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DOI: 10.1148/radiol.2371031757
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(Radiology 2005;237:101-105.)
© RSNA, 2005


Diagnosis Please

Case 87: Subacute Combined Degeneration1

Michelle J. Naidich, MD and Sam U. Ho, MD

1 From the Departments of Radiology (M.J.N.) and Neurology (S.U.H.), Feinberg School of Medicine, Northwestern University and Northwestern Memorial Hospital, 676 N St Clair St, Suite 800, Chicago, IL 60611. Received October 31, 2003; revision requested January 20, 2004; revision received January 27; accepted February 24.

Correspondence: Address correspondence to M.J.N. (e-mail: m-naidich{at}northwestern.edu).


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A 59-year-old man with non–insulin-dependent diabetes mellitus underwent laparoscopic cholecystectomy for biliary stones. He was able to return to work 8 days after surgery. The patient started to experience numbness and tingling in all four limbs 2–3 weeks later. The symptoms progressed to the point that he had difficulty driving, walking, and using his hands. Bladder function was intact. The patient was hospitalized for a complete neurologic evaluation 8 weeks after surgery. A cervical spine magnetic resonance (MR) imaging examination was performed at that time.


    IMAGING FINDINGS
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The sagittal T2-weighted MR image (Fig 1) demonstrates abnormal hyperintensity within the posterior aspect of the cervical spinal cord extending from the level of C2 to C6. Transverse T2-weighted MR images obtained at these levels (Fig 2) show symmetric abnormal hyperintensity within the posterior spinal cord corresponding to the dorsal columns. The areas of abnormal T2 hyperintensity within the dorsal columns are enhanced on T1-weighted images (Fig 3). This distinctive pattern of abnormal signal intensity was considered characteristic of subacute combined degeneration of the spinal cord. A serum vitamin B12 test was performed and showed a diminished serum B12 level of 43 pg/mL (32 pmol/L); this abnormal result was confirmed with a repeat test, which indicated a B12 level of 51 pg/mL (38 pmol/L) (normal range, 200–1000 pg/mL [148–738 pmol/L]). Intrinsic factor antibody was present, and the serum homocysteine level was elevated. Findings were negative for human immunodeficiency virus and syphilis. These findings confirmed the diagnosis of subacute combined degeneration, and 1000 µg of B12 was administered intramuscularly every day for 1 week and was followed with maintenance injections. At 3-week follow-up, the patient had made substantial clinical improvement. Review of the anesthesia note from surgery showed nitrous oxide was administered for 1 hours during surgery.



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Figure 1. Sagittal T2-weighted fast spin-echo MR image (repetition time msec/echo time msec, 3894/130) of the cervical spinal cord shows hyperintensity (arrows) in the dorsal aspect of the cord spinal, extending from the level of C2 to the level of C5.

 


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Figure 2a. Transverse T2-weighted fast spin-echo MR images (5703/130) obtained through the cervical spinal cord at three separate levels from C3 to C4. (a–c) Images demonstrate bilateral symmetric signal intensity abnormality within the dorsal columns (arrows). All transverse images obtained through the area of posterior signal abnormality provided identical imaging findings.

 


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Figure 2b. Transverse T2-weighted fast spin-echo MR images (5703/130) obtained through the cervical spinal cord at three separate levels from C3 to C4. (a–c) Images demonstrate bilateral symmetric signal intensity abnormality within the dorsal columns (arrows). All transverse images obtained through the area of posterior signal abnormality provided identical imaging findings.

 


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Figure 2c. Transverse T2-weighted fast spin-echo MR images (5703/130) obtained through the cervical spinal cord at three separate levels from C3 to C4. (a–c) Images demonstrate bilateral symmetric signal intensity abnormality within the dorsal columns (arrows). All transverse images obtained through the area of posterior signal abnormality provided identical imaging findings.

 


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Figure 3. Transverse T1-weighted fast spin-echo MR image (747/12) obtained after contrast material administration through the cervical spinal cord at the level of C4 shows symmetric enhancement (arrows) within the dorsal columns.

 

    DISCUSSION
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 HISTORY
 IMAGING FINDINGS
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Vitamin B12 cobalamin can be found in food from animal and some plant sources. The average adult ingests 5–30 µg of vitamin B12 per day, of which 1–5 µg are absorbed. There is a total body store of 2–5 mg of B12, of which 1 mg is stored in the liver (1,2). Consequently, the effects of vitamin B12 deficiency may not be appreciated until several years later, when these stores are depleted. Once ingested, B12 is released from the source substance by the actions of the peptic enzymes. Absorption occurs via the ileal microvilli after binding to the intrinsic factor. Any abnormality along this pathway, such as inadequate B12 intake related to diet or poor intestinal absorption, increased B12 requirement, or impaired B12 use can result in effective vitamin B12 deficiency (3). The most common cause of vitamin B12 deficiency is pernicious anemia. In this disease, there are autoimmune antibodies against the parietal cells that make intrinsic factor (4). Several laboratory tests are used to directly or indirectly measure the amount of cobalamin and enable detection of a deficiency (1).

Vitamin B12 cobalamin is a required coenzyme for two important enzymatic reactions. In the first reaction, cobalamin facilitates the methylation of homocysteine by methyltetrahydrofolate into methionine and tetrahydrofolate. Tetrahydrofolate is necessary for normal DNA synthesis by all cells, including blood cell precursors and myelin-producing oligodendrocytes. Methionine is subsequently converted to S-adenosyl-methionine. S-adenosyl-methionine is necessary for methylation of myelin sheath phospholipids. In the second reaction, cobalamin is a coenzyme that converts methylmalonyl coenzyme A into succinyl coenzyme A. Failure of this second reaction to occur results in elevated levels of methylmalonic acid. Excessive methylmalonic acid will prevent normal fatty acid synthesis, or it will be incorporated into fatty acid itself rather than normal malonic acid. If this abnormal fatty acid subsequently is incorporated into myelin or if the methylation of the myelin sheath phospholipids fails to occur, the resulting myelin will be too fragile, and demyelination will occur (14).

Active vitamin B12 cobalamin exists in a reduced form. Nitrous oxide oxidizes the reduced form to inactive cobalamin, which is excreted. This oxidation is not reversible. Even after relatively short periods of exposure to nitrous oxide, the amount of methionine synthase-vitamin complex is measurably reduced (4). Once inactivated, this complex requires 3–4 days to recover; during this time, new enzyme-vitamin complexes are synthesized. Healthy individuals have sufficient stores of cobalamin to compensate; however, there is no reserve in patients with vitamin B12 deficiency. Thus, nitrous oxide may bring about manifestations of vitamin B12 deficiency in a patient who had yet to experience symptoms of vitamin B12 deficiency, as was the case in this patient (4,5).

Vitamin B12 deficiency may manifest with megaloblastic anemia because of impairment of DNA synthesis or as one of a few neurologic syndromes. These neurologic syndromes include mental status changes (eg, memory impairment, poor attention span, diminished intellectual function, and abnormalities of behavior, mood, or logical thought), optic neuropathy, or subacute combined degeneration. The term subacute combined degeneration was introduced in the late 1800s (6,7) and used to describe myelopathy that develops over the course of a few weeks to a few months. Myelopathy was later found to be associated with vitamin B12 deficiency. Numbness, weakness, and paresthesia of the extremities primarily affects the lower extremities, is often symmetric, and progresses in a distal-to-proximal manner. Later, this myelopathy progresses to unsteady gait, poor coordination, sensory deficits, and bowel or bladder dysfunction. At physical examination, signs of dorsal column involvement include loss of position and vibration sense and ataxia. Lateral column involvement includes spasticity, hyperreflexia, and a positive Babinski sign. There may be involvement of the spinothalamic tracts with a sensory level (24,8,9). These neurologic findings may predate the development of anemia. In fact, there may be an inverse relationship between the degree of neurologic deficits and the occurrence of hematologic abnormalities (1,2,7).

Pathologically, there is demyelination involving the dorsal columns, predominately in the lower cervical and upper thoracic region. Focal swelling of the myelin tubes progresses to larger areas of vacuolization of myelin. This process eventually involves the entire dorsal columns symmetrically, with spread in the cranial and caudal directions and into the lateral columns. If uncontrolled, this process may advance to other long fiber tracts (913).

This demyelination is seen as hyperintensity on the T2-weighted images and involves the dorsal columns. On sagittal images, there is a vertically oriented segment of variable length at the posterior aspect of the spinal cord, as is seen in this patient. On cross-section images, bilateral paired areas of T2 hyperintensity are seen as an "inverted V" or "inverted rabbit ears" in the expected anatomic location of the dorsal columns. Case reports demonstrate occasional lateral column involvement and enhancement. After treatment for vitamin B12 deficiency, there is interval improvement in the region of signal abnormality (9,1417).

Patients with acquired immunodeficiency syndrome and vacuolar myelopathy present with clinical symptoms similar to those of patients with subacute combined degeneration. Furthermore, images obtained in patients with this disease show symmetric T2 hyperintensity within the posterior columns that extends for several vertebral segments. The pathologic changes are also nearly identical (1113,17,18). The cause of vacuolar myelopathy is not known exactly, but research (18) has demonstrated impairment of the methylation pathway, perhaps by the virus itself. Given the complexity of the B12-dependent transmethylation pathway, it is not surprising that errors anywhere along the course can result in identical clinical, gross pathologic, and imaging findings, even in patients with normal levels of B12. Consequently, although imaging findings of vacuolar myelopathy will look identical to those of subacute combined degeneration, this former diagnosis is strictly reserved for those individuals who have the human immunodeficiency virus. In the absence of this clinical data, however, both diagnoses need to be considered.

Authors have suggested that similar findings could be seen in patients with multiple sclerosis (19). Although multiple sclerosis certainly involves the dorsal columns, the exquisite symmetry of the signal abnormality confined to the dorsal columns over several vertebral segments, as in this case, would be unlikely. Tabes dorsalis, with its preferential involvement of the posterior columns, has been postulated to yield similar findings. A search of the literature failed to reveal any magnetic resonance (MR) studies of tabes dorsalis. This is presumably related to the introduction of penicillin predating the development of MR imaging and the number of cases of neurosyphilis having decreased drastically since that time. Although the incidence of tabes dorsalis is increasing, mainly as a consequence of human immunodeficiency virus infection, most new cases are of the meningovascular form (2023).

The synergistic effect of nitrous oxide in patients with clinically silent or borderline vitamin B12 deficiency is not commonly known. Consequently, it may be the radiologist who is called to evaluate a patient with new-onset myelopathy and a remote postoperative history. Bilateral paired T2 hyperintensity within the dorsal columns, when seen on MR images, is strongly suggestive of subacute combined degeneration, even in the absence of confirmation of the neurologic signs and symptoms.


    FOOTNOTES
 

Part one of this case appeared 4 months previously and may contain larger images.

 


    References
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 HISTORY
 IMAGING FINDINGS
 DISCUSSION
 References
 

  1. Green R, Kinsella LJ. Current concepts in the diagnosis of cobalamin deficiency. Neurology 1995;45:1435–1440.[Free Full Text]
  2. Clementz GL, Schade SG. The spectrum of vitamin B12 deficiency. Am Fam Physician 1990;41:150–162.[Medline]
  3. Beck WS. Neuropsychiatric consequence of cobalamin deficiency. In: Stollerman GH, ed. Advances in internal medicine. Vol 36. St Louis, Mo: Mosby-Year Book, 1991;33–56.
  4. Holloway KL, Alberico AM. Postoperative myeloneuropathy: a preventable complication in patients with B12 deficiency. J Neurosurg 1990;72:732–736.[Medline]
  5. Hadzic A, Glab K, Sanvorn KV, Thys DM. Severe neurologic deficit after nitrous oxide anesthesia. Anesthesiology 1995;83:863–866.[CrossRef][Medline]
  6. Healton EB, Savage DG, Brust JC, Garrett TJ, Lindenbaum J. Neurologic aspects of cobalamin deficiency. Medicine 1991;70:229–245.[Medline]
  7. Hughes JT. Pathology of the spinal cord. 2nd ed. In: Bennington J, ed. Major problems in pathology. Vol 6. Philadelphia, Pa: Saunders, 1978;192–196.
  8. Tartaglino LM, Flanders AE, Rapoport RJ. Intramedullary causes of myelopathy. Semin Ultrasound CT MR 1994;15:158–188.[CrossRef][Medline]
  9. Ravina B, Loevner LA, Bank W. MR findings in subacute combined degeneration of the spinal cord: a case of reversible cervical myelopathy. AJR Am J Roentgenol 2000;174:863–865.[Free Full Text]
  10. Friedman DP, Tartaglino LM, Fisher AR, Flanders AE. MR imaging in the diagnosis of intramedullary spinal cord diseases that involve the specific neural pathways or vascular territories. AJR Am J Roentgenol 1995;165:515–523.[Abstract/Free Full Text]
  11. Petito C, Navia B, Cho E, Jordan B, George D, Price R. Vacuolar myelopathy pathologically resembling subacute combined degeneration in patients with the acquired immunodeficiency syndrome. N Engl J Med 1985;312:874–879.[Abstract]
  12. Sartoretti-Schefer S, Blattler T, Wichmann W. Spinal MRI in vacuolar myelopathy, and correlation with histopathological findings. Neuroradiology 1997;39:865–869.[CrossRef][Medline]
  13. Santosh CG, Bell JE, Best JJ. Spinal tract pathology in AIDS: postmortem MRI correlation with neuropathology. Neuroradiology 1995;37:134–138.[Medline]
  14. Timms SR, Cure JK, Kurent JE. Subacute combined degenration of the spinal cord: MR findings. AJNR Am J Neuroradiol 1993;14:1224–1227.[Abstract]
  15. Pema PJ, Horak H, Wyatt RH. Myelopathy caused by nitrous oxide toxicity. AJNR Am J Neuroradiol 1998;19:894–896.[Abstract]
  16. Locatelli ER, Laureno R, Ballard P, Mark AS. MRI in vitamin B12 deficiency myelopathy. Can J Neurol Sci 1999; 26(1):60–63.[Medline]
  17. Kuker W, Thron A. Subacute combined degeneration of the spinal cord: demonstration of contrast enhancement (letter). Neuroradiology 1999; 41(5):387.[CrossRef][Medline]
  18. Thurnher MM, Post MJ, Jinkins JR. MRI of infections and neoplasms of the spine and spinal cord in 55 patients with AIDS. Neuroradiology 2000;42:551–563.[CrossRef][Medline]
  19. Di Rocco A, Bottiglieri T, Werner P, et al. Abnormal cobalamin-dependent transmethylation in AIDS-associated myelopathy. Neurology 2002; 58(5):730–735.[Abstract/Free Full Text]
  20. Beltramello A, Puppini G, Cerini R, et al. Subacute combined degenerationof the spinal cord after nitrous oxide anesthesia: role of magnetic resonance imaging. J Neurol Neurosurg Psychiatry 1998; 64(4):563–564.[Free Full Text]
  21. Brightbill TC, Ihmeidan IH, Post JD, Berger JR, Katz DA. Neurosyphilis in HIV-positive and HIV-negative patients: neuroimaging findings. AJNR Am J Neuroradiol 1995;16:703–711.[Abstract]
  22. Nieman EA. Neurosyphilis yesterday and today. J R Coll Physicians Lond 1991; 25(4):321–324.[Medline]
  23. Simon RP. Neurosyphilis. Arch Neurol 1985;42:606–613.[Abstract]
Congratulations to the 171 individuals and two resident groups who submitted the most likely diagnosis (subacute combined degeneration) for Diagnosis Please, Case 87. The names and locations of the individuals and resident groups, as submitted, are as follows:

Individual responses

Hisashi Abe, Osaka, Japan
Gholamali Afshang, MD, Tinley Park, Ill
Dr Jorge Ahualli, Tucuman, Argentina
Okan Akinci, MD, Istanbul, Turkey
Canan Altay, MD, Izmir, Turkey
Aaron Scott Bailey, MD, Coppell, Tex
Ken Baliga, Rockford, Ill
Fabrice Basseau, Tarbes, France
Richard Beedie, Auckland, New Zealand
D. Lee Bennett, Iowa City, Iowa
Ashish Bhagat, Hemel Hempstead, England, United Kingdom
Miguel Blanco Ulla, MD, Santiago de Compostela, Spain
Susan Blaser, MD, FRCPC, Toronto, Ontario, Canada
A. Joseph Borelli, Jr, MD, Bluffton, SC
Dr Adrian Brady, FFRRCSI, Cork, Ireland
Ray A. Brinker, MD, Toledo, Ohio
Daniel F. Broderick, MD, Jacksonville, Fla
Douglas C. Brown, MD, Virginia Beach, Va
Michael P. Buetow, MD, Okemos, Mich
Peter Buetow, MD, Bellingham, Wash
Stephen J. Buetow, Bagram, Afghanistan
Marcio Bustamante, Rio de Janeiro, Brazil
Océlio Cartaxo, Recife, Brazil
Luisa Fernanda Cervantes, Miami, Fla
N. Chidambaranathan, MD, Chennai, India
John J. Combs, MD, Heidelberg, Germany
Carla Conceição, Amadora, Portugal
Neal R. Conti, MD, Seattle, Wash
Y. S. Cordoliani, MD, Paris, France
Joel Curé, MD, Indian Springs, Ala
Trupti Prabhu Dabholkar, Nassau, Bahamas
Anil Kumar Dasyam, Pittsburgh, Pa
Marc G. de Baets, MD, Lugano, Switzerland
Peter C. De Baets, MD, Damme, Belgium
Helder de Castro Marques, Juiz de Fora, MG, Brazil
Jose Luiz F. De Mendonca, MD, Brasilia, Brazil
J. F. K. de Villiers, Gisborne, New Zealand
Jon De Witte, Athens, Ga
Mustafa Kemal Demir, MD, Istanbul, Turkey
Thaworn Dendumrongsup, MD, Songkla, Thailand
Nam Ky Do, Duluth, Ga
Heratch O. Doumanian, MD, Merrillville, Ind
Steven Falcone, Miami, Fla
Juliet H. Fallah, MD, Chicago, Ill
Francis Flaherty, MD, Ridgefield, Conn
Nelson Fortes Ferreira, MD, São Paulo, Brazil
Jordi Catala Forteza, Barcelona, Spain
Kai Frentzel, MD, Hopsten, Germany
Akira Fujikawa, Tokyo, Japan
Ram Prakash Galwa, MD, Chandigarh, India
Douglas Gardner, MD, Windsor, Ontario, Canada
Gilles Genin, MD, Annecy, France
Ted A. Glass, MD, Ridgeland, Miss
Trevor N. Golding, MD, Kingston, Jamaica, West Indies
Mark Goldshein, MD, Andover, Mass
Alvaro Gomez Naar, Salta, Argentina
Eduardo Gonzalez Toledo, MD, PhD, Shreveport, La
Christopher Govea, MD, Austin, Tex
Daniel Gridley, MD, Goodyear, Ariz
Philippe Grouwels, Genk, Belgium
Flavius Guglielmo, MD, Basking Ridge, NJ
Gowthaman Gunabushanam, New Delhi, India
Ferris M. Hall, MD, Boston, Mass
Yukihiro Hama, MD, PhD, Bethesda, Md
Andreas Harzheim, MD, Cologne, Germany
Raúl Hernández Muñiz, Madrid, Spain
Thomas L. Huang, Brookline, Mass
Alberto Iaia, MD, Wilmington, Del
Rajapandian Ilangovan, Grimsby, United Kingdom
Ganesh Iyer, MD, Mumbai, India
Shinichi Kan, MD, Kanagawa, Japan
S. Pinar Karakas, New York, NY
Nurettin Katranci, MD, Antalya, Turkey
Dr Sashidhar Kaza, Hyderabad, India
Eung Yeop Kim, MD, Seoul, Korea
Takuji Kiryu, MD, Gifu, Japan
Steven A. Klein, MD, Shrewsbury, Mass
Yoshihisa Kurosaki, MD, Tokyo, Japan
Mark Kutler, MD, Dallas, Tex
Stefanos Lachanis, MD, Athens, Greece
Alexis Lacout, MD, Paris, France
Mario Laguna, West Allis, Wis
Eduardo Lassalle, MD, Quilmes, Argentina
D. Wayne Laster, MD, San Antonio, Tex
Richard A. Levy, MD, Saginaw, Mich
John T. Lim, MD, Newport Coast, Calif
David A. Lisle, Brisbane, Australia
Humberto Lobato Mcphee, Belém Pará, Brazil
Patricia Lowry, MD, Richmond, Va
Andrew B. MacKersie, Niceville, Fla
Antonio Maia, Jr, São Paulo, Brazil
Walter Mak, MD, Peoria, Ill
N. B. S. Mani, MD, Nassau, Bahamas
Javier E. Martínez, MD, Chubut, Argentina
John A. Mattingly, MD, Belleville, Ill
Frank McKowne, MD, Vancouver, Wash
Edward Menges, Aptos, Calif
Koen Mermuys, MD, Heverlee, Belgium
Jonathan Meyer, MD, Chicago, Ill
Gary M. Miller, MD, Rochester, Minn
Manabu Minami, MD, Ibaraki, Japan
Mansour Mirfakhraee, MD, Shreveport, La
Robert L. Mittl, Jr, MD, Charlotte, NC
Sankar Ranjan Mondal, MD, Nassau, Bahamas
Eduardo Mondello, MD, Buenos Aires, Argentina
S. Namasivayam, MD, DNB, DHA, Atlanta, Ga
R. Nandhagopal, Andhra Pradesh, India
Tammam Nehme, East Wenatchee, Wash
Alexander J. Nemeth, MD, Boston, Mass
Mizuki Nishino, MD, Boston, Mass
Diego B. Nunez, Jr, MD, MPH, New Haven, Conn
Edward S. Oh, Tucson, Ariz
Michael T. O'Loughlin, MD, West Hartford, Conn
Sanford M. Ornstein, MD, Phoenix, Ariz
Neeraj J. Panchal, MD, San Diego, Calif
Anoop Kumar Pandey, Varanasi, India
Young Jin Park, MD, Busan, Korea
Narendrakumar P. Patel, MD, Newburgh, NY
Christopher Payne, MD, Greensboro, NC
Alexander Petersen, MD, Nowra, Australia
Hilton W. Pittman, Pensacola, Fla
Cecilio Poyatos, MD, Valencia, Spain
Henry W. Pribram, MD, Laguna Beach, Calif
G. Lee Pride, Jr, MD, Dallas, Tex
Anuradha T. N. Rao, Toronto, Ontario, Canada
John F. Rice, MD, FACR, Anchorage, Ky
Antônio Rocha, São Paulo, Brazil
Mathieu H. Rodallec, Paris, France
Jordi Roldan i Busto, Illes Balears, Spain
Dr Luis San Román Manzanera, Barcelona, Spain
H. Tuba Sanal, MD, Ankara, Turkey
Satyajit Sarangi, MD, Lewes, Del
Pierre J. Sauvage, MD, Mâcon, France
Janet Scheraga, Tully, NY
Steven M. Schultz, MD, Fort Worth, Tex
Simona Secci, MD, Cagliari, Italy
Matt Shapiro, MD, Charlottesville, Va
Niall Sheehy, MD, Dublin, Ireland
Waka Shimada, Tochigi, Japan
Taro Shimono, MD, Osaka, Japan
Grady Shue, Heidelberg, Germany
Ken Simmons, Sydney, Australia
Dr Nitin Singh, Nassau, Bahamas
David F. Sobel, MD, La Jolla, Calif
James D. Sprinkle, Jr, MD, Spotsylvania, Va
Scott D. Steenburg, MD, Mount Pleasant, SC
Jonathan D. Stephenson, MD, Hershey, Pa
C. V. Subbarao, Nassau, Bahamas
Kouichi Sugiyama, Hamamatsu, Japan
Vinod Sukumaran, Davangere, India
Amit Suri, MD, Kings Lynn, Norfolk, United Kingdom
Norio Takahashi, MD, Fukui, Japan
Eliko Tanaka, Yokohama, Japan
Robert Tash, MD, Nyack, NY
Douglas L. Teich, MD, Brookline, Mass
Kazuma Terauchi, MD, Fukuoka, Japan
Eugene Tong, MD, Austin, Tex
Meriç Tüzün, Ankara, Turkey
Hiroyuki Ueda, Kyoto, Japan
J. Valk, MD, PhD, Amsterdam, The Netherlands
Geert Verswijvel, MD, Genk, Belgium
B. Vijayalakshmidevi, Tirupathi, India
Joan C. (Kai) Vilanova, MD, Girona, Spain
Christopher Vittore, MD, Rockford, Ill
Dr Silvio Alejandro Vollmer, Rio Negro, Argentina
Lynne Voutsinas, MD, Staten Island, NY
Yukari Wakabayashi, MD, Tokyo, Japan
Xinjiang Wang, MD, Xinjiang, P. R. China
Susan W. Weathers, MD, Houston, Tex
Jiang Yi Yi, Zhe Jiang, China
Satoru Yoshida, MD, Muroran City, Japan

Resident group responses

Hospital of the University of Pennsylvania Radiology Residents, Philadelphia, Pa
Oregon Health & Science University Radiology Residents, Portland, Ore

For "Case 85: Pelvic Actinomycosis in Association with an Intrauterine Device" (Radiology 2005; 236:492--494), the following individual should have been listed among those submitting the most likely diagnosis:

Roger Antonelli, MD, Dayton, Ohio





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