Journal of Clinical Neuroscience 16 (2009) 867876

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Journal of Clinical Neuroscience

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Review

Neurocysticercosis: A review of current status and management

Sumit Sinha *, B.S. Sharma
Department of Neurosurgery, Neurosciences Centre, All India Institute of Medical Sciences, Ansari Nagar, Aurobindo Marg, New Delhi 110 029, India

a r t i c l e

i n f o

a b s t r a c t
Neurocysticercosis (NCC) is an infection of the brain and its coverings by the larval stage of the tapeworm Taenia solium. It is the most common helminthic infestation of the central nervous system and a leading cause of acquired epilepsy worldwide. NCC induces neurological syndromes that vary from an asymptomatic infection to sudden death. Neuroimaging is the mainstay of diagnosis. The diagnosis is suggested in patients living in endemic areas with typical CT scan ndings and a compatible clinical picture. Since the late 1980s, successful medical treatment has been established with relatively short courses of either albendazole or praziquantel. The selection of cases for medical or surgical treatments has improved and these two forms of therapy are complementary. In general, indications of surgery are: cysts that compress the brain and cranial nerves locally, intracranial hypertension or edema refractory to medical treatment, intraventricular NCC, spinal NCC with cord or root compression and ocular cysts. Recently, endoscopic approaches for ventricular NCC have been developed, which are now the treatment of choice for ventricular NCC with hydrocephalus. 2009 Elsevier Ltd. All rights reserved.

Article history: Received 14 September 2008 Accepted 31 October 2008

Keywords: Neurocysticercosis Cysticidal therapy Surgical management Endoscopy

1. Introduction Neurocysticercosis (NCC) is an infection of the brain and its coverings by the larval stage of the tapeworm Taenia solium. It is the most common helminthic infestation of the central nervous system (CNS) and a leading cause of acquired epilepsy worldwide.16 NCC results from ingestion of the eggs of T. solium. The oncospheres hatch in the intestine, penetrate the intestinal wall and disseminate to several body tissues, showing strong tropism to the CNS. The clinical manifestations of NCC are non-specic and varied and depend on the number of lesions and the developmental stage of the cysticercus. Seizures are the commonest manifestation, occurring in 50% to 80% of patients.3,4 NCC has been classied depending on the location of cysts, its clinical presentation, prognosis and cyst viability.710 2. Pathogenesis and life cycle T. solium has a complex life cycle, requiring two hosts (Fig. 1). Humans are the denitive host whereas pigs are the intermediate host.3,4 Humans can also act as intermediate hosts after ingestion of Taenia eggs. The disease manifests itself as two distinct clinical entitites: taeniasis and cysticercosis.

3. Clinical presentation NCC induces neurological syndromes that vary from an asymptomatic infection to sudden death. Differences in the clinical picture depend on the number, size, stage and localization of cysts and the patients immune response. Patients commonly present with seizures or headaches.5,6 The clinical manifestations of NCC are listed in Table 1. 3.1. Parenchymatous form (Figs. 2-6) In the parenchymatous form, the parasite lodges in the brain parenchyma as single (Fig. 2) or multiple cysts forming clumps. Epilepsy is the most common clinical manifestation. Pericystic inammation results in a granuloma formation, which is the cause of epilepsy in most patients (Fig. 2). The cysts may continue to grow and produce a tumor-like syndrome. In India, the single small enhancing lesion (SSEL) is the commonest form of parenchymatous NCC.1113 It commonly presents with simple partial seizures, partial complex seizures, simple partial seizures with secondary generalization or generalized seizures. Tuberculous granuloma, microabscess, focal meningo-encephalitis, neoplasms and vascular lesions should be considered in the differential diagnosis.1416 Chandy et al. reported that 12 out of 15 patients with SSELs were shown to have cysticercosis.17 In disseminated or miliary NCC, there are multiple cysts in varying stages of development (i.e. living, dying and calcied cysts) (Fig. 3). There may be associated extracranial (i.e. conjunctival, subcutaneous or muscle) cysts. This variety is uncommon but

* Corresponding author. Tel.: +91 11 26731172/+91 9868398244; fax: +91 11 26106803. E-mail addresses: sumitaiims@yahoo.com, sumitneuro@gmail.com (S. Sinha). 0967-5868/$ - see front matter 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2008.10.030

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Ingestion raw pork HUMAN Cysticerci in brain, muscle, eyes HUMAN Cysticerci in small intestine PIG Cysticerci in brain, muscle, eyes, other organs Cross GIT HUMAN Cestode in small intestine PIG Oncospheres in stomach

Cross GIT HUMAN Oncospheres in stomach

Feco-oral contamination

Ingestion of human feces

Proglottids and eggs excreted in feces

Fig. 1. Life cycle of Taenia solium. Cysticerci are the larval cyst of the parasite, oncospheres are the embryonic form and the cestode is the adult form of the tapeworm. Proglottids are the segments of the tapeworm, which can detach and reproduce independently. Taeniasis is intestinal infection with the adult tapeworm (gray shaded boxes) while cysticercosis is systemic infection with larval cysts (unshaded boxes). GIT = gastrointestinal tract.

Table 1 Clinical manifestations of neurocysticercosis (after91) Clinical manifestation Epilepsy Raised intracranial pressure Pathology Pericyst inammation, granuloma formation Hydrocephalus (arachnoiditis, ependymitis, ventricular cysts), pseudotumor (edema), giant cysts, cysticercal encephalitis Direct compression by large or multiple cysts Widespread subarachnoid inammation Inammation, local mass effect, vasculitis Multiple parenchymatous cysts Intense inammation and edema Inammatory aneurysm27 Arachnoiditis28 Collection of multiple cysts29 Angiitis30,31 Intermittent CSF obstruction Sellar/intraocular cysts

Focal decits Meningitis Myelo radiculopathy Others Mental changes (dementia) Encephalitis SAH Trigeminal neuralgia Subdural hematoma Stroke/TIA Dizziness Endocrinological or ophthalmic symptoms CSF = cerebrospinal ischaemic attack. uid,

SAH = subarachnoid

haemorrhage,

TIA = transient

may have a malignant course with unfavourable prognosis. It is most frequently seen in children and adolescents and presents like an acute or subacute allergic or viral encephalitis.18 There are four stages of development of a parenchymal larval cyst: vesicular, colloidal, nodular and calcied. The vesicular cyst is viable, where the scolex exists as an eccentric nodule within the cyst, and there is little or no enhancement due to a minimal host immune response (Figs. 46). As the scolex dies after cysticidal treatment or an effective immune response, the transparent vesicular uid is replaced by a viscous and turbid uid, which is readily identiable on MRI.19 The uid migrates from the degenerating cyst into the surrounding parenchyma and incites a strong

Fig. 2. Contrast enhanced axial CT Scan of a patient with neurocysticercosis showing a single dying parenchymal cyst (solitary cerebral cysticercal granuloma) (arrow) with a scolex of Taenia solium and surrounding perilesional edema.

immune response, characterized by strong enhancement on contrast CT scans or MRI. This is the colloidal cyst, which has contrast enhancement but lacks a well-dened scolex. As the cyst further degenerates, it develops into a nodular cyst, which still shows some contrast enhancement. Finally, the degenerated cyst calcies and is recognized as a punctuate calcication on CT scan (Fig. 3).

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3.3. Intraventricular and subarachnoid (cisternal) forms (Figs. 712) The intraventricular and subarachnoid (cisternal) forms of NCC are seen in 15% to 54% of patients and present clinically in a more aggressive manner as compared to the parenchymatous form.2123 The oncosphere reaches the ventricular cavity via the choroid plexus. The parasite migrates through the ventricular system, occluding CSF communication corridors, causing acute episodes of ventriculomegaly with sudden death, or mass effect with focal compression. About 38% of patients present with rapid clinical deterioration. Larval death initiates ependymitis and occlusion of ventricular outlets, producing hydrocephalus.21,24 Patients commonly present with raised intracranial pressure caused by large cyst size or load, occlusion of CSF pathways, associated ependymitis and basal arachnoiditis.22 Ventricular entrapment may occur secondary to ependymitis and cause double compartment syndrome.21 The intraventricular form has a rapidly progressive clinical course and demands prompt action. It tends to occur in isolation in most patients; however, parenchymatous disease may be associated in 24% of patients.23 The fourth ventricle is the commonest site (53%) (Figs. 810), followed by the third ventricle (27%), lateral ventricle (11%) and the aqueduct (9%) (Fig. 7). Isolated cystic lesions within the lateral ventricle are mobile (migratory); transventricular migration is towards the fourth ventricle due to the effects of gravity. This results in entrapment of the cyst in the fourth ventricle because of the size of the foraminae of Luschka and Magendie.

3.4. Spinal form

Fig. 3. Noncontrast axial CT Scan of a patient with neurocysticercosis showing multiple (arrows) punctate calcied lesions in the disseminated variety of neurocysticercosis.

3.2. Meningeal form The meningeal form commonly presents with raised intracranial pressure secondary to widespread subarachnoiditis, arachnoiditis and adhesions resulting in cerebrospinal uid (CSF) obstruction and hydrocephalus. It may also manifest as focal decits due to vasculitis and brous entrapment of cranial nerves.7,20

The spinal form occurs in 1.6% to 13% of patients with NCC. The clinical features depend on the lodgment site of the parasite. Two forms of spinal NCC are recognized: (i) leptomeningeal (extramedullary) and (ii) intramedullary. The leptomeningeal (extramedullary) form is 6 to 8 times more common than the intramedullary form. This form occurs as a consequence of downward migration of larvae from the cerebral to the spinal subarachnoid space. The intramedullary form is uncommon. It occurs through hematogenous or ventriculoependymal migration. The parasite commonly lodges in the thoracic spinal cord according to percentage distribution of blood ow to the spinal cord.25,26

Figs. 46. (left to right) 4: Viable parenchymal cyst. Fluid attenuated inversion recovery (FLAIR) axial MRI showing a viable parenchymal cyst. 5: T2-weighted coronal MRI showing a cyst with the scolex seen as a central low density lesion. 6: Contrast enhanced axial T1-weighted MRI showing a viable cyst (vesicular cyst) with the scolex seen as an eccentric nodule within the cyst. Note the minimal contrast enhancement due to a weak host immune response.

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Fig. 7. Noncontrast axial CT Scan showing a cyst in the aqueduct (arrow) causing obstructive hydrocephalus.

Fig. 8. Noncontrast axial CT Scan showing a fourth ventricular cyst with obstructive hydrocephalus. Note the deformation of the shape of the ventricular cavity and the same density of the cyst and cerebrospinal uid, making them indistinguishable.

4. Diagnosis of NCC The diagnosis of NCC is suspected in patients living in endemic areas presenting with a compatible clinical picture and lesions suggestive of NCC on CT scans. Neuroimaging is the mainstay of diagnosis of NCC. Table 2 shows proposed objective diagnostic criteria.32 These criteria are complex and need validation in population or hospital-based studies. The major drawback of these criteria is that they do not differentiate between NCC and tuberculoma, which is of utmost importance in endemic countries, such as India.3335 Moreover, access to enzyme-linked immunoelectrotransfer blot assay (EITB) is limited in India and consequently the usefulness of these criteria has been questioned.36,37 4.1. Radiological investigations 4.1.1. Plain X-ray Plain X-rays of muscles and the skull may show cigar-shaped calcications.
Table 2 Diagnostic criteria for denitive or probable diagnosis of neurocysticercosis (after32) Level of criteria Absolute Major Minor Epidemiologic

4.1.2. CT scan of the head CT scans have a sensitivity and specicity of over 95% in the diagnosis of NCC,38,39 but it is much lower for diagnosing ventricular or cisternal forms of the disease. CT scans are optimal for detecting calcications, which occur in about 50% of patients. On a CT scan, cysts may appear as single or multiple, rounded lesions of variable size and low density, with a small, hyperdense, eccentric mural nodule representing the scolex. This gives a starry night effect in the parenchyma (Fig. 3). Ring enhancement occurs with an inammatory reaction or a granuloma formation. Perilesional edema is seen around dying cysts (Fig. 2). The ventricles may be either small or there may be hydrocephalus. In fourth ventricular cysts, there may be deformation or rounded enlargement of the ventricular cavity (Fig. 8). Ventricular or periventricular enhancement suggests ependymitis. The encephalitic variety shows extensive edema. Degenerative cysts are seen as single or multiple pinhead-sized calcied dots without preferential localization (Fig. 3). A honeycomb appearance may be due to additional

Findings Pathologic demonstration of the parasite; CT scans or MRI showing a cystic lesion with scolex; direct funduscopic visualization of parasite Lesions highly suggestive of neurocysticercosis on neuroimaging; positive serum enzyme-linked immunoblot assay for cysticercal antibodies; resolution of cysts after antiparasitic therapy; spontaneous resolution of a small solitary enhancing lesion Lesions compatible with neurocysticercosis on neuroimaging; clinical manifestations suggestive of neurocysticercosis; positive cerebrospinal uid enzymelinked immunosorbent assay for anticysticercal antibodies or cysticercal antigens; cysticercosis outside of the central nervous system Household contact with Taenia solium infection; immigrants from or living in an endemic area; history of frequent travel to disease-endemic areas

Diagnosis: denitive one absolute criterion or two major + one minor + one epidemiologic criterion; probable one major + two minor criteria, or one major + one minor + one epidemiologic criterion, or three minor + three epidemiologic criteria.

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extracranial cysts in temporalis or nuchal muscles.38 On positive contrast ventriculography, the presence of a regular, rounded lling defect similar to an inverted cup suggests the presence of a cyst and denes its extent, contour and mobility,40 whereas a cul-desac suggests inammatory obstruction. A cyst within the third ventricle may mimic a colloidal cyst.41,42 The patients with epilepsy frequently have SSELs. SSELs are the commonest cause of partial seizures in children in India.35,37,38 Most of these lesions represent solitary cerebral cysticercus granuloma (SCCG). SCCG is the granulonodular form of the parenchymal cyst and accounts for nearly 60% to 70% of all forms of NCC seen in patients in India.38 The differential diagnosis of SSEL includes tuberculoma, pyogenic brain abscesses, fungal abscess, toxoplasmosis, a primary or metastatic brain tumor and infectious vasculitis. The diagnosis relies on associated features, especially in those with uncertain imaging. Serology is also often negative in patients with SCCG, because the parasite is already dead or because a sole parasite does not elicit a strong antibody response. However, many patients with tuberculoma do not have detectable tuberculosis in the lungs or in any other location to conrm the diagnosis. Rajshekhar et al.16 described CT scan criteria for differentiating NCC and tuberculoma. An enhancing ring lesion that is <20 mm in size, regular in outline and not producing a midline shift is likely to be NCC. However, the authors themselves believe that these criteria are not absolute and it may be difcult to differentiate a small tuberculoma from NCC on a CT scan alone. MRI has better sensitivity to differentiate tuberculomas from NCC. Preliminary experience with proton magnetic resonance spectroscopy has shown promise in differentiating tuberculoma from NCC.43 4.1.3. MRI of the brain MRI is the most accurate technique to assess degree of infection, location and evolutionary stage of the parasite. MRI is able to detect perilesional edema and degenerative changes of the parasite and is suitable for small cysts or those located in the ventricles, brainstem, cerebellum, base of the brain, eye and spine.44 The main disadvantages of MRI are its high cost and limited availability. Thus, in our Indian center, a CT scan may be the rst investigation, reserving MRI for patients with inconclusive CT ndings. It is possible to differentiate the various cyst stages on MRI.45 The intensity of uid in live cysts is similar to CSF. The scolex appears as a mural nodule of high signal intensity on T1-weighted MRI and of low signal intensity on T2-weighted MRI (like a hole with a dot, or a pea in a pod) (Fig. 5). There is no perilesional edema at this stage.46 In a degenerated cyst, the uid becomes turbid (colloid vesicular stage), appearing as high intensity on a T1-weighted MRI. In the granulonodular stage, ring enhancement occurs on gadolinium injection (isointense on T1-weighted and hypointense on T2-weighted MRI) and there is variable perilesional edema. However, calcied cysts are better delineated on CT scans. The racemose type of cyst is a large lobulated cyst without a scolex whereas the cellulose type contains a scolex inside a vesicle. Intraventricular cysts (Figs. 912) are well delineated with a small metacystode inside the cyst.47 Abnormal enhancement after gadolinium suggests ependymitis or ventricular entrapment (Fig. 12).48 MRI is useful in follow-up to assess reduction in the number or size of cysts with treatment. 4.2. Serology The available serological tests are of little value in clinical practice. These have a sensitivity of 65% to 98% and a specicity of 67% to 100%, depending on the specic test used, and the cyst burden, location, and phase of infection.4951 The most commonly used enzyme-linked immunosorbent assay is neither sensitive nor speFig. 9. T1-weighted Axial MRI showing a well-delineated fourth ventricular cyst.

Fig. 10. T1-weighted sagittal MRI showing a well-delineated fourth ventricular cyst with obstructive hydrocephalus.

cic.49 EITB is reported to have a sensitivity of 98% and specicity of 100%, and it is the test of choice as a major diagnostic criterion.50 However, its sensitivity in a patient with a single enhancing or calcied lesion is much lower.51

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Dilated ophthalmologic examination is sensitive for the detection of ocular cysts and is necessary for anyone diagnosed with cysticercosis to rule out ocular involvement.54 5. Treatment The treatment modalities available to patients with NCC include: 1. cysticidal agents to kill larvae 2. corticosteroids to decrease or prevent the inammatory reaction. 3. anti-epileptic drugs (AEDs) to prevent or decrease the severity and number of seizures 4. surgery to remove the cyst or insert a shunt for hydrocephalus. Garcia et al. analyzed the current evidence and reported consensus guidelines for the management of NCC56 (Table 3).

5.1. Cysticidal agents 5.1.1. Is cysticidal therapy needed? There are three major arguments against the use of cysticidal therapy in NCC: (i) immediate risks due to acute inammation from the death of cysts; (ii) worsening of long-term prognosis of seizures with increased scarring due to acute inammation,57 and (iii) treatment may be unnecessary due to natural death of the parasites within a short period.58 According to a Cochrane Database Systematic Review, there is insufcient evidence to assess the benecial effects of cysticidal drugs in NCC.59 However, in a double-blind, placebo-controlled study in patients with seizures resulting from viable parenchymal cysts, cysticidal therapy decreased the burden of parasites and was effective in reducing the number of generalized seizures.60 A recent meta-analysis showed that there is a reduced seizure rate and increased resolution of parenchymal lesions with cysticidal therapy.61 The clinical benet from cysticidal therapy in the treatment of SSELs is also controversial. A few trials from India have assessed the efcacy of cysticidal therapy for SSEL in adults and children.15,6264 More complete resolution on imaging and fewer seizures during follow-up were reported in an albendazole group in two of these trials.63,64 In contrast, Gogia et al.65 did not show any benet of albendazole in hastening resolution of CT lesions.

Fig. 11. A,B. T2-weighted coronal (A) and sagittal (B) MRI showing a rounded welldened cyst in the fourth ventricular cavity with a hyperintense scolex.

Table 3 Guidelines for the treatment of neurocysticercosis (after56) Type of neurocysticercosis Fig. 12. Gadolinium-enhanced sagittal MRI of a patient showing an inammatory cyst with enhancement of the cyst wall and surroundings. Parenchymal neurocysticercosis Viable cysts Calcied Enhancing lesions Cysticercotic encephalitis Extraparenchymal neurocysticercosis Intraventricular cyst Subarachnoid cyst Hydrocephalus with no viable cyst Hydrocephalus + intracranial cyst Ocular cysticercosis Spinal cysticercosis Treatment

Serology should be used together with clinical and neuroimaging data. Antigen detection assays are also available, which perform well in comparison with other available tests on CSF samples.52 Antibodies can persist after cysts die; therefore, serology should always be reviewed in light of the presenting clinical picture and imaging studies.36 4.3. Other tests Biopsy of brain, skin or muscle can provide a denitive diagnosis in an otherwise ambiguous clinical situation and may be the diagnostic method of choice for ocular, extraocular muscle, or painful muscular or subcutaneous cysts.5,5355

Cysticidal treatment + steroids AED no cysticidal therapy Single AED, cysticidal drugs if persistent Multiple AED, cysticidal drugs + steroids High dose steroids + osmotic diuretic or immunosuppressive therapy + cysticidal therapy

Neuroendoscopic removal Cysticidal treatment + steroids; VP shunt if required VP shunt, no cysticidal treatment Shunt before cysticidal therapy Surgery (cysticides avoided) Surgical treatment

AED = antiepileptic drugs, VP = ventriculoperitoneal.

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However, some authors would not recommend leaving a live parasite untreated in the brain.60 Thus, although there is controversy regarding the routine use of cysticidal drugs in SSELs, cysticidal drugs are generally considered helpful in the management of some patients (such as those with persisting lesions) as they hasten the resolution of the lesion, and thus, may avoid diagnostic pitfalls. 5.1.2. Cysticides Cysticidal drugs, albendazole and praziquantel, are effective in all forms of NCC.1,7,61,66,67 Praziquantel (an isoquinolone) produces spastic paralysis of the parasite and destroys the scolex. About 60% to 70% of parenchymal cysticerci disappear after a 15-day treatment at doses of 50 mg/kg per day.6870 Recently, ultrashort single-day therapy with praziquantel has been introduced, and the reduction in cyst number has been the same as for longer courses of treatment.7174 Albendazole (an imidazole) acts by inhibiting glucose uptake by parasitic membranes thereby causing energy depletion. About 75% to 90% of parenchymal cysts disappear, and albendazole is considered superior to praziquantel in several trials.7577 Other points favoring albendazole are its efcacy against meningeal, subarachnoid and ventricular cysticerci, and its lower cost. Albendazole does not interact with corticosteroids or antiepileptic drugs.78 It was initially recommended to be administered at a dosage of 15 mg/kg per day for 1 month, but later studies showed that a 1 week course of albendazole is equally effective and is probably more effective than praziquantel.60,79,80 Infections with more than a few lesions may require longer courses of anti-parasitic medication.61 The optimal duration of cysticidal therapy for other less common forms such as giant cysts or subarachnoid forms is unknown but should perhaps be longer than for parenchymal NCC.56 An additional course of praziquantel can be given if cystic lesions remain unchanged on repeat MRI after 1 month to 2 months of therapy. However, with a partial response to one cysticidal drug, administration of the other cysticide (such as albendazole 15 mg/ kg per day in 2 divided doses for 8 days) is probably better than repetition of the same drug course.66 Intraventricular cysts have generally been excised, but many authors have reported disappearance of intraventricular and subarachnoid cysts with cysticidal therapy.48 A recent trial suggests that a high dose of albendazole (30 mg/kg per day) increases clearance of subarachnoid and intraventricular cysts, as compared with usual dosing.81 However, regardless of the treatment chosen, a ventriculoperitoneal shunt should be placed in all patients with evidence of signicant obstructive hydrocephalus. Steroids should be commenced prior to cysticidal treatment to reduce the risk of shunt obstruction. There are concerns of catastrophic complications with cysticidal treatment due to ventriculitis and recurrent obstruction of the ventricular drainage system.42 Corral et al.26 successfully treated intramedullary spinal cysticercosis with cysticidal therapy. In the meningeal form, cysticidal treatment may give only marginal benet and the prognosis is poor due to hydrocephalus, meningeal brosis and multiple brain infarcts secondary to vasculitis. In these patients administration of 50 mg prednisolone 3 times per week may be useful to prevent or diminish chronic inammation.66,67 5.2. Corticosteroids Corticosteroids are used as adjuncts to cysticidal therapy to alleviate symptoms due to the inammatory reaction caused by the death of larvae, which occurs from 2 days to 5 days after initiating therapy. There is conicting evidence to support corticosteroid use as the primary treatment in SSELs;82,83 however, high dose corticosteroids are the primary therapy for cysticercotic

encephalitis. Steroids should be given with cysticidal drugs for patients with subarachnoid cysts, chronic meningitis or multiple viable cysts. Oral prednisolone is preferred and should be commenced 2 days to 3 days before cysticidal therapy and continued for 7 days to 10 days, since maximum exacerbation occurs during this period. Long-term steroid therapy depends on the parasite load and inammation. All trials to evaluate cysticidal therapy have used steroids for a variable period of time.64,82 5.3. Anti-epileptic drugs A single agent rst-line AED such as phenytoin or carbamazepine usually results in adequate seizure control. The optimal duration of AED therapy has been debated and is estimated by identifying the parasite stage at the time of the seizure.84 Patients with degenerating cysticerci develop acute symptomatic seizures because of the inammatory response of the brain. Therefore, these patients may be treated for the duration of the acute condition only, perhaps several months, during the active inammatory response. There are, however, no guidelines for how long AEDs should be continued after an acute episode. For patients with SCCG, it is most appropriate to monitor cyst activity with neuroimaging and to continue AEDs until resolution of the acute lesion. Most physicians repeat MRI or CT scans after 6 months in patients with parenchymal cysticercosis (earlier if the patient is symptomatic). Once the lesion has resolved on neuroimaging, the AED may be tapered off over the next 12 weeks. However, seizures in a patient with inactive or calcied parasites may be categorized as unprovoked seizures. The treatment should last until the patient has experienced a seizure-free period of 2 years. Treatment in patients with multiple lesions or extraparenchymal NCC should be tailored to the individual. 5.3.1. Future research More studies are needed to study the prevention of disease spread and to further elucidate treatment regimes. The Center for Disease Control and Prevention Working Group on Parasitic Diseases has classied cysticercosis as a potentially eradicable disease.85 Recent studies have demonstrated the potential utility of various vaccines against Taenia solium for use in pigs, but their widespread use is not yet a reality.86,87 5.4. Surgery In general, indications for surgery are: 1. 2. 3. 4. 5. 6. 7. cysts exhibiting local compression of brain and cranial nerves. pseudotumor (edema) refractory to medical treatment. hydrocephalus. intraventricular cysticercosis. intracranial hypertension. spinal cysticercosis with cord/ root compression. ocular cysts.54

5.4.1. Extraparenchymal forms 5.4.1.1. Cisternal forms. Patients with the cisternal form of NCC usually have racemose cysts in the basal cisterns and are prone to symptoms that result from local compression. Direct excision of these cysts is not recommended and can be dangerous due to severe adhesions. However, excising individual cysts that cause local compression can be benecial for local compressive symptoms, but is not helpful to reduce the inammatory reaction. 5.4.1.2. Ventricular forms. The indications for excision of a viable ventricular cyst are: (i) mass effect, (ii) CSF obstruction, (iii) uncertain diagnosis, and (iv) fourth ventricular cysts, as they may cause

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brainstem compression even after shunt placement. The treatment options for ventricular NCC include medical therapy, CSF diversion and surgical resection by microsurgery and/or endoscopy. Repeat imaging should be performed immediately before surgical intervention, to exclude cyst migration between the time of diagnosis and surgery. The development of acute hydrocephalus requires an emergency ventriculostomy, especially if the patient has an altered level of consciousness, followed by denitive resection of cysts. A ventriculoperitoneal shunt may be required thereafter, once the cysts have been resected, especially in the presence of ependymitis.41 Due to the frequency of ventriculitis, shunt failure rates have been reported as high as 30% to 67%. Therefore, multiple shunt revisions may be required in these patients, with a high mortality rate (50% in 2 years).8891 Direct microsurgical excision via a posterior fossa exploration is invasive and carries a high risk of morbidity and mortality. Sharma et al. reported posterior fossa craniotomy for fourth ventricle cysts and supratentorial open or stereotactic craniotomy for third or lateral ventricular cysts.91 Endoscopic approaches for ventricular NCC have been described92102 and have become the treatment of choice for ventricular NCC with hydrocephalus. The neuroendoscopic approaches to treatment of NCC have many advantages including the avoidance of a shunt with its attendant complications,89,92,94,96,97,99 quick and easy navigation within the ventricles and excision of multiple ventricular cysts with minimal postoperative complications. Proano et al. reported endoscopic exploration of the fourth ventricle entrapped secondary to vasculitis.48 Later, Bergsnaider et al. reported a transvalecular exploration of fourth ventricular NCC with removal of cysts in 5 patients.96,97 The transfrontal transaqueductal approach was rst described by Schroeder and Gaab for the treatment of aqueductal stenosis.103 The use of this approach for the removal of ventricular NCC was reported by Anandh et al. (using a exible endoscope)99 and Zymberg et al. (using a rigid endoscope).102 Hussain et al. recommend a transventricular transforaminal approach to remove a third or even a fourth ventricular cyst and to perform an endoscopic third ventriculostomy at the same time, through a single burr hole. They used a 5 Fr. angiographic catheter and passed it through the rigid endoscope to negotiate through the aqueduct. In their series, minimal periaqueductal contusions developed in 3 patients due to catheter negotiation, although none had any sequelae.9294 In their series of 13 patients, Suri et al. used a exible endoscope and passed it through a rigid scope to negotiate the catheter through the aqueduct under direct vision. A long exible biopsy forceps was then used to excise the fourth ventricular NCC. This avoided the chance of periqueductal injury and all their patients had normal extra-ocular movements postoperatively.104,105 Many series have reported aspiration of the contents of the cyst prior to its removal, as a collapsed cyst is easier to handle and retrieve.92,94,101 Although there are some concerns regarding ventriculitis after perioperative cyst rupture, techniques such as preoperative continuous irrigation with Ringers solution and postoperative lumbar drainage can clear debris and maintain ventricular patency. However, despite advantages, neuroendoscopic procedures have some potential drawbacks and limitations.48,97,99,101 Firstly, endoscopic excision may be hazardous in presence of ependymitis and dense adhesions. Therefore, patients in whom MRI demonstrates signicant ependymal enhancement are considered poor candidates for this procedure and should probably undergo shunt placement. Secondly, intraventricular bleeding can be problematic. 5.4.1.3. Encephalitic forms. Patients with the encephalitic form of NCC have diffuse cerebral edema due to multiple cysticerci in the

brain parenchyma. Treatment of this form is primarily medical in order to reduce the raised intracranial pressure. However, decompressive craniotomy has been recommended for these patients with only transient benets; now, with more effective means to control raised intracranial pressure, most authors would not advise this.106 5.4.1.4. Parenchymal forms. For parenchymatous NCC, the following surgical approaches are recommended:1,21,24,88,107109 1. Stereotactic excisonal biopsy or open craniotomy and cyst removal is recommended for a single giant cortical cyst or large clumps exhibiting tumor-like behavior, provided that the lesion is surgically accessible, is producing progressive decits or is not responding to cysticidal treatment. This approach may also be used when diagnosis is uncertain (e.g. a SSEL is not responding to cysticides) or multiple lesions. Supratentorial decompressive craniotomy, craniectomy or lobectomy is undertaken when the psuedotumor-type edema is refractory to medical treatment, particularly in the disseminated variety. 2. For spinal cysticercosis, excision needs to be undertaken. Intramedullary and clumped leptomeningeal cysts producing symptoms by mass effect and not responding to cysticidal drugs can be removed via laminectomy. When diagnosis is in doubt, surgery helps in getting a histopathological diagnosis.108 References
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