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DOI:10.2214/AJR.07.3139
AJR 2008; 191:582-588
© American Roentgen Ray Society

Clinical Observations

MRI in Cerebral Schistosomiasis: Characteristic Nodular Enhancement in 33 Patients

Hanqiu Liu1, C. C. Tchoyoson Lim2,3, Xiaoyuan Feng1, Zhenwei Yao1, Yuanjun Chen4, Huaping Sun1 and Xingrong Chen1

1 Department of Radiology, Huashan Hospital, Fudan University, 12 Wulumuqi Zhong Rd., Shanghai, P.R. China, 200040.
2 Department of Neuroradiology, National Neuroscience Institute, Singapore.
3 Department of Radiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
4 Department of MRI, Yijishan Hospital, Wannan Medical College, Wuhu, P.R. China.

Received August 30, 2007; accepted after revision February 4, 2008.

 
Address correspondence to X. Feng (xyfeng{at}shmu.edu.cn).

CME

This article is available for CME credit. See www.arrs.org for more information.


Abstract
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 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
OBJECTIVE. The purpose of our study was to describe the characteristic MRI appearance of cerebral infection with Schistosoma japonicum.

CONCLUSION. Cerebral infection with S. japonicum can cause a characteristic MRI pattern of a large mass comprising multiple intensely enhancing nodules, sometimes with areas of linear enhancement. The typical appearance may be useful for diagnosis in endemic regions and may potentially be useful in cases imported into countries in which the disease is not endemic.

Keywords: cerebral schistosomiasis • diagnosis • MRI


Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Schistosomiasis is a chronic parasitic infection caused by trematode blood flukes of the genus Schistosoma [1–3]. Although schistosomiasis affects more than 200 million people in 77 countries, with an estimated annual mortality rate of 200,000, its public health importance is often underrated [1, 2]. Chronic schistosomiasis can lead to severe liver disease with fibrosis, portal hypertension, ascites, ruptured varices, and hepatic coma. Considerable morbidity and mortality can also result from intestinal complications, as well as cocarcinogenesis in the bladder and liver and rectal carcinoma. Three species of schistosomes commonly affect man: Schistosoma hematobium, Schistosoma mansoni, and Schistosoma japonicum [1, 2]. Endemic human schistosomiasis is ecologically most dependent on the presence of the snail intermediate host and the deposition of infected human excreta into freshwater habitat. Thus, schistosomal flukes are snail species-specific, and frequently geographically specific, distributed throughout much of the tropics and subtropics. S. mansoni is endemic to tropical Africa and parts of the Near East, northeastern South America, and the eastern Caribbean islands. S. hematobium is found in Africa and the Middle East, and S. japonicum is found exclusively in Asia, where it is endemic to southern and eastern China (including the middle and lower reaches of the Yangtze River), Taiwan, Japan, and the Philippines.

Ectopic migration of worms and oviposition can occur, resulting in a variety of lesions outside the gastrointestinal system, including the lungs and CNS, with S. japonicum typically affecting the brain, whereas S. mansoni and S. hematobium infections characteristically result in spinal cord lesions [4]. Despite the facts that CNS schistosomiasis is an important cause of focal epilepsy in endemic areas of the Far East and that cerebral involvement occurs in 1.6–4.3% of infected individuals [3, 5, 6], few studies of cerebral schistosomiasis have been reported [7–10]; the largest series of S. japonicum cerebral infection dates back to a review of 27 U. S. servicemen infected during the military reinvasion of Leyte in the Philippines during World War II [4]. Although there have also been several reports of cerebral schistosomiasis in the Chinese-language literature [11–15], recent neuroimaging descriptions in the English-language literature have been limited to case reports or small series of cerebral S. japonicum infection [7, 16], or descriptions of uncommon cerebral infection by S. mansoni or S. hematobium [17–22].

The clinical manifestations of cerebral schistosomiasis are variable; patients typically present with headache, acute encephalopathy, seizure disorders, and hemiparesis, which can simulate neoplasm both clinically and on neuroimaging [4, 21, 23]. In addition to being an important health problem in endemic areas, schistosomal infection can also be imported into nonendemic areas via immigration or travel. In such cases the diagnosis may not be straightforward if physicians and radiologists are unfamiliar with this disease. Therefore, knowledge of the typical MRI findings is valuable to confidently direct correct treatment and avoid unnecessary surgery. In this study, we describe the characteristic MRI findings of patients with cerebral schistosomal infection by S. japonicum.


Materials and Methods
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 Materials and Methods
Results
 Discussion
 References
 
We searched the radiology and pathology databases of two hospitals in Anhui province and Shanghai city for patients diagnosed with CNS schistosomiasis who underwent MRI between 2000 and 2005. These hospitals were both located in the Yangtze delta in China and are major tertiary referral centers for parasitology and neurologic diseases. Patient charts were reviewed for clinical presentation, neuroimaging, and final diagnosis by either examination of stool samples, serology for S. japonicum using the circumoval precipitin reaction test (COPT), or histologic examination of surgical samples. Thirty-three patients (23 male, 10 female; mean age, 41.8 years; range, 12–72 years) with a final diagnosis of cerebral schistosomiasis established by histologic examination or positive serology and serial neuroimaging were included in our study; patients with uncertain diagnosis or without neuroimaging were excluded. Informed consent was waived by the institutional review boards for this retrospective study.

MRI was performed using a 1.0- or 1.5-T MRI scanner equipped with the standard head coil with a 240 x 240 mm field of view. All MR examinations comprised at least a transverse T2-weighted fast spin-echo sequence (TR/TE, 3,800/98; section thickness, 8 mm), transverse FLAIR sequence (10,000/103; 8-mm section thickness), and T1-weighted sequences before and after IV contrast injection (320/12, 5- to 8-mm section thickness; gadopentetate dimeglumine, 0.1 mmol/kg). CT was performed using a variety of scanners and protocols, including contrast enhancement studies. All initial pretreatment MR images, as well as CT and MR images obtained during follow-up studies after treatment, were reviewed by unblinded consensus reading. The maximum diameter of the contrast-enhancing lesion was measured, and the location, appearance, and perilesional edema, if any, were recorded.


Results
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 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Clinical and Laboratory Findings
Twenty eight of the 33 patients lived in areas endemic for schistosomiasis, and the remaining five patients worked in endemic areas and were exposed to potentially contaminated fresh water. The clinical and MRI findings in patients with cerebral schistosomiasis are shown in Table 1. Twenty-three patients presented with headache, 12 had epilepsy or limb-jerking, and nine had focal neurologic signs such as hemiplegia, visual symptoms, or unsteady gait. The duration of symptoms ranged from 1 to 24 weeks. All were suspected of schistosomal infections and COPT serology was positive in 29 patients; stool samples were positive for Schistosoma species ova in nine patients.


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  		TABLE 1: Clinical and MRI Findings in Patients with Cerebral Schistosomiasis

 

Imaging Findings
Initial MR images at diagnosis showed a single mass lesion in 20 patients and multiple masses in 13 patients, yielding a total of 62 lesions for analysis. These lesions were located in the frontal (n = 27), temporal (n = 8), parietal (n = 6), and occipital (n = 4) lobes. Another seven lesions occupied multiple lobes, including the parietooccipital, frontoparietal, and frontotemporal regions. Six lesions were located in the cerebellar hemispheres, three in the basal ganglia and insula, and one in the mid brain. The maximum diameter of these lesions ranged from 0.9 to 7.2 cm (mean, 3.52 ± 1.48 cm). All cerebral lesions displayed long T1 and T2 signals and had prominent surrounding vasogenic edema and mass effect, such as ventricular or sulcal effacement and shift of midline structures. In 18 patients, the perilesional vasogenic edema showed a deeper edge that was smooth with regular and multiple finger-like projections into the subcortical white matter (Fig. 1A).


Figure 1
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  		Fig. 1A —47-year-old woman with cerebral schistosomiasis and 2-week history of headache and seizures. Sagittal T2-weighted (A) and axial T1-weighted (B) MR images show prominent vasogenic edema in frontal and parietal lobes, with well-defined deep surface and fingerlike projections (arrow, A) into subcortical white matter.

 
After IV contrast administration, all lesions were noted to comprise multiple intensely enhancing nodules clustered together in a large mass (Figs. 1A, 1B, 1C, 1D, 2A, 2B, 3A, and 3B). These were usually small discrete nodules, 1–3 mm in diameter with well-defined margins, but in some patients they consisted of larger central confluent enhancing masses surrounded by smaller discrete nodules in the periphery of the lesion (Figs. 2A and 2B). Although two patients had a focal area of intralesional hemorrhage, no evidence of cystic degeneration or necrosis was seen. Seventeen patients had areas of linear enhancement in addition to the enhancing nodules (Fig. 3B).


Figure 2
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  		Fig. 1B —47-year-old woman with cerebral schistosomiasis and 2-week history of headache and seizures. Sagittal T2-weighted (A) and axial T1-weighted (B) MR images show prominent vasogenic edema in frontal and parietal lobes, with well-defined deep surface and fingerlike projections (arrow, A) into subcortical white matter.

 

Figure 3
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  		Fig. 1C —47-year-old woman with cerebral schistosomiasis and 2-week history of headache and seizures. Axial (C) and coronal (D) T1-weighted images after IV administration of contrast material show multiple intensely enhancing small nodules, 1–3 mm in diameter (arrows), clustered closely together. Second cluster in right frontal lobe superiorly is poorly seen because of partial volume effects.

 

Figure 4
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  		Fig. 1D —47-year-old woman with cerebral schistosomiasis and 2-week history of headache and seizures. Axial (C) and coronal (D) T1-weighted images after IV administration of contrast material show multiple intensely enhancing small nodules, 1–3 mm in diameter (arrows), clustered closely together. Second cluster in right frontal lobe superiorly is poorly seen because of partial volume effects.

 

Figure 5
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  		Fig. 2A —67-year-old woman with headache and seizures for 1 week. Axial contrast-enhanced MR images show large confluent enhancing mass (arrows) in left frontal lobe and multiple small nodules in periphery (arrowheads).

 

Figure 6
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  		Fig. 2B —67-year-old woman with headache and seizures for 1 week. Axial contrast-enhanced MR images show large confluent enhancing mass (arrows) in left frontal lobe and multiple small nodules in periphery (arrowheads).

 

Figure 7
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  		Fig. 3A —13-year-old boy with headache and seizures for 1 week. Axial (A) and sagittal (B) contrast-enhanced MR images show multiple discrete enhancing nodules (arrows) clustered around area of central linear enhancement (arrowheads).

 

Figure 8
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  		Fig. 3B —13-year-old boy with headache and seizures for 1 week. Axial (A) and sagittal (B) contrast-enhanced MR images show multiple discrete enhancing nodules (arrows) clustered around area of central linear enhancement (arrowheads).

 
Diagnosis, Treatment, and Follow-Up Imaging
Eleven patients underwent surgical resection; histologic examination showed chronic granulomatous inflammation with giant cells, lymphocytes, and fibroblasts surrounding refractile ovoid structures that could be identified as schistosome eggs (Fig. 4). No adult worms were seen in any of the specimens. The remaining 22 patients were treated non-surgically with praziquantel and corticosteroid therapy, with resolution of clinical symptoms and seizures. In all patients, follow-up CT (six patients) or MRI (16 patients) obtained 2 months after treatment showed complete resolution of the enhancing lesions and perilesional edema (Figs. 5A, 5B, 5C, and 5D).


Figure 9
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  		Fig. 4 —51-year-old man with cerebral schistosomiasis and 4-week history of right hand jerking. Photomicrograph of histologic section shows granuloma formation around characteristic Schistosoma japonicum ova (arrows). Note absence of protruding spines, unlike other schistosomal species. (H and E, x200)

 

Figure 10
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  		Fig. 5A —52-year-old man with 8-week history of headache and right hemianopia. FLAIR (A) and coronal contrast-enhanced (B) MR images show enhancing nodules (arrow, B) surrounded by vasogenic edema in left occipital, parietal, and bilateral frontal lobes.

 

Figure 11
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  		Fig. 5B —52-year-old man with 8-week history of headache and right hemianopia. FLAIR (A) and coronal contrast-enhanced (B) MR images show enhancing nodules (arrow, B) surrounded by vasogenic edema in left occipital, parietal, and bilateral frontal lobes.

 

Figure 12
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  		Fig. 5C —52-year-old man with 8-week history of headache and right hemianopia. Two months after treatment, images corresponding to A and B show near-complete resolution of abnormal FLAIR signal and enhancement.

 

Figure 13
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  		Fig. 5D —52-year-old man with 8-week history of headache and right hemianopia. Two months after treatment, images corresponding to A and B show near-complete resolution of abnormal FLAIR signal and enhancement.

 

Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
We found that in 33 patients with a presumptive diagnosis of cerebral schistosomiasis caused by S. japonicum, MRI showed large discrete lesions with prominent perilesional edema; the lesions were composed of characteristic multiple enhancing nodules, sometimes with areas of linear enhancement. Early CT reports of cerebral schistosomiasis have described single or multiple hyperdense lesions with variable enhancement surrounded by low-density edema and associated mass effect [16, 17, 19, 23]. Previous case reports of MRI findings in cerebral schistosomiasis caused by S. mansoni and S. hematobium have also described a variable enhancement pattern, using such terms as "diffuse," "spotty," or "nodular" [18, 19, 22, 24]. In one study of two cases of S. mansoni cerebral schistosomiasis and one case of mye lopathy, a pattern of large lesions with linear and nodular enhancement was described, similar to that seen in our patients [21].

Our review of cerebral schistosomiasis caused by S. japonicum shows similar MRI features as in the lesions caused by S. mansoni, although linear enhancement may not be detected in all patients and may be due to unresolved tiny adjacent nodules aligned in a row. Similarly, several reports in Chinese-language journals have also documented multiple punctuate enhancing lesions on MRI in S. japonicum [11–14]. As far as we are aware, this study represents the largest series of MRI describing these characteristic nodular and linear enhancing features. With the limited reports available, our findings suggest that this appearance may be common to cerebral schistosomiasis caused by both endemic S. japonicum and imported cases of S. mansoni.

This pattern of discrete nodular and linear enhancing nodules has not been described in association with other CNS worm infections (such as neurocysticercosis or paragonimiasis), tuberculoma, or neoplastic disease processes; it has been suggested that when this unique "arborized" pattern is observed, a diagnosis of CNS schistosomiasis should be considered [21]. Although the definitive diagnosis of cerebral schistosomiasis is based on the visualization of eggs or adult worms in the CNS tissue at histologic examination, a presumptive diagnosis can be made on the basis of coincidence of brain lesions on CT or MRI, evidence of schistosome infection, and exclusion of other causes of neurologic disease [1, 2]. Hence, in patients with a combination of neurologic symptoms, positive exposure, and serology or stool samples positive for schistosomiasis, and the typical MRI appearance of clustered linear and nodular enhancement, it may be possible to make a prospective diagnosis. In 22 of our patients, the current treatment regimen of praziquantel [7] combined with corticosteroids resulted in resolution of clinical and neuroimaging abnormalities; in these patients the characteristic MRI features allowed a confident prospective diagnosis and played a role in avoiding unnecessary surgery.

The enhancing nodules seen in our patients are probably granuloma formation surrounding the schistosome egg; these lesions are believed to represent miliary pseudotubercles similar to those of Mycobacterium tuberculosis [10]. On histologic examination, the morphology and location of the ova spine (absent, lateral, or terminal in S. japonicum, S. mansoni, and S. hematobium, respectively) can be useful for identifying the schistosomal species even if the MRI features may not be useful for distinguishing them.

Schistosoma species have a complex life cycle [1, 2]: Cercariae released into streams or lakes by freshwater snails (the intermediate hosts) penetrate human skin and migrate to the lungs and liver, where they mature to form mating pairs of male and female adult worms in the mesenteric veins. The S. japonicum worms complete the cycle by fecal shedding of eggs into contaminated waterways and the snail host is subsequently invaded. The leading theory proposed to explain how the ova reach the CNS to cause ectopic schistosomiasis postulates that during periods of increased intraabdominal pressure (e.g., during defecation), the adult worms may enter the intercommunicating Batson's plexus, which drains into the internal jugular vein, and gain access to the dural sinus [3]. The worms are thus carried to the CNS through retrograde venous blood flow via venous anastomosis, reaching the brain directly from the abdominal cavity without going by way of the heart or lungs. Physical egg characteristics appear to influence venous access to the CNS: S. japonicum eggs are smaller and are shed in much greater numbers (an adult worm typically sheds hundreds to thousands of eggs daily); hence, they travel relatively easily to reach the brain. On the other hand, S. mansoni and S. hematobium eggs, which are larger and bear protruding spines, have a tendency to lodge in the lower vertebral plexus to infect the lower spinal cord and only rarely affect the brain [2].

The cause of linear enhancement on MRI is more obscure, and there have been no previous studies with histologic correlation. In the only other report describing nodular and linear enhancement, the authors postulate that these findings may be the result of worms causing local leptomeningeal vein obstruction and slow blood flow, leading to ova concentration and forming a nodular mass [21].

This article focuses exclusively on patients in a geographically endemic area and is limited by selection bias and incomplete retrospective review of clinical characteristics. Praziquantel, the treatment of choice for schistosomiasis, is effective against many worm species, and concurrent infection with other parasites in our patients cannot be completely excluded. Future prospective studies may benefit from better documentation of serology and may examine whether there are imaging features of hepatic schistosomiasis that may predict ectopic CNS infection.

Although imported schistosomiasis is rare in nonendemic countries because of better sanitation and the absence of appropriate snail intermediate hosts, the presence of an immigrant population from endemic areas and the increase in worldwide travel for business and pleasure mean that the number of individuals exposed to schistosomal infection may be increasing. A positive history of travel in endemic areas and exposure to contaminated fresh water, including activities such as swimming, bathing, boating, or washing clothes, should be sought. Travelers at greatest risk include backpackers, boating enthusiasts, soldiers, and local workers such as Peace Corp volunteers and missionaries [2]. As with other parasitic infections uncommonly encountered in developed countries, the key to establishing the diagnosis of schistosomiasis is to consider the possibility in the first place [2]. In cases of suspected cerebral schistosomiasis, the characteristic MRI pattern of clustered nodular enhancement may be useful for noninvasive diagnosis and to avoid unnecessary surgery.


References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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