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Case 21: Glomus Vagale Tumor¹

¹ From the Departments of Radiology and Otolaryngology, University of Pittsburgh, Pa. Received October 30, 1998; revision requested December 28; revision received February 2, 1999; accepted July 1. Address reprint requests to the author, Departments of Radiology and Otolaryngology, Oregon Health Sciences University, Mail Code CR-135, 3181 S.W. Sam Jackson Park Rd, Portland, OR 97201 (e-mail: weissmaj@ohsu.edu).

Index terms: Carotid arteries, angiography, 90.122 • Diagnosis Please • Magnetic resonance (MR), maximum intensity projection, 27.12141 • Magnetic resonance (MR), three-dimensional, 27.12141 • Magnetic resonance (MR), time of flight, 27.12141 • Neck, CT, 27.1211 • Neck, MR, 27.12141 • Paraganglioma, 27.3642

	HISTORY

TOP HISTORY IMAGING FINDINGS DISCUSSION References

 
A 77-year-old woman realized her voice had become hoarse, though she was unable to say when it had changed. Her physician palpated a mass high on the left side of her neck. Inspection of the oral cavity showed medial bulging of the left pharyngeal wall and tonsil. Indirect laryngoscopy revealed a paralyzed left vocal cord. Information from a computed tomographic (CT) scan of the neck (Fig 1) was supplemented with magnetic resonance (MR) images (Fig 2). Because the woman had severe congestive heart failure and an ejection fraction of 19%, she and her physician agreed surgery was not the best option. She therefore underwent conventional angiography (Fig 3a) and therapeutic embolization (Fig 3b).

View larger version (142K): [in this window] [in a new window] [Download PPT slide]   Figure 1. Transverse contrast material-enhanced CT image at the level of the mandible shows the intensely enhancing glomus vagale tumor (gv) displacing the internal carotid artery (ic) anteriorly and the internal jugular vein (ij) posteriorly. The tumor makes the lateral pharyngeal wall bulge into the pharyngeal lumen.

View larger version (155K): [in this window] [in a new window] [Download PPT slide]   Figure 2a. (a) Transverse T2-weighted MR image (3,500/80 [repetition time msec/echo time msec]; number of signals acquired, two) through the tumor shows the hyperintense tumor ("salt") interspersed with signal voids of tumor vessels ("pepper"). The tumor widely separates the internal carotid artery (ic) and the internal jugular vein (ij). (b) Transverse three-dimensional time-of-flight image (26/4.3 fractionated, 1-mm-thick section) shows the internal (i) and external (e) carotid arteries anterior to the tumor and the internal jugular vein (v) posterior to the tumor. The small tumor vessels are not hyperintense with this sequence. (c) Transverse three-dimensional time-of-flight image (26/4.3 fractionated, 1-mm-thick section) shows the normal internal (i) and external (e) carotid arteries at the carotid bifurcation. (d) Sagittal maximum intensity projection image of the left side of the neck, which was created from the transverse three-dimensional time-of-flight data, shows anterior displacement of the internal (i) and external (e) carotid arteries and posterior displacement of the internal jugular vein (v). (e) Sagittal phase-contrast image of the left side of the neck (33/8.5 fractionated; flip angle, 25°; velocity encoded 40 cm/sec) shows the normal internal (i) and external (e) carotid arteries at the carotid bifurcation. The internal carotid artery is pushed forward (open arrows) by the tumor. The tumor pushes the external carotid artery laterally and anteriorly, so the upper external carotid artery is not included in the area imaged. The tumor vessels are not conspicuous. The internal jugular vein is not seen.

View larger version (159K): [in this window] [in a new window] [Download PPT slide]   Figure 2b. (a) Transverse T2-weighted MR image (3,500/80 [repetition time msec/echo time msec]; number of signals acquired, two) through the tumor shows the hyperintense tumor ("salt") interspersed with signal voids of tumor vessels ("pepper"). The tumor widely separates the internal carotid artery (ic) and the internal jugular vein (ij). (b) Transverse three-dimensional time-of-flight image (26/4.3 fractionated, 1-mm-thick section) shows the internal (i) and external (e) carotid arteries anterior to the tumor and the internal jugular vein (v) posterior to the tumor. The small tumor vessels are not hyperintense with this sequence. (c) Transverse three-dimensional time-of-flight image (26/4.3 fractionated, 1-mm-thick section) shows the normal internal (i) and external (e) carotid arteries at the carotid bifurcation. (d) Sagittal maximum intensity projection image of the left side of the neck, which was created from the transverse three-dimensional time-of-flight data, shows anterior displacement of the internal (i) and external (e) carotid arteries and posterior displacement of the internal jugular vein (v). (e) Sagittal phase-contrast image of the left side of the neck (33/8.5 fractionated; flip angle, 25°; velocity encoded 40 cm/sec) shows the normal internal (i) and external (e) carotid arteries at the carotid bifurcation. The internal carotid artery is pushed forward (open arrows) by the tumor. The tumor pushes the external carotid artery laterally and anteriorly, so the upper external carotid artery is not included in the area imaged. The tumor vessels are not conspicuous. The internal jugular vein is not seen.

View larger version (155K): [in this window] [in a new window] [Download PPT slide]   Figure 2c. (a) Transverse T2-weighted MR image (3,500/80 [repetition time msec/echo time msec]; number of signals acquired, two) through the tumor shows the hyperintense tumor ("salt") interspersed with signal voids of tumor vessels ("pepper"). The tumor widely separates the internal carotid artery (ic) and the internal jugular vein (ij). (b) Transverse three-dimensional time-of-flight image (26/4.3 fractionated, 1-mm-thick section) shows the internal (i) and external (e) carotid arteries anterior to the tumor and the internal jugular vein (v) posterior to the tumor. The small tumor vessels are not hyperintense with this sequence. (c) Transverse three-dimensional time-of-flight image (26/4.3 fractionated, 1-mm-thick section) shows the normal internal (i) and external (e) carotid arteries at the carotid bifurcation. (d) Sagittal maximum intensity projection image of the left side of the neck, which was created from the transverse three-dimensional time-of-flight data, shows anterior displacement of the internal (i) and external (e) carotid arteries and posterior displacement of the internal jugular vein (v). (e) Sagittal phase-contrast image of the left side of the neck (33/8.5 fractionated; flip angle, 25°; velocity encoded 40 cm/sec) shows the normal internal (i) and external (e) carotid arteries at the carotid bifurcation. The internal carotid artery is pushed forward (open arrows) by the tumor. The tumor pushes the external carotid artery laterally and anteriorly, so the upper external carotid artery is not included in the area imaged. The tumor vessels are not conspicuous. The internal jugular vein is not seen.

View larger version (126K): [in this window] [in a new window] [Download PPT slide]   Figure 2d. (a) Transverse T2-weighted MR image (3,500/80 [repetition time msec/echo time msec]; number of signals acquired, two) through the tumor shows the hyperintense tumor ("salt") interspersed with signal voids of tumor vessels ("pepper"). The tumor widely separates the internal carotid artery (ic) and the internal jugular vein (ij). (b) Transverse three-dimensional time-of-flight image (26/4.3 fractionated, 1-mm-thick section) shows the internal (i) and external (e) carotid arteries anterior to the tumor and the internal jugular vein (v) posterior to the tumor. The small tumor vessels are not hyperintense with this sequence. (c) Transverse three-dimensional time-of-flight image (26/4.3 fractionated, 1-mm-thick section) shows the normal internal (i) and external (e) carotid arteries at the carotid bifurcation. (d) Sagittal maximum intensity projection image of the left side of the neck, which was created from the transverse three-dimensional time-of-flight data, shows anterior displacement of the internal (i) and external (e) carotid arteries and posterior displacement of the internal jugular vein (v). (e) Sagittal phase-contrast image of the left side of the neck (33/8.5 fractionated; flip angle, 25°; velocity encoded 40 cm/sec) shows the normal internal (i) and external (e) carotid arteries at the carotid bifurcation. The internal carotid artery is pushed forward (open arrows) by the tumor. The tumor pushes the external carotid artery laterally and anteriorly, so the upper external carotid artery is not included in the area imaged. The tumor vessels are not conspicuous. The internal jugular vein is not seen.

View larger version (127K): [in this window] [in a new window] [Download PPT slide]   Figure 2e. (a) Transverse T2-weighted MR image (3,500/80 [repetition time msec/echo time msec]; number of signals acquired, two) through the tumor shows the hyperintense tumor ("salt") interspersed with signal voids of tumor vessels ("pepper"). The tumor widely separates the internal carotid artery (ic) and the internal jugular vein (ij). (b) Transverse three-dimensional time-of-flight image (26/4.3 fractionated, 1-mm-thick section) shows the internal (i) and external (e) carotid arteries anterior to the tumor and the internal jugular vein (v) posterior to the tumor. The small tumor vessels are not hyperintense with this sequence. (c) Transverse three-dimensional time-of-flight image (26/4.3 fractionated, 1-mm-thick section) shows the normal internal (i) and external (e) carotid arteries at the carotid bifurcation. (d) Sagittal maximum intensity projection image of the left side of the neck, which was created from the transverse three-dimensional time-of-flight data, shows anterior displacement of the internal (i) and external (e) carotid arteries and posterior displacement of the internal jugular vein (v). (e) Sagittal phase-contrast image of the left side of the neck (33/8.5 fractionated; flip angle, 25°; velocity encoded 40 cm/sec) shows the normal internal (i) and external (e) carotid arteries at the carotid bifurcation. The internal carotid artery is pushed forward (open arrows) by the tumor. The tumor pushes the external carotid artery laterally and anteriorly, so the upper external carotid artery is not included in the area imaged. The tumor vessels are not conspicuous. The internal jugular vein is not seen.

View larger version (103K): [in this window] [in a new window] [Download PPT slide]   Figure 3a. (a) Left common carotid arteriogram, lateral view, midarterial phase obtained at the initial diagnostic study shows the very vascular tumor surrounding the internal (i) and external (e) carotid arteries and displacing the internal carotid artery anteriorly. A hypertrophied ascending pharyngeal artery (solid arrows) supplies the tumor. The tumor extends to the skull base (open arrows) but not through it. The carotid bifurcation is normal. (b) Left common carotid arteriogram, lateral view, midarterial phase obtained at the concluding study after therapeutic embolization shows most of the tumor neovascularity is no longer present, but the persistent displacement of the internal carotid artery (i) provides indirect evidence that the mass remains.

View larger version (94K): [in this window] [in a new window] [Download PPT slide]   Figure 3b. (a) Left common carotid arteriogram, lateral view, midarterial phase obtained at the initial diagnostic study shows the very vascular tumor surrounding the internal (i) and external (e) carotid arteries and displacing the internal carotid artery anteriorly. A hypertrophied ascending pharyngeal artery (solid arrows) supplies the tumor. The tumor extends to the skull base (open arrows) but not through it. The carotid bifurcation is normal. (b) Left common carotid arteriogram, lateral view, midarterial phase obtained at the concluding study after therapeutic embolization shows most of the tumor neovascularity is no longer present, but the persistent displacement of the internal carotid artery (i) provides indirect evidence that the mass remains.

	IMAGING FINDINGS

TOP HISTORY IMAGING FINDINGS DISCUSSION References

The T2-weighted MR image (Fig 2a) showed a hyperintense tumor lying between the internal carotid artery and the internal jugular vein. The tumor contained the punctate signal voids of many small tumor vessels.

The three-dimensional time-of-flight transverse images showed the hyperintense (patent) internal carotid artery and the internal jugular vein (Fig 2b–2d). These two vessels were widely separated by the tumor, which was not seen well on these flow-sensitive images. The small tumor vessels seen on the T2-weighted image (Fig 2a) were also not conspicuous on these images. The external carotid artery ran along the anterior surface of the tumor, lateral to the internal carotid artery. An image obtained lower in the neck (Fig 2c) showed that the carotid bifurcation was normal.

A sagittal view reconstructed from time-of-flight transverse images (Fig 2d) showed the anterior displacement of the internal carotid artery and the posterior displacement of the internal jugular vein; the tumor's location could be inferred only from the vascular displacement. The sagittal phase-contrast image (Fig 2e) demonstrated anterior displacement of the internal carotid artery and a normal carotid bifurcation. High in the neck at the level of the tumor, the external carotid artery, displaced laterally and anteriorly, lay lateral to the locations used to generate this image.

Injection of contrast material into a catheter in the left common carotid artery (lateral view, midarterial phase) showed anterior displacement of the internal and external carotid arteries by a vascular mass (Fig 3a). The tumor was partially supplied by a hypertrophied ascending pharyngeal artery. The carotid bifurcation was normal. After embolization with polyvinyl alcohol particles, the mass remained, displacing the internal carotid artery, but the tumor vascularity was markedly diminished (Fig 3b).

	DISCUSSION

TOP HISTORY IMAGING FINDINGS DISCUSSION References

 
The patient had a glomus vagale tumor. The tumor, also called a "glomus intravagale tumor" or "vagal paraganglioma," arises from paraganglia in and around the vagus nerve (1–3).

Normal Anatomy
Paraganglia are normal structures that develop from the neural crest; they accompany cranial nerves and cluster around cranial nerve ganglia (4). The function of most paraganglia remains obscure (5), though the carotid body is a known chemoreceptor, and other paraganglia may play similar roles (4).

There are three large vagal ganglia in the upper neck. The nodose ganglion, the largest and most caudal of the three, lies posterior to the internal carotid artery within the carotid sheath (6,7).

Paragangliomas
Tumors of the paraganglia are called "paragangliomas," "glomus tumors," and "chemodectomas." "Paraganglioma," the most accurate name, reflects their origin (1). Most paragangliomas of the head and neck are hormonally inactive (8,9). For these, the term "nonchromaffin paragangliomas" has been used to differentiate them from the epinephrine- and norepinephrine-secreting chromaffin tissue and tumors of the adrenal medulla and organs of Zuckerkandl (paraaortic bodies) (4).

The most frequent head and neck paragangliomas are carotid body tumors. Next most frequent are glomus jugulare tumors, which arise in the jugular fossa from paraganglia in the adventitia of the jugular bulb (10). Glomus vagale tumors are the third most frequent (7,9). Glomus bodies are found within the vagus nerve and its ganglia and beneath the perineurium (1,7,11); a glomus vagale tumor may arise in any of these locations but most often in or near the nodose ganglion (1,2). Glomus tympanicum tumors arise from the glomus bodies of the Jacobson nerve in the middle ear (5). Glomus tumors of the facial nerve, the larynx, the thyroid, and the orbit are rare (1,8).

Clinical Presentation
Most glomus vagale tumors manifest as a painless neck mass near the angle of the mandible (1,7,9,11–13), usually between the skull base and the hyoid bone. Glomus vagale tumors lower in the neck are rare. Less than half of the patients are hoarse, which is the clinical manifestation of vagal dysfunction (vocal cord paralysis) (7,9). Glomus vagale tumors cause other lower cranial neuropathies: dysphagia, palatal weakness, and tongue hemiatrophy (3,7,8,14). Pressure on the cervical sympathetic chain causes Horner syndrome (1). Although most head and neck glomus tumors are nonsecretory, screening for catecholamines and their metabolites (urinary metanephrines and vanillylmandelic acid) may be performed before angiography or surgery.

Ten percent of people with glomus tumors have the hereditary form (9), which is transmitted as an autosomal dominant trait with incomplete, variable penetrance (7). About one-third of people with hereditary paragangliomas have multiple tumors; only 10% of those with the sporadic (nonhereditary) form have multiple tumors (7). Glomus tumors are more frequent in women than in men.

Histologic Features
The characteristic histologic features of glomus tumors are Zellballen, which are nests of neoplastic chief cells surrounded by reticulin fibers and many blood vessels (1). Malignancy is not a histologic diagnosis (1), as both benign and malignant tumors may contain pleomorphic and multinuclear cells and mitoses (10). Malignancy is a clinical diagnosis made when local invasion or metastases are present (1,12).

Radiologic Appearance
Cross-sectional imaging studies can be used to accurately diagnose a glomus vagale tumor (3,15,16). This highly vascular, intensely enhancing tumor displaces the internal and the external carotid arteries anteriorly (3) and the internal jugular vein posteriorly (3,5,6) (Figs 1, 2a, 2b, 2d, 2e, 3). Both the location and the enhancement of the tumor are characteristic.

Large tumors may contain necrotic or hemorrhagic foci that enhance heterogeneously or not at all (3,16). The salt-and-pepper appearance on contrast-enhanced T1-weighted MR images represents the intensely enhancing tumor stroma ("salt") interspersed with many small tumor vessels ("pepper") (3,15). On T2-weighted images, the "salt" is tumor matrix, hemorrhage, and slow flow; the "pepper" is the signal void of rapid flow (15,16).

At dynamic CT, which is rarely used today, a plot with respect to time of the attenuation of a paraganglioma during administration of contrast material demonstrates a sharp upswing followed by a rapid decline, or washout (3,16). The pattern closely parallels the curve for blood vessels (3,16). Delayed scanning may demonstrate only minimal enhancement of the tumor because the washout of contrast material is so rapid (16). Dynamic MR imaging of skull base glomus tumors after intravenous administration of high-dose contrast material yields a characteristic dip in the curve plotting jugular signal intensity over time (17). This dip is presumed to represent T2 shortening by the high concentration of contrast material passing through these highly vascular tumors (17).

MR angiograms may be obtained by using time-of-flight or phase-contrast techniques. The three-dimensional time-of-flight images (transverse "base" images [Fig 2b, 2c] and maximum intensity projection image [Fig 2d]) demonstrate arteries well and also show large venous structures, such as the internal jugular vein, that are not visible on phase-contrast images (Fig 2e). Three-dimensional time-of-flight images obtained without contrast material demonstrate displacement of the large vessels, but most of the small tumor vessels remain invisible (Fig 2b, 2d). Contrast-enhanced three-dimensional time-of-flight MR angiograms obtained during the arterial phase show even very small arteries. Delayed, or venous phase, images may be less valuable because the venous structures are as conspicuous as the arteries.

Bilateral carotid or carotid and vertebral conventional angiography were formerly advocated in all patients with glomus tumors (12). This is no longer necessary, as detailed cross-sectional imaging studies depict even "occult" tumors (8,9).

Arteriography of a glomus vagale tumor demonstrates anterior displacement of the internal and external carotid arteries (Fig 3). The tumor is usually supplied by a hypertrophied ascending pharyngeal artery (18) (Fig 3) and may be supplied by the occipital, lingual, facial, vertebral, and deep cervical arteries (18,19) and by hypertrophied, unnamed arteries (13,19,20). Early, intense opacification of many abnormal tumor vessels (12) is often followed by early venous filling (18).

Treatment Options
Because glomus vagale tumors grow within the vagus nerve, it is almost impossible to remove the tumor without sacrificing the nerve (2,9). Nearly all patients have vocal cord paralysis after surgery (7,9), whether or not they were hoarse preoperatively. Therefore, some surgeons perform an intraoperative thyroplasty at the same time the tumor is removed (3,7,9) to move the vocal cord closer to the midline and reduce hoarseness and aspiration. After complete surgical removal of the tumor, recurrence is unlikely (3).

Surgery may not be a feasible option for patients with an underlying disease, such as the woman presented here, and in patients with certain combinations of bilateral glomus tumors. Vocal cord paralysis may follow removal of both a glomus vagale tumor and a glomus jugulare tumor. Bilateral vocal cord paralysis is extremely debilitating and may be fatal (2,7,8). Therefore, bilateral glomus vagale or glomus jugulare tumors, or a glomus vagale tumor and a contralateral glomus jugulare tumor, present a surgical dilemma, as removal of both tumors may be contraindicated. When surgery is not an option, therapeutic embolization and radiation therapy are important alternatives.

Therapeutic embolization decreases the size of a tumor. It is sometimes possible to embolize the tumor completely (19), though new vessels may replace those that were embolized. Preoperative embolization of a glomus tumor reduces intraoperative blood loss (7,13). When surgery is not an option, embolization may be the definitive treatment.

Radiation therapy controls the growth of glomus tumors and may cure them (3). In patients with bilateral tumors, one approach is to remove the larger tumor and irradiate the smaller one (9). Radiation therapy may also be used to treat tumor left behind at surgery and recurrent tumor after surgery (3).

Differential Diagnosis
A mass between the internal carotid artery and internal jugular vein usually arises from one of the structures within the carotid sheath, or poststyloid parapharyngeal space. Lymph nodes are not found within the carotid sheath, so adenopathy would be an unlikely cause of splaying of these vessels, though a large node could insinuate itself between the vessels. Vascular (enhancing) lymph nodes may be found in Castleman disease, angioimmunoblastic lymphadenopathy, and Kaposi sarcoma.

A carotid body tumor also lies between two vessels, as does a glomus vagale tumor (Fig 4a). However, a glomus vagale tumor splays the internal jugular vein and the internal carotid artery; a carotid body tumor splays the internal and external carotid arteries (Fig 4a). The carotid bifurcation is normal in a patient with a glomus vagale tumor (Fig 2c), unless the patient also has a carotid body tumor (Fig 4b). Glomus vagale tumors occur higher in the neck than carotid body tumors (12). The hyoid bone is a useful landmark for the carotid bifurcation and so for carotid body tumors (Fig 4a). Carotid body tumors rarely grow up to the skull base (12).

View larger version (109K): [in this window] [in a new window] [Download PPT slide]   Figure 4a. Carotid body tumors in two patients. (a) Transverse enhanced CT scan of the carotid bifurcation shows the intensely enhancing tumor (T) between the left internal (i) and external (e) carotid arteries; j = internal jugular vein. The right carotid bifurcation is normal. (b) Right common carotid arteriogram, lateral view, arterial phase shows a small carotid body tumor (black arrow) at the bifurcation of the internal (I) and external (E) carotid arteries. There is also a large glomus vagale tumor (white arrow) displacing the internal carotid artery anteriorly. The vagale tumor separates the internal carotid artery from the internal jugular vein (J). The vein can be seen as a black structure because a venous-phase mask was used to create this subtraction image.

View larger version (104K): [in this window] [in a new window] [Download PPT slide]   Figure 4b. Carotid body tumors in two patients. (a) Transverse enhanced CT scan of the carotid bifurcation shows the intensely enhancing tumor (T) between the left internal (i) and external (e) carotid arteries; j = internal jugular vein. The right carotid bifurcation is normal. (b) Right common carotid arteriogram, lateral view, arterial phase shows a small carotid body tumor (black arrow) at the bifurcation of the internal (I) and external (E) carotid arteries. There is also a large glomus vagale tumor (white arrow) displacing the internal carotid artery anteriorly. The vagale tumor separates the internal carotid artery from the internal jugular vein (J). The vein can be seen as a black structure because a venous-phase mask was used to create this subtraction image.

A schwannoma, or neurilemoma, of one of the nerves within the carotid sheath can mimic a glomus vagale tumor (Fig 5). The nerve sheath tumor often (Fig 5a) but not always (Fig 5b) enhances less intensely than a glomus tumor. Cranial nerves and the sympathetic trunk all give rise to nerve sheath tumors. Even the surgeon may not be able to tell the nerve of origin (12), though Horner syndrome after surgery strongly suggests an origin from the cervical sympathetic trunk.

View larger version (128K): [in this window] [in a new window] [Download PPT slide]   Figure 5a. Nerve sheath tumors in two patients. (a) Transverse contrast-enhanced CT image shows a heterogeneously enhancing schwannoma (S) medial to the internal (I) and external (E) carotid arteries and the internal jugular vein (J). (b) Transverse T1-weighted MR image (600/15; number of signals acquired, one) obtained with the use of contrast material shows an intensely enhancing sympathetic schwannoma (S) between the right internal (I) and external (E) carotid arteries. The relationship of the tumor to the arteries is similar to that in a carotid body tumor, but this is higher in the neck than the bifurcation, at a level more typical of a glomus vagale tumor. J = internal jugular vein.

View larger version (140K): [in this window] [in a new window] [Download PPT slide]   Figure 5b. Nerve sheath tumors in two patients. (a) Transverse contrast-enhanced CT image shows a heterogeneously enhancing schwannoma (S) medial to the internal (I) and external (E) carotid arteries and the internal jugular vein (J). (b) Transverse T1-weighted MR image (600/15; number of signals acquired, one) obtained with the use of contrast material shows an intensely enhancing sympathetic schwannoma (S) between the right internal (I) and external (E) carotid arteries. The relationship of the tumor to the arteries is similar to that in a carotid body tumor, but this is higher in the neck than the bifurcation, at a level more typical of a glomus vagale tumor. J = internal jugular vein.

Our congratulations to the 102 individuals who submitted the most likely diagnosis (glomus vagale tumor) for Diagnosis Please, Case 21. Credit was given only if the vagus nerve was mentioned. The names and locations of the individuals, as submitted, are as follows:

• Hisashi Abe, Osaka-city, Japan
  
• Gholamali Afshang, MD, Tinley Park, Ill
  
• Julio Almeida Llanos, MD, Rosario, Argentina
  
• Roger Antonelli, MD, Dayton, Ohio
  
• Yasutaka Baba, Kagoshima, Japan
  
• Ken Baliga, Rockford, Ill
  
• Helene Bänziger, Basel, Switzerland
  
• Frank S. Bonelli, MD, PhD, Rockford, Ill
  
• Adrian Brady, FFRRCSI, FRCR, Cork, Ireland
  
• Eric L. Bressler, MD, Minnetonka, Minn
  
• José Burgos Flor, MD, La Rioja, Argentina
  
• Yvette Cheong, MD, Vancouver, British Columbia, Canada
  
• Kenneth R. Curtin, MD, Petoskey, Mich
  
• Marc G. de Baets, MD, Lugano, Switzerland
  
• J. F. K. de Villiers, Gisborne, New Zealand
  
• Kemal Demir, Istanbul, Turkey
  
• Dra. Estela Di Nella, Buenos Aires, Argentina
  
• Seyed A. Emamian, MD, PhD, Washington, DC
  
• Keith D. Epperson, MD, Milwaukee, Wis
  
• Gabriel C. Fernandez, Vigo, Spain
  
• Manohar P. Gandhi, MD, Encino, Calif
  
• Marcelo García Arnedo, MD, Rosario, Argentina
  
• Teresa Adriana Garcia, MD, Buenos Aires, Argentina
  
• H. Gaucher, MD, Metz, France
  
• David D. Goltra, Jr, MD, Mt Pleasant, SC
  
• Walter O. Grauer, MD, Zurich, Switzerland
  
• J-P Guichard, Paris, France
  
• Dr. Isaac Hassan, Bolton, United Kingdom
  
• Rufus W. Head, MD, North Bridgton, Me
  
• Maureen Heldmann, MD, Shreveport, La
  
• Waleed Ibrahim, MD, Detroit, Mich
  
• Christophe Ide, MD, Namur, Belgium
  
• Timothy Kadlecek Hirotsugu Kado, Fukui, Japan
  
• Nuri Karabay, MD, nciralt/zmir, Turkey
  
• Douglas S. Katz, MD, Mineola, NY
  
• Norbert Keune, Karlsruhe, Germany
  
• Paul H. Kim, MD, LaSalle, Ill
  
• Mitchell A. Klein, MD, Milwaukee, Wis
  
• Stephanos Lachanis, MD, Athens, Greece
  
• Jeffrey Neal Lang, MD, New York, NY
  
• Eduardo Lassalle, MD, Quilmes, Argentina
  
• Steven Lev, MD, Great Neck, NY
  
• Han Lixin, MD, Guangzhou, China
  
• Alain Luciani, MD, Paris, France
  
• Goetz Lutterbey, MD, Bonn, Germany
  
• Antonio Jose Madureira, MD, Porto, Portugal
  
• N. B. S. Mani, MD, Chandigarh, India
  
• Menahem M. Maya, MD, Los Angeles, Calif
  
• Jaime Mejia, MD, Miami, Fla
  
• Edward Menges, MD, Aptos Calif
  
• Leslie Miller, MD, Mineola, NY
  
• Gary M. Miller, Rochester, Minn
  
• Mansour Mirfakhraee, Shreveport, La
  
• Hidetoshi Miyake, MD, Oita, Japan
  
• Sergio J. Moguillansky, MD, Rio Negro, Argentina
  
• Peter Mollet, MD, Gent, Belgium
  
• Eduardo Mondello, Buenos Aires, Argentina
  
• Toshio Moritani, Rochester, NY
  
• Shinji Naganawa, MD, Nagoya, Japan
  
• Hiroyuki Nakagawa, MD, Nara, Japan
  
• Vung Duy Nguyen, San Antonio, Tex
  
• Sanford M. Ornstein, MD, Phoenix, Ariz
  
• Ann B. Owen, MD, Murfreesboro, Tenn
  
• Frank A. Pameijer, MD, PhD, Amsterdam, the Netherlands
  
• Harish Panicker, MD, Pontiac, Mich
  
• David M. Pelz, MD, London, Ontario, Canada
  
• Donald B. Price, MD, Mineola, NY
  
• Shawn P. Quillin, MD, Charlotte, NC
  
• Danny Rappaport, Toronto, Ontario, Canada
  
• Randall Rhodes, MD, Rockford, Ill
  
• Javier Rodríguez Lucero, Rosario, Argentina
  
• Dr. Francisco J. Romero-Vidal, Barcelona, Spain
  
• Gerald J. Ross, MD, Pittsburgh, Pa
  
• Eric J. Russell, MD, Chicago, Ill
  
• Pierre-Jean Sauvage, MD, Mâcon, France
  
• Janet Scheraga, Syracuse, NY
  
• Steven M. Schultz, MD, Ft Worth, Tex
  
• Anthony J. Scuderi, MD, Johnstown, Pa
  
• Dr. Carlos Antonio Serrano, Olavarria, Argentina
  
• Matt Shapiro, MD, Lowell, Mass
  
• Taro Shimono, MD, Kyoto, Japan
  
• Paolo Siotto, MD, Cagliari, Italy
  
• David Sobel, MD, La Jolla, Calif
  
• Juan Carlos Spina, MD, Buenos Aires, Argentina
  
• Stacy Stevens, MD, San Antonio, Tex
  
• Peter M. Stroz, MD, Toronto, Ontario, Canada
  
• Franz Sulzer, MD, Kapfenberg, Austria
  
• Eugenio L. Suran, MD, Framingham, Mass
  
• J. Takasugi, Mercer Island, Wash
  
• Douglas L. Teich, MD, Brookline, Mass
  
• Shendee Teng, MD, Woodbridge, NJ
  
• Tapani Tikkakoski, MD, Kokkola, Finland
  
• Dr. Edgardo F. Torres, Rio Negro, Argentina
  
• Carlos E. Triana Rodriguez, Santafe de Bogota, Columbia
  
• Masataka Uetani, MD, Nagasaki, Japan
  
• Ruediger von Kummer, MD, Dresden, Germany
  
• Andrew L. Wagner, MD, Harrisonburg, Va
  
• Edward Williams, FRCR, Cayman Islands, BWI
  
• Peter Yang, La Mesa, Calif
  
• Joe Yut, Olathe, Kan
  
• Yu Zhang, Nagoya, Japan
  

	Acknowledgments

 
The author is grateful to Sabrina Jennings for her expert word-processing assistance throughout the preparation of this manuscript and to Ruth Gerger, who created maximum intensity projection images and provided MR technical assistance and expertise.

	References

TOP HISTORY IMAGING FINDINGS DISCUSSION References

 

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