MR Findings of Degenerating Parenchymal N eu rocyst icercos is 1

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1 Journal of the Korean Radiologica l Society 1996 : 34(6) : MR Findings of Degenerating Parenchymal N eu rocyst icercos is 1 Yul Lee, M.D., EunA Chung, M.D., IkYang, M.D., HaeJung Park, M.D., Soo Young Chung, M.D. Purpose: To evaluate MR imaging findings of degenerating parenchymal neurocysticercosis and to determine the characteristics which distinguish it from other brain diseases. Methods : MR imagings of 19 patients (56 lesions) of degenerating parenchymal neurocysticercosis were retrospectively evaluated, focusing on the size and location of lesions, signal intensity patterns of cyst fluid and wal l. the extent of the surround ing edema and features of contrast enhancement. Results: Degenerating parenchymal neurocysticercosis was located in gray or subcortical white matter in 89.3% of 56 lesions{50/ 56); most of these (98.2%) were smallerthan 2cm in diameter. Cyst fluid signal was hyperintense relativeto CSF on T1 and proton density weighted images (92.9%). A hypointensesignal rim of the cyst wall was noted i n the lesions on proton density (92.9%) and T2 weighted (98.2%) images. Surrounding edema was mostly mild. Peripheral rim enhancement was noted in all lesions, and this was frequently irregular and lobulated (67.9%) with a focal defect in the enhancing rim (41.1 %). Conclusion: Findings which could be helpf 비 in distinguishing degenerating parencymal neurocysticercosis from other brain diseases are as follows: small, superficiallesions ; hyperintense signal of the cyst fluid on T1 and proton density weighted images; hypointense signal of the cyst wall on proton density and T2 weighted images; relatively mild extent of surrounding edema, and peripheral rim enhancement which is frequently irregular and lobulated with a focal defect in the enhancing rim. Index Words: Brain, MR Brain, parasites Cysticercosis Parasites INTRODUCTION Neu rocysticercosis is a central nervous system manifestation of cysticerci, the la rvae of Taenia solium and worldwide is the most common par asitic disease affecting the brain (1-4). The usual-and well knowncomputed tomography (CT) and magnetic resonance imaging (MR I) findings of parenchymal neurocysticercosis are multiple cystic masses contain ing a characteristic scolex (4-9). Degeneration of the worm, how- ever, causes inflammation, edema and contrast enhancement and it is sometimes difficult to distinguish it from other diseases such as metastases, primary brain tumors, abscesses, or other inflammatory granulomas (4-1 1). We retrospectively evaluated the MRls of 19 cases (56 cysts) of parenchymal neurocysticercosis showing manifestations of degeneration to determine the characterstics which distinguish it from other brain diseases MATERIALS and METHODS 'Department olradiology, Kangnam Sungshim Hospital, Hallym University MRls of 28 cases of parenchymal neurocysticercosis Received October 25, 1995: Accepted January 15, 1996 were retrospectively reviewed ; cases of cisternal and Address reprint requests to :Yul Lee, M.D., Department 01 Radiology. ventricular cysticercosis were not included in this Kangnam Sungshim Hospi tal, Hall ym University, 948-1, Daerim.1-Dong, Youn gdeungpo.ku,seoul, Korea study. The criteria of degeneration were asfollows : Te l (exl 278) Fax increased signal intensity of the cyst fluid on T

2 Journal of the Korean Radiological Society 1996: 34(6) weighted (T1 WI) and proton density-weighted image (PDWI) relative to CSF ; hyperintense signal around the cyst on PDWI and T2-weighted image (T2WI) suggesting edema, inflammation or gliosis; and contrast enhancement in the lesion. The above three findings have been reported as the signs of degeneration of parenchymal neurocysticercosis (4-1 1). Cysts showing more than two of the above mentioned criteria were regarded as cases of degenerati ng parenchymal neurocysticercosis (DPNCC). Cysts smaller than 0.5 cm in diameter were excluded because of difficulty of analysis. Of the 28 cases, 19 (56 lesions) were the included in this study. Eleven were males and eight were females; their ages ranged between 26 and 71(mean 45). In two cases, neurocysticercosis was diagnosed by sugery, and in 14 cases by a positive ELl SA (enzyme - linked immunosolvent assay) for cysticercus specific immunoglobulin G (Ig G) antibody in serum and CSF. The remaining three cases were included in this study because they had multiple cysts containing a ti ny eccentric nodule representing a scolex of the worm virtually pathognomonic of neurocysticercosis particularly in an endemic area such as Korea, and also had DPNCC fulfilling the above mentioned criteria. AII studies were performed using a 1.0 T MR system ; T1WI was obtained using spin echo sequence /15/2 (repetition time/echo time/excitations) and PDWI and T2WI were obtained using fast spin echo sequence /17, 85-90/5/2 (repetition time/ echo time/echo train length/excitations). Other scan parameters were 5 mm section thickness, 1.5 mm interslice gap, 20cm field ofview, and 192 or 256 X 256 matrix size. Contrast enhancement was performed in all patients with intravenous injection of 0.1 mmol/kg of gadopentetate dimeglumine. In three cases gradient echo image was also obtained using FLASH (fast low angle shot) sequence 600/26/20/2 (repetition time/echo time/flip angle/excitations) Location and size of the cyst, signal intensity of the cyst fluid and cyst wall, extent of hyperintense signal around the cyst on PDWI and T2WI, and featu res of contrast enhancement were evaluated. RESUlTS Size and location of DPNCC In 55Iesions(98.2%), maximum diameter of the cyst was less than 2 cm. Only one cyst was larger than 2 a b Fig. 1. Degenerating parenchymal neur cysticercosis. 71 -year-old male patien t. Fast spin echo (a) proton density weighted and (b) T2 weighted image (3000 /17, 85 /5). A lobulated cystic mass with a hypointense signal rim (arrow) is noted in right Irontal subcortical white matter. Signal of the cyst fluid is hyperintense relative to CSF on proton density weighted image and isointense n T2 weighted image. Signal intensity of the cyst wall is similar to the white matter signal. (c) T1 weighted image (600 /15) Signal of the cyst fluid (white arrow) is hyperintense relative to CSF. The cyst wall is not identified. (d) Contrast enhanced T1 weighted image (600 /15). Peripheral rim enhancement is noted along the wall 01 the cyst with a focal non-enhancing defect (ar row) in its lateral border probably due to lobulation ofthecyst. c d 696-

3 Yu l Lee, e t al : MR Findin gs of Degeneratin g Paren chymal Neurocysticercosis cm. 50 lesions (89.3%) were located in the cortex or subcortical white matter. five (8.9 % ) in deep periventricular white matter, and one (1.8%) at the junction of the lower medulla and upper cervical cord Signal intensity of cyst fluid and cyst wall On T1WI and PDWI, cyst fluid signal was hyperintense relative to CSF in 52 lesions (92.9%). On T2WI, it was isointense relative to CSF in 37 lesions (66.1 %) and hypointense in 19 lesions (33.9%) (Fig. 1) (Table 1). A hypointense signal rim was noted along the wall of the cyst in 551esions (98.2%) on T2WI and in 52 lesions (92.9 % ) on PDWI (Fig. 1, 2, 3). cyst wall signal was usually iso or hypointense relative to white matter (Table 2). Even in lesions showing a hyperintense signal rim relative to white matter, the cyst wall could be identified between the hyperintense signal of cyst fluid and surrounding edema, inflammation or gliosis. In eight lesions, cyst wall signal intensity Table 1. Signal Intensity 01 the Cyst Fluid 01 Degenerating Parenchymal Neurocysticercosis Relative to CSF Signal Signallntensity relative NO.oICases(%) to CSF Signal (n = 56) T1WI Hyperintense 52 (92.9) Isointense 4( 7.1) PDWI Hyperintense 52 (92.9) Isointense 4 ( 7.1) T2WI Isointense 37(66.1) Hypointense 19(33.9) Fig. 2. Degenerating parenchymal neurocysticercosis. 51-year-old male patien t. Fast spin echo (a) proton density weighted and (b) T2 weighted image (3000/17, 85/5). Multiple cysts are noted in both high parietal subcortical white matter (arrowheads) and right centrum semiovale (arrow). A hypointense signal rim is noted along the wall in all Ithecysts a b a Fig. 3. Degenerating parenchymal neurocysticerco, is. 28-year-old male patient a. Fast spin echo T2 weighted image (3000 /85 /5) shows about 2.5 cm sized cyst in right Irontal deep periventricular white matter. Signal intensity 01 the cyst Iluid is heterogeneous and hypointense relative to CSF. A hypointense signal rim along the cyst wall (arrow) is well noted b. Contrast enhanced T1 weighted image (630/15) shows irregular marginated peripheral rim enhancement (arrow). Signal 01 the cyst Iluid is hyperintense relative to CSF c. On the gradient echo image (600 /26 /20), the hypointense signal rim (arrow) along the cyst wall is less well delined than on T2 weighted image suggesting that there is no magnetic suscepti 이 lityeffe c t

4 Journal of the Korean Radiological Society 1996; 34(6 ) : Table 2. Signal Intensity 01 the Cyst Wall 01 Degenerating Parenchym al Neurocysticercosis relative to White Matter Signal Signallntensity relative No. oicases( %) to White Matter Signal (n = 56) T1WI Isointense 56 (100.0) PDWI Hypointense 17 ( 30.4) Isointense 30 ( 53.6) Hyperintense 5( 89) NoRim 4( 7.1) T2WI Hypointense 19( 33.9) Isointense 31 ( 55.4) Hyperintense 5( 8.9) NoR im 1 ( 1.8) Table 3. Extent 01 Hyperintense Signal around the Cyst on PDWI andt2wi Extent 01 Hyperintense Signal Grade 0 Grade 1 Grade 2 Grade 3 Note. - Grade 0 : No surrounding hyperin tense signal Grade1 ; 0 미 y in subcortical white matter Grade 2 : Extend to deep periventricular white matter Grade 3: Extend beyond one lobe No. 01 Cases (%) (n = 55) 2 ( 3.6) 46(83.6) 7 (12. 7l O( 00) was!ower on T2WI than on PDWI, and in six lesions lower, on PDWI than on T2WI. On T1 WI, the cyst wall coulcj not be identified in alllesions because they were isointense to the surrounding brain parenchyme. On gradient echo image, the cyst wall was less well identifiedthan on PDWI and T2WI in all three cases (eight lesions) suggesting that there was no magnetic susceptibi I ity effect (Fig. 3). Hyperintense signal around the cyst On PDWI and T2WI, a hyperintense signal suggesting edema, inflammation or gliosis was observed in 54 lesions (96.4 %). The extent of hyperintense signal was graded from 0 to 3 (grade 0 : no hyperintense signal ; grade 1 : hyperintense signal localized to subcortical white matter ; grade 2: hyperintense signal extending to deep periventricular white matter within one lobe ; grade 3: hyperintense signal extending beyond one lobe). The five lesions located in deep periventricular white matter were all regarded as grade 2 because the hyperintense signal did not extend beyond one lobe. One lesion located in the junction of the lower medulla and upper cervical cord was not graded. As a result, the extent of the hyperintense signal was grade 1 in 46 lesions (83.6%) and grade 2 in seven lesions (12.7%). Fig. 4. Degenerati ng parenchymal neurocysticercosis. 41- year- 이 d lemale patien t. Fast sp in echo T2 weighted image (3400/85/5). Multiple cysts (arrowheads) are noted in gray matter and subcortical white matter 01 both cerebr al hemispheres. Surrounding hyperintense signal does not extend to deep periven tricul ar white matter in all olthe cysts There were no grade 31esions (Fig. 1, 2, 4) (Table 3) Features of contrast enhancement Peripheral rim enhancement was noted in all 56 lesions. The contrast enhancing rim was irregular and lobulated in 38 lesions (67.9%) and regular in 18 lesions (32.1 %). In 23 lesions (41.1 %) a focal defect of the enhancing rim was observed (Fig. 1, 2, 3, 5) DISCUSSION Cysticercosis is an infection caused by the larval stage ofthe tapeworm, Tania -solium, and can develop in any human organ, though is more common in the skin, subcutaneous tissue and brain. In the brain, the location of involvement can be parenchymal, ventricular, cisternal or a combination of these sites. Of these, parenchymal involvement is most common (7, 1 이 Pathologically, parenchymal neurocysticercosis undergoes four stages during its evolution (12). In the vesicular stage the worm is alive and has a cyst with clear fluid surrounded by a thin caps 미 e and a mu ral nodule (scolex) invaginated into the cyst ; at this stage, patients are usually asymptomatic. I n the colloidal vesicular stage the worm begins to degenerate with surounding edema and inflammation due to host immune reaction. The cyst fluid becomes turbid or jellylike and the capsule thickens. The degeneration of the worm progresses during the succeeding granular nodular stage, with further retraction of the cyst and thickening of the capsule. Its contents begin to mineralize with involution and granuloma formation. The lesion is completely mineralized in the final nodular calcified stage. In the vesicular stage, MRI and CT 698 -

5 Yul Lee, et al : I\~R Findings of Degenerating Parenchymal Neurocysticercosis Fig. 5. Degenerating parenchymal neurocysticercosis. 50-year-old male patien t. a. Fast spin echo T2 weighted image ( /5). A lobular marginated cyst (arrow) is noted in the junction 01 lower medulla and upper cervical cord with surrounding hyperintense signal suggesting edema. A hypointense signal rim is noted along the cystwal l. b. Constrast enhanced T1 weighted image (600/15) shows lobular marginated peripheral rim enhancement (white arrow) a b usually show a characteristic mural nodule indicating a scolex within the cyst ; in the final nodular calcified stage only small punctate calcifications are noted. During these live and dead stages of the worm, there is therefore usually no problem in diagnosis. During the colloidal vesicular and granular nodular stages, however, the so called degenerating stages, MRI and CT show surrounding edema and contrast enhancement mimicking other brain diseases, such as metastases, primary brain tumors, abscesses or other inflammatory granulomas and the patient" s symptoms usually occur in this degenerating stage. The differentiation of DPNCC from other brain diseases is therefore considered to be the most difficult problem in the diagnosis of parenchymal neurocysticercosis (13, 14). Michael et al(14) reported two cases of DPNCC who had undergone surgery after pre-operative diagnosis of a brain tumor. In the two surgical cases in this study, pre-operative diagnosis was also a brain tumor ; one was a metastasis and the other was a glioma. The purpose of this study to determine, therefore, whether there are which could lead to a diagnosis of DPNCC and thus prevent unnecessary surgery. We thought that the peripheral hyp 이 ntense signal rim observed in most lesions on PDWI and T2WI was a finding suggesting DPNCC and it has also been reported by several authors as being an MRI finding of DPNCC (8-1 이 It is not unigue to DPNCC, however, but can be seen in brain abscesses, etastases, chronic intracerebral hematomas or other inflammatory granulomas (15-18). It is especially well known in brain abscesses and the magnetic susceptibility effect of oxygen free radicals produced by macrophages in the abscess caps 비 e was stated to be the cause of the hyp이 ntense signal rim on T2WI (15, 16). It was also stated that this magnetic susceptibility effect of free radicals could also be attributable to the hypointense signal rim of other inflammatory lesions (15). But on the basis of our results, it is considered unlikely that the hypointense signal rim can be explained by this magnetic susceptibility effect in DPNCC. On gradient ech images of three cases (eight lesions) there was no magnetic susceptibility effect, and the hypointense signal rim was observed in most of the lesions with the same degree of signal intensity on both PDWI and T2WI ; if due to magnetic susceptibility effect, the degree of hypointense signal should be lower on T2WI than on PDW I. We thought that the hypointense signal rim could be mainly due to the fibrous capsule around the cyst; when the worm is alive the cyst is surrounded by a very thin caps 비 e, but as the worm degenerates the capsule becomes thick (12). On pathologic examination of the two surgical cases in this study, a thick collagenous caps비 e was noted. Calcification was also noted in some portion of the capsule and this could contribute to the hyp이 ntense signal of the cyst wall. Even though this signal rim can be seen in other brain diseases, it can at least be stated that if there is no hypointense signal rim, the possibility of DPNCC is very low % of the cysts were less than 2 cm in diameter ; parasitologically, cysticerci are about 1-2 cm in diameter when f미 Iy developed (12). Occasionally a cyst grows larger than 2 cm, but this is mostly in the cisternal type and it is very unusual for a parenchymal cyst to be larger than 2 cm, as our result shows (7, 9, 12) % of the cysts were located in gray or subcortical white matter and this is common to other hematogeneously spreading lesions such as metastasis. A size of less than 2 cm in diameter and a superficial 10- cation could be helpful in the diagnosis of DPNCC. Signal intensity of the cyst fluid was mostly hyperintense relative to CSF on T1WI and PDWI. Increased signal intensity of the cyst fluid was also reported as a sign of the degeneration which occurs in neuro

6 Journal of the Korean Radiological Society 1996: 34(6) : cysticercosis (4, 6-1 1). This is because as the worm degenerates the cyst fluid becomes turbid with increased protein content in contrast to a clear fluid when the worm is al ive (12). If on T1 WI and PDWI the signal intensity of a cystic lesion is the same as that of CSF, then DPNCC is unlikely On PDWI and T2WI, a hyperintense signal around the cyst (usualy called surrounding edema) was observed in most of the lesions, though this can in fact be due not only to edema but also to inflammation or gliosis (9, 12) It is interesting that the hyperintense signal was usually localized to the subcortical white matter adjacent to the cyst. Of the seven lesions showing a grade 2 hyperintense signal (extending to deep periventricular white matter), five were located in this region. Only two lesions located in gray or subcortical white matter showed a grade 2 hyperintense signal and no lesion showed grade 3 (extending beyond one lobe). This result may be due to the fact that the lesions are small, but may help in the differentiation of DPNCC from metastases or abscesses that are frequently accompanied by surrounding edema which is extensive relative to the size ofthe lesions. Contrast enhancement is also known to be a sign of degenerative neurocysticercα~is (4, 8). It was reported thatthe enhancement is usually ring - like along the periphery of the cyst and that occasionally a solid nodular enhancement could be seen (4, 8). In some of the lesions which were excluded from this study because they were too small (below 0.5 cm in diameter), solid nodular enhancement was noted, but all of the lesions in this study showed peripheral rim enhancement. This result suggests that a solid nodular enhancing lesion larger than 0.5 cm in diameter is unlikely to be caused by DPNCC. The outer margin of the enhancing rim was irregular and lobulated in about two-thirds of the 56 lesions. This is not strange because as the worm degenerates the cyst fluid is extravasated, resulting in scalloping of the cyst wall (12). The defect of the enhancing rim which was observed in 41.1 % of cases is also thought to be due to lobulation of the cyst wall, with a partial volume effect. In summary, cysts caused by DPNCC are usually small (below 2cm in diameter) and superficially located. The cyst fluid signal is usually hyperintense relative to CSF on T1 WI and PDWI. The cyst wall signal is mostly hyp 이 ntense on PDWI and T2WI, in contrastto the hyperintense signal of the cyst fluid and is frequently irregular and lobulated with a focal defect in the enhancing rim. REFERENCES 1. Del 8rutto OH, Santibnez R, Noboa CA, et al. Epilepsy due to neurocysticercosis: Analysis patients. Neurology 1992 : 42: Medina MT, Rosas E, Rubio-Donnadieu F, Sotelo J. Neurocysticercα, is as the main cause 01 late-onset epilepsy in Mexico. Arch Int Med : Couldwell WT, Zee C-S, Apuzzo MLJ. Delinition olthe roleolcontemporary surgical management in cisternal and parenchymatous cysticercosis cerebr i. Neurosurgery 1991 : 28: Chang KH, Cho SY, Hesselink JR., Han MH, Han MC. Parasitic diseases 01 the central nervous system. Neuroimag Clin North Am 1991 : 1 : yrd SE, Locke GE, 8iggers S, Persy AK. The computed tomographic appearance 01 cerebral cysticercosis in adults and children. Radiology 1982: 144: Suss RA, Maravilla KR, Thompson J. MR imaging 01 intracranial cysticercosis : comparison with CT and anatomopathologic leatures. AJNR 1989 : 7 : Teitelbaum GP, Otto RJ, Lin M, et al. MR imaging 01 neurocystlcerco,is. AJNR 1989 : 1 0: Chang KH, Lee JH, Han MH, et al. The role 01 contrast-enhanced MR imaging in the diagnosis 01 neurocysticercosis. AJNR : Lotz J, Howlett R, Alheit 8, 80wen R. Neurocysticercosis: correlative pathomorphology and MR imaging. Neuroradiology 1988: 30 : Zee C-S, Segall HD 80swell W, Ahmadi J, Nelson M, Colletti P MR imaging 01 neurocysticercosis. J Comput Assist Tomogr 1988 : 12 : Martinez HR, Rangel-Guerra R, Elizondo G, et al. MR imaging in neurocysticercosis: a study cases. AJNR 1989 : Escobar A, The pathology of neurocysticercosis. In : Palacios E Rodriguez-Carbajal J, Taveras JM, ed. Cysticercosis of the central nervous system. Springlield : Thomas, 1983 : Suh DC, Chang KH, Han MH, Lee SR, Han MC, Kim Cw. Unusual MR manilestations 01 neurocysticercosis. Neuroradiology 1989: 31 : Michael AS, Levy JM, Paige ML. Cysticercosis mimicking brain neoplasm : MR and CT appearance. J Comput Assist Tomogr 1990 ; 14 : Hai rr. es A8, Zimmerman RD, Morgello S, et al. MR imaging 01 brain abscesses. AJNR 1989; Zimmerman RD, Weingarten K. Neuroimaging 01 cerebral abscesses. Neuroimag Clin North Am 1991 ; 1 : Gomori JM, Grossman RI, Goldberg HI, Zimmerman RA, 8ilaniuk L T. Intracranial hematomas: imaging by high lield MR Radiology 1985 ; 157: Gupta AK, Jena A, Sharma A, Guha DK, Khushu S, GuptaAK. MR imaging 01 intracranial tuberculomas. J Comput Assist Tomogr 1988; 12 : 一 700 -

7 Yul Lee. et al : MR Findings of Degenerating Parenchymal Neurocysticercosis 대한방사선의학회지 1996:34(6) : 변성중인뇌실질낭미충증의특징적인자기공명영상소견 1 1 한립대학교의과대학방사선과학교실 이열 정은아 양익 박해정 정수영 목적 : 변성이되고있는뇌실질낭미충증의자기공명영상소견을다른뇌질환들과의감별점을중심으로알아보고자하였다- 대상및방법 : 수술. ELlSA 검사및특징적인자기공명영상소견으로뇌실질낭미충증으로확진된 19 명의환자에서변성중인 56부위의병변의자기공명영상을병변의크기, 위치, 낭액과낭벽의신호강도, 주위부종의정도, 조영증강의앙상을중심으로후향적으로분석하였다. 결과 : 병변은대부분뇌회질혹은뇌회질과뇌백질의경계부위에위치하였으며 (89.3%) 크기는 2cm 미만이었다 (98. 2%). 낭액은 T1 및앙자밀도강조영상에서고신호강도를 (92.9%) 낭벽은 T2 (98.2% ) 및앙자밀도강조영상 (92.9%) 에서저신호강도를나타내었다. 주위부종은심하지않았고모든예에서변연부조영증강이관찰되었는데조영증감되는낭벽의경계가불규칙한경우가많았으며 (67.9%) 조영증강의국소적인걸손부위가 % 에서관찰되었다. 결론 : T1 및양자밀도강조영상에서낭액의고신호강도. T2 및양자밀도강조영상에서낭벽의저신호강도, 변연부조영증강, 심하지않은주위부종, 표재성위치와 2cm 미만의병변의크기와같은자기공명영상소견은변성이동반된뇌실질낭미충증을다른뇌질환들과감별진단하는데도움이될것으로사료된다

8 가. 일시 : 1996 년 10 월 17 일 ( 목 ) - 19 일 ( 토 ) 나. 장 소 : 호텔롯데월드 3 층크리스탈볼룸 ( 서울시송파구잠실소재깝 ) 다. 초 록 : 1996 년 8 월 17 일 ( 토 ) 전시작품 : 1996 년 10 월 16 일 ( 수 ) 20: 00 - 이후학술대회장의전시장에직접부착 라. 접수처본학회사무국 (TEL , 8005, FAX ) 서울시서초구양재동 121-8번지 PC통신을통해서초록을접수할수도있습니다. ( 학회 PC 통신 ID, 천리안 : KKRS) 마. 호텔예약 : 호텔객실을이용하실분은 9 월 30 일까지호텔롯데월드 ( 전화 : , 담당자 : 명노훈과장 ) 로직접예약하시기바랍니다. 객실료는정상가에서 20% 할인된금액으로이용하실수있습니다. m