />

pseudoaneursym<br />

26<br />

Paper 51 Starting at 10:10 AM, Ending at 10:18 AM<br />

Prospective Evaluation of Complications in 23,649<br />

Consecutive Cases of Diagnostic Cervicocerebral<br />

Angiography<br />

Kaufmann, T. J. · Huston, J. · Mandrekar, J. · Schleck, C. ·<br />

Kallmes, D. F.<br />

Mayo Clinic<br />

Rochester, MN<br />


Cervicocerebral angiographic imaging continues to shift<br />

from catheter angiography to noninvasive means. With the<br />

decreasing size of patient cohorts undergoing catheter<br />

angiography, the ability to carry out studies of the complications<br />

associated with the test will diminish. We report herein<br />

the largest study to date regarding the adverse event rate in<br />

cervicocerebral angiography.<br />


We prospectively have completed data forms on all patients<br />

receiving diagnostic cervicocerebral angiography at our<br />

institution, a tertiary and quaternary academic medical center,<br />

from 1981 through 2003. The data fields on the form<br />

include demographic data, comorbidities, indication for the<br />

examination, access site, procedure duration, number of<br />

catheters employed, type and volume of iodinated contrast<br />

material employed, presence or absence of trainee operator,<br />

and type of any neurologic, systemic, or local complication<br />

of the procedure. Clinical follow up was performed by a<br />

radiology nurse at 24 hours after every procedure, either by<br />

visiting inpatients and searching the medical record or by<br />

telephone interview with outpatients. Complications were<br />

recorded if they occurred within 24 hours of the angiogram,<br />

regardless of whether it was thought that the angiogram<br />

directly contributed to the complication. Descriptive statistics<br />

were generated of patient and procedural characteristics<br />

and of procedural complications. Univariate and multivariate<br />

analysis of complications was performed.<br />


Records were reviewed for 23,649 consecutive cases,<br />

involving 20,015 patients. Mean patient age was 53, and<br />

55% were male. The most common indication for imaging<br />

was cerebrovascular disease (36%). Comorbidities included:<br />

hypertension (31%), serum creatinine greater than 1.2<br />

(16%), and frequent TIAs (10%). Retrograde, femoral arterial<br />

puncture was used in 98% of cases. A single catheter,<br />

alone, was used in 70% of cases. Mean procedure duration<br />

was 67 minutes. Access site hematoma occurred in 4%, and<br />

hematoma requiring surgery occurred in 0.08% of cases.<br />

Nausea/vomiting/hypotension occurred in 1%, anaphylaxis/circulatory<br />

collapse in 0.03%, and death in 0.05% (n = 13<br />

deaths; 11 of these related to neurologic conditions).<br />

Neurologic deficits occurred in 2.2% of cases (n = 523):<br />

transient in 1.8% (n = 419), reversible in 0.31% (n = 72), and<br />

permanent in 0.14% (n = 32). For all neurologic complications,<br />

including death related to neurologic events, independently<br />

correlating factors at multivariate analysis included<br />

patient age (p = .0008), history of frequent TIAs (p <<br />

.0001), and amount of contrast material used (p = .0205).<br />

The preprocedure imaging indication of cerebrovascular disease<br />

was more likely to correlate with neurologic complication<br />

of angiography.


This study, comprising a prospective assessment of greater<br />

than 20,000 consecutive examinations, confirms the relative<br />

safety of diagnostic conventional cervicocerebral angiography.<br />

This true risk profile of cervicocerebral angiography<br />

should be weighed against its potential benefits in deciding<br />

between it and noninvasive imaging modalities.<br />

KEY WORDS: Angiography, complications, stroke<br />

Paper 52 Starting at 10:18 AM, Ending at 10:26 AM<br />

MR Angiography of Radiation-Induced Extracranial<br />

Stenosis: Patterns and Correlation with Catheter<br />

Angiography<br />

Kane, A. G.<br />

Tripler Army Medical Center<br />

Honolulu, HI<br />


Radiation treatment of head and neck cancer can result in<br />

stenoses of the carotid and vertebral vessels. In order to identify<br />

such stenoses, noninvasive testing must distinguish radiation-induced<br />

stenosis from more frequent atherosclerotic<br />

stenoses in the carotid bifurcation.<br />


Seven high-grade (> 70%) stenosis in craniocervical vessels<br />

in patients who had undergone whole neck radiation therapy<br />

of head and neck cancer, and who subsequently were imaged<br />

with both MR imaging and catheter angiography, were<br />

reviewed.<br />


All but one patient had smooth and long-segment common<br />

carotid stenoses (Figs. 1A, 1B arrows), and three of these<br />

had coincident proximal internal carotid bifurcation stenosis<br />

(two ulcerated) ipsilateral to the common carotid stenosis.<br />

Two patients had ipsilateral vertebral long-segment irregular<br />

stenoses. One patient treated with carotid stenting developed<br />

rapid restenosis within 4 months, underwent repeat angioplasty<br />

and is without restenosis 5 months later.<br />

27<br />


Large vessel radiation injury commonly effects long segments<br />

of the common carotid artery, distinguishing this entity<br />

in location from more common diseases such as atherosclerotic<br />

stenosis, fibromuscular dysplasia, and dissection.<br />

Ulceration may be more common than in atherosclerotic<br />

lesions when radiation stenosis affects the carotid bifurcation.<br />

MR angiography, with its ability to rapidly image the<br />

entire craniocervical region, is ideally suited to screening<br />

these patients for potential intravascular therapy when radiation<br />

or encasement are suspected.<br />


1. Santoro A, Bristot R, Paolini S, Di Stefano D, Cantore G.<br />

Radiation injury involving the internal carotid artery.<br />

Report of two cases. J Neurosurg Sci 2000;44(3):159-164<br />

2. Gauvrit JY, Leclerc X, Gautier C, Pruvo JP. Techniques for<br />

evaluating the degree of carotid artery stenosis J<br />

Neuroradiol 2001;28(1):17-26<br />

3. Ohta H, Sakai N, Nagata I, Sakai H, Higashi T, Takahashi J.<br />

Bilateral carotid stenting for radiation-induced arterial<br />

stenosis. No Shinkei Geka 200129(6):559-563<br />

KEY WORDS: Radiation, vasculopathy, stenosis<br />

Paper 53 Starting at 10:26 AM, Ending at 10:34 AM<br />

Endovascular Management of Extracranial Carotid and<br />

Vertebral Artery Dissections by Means of Stent-<br />

Supported Angioplasty<br />

Gomori, J. M. · Cohen, J. E.<br />

Hadassah Hebrew University Medical Center<br />

Jerusalem, ISRAEL<br />


Supraaortic dissection may lead to stenosis, occlusion, and<br />

pseudoaneurysms formation with subsequent embolic<br />

infarcts despite anticoagulation. Our purpose is to determine<br />

the therapeutic value of stent-supported endovascular reconstruction<br />

in a subgroup of patients who are poor candidates<br />

for medical therapy.<br />


The patient population was composed of 12 patients; 8 men<br />

and 2 women, with ages ranging from 17-64 years (mean 51<br />

years). Nine dissections were located on the ICA and 3 on<br />

the VA. Patients were considered for endovascular stenting<br />


Monday<br />

when symptomatic despite anticoagulation, contraindication<br />

for anticoagulation, clinical instability, or angiographic evidence<br />

of hemodynamic insufficiency. Before the procedure<br />

cranial CT/MR imaging and DSA of supraaortic vessels and<br />

cerebral parenchymography were performed.<br />


The treatment significantly improved dissection-related<br />

stenosis from mean 75% stenoses to 8%. Two complete<br />

occlusions were recanalized. Multiple overlapping stents<br />

were used in 9 of the cases. No clinical complications were<br />

assessed in a mean follow-up period of 4 months (range 2<br />

months - 2 years). Postoperative morbidity: pneumonia, 1<br />

case. Postoperative mortality: 0%.<br />


In selected cases of carotid and vertebral artery dissection,<br />

endovascular reconstruction by means of stents appears to be<br />

a safe and effective method of restoring arterial lumen with<br />

good clinical outcome.<br />

KEY WORDS: Dissection, stent, angioplasty<br />

Paper 54 Starting at 10:34 AM, Ending at 10:42 AM<br />

High-Resolution Dynamic Time-Resolved MR<br />

Angiography: Initial Experience in the Neurovascular<br />

Patient<br />

Hopkins, J. K. · Cashen, T. · Walker, M. · Carr, J. · Futterer,<br />

S. · Parkinson, R. · Carroll, T. J.<br />

Northwestern University<br />

Chicago, IL<br />


Time-resolved contrast-enhanced MR angiography (CE<br />

MRA) is a promising technique, providing dynamic temporal<br />

information without significant degradation of spatial<br />

resolution. Rapid arteriovenous transit time and requirements<br />

for high spatial resolution make time-resolved imaging<br />

of neurovascular abnormalities particularly challenging.<br />

Additionally, spatial resolution is sacrificed incrementally in<br />

order to achieve an adequate frame rate. We have developed<br />

a CE MRA pulse sequence for high-resolution dynamic<br />

time-resolved MRA of the neurovascular system, combining:<br />

echo-sharing (TREAT), ultrashort TR and parallel imaging<br />

(GRAPPA). The purpose of this study is to evaluate this<br />

novel pulse sequence in a series of patients with a range of<br />

neurovascular abnormalities.<br />


Patients with suspected/known vascular disease were<br />

imaged using a 1.5 T whole body MR scanner (Avanto,<br />

Sonata, Siemens Medical Solutions, Erlangen, Germany)<br />

with a 2-channel neck coil and/or a 4-channel head coil. A<br />

3D multiphase TREAT (time-resolved echo-shared angiographic<br />

technique) pulse sequence was combined with parallel<br />

imaging (GRAPPA). The 3D TREAT sequence is a segmented<br />

k-space acquisition using the TRICKS variable rate<br />

k-space acquisition. Typical acquisition parameters were:<br />

(FOV = 300 x 135 x 64 mm, image matrix = 320 x 144 x 64,<br />

spatial resolution = 1.0 x 1.0 x 1.0 mm, temporal resolution<br />

= 6.0 s/frame, TR/TE = 2.44/0.91 ms, flip = 25, bandwith =<br />

980 Hz/pixel, R-L/A-P partial Fourier factors = 0.75/0.75).<br />

Gadolinium-based contrast material was administered as a<br />

28<br />

single dose in an antecubital vein at an injection rate of 4.0<br />

ml/s.<br />


We have successfully imaged AVMs, STAMCA bypass, an<br />

intratumoral shunt, and stenosis of the carotid bifurcation.<br />

We have found the 6-second frame rate used for our standard<br />

submillimeter high-resolution CE MRA insufficient for high<br />

flow lesions, such as fistulae. In these cases, frame rates of 2<br />

to 3 seconds were desired and achieved through reducing the<br />

number of partitions, while maintaining in-plane resolution.<br />

Fig. 1 shows a series of coronal MIP images from a patient<br />

with intratumoral AV shunting (arrow) at temporal resolution<br />

of 4.5 seconds.<br />


We have successfully combined echo-sharing and parallel<br />

imaging for high-resolution, high-frame rate neurovascular<br />

MRA. With continued improvements in temporal and spatial<br />

resolution, this technique could approach the gold standard<br />

examination, DSA. The potential to diagnose flow-related<br />

pathologies and assess or monitor treatment effects is exciting<br />

and could result in improvement in the morbidity and<br />

mortality associated with the typical work up of these types<br />

of lesions.<br />

KEY WORDS: Time resolved, contrast-enhanced MR angiography,<br />


Paper 55 Starting at 10:42 AM, Ending at 10:50 AM<br />

Relationship between Carotid Artery Bifurcation<br />

Calcification and White Matter Changes<br />

Fanning, N. F. 1 · Walters, T. D. 2 · Symons, S. 1 · Fox, A. 1<br />

1Sunnybrook and Women’s College Health Sciences Center,<br />

Toronto, ON, CANADA, 2Hospital for Sick Children,<br />

Toronto, ON, CANADA<br />


Carotid bulb scores for calcified plaque have been proposed<br />

for future stroke risk, similar to acceptance of coronary<br />

artery calcification scores for future heart disease risk (1).<br />

Relative future stroke risk already has been correlated with<br />

white matter change severity. We sought to link associations<br />

between carotid calcification and white matter severity on<br />

CT to predict relative risk for future stroke, based on calcification<br />

grade.<br />


We retrospectively reviewed neuroradiologic findings in 221<br />

patients with unenhanced neck and brain CT for carotid bulb<br />

calcification and white matter changes. Degree of carotid<br />

calcification was scored by the Agatston method (2), calculating<br />

the calcific plaque load as the sum of all single calcific<br />

plaques in the carotid bulb, with each plaque calculated as<br />

a function of its Hounsfield density and area. White matter<br />

change severity was graded on CT according to the<br />

European Task Force for Age-Related White Matter Change<br />

scale (3). Each variable was measured in a blinded fashion.<br />

Demographic details, including age and gender, were recorded.<br />

Univariate and multivariate analyses were used to examine<br />

for evidence of association.<br />


Both carotid calcification and white matter scores were<br />

strongly, and independently, associated with increasing age<br />

(r = 0.65, p < 0.001 and r = 0.67, p < 0.001 respectively).<br />

Despite apparent association between carotid calcification<br />

and white matter scores on univariate analysis, there was no<br />

independent effect evident after adjusting for age as a covariant<br />

(r = 0.006, p = 0.93). Gender had no independent effect<br />

on white matter scores; however, males had a marginally<br />

higher mean calcified carotid plaque load than females after<br />

controlling for age (p = 0.025).<br />


Carotid bulb CT calcification scores do not independently<br />

predict severity of white matter changes. Future stroke risk,<br />

assessed by white matter severity scores, cannot be predicted<br />

from carotid calcific score. It is premature to suggest that<br />

screening CT for carotid calcification has potential benefit.<br />


1. Pletcher MJ, Tice JA, Pignone M, Browner WS. Using the<br />

coronary artery calcium score to predict coronary heart disease<br />

events: a systematic review and meta-analysis. Arch<br />

Intern Med 2004;164:1285-1292<br />

2. Agatston AS, Janowitz WR, Hildner FJ, Zusmer NR, Viamonte<br />

M, Detrano R. Quantification of coronary artery calcium<br />

using ultrafast computed tomography. J Am Coll Cardiol<br />

1990;15:827-832<br />

29<br />

3. Wahlund LO, Barkhof F, Fazekas F et al. A new rating scale<br />

for age-related white matter changes applicable to MRI and<br />

CT. Stroke 2001;32:1318-1322<br />

KEY WORDS: Carotid bulb calcification, white matter<br />

changes, stroke risk<br />

Paper 56 Starting at 10:50 AM, Ending at 10:58 AM<br />

Validity of Millimeter Carotid Stenosis CT Angiography<br />

Measurements for Endarterectomy<br />

Bartlett, E. S. 1 · Walters, T. D. 2 · Symons, S. P. 1 · Fox, A. J. 1<br />

1Sunnybrook and Women’s College Health Sciences Center,<br />

Toronto, ON, CANADA, 2Hospital for Sick Children,<br />

Toronto, ON, CANADA<br />


Millimeter carotid stenosis measurements from high speed CT<br />

angiography (CTA) are direct, accurate, and have a linear relationship<br />

with NASCET-style ratios. Millimeter measurements<br />

can be used as guidelines for management of carotid stenosis<br />

in lieu of ratio calculations that NASCET and other trials have<br />

defined previously to support surgical versus medical management<br />

of carotid artery disease. The guidelines from these<br />

prior trials are based upon ratio measurements, since direct<br />

measurement of stenosis is not possible with standard catheter<br />

digital subtraction angiography (DSA).<br />


Two neuroradiologists separately reviewed 267 carotids<br />

imaged on CTA blinded to other information. The narrowest<br />

portion of carotid stenosis was measured in millimeters.<br />

Distal internal carotid (ICA) was measured well beyond the<br />

carotid bulb. NASCET-style ratio was calculated for each<br />

ICA, excluding suspected near-occlusion cases. Correlation<br />

coefficients were calculated to determine the degree of interobserver<br />

variation in mm measurements. ROC curves were<br />

utilized to determine the millimeter stenosis value equivalent<br />

to the 70% severe stenosis NASCET guideline with the<br />

greatest sensitivity, specificity, and predictive value.<br />


Excellent interobserver correlation (0.78 to 0.89, 2-tail significance<br />

= 0.01) permitted averaging of millimeter stenosis<br />

and distal ICA measurements from the CTA luminogram for<br />

each carotid. These values were used to calculate mean percent<br />

stenosis. Regression analysis of mean percent stenosis<br />

as a function of mean millimeter stenosis proves a linear<br />

relationship between these values (Pearson’s correlation of -<br />

0.95, N = 136). ROC curve analysis demonstrates a direct<br />

millimeter measurement of 1.3 mm identifies severe carotid<br />

stenosis (70% as in NASCET) with a sensitivity of 88.2%,<br />

specificity 92.4%, and negative predicted value 98.2%.<br />


Direct measurement of carotid stenosis by CTA can be utilized to<br />

determine the appropriateness of endarterectomy for severe<br />

symptomatic stenosis with relatively high sensitivity and specificity,<br />

based upon previously published percent stenosis guidelines<br />

from NASCET. With a negative predicted value of 98.2%,<br />

clinicians can be assured that patients with carotid stenosis measurements<br />

greater than 1.3 mm are without severe carotid disease.<br />

KEY WORDS: CT angiography, carotid stenosis, endarterectomy<br />


Monday<br />

Paper 57 Starting at 10:58 AM, Ending at 11:06 AM<br />

Direct CT Angiographic Measurements of Vessels<br />

Alleviates Cumbersome Estimates for Ratio Calculations<br />

Bartlett, E. S. 1 · Walters, T. D. 2 · Symons, S. P. 1 · Fox, A. J. 1<br />

1Sunnybrook and Women’s College Health Sciences Centre,<br />

Toronto, ON, CANADA, 2Hospital for Sick Children,<br />

Toronto, ON, CANADA<br />


CT angiography of the carotid arteries allows for the direct<br />

measurement of diseased and normal vessels, alleviating the<br />

need for cumbersome and novel ratio calculations. This is<br />

especially true when regarding the ambiguities of some ratio<br />

calculations from studies such as the European Carotid<br />

Surgery Trial (ECST) and the Carotid Stenosis Index (CSI)<br />

method (1). The ECST method calculates a ratio based upon<br />

an estimate of an unseen carotid bulb. The CSI estimates the<br />

size of the carotid bulb by an equation: 1.2 x CCA diameter,<br />

based upon previously published anatomical relationships<br />

(2).<br />


Two neuroradiologists reviewed 261 carotid CTAs with<br />

carotid disease. Millimeter measurements were obtained of<br />

the residual stenotic lumen in the narrowest diameter, the<br />

actual carotid bulb diameter at the level of the greatest stenosis,<br />

and at the common carotid artery, measured between 3-<br />

5 centimeters prior to the carotid bifurcation. Interobserver<br />

variation correlation was calculated for all measurements.<br />

Pearson correlation coefficients compared the CSI estimate<br />

of the carotid bulb to the actual carotid bulb measurement<br />

from CTA. Ratio calculations of the stenosis were performed<br />

using the CSI carotid bulb estimate as denominator data and<br />

then repeated using the actual carotid bulb measurement as<br />

denominator data [(1-stenosis/carotid bulb)*100]. A pairedsample<br />

Wilcoxon Signed Rank test was performed to compare<br />

the results of these two ratio measurements per carotid.<br />


Interobserver variability was good, ranging from 0.63 to<br />

0.81. The CSI estimate of the carotid bulb size routinely<br />

overestimated the actual measured carotid bulb value by an<br />

average of 1.5 mm. The overestimation was randomly distributed,<br />

as evidenced by the poor correlation between the<br />

CSI estimate and the actual bulb measurements (Pearson’s<br />

correlation coefficient = 0.4, N = 151). Paired-sample<br />

Wilcoxon Signed Rank test (2-tailed, equal variance)<br />

demonstrated a significant difference between the two sets of<br />

ratios with a Z-value of -9.51 (p < 0.001).<br />


With the high-resolution anatomical data present in highspeed<br />

CTA, direct measurement of vessel diameter is possible.<br />

Cumbersome ratio calculations using visual or mathematical<br />

estimates of vessel diameter are no longer necessary.<br />


1. Bladin CF, Alexandrov AV, Murphy J, Maggisano R, Norris JW.<br />

Carotid stenosis index: A new method of measuring internal<br />

carotid artery stenosis. Stroke 1995;26:230-234<br />

30<br />

2. Williams MA, Nicolaides AN. Predicting the normal dimensions<br />

of the internal and external carotid arteries from the<br />

diameter of the common carotid. Eur J Vasc Surg 1986;1:91-<br />

96<br />

KEY WORDS: CT angiography, carotid disease<br />

Paper 58 Starting at 11:06 AM, Ending at 11:14 AM<br />

Cross-Sectional Mm 2 Area of Carotid Stenosis CT<br />

Angiography<br />

Bartlett, E. S. · Symons, S. P. · Fox, A. J.<br />

Sunnybrook and Women’s Health Sciences Center<br />

Toronto, ON, CANADA<br />


New tools integrated in the current versions of PACS workstations<br />

allow for a more precise calculation of the carotid<br />

geometry. Carotid stenosis quantification has relied traditionally<br />

upon measurements from catheter angiography of<br />

the carotid artery. The validity of such measurements can be<br />

questioned since a stenotic carotid lumen often is shaped<br />

irregularly. Trials regarding this question have resulted in<br />

recommending digital subtraction angiography (DSA) imaging<br />

in at least 2 different planes and the provision of qualifying<br />

statements such as “narrowest diameter.”<br />


During an 8-month review of consecutive carotid CT<br />

angiography (CTA) in a single institution, two neuroradiologists<br />

evaluated 178 stenosed carotids in a blinded protocol.<br />

Carotid artery bulb stenosis was identified on axial CTA.<br />

AGFA Impax 4.5 volume tool (VT) utilizing Houndsfield<br />

units was used to estimate the cross-sectional area of the<br />

contrast luminogram. The narrowest diameter of a carotid<br />

stenosis was measured also by manually placing measurement<br />

calipers. Correlation coefficients were calculated to<br />

determine the degree of interobserver variation. Pearson correlation<br />

coefficients were calculated between the millimeter<br />

stenosis and the VT area, as well as between the VT area and<br />

the calculated area (based upon the narrowest diameter and<br />

assuming a circular residual lumen using a formula of: area<br />

= Pi x radius 2 ).<br />


Excellent interobserver correlation (0.71 to 0.81, 2-tail significance<br />

= 0.01) permitted averaging of narrowest diameter<br />

stenosis measurement and the VT area values per carotid.<br />

There is excellent correlation between the VT area of the<br />

often irregular carotid stenosis and the narrowest diameter<br />

mm measurement (Pearson’s correlation of 0.77, N = 178).<br />

The VT area was generally greater than the calculated area<br />

by an average of 2.03 mm 2 . This difference is due to the often<br />

irregular shape of the residual lumen. Nonetheless, there is<br />

excellent correlation between the VT area and the calculated<br />

area (Pearson’s correlation of 0.76, N = 178).

Carotid measurement and example of volumetric tool: A:<br />

Measurement in centimeters of a right ICA with proximal<br />

stenosis. B: AGFA Impax 4.5 volume tool at the same level<br />

as in figure A, with perimeter and area in centimeters and<br />

squared centimeters, respectively.<br />


Measurement of the narrowest portion of a carotid stenosis<br />

remains an acceptable method to characterize carotid disease.<br />

There is excellent correlation to more precise area calculations<br />

of an often irregular residual lumen.<br />

KEY WORDS: CT angiography, carotid stenosis, volume tool<br />

Paper 59 Starting at 11:14 AM, Ending at 11:22 AM<br />

Identification of Carotid Near Occlusion by CT<br />

Angiography<br />

Bartlett, E. S. 1 · Walters, T. D. 2 · Symons, S. P. 1 · Fox, A. J. 1<br />

1 Sunnybrook and Women’s College Health Sciences Center,<br />

Toronto, ON, CANADA, 2 Hospital for Sick Children,<br />

Toronto, ON, CANADA<br />


CT angiography is a valuable tool for evaluation of carotid<br />

stenosis. However, near occlusion with secondary distal<br />

carotid artery reduction remains a confounder for calculation<br />

of NASCET-style percent stenosis. Using criteria to identify<br />

subtle findings of near occlusion (1), a recent review of<br />

NASCET and ECST angiograms diagnosed 262 near occlusions,<br />

only 16 having significant luminal collapse.<br />

Identification of near occlusion is essential prior to attempted<br />

percent stenosis ratio calculation, since these calculations<br />

yield fallacious numbers. The implications relate to proper<br />

stenosis quantification and treatment, since the risk of ipsilateral<br />

stroke in near occlusion is less than in severe stenosis (1).<br />


Two hundred and forty carotid artery CTAs for known or<br />

suspected carotid disease were evaluated independently by 2<br />

neuroradiologists with a blinded protocol. Besides identifying<br />

arteries with criteria for near occlusion, millimeter measurements<br />

were obtained at narrowest diameter of the stenotic<br />

bulb, distal ICA well beyond the tapering carotid bulb, and<br />

distal ECA prior to its terminal branching. Forty-three<br />

carotid arteries were labeled near occlusion. All interpretative<br />

disagreement cases were reviewed at consensus meeting.<br />

Interobserver variance was calculated for all measurements.<br />

Threshold values best predicting near occlusion were<br />

devised with ROC curve analysis for: 1) ICA stenosis, 2) distal<br />

ICA, 3) distal ICA:distal ICA, and 4) distal ICA:ECA.<br />

Combinations of variables also were evaluated.<br />

31<br />


Based upon threshold values for the independently measured<br />

variables, the sensitivity range = 88.4-100; specificity = 83.9<br />

-92.9; PPV = 57.6-73.1 and NPV = 96.6-100. The range for<br />

paired permutations is: sensitivity = 76.3-84.2; specificity =<br />

93.8-97.1; PPV = 72.5-89.5 and NPV = 93.6-96.1.<br />

Fig. 1. The partially collapsed ICA called near occlusion on<br />

right is about the diameter of ECA, far narrower than usual<br />

relationship as seen on the left (arrow = distal ICA).<br />


Threshold values are most helpful in providing guidelines to<br />

the CTA interpreter when assessing carotid artery disease<br />

and for the presence of near occlusion. Ultimate identification<br />

of near occlusion requires the judgment of the interpreter,<br />

with attention to the following criteria: 1) notable<br />

stenosis of the ICA bulb, and 2) distal ICA caliber reduction<br />

compared to: a) expected size, b) contralateral ICA, and c)<br />

ipsilateral ECA.<br />


1. Fox AJ, Eliasziw M, Rothwell PM, Schmidt MH, Warlow CP,<br />

Barnett HJM. Identification, prognosis, and management of<br />

patients with carotid artery near occlusion. AJNR Am J<br />

Neuroradiol in press<br />

KEY WORDS: Near occlusion, CT angiography, carotid disease<br />

Discussion<br />

Monday Morning<br />

10:15 AM - 11:45 AM<br />

Room 103<br />

(8) ELC Workshop B: Advanced<br />

PowerPoint<br />

— Richard H. Wiggins, III, MD<br />

— H. Christian Davidson, MD<br />


Monday<br />

Monday Afternoon<br />

1:00 PM - 1:30 PM<br />

Room 205<br />

(9) ELC Lecture B: High Speed<br />

Connectivity Update<br />

Monday Afternoon<br />

1:00 PM - 2:30 PM<br />

Theatre<br />

(10) Vascular Malformations of the<br />

Head and Neck (ASITN)<br />

(63) Imaging of Head and Neck Vascular<br />

Malformations<br />

— Anton N. Hasso, MD, FACR<br />

(64) Treatment of Hi-Flow Lesions<br />

— Wayne F. Yakes, MD<br />

(65) Treatment of Low-Flow Lesions<br />

— Patricia E. Burrows, MD<br />

Discussion<br />

Moderator: Mary E. Jensen, MD<br />

— Gerard J. Muro, MD<br />

Imaging of Head and Neck Vascular Malformations<br />

Anton N. Hasso, MD, FACR<br />


Upon completion of this presentation, participants will be<br />

able to:<br />

1) Discuss the classification system of vasoformative anomalies.<br />

2) Review MR imaging findings in hemangiomas and vascular<br />

malformations.<br />

3) Construct a table listing the optimal treatment of vasoformative<br />

anomalies.<br />

32<br />


Vascular anomalies can be divided into hemangiomas and<br />

vascular malformations based on histologic features, natural<br />

history, and biologic behavior. Hemangiomas are benign<br />

endothelial tumors that appear during infancy, undergo a<br />

period of rapid proliferation, and eventually regress.<br />

Accordingly, hemangiomas can be subclassified as either<br />

proliferating or involuting. Vascular malformations, on the<br />

other hand, are developmental defects of the vasculature that<br />

are present at birth, grow in parallel with the individual, and<br />

never involute. These lesions are subdivided based on the<br />

predominant vascular channel that is affected, namely arterial,<br />

venous, capillary, lymphatic, or combined. MR imaging<br />

is critical in the characterization of vascular anomalies as it<br />

can determine hemodynamic flow properties, delineate<br />

extent of disease, and guide treatment. High-resolution, 3dimensional<br />

capabilities, and noninvasiveness make MR<br />

imaging the gold standard in the treatment planning of craniofacial<br />

vascular lesions. The hallmark imaging features of<br />

hemangiomas and vascular malformations are coupled<br />

closely to clinical decision-making strategies. Current therapeutic<br />

options include steroids, laser photocoagulation, percutaneous<br />

sclerotherapy, endovascular embolization, and<br />

surgical resection. The impetus for treatment of head and<br />

neck lesions is to improve cosmetic appearance, eliminate<br />

functional impairment, and preclude life-threatening complications.<br />

A number of effective treatments currently are<br />

employed in the management of vascular anomalies, including<br />

pharmacotherapy, laser photocoagulation, sclerotherapy,<br />

cryosurgery, embolization, and surgical resection. In this<br />

presentation, we will review the salient MR findings for various<br />

vascular anomalies and discuss strategies for selecting<br />

optimal treatments for lesions of the head and neck.<br />


1. Mulliken JB, Glowacki J. Hemangiomas and vascular malformations<br />

in infants and children: a classification based on<br />

endothelial characteristics. Plast Reconstr Surg 1982;69:412-<br />

422<br />

2. Meyer JS, Hoffer FA, Barnes PD, Mulliken JB. Biological classification<br />

of soft-tissue vascular anomalies: MR correlation.<br />

AJR Am J Roentgenol 1991;157:559-564<br />

3. Jackson IT, Carreno R, Potparic Z, Hussain K. Hemangiomas,<br />

vascular malformations, and lymphovenous malformations:<br />

classification and methods of treatment. Plast Reconstr Surg<br />

1993;91:1216-1230<br />

4. Van Aalst JA, Bhuller A, Sadove AM. Pediatric vascular<br />

lesions. J Craniofac Surg 2003;14:566-583<br />

5. Enjolras O, Mulliken JB. The current management of vascular<br />

birthmarks. Pediatr Dermatol 1993;10:311-313<br />

Treatment of Hi-Flow Lesions<br />

Wayne F. Yakes, MD<br />


Upon completion of this presentation, participants will be<br />

able to:<br />

1) Be facile in the understanding of the various types of congenital<br />

types of vascular malformations.<br />

2) Be familiar with the rationale for endovascular treatment<br />

with the philosophy of permanent treatment.<br />

3) Be aware of various approaches for managing head and

neck vascular malformations with ethanol embolization.<br />

4) Understand the minimally invasive endovascular<br />

approaches to manage these complex and vexing lesions.<br />


Interventional Radiology and Interventional Neuroradiology<br />

have pioneered a minimally invasive therapeutic specialty to<br />

treat a wide variety of vascular and nonvascular lesions of the<br />

body, the brain, spine, spinal cord and head and neck areas.<br />

Interventional procedures routinely use minimally invasive,<br />

direct puncture, and transcatheter techniques to treat various<br />

conditions. In the head/neck and paraspinal area the vast<br />

majority of entities that are treated are largely of vascular origin.<br />

The extensive array of catheters, guidewires, embolic<br />

agents, digital imaging systems and the pharmaceutical products<br />

that commonly are used are a tribute to the hard work,<br />

insight, and imagination of the many dedicated investigators<br />

in this area. Because of significant laboratory research, clinical<br />

research, and extensive clinical experience, the judicious<br />

use of endovascular therapy is now commonplace in modern<br />

clinical practice. Now that it is firmly established as an essential<br />

therapeutic tool, its role will only continue to grow. In the<br />

head and neck and paraspinal region, embolotherapy procedures<br />

have become an essential therapeutic modality that has<br />

assisted our colleagues in otolaryngology, plastic and reconstructive<br />

surgery, neurosurgery, ophthalmology, vascular surgery<br />

and various pediatric surgical specialties. After the diagnosis<br />

has been established, the next major decision is to determine<br />

whether therapy is warranted. The interventional radiologist/interventional<br />

neuroradiologist should plan and direct<br />

the patient’s care with surgical specialists who are familiar<br />

with the management of hemangioma and vascular malformations<br />

and the problems they present. It is extremely important<br />

that appropriate surgical, medical, pediatric, and anesthesiology<br />

specialists be involved for optimal patient care. They<br />

would function much like a tumor board team in the management<br />

of cancer. I classify vascular malformations as either<br />

high-flow or low-flow lesions. The high-flow lesions are<br />

shunting malformations such as arteriovenous malformations<br />

(AVMs) and congenital or acquired arteriovenous fistulae<br />

(AVF). The low-flow lesions include venous malformations,<br />

lymphatic malformations, and mixed lesions. The arteriography<br />

of these lesions demonstrates normal arteries and normal<br />

capillary beds. The malformation is truly a postcapillary<br />

lesion. The terms “cavernous hemangioma," “vertebral body<br />

hemangioma," and “hepatic hemangioma” should be replaced<br />

with the term “venous malformation." If they were truly<br />

hemangiomas, they should not be present in the adult population.<br />

Vascular malformations are treated best where these<br />

patients are seen on a regular basis. The interventional radiologist<br />

or interventional neuroradiolgist who occasionally evaluates<br />

these patients will never gain enough experience or<br />

knowledge to manage these challenging lesions effectively.<br />

All too frequently the patient ultimately pays for the interventionalist’s<br />

initial enthusiasm, inexperience, folly, and lack of<br />

necessary clinician backup. To optimally manage these<br />

patients, a dedicated team should be in place.<br />

Interventionalists, combined with the various surgical and<br />

medical subspecialties, function together much like the tumor<br />

board team of specialists. When patients are seen and treated<br />

regularly, then experience can be gained, rational decisions<br />

made, complications appropriately managed, and patient care<br />

then is optimized. It cannot be emphasized enough that, as a<br />

group, vascular malformations pose one of the most difficult<br />

challenges in the practice of medicine. A cavalier approach to<br />

33<br />

their management always will lead to significant complications<br />

and dismal outcomes for the patients.<br />


1. Mourao GS, Hodes JE, Gobin YP, Casasco A, Aymard A,<br />

Merland JJ. Curative treatment of scalp AV fistulas by direct<br />

puncture and embolization with absolute alcohol. J<br />

Neurosurg 1991;75:634-637<br />

2. Yakes WF. Interventional neuroradiologic procedures in the<br />

head and neck: ENT perspective. In: English GM, (ed).<br />

Otolaryngology. New York: Lippincott-Raven publishers,<br />

1996;1-26<br />

3. Yakes WF. Diagnosis and management of AVMs. In: Haskal<br />

ZJ, Kerlan RK, Trerotola SO (eds). SCVIR Syllabus: Thoracic<br />

and Visceral Vascular Interventions. Fairfax: Society of<br />

Cardiovascular and Interventional Radiology Publishers,<br />

1996;314-322<br />

4. Yakes WF, Rossi P, Odink H. How I do it: arteriovenous malformation<br />

management. Cardiovasc Intervent Radiol<br />

1996;19:65-71<br />

5. Yakes WF. Endovascular management of high-flow AVMs.<br />

Semin Intervent Radiol 2004;21:49:49-58<br />

Treatment of Low-Flow Lesions<br />

Patricia E. Burrows, MD<br />

Dr. Burrows obtained her MD in Winnipeg, Manitoba,<br />

Canada and did fellowships in Pediatric Radiology,<br />

Pediatric Special Procedures, and Interventional<br />

Neuroradiology. She has been involved in imaging and treatment<br />

of vascular anomalies since 1985 and currently is the<br />

Co-Director of the Vascular Anomalies Program at<br />

Children's Hospital, Boston, where she has worked for the<br />

past 12 years. Her clinical and research activities are almost<br />

entirely related to endovascular treatment of vascular malformations.<br />

She has published over 140 original papers and<br />

50 reviews on the subject of pediatric vascular disease.<br />


Upon completion of this presentation, participants will be<br />

able to:<br />

1) Diagnose various forms of low-flow vascular malformations<br />

by imaging and clinical characteristics.<br />

2) Determine appropriateness for treatment of patients with<br />

low-flow vascular malformations.<br />

3) Be familiar with the drugs and techniques that are useful<br />

in treating vascular malformations.<br />

4) Recognize complications of treatment of low-flow vascular<br />

malformations.<br />


Low-flow vascular malformations include venous malformations<br />

(VM), lymphatic malformations (LM) and capillary malformations<br />

(CM) as well as combined forms. Sclerotherapy or<br />

injection of sclerosing drugs into the vascular spaces is the current<br />

standard method of treatment. Commonly used sclerosants<br />

for venous malformations include ethanol, sodium tetradecyl,<br />

and other detergent type sclerosants. For lymphatic malformations,<br />

injection of ethanol, OK432, and doxycycline have been<br />

found to be effective. Venous malformations can be diffuse,<br />

focal, or multifocal. The soft tissues of the head and neck can<br />

be involved. The most extensive lesions involve the cerebral<br />

and cranial veins as well. Focal and multifocal lesions respond<br />


Monday<br />

best to sclerotherapy. Intraorbital venous malformations are<br />

almost impossible to treat safely by injection techniques<br />

because of the risk of orbital compartment syndrome and loss<br />

of vision. Venous malformations of the oral cavity and more<br />

distal airway require prolonged airway protection after sclerotherapy.<br />

Direct injection of supraglottic VM can be accomplished<br />

through a rigid laryngoscope. Varicocoele expansion of<br />

superficial neck veins can be treated but require more complicated<br />

techniques. Lymphatic malformations (LM) are classified<br />

as macrocystic or microcystic. Most cystic forms can be<br />

injected with sclerosant, using ultrasound guidance. Orbital<br />

LM with a visual impairment due to repeated bleeds and infections<br />

can be sclerosed cautiously, although there is a risk of<br />

orbital compartment syndrome. Complications include damage<br />

to skin and nerves, infection, orbital compartment syndrome,<br />

and airway obstruction. Patient follow-up surveys indicate<br />

good to excellent results in at least 75% of cases.<br />

Discussion<br />

Monday Afternoon<br />

1:00 PM - 2:30 PM<br />

Room 105/106<br />

(11) Neuropathies of the Head and<br />

Neck (ASNHR)<br />

(66) Upper Cranial Nerves (III-VI)<br />

— William P. Dillon, MD<br />

(67) Lower Cranial Nerves (IX-XII)<br />

— Wendy R.K. Smoker, MD, FACR<br />

(68) Brachial Plexopathy<br />

— Brian C. Bowen, PhD, MD<br />

Moderators: Wendy R.K. Smoker, MD, FACR<br />

William P. Dillon, MD<br />

Upper Cranial Nerves (III-VI)<br />

William P. Dillon, MD<br />


Upon completion of this presentation, participants will be able<br />

to:<br />

1) Recognize the anatomy and function of cranial nerves 3-6<br />

on MR imaging.<br />

2) Be familiar with the MR imaging protocol for and appearance<br />

of cranial nerve pathology.<br />

34<br />


Cranial nerve dysfunction is a disturbing problem that in most<br />

cases quickly brings the patient to medical attention.<br />

Symptoms are usually a manifestation of the particular nerve<br />

that is involved. The new onset of cranial nerve palsy may be<br />

the first sign of malignancy or other serious medical or vascular<br />

disease. For instance, acute third nerve palsy may be the<br />

harbinger of an expansile cerebral aneurysm; benign and<br />

malignant neoplasms, infection, noninfectious inflammatory<br />

abnormalities, radiation damage, and vascular infarctions may<br />

result in various cranial neuropathies. In addition, a number of<br />

idiopathic disorders may result in either single or multiple cranial<br />

neuropathies. Imaging of the cranial nerves has taken on<br />

more importance with the use of contrast-enhanced fat-suppressed<br />

MR techniques, which is the study of choice. Using<br />

MR imaging, the nerve itself is visualized throughout its intra<br />

and extracranial course. While a complete evaluation of cranial<br />

nerve dysfunction is beyond this short communication,<br />

the anatomical and pathologic features of dysfunction of cranial<br />

nerves 3-6 will be covered. There are several basic concepts<br />

that are useful to remember when designing a protocol<br />

for the patient with cranial neuropathy. Imaging should be performed<br />

in at least two planes encompassing the nucleus, the<br />

nerve, and its distal muscle of innervation. Imaging with both<br />

T1- and T2-weighted sequences with fat saturation is necessary.<br />

Contrast-enhanced, fat-suppressed T1-weighted imaging<br />

is essential for diagnosis of many disorders. Secondary signs<br />

of damage to cranial nerves, such as atrophy of denervated<br />

muscles, are often helpful signs.<br />


1. Fischbein NJ, Dillon WP, Barkovich AJ, eds. A Teaching<br />

Atlas: Brain. Thieme;2000<br />

2. Wilson-Pauwels L, Akesson EJ, Stewart PA. Cranial Nerves:<br />

Anatomy and Clinical Comments. Toronto: B.C. Decker<br />

Inc.;1988<br />

3. Waxman SG, de Groot J. Correlative Neuroanatomy, 22nd<br />

edition. Connecticut:Appleton and Lange;1995<br />

4. Kelly WM, guest editor. Cranial Neuropathy. Neuroimag<br />

Clin North Am 1993;3<br />

5. Harnsberger HR. Handbook of Head and Neck Imaging. St.<br />

Louis:Mosby;1995<br />

Lower Cranial Nerves (IX-XII)<br />

Wendy R.K. Smoker, MD, FACR<br />


Upon completion of this presentation, participants will be<br />

able to:<br />

1) Define the course (intracranial and extracranial) of the<br />

lower four cranial nerves.<br />

2) Name the muscles innervated by each of the lower four<br />

cranial nerves and identify them on cross-sectional images.<br />

3) Learn the imaging appearance of different stages of denervation<br />

atrophy.<br />

4) Name common pathologies that affect the lower four cranial<br />

nerves in their cisternal, skull base, high carotid space,<br />

and distal segments.<br />


Radiologic evaluation of the patient with deficits of the lower<br />

four motor cranial nerves requires knowledge of the course of

each nerve as well as muscles innervated by these nerves.<br />

Cranial nerves IX, X, and XI are complex nerves having both<br />

motor and sensory/parasympathetic fibers. However, symptoms<br />

of motor denervation are those that are typically appreciated<br />

and cause patients to present for radiologic evaluation.<br />

The hypoglossal nerve has complete motor function.<br />

Glossopharyngeal Nerve: Nucleus (ambiguus) in rostral<br />

medulla; exits brainstem between olives and inferior cerebellar<br />

peduncle; exits skull through pars nervosa of jugular<br />

foramen to enter high carotid space. Innervates stylopharyngeus<br />

muscle and contributes to pharyngeal plexus (along<br />

with the vagus nerve), providing innervation to levator veli<br />

palatini, superior and middle pharyngeal constrictor,<br />

palatopharyngeus, and palatoglossus muscles.<br />

Vagus Nerve: Nucleus (ambiguus) in rostral medulla; exits<br />

brainstem between olive and inferior cerebellar peduncle;<br />

exits skull base through pars vascularis of jugular foramen<br />

and courses within carotid sheath. Innervates inferior pharyngeal<br />

constrictor and cricothyroid muscles via the superior<br />

laryngeal nerve, the endolaryngeal muscles via the recurrent<br />

laryngeal nerve, and contributes to pharyngeal plexus.<br />

Spinal Accessory Nerve: Nucleus in anterior lateral gray of<br />

upper 5 or 6 cord segments; rootlets ascend through foramen<br />

magnum and exit skull base through pars vascularis of jugular<br />

foramen; Innervates trapezius and sternocleidomastoid<br />

muscles.<br />

Hypoglossal Nerve: Nucleus in rostral medulla, anteromedial<br />

to dorsal motor nucleus of X; rootlets exit brainstem in<br />

preolivary sulcus; coalesce to exit skull base through<br />

hypoglossal canal and course within high carotid space<br />

before coursing to terminate in sublingual space. Innervates<br />

intrinsic and extrinsic tongue muscles. The lower four cranial<br />

nerves may be affected by supranuclear, nuclear (brainstem),<br />

or infranuclear pathology. (This discussion does not<br />

address supranuclear pathology). Common nuclear pathology<br />

includes multiple sclerosis, infarction, neoplasms (primary<br />

and metastatic), syringobulbia, etc. Infranuclear<br />

pathology is subdivided into cisternal, skull base, carotid<br />

space, and distal segments. Nuclear, cisternal, skull base, and<br />

carotid space pathology often produces deficits of all four<br />

lower cranial nerves due to their close proximity in these<br />

locations. More distal pathology, however, often produces<br />

isolated cranial deficits. Various patterns of denervation atrophy<br />

often help distinguish proximal from distal pathology.<br />

Common cisternal pathology: meningitis, vertebrobasilar<br />

dolichoectasia, neoplasms (especially neurogenic tumors,<br />

and meningiomas).<br />

Common skull base pathology: trauma, neoplasms (especially<br />

metastases, paragangliomas, neurogenic tumors, and<br />

meningiomas), and infections.<br />

Common carotid space pathology: primary and nodal SCCa,<br />

lymphoma, neoplasms (especially paragangliomas and neurogenic<br />

tumors), infection, and vascular pathology (carotid<br />

dissection/aneurysm, jugular thrombophlebitis).<br />

Brachial Plexopathy<br />

Brian C. Bowen, PhD, MD<br />


Upon completion of this presentation, participants will be<br />

able to:<br />

1) Identify plexus intrinsic and extrinsic anatomy, as dis-<br />

35<br />

played on MR images.<br />

2) Recognize the MR appearance of motor denervation.<br />

3) Identify the MR imaging features that are used to differentiate<br />

between normal and abnormal peripheral nerves.<br />

4) Recognize, and potentially avoid, pitfalls and artifacts in<br />

the acquisition and interpretation of plexus MR images.<br />


The clinical evaluation of plexopathy and peripheral neuropathy<br />

increasingly involves the use of high-resolution MR<br />

imaging to facilitate diagnosis and management. MR studies<br />

(MR neurography) of the brachial plexus are especially challenging<br />

because of the oblique course, complex intrinsic<br />

anatomy of the plexus components (roots, trunks, divisions,<br />

cords) and their extrinsic anatomical relationships (interscalene<br />

triangle, subclavian/axillary arteries/veins, and bony<br />

landmarks), as well as regional susceptibility effects and<br />

physiologic (vascular, respiratory) motion artifacts that can<br />

degrade image quality. Current imaging techniques emphasize<br />

the use of dedicated phase array coils, high spatial resolution<br />

acquisitions in the coronal (plexus in-plane) and sagittal<br />

or oblique-sagittal imaging planes (plexus in cross-section)<br />

of the involved plexus, predominantly spin-echo (T1weighted<br />

+ fat sat, T2-weighted + fat sat) and STIR<br />

sequences, and the use of a gadolinium contrast agent, in<br />

order to obtain diagnostic images of the component nerves<br />

themselves (approximately 2 - 6 mm diameter). In the<br />

patient with plexopathy, the MR study usually is requested to<br />

evaluate a clinically known or suspected (1) neoplastic or<br />

inflammatory mass (intrinsic versus extrinsic to plexus components),<br />

(2) traumatic injury (at sites ranging from neural<br />

foramina to cords and their branches), (3) entrapment or<br />

nontraumatic compressive lesion, or to provide evidence<br />

favoring (4) intrinsic structural abnormalities (hereditary<br />

hypertrophic neuropathy) or idiopathic conditions (brachial<br />

plexitis). MR imaging in the (5) posttreatment (surgery,<br />

radiotherapy) patient with a history of cancer usually is<br />

requested to help distinguish between radiation injury to the<br />

plexus and recurrent tumor. Examples of these clinical “indications”<br />

for brachial plexus imaging will be presented and<br />

discussed. The discussion also will include technical and<br />

anatomical considerations, such as magic angle effects in<br />

peripheral nerve imaging.<br />


1. Bowen BC, Pattany PM, Saraf-Lavi E, Maravilla KR. The<br />

brachial plexus: normal anatomy, pathology, and MR imaging.<br />

In: Bowen BC, Maravilla KR, Naidich T (eds). Imaging of<br />

the peripheral nervous system. Philadelphia, Elsevier Science<br />

(USA), Neuroimag Clin N Am 2004; pp59-85<br />

2. Chappell KE, Robson MD, Stonebridge-Foster A, Glover A,<br />

Allsop JM, Williams AD, Herlihy AH, et al. Magic angle<br />

effects in MR neurography. AJNR Am J Neuroradiol<br />

2004;25:431-440<br />

3. Bowen BC. Peripheral nerve imaging and the magic angle.<br />

Editorial. AJNR Am J Neuroradiol 2004;25:352-354<br />


Monday<br />

Monday Afternoon<br />

1:00 PM - 2:30 PM<br />

Room 107<br />

(12) NeuroNews Scientific Paper<br />

Session<br />

Moderators: TBD<br />

Monday Afternoon<br />

1:00 PM - 2:30 PM<br />

Room 201B<br />

(13) <strong>ASNR</strong> Business Center - Part I<br />

(69) Welcome and Introduction to Business Issues<br />

in Radiology<br />

— Gregory L. Katzman, MD<br />

(70) Net Present Value and Finance for Practicing<br />

Radiologists<br />

— Jonathan Breslau, MD<br />

(71) Managerial Accounting Applications in<br />

Radiology<br />

— Frank Lexa, VII, MD, MBA<br />

Moderators: Gregory L. Katzman, MD<br />

Monday Afternoon<br />

1:00 PM - 2:30 PM<br />

Room 103<br />

(14) ELC Workshop C: Website<br />

Creation for the Novice<br />

— Richard H. Wiggins, III, MD<br />

36<br />

Monday Afternoon<br />

1:30 PM - 2:00 PM<br />

Room 205<br />

(15) ELC Lecture C: Capturing and<br />

Using Image Files<br />

Monday Afternoon<br />

3:00 PM - 4:00 PM<br />

Room 103<br />

(16) National Library of Medicine<br />

(NLM) Workshop: PubMed ® /Medline<br />

Plus: Advanced Tips and Tricks<br />

Monday Afternoon<br />

3:00 PM - 4:30 PM<br />

Room 105/106<br />

— Barton F. Branstetter, IV, MD<br />

— Linda Milgrom<br />

(17a) HEAD AND NECK: Neck and<br />

Extracranial Carotid<br />

(Scientific Papers 75 - 86)<br />

See also Parallel Sessions<br />

(17b) INTERVENTIONAL: Arteriovenous<br />

Malformations/Fistulae<br />

(17c) HEAD AND NECK: Neck, New Techniques,<br />

and Excerptas<br />

(17d) ADULT BRAIN: Infarction and Vasospasm<br />

Moderators: Anton N. Hasso, MD, FACR<br />

Wendy R.K. Smoker, MD, FACR

Paper 75 Starting at 3:00 PM, Ending at 3:08 PM<br />

Role of Diffusion-Weighted MR Imaging in Pediatric<br />

Head and Neck Masses<br />

Abdel Razek, A. A. · Hafez, M. · Bilal, M. · Monier, S. ·<br />

Elmogy, S. · Rudwan, W.<br />

Mansoura University Faculty of Medicine<br />

Mansoura, EGYPT<br />


To determine the role of diffusion-weighted MR imaging in<br />

pediatric head and neck masses.<br />


This study included 37 patients (24 boys and 13 girls aged 3<br />

months-15 years: mean 6 years) with head and neck mass.<br />

Routine MR imaging and diffusion-weighted MR imaging<br />

were done on a 1.5 T MR unit (Symphony, Siemens).<br />

Diffusion MR imaging was done using a single-shot echoplanar<br />

imaging (EPI) with a diffusion-weighted factor, factor<br />

b of 0.500 and 1000 sec/mm2. The ADC map was reconstructed<br />

with calculation of apparent diffusion coefficient<br />

(ADC) values. Image analysis was performed qualitatively<br />

and quantitatively. The signal intensity was assessed visually<br />

on ADC maps and ADC value was measured in the suspected<br />

lesion. The final diagnosis proved by pathology, MR<br />

appearance, and clinical examination.<br />


Adequate ADC maps were obtained in 34 patients. This<br />

study included malignant tumor (n = 13), benign lesions (n =<br />

21). Restricted diffusion (high SI at B = 1000 images and<br />

low SI at ADC map) was seen in 10 lesions. Free diffusion<br />

(low SI at B = 1000 images and high SI at ADC map) was<br />

seen in 16 lesions. Mixed pattern of diffusion (areas of low<br />

and high SI at B = 1000 images and ADC map) were seen in<br />

8 lesions. The mean ADC value of the malignant tumor (1.07<br />

± 0.17 X 10-3 mm2/sec) was smaller than that of benign<br />

lesions (1.99 ± 0.17 X 10-3 mm2/sec). There was significant<br />

difference in ADC values of benign and malignant pediatric<br />

head and neck tumors (p < 0.021).<br />


Diffusion-weighted MR imaging is a new promising imaging<br />

modality for differentiating malignant pediatric head and<br />

neck tumors from benign lesions. It can be added to routine<br />

MR imaging of pediatric head and neck masses.<br />

KEY WORDS: Pediatric, diffusion<br />

Paper 76 Starting at 3:08 PM, Ending at 3:16 PM<br />

Recurrent Head and Neck Neoplasms: Quantitative<br />

Assessment by Means of Dynamic MR Imaging with<br />

Analysis of Perfusion<br />

Maroldi, R. · Farina, D. · Piazzalunga, B.<br />

University of Brescia<br />

Brescia, ITALY<br />


To assess the role of dynamic MR sequence in the detection<br />

of recurrent head and neck neoplasms.<br />

37<br />


Forty-one patients previously treated for a head and neck<br />

tumor (28/41 squamous cell carcinoma, 10/41 adenoid cystic<br />

carcinoma, 1/41 adenocarcinoma, 1/41 olfactory neuroblastoma,<br />

1/41 rhabdomyosarcoma; 13/41 nasopharynx,<br />

12/41 paranasal sinuses, 10/41 oral cavity, 6/41 oropharynx,)<br />

had follow-up MR studies. Patients had been treated by surgery<br />

alone (3/41), RT (13/41). or both (25/41). In all patients<br />

a dynamic MR sequence (GE T1, TR813, matrix 2562;<br />

repeated acquisition of a single slice for 60 sec) was added<br />

to the standardized protocol. On images acquired, regions of<br />

interest (ROI) were placed on ICA, on the area of suspected<br />

relapse, and on normal mucosa and muscle. Slope of<br />

enhancement curves as well as average of maximum signal<br />

intensities (AMS) within ROI were statistically analysed (ttest).<br />

MR findings were confirmed by histology or subsequent<br />

follow-up studies.<br />


Slope of enhancement curves of positive lesions (1.67 ± 0.6)<br />

was significantly steeper than in negative lesions (0.76 ± 0.6)<br />

(p = 0.00009). This finding was confirmed also when the<br />

steepest slope tracts of the curves were compared (p =<br />

0.00001). Significant difference was observed between AMS<br />

of recurrent (90 ± 18) and negative patients (66 ± 18) (p =<br />

0.0008). ROC curves analysis shows that a cut-off value of<br />

selective slope > = 1.4 enables to detect all recurrences with<br />

a 100% negative predictive value and 85.2% positive predictive<br />

value.<br />


This dynamic sequence provides additional data on the<br />

enhancement pattern that are useful to discriminate recurrences<br />

from nonneoplastic tissues.<br />

KEY WORDS: Recurrence, head and neck neoplasm, MR<br />

imaging<br />

Paper 77 Starting at 3:16 PM, Ending at 3:24 PM<br />

Reliable Fat Signal Suppression in Head and Neck<br />

Imaging Using a Three-Point Dixon Technique<br />

Barger, A. · DeLone, D. · Bernstein, M. · Welker, K.<br />

Mayo Clinic<br />

Rochester, MN<br />


MR imaging of the extracranial head and neck is made difficult<br />

by multiple factors, including unreliable fat suppression.<br />

The effectiveness of frequency-selective RF excitation or<br />

saturation pulses is dependent on main magnetic field (B0)<br />

homogeneity. Tissue-induced magnetic field inhomogeneity<br />

in head and neck imaging is substantial and is very difficult<br />

to remove completely by shimming, thus limiting the reliability<br />

of frequency selective fat saturation. Dixon techniques<br />

use multiple acquisitions with differing phase information to<br />

generate fat and water images (1). The original Dixon<br />

method is also unreliable in the presence of B0 inhomogeneity.<br />

However, modified Dixon techniques can account for<br />

effects of inhomogeneity-induced off-resonance (2, 3). In<br />

this work we investigated the feasibility of using a modified,<br />

three-point Dixon technique to obtain reliable fat-water separation<br />

in the soft-tissue neck.<br />


Monday<br />


Imaging was performed using a 1.5 T Signa scanner with<br />

EXCITE 11.0 software (GE Medical Systems, Milwaukee,<br />

WI). Coils used included five- and eight-channel neuro-vascular<br />

phased-array coils (Medrad, Indianola, PA, and MRI<br />

Devices, Gainesville, FL, respectively). A three-point Dixon<br />

protocol was performed on three volunteers and one patient.<br />

FSE T1-weighted scans were performed using TR 600,<br />

TEeff 11.5, 256 x 192 matrix, ETL 4. FSE T2-weighted<br />

scans were performed using TR 2553, TEeff 97.3, 256 x 192<br />

matrix, ETL 11. Scan time is quite manageable (generally<br />

several minutes per pack), and was proportional to the phase<br />

encoding matrix size divided by the ETL, the number of<br />

passes, the number of Dixon “points” (i.e., 3), and the repetition<br />

time. GE Dixon reconstruction software was used for<br />

postprocessing the acquired data. For volunteer studies, the<br />

Dixon FSE T1 was done without gadolinium; in the single<br />

patient study, the Dixon FSE T1 was done after intravenous<br />

administration of gadolinium.<br />


Resultant separate fat, water, and combined images from the<br />

method were reviewed. In all subjects the water images<br />

obtained using three-point Dixon technique demonstrated<br />

effective, uniform fat suppression. In two of the cases the<br />

Dixon method caused some erroneous, nonanatomical mapping<br />

of fat signal, which was irrelevant to clinical interpretation<br />

in the one clinical case.<br />


Three-point Dixon imaging promises to be an effective,<br />

robust, and practical method of fat suppression in the<br />

extracranial head and neck. The method does require three<br />

acquisitions for each phase encode, which imposes limitations<br />

of coverage and resolution to maintain a reasonable<br />

scan time. However, the signal-to-noise ratio is also<br />

improved and is roughly equivalent to a 2.7 NEX acquisition<br />

(2). In this preliminary investigation some erroneous mapping<br />

of fat signal was observed. Although this appears nonlimiting,<br />

a larger series of patients is needed.<br />


1. Dixon WT. Simple proton spectroscopic imaging. Radiology<br />

1984;153:189-194<br />

2. Glover GH, Schneider E. Three-point Dixon technique for<br />

true water/fat decomposition with B0 inhomogeneity correction.<br />

Magn Reson Med 1991;18(2):371-383<br />

3. Reeder SB, Wen Z, Yu H, Pineda AR, Gold GE, Markl M, Pelc<br />

NJ. Multicoil Dixon chemical species separation with an<br />

iterative least-squares estimation method. Magn Reson Med<br />

2004;1(1):35-45<br />

KEY WORDS: Dixon, fat suppression, head and neck<br />

38<br />

Paper 78 Starting at 3:24 PM, Ending at 3:32 PM<br />

Radiologic Features of Solitary Fibrous Tumors of the<br />

Head and Neck<br />

Stambuk, H. E. · Ganly, I. · Carlson, D. · Ghossein, R. · Shah,<br />

J. P. · Patel, S. G.<br />

Memorial Sloan-Kettering Cancer Center<br />

New York, NY<br />


To illustrate the salient radiologic features in the rare, generally<br />

benign, solitary fibrous tumors of the head and neck.<br />


Seven patients with a histopathologic diagnosis of solitary<br />

fibrous tumor (SFT) treated between the years 1990-2004<br />

were identified from institutional databases. Retrospective<br />

review of available CT (5) and MR (5) scans was performed<br />

by a CAQ certified neuroradiologist. Imaging findings were<br />

correlated with clinical data and pathologic features with the<br />

aim of identifying radiographic traits that would suggest the<br />

diagnosis of SFT.<br />


Solitary fibrous tumors occurred more commonly in women<br />

than men (4:3). Age at presentation ranged from 46 to 78<br />

years (median 57 years). Symptoms at presentation varied<br />

according to the anatomical site of the primary tumor: palpable<br />

mass (3), nasal obstruction (2), arm pain (1), and ptosis<br />

(1). Most tumors presented as a slow-growing, painless<br />

mass with a history ranging in duration from 2 months to 3<br />

years. Anatomical sites of tumor included the sinonasal cavity<br />

(3), oral cavity (2), infratemporal fossa (1), and<br />

paraspinal soft tissues of the cervical spine (1). On imaging,<br />

all lesions were well defined including the two malignant<br />

lesions that had extended intracranially. Tumors ranged in<br />

size from 1.5 x 1.4 cm to 6.3 x 3.2 cm. All tumors were<br />

densely enhancing on imaging with tumor generally isodense<br />

to muscle on noncontrast CT and isointense to muscle<br />

on precontrast T1-weighted images. Most tumors were low<br />

to intermediate signal on T2-weighted images; however two<br />

had high-signal intensity. All lesions that were adjacent to<br />

bone caused expansile regressive remodeling. In addition,<br />

both patients with malignant SFT had areas of bone destruction<br />

one of which also had sclerosis of the fovea ethmoidalis,<br />

crista galli, and several ethmoid septa. All patients were<br />

managed by surgical resection. Five of the seven lesions<br />

were benign and two were malignant on histopathologic<br />

examination. The margins of surgical resection were positive<br />

in 3 patients (2 malignant and 1 benign SFT). None of the<br />

tumors recurred and all patients were alive with follow-up<br />

periods ranging from 2 to 76 months.<br />


Solitary fibrous tumors of the head and neck region are rare<br />

and are most commonly benign. Although imaging findings<br />

are not diagnostic, the presence of an intensely enhancing,<br />

well defined mass with regressive remodeling of bone can be<br />

suggestive of SFT. Bone destruction is suggestive of malignant<br />

SFT, but even malignant lesions tend to remain well<br />

defined in appearance.

KEY WORDS: Mesothelioma/*diagnosis/pathology/surgery,<br />

paranasal sinus neoplasms/*diagnosis/pathology/surgery,<br />

neoplasm invasiveness<br />

Paper 79 Starting at 3:32 PM, Ending at 3:40 PM<br />

Pathologic Changes of the Lateral Pterygoid Muscle in<br />

Patients with Temporomandibular Joint Disk<br />

Derangement: Objective Measures at MR Imaging<br />

Finden, S. G. · Enochs, W. · Rao, V.<br />

Thomas Jefferson University<br />

Philadelphia, PA<br />


The lateral pterygoid muscle, specifically the superior head,<br />

has been implicated in anterior dislocation of the disk in<br />

internal derangement of the temporomandibular joint (TMJ).<br />

In patients with occlusal disorders, the superior head of the<br />

lateral pterygoid muscle (SHLPM), which inserts on the disk<br />

and anterior capsule of the TMJ, has been postulated to<br />

undergo spasm and contraction, which results in forward<br />

traction and anterior displacement of the disk (1). In longstanding<br />

TMJ dysfunction, the SHLPM is expected to show<br />

subsequent edema and/or atrophy (2). The goal of the present<br />

study is to examine the corresponding changes of the<br />

SHLPM on MR imaging using objective measures of signal<br />

intensity and morphology.<br />


Patients with abnormalities involving the TMJ were identified<br />

through a retrospective review of MR imaging reports at<br />

our institution from January 1997 through August 2003.<br />

Relative signal intensities were measured for representative<br />

regions of interest (ROI) within the superior and inferior<br />

heads of the LPM bilaterally on T2-weighted, sagittal<br />

oblique images. In addition, relative thickness between the<br />

two muscle heads was measured as a morphologic parameter.<br />

Statistically significant differences in relative signal<br />

intensity and muscle thickness between the superior and<br />

inferior heads of the LPM then were identified and correlated<br />

with the presence or absence of anterior displacement,<br />

with or without reduction.<br />


In patients with anterior disk displacement without reduction,<br />

17 of 19 joints (89.5%) demonstrated a significant<br />

increase in relative T2 signal intensity within the SHLPM<br />

compared to the inferior head. By contrast, no patients with<br />

anatomically normal disks demonstrated a statistically significant<br />

difference in signal between the superior and inferior<br />

heads of the LPMs. Variation in relative thickness<br />

between normal and abnormal muscles overlapped to an<br />

extent that precluded its use as a distinguishing parameter.<br />


Pathologic alterations in the superior head of the lateral<br />

pterygoid muscle can be identified using ROI values as an<br />

objective measurement of relative T2 signal intensity.<br />

Comparing these values between the superior and inferior<br />

heads demonstrated a strong correlation (89.5%) between<br />

increased T2 signal intensity and pathologic alteration of the<br />

condylar head/disk relationship. This increased signal may<br />

reflect increased fluid signal related to muscle edema and/or<br />

fatty change secondary to atrophy. By contrast, relative<br />

39<br />

thickness between the two muscle heads as a morphologic<br />

measure is not useful in identifying this pathology.<br />


1. Wongwatana S, Kronman JH, Clark RE, Kabani S, Mehta N.<br />

Anatomic basis for disk displacement in temporomandibular<br />

joint (TMJ) dysfunction. Am J Orthod Dentofacial Orthop<br />

1994;105(3):257-264<br />

2. Yang X, Pernu H, Pyhtinen J, Tiilikainen PA, Oikarinen KS,<br />

Raustia AM. MR abnormalities of the lateral pterygoid muscle<br />

in patients with nonreducing disk displacement of the<br />

TMJ. Cranio 2002;20(3):209-221<br />

KEY WORDS: Temporomandibular joint, lateral pterygoid<br />

Paper 80 Starting at 3:40 PM, Ending at 3:45 PM<br />

Extracranial Extramedullary Hematopoiesis in Two<br />

Teenagers with Sickle-Cell Disease<br />

Coopersmith, H. · Bello, J.<br />

Montefiore Medical Center<br />

New York, NY<br />


The purpose of this abstract is to describe intracranial<br />

epidural and extracranial soft tissue manifestations of<br />

extramedullary hematopoiesis (EMH) in two adolescent<br />

males homozygous for sickle-cell disease.<br />


Preceding vaso-occlusive crises in both patients suggest a<br />

direct causal relationship between the crisis, and the development<br />

of EMH. D.L. presented to the hospital with a<br />

bifrontal headache, and anterior chest pain. He was afebrile,<br />

and his lungs were clear to auscultation. D.L. was maintained<br />

on his routine daily doses of hydroxyurea and folic<br />

acid. Morphine, zithromax, prednisone, and cefzil were<br />

added to his treatment regimen. On hospital day (HD) #6,<br />

D.L.’s admission hemoglobin of 8.8 g/ml reached a low of<br />

6.8 g/ml. Four days later, he was discharged from the hospital,<br />

only to return the next day complaining of a severe retroorbital<br />

and bifrontal headache, and sternal chest pain. Three<br />

days later, D.L. developed bilateral parieto-occipital tender,<br />

fluctuant masses measuring 4 cm by 4 cm in size, as well as<br />

bilateral fronto-parietal swelling. On HD #5, MR imaging<br />

was performed. D.V. presented to the hospital with a productive<br />

cough, severe chest pain, and bilateral upper leg<br />

pain. After 24 hours, he developed a fever. A chest X-ray<br />

demonstrated a left lower lobe infiltrate. D.V. was started on<br />

intravenous cefuroxime, azithromax, and albuterol nebulizers<br />

in addition to the hydroxurea, folic acid, morphine,<br />

toradol, oxygen, and intravenous fluids he had been receiving<br />

already. Over his first three hospital days, D.V.’s hemoglobin<br />

dropped from 9.4 g/ml to 5.1 g/ml. He received 2<br />

units of packed red blood cells on HD #4, and was discharged<br />

from the hospital the following day. D.V. returned 1<br />

day later with swelling over the left side of his scalp, a history<br />

of fever to 101 degrees, and worsening bilateral leg<br />

pain. A CT scan of the brain was performed that day, as well<br />

as an MR image 5 days later. D.L.’s MR image showed diffuse<br />

expansion of the calvarium with multiple areas of calvarial<br />

high signal in the biparietal and bifrontal regions on<br />

T2, Flair, and T1-weighted sequences. In addition, there was<br />

an extracranial lobular soft tissue mass adjacent to the left<br />


Monday<br />

parietal bone, measuring 4.2 by 1.7 cm in size. The mass<br />

demonstrated high signal on both T1- and T2-weighted<br />

sequences. Small additional areas of high signal were present<br />

in the left parietal and right frontal epidural regions<br />

intracranially. D.V.’s CT scan demonstrated high attenuation<br />

regions in the left epidural space and left subgaleal space<br />

near the convexity measuring 3.1 cm and 5.9 cm in size,<br />

respectively. There was no evidence of bone erosion. The<br />

MR image showed high signal on T1- and T2-weighted<br />

sequences in the left frontal epidural space and the left subgaleal<br />

region, with minimal postcontrast enhancement.<br />


Our case series is significant for several reasons. First, these<br />

may represent the first reported cases of EMH in the<br />

extracranial soft tissues. Second, there are few reported cases<br />

of EMH in patients homozygous for sickle-cell disease.<br />

Third, the time-course of EMH shadowed the time-course of<br />

the vaso-occlusive crises, suggesting a direct causal relationship.<br />

KEY WORDS: Extramedullary hematopoiesis, extracranial<br />

mass, sickle-cell disease<br />

Paper 81 Starting at 3:45 PM, Ending at 3:50 PM<br />

Subarachnoid Perfluorocarbon Droplets after Attempted<br />

Retinal Detachment Treatment<br />

Malin, D. R. · Aulino, J. M. · Recchia, F. M.<br />

Vanderbilt University Medical Center<br />

Nashville, TN<br />


We present a case of a gunshot wound resulting in severe<br />

orbital trauma treated with vitreoretinal surgery and perfluorocarbon<br />

(PFC) liquid injection. Postoperative CT demonstrated<br />

migration of PFC into the subarachnoid space.<br />


A 22-year-old man suffered a gunshot wound to the face<br />

which produced multiple facial fractures and orbital trauma<br />

including retinal detachment. Surgical repair and exploration<br />

for a left open-globe injury was performed including vitreoretinal<br />

surgery with PFC liquid injection to treat retinal<br />

detachment. Optic nerve avulsion was discovered which rendered<br />

the treatment unsuccessful. Postoperative CT imaging<br />

demonstrated subarachnoid hyperdense PFC droplets.<br />


Initial trauma head CT demonstrated extensive facial fractures<br />

and orbital trauma. After vitreoretinal surgery with<br />

PFC liquid injection to treat retinal detachment, unusual<br />

hyperdense small droplets were seen within the subarachnoid<br />

space and within the left intraconal orbit.<br />


Perfluorocarbon liquids and silicone oil have been used as an<br />

aid in vitreoretinal surgery for the treatment of complex retinal<br />

detachments. As a highly dense substance, PFC may provide<br />

significant tamponade to displace subretinal fluid and<br />

blood and to stabilize and flatten the retina. Known complications<br />

include subretinal retention of PFC and migration of<br />

silicone oil along the optic nerve into the subarachnoid<br />

space. We do not believe that subarachnoid migration of PFC<br />

40<br />

has been reported previously. Our case illustrates orbital<br />

trauma with attempted retinal detachment repair resulting in<br />

subarachnoid migration of PFC droplets.<br />

KEY WORDS: Perfluorocarbon, subarachnoid, orbit trauma<br />

Paper 82 Starting at 3:50 PM, Ending at 3:58 PM<br />

Multislice Carotid Wall Imaging at 1.5 T and 3.0 T<br />

Koktzoglou, I. 1 · Carroll, T. J. 1 · Walker, M. T. 1 · Morasch, M.<br />

D. 1 · Mani, V. 2 · Mizsei, G. 2 · Fayad, Z. A. 2 · Simonetti, O. P. 3<br />

· Li, D. 1<br />

1 Northwestern University, Chicago, IL, 2 Mount Sinai School<br />

of Medicine, New York, NY, 3 Siemens Medical Solutions,<br />

Chicago, IL<br />


Noninvasive MR imaging of the carotid artery wall has been<br />

shown to be capable of detecting and characterizing carotid<br />

atherosclerotic plaque at 1.5 T. However, achievable image<br />

signal-to-noise ratio (SNR) is limited by spatial resolution.<br />

One way to improve SNR is to image at higher magnetic<br />

field strengths. The objective of this work was to compare<br />

the SNR efficiency of carotid artery wall imaging at 1.5 T<br />

and 3.0 T using multislice turbo spin-echo (TSE) imaging.<br />


Six healthy volunteers (4 males, 2 females, mean age = 37<br />

years) were imaged on 1.5 T and 3.0 T whole-body scanners<br />

(Magnetom Sonata and Trio, Siemens Medical Solutions,<br />

Erlangen, Germany). Four channel phased-array coils consisting<br />

of two left and two right channels (1.5 T: Machnet<br />

BV, The Netherlands; 3.0 T: in-house coil) were used for signal<br />

reception. In each volunteer, 12 cross-sectional slices<br />

through the carotid bifurcation were imaged using fat-saturated<br />

proton density-weighted, T2-weighted, and T1-weighted<br />

regional saturation (RSAT) TSE. Imaging time (~4 min)<br />

and imaging resolution (0.47 x 0.47 x 3 mm 3 ) was matched<br />

on both 1.5 T and 3.0 T scanners. Carotid wall SNR and was<br />

measured at both 1.5 T and 3.0 T.<br />


MR imaging was completed successfully in all volunteers.<br />

Mean carotid artery wall SNR at 1.5 T was 17 ± 4 (proton<br />

density-weighted), 11 ± 2 (T2-weighted), and 12 ± 3 (T1weighted).<br />

At 3.0 T mean carotid artery wall SNR was 36 ±<br />

18 (proton density-weighted), 23 ± 9 (T2-weighted), and 30<br />

± 13 (T1-weighted). Siganl-to-noise ratio efficiency at 3.0 T<br />

was roughly 2.2 fold higher than that of 1.5 T. Based on<br />

these results, three patient studies were performed at 3.0 T<br />

using RSAT TSE. Carotid plaques were clearly delineated in<br />

all patients. A T2-weighted image acquired from a patient at<br />

3.0 T is shown. The atherosclerotic plaque is well delineated,<br />

and exhibits what appears to be a fibrous cap (gray<br />

arrow) and a lipid core (white arrow).


Carotid wall imaging benefits from higher SNR at 3.0 T. In<br />

this study the SNR gain at 3.0 T over 1.5 T was roughly 2.2<br />

fold. The higher SNR afforded by 3.0 T may allow for even<br />

higher resolution imaging of the carotid artery wall. Further<br />

studies with pathologic correlation are needed to validate the<br />

findings in the MR images.<br />

KEY WORDS: MR imaging, carotid artery, vessel wall imaging<br />

Paper 83 Starting at 3:58 PM, Ending at 4:06 PM<br />

Evaluation of Intracranial and Cervical Arteries with 3D<br />

CT Angiography Using a 16-Detector Multidetector Row<br />

CT: Continuous Scanning of the Head and Neck Using a<br />

Single Injection of Contrast Medium<br />

Matsumoto, M. · Endo, Y. · Kodama, N. · Sakuma, J. ·<br />

Suzuki, K. · Sasaki, T.<br />

Fukushima Medical University<br />

Fukushima, JAPAN<br />


Extracranial carotid atherosclerosis is well established as an<br />

important risk factor for the development of thromboembolic<br />

cerebrovascular disease. To detect cervical vascular lesions in<br />

50 patients with known or suspected intracranial cerebrovascular<br />

disease, we performed 3D CTA of the head and neck<br />

using a multidetector CT (MD CT) with 16 detectors.<br />


The head and neck were scanned continuously with a 20 s<br />

scan delay after a bolus injection of contrast medium<br />

(3ml/sec, total 100 ml). The data then were transferred to a<br />

workstation (ZIO M900; Amin Corp., Tokyo, Japan). A volume-rendering<br />

method was used for the extraction of vessels<br />

at a 140-200 HU threshold. We also created multiplanner<br />

reconstruction (MPR) images and maximum intensity projection<br />

(MIP) images of the cervical arteries and evaluated<br />

the visualization of the cervical arteries.<br />

41<br />


We obtained excellent 3D CTA from the origin of the common<br />

carotid arteries to the superior sagittal sinus in all<br />

patients. A small aneurysm (1.2 mm in a diameter) was<br />

detected in this method. The quality of the 3D images of this<br />

method was equal or superior to that of conventional 3D<br />

CTA which target on head only. The CT numbers of the cervical<br />

carotid bifurcation, vertebral artery, and jugular veins<br />

at C4 level were 360.1 HU (n = 100), 322.7 HU (n = 100)<br />

and 189.8 HU (n = 100), respectively. Because of the high<br />

CT number of the carotid arteries, it was possible to extract<br />

arteries upon setting a threshold CT number. Using 3D CTA,<br />

whole course of the vertebral arteries were well demonstrated,<br />

especially at the cranio-vertebral junction. Since the CT<br />

number of the VA was 40HU lower than that of the carotid<br />

artery at the same level, we should set a scan delay late to<br />

evaluate the vascular lesions in the VA. To visualize the cervical<br />

segment of the VA within the transverse foramens of<br />

C6 to C2, we deleted vertebral arches at an imaginary line<br />

that linked transverse foramens of the cervical vertebrae.<br />


The head and neck 3D CTA using the MD CT with 16-detectors<br />

provides valuable diagnostic information regarding vascular<br />

lesions of the intracranial and cervical arteries. This<br />

method facilitates the screening for vascular lesions in the<br />

cervical arteries as well as intracranial arteries in a single<br />

procedure.<br />

KEY WORDS: Multidetector CT, 3D CT angiography, multiplanar<br />

reconstruction<br />

Paper 84 Starting at 4:06 PM, Ending at 4:14 PM<br />

Measuring Carotid Arterial Distensibility: Comparison<br />

of Measurements of Common Carotid Cross-Sectional<br />

Area on Catheter and CT Angiography<br />

Sherman, P. M. · Takhtani, D.<br />

The Johns Hopkins Medical Institutions<br />

Baltimore, MD<br />


We hypothesized that catheter angiography causes arterial<br />

distensibility due to direct injection whereas CT angiography<br />

does not. To measure the degree of distensibility, comparison<br />

was made between common carotid arterial area on both<br />

catheter and CT angiography.<br />


We retrospectively reviewed 25 common carotid arteries in<br />

15 patients in which both catheter angiography and neck CT<br />

angiography were performed during the past 2 years.<br />

Catheter angiograms were performed using hand injections.<br />

We included patients in whom both studies were performed<br />

within a 3-month period. There were 7 males and 8 females,<br />

ranging in age from 9 to 84 years. Common carotid diameter<br />

was measured on the lateral catheter angiogram image, 1<br />

centimeter below the carotid bifurcation. An intraluminal<br />

surface area was measured at the same location on the CTA<br />

using commercially available software after correcting for<br />

obliquity. The third or fourth cervical vertebral body was<br />

measured in the antero-posterior dimension at the midbody<br />

on the lateral carotid angiogram image and on the 3 D MIP<br />

lateral CT image to calculate the correction factor, using the<br />


Monday<br />

CT measurement as the reference standard. After applying<br />

appropriate magnification factor, the angiographic cross-sectional<br />

area was calculated using the formula π r2.<br />


The arterial distensibility, defined as percent increase in area<br />

on catheter angiography compared to CTA, ranged from 12<br />

% to 58.4% in 23 arteries. In one common carotid artery in<br />

an 9-year-old girl who had complete internal carotid occlusion,<br />

the increase was 116%, and in another common carotid<br />

artery in a 52-year-old man with 90% internal carotid stenosis,<br />

the increase was 63.4%.<br />


We demonstrated carotid distensibility in all vessels. This<br />

may be one of the factors in discordance between CTA and<br />

catheter angiography in the assessment of stenosis. This new<br />

way of measuring arterial distensibility also may find new<br />

applications in assessing arterial stiffness which has been<br />

found to predispose to atherosclerosis. Usually arterial distensibility<br />

is measured by doppler ultrasound. The degree of<br />

variation in distensibility in different subjects could be<br />

attributed to distal stenosis, differences in hand injection<br />

technique, inherent stiffness of varying degrees in the arteries,<br />

and intraobserver measurement differences.<br />

KEY WORDS: Carotid artery; distensibility, carotid angiography,<br />

neck CT angiography<br />

Paper 85 Starting at 4:14 PM, Ending at 4:22 PM<br />

Zero Filling Interpolation Processing Technique Can<br />

Efficiently Suppress Segmental Stenosis Artifact on<br />

Small Artery of Anatomical Phantoms<br />

Lin, R. 1 · Wu, R. H. 1 · Xiao, Z. W. 1 · Liu, G. R. 1 · Kong, K.<br />

M. 1 · Lang, Z. J. 2<br />

1 Shantou University Medical College, Shantou, CHINA,<br />

2 Dalian Medical University, Dalian, CHINA<br />


The purpose of this study was to evaluate the zero-filling<br />

interpolation processing (ZIP) technique for contrastenhanced<br />

MR angiography (CE MRA).<br />


Phantoms of arteries were made with different lumen diameter.<br />

Gadolinium-enhanced three-dimensional MR angiography<br />

was performed on a GE 1.5 T scanner. The parameters<br />

of FSPGR pulse sequence were: flip angle 30°, TR 6 ms, TE<br />

1.4 ms, bandwidth 31.25 kHz, slice thickness 1.2 mm, matrix<br />

256 × 256. The sequence parameters were kept constant for<br />

the studies, whereas four selections were chosen: (1) with<br />

ZIP1024 and ZIP×4 techniques; (2) only with ZIP1024 technique;<br />

(3) only with ZIP×4 technique; (4) without ZIP technique.<br />

For image quality evaluation, MR maximum intensity<br />

projection (MIP) images were created. Signal-to-noise<br />

ratio (SNR) was measured on MIP images. Vessel edge was<br />

determined using full width at half maximum (FWHM) for<br />

lumen diameter calculation and calculated results were compared<br />

with the actual lumen diameter. The distinctness of the<br />

vessel edge and the artifacts on the phantoms were compared<br />

for all sequences.<br />

42<br />


Three experienced radiologists made consensus evaluation.<br />

The FWHM results of lumen measurements for all the<br />

sequences with ZIP techniques were more accurate than that<br />

of the sequence without ZIP technique in all phantoms, no<br />

matter what was the size the artery. The vessel edge with<br />

ZIP1024 technique was more distinct. But the highest average<br />

SNR was obtained with the sequence without ZIP technique.<br />

The segmental stenosis artifacts on small artery of<br />

phantoms were only efficiently suppressed with ZIP×4 technique.<br />


ZIP technique is excellent for CE MRA to obtain high quality<br />

MR angiography; it not only can improve the spatial resolution<br />

and the distinctness of the vessel edge on CE MRA,<br />

but also can efficiently suppress segmental stenosis artifact<br />

on small artery of phantoms.<br />

KEY WORDS: Zero<br />

Paper 86 Starting at 4:22 PM, Ending at 4:27 PM<br />

Intraventricular Migration of Silicone Oil after<br />

Intravitreous Injection of Silicone<br />

Singla, R. · Magalhaes, A. C. A. · Kish, K.<br />

Wayne State University<br />

Detroit, MI<br />


Intravitreous silicone injection has become the standard for<br />

the treatment of retinal detachment. MR findings of intraocular<br />

silicone oil have been well described. However there are<br />

only few pathologic reports of the migration of silicone into<br />

the ventricles and to our best knowledge, no corresponding<br />

reports of CT imaging findings. This is an uncommon entity<br />

and it is important to recognize the radiologic findings of<br />

presence of intraventricular silicone and differentiate it from<br />

other intraventricular pathologies.<br />


A 43-year-old female with human immunodeficiency viral<br />

infection who had undergone intravitreous injection of silicone<br />

for retinal detachment as a complication of CMV retinitis<br />

presented with headaches. Noncontrast CT scan showed<br />

multiple small spherical areas in the nondependent portion of<br />

the lateral, third and fourth ventricles. Subsequently MR<br />

imaging was performed and a diagnosis of intraventricular<br />

silicone migration from the inraoccular injection of silicone<br />

oil was made based on the MR findings.<br />


Noncontrast CT scan showed multiple spherical hyperdense<br />

lesions in the nondependent portion of the ventricles.<br />

Contrast-enhanced CT scans did not show any enhancement.<br />

Subsequent scanning in the prone position revealed migration<br />

of these lesions to the nondependent posterior portion.<br />

Nonenhanced MR imaging revealed hyperintense lesions in<br />

the nondependent parts of the ventricles on T1-weighted<br />

images and fluid-attenuated inversion recovery images. The<br />

lesion was hypointense when compared with vitreous in the<br />

globe and CSF in the ventricles on fat saturated T2-weighted<br />

images. A prominent chemical shift artifact was present<br />

along the frequency encoding direction that changed appro-

priately as the phase and frequency encoding directions were<br />

swapped. Retrospective consultation of the records of the<br />

patient revealed she had developed raised intraocular pressure<br />

after the silicone injection.<br />


The migration of intravitreous silicone to the ventricles has<br />

been reported only recently and is not a well known entity.<br />

Most of the patients who had intraventricular silicone were<br />

reported to have developed raised intraocular pressure after<br />

the silicone injection. MR and CT findings of the intraventricular<br />

silicone are diagnostic. The mechanism of migration<br />

of intravitreous silicone into the ventricles is not well established;<br />

there are hypothesis to explain the migration but<br />

these need further evaluation to establish the facts.<br />

Consequences of migration of silicone into the ventricles are<br />

not known at this time; however, wide spread knowledge of<br />

radiologic findings and subsequent establishment of radiologic<br />

diagnosis can prevent further intervention and biopsy<br />

unless some adverse effects are noticed.<br />

KEY WORDS: Silicone oil, intraventricular, MR imaging<br />

43<br />

Monday Afternoon<br />

3:00 PM - 4:30 PM<br />

Theatre<br />


Arteriovenous Malformations/Fistulae<br />

(Scientific Papers 87 - 98)<br />

See also Parallel Sessions<br />

(17a) HEAD AND NECK: Neck and Extracranial<br />

Carotid<br />

(17c) HEAD AND NECK: Neck, New Techniques,<br />

and Excerptas<br />

(17d) ADULT BRAIN: Infarction and Vasospasm<br />

Moderators: Philippe E. Gailloud, MD<br />

John D. Barr, MD<br />

Paper 87 Starting at 3:00 PM, Ending at 3:08 PM<br />

Ethanol Embolization of Tongue Vascular<br />

Malformations<br />

Yakes, W. F.<br />

Vascular Malformation Center<br />

Englewood, CO<br />


To determine the efficacy of ethanol embolization in management<br />

of tongue vascular malformations.<br />


Forty-seven patients (26 female, 21 male; mean age: 38<br />

years) presented to my service with tongue vascular malformations<br />

(8 AVMs; 39 venous-lymphatic). Forty-seven<br />

patients had undergone 61 failed previous procedures (embo,<br />

laser, surgery, steroid injection, alpha-interpheron, radiation).<br />

All patients had baseline arteriograms and MR images.<br />

All patients underwent transcath and/or direct puncture<br />

ethanol therapy.<br />


Of 8 AVM patients, 5 cured and 3 treatment on-going (mean<br />

f/up: 40 months); of 39 patients with venous-lymphatic malformations,<br />

18 patients had dramatic reduction and 21<br />

patients’ therapy on-going with concurrent reductions (mean<br />

f/up: 60 months). One patient with AVM required additional<br />

surgery and 1 patient with mixed veno-lymphatic malformation<br />

required surgical debulking of excess tissues. Minor<br />

complications such as tongue blisters (9 instances) healed<br />

spontaneously; 3 tongue injuries healed spontaneously; 3<br />

infections responded to antibiotic treatment; 1 focal numbness<br />

resolved.<br />


Monday<br />


Ethanol embolotherapy is a primary form of therapy to eradicate<br />

high-flow and low-flow vascular malformations of the<br />

tongue permanently at long-term follow-up. Rarely is concurrent<br />

surgery required.<br />

KEY WORDS: Vascular malformations, embolization, ethanol<br />

Paper 88 Starting at 3:08 PM, Ending at 3:13 PM<br />

Unusual Imaging Findings following Ethanol Ablation of<br />

a Glomus Jugulare Tumor<br />

Wallace, M. A. · Rothfus, W. E. · Bartynski, W. S.<br />

University of Pittsburgh Medical Center<br />

Pittsburgh, PA<br />

Stroke is a known complication of alcohol ablation of<br />

meningohypophyseal arterial supply of indirect carotid-cavernous<br />

sinus fistulae and tumors from inadvertent distal ablation.<br />

However, there is no published data that describes the<br />

imaging characteristics of the ethanol during such complications.<br />

We d