(Radiology. 1999;211:472-476.)
© RSNA, 1999
Case 10: Neurocysticercosis1
Andrew W. Litt, MD and
Tamara Mohuchy, MD
1 From the Department of Magnetic Resonance Imaging, New York University Medical Center, 530 First Ave, New York, NY 10016. Received March 2, 1998; revision requested April 16; revision received July 22; accepted August 17. Address reprint requests to A.W.L.
Index terms: Brain, CT, 10.12112 • Brain, MR, 10.121411, 10.12143 • Brain, parasites, 10.2083 • Cysticercosis, 10.2083 • Diagnosis please
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HISTORY
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The patient is a 33-year-old, right-handed woman with no noteworthy medical history. She presented with a chief complaint of three distinct episodes of focal seizures of the left side of the face and left arm that lasted for approximately 3 minutes each. Historical information includes no loss of consciousness, no history of trauma, and no dental work or foreign travel. She is a practicing Orthodox Jew, and her religion prohibits ingestion of pork. She has employed a Mexican housekeeper in her home for several years. On physical examination, the patient displayed a mild left facial paresis, otherwise the remainder of her neurologic examination was intact. She was seen in the emergency department, and imaging was performed.
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IMAGING FINDINGS
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Contrast material–enhanced computed tomographic (CT) (GE Medical Systems, Milwaukee, Wis) and magnetic resonance (MR) imaging (Siemens, Iselin, NJ), including an echo-planar perfusion study, were performed. Axial T1-weighted images obtained following the intravenous administration of 469.01 mg/mL gadopentetate dimeglumine (Magnevist; Berlex, Wayne, NJ) demonstrated the presence of a single, small, spherical ring-enhancing lesion at the corticomedullary junction of the right frontal lobe. The ring is regular in its margins; however, it appears to contain a focal thickening posteriorly consistent with a mural nodule. The center is hypointense to brain yet appears higher in signal intensity than cerebrospinal fluid (Fig 1a). On corresponding T2-weighted images, the ring and the posterior mural nodule appear hypointense with a hyperintense center. A substantial amount of perilesional vasogenic edema is present (Fig 1b).
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Figure 1a. (a) Postcontrast axial T1-weighted spin-echo MR image (600/14 [repetition time msec/echo time msec], 5-mm section thickness, 250-mm field of view, 250 x 256 matrix, acquisition time of 4 minutes 9 seconds) shows a 1-cm mass with ring enhancement (long arrow), slightly thickened posteriorly (short arrow), at the corticomedullary junction in the right frontal lobe. The center of the lesion is mildly hypointense to white matter. A small amount of decreased signal intensity in adjacent white matter represents vasogenic edema (arrowhead). (b) Corresponding axial T2-weighted turbo spin-echo MR image (3,400/119, 5-mm section thickness, 250-mm field of view, 250 x 256 matrix, acquisition time of 2 minutes 58 seconds) shows a well-defined, thin, hypointense capsule (long arrow) with posterior thickening (short arrow). The center of the lesion is hyperintense. Vasogenic edema (arrowhead) is clearly depicted.
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Figure 1b. (a) Postcontrast axial T1-weighted spin-echo MR image (600/14 [repetition time msec/echo time msec], 5-mm section thickness, 250-mm field of view, 250 x 256 matrix, acquisition time of 4 minutes 9 seconds) shows a 1-cm mass with ring enhancement (long arrow), slightly thickened posteriorly (short arrow), at the corticomedullary junction in the right frontal lobe. The center of the lesion is mildly hypointense to white matter. A small amount of decreased signal intensity in adjacent white matter represents vasogenic edema (arrowhead). (b) Corresponding axial T2-weighted turbo spin-echo MR image (3,400/119, 5-mm section thickness, 250-mm field of view, 250 x 256 matrix, acquisition time of 2 minutes 58 seconds) shows a well-defined, thin, hypointense capsule (long arrow) with posterior thickening (short arrow). The center of the lesion is hyperintense. Vasogenic edema (arrowhead) is clearly depicted.
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A CT scan obtained after the administration of 150 mL of iothalamate meglumine (Conray; Mallinckrodt, St Louis, Mo) more clearly demonstrates the regularity of the ring and the presence of a small enhancing mural nodule with surrounding vasogenic edema (Fig 2). Nonenhanced imaging was not performed. Perfusion imaging of the lesion and surrounding T2 signal intensity abnormality revealed absence of hyperperfusion. Normal perfusion of the surrounding cortex was clearly visible (Fig 3).
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Figure 2. Postcontrast axial CT scan also shows thin, regular ring enhancement (long arrow). A discrete mural nodule (short arrow) enhances along the posterior aspect of the capsule. Subtle edema is present (arrowhead).
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Figure 3. Color overlay on a T2*-weighted echo-planar MR image (0.8/54; 90° flip angle; 5-mm section thickness; 215-mm field of view; 128 x 128 matrix; acquisition time of 1 minute, seven sections, 60 measures) shows no demonstrable perfusion abnormality in the underlying region of increased T2 signal intensity and reflects the perilesional edema (arrowhead). The color overlay image has a threshold to depict normal cortical perfusion as green (arrow).
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DISCUSSION
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The diagnostic considerations of a small, spherical, ring-enhancing lesion with a regular margin located at the corticomedullary junction and displaying a substantial amount of vasogenic edema include a variety of lesions in a patient seemingly without a contributory history. The leading differential diagnosis to be excluded in an adult presenting with a seizure in this country is metastases, which characteristically lodge at the corticomedullary junction, can enhance in a ringlike pattern, and often incite more edema than expected for the size of the lesion. Primary neoplasms are more likely to be heterogeneous with irregular borders.
Cerebral abscesses may also be considered because of the typical location at the corticomedullary junction and the thin, regular capsule formation that appears hypointense on T2-weighted images (1). Causes include bacterial, fungal, or granulomatous agents that evolve from an early cerebritis and extensive T2 signal intensity abnormality to central necrosis and capsule formation. Parasitic infection, such as neurocysticercosis, paragonimiasis, or echinococcus infection, can be considered, especially with knowledge of patient origin or travel to a region where the disease is endemic (2). Less likely, a subacute infarction or resolving hematoma of the cortex rarely enhances in a ring pattern; however, the patient's history should include prior symptoms.
The lack of hyperperfusion of the lesion makes the diagnosis of a neoplastic process unlikely, which leads us to an infectious cause. In this case, however, the differential diagnosis can be further narrowed because of the additional imaging finding of a discrete mural nodule that enhances following the intravenous administration of contrast material and appears hypointense on T2-weighted images. These imaging findings point to neurocysticercosis as the most likely diagnosis rather than to a bacterial abscess.
Moreover, the small size and spherical shape of the lesion are typical of a parenchymal cysticercal abscess, which is usually approximately 1 cm in diameter (range, 4–20 mm) and displays a characteristic spherical shape (3). The mural nodule is consistent with the scolex, which is usually 2–3 mm in diameter. The surrounding edema suggests that the parasite is in its degenerative or colloidal state, and, therefore, enhancement of the abscess capsule and scolex will occur avidly. In addition, the central T1 signal that appears hypointense to white matter but hyperintense to cerebrospinal fluid and appears markedly hyperintense on T2-weighted images reflects the proteinaceous nature of the cyst fluid during involution of the cysticercus (4). Enhancement is unusual in the earlier vesicular stage, when the larva is still viable and the cyst is antigenically inert and therefore does not incite an edematous reaction. Also, in the nodular calcified stage, when the cystic lesion is mineralized and shrunken and a nonenhanced CT scan is diagnostic, enhancement is unusual (5).
Although the patient's age, the size and imaging appearance of the abscess capsule, the presence of a mural nodule and perilesional edema, and the lack of hyperperfusion support the diagnosis of a cysticercal abscess, the lack of contributory history at the time of presentation confounded the imaging evidence, and the option of surgical biopsy was pursued by the referring physicians to confirm the diagnosis of an abscess caused by cysticercosis. We were initially averse to the diagnosis of neurocysticercosis because of the patient's abstinence from pork ingestion. However, as a more detailed history was uncovered, it was learned that the housekeeper emigrated from Mexico and was infected with cysticercosis. The patient was infected either by ingesting ova in contaminated food or after direct contact and transfer of ova from hand to mouth.
Neurocysticercosis is the most common parasitic infection involving the central nervous system in developing countries. It is endemic to Mexico, South America, Africa, eastern Europe, Asia, and Indonesia, where neurocysticercosis is the most common cause of adult-onset epilepsy. The disease has also become more prevalent in developed countries secondary to an increase in immigration and travel (6).
Humans become infested with the causative agent, the adult pork tapeworm, Taenia solium, by ingesting ova residing in contaminated food or water or in undercooked pork containing its larvae. Neurocysticercosis is acquired by ingesting ova in food contaminated by infected human feces and, less commonly, by autoinfection through the fecal-oral route. The ingested ovum matures to its larval stage, which penetrates human intestinal mucosa and spreads hematogenously to finally encyst in the central nervous system, eyes, muscle, and skin (2). Although this patient did not ingest pork because of her religious background, her housekeeper and baby-sitter was from Mexico and was later shown to be infected with cysticercosis. Transmission was probably through poor sanitation in the handling of food. This is an increasingly common method of infection in the United States (7).
In the central nervous system, cysticercosis can affect the brain parenchyma and can seed the subarachnoid space, intraventricular system, and spine, usually in a subarachnoid location and, less commonly, within the cord itself. Symptoms and imaging findings depend on the location of the infection. In the brain parenchyma, the larva undergoes an orderly life cycle, from cysticercus to involution. These pathologic stages can be correlated with the progressive radiologic appearance of the lesion (8).
The first stage, described as the larval tissue invasion phase, is not normally imaged owing to lack of symptoms at this very early stage. However, as observed in one study (9) in which imaging was performed regularly to follow anticysticercal therapy, this phase appears as a localized focus of edema on T2-weighted images and displays nodular tissue enhancement following the administration of gadopentetate dimeglumine.
The second stage is referred to as the vesicular stage and describes the formation of a cyst that encircles the scolex. These cysts are typically 1-2 cm, and the scolex is approximately 2–4 mm (2). The cyst is thin walled and contains clear fluid. The lesion is antigenically inert and therefore does not incite an inflammatory reaction or circumferential edema (8). At MR imaging and CT, these features correspond to a cystic structure with a thin-walled capsule that rarely enhances. Internally, the cyst fluid parallels cerebrospinal fluid intensity, and the scolex appears as a mural nodule that is isointense with brain parenchyma. The patient will also usually remain asymptomatic at this stage (9).
The third stage is the colloidal stage in which the parasite dies, and as a result the cysticercus becomes nonviable. The metabolic breakdown results in a local inflammatory response and capsule and granulation tissue formation with breakdown of the blood-brain barrier, resulting in avid ring enhancement (10). As the scolex dies, the cyst fluid transforms into a colloidal suspension containing protein solutes, which results in T1 shortening. The scolex and cyst capsule are decreased in T2 signal intensity. At CT, cystic contents increase in attenuation (11). Symptoms become evident during this stage of evolution secondary to the presence of inflammation and edema. The most common manifestation is seizure, followed by headache and signs of increased intracranial pressure (9).
The fourth stage is the nodular granular stage and represents the degeneration of the cysticercus. The perilesional edema begins to subside gradually, the cyst involutes, and the contents begin to mineralize. The lesion becomes isointense with brain parenchyma on T1-weighted MR images and hypointense on T2-weighted MR images. At CT, the lesion becomes isoattenuating, and a thick nodular ring continues to enhance (10).
The final stage is the calcified stage, which describes complete involution of the lesion with continued mineralization. The calcifications are obvious at CT and show susceptibility at MR imaging, particularly on gradient-echo images (9). This phase is generally asymptomatic, although recent study findings (4) suggest that persistent contrast enhancement is associated with continued posttreatment seizures.
Subarachnoid (racemose) neurocysticercosis usually infiltrates the basal cisterns and sylvian fissures. The cysts may grow to several centimeters. They are nonviable and do not contain a scolex. They are associated with a local meningeal inflammatory reaction that results in fibrosis and hydrocephalus. Therefore, symptoms are obstructive in nature (9). Rarely, neurocysticercosis can manifest merely as leptomeningeal enhancement in the basal cisterns without actual cyst formation. This inflammatory response can incite a vasculitic phenomenon that affects the basal perforating vessels and results in scattered infarctions. Administration of contrast material is necessary for evaluation (12).
Intraventricular cysts also manifest as symptoms of increased intracranial pressure. However, the lesions are usually clinically silent until obstruction occurs, secondary to either the location of the cystic lesion or associated ependymitis caused by an adjacent granulomatous response. Owing to the isoattenuating characteristics of the intracystic fluid, the lesions are occult at CT (12). They are, however, more conspicuous at MR imaging and are also associated with aqueductal stenosis, which may be secondary to coexisting ependymitis or adhesions from prior ventricular inflammation (9).
Spinal lesions are not common, and they are usually subarachnoid and result in arachnoiditis. Intramedullary lesions have been reported and manifest as myelopathic symptoms. Differential diagnosis includes a cystic neoplasm (13).
Our congratulations to the 179 individuals who submitted the most likely diagnosis (neurocysticerosis) for Diagnosis Please, Case 10. Their names and locations, as submitted, are as follows:
- Gholamali Afshang, MD, Tinley Park, Ill
- Anjali Agrawal, MD, Houston, Tex
- David R. Anderson, MD, Richmond, Va
- Günther Antes, MD, Kempten, Germany
- Roger L. Antonelli, MD, Dayton, Ohio
- Lionel Arrivé, MD, Paris, France
- William W. Atherton, DC, Chesterfield, Mo
- Edward L. Baker, MD, San Francisco, Calif
- Kenneth Baliga, MD, Rockford, Ill
- Zubin N. Balsara, MD, Fort Smith, Ark
- Dr. Hans Bender, Krefeld, Germany
- Richard Benedikt, MD, San Antonio, Tex
- Sonia Bermúdez, Santafé de Bogotá, Colombia
- Rita J. Blom, Errington, British Columbia, Canada
- Antonio Botero, MD, Bogota, Colombia
- Adrian Brady, FFRRCSI, FRCR, Cork, Ireland
- Giuseppe Brancatelli, Palermo, Italy
- Eric Bressler, MD, Minnetonka, Minn
- Michael P. Buetow, MD, Okemos, Mich
- Steven J. Burbidge, MD, Minneapolis, Minn
- Claudio Campi de Castro, Sao Paulo, Brazil
- Ramón Carabajal, MD, Tucamán, Argentina
- Betty Ann Caravella, MD, Port Washington, NY
- James Carrico, MD, Ashland, Kan
- Tirso Cascajares Murillo, Los Mochis, Sin, Mexico
- Nancy Chandler, MD, Greenville, Miss
- Hearns W. Charles, MD, New York, NY
- Chris Chernesky, MD, Oakland, Calif
- Royce A. Chrys, MD, Oakland, Calif
- Wiluck Chu-Ongsakul, MD, Bangkok, Thailand
- Allen J. Cohen, PhD, MD, Orange, Calif
- Martin I. Cohen, MD, Westlake Village, Calif
- Michael A. Cook, DO, Staten Island, NY Y-S Cordoliani, MD, Paris, France
- David A. Cory, MD, South Bend, Ind
- Burkhardt Danz, MD, Ulm, Germany
- David R. DeLone, Madison, Wis
- Jacques F. Demers, MD, La Pocatière, Québec, Canada
- Dra. Estela Di Nella, Buenos Aires, Argentina
- Dra. Monica S. Donadi, Olavarria, Argentina
- Luiz Carlos Donoso Scoppetta, Sao Paulo, Brazil
- Kenneth H. Elson, Jr, MD, Omaha, Neb
- Keith D. Epperson, MD, Milwaukee, Wis
- Richard Farb, MD, Toronto, Ontario, Canada
- Nancy J. Fischbein, MD, San Francisco, Calif
- Andrew Fisher, MD, St Louis, Mo
- Eric K. Fitzcharles, MD, Lexington, Ky
- Lee Foo Cheung, MD, Angouleme, France
- Rainer Frank, MD, Krefeld, Germany
- Arnold C. Friedman, MD, New York, NY
- Akira Fujikawa, MD, Tokyo, Japan
- Raimundo Sergio Furtado de Oliveira, MD, Rio de Janeiro, Brazil
- Gary E. Galens, MD, Farmington Hills, Mich
- Martin Garcia Perez, Almeria, Spain
- Jorge M. Garin Ferreira, Caceres, Spain
- Dietrich Gerhardt, MD, Iowa City, Iowa
- Abner Gershon, MD, Hartford, Conn
- Mazen Ghani, MD, Springfield, Mass
- Ronald B. J. Glass, MD, New York, NY
- Ken Goldberg, MD, Maywood, Ill
- Mark Goldshein, MD, Andover, Mass
- Daniel S. Gordon, MD, Sanford, NC
- Walter O. Grauer, MD, Zurich, Switzerland
- Harold R. Griffith, MD, La Jolla, Calif
- Hugo R. Guerra, MD, Quito, Ecuador
- Flavius Guglielmo, MD, Basking Ridge, NJ
- F. Tahsin Guneysu, MD, Brussels, Belgium
- Ferris Hall, MD, Boston, Mass
- Robert T. Harvey, MD, Philadelphia, Pa
- Rufus W. Head, MD, No Bridgton, Me
- Richard Herman, MD, Newton, Mass
- Helen T. Ho, MD, Chicago, Ill
- Carlos Holguera Blazquez, MD, Madrid, Spain
- Lowrey H. Holthaus, MD, Richmond, Va
- Christophe Ide, MD, Namur, Belgium
- Maurillio Indiani, S J dos Campos, Brazil
- Victor Iyer, MD, Stockholm, Sweden
- Dany Jasinowodolinski, Sao Paulo, Brazil
- Blake Johnson, MD, Minneapolis, MN
- James C. Johnson, MD, Salisbury, NC
- Aron Judkiewicz, MD, Tarzana, Calif
- Douglas S. Katz, MD, Mineola, NY
- Jennifer L. Kemp, MD, Denver, Colo
- Scott Kennedy, MD, Concord, NC
- H. Khoshnevis, MD, Copperas Cove, Tex
- Arlene Klink, MD, Bronx, NY
- Craig D. Korbin, Weston, Mass
- Richard Krauthamer, MD, Torrance, Calif
- David P. Kunz, MD, Newburgh, NY
- Jeffrey N. Lang, MD, New York, NY
- David S. Liebeskind, MD, Los Angeles, Calif
- Joseph H. Lock, Jr, MD, Mankato, Minn
- Jesus M. Longo, MD, Oviedo, Spain
- David R. Ludwig, MD, Amherst, NY
- Stephen C. Machnicki, MD, New York, NY
- Frank Maguire, MD, St Paul, Minn
- Leslie Marshall, Kensington, Md
- Kathlyn Marsot Dupuch, Paris, France
- Jeffrey J. McClure, MD, Grand Rapids, Mich
- Andrew McDonnell, MD, Corning, NY
- Dr. Breda Mc Manus, MBBCh, BAO, MRCP, Manchester, United Kingdom
- Mitesh Mehta, MD, Toronto, Ontario, Canada
- Edward Menges, MD, Aptos, Calif
- Dina Miklic, MD, Zagreb, Croatia
- Mansour Mirfakhraee, MD, Shreveport, La
- Hidetoshi Miyake, MD, Oita, Japan
- Sergio J. Moguillansky, MD, Rio Negro, Argentina
- Dr. Eduardo Mondello, Buenos Aires, Argentina
- Kirk Moon, MD, San Francisco, Calif
- Toshio Moritani, MD, Tokyo, Japan
- Bernard Mouillet, MD, Angouleme, France
- Lyn Nadel, MD, Miami, Fla
- Miguel E. Nazar, MD, Capital Federal, Argentina
- Vung D. Nguyen, MD, San Antonio, Tex
- Albert Nizzero, MD, Sudbury, Ontario, Canada
- Samir E. Noujaim, MD, Royal Oak, Mich
- Juliana Oliveira, MD, Porto Alegre, Brazil
- Sanford M. Ornstein, Phoenix, Ariz
- David M. Panicek, MD, New York, NY
- Ulisses C. Parente, MD, Belo Horizonte, Brazil
- Narendrakumar Patel, MD, Newburgh, NY
- Maria Carolina Perez, Santafe de Bogota, Colombia
- Dr. Roberto Perez Gautrin, Sonora, Mexico
- Amir B. Perez Lanz, MD, Tabasco, Mexico
- Dirk Perdieus, MD, Bonheiden, Belgium
- Carlo L. Petralli, MD, Bruderhold, Switzerland
- John M. Plotke, MD, Naperville, Ill
- P. B. Pressel, Rixheim, France
- G. Lee Pride, Jr, Dallas, Tex
- Nasrollah Rahbar, MD, Missouri City, Tex
- Sandeep K. Rao, MD, Farmington Hills, Mich
- Enrique Remartinez Escobar, MD, Melilla, Spain
- Marco A. Rocha Mello, MD, Sao Paulo, Brazil
- Javier Rodriguez Lucero, MD, Rosario, Argentina
- Derek J. Roebuck, FRACR, Hong Kong, China
- Gerald Ross, MD, Pittsburgh, Pa
- Arnold Rotter, MD, Duarte, Calif
- Scott J. Rowen, MD, Orange, Calif
- Joel Rubenstein Siram Satyanath, Hauppauge, NY
- Dr. Bernhard Schulte, Cologne, Germany
- Steven M. Schultz, MD, Fort Worth, Tex
- Joel Schwartz, MD, Irvington, NY
- James N. Scott, MD, Calgary, Alberta, Canada
- Anthony J. Scuderi, MD, Johnstown, Pa
- Kevin J. Sentell, MD, Jackson, Tenn
- Matt Shapiro, MD, Boxborough, Mass
- David L. Sherr, MD, Manhasset, NY
- Dr. Alessandro Sias, Cagliari, Italy
- PD Dr. Guenther Sigmund, Trier, Germany
- Michael Silberman, MD, Durham, NC
- Martin D. Simms, MD, FRCPC, Chattanooga, Tenn
- Cory Singer, MD, Bedford, NY
- Paolo Siotto, MD, Cagliari, Italy
- James F. Smith, Columbia, Mo
- David Sobel, La Jolla, Calif
- Thomas Solbach, Ulm, Germany
- Paul Stark, MD, Palo Alto, Calif
- Michael S. Stecker, MD, Iowa City, Iowa
- Janio Szklaruk, MD, PhD, Philadelphia, Pa
- Jean-Bernard Tallon, MD, D'Angouleme, France
- Luciano Targa, MD, Porto Alegre, Brazil
- Helena M. Taylor, MD, London, United Kingdom
- Douglas L. Teich, MD, Hermosa Beach, Calif
- Magnus Tengvar, MD, Stockholm, Sweden
- Andrew L. Tievsky, MD, Washington, DC
- John S. To, MD, Iron Mountain, Mich
- Carlos E. Triana Rodriguez, Santafe de Bogota, Colombia
- Juan Antonio Valdez, MD, Miami, Fla
- Edwin J. R. van Beek, MD, PhD, Sheffield, United Kingdom
- H. Wouter van Es, MD, Nieuwegein, the Netherlands
- Pedro T. Vieco, MD, Woodinville, Wash
- Andrew L. Wagner, MD, Durham, NC
- George Wakefield, MD, Montgomery, Ala
- K. Ted Wickstrom, MD, Glendale, Ariz
- Joseph T. Wroblicka, MD, Iowa City, Iowa
- Peter J. Yang, La Mesa, Calif
- Jorge Massayuki Yokochi, MD, Curitiba, Brazil
- Dahua Zhou, MD, East Meadow, NY
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HISTORY
IMAGING FINDINGS
