Karin Leder, MBBS, FRACP, MPH, DTMH
Peter F Weller, MD, FACP
UpToDate performs a continuous review of over 375 journals and other resources. Updates are added as important new information is published. The literature review for version 15.1 is current through December 2006; this topic was last changed on October 19, 2006. The next version of UpToDate (15.2) will be released in June 2007.
INTRODUCTION — Cysticercosis is caused by the metacestode or larval stage of Taenia solium, the pork tapeworm. Clinical syndromes related to this parasite are divided into neurocysticercosis (NCC) and extraneural cysticercosis.
The clinical features and diagnosis of cysticercosis will be reviewed here. The epidemiology, life cycle, transmission and treatment of this infection are discussed separately. (See "Epidemiology and transmission of cysticercosis" and see "Treatment and prevention of cysticercosis" and see "Intestinal tapeworms").
PATHOGENESIS — Cysticerci that enter the cerebrospinal fluid (CSF) are initially viable but do not cause much inflammation in surrounding tissues; this phase of infection is usually asymptomatic. The host develops a state of immune tolerance to the parasite, and cysticerci can remain in this stage for many years.
There are a number of postulated mechanisms underlying this immune tolerance. Taenia parasites have elaborate means of evading complement-mediated destruction. Metacestodes elaborate a variety of substances (paramyosin, taeniaestatin, sulfated polysaccharides) that either inhibit or divert complement pathways away from the parasite [1]. Additionally, humoral antibodies do not kill the mature metacestode. Taeniaestatin and other poorly defined factors may also interfere with lymphocyte proliferation and macrophage function thus, inhibiting normal cellular immune defenses [1].
Clinical manifestations frequently develop when an inflammatory response develops around a degenerating cysticercus. It is not known what triggers this degeneration, but after a variable number of years, the cyst seems to lose its ability to modulate the host immune response [2].
NEUROCYSTICERCOSIS — Postmortem studies in endemic areas suggest that 80 percent of neurocysticercal infections are asymptomatic. Consequently, many cases are never diagnosed or are found accidentally during imaging procedures.
If symptoms are present, these are mainly due to mass effect, an inflammatory response, or obstruction of the foramina and ventricular system of the brain [3]. The symptoms of NCC depend upon the stage, site, and number of cysticerci [4]. The most common symptoms include seizures, focal neurological signs, and intracranial hypertension [5,6].
The peak of NCC has been estimated to occur three to five years after infection, but it can be delayed for >30 years [7]. After a variable period of degeneration, cysts can become calcified and may then become inactive. Once they are calcified, they may cease to cause symptoms or may serve as a focus for epileptic activity. Patients frequently have cysts in more than one location, and it is not uncommon to have active and inactive cysts present in the same patient [8].
NCC can be further classified into parenchymal or extraparenchymal infection, the latter of which includes intraventricular, subarachnoid, or spinal involvement. Infection and disease are also classified in terms of parasite viability, which result in diverse clinical entities [9].
Parenchymal cysts — Active parenchymal disease is the most common form of NCC and is present in >60 percent of patients. In the brain parenchyma, cysticerci tend to lodge in the cerebral cortex or the basal ganglia. The cysts are usually <1 cm in diameter but can be much larger.
Generalized or focal seizures are a common manifestation of symptomatic disease [2,10-12]. In many endemic countries, NCC is the most common cause of adult-onset seizures [13,14]. The risk of seizures in seropositive individuals is two to three times higher than in seronegative controls [15].
Neurologic examinations of patients with neurocysticercosis are usually normal. Severe headaches are a common presenting feature. Symptoms of elevated intracranial pressure, such as nausea and vomiting, may develop. Intellectual deterioration and psychiatric presentations also occur. Rarely do these patients have fever, signs of meningeal irritation, or focal findings on neurologic examination.
Calcific cysts — Parenchymal cysts provoke an immune response that often leads to cystic degeneration, granuloma formation, and calcification. In endemic populations, punctate calcifications are the most frequent finding on neuroimaging of the brain [16-18]. These lesions were once thought to be clinically inactive, but growing evidence suggests they are an important cause of seizures and focal neurologic symptoms [19]: There is a high prevalence of typical cerebral calcifications in patients with seizures or epilepsy in the absence of other etiologies. A positive correlation has been found between endemic populations with increased proportions of calcifications and seizure activity. There is an increased risk of seizure activity in patients with a single calcific granuloma.
Calcific cysts may also exhibit periodic or episodic perilesional edema that is best visualized on magnetic resonance imaging (MRI) of the brain as bright signal with fluid attenuated inversion recovery (FLAIR) or T2 sequences; the cysts typically enhance with contrast [19-22]. Perilesional edema may be associated with severe symptoms including seizures and focal neurologic deficits but may also be without any overt symptoms.
Cysticercal encephalitis — An intense immune response can occur in patients with massive numbers of cysts in the brain parenchyma, resulting in encephalitis and diffuse brain edema. This syndrome can manifest as fever, headache, and hydrocephalus, with vomiting, impaired consciousness, reduced visual acuity, and seizures. This reaction can occur spontaneously, or it can be provoked by therapy that causes a large number of cysts to degenerate simultaneously. For unknown reasons, this presentation is most common in children and young females.
Subarachnoid cysts — Cysticerci that lodge in the subarachnoid space may grow to 10 cm or larger since they are not limited by pressure from the brain parenchyma [13]. This can result in meningeal inflammation and abnormal thickening of the leptomeninges at the base of the brain. In turn, this can lead to entrapment of the cranial nerves arising from the brainstem. This entrapment can result in visual field defects and cranial nerve palsies. Hydrocephalus can also develop from arachnoiditis and secondary occlusion of the foramen of Luschka or Magendie. In one study of neurocysticercosis in Mexico, this clinical presentation was more common in adults than in children, who were more likely to have a single parenchymal cyst [6].
Inflammation can also involve the walls of blood vessels, leading to a proliferative angiitis and vascular obstruction with secondary cerebral infarcts [23]. Focal neurologic motor signs, ataxia, and sensory dysfunction can ensue; this presentation tends to be associated with a relatively poor prognosis.
Racemose cysticercosis — Racemose cysticercosis is characterized by proliferating lobulated cysts without scolices, which are usually found in the ventricular system and subarachnoid space. These cysticerci undergo disproportionate growth of their membrane, with extensions of membranes that group in clusters, resembling bunches of grapes. While infrequent, this is one of the most serious presentations of NCC since it is often associated with arachnoiditis, basilar meningitis, and hydrocephalus.
Ventricular cysts — In approximately 10 to 20 percent of patients, cysticerci develop in the ventricular system, either as free floating cysts in the ventricular cavity or attached to the choroid plexus. The cysticerci in the ventricles can elicit inflammatory responses leading to granular ependymitis, with consequent obstructive hydrocephalus and increased intracranial pressure of gradual or acute onset. Associated symptoms can include seizures, focal neurologic signs, or dementia. Mobile cysts in the fourth ventricle can occasionally cause intermittent obstruction, leading to episodes of sudden loss of consciousness related to head movements (Bruns' syndrome) [24].
Spinal cysticercosis — Involvement of the spinal cord occurs in approximately one to three percent of cases of NCC [25]. Although spinal neurocysticercosis is relatively rare, it represents a distinct clinical entity which can have devastating consequences, due to the limited size of the spinal canal.
Spinal cysticerci can be intramedullary or located in the subarachnoid space. They can lead to inflammatory and demyelinating changes in the peripheral nerve roots. Patients typically present with radicular pain or paresthesias and may also have sphincter disturbances. Neurological deficits vary with the location of the lesion and may not be distinguishable from other spinal cord lesions on clinical grounds alone. Lesions in the thoracic segments are most common.
EXTRANEURAL CYSTICERCOSIS — Extraneural cysticercosis typically involves the eye, muscle, or subcutaneous tissue. It is not known whether oncospheres actively migrate to muscle, subcutaneous tissues, and the brain, or whether they enter tissues passively during high blood flow [2].
Ocular cysticercosis — Ocular cysticercosis occurs in approximately one to three percent of all infections [15]. Patients with ocular cysticercosis may have parasites located in the subretinal space or vitreous humor. These are often asymptomatic, but inflammation around degenerating cysticerci can threaten vision by causing chorioretinitis, retinal detachment, or vasculitis. Parasites may also be present in the anterior chamber or may affect the conjunctiva or extraocular muscles. Ocular cysticercosis should be excluded by a proper ophthalmologic examination in all patients with NCC prior to initiating therapy.
Subcutaneous and intramuscular cysticercosis — Cysticerci can develop in almost any body site, but tend to have a predilection for muscle or subcutaneous tissues. Cysticerci at these sites are usually asymptomatic, but the patient may notice subcutaneous, pea-like or walnut-sized nodules. Subcutaneous nodules are more common in patients from Asia and Africa than from Latin America.
In cases of major muscle involvement, acute myopathy can develop. Both subcutaneous and intramuscular cysts often undergo calcification and may be detected incidentally when radiographs are performed for unrelated problems. (See "MRI versus CT scanning" below).
Cysts have also been found in the heart. Depending upon the location of the cysts, these may be asymptomatic or may result in arrhythmias and/or conduction abnormalities [8].
DIAGNOSTIC TESTS — The diagnosis of neurocysticercosis is often based on clinical presentation, neuroimaging abnormaIities, and serology [5,26]. Occasionally, more invasive procedures, such as a brain biopsy, are required.
The extent of diagnostic work-up that is needed may depend upon the clinical presentation [27]. In an asymptomatic patient, an incidental finding during testing for unrelated reasons may not warrant further diagnostic procedures, except for serologic testing. A trial of antiparasitic therapy may be administered and the patient monitored to see if there has been an adequate response. However, a patient who presents with seizures or neurologic symptoms may require further investigation. We recommend a brain biopsy to confirm the diagnosis in symptomatic patients with equivocal serology and radiologic tests; however, this is often not feasible in countries where the infection is endemic.
Routine laboratory tests — Most patients with cysticercosis have no specific diagnostic finding on routine blood counts and liver function tests. Individuals with cysticercosis often have no peripheral eosinophilia unless a cyst is leaking, in which case the eosinophilia may be pronounced.
Stool examinations can be performed; however, eggs are typically not found, since the majority of people diagnosed with cysticercosis do not have a viable T. solium tapeworm in their intestines.
Imaging — Imaging is an important modality for diagnosing neurocysticercosis and extraneural cysticercosis.
  Radiography — Plain radiography can be helpful in identifying neurocysticercosis or extraneural cysticercosis. Calcified cysticercal lesions in muscle or subcutaneous tissue may be seen on routine skeletal radiographs or intracranial calcifications may be seen on skull x-rays.
  Brain imaging — Any case of suspected NCC should be evaluated with a computed tomographic (CT) scan or magnetic resonance imaging (MRI). The appearance can depend upon the location and stage of the lesion(s) and upon the host immune response. In parenchymal NCC, viable cysts are seen as nonenhancing hypodense lesions. Degenerating cysts may enhance with contrast and may have variable degrees of surrounding edema and flare. Old cysts often appear as calcified lesions.
Intraventricular cysts, subarachnoid cysts, leptomeningeal enhancement, or hydrocephalus with ventricular enlargement, can also be detected with cerebral imaging, depending upon the location of the lesions. In addition, complications such as cerebral infarcts may be visible. Individuals may have giant cysts measuring >10 cm and/or may have multiple cysts, sometimes numbering >50 to 100.
In some patients, the radiologic appearance is specific for cysticercosis. The pathognomonic lesion is one in which a scolex can be identified as a mural nodule within the cyst. There will often be other areas of punctate calcification seen in association. However, the appearance on imaging by CT or MRI is frequently nonspecific, and it may not be possible to differentiate NCC from other brain lesions, such as abscesses or malignancies.
Additional imaging may be helpful in making the diagnosis of neurocysticercosis. In a study performed in Peru, 25 patients with calcified intraparenchymal brain lesions underwent a non-contrast CT scan of the thighs; 13 (52 percent) had one or more muscle calcifications consistent with extraneural cysticercosis [28]. Patients with a positive CT scan for muscle calcifications also had plain radiographs of their thighs to compare both methods; only 6 of 13 had visible calcifications on x-ray.
CT scanning is also useful in the diagnosis of cysticercal infestation of extraocular muscles [29].
  MRI versus CT scanning — MRI is preferred over CT scanning, since MRI is more sensitive in detecting small lesions, brainstem or intraventricular lesions, perilesional edema around calcific lesions, and is better at visualizing the scolex [30-34]. MRI is also more useful in evaluating degenerative changes in the parasite [35,36]. However, CT scanning is cheaper and is better at detecting small areas of calcification.
A reasonable practical approach is to perform a CT scan first followed by an MRI in patients with inconclusive findings or in those patients with negative CT scans where a strong clinical suspicion of cysticercosis persists [13,37].
For spinal cord lesions, MRI is better at detecting lesions than CT. Myelography may also be helpful in patients with spinal cord involvement.
Serology — All patients with suspected cysticercosis should have serologic testing. As with all serologic tests, results need to be interpreted with caution in individuals from highly endemic areas where a positive serology may be due to past infection and may not prove current active disease. Negative serology lowers the suspicion for cysticercosis, but does not exclude the diagnosis in patients with a compatible clinical presentation and radiographic findings.
A number of different serologic tests have been developed. Some assays detect anticysticercal antibodies, and others identify cysticercal antigens. Some can only be performed on blood, while others can be done on other fluids, such as CSF or saliva [38]. Various techniques can be used, including enzyme linked immunosorbent assay (ELISA), complement fixation (CF), radioimmunoassay, hemagglutination or immunoblot. The sensitivity and specificity of all these tests can be influenced by the stage of disease, site of infection, and host immune response.
In general, the test of choice is the enzyme-linked immunoelectrotransfer blot assay.
  Enzyme linked immunoelectrotransfer blot assay — An enzyme-linked immunoelectrotransfer blot (EITB) assay is the test of choice for detecting anticysticercal antibodies [39]. This assay uses affinity-purified glycoprotein antigens and has higher sensitivity (83 to 100 percent) and specificity (93 to 98 percent) than older ELISA tests [40,41].
However, the diagnostic performance of the EITB can vary in different patient populations depending on the activity of the cyst and number of lesions [42,43]. As an example, in a study of patients with pathologically confirmed neurocysticercosis, 94 percent with two or more lesions had detectable antibodies by EITB compared to only 28 percent with a single lesion [43]. Patients with only calcified cysts (single or multiple) were also less likely to have EITB-positive results than were those with noncalcified, enhancing lesions.
The EITB assay can be performed on serum or CSF but has a higher sensitivity on serum [43-45]. Antibodies can persist for years after the death of parasites, so a positive antibody test does not necessarily indicate the presence of live parasites or active disease [15].
  Serologic testing on CSF — Serologic testing for anticysticercal antibodies or parasite antigens can also be performed on CSF specimens. A study that used ELISA for the detection of CSF antigen in patients who had a CT or serum EITB positive for cysticercosis showed the sensitivity of this assay to be 86 percent [46]. Levels of parasite antigen were positively correlated with the number of live cysts detected by CT and were also proportional to the number and intensity of antibody reactions recognized by the EITB test. In contrast, there was a negative correlation with the number of enhancing lesions revealed by CT, supporting the hypothesis that enhancing lesions correspond to a terminal, moribund stage of the parasite.
Antigen testing — Newer assays using different, more purified T. solium antigens are being developed and are applicable both in immunoblot and ELISA assays. Some studies using these highly purified antigens have suggested that the sensitivity is as high using ELISA as with immunoblot, although the specificity is generally better with immunoblot assays [47,48]. One study reported on detection of IgG in CSF by ELISA assay using newer specific antigens [49]. It showed the ELISA sensitivity to be 85 to 100 percent and the specificity to be 98 to 100 percent. Another study using ELISA assays with synthetic and recombinant antigens, demonstrated high sensitivity (90 to 95 percent with serum and 90 to 100 percent with CSF) and high specificity (90 to 100 percent). However, optimal purified antigens have not been defined, and recombinant antigens are not yet commercially available [50-53].
Antigen detection tests are also being developed that detect live parasites. Studies using monoclonal antibody-based ELISA tests have shown detection of circulating antigen to be both sensitive and useful in monitoring patients following therapy, with a high degree of correlation between circulating antigen detection and CT scanning results during follow-up [52,54-56]. Parasite antigen levels typically fall by three months after successful treatment.
CSF examinations — A lumbar puncture for CSF examination is usually not necessary for the diagnosis of NCC. This procedure is also contraindicated when there is a suspicion of increased intracranial pressure.
If a lumbar puncture is performed, examination of the CSF typically shows a normal glucose concentration and protein and white cell counts that are usually only mildly elevated. CSF eosinophilia can be present and prominent on examination of cerebral spinal fluid in individuals who have leaking cysts that communicate with the CSF [57,58]. These individuals may be at risk of developing chemical arachnoiditis. The differential diagnosis of an eosinophilic CSF pleocytosis includes coccidioidomycosis and angiostrongyloidiasis. (See "Eosinophilic meningitis").
Pathology — Patients suspected of NCC who have a single brain lesion with no characteristic scolex and who have negative serology can be managed either with presumptive therapy or with a biopsy. The decision will depend upon the likelihood of the diagnosis (including epidemiologic characteristics that influence the pretest probability of NCC), the chances of missing other diagnoses that need urgent therapy, and the cyst location.
Occasionally, the diagnosis of extraneural cysticercosis is made via excisional biopsy of a skin or muscle lesion. The cysticercus will appear as a white fluid-filled bladder about 5 to 10 mm in diameter containing a solid 2 mm long larval tapeworm scolex.
Polymerase chain reaction — No polymerase chain reaction (PCR) tests are available for the diagnosis of cysticercosis. A PCR for diagnosis of taeniasis from human fecal samples has been developed but is not yet commercially available [59].
DIAGNOSTIC CRITERIA — A set of diagnostic criteria has been proposed based upon objective clinical, imaging, immunologic, and epidemiologic data [60,61]. The criteria are stratified on the basis of their diagnostic strength as follows: Absolute criteria: Histologic demonstration of the parasite, cystic lesions showing the scolex on CT or MRI, and direct visualization of ocular parasites by fundoscopic examination Major criteria: Lesions highly suggestive of neurocysticercosis on neuroimaging, positive serum enzyme-linked immunoblot for anticysticercal antibodies, resolution of cysts after therapy after antiparasitic therapy, and spontaneous resolution of small single enhancing lesions Minor criteria: Lesions compatible with neurocysticercosis on neuroimaging, clinical manifestations suggestive of neurocysticercosis, positive CSF ELISA for anticysticercal antibodies or cysticercal antigens, and cysticercosis outside the CNS. Epidemiologic criteria: Evidence of a household contact with Taenia solium infection, individuals coming from or living in an area where cysticercosis is endemic, and history of frequent travel to disease-endemic areas.
Combinations of these criteria permit two levels of diagnostic certainty: Definitive diagnosis: Patients who have one absolute criterion or two major plus one minor and one epidemiologic criterion Probable diagnosis: Patients who have one major plus two minor criteria, one major plus one minor and one epidemiologic criterion, or three minor plus one epidemiologic criterion.
These criteria are complex and still require proper validation [62].
SUMMARY AND RECOMMENDATIONS Cysticercosis is estimated to affect approximately 50 million people worldwide. Cysticercosis is endemic in many areas, particularly in Central and South America, sub-Saharan Africa, India, and Asia. The prevalence of NCC varies within these countries and is often higher in places where pigs are raised. (See "Epidemiology and transmission of cysticercosis"). Humans develop cysticercosis by ingestion of eggs of T. solium, which invade the bowel wall and disseminate hematogenously to other tissues. (See "Epidemiology and transmission of cysticercosis"). Clinical syndromes are divided into neurocysticercosis (NCC) and extraneural cysticercosis. Postmortem studies in endemic areas suggest that most neurocysticercal infections are asymptomatic. Clinical manifestations include seizures, encephalitis, visual field defects, hydrocephalus, and cranial nerve palsies. Extraneural cysticercosis typically involves the eye, muscle, or subcutaneous tissue. (See "Neurocysticercosis" above). For initial evaluation, we recommend CT imaging and serology with an enzyme-linked immunoelectrotransfer blot assay. If the CT scan is negative or non-specific, we recommend MRI imaging due to its increased sensitivity in detecting small lesions, brainstem or intraventricular lesions, and better visualization of the scolex. No routine laboratory studies are necessary; patients often have no peripheral eosinophilia unless a cyst is leaking (See "Diagnostic tests" above). As with all serologic tests, results need to be interpreted with caution in individuals from highly endemic areas where a positive serology may be due to past infection and may not prove current active disease. The sensitivity of this test depends on the activity of the cyst and the number of lesions. Diagnostic criteria have been proposed which include clinical, imaging, immunologic, and epidemiologic data. The strength of these criteria are divided into absolute, major, minor, and epidemiologic categories that enable either a definitive or probable diagnosis of neurocysticercosis. However, these criteria are complex and still require proper validation. (See "Diagnostic criteria" above). Serological screening of the contacts of patients should also be considered in the management of cysticercosis. This is particularly relevant in nonendemic countries when transmission may have occurred within a household (eg, via food prepared by a household worker from an endemic country).
Use of UpToDate is subject to the Subscription and License Agreement. REFERENCES 1. White, A, Robinson, P, et al. Taenia solium cysticercosis: host-parasite interactions and the host immune response. Chem Immunol 1997; 66:209.
2. White, AC Jr. Neurocysticercosis: a major cause of neurological disease worldwide. Clin Infect Dis 1997; 24:101.
3.  Gordon, E, Cartwright, M, Avasarala, J. Ventricular obstruction from neurocysticercosis. Arch Neurol 2005; 62:1018.
4.  Takayanagui, O. Parasitol Int. 2006; 55:S111.
5. Del Brutto, OH. Neurocysticercosis. Semin Neurol 2005; 25:243.
6. Saenz, B, Ruiz-Garcia, M, Jimenez, E, et al. Neurocysticercosis: clinical, radiologic, and inflammatory differences between children and adults. Pediatr Infect Dis J 2006; 25:801.
7. Flisser, A. Taeniasis and cysticercosis due to Taenia solium. Prog Clin Parasitol 1994; 4:77.
8. Botero, D, Tanowitz, HB, Weiss, LM, Wittner, M. Taeniasis and cysticercosis. Infect Dis Clin North Am 1993; 7:683.
9. Patel, R, Jha, S, Yadav, RK. Pleomorphism of the clinical manifestations of neurocysticercosis. Trans R Soc Trop Med Hyg 2006; 100:134.
10. Medina, MT, Rosas, E, Rubio-Donnadieu, F, Sotelo, J. Neurocysticercosis as the main cause of late-onset epilepsy in Mexico. Arch Intern Med 1990; 150:325.
11. Garcia, HH, Gilman, R, Martinez, M, et al. Cysticercosis as a major cause of epilepsy in Peru. The Cysticercosis Working Group in Peru (CWG). Lancet 1993; 341:197.
12. Del Brutto, OH, Santibanez, R, Noboa, CA, et al. Epilepsy due to neurocysticercosis: analysis of 203 patients. Neurology 1992; 42:389.
13. Garcia, HH, Del Brutto, OH. Taenia solium cysticercosis. Infect Dis Clin North Am 2000; 14:97.
14. Montano, SM, Villaran, MV, Ylquimiche, L, et al. Neurocysticercosis: association between seizures, serology, and brain CT in rural Peru. Neurology 2005; 65:229.
15. Garcia, HH, Gonzalez, AE, Evans, CA, Gilman, RH. Taenia solium cysticercosis. Lancet 2003; 362:547.
16. Sanchez, AL, Lindback, J, Schantz, PM, et al. A population-based, case-control study of Taenia solium taeniasis and cysticercosis. Ann Trop Med Parasitol 1999; 93:247.
17. Cruz, ME, Schantz, PM, Cruz, I, et al. Epilepsy and neurocysticercosis in an Andean community. Int J Epidemiol 1999; 28:799.
18. Garcia-Noval, J, Moreno, E, de Mata, F, et al. An epidemiological study of epilepsy and epileptic seizures in two rural Guatemalan communities. Ann Trop Med Parasitol 2001; 95:167.
19. Nash, TE, Del Brutto, OH, Butman, JA, et al. Calcific neurocysticercosis and epileptogenesis. Neurology 2004; 62:1934.
20. Sheth, TN, Pillon, L, Keystone, J, Kucharczyk, W. Persistent MR contrast enhancement of calcified neurocysticercosis lesions. AJNR Am J Neuroradiol 1998; 19:79.
21. Nash, TE, Patronas, NJ. Edema associated with calcified lesions in neurocysticercosis. Neurology 1999; 53:777.
22. Nash, TE, Pretell, J, Garcia, HH. Calcified cysticerci provoke perilesional edema and seizures. Clin Infect Dis 2001; 33:1649.
23. Cantu, C, Barinagarrementeria, F. Cerebrovascular complications of neurocysticercosis. Clinical and neuroimaging spectrum. Arch Neurol 1996; 53:233.
24. Salazar, A, Sotelo, J, Martinez, H, Escobedo, F. Differential diagnosis between ventriculitis and fourth ventricle cyst in neurocysticercosis. J Neurosurg 1983; 59:660.
25. Alsina, GA, Johnson, JP, McBride, DQ, et al. Spinal neurocysticercosis. Neurosurg Focus 2002; 12:e8.
26. Del Brutto, OH, Wadia, NH, Dumas, M, et al. Proposal of diagnostic criteria for human cysticercosis and neurocysticercosis. J Neurol Sci 1996; 142:1.
27. Garcia, HH, Del Brutto, OH. Neurocysticercosis: updated concepts about an old disease. Lancet Neurol 2005; 4:653.
28. Bustos, JA, Garcia, HH, Dorregaray, R, et al. Detection of muscle calcifications by thigh CT scan in neurocysticercosis patients. Trans R Soc Trop Med Hyg 2005; 99:775.
29. Rauniyar, RK, Thakur, SK, Panda, A. CT in the diagnosis of isolated cysticercal infestation of extraocular muscle. Clin Radiol 2003; 58:154.
30. Chang, KH, Han, MH. MRI of CNS parasitic diseases. J Magn Reson Imaging 1998; 8:297.
31. Ng, SH, Tan, TY, Fock, KM. The value of MRI in the diagnosis and management of neurocysticercosis. Singapore Med J 2000; 41:132.
32. Creasy, JL, Alarcon, JJ. Magnetic resonance imaging of neurocysticercosis. Top Magn Reson Imaging 1994; 6:59.
33. do Amaral, LL, Ferreira, RM, da Rocha, AJ, Ferreira, NP. Neurocysticercosis: evaluation with advanced magnetic resonance techniques and atypical forms. Top Magn Reson Imaging 2005; 16:127.
34. Hauptman, JS, Hinrichs, C, Mele, C, Lee, HJ. Radiologic manifestations of intraventricular and subarachnoid racemose neurocysticercosis. Emerg Radiol 2005; 11:153.
35. Martinez, HR, Rangel-Guerra, R, Arredondo-Estrada, JH, et al. Medical and surgical treatment in neurocysticercosis a magnetic resonance study of 161 cases. J Neurol Sci 1995; 130:25.
36. Teitelbaum, GP, Otto, RJ, Lin, M, et al. MR imaging of neurocysticercosis. AJR Am J Roentgenol 1989; 153:857.
37. Garcia, HH, Del Brutto, OH. Imaging findings in neurocysticercosis. Acta Trop 2003; 87:71.
38. Flisser, A, Plancarte, A, Correa, D, et al. New approaches in the diagnosis of Taenia solium cysticercosis and taeniasis. Ann Parasitol Hum Comp 1990; 65 Suppl 1:95.
39. Garcia, HH, Herrera, G, Gilman, RH, et al. Discrepancies between cerebral computed tomography and western blot in the diagnosis of neurocysticercosis. The Cysticercosis Working Group in Peru (Clinical Studies Coordination Board). Am J Trop Med Hyg 1994; 50:152.
40. Tsang, VC, Brand, JA, Boyer, AE. An enzyme-linked immunoelectrotransfer blot assay and glycoprotein antigens for diagnosing human cysticercosis (Taenia solium). J Infect Dis 1989; 159:50.
41. Mason, P, Houston, S, Gwanzura, L. Neurocysticercosis: experience with diagnosis by ELISA serology and computerised tomography in Zimbabwe. Cent Afr J Med 1992; 38:149.
42. Mandal, J, Singhi, PD, Khandelwal, N, Malla, N. Evaluation of ELISA and dot blots for the serodiagnosis of neurocysticercosis, in children found to have single or multiple enhancing lesions in computerized tomographic scans of the brain. Ann Trop Med Parasitol 2006; 100:39.
43. Wilson, M, Bryan, RT, Fried, JA, et al. Clinical evaluation of the cysticercosis enzyme-linked immunoelectrotransfer blot in patients with neurocysticercosis. J Infect Dis 1991; 164:1007.
44. Chang, KH, Kim, WS, Cho, SY, et al. Comparative evaluation of brain CT and ELISA in the diagnosis of neurocysticercosis. AJNR Am J Neuroradiol 1988; 9:125.
45. Proano-Narvaez, JV, Meza-Lucas, A, Mata-Ruiz, O, et al. Laboratory diagnosis of human neurocysticercosis: double-blind comparison of enzyme-linked immunosorbent assay and electroimmunotransfer blot assay. J Clin Microbiol 2002; 40:2115.
46. Garcia, HH, Harrison, LJ, Parkhouse, RM, et al. A specific antigen-detection ELISA for the diagnosis of human neurocysticercosis. The Cysticercosis Working Group in Peru. Trans R Soc Trop Med Hyg 1998; 92:411.
47. Gekeler, F, Eichenlaub, S, Mendoza, EG, et al. Sensitivity and specificity of ELISA and immunoblot for diagnosing neurocysticercosis. Eur J Clin Microbiol Infect Dis 2002; 21:227.
48. Dorny, P, Brandt, J, Zoli, A, Geerts, S. Immunodiagnostic tools for human and porcine cysticercosis. Acta Trop 2003; 87:79.
49. Barcelos, IS, Mineo, JR, de Oliveira, Silva DA, et al. Detection of IgG in cerebrospinal fluid for diagnosis of neurocysticercosis: evaluation of saline and SDS extracts from Taenia solium and Taenia crassiceps metacestodes by ELISA and immunoblot assay. Trop Med Int Health 2001; 6:219.
50. Shiguekawa, KY, Mineo, JR, de Moura, LP, Costa-Cruz, JM. ELISA and western blotting tests in the detection of IgG antibodies to Taenia solium metacestodes in serum samples in human neurocysticercosis. Trop Med Int Health 2000; 5:443.
51. da Silva, AD, Quagliato, EM, Rossi, CL. A quantitative enzyme-linked immunosorbent assay (ELISA) for the immunodiagnosis of neurocysticercosis using a purified fraction from Taenia solium cysticerci. Diagn Microbiol Infect Dis 2000; 37:87.
52. Garcia, HH, Parkhouse, RM, Gilman, RH, et al. Serum antigen detection in the diagnosis, treatment, and follow-up of neurocysticercosis patients. Trans R Soc Trop Med Hyg 2000; 94:673.
53. Ito, A, Plancarte, A, Ma, L, et al. Novel antigens for neurocysticercosis: simple method for preparation and evaluation for serodiagnosis. Am J Trop Med Hyg 1998; 59:291.
54. Erhart, A, Dorny, P, Van De, N, et al. Taenia solium cysticercosis in a village in northern Viet Nam: seroprevalence study using an ELISA for detecting circulating antigen. Trans R Soc Trop Med Hyg 2002; 96:270.
55. Nguekam, , Zoli, AP, Ongolo-Zogo, P, et al. Follow-up of neurocysticercosis patients after treatment using an antigen detection ELISA. Parasite 2003; 10:65.
56. Garcia, HH, Gonzalez, AE, Gilman, RH, et al. Circulating parasite antigen in patients with hydrocephalus secondary to neurocysticercosis. Am J Trop Med Hyg 2002; 66:427.
57.  Coyle, C, Wittner, M, Tanowitz, HB. Cysticercosis. In: Tropical Infectious Diseases: Principles, Pathogens and Practice, vol 2, Guerrant, R, Walker, DH, Weller, PF, (Eds), Churchill Livingstone, Philadelphia 1999. p.993.
58. Wang, CH, Gao, SF, Guo, YP. Diagnostic significance of eosinophilia of the cerebrospinal fluid in cerebral cysticercosis. Chin Med J (Engl) 1993; 106:282.
59. Nunes, CM, Lima, LG, Manoel, CS, et al. Taenia saginata: polymerase chain reaction for taeniasis diagnosis in human fecal samples. Exp Parasitol 2003; 104:67.
60. Del Brutto, OH, Rajshekhar, V, White, AC Jr, et al. Proposed diagnostic criteria for neurocysticercosis. Neurology 2001; 57:177.
61. Garcia, HH, Evans, CA, Nash, TE, et al. Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev 2002; 15:747.
62. Carpio, A. Neurocysticercosis: an update. Lancet Infect Dis 2002; 2:751