B ritish Jour nal of N eurosurger y 2000; 14(3): 211± 218 ORIG INA L ART ICLE Experience with neurocysticercosis in the U K: correct diagnosis and neurosurgical m anagem ent of the sm all enhancing brain lesion 1 2 Br J Neurosurg Downloaded from informahealthcare.com by SUNY State University of New York at Stony Brook on 10/26/14 For personal use only. J. P. WADLEY , R. A. SHAK IR & J. M . RICE EDWARD S 1 1 2 D epartm ents of N eurosurger y and N eurology,West Londo n N eurosciences Centre, Charing Cross Hospital, Fulham Palace Road, London , UK Abstract Neurocysticercosis is a major cause of epilepsy and other neurological morbidity in endemic areas of the world but is exceptionally rare in the West. We have recently had experience of eight patients with this condition, seven presenting with epilepsy and single or m ultiple small, enhancing parenchymal lesions and one with hydrocephalus caused by a midbrain lesion. One lesion was stereotactically excised after it persisted, but in ® ve other cases spontaneous cyst resolution was observed during expectant management with anticonvulsants. Two patients with multiple lesions were referred to us for further management but were free of active infection. Recent studies show that neurocysticercosis m ay often be diagnosed based upon the clinical, epidemiological and radiological features. Spontaneous cyst resolution is to be expected in this condition and suspected patients should be carefully observed and surgery avoided. We believe that this disease presents more com monly than has been appreciated in the U K and propose a protocol for management. Key words: Diagnostic cr iteria, epilepsy, expectant m anagement, neuroc ysticercosis, spontaneou s resolution . tory reaction elicited by the release of lar val antigens. The cyst then shrinks, and the resulting granulom a calci® es or disappears com pletely. 3 ,5 ,1 6± 1 9 This clinicopathological pattern of spontaneous resolution has im portant im plications for the correct diagnosis and treatm ent of the disease. Introduction Neurocysticercosis is a disease that is unlikely to be fam iliar or even known to m ost clinicians in the UK and Western Europe. D espite being the most common parasitic disease of the central nervous system worldwide and a m ajor cause of epilepsy and death in endem ic areas such as M exico and India. 1± 12 W ith perhaps the exception of the South-Western USA,1 ,4,1 3 it is exceptionally rare for it to present in developed 4 ,5 ,1 3 ,1 4,1 5 countries. The condition is caused by the encysted larval stage, Cysticercus cellulosae, of the pork tapeworm Taenia solium. M an is the usual ® nal host, but may unwittingly become the interm ediate host, rather than the pig by ingesting the ova shed in the 5 faeces. Serious neurological sequelae m ay result when the subsequent larvae preferentially settle in the brain, and more rarely the spinal cord. The solitary paren17 chymal lesion is the m ost comm on form and the pre sen ting sym ptom in 52± 94% o f cases is epilepsy, 1 ,3 ,5 ,9 ,11 ,12 but the lesions m ay be multiple and cause mass effect, hydrocephalus, basal arachnoiditis and cerebral infarction.1 ,5 ,9 ,10 It is now know n that parenchym al cysts usually lie d or m ant fo r m any years an d sym pto m s u su ally coincide with larval death and an intense in¯ am m a- Clinical m aterial Patient data are sum m arized in Table I. A total of eight patients were adm itted to the Regional N eurosciences Service at C haring C ross H ospital d uring a period of just un der 2 years, between August 1995 and M ay 1997, in w hom a de® nitive diagnosis of cerebral cysticercosis was m ade. Five patients were urgent neurosurgical referrals from district general hospitals with enhancing cerebral lesions initially diagnosed by a radiologist as tum ours (4) o r tuberc ulom a (1) and thre e p atients w ere referred to the neurology service, two for further m anagement w ith m ultiple lesions and a previous diagnosis of neurocysticercosis and one with a single enhancing lesion, initially diagnosed as a tubercu lom a, in whom joint consultation was effected. T here were three m ale patients and ® ve fem ale patients with a m ean age of 32 years (range 19± 69). Correspondence: Mr John Wadley, U niversity Departm ent of Neurosurgery, Institute of Neurology, Queen Square, London W C1N 3BG , U K. Tel: 020 783 7 3611 . Fax: 020 727 8 7894. E-m ail: J.Wadley@doctors.org.uk. Received for publication 17 February, 1999. Accepted 11 January 2000 ISSN 0268± 8697 print/ISSN 1360± 046 X online/00/030211± 08 ½ The Neurosurgical Foundation Male Fem ale Fem ale Fem ale Male Fem ale Male Fem ale 2 3 4 5 6 7 8 M/F 1 Case 45 23 31 27 21 23 19 69 Age (years) TABLE I. Patient data Epilepsy (1985) Recurrent seizures (1997) Epilepsy Epilepsy (1994) Recurrent seizures (1996) Epilepsy Epilepsy Epilepsy Epilepsy Hydrocephalus Presentation T hailand (Born & Travel) India (Travel) South Am erica (Travel) India (Born, U K 3 years) India M alaw i (Travel) India (Born, U K 3 years) India (Travel) India M . East (Travel) Epidem iology Multiple cerebral calci® cations Single enhancing cyst R. tem poral scolex Single enhancing cyst R. frontal scolex Multiple calci® cations & enhancing cysts (1994± 1996) Single enhancing cyst R. frontal scolex Single enhancing cyst brainstem scolex Single enhancing cyst L. temporal scolex Single enhancing cyst L. frontal, scolex Multiple calci® cations CT/M RI Positive Calci® cations Negative Positive Calci® cations Negative Negative Positive Calci® cations Negative Negative X -ray thighs Positive (1985) Negative (1997) Negative Positive Positive (1994) Negative (1996) Negative Negative Negative Negative Serology Negative (1997) Negative Negative (1995 & 1998) Negative Negative Negative Negative Negative Stools (ova) Neurocysticercosis (1985) Neurocysticercosis inactive (1997) Tumour Neurocysticercosis (1994) Tuberculom a Tuberculom a Tumour Tumour Tumour Referral diagnosis M anagem ent Restart anticonvulsants Follow -up scans Anticonvulsants Follow -up scans Change anticonvulsants Follow -up scans Anticonvulsants Follow -up scans Anticonvulsants Follow -up scans Anticonvulsants Follow -up scans Anticonvulsants Follow -up scans VP Shunt Follow -up scans Br J Neurosurg Downloaded from informahealthcare.com by SUNY State University of New York at Stony Brook on 10/26/14 For personal use only. M RI 4/12: resolving M RI 16/12: disappeared seizure-free 18/12 M RI 9/12: no new cysts all lesions calci® ed seizure free 9/12 M RI 3/12: resolving M RI 18/12: disappeared stopped anticonvuls 1 year seizure-free 18/12 Seizure-free 1 year stop anticonvulsants if seizure-free 2 years M RI 2 m onths: no resolution Stereotactic excision (Neurocysticercosis) Seizure 3/12 M RI: resolution but new cyst R frontal M RI 14/12: disappeared stopped anticonvuls 18/12 seizure-free 1 year later M RI 8/12: disappeared stopped anticonvuls seizure-free 2 years M RI 4 m onths Lesion disappeared Sym ptom free 2 years Follow up 212 J. P. Wadley et al. Br J Neurosurg Downloaded from informahealthcare.com by SUNY State University of New York at Stony Brook on 10/26/14 For personal use only. N eurocysticercosis in the UK Presen tation was with focal and/or generalised epilepsy in seven and obstructive hydrocephalus in o n e. O n ly o n e p atien t exp er ien ced p ro d ro m a l sym ptom s of headaches for several weeks. N o patients w ith ep ilep tic s eiz u r es h ad a d em o n stra ble n eurolo gical d e® cit u pon pre sen tatio n. T he ® rst p atien t in th e series, w h o p resen ted w ith hydrocephalus, had experienced 6 m onths of erratic driving and 10 days of progressive gait disturbance and confusion. All eight patients had a history of travel to or had been born in endem ic areas for cysticercosis (Table I). T he countr y com m on to six patients was India: two patients were born in India and had both been resident in the U K for 3 years prior to presentation. Results Radiological features All patients underwent contrast CT and M RI of the brain, either at the referring hospital or after adm issio n . A ll ca ses d em o n strated th e cau se o f th e sym ptom s as a spherical ring-enhancing cystic lesion between 8 and 12 m m in diam eter. In ® ve patients the lesion was single (Fig. 1); one patient showed a sin gle en han cin g lesio n w ith add itio nal m u ltiple cerebral calci® cations (Fig. 2), and two patients w ith a p rev io u s d iag n o sis o f n eu ro c y sticerco sis d em o n strated m u ltip le lesio n s, o n e o f m ixed enhancing and calci® ed cysts, and one of m ultiple calci® cations only. All enhancing cortical cysticerci elicited a m arked degree of surrounding oedem a, particularly well demonstrated on T2 M R sequences (Fig. 2B,C). In the six patients with a solitary cysticercus the 213 larval scolex was clearly dem onstrated on M RI and som etim es also on C T, as a characteristic `spot’ irregularity w ithin the cyst wall (Fig. 4). In the ® ve presenting with epilepsy the lesion was cortical or subcor tical. T he ® rst patient, who presented with obstructive hydrocephalus, harboured a single cysticercus that was visible on CT and M RI situated within the m idbrain, causing aqueductal obstruction (Fig. 1A). Further investigations All patients were questioned for a history of, or contact with, tuberculosis. This was negative in all cases and all patients had norm al chest radiographs. There was no clinical or laboratory evidence of system ic or intracranial bacterial infection in any case. S ero lo g ical tests o f ser u m o r C S F fo r an ti cysticercal antibodies were perform ed in all cases: enzym e-linked im m unosorbent assay (ELISA) or the enzym e-linked im m unotransfer blot (im m unoblot), or both. Serology was negative in ® ve cases and positive in three. O f the three patients w ith positive serology, only one had a single enhancing lesion. T he other two harboured m ultiple lesions; both had positive serology at original diagnosis, but negative tests at referral. T hree patients with multiple cerebral lesions were seen to have `cigar-sh aped’ calci® cations caused by la r vae in th e th igh m u scles v isib le u p o n p lain rad io g rap hy (F ig. 3) . S to o l exa m in atio n w as perform ed in all cases to search for ova (proglottids) to rule out co-existing taeniasis (gut tapeworm s) and thus the possibility of continuing auto-infection. T his was negative in all eight cases. F IG . 1. Patient 1. (A ) Axial T1 -weighted M R scan with gadolineum at presentation. There is a discrete enhancing lesion within the midbrain and obvious hydrocephalus. The scolex of the cysticercus is visible as an irregularity within the wall of the cyst. ( B ) Axial T1 -weighted M RI scan with gadolineum at 4 m onths and after VP shunt insertion. There has been spontaneous and complete resolution of the m idbrain lesion and the cerebral aqueduct is clearly visible and patent. Br J Neurosurg Downloaded from informahealthcare.com by SUNY State University of New York at Stony Brook on 10/26/14 For personal use only. 214 J. P. Wadley et al. F IG . 2. Patient 3. (A ) Axial CT scan with contrast after presentation with grand mal seizures. There is a small left frontal enhancing lesion with a considerable amount of surrounding oedema. There are also two small calci® cations in the opposite frontal lobe, but without oedem a. (B ) Axial and ( C ) sagittal T2-weighted M R scans demonstrate very well the oedem a surrounding the cysticercus and the `dot and spot’ appearance of the larval scolex is clearly appreciated. (D ) Enhanced CT scan at 3 m onths after a further generalized seizure. The previous left frontal lesion has almost disappeared, but there is a new cysticercus with surrounding oedem a in the right frontal lobe. M anagement The changing m anagem ent of the patients in this series from the second case onwards re¯ ects our growing experience and the evolution of a de® ned managem ent protocol for patients presenting with epilepsy and sm all en hancing cerebral lesion s or calci® cations. Patient 1, the only patient not to present w ith ep ilep sy, u n d er w en t ven tr icu lo p er ito n eal shunting for obstructive hydrocephalus and m ade a rapid recover y. Follow -up M RI at 4 m onths surpris- in gly show ed co m plete reso lu tio n o f th e in itial m idbrain cyst. The diagnosis was initially uncertain, but in the light of the com plete disappearance of the lesion and review of the radiology a retrospective diagnosis of cerebral cysticercosis was m ade. N o further treatm ent was necessary and he was well at review 2 years later. The second patient presented w ith a sim ilar single enhancing lesion, in a subcortical position in the left temporal lobe. It was decided to treat with N eurocysticercosis in the UK 215 neurocysticercosis. Both were considered to be free of live cysticerci during follow -up and repeat serology was negative having been positive in the past. Anticysticercal treatm ent was not required. Br J Neurosurg Downloaded from informahealthcare.com by SUNY State University of New York at Stony Brook on 10/26/14 For personal use only. Discussion F IG . 3. Patient 3. Plain radiograph of the thighs. Three `cigar-shaped’ calci® cations are clearly demonstrated within the thigh muscles (arrows). anti-epileptic drugs (AED s) in the light of the history of recent travel to rural India. T he lesion persisted at 8 weeks, however, and it was therefore excised. Histological features of the cyst showed a chronic encapsulated in¯ am m ator y process in keeping with a cysticercus, but unfortunately the central pearly white scolex seen at surgery was lost in the laboratory. In hindsight it was felt that a longer period should have been allowed before deciding upon surgery. F rom the third case onwards, we felt con® dent about the typical CT and M RI appearances of the lesions of neurocysticercosis. A de® ned m anagem ent protocol was aided by the recent diagnostic criteria form ulated by D el Brutto et al. 8 In this way the four rem aining patients who were referred as emergencies to our service with sm all enhancing lesions and epilepsy were m anaged w ith AED s alone and repeat im ag ing at follow -up. In all cases this o b ser va n t ap p ro ach w a s ju st i® ed b y com plete disappearance of the enhancing lesions at inter vals of between 8 and 18 m onths. Patient 3 was in teresting in that a further seizure at 3 m onths resulted in repeat M RI, which showed that the initial cy sticercu s had reso lve d b u t a n ew lesio n h ad appeared in the opposite frontal lobe (Fig. 3a± d). T he patient was continued on AED s and this second lesion had resolved at 14 m onths. Subsequently, all fo ur o f th ese p atien ts rem ain ed seizu re -free, at follow -up intervals between 18 m onths and 2 years. AED s were successfully stopped in three patients after cyst resolution. Patients 6 and 8 were different in that they were referre d for fur ther m anag em en t with m ultiple cerebral lesions and a previous diagnosis of Although cerebral cysticercosis is a disease that has been recognized in endemic areas since the m iddle of the last century, it is really only since the advent of m odern neuroim ag ing w ith CT and M RI that the natural history, and true prevalence of this infestation have been realized. T he m o st w or r y in g co n cer n w ith su ch sm all enhancing lesions is that they m ight represent prim ary or m etastatic malignancy, and is the reason why stereotactic biopsy or excision m ay initially be advocated unless thought is given to alternative conditions. Other lesions that might present with sim ilar radiological features are bacterial abscess, mycotic granulom a, toxo p lasm osis, hy d atid cyst, lar va m ig ran s an d sarcoidosis. A controversy since C T becam e widely available is the distinction between the lesions of neurocysticer1 7 ,1 8 ,2 0 ± 2 3 cosis and cerebral tuberculom a. T his is because both diseases are comm on in endemic areas, m ay coexist in the sam e patient and m ay both present with epilepsy. Recent studies from India 1 7 ,1 8 have revealed that the m ajority of sm all enhancing lesions in epileptic patients disappear spontaneously on AED s 18 alone and are actually cysticerci. R ajshekar has found that cysticerci are usually round in shape, 20 m m or less in size w ith ring enhancement or a visible scolex, and m idline shift or neurological deficit are never seen. Tuberculom as by contrast are usually irregular, solid, greater than 2 cm in size, usually with shift and presenting w ith a progressive de® cit. T his distinction is an im portant issue since parenchym al cysticercosis is a benign and self-lim iting condition, whereas a tuberculom a is an active infection that requires prolonged therapy w ith potentially toxic 1 7 ,1 8 drugs. M odern neuroim ag ing has clearly established the pattern of larval death that leads to in¯ am m ation and oedema and the onset of sym ptom s, followed by sp o n tan eo u s g ran u lo m a reso rp tion o r ca lci® ca 3 ,5 ,9,1 3 ,1 7,1 8 13 tio n . M iller d o cu m en ted th is phenom enon and questioned the need for surgical intervention. It is known that cerebral lar vae m ay lie 3 ,5 ,1 3 dorm ant with no sym ptom s for 10 years or m ore an d altho u gh the p er io d fr o m p resen tatio n to 17 spontaneous resolution is variable, 65% of lesions 18 disappear within 12± 16 weeks and 85% by 6± 8 m onths. 1 9 As well as clearly delineating the different stages of the disease described above, CT and M RI has also been used to identify the characteristic radiological fe atu res o f the in d ividu al pare nchym al cysticer1 ,8 ,9 ,1 1 ,1 7 ,2 4 cus. Although live asymptomatic cysts m ay be several centim etres in diam eter, dying enhancing Br J Neurosurg Downloaded from informahealthcare.com by SUNY State University of New York at Stony Brook on 10/26/14 For personal use only. 216 J. P. Wadley et al. F IG . 4. Enlarged view of cysticercus from T2 -weighted M R scan to highlight the characteristic appearance of the larval scolex. The scolex is seen as the `spot’ irregularity in the cyst wall (black arrow), the cyst wall itself (hollow arrow) and the cyst ¯ uid which is of high intensity in the T2 sequence (headed arrow). cysticercus granulom as are always 20 m m or less in size. 1 8 In m ost cases the scolex m ay be seen within the cyst wall as an eccentric, enhancing hyperdense spot on T1 sequences and is regarded as a pathogne1 ,5 ,8 ,1 1 monic feature (Fig. 4). T here is usually m arked oedem a surrounding the cyst and contrast enhance24 m en t d u r in g th e tra n sitio n al p h ase, w hich dim inishes during resolution. In 65% of cases with 1 multiple lesions sm all calci® cations will also be seen, although each cysticercus m ay not necessarily calcify before resolution. T he two principal serological tests in use are the enzym e-linked im m unosorbent assay (ELISA) and the enzym e-linked im m unotransfer blot (im m unob lot, EITB). The im m unoblot is regarded as m ore reliable, with a speci® city of 100% and a sensitivity of 5 ,1 6 up to 97% in both blood and C SF. However, it is recognized that these tests display poor sensitivity in 5 ,1 7 ,1 8 detecting antibodies in cases of solitary lesions 16 when the sensitivity drops to 18± 46%. Positive tests may help to con® rm the diagnosis, but a negative test cannot be used to exclude neurocysticercosis. 8 ,1 6 Tw o an ticisticerca l d r u gs are w id ely u sed in 5± 7 ,1 2 endemic areas: praziquantel and albendazole. It is our policy not to use these drugs w ith single lesions since the enhancing cysticerci dem onstrated upon im ag ing are by de® nition dyin g anyway and will sp o n tan eo u sly reso lve, a v iew sh ared b y others. 5 ,1 1 ,1 8 ,1 7 ,2 1 These drugs m ay accelerate cyst resolution and som e authors advocate their use even with solitary lesions. The m ainstay of treatm ent in this patient group during observation has been seizure control with AED s. Seizures caused by a single cysticercus are 5 ,7 ,1 1 19 generally very well controlled and Rajshekhar found that 58 of 62 patients with solitary lesions rem ained seizure-free in the long term after AED withdrawal between 2 and 4 weeks after cyst disapp earan ce. T he pr in cipal in dicatio ns fo r su rg ical intervention in neurocysticercosis are the treatm ent of hydrocephalus, the rem oval of m obile intraven tricular cysts, spinal cysts, accessible racemose cysts in the basal cisterns and large supratentorial cysts 1 , 3 ± 6 , 1 2 , 1 9 ,2 0 , 2 5 cau sing m ass effect. Sm all co r tical granulom as such as those in this series should not be biopsied or rem oved since the parasite is dying and 1 ,7 ,8 , 1 0 ,1 8 , 2 5 will disappear spontaneously. Additionally, stereotactic biopsy m ay be difficult owing to the toughness and m obility of the cysticercus, and hazardous owing to the usual site of lesions at the grey-white m atter junction w ith the 17 subsequent risk of haem orrhage. In the rare situatio n w h ere a cyst enlarges o r cau se s in creasing n euro logical d e® cit we wou ld treat w ith an ticisticercal therapy in the ® rst instance if the diagnosis is de® nite. If the lesion still does not respond to this therapy then surger y is inevitable. In the light of the above inform ation, how m ay a con® dent diagnosis of neurocysticercosis be m ade fro m the p resen tin g clin ica l ev id en ce a n d th e radiological ® ndings? T his controversy has recently been addressed by an international panel led by D el Brutto 8 which has summ arized diagnostic criteria and degrees of diagnostic certainty (Tables II and III). T he criteria are subdivided into separate categories according to the weight attached to each feature: a b so lu te, m a jo r, m in o r a n d ep id e m io lo g ica l. In terpretation of the cum ulative criteria in each patient allow the calculation of three degrees of diagnostic certainty: de® nitive, probable and possible. Since spontaneous cyst resolution is typical of this TABLE II. Diagnostic criteria (after Del Brutto)8 Absolute M ajor M inor Epidemiological 1. Histological demonstration of parasite. 2. Fundoscopic visualization of parasite. 3. Cystic lesions with scolex on CT or M RI. 1. Lesions suggestive of neurocysticercosis on CT or MRI. 2. Positive anticysticercal antibodies in serum or CSF. 3. Calci® cations on plain X -rays of thighs. 1. Subcutaneous nodules. 2. Clinical manifestations suggestive of cysticercosis. 3. Disappearance of brain lesions with anticysticercal therapy. 1. Imm igration from or living in endemic area. 2. Travel to endem ic area. 3. Household contact with T. solium infection. N eurocysticercosis in the UK 217 8 TABL E III. Degrees of certainty for diagnosis (after Del Brutto ) De® nitive diagnosis Probable diagnosis Br J Neurosurg Downloaded from informahealthcare.com by SUNY State University of New York at Stony Brook on 10/26/14 For personal use only. Possible diagnosis 1. One absolute criterion. 2. Two major criteria. 3. One m ajor, two minor and one epidem iological criteria. 1. One m ajor and two minor criteria. 2. One m ajor, one minor and one epidem iological criteria. 3. Three minor and one epidemiological criteria. 1. One m ajor criterion. 2. Two minor criteria. 3. One m inor and one epidem iological criteria. F IG . 5. M anagement protocol of a patient presenting with epilepsy and small enhancing lesion(s). condition, it m ight be suggested that this is also included as a m inor criterion. In all cases in our series the criteria accum ulated perm itted a de® nitive diagnosis to be m ade. W ith increasing experience d u rin g th e series descr ibed w e h ave ad op ted a coherent m anagem ent strategy for patients presenting with sm all enhancing cerebral lesions and epilepsy (Fig. 5). For patients with a de® nitive or probable diagnosis after investigation, the m anagem ent should be expectant w ith AED s alone and repeat im aging initially at 8± 10 weeks. Stereotactic or image guided excision should be reserved for lesions that enlarge or persist despite additional anticysticercal treatm ent or when the diagnosis is not certain. industrialised nations in the era of m odern travel and im m igration from endemic areas. Lesions such as those described m ay have been m istakenly biopsied or rem oved in the past w hen thought to be tubercu lom as or sm all tum ours, resulting in non -speci® c histological ® ndings. Correct differential diagnosis with other ring-enhancing lesions is essential, since neurocysticercosis with a solitary or a sm all num ber of cerebral lesions is a self-lim itin g d isease, an d u nn ecessa r y su rger y o r prolo nged therapy w ith potentially toxic drugs should be avoided since the pattern is of spontaneous cyst resolution. References Conclusions We have aim ed to highlight a new clinical problem that m ust be considered as a differential diagnosis in 1 M cC orm ick G F, Zee C S, Heiden J. C ysticercosis cerebr i. R ev iew o f 127 cases. A rch N eu rol 1982;39 :534± 9. 2 Sotelo J, Guerrero V, Rubio F. Neurocysticercosis: a Br J Neurosurg Downloaded from informahealthcare.com by SUNY State University of New York at Stony Brook on 10/26/14 For personal use only. 218 J. P. Wadley et al. new classi® cation based on active and inactive forms. Arch Inter n M ed 1985;14 5:442± 5. 3 Shakir RA, P® ster HW. Parasitic Infections. 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Solitary cysticercus granulomas. J Neurosurg 1995;82:911 (letter). 22 Wadley JP. Differential diagnosis of cerebral tubercu loma. J R oy Soc M ed 1997;90: 469± 70 (letter). 23 Bansal BC, Abha Dua, Gupta R, Gupta M S. Appearing and disappearing C T scan abnormalities in epilepsy in India: an enigma. J Neurol Neurosurg Psychiatr y 1989;52: 1185± 7. 24 Chang HK, Lee HJ, Han M H, Han M C. The role of contrast enhanced M R imaging in the diagnosis of neurocysticercosis. AJN R 1991;12 :509± 12. 25 Carpio A, Placenua M. De® nition of contem porary surgical management in cisternal and parenchym atous cysticercosis cerebri. N eu rosu rger y 19 92;30:968± 9 (letter).