Home Print this page Email this page Small font sizeDefault font sizeIncrease font size
Users Online: 672
Home | About us | Editorial board | Search | Ahead of print | Current issue | Archives | Submit article | Instructions | Subscribe | Contacts | Login 

 Table of Contents  
Year : 2013  |  Volume : 3  |  Issue : 2  |  Page : 106-113  

Neurocysticercosis: A disease of neglect

Department of Medical Parasitology, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Date of Submission20-Oct-2013
Date of Web Publication26-Nov-2013

Correspondence Address:
Rakesh Sehgal
Department of Medical Parasitology, Postgraduate Institute of Medical Education and Research, Chandigarh 160 012
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2229-5070.122111

Rights and Permissions

Neurocysticercosis (NCC) is a neglected tropical disease caused by larval forms of the parasite Taenia solium lodging in central nervous system (CNS). There is a huge morbidity and debilitation due to CNS manifestations of NCC in developing and underdeveloped regions of the globe, mainly Asian, African and Latin American countries. It is the cause of epilepsy in about 1% of the population of endemic countries and is the underlying etiology in about 15-50% persons with epilepsy, depending upon the geographical region. There is no perfect diagnostic method and the diagnosis relies on a combination of clinical, radio-imaging, immunologic and epidemiologic data. Treatment includes anti-parasitic treatment by cysticidal drugs and management of associated symptoms and complications. The disease is eradicable and control depends on an integrated and coordinated involvement of international bodies like the World Health Organization along with scientific institutions and political and administrative strata of the endemic countries to provide the essential tools such as adequate sanitation, live-stock management, health education and improved socio-economic conditions.

Keywords: Neglected tropical disease, neurocysticercosis, Taenia solium

How to cite this article:
Mewara A, Goyal K, Sehgal R. Neurocysticercosis: A disease of neglect. Trop Parasitol 2013;3:106-13

How to cite this URL:
Mewara A, Goyal K, Sehgal R. Neurocysticercosis: A disease of neglect. Trop Parasitol [serial online] 2013 [cited 2022 Nov 28];3:106-13. Available from: https://www.tropicalparasitology.org/text.asp?2013/3/2/106/122111

   Introduction Top

Cysticercosis, caused by metacestodes of Taenia solium, a two-host zoonotic cestode of the order cyclophyllidea, is a disease of antiquity. The ancient vedic texts describe infestations of head and eyes by parasites and Greek physicians Hippocrates and Theophratus were aware of human infection with a tape worm. [1],[2] The name "cysticercosis" was given by Laennec derived from the Greek word "Kystic" meaning bladder and "Kercos" signifying tail. In 1809, Rudolphi gave the second name of "cellulose" due to its great affinity for connective tissue and in 1853, Beneden was the first to suspect its relationship to Taenia worm. [2] Humans acquire cysticercosis through feco-oral contamination with T. solium eggs from tapeworm carriers. [3] Though, cysticerci (larval cysts) can develop in any organ in the body, cystercerci in the brain or spinal cord, neurocysticercosis (NCC) is the most serious form of infection.

Cysticercosis is of much economic and public health importance causing morbidity and mortality in many developing countries of Asia, Africa and Latin America. [4] Until recently, NCC and echinococcosis were referred to as "neglected" diseases, but are now recognized by the World Health Organization (WHO) as "major neglected diseases". [5],[6] It is one of the most common parasitic diseases of the central nervous system (CNS) and is considered a "biological marker" of the social and economic development of a community. In many endemic communities, NCC is the cause of epilepsy in about 1% of the population. [5] It the past few decades, it has gained even more importance as it has spread to areas previously unknown to be endemic like the United States of America (USA) and Australia. This epidemiological diversity can be attributed to intensification of animal products, increase in world meat and live animal trade, large scale intra-and inter-country migration of agricultural and other workers such as domestic employers and international tourism. [7],[8]

   Epidemiology Top

The disease is world-wide in distribution, though major endemic regions are the world's poorer countries where families raise free-roaming pigs that are able to ingest human feces. [5],[9] These regions include Latin America, most parts of Asia (including China and the Indian subcontinent), Eastern Europe and most of Africa. The world-wide prevalence of NCC still remains to be known, though, initiatives are underway to determine the burden in endemic countries as well as in developed nations like USA. [9],[10],[11],[12] The data on the burden of NCC associated with epilepsy is relatively well-documented, hence is used to provide estimates of prevalence and incidence of NCC in endemic regions. [9],[10] The estimated numbers of people suffering from epilepsy due to NCC are as high as 0.31-4.6 million in sub-Saharan Africa, 0.45-1.35 million in Latin America, 1 million in India and 0.3-0.7 million in China. [5] In a community-wide screening survey from rural Peru, the seroprevalence was 24% and was associated with seizures with an odd's ratio of 2.1, [13] with an additional 13% of those with negative serology demonstrating calcifications typical of NCC in computed tomography (CT) scans, thereby giving an overall estimate of 37% prevalence of cysticercosis. [5],[13] Estimates of prevalence from other Latin American countries range from 15% to 38%. [5] In a systematic review conducted to estimate the frequency of NCC world-wide, the proportion of NCC among persons with epilepsy was consistently found to be about 29% (95% CI: 23.5-36.1%) from Latin America, sub-Saharan Africa and Southeast Asia. [10] The average incidence of T. solium infection in China has been estimated to be 0.11%, with 1.26 million suffering from teniasis and 3-6 million from cysticercosis. [6]

In the Indian subcontinent, the disease is documented to be endemic in India, Bhutan, parts of Indonesia (Bali and Papua), Nepal and Timor-Leste. In India, it is prevalent in all states, with WHO estimating NCC to be the cause of epilepsy in up to 50% of Indian patients who present with partial seizures; ocular cysticercosis also being common. [6] In a community survey in Vellore in southern India, among those suffering from active epilepsy, NCC was found in 28% by CT scan and 13% by the enzyme-linked immunoelectrotransfer blot (EITB). Overall, 34% of patients were diagnosed with NCC. Moreover, there was no significant difference in prevalence of NCC in urban and rural areas. [14] In Puducherry in south India, seroprevalence was observed to be 16% in patients with epileptic seizures [15] and 6% in blood donors when tested for both antibodies and antigens. [16] In Chandigarh in northern India, overall seroprevalence in the general population was found to be 17%, with 24% in slum areas, 20% in rural and 8% in organized urban sectors, with only 8% of the seropositive individuals having history suggestive of NCC. [17] Another study carried out in a rural pig farming community across 30 villages in north India showed a very high prevalence with 48% of those suffering from active epilepsy fulfilling the definitive or probable diagnostic criteria for NCC; epilepsy in the family and no separate place to keep pigs being the major risk factors. [18]

   Disease Top

Human beings acquire cysticercosis through feco-oral contamination with T. solium eggs from tapeworm carriers. [3] Thus, vegetarians and other people who do not eat pork can acquire cysticercosis; exogenous autoinfection due to ano-oral contamination and endogenous autoinfection due to reverse peristalsis can also give rise to cysticercosis. After ingestion of eggs, the oncospheres are liberated in the duodenum, can penetrate the intestinal mucosa and enter the local lymphatics and mesenteric vessels and may migrate to locate anywhere in the body as larval cysts. [19] Within 2-3 months, the oncospheres lose the hooks and develop into fluid filled bladder worms or cysticerci. The most frequent site of cysticerci is subcutaneous and intramuscular tissues, followed by the brain and eye. These can also occur in heart, liver, lung, abdominal cavity and rarely spinal cord. Symptomatic disease results almost exclusively from invasion of the nervous system, i.e., NCC and the eye; there are case reports, though, of extraneural forms presenting as cystic masses involving skeletal muscles, subcutaneous tissues, buccal mucosa, tongue and lips [20],[21] and rare cases of disseminated cysticercosis. [22]

NCC is polymorphic in clinical presentation and ranges from asymptomatic individuals to cases with severe neurological problems. The infected persons grossly vary in terms of the number of active episodes and recurrences, incidence of serious complications, as well as incidence of co-infections with Japanese Encephalitis and HIV. [23] Carabin et al. systematically reviewed estimates of frequencies of different manifestations, complications and disabilities associated with NCC and documented about 79% having seizures/epilepsy, 38% severe headaches, 16% focal deficits and 12% signs of increased intracranial pressure; all other manifestations such as cranial nerve palsy, gait abnormality/ataxia, focal deficits, visual changes, altered mental state/psychiatric symptoms and pyramidal signs occurring in lesser than 10% of symptomatic NCC patients. [24] The clinical presentation is clearly different in parenchymal and extraparenchymal NCC. The most common presentation of parenchymal NCC is with seizures, while extraparenchymal NCC may cause hydrocephalus by mechanical obstruction of the ventricles or the basal cisterns. [19],[25],[26]

NCC is common in adults as well as in children. Although it usually manifests after 5 years of age, symptomatic NCC is seen even in infants and preschool children. The prevalence of epilepsy in Mexico was seen to increase with age. [27] There are also age-related differences in the manifestation of NCC. Most of the cases of childhood NCC present with mild to moderate symptoms and single lesions and extraparenchymal NCC seen in adults are rarely seen in children. [28] There is also clinical heterogeneity across countries; most cases from the Indian subcontinent present with single degenerating lesions, whereas those from Latin America and China present with few viable lesions. [29] Extraparenchymal NCC is frequently seen in Latin American countries, whereas it is uncommon in the Indian subcontinent. These variations are perhaps due to complex interactions between the host, parasite and environmental factors. [30] Genetic differences in T. solium cysticerci have been reported from different countries and may contribute towards the clinical variations across countries. [31] A significantly increased frequency of HLA-A28 (39% vs. 15%) and decreased frequency of HLA-DQW2 (4% vs. 31%) has been reported from a Mexican cohort with parenchymal NCC when compared to healthy controls, with a relative risk of 3.5 for developing the disease in HLA-A28 positive individuals. [32] From India, in patients with single, small, contrast enhancing CT lesions, a positive association of HLA-DRB1* 13, HLA-B63 and HLA-B58 and a decrease in persons with HLA-A11 has been shown. [33],[34] The environmental factors determining solitary cysts are young age and a patient being from the Indian subcontinent or travelers from non-endemic countries. Such patients are usually young teenagers or young adults (majority under 20 years of age) presenting with newly developed seizures. [35],[36] Though not clearly known, the factors responsible could be that in India only a few individuals raise pigs and a vast subgroup is vegetarian or not eating pork. [35] The cooking habits in India where heating the food to high temperatures is commonly practiced, in contrast to South American countries and China where undercooked food is commonly used in recipes, may also be aiding milder egg challenges and thus low parasite loads and milder infections.

   Diagnosis Top

The lack of specificity of the neurological symptoms makes it impossible to diagnose the disease on clinical grounds alone. Thus clinical presumptive diagnosis is usually substantiated with radio-imaging techniques and serodiagnosis. An ideal test for diagnosis of NCC should be a non-expensive, simple-to-perform, point-of-care method with good sensitivity and specificity not only for multiple lesions but also for solitary cyst lesions. Such method is not yet available; hence the diagnosis depends on objective clinical, radio-imaging, immunologic and epidemiologic data, the only absolute diagnostic criteria being histologic demonstration of the parasite from biopsy of the brain or spinal cord, cystic lesions showing scolex on CT or magnetic resonance imaging (MRI), or direct visualization of subretinal parasites by funduscopy [Table 1]. [19]
Table 1: Diagnostic criteria for NCC*

Click here to view


In most cases, NCC diagnosis is based on neuroimaging studies (CT and MRI). CT and MRI also provide information about the parasite stage and location. [37],[38] Three main stages have been described: Vesicular (viable), colloidal (degenerative) and calcified (inactive). [39] CT is the best radiological method for detection of intraparenchymal calcification, while MRI is more sensitive for the identification of cysts in the ventricles. [7] Radioimaging methods may serve the useful purpose, but due to the unavailability of the facilities at many cities and high cost, its use is limited in the developing countries. Moreover, imaging findings may mimic with other types of neurological diseases, thus posing problems in the diagnosis. [40],[41] In some cases, particularly when parasites are located in the subarachnoid basal cisterns, neither CT nor MRI can detect the parasite. In these cases, NCC diagnosis is supported by clinical, epidemiological and serological data as well as by the response to cysticidal treatment. [42]


Immunodiagnosis of NCC by detecting an antigen and/or antibodies is an accessible, low-cost diagnostic tool in areas of endemicity.

Antibody detection

A variety of immunodiagnostic techniques and antigens (total metacestode soluble antigens, metacestode membrane or scolex soluble extracts, semi-purified proteins) have been assessed for the diagnosis of NCC with variable sensitivity and specificity. [43],[44],[45],[46],[47],[48] It has been observed that immunodiagnostic tests based on crude antigen preparations have, at best, moderate sensitivity and specificity. [49] Using semi-purified/purified antigens could constitute a better alternative, but purification procedures are often complex and require considerable technical expertise.

Currently, the most reliable immunological test is an EITB assay with serum samples using lentil lectin glycoprotein antigens of T. solium cysts and is reported to have a 100% specificity for detection of antibodies in serum and cerebrospinal fluid (CSF). [7],[50] Although, 90% sensitivity has been reported in patients with more than two lesions, it declines to 50-62% with a single lesion and for calcified lesions. [51] It is also estimated that most cured patients remain seropositive when followed-up for 1 year after anti-parasitic therapy, mainly due to persistence of antibodies after resolution of active infection. [52] Extraneural cysticercosis and cross-reactions with other cestodes and helminths can also contribute to false-positive results obtained by using serum antibodies. [52],[53] Atluri et al. have shown a high sensitivity (100%) in all the thirteen NCC seropositive children (11 had solitary NCC lesion and 2 had multiple NCC lesions) and 60% sensitivity among suspected cases of NCC children who were seronegative for NCC (36% had solitary NCC lesion and 24% had multiple NCC lesions), with specificity of 92% by two-dimensional polyacrylamide gel electrophoresis EITB. [54] This could be a useful diagnostic modality in endemic countries for the serodiagnosis of NCC, however it requires expertise and facilities. EITB has been extensively used for diagnosis of human and porcine cysticercosis and is commercially available. [55] The drawback, however, is that it depends on infected pigs for supplying the source material. Preparation of the antigen and performance of western blot require considerable technical expertise. Furthermore, batch differences can exist between different antigen preparations and the antigen mixture is not suitable for use in an enzyme-linked immunosorbent assay (ELISA) format due to the presence of non-specific fractions. Further, a western blot assay is not suitable for field studies, nor is it a suitable or affordable assay for diagnosis in countries where cysticercosis is endemic. [56]

The development of numerous serodiagnostic tests using different parasitic antigens is indicative of the fact that none of them is 100% sensitive and specific, particularly in single-lesion parenchymal NCC. Michelet et al. compared the diagnostic efficacy of EITB and HP10 antigen detection by ELISA and found the sensitivities of antibody detection by both tests not to be significantly different, with ELISA identifying HP10 even when vesicular cysticerci were located in the subarachnoideal basal cisterns. [57] Other tests like dot-blots have also been used for the serodiagnosis of several parasitic infections and can give sensitivities as high as those observed with ELISA, at the same time being rapid, easy to carry out and read. Mandal et al. have shown that ELISA and dot-blot assays developed "in-house" can give good sensitivity in the detection of anti-cysticercal IgG, especially among the pediatric cases of NCC who have multiple brain lesions (100%) when compared to those with single-lesion (87%). [58]

Antigen detection

Antigen detection assays have also been described. The detection of secreted cysticercal Ag by ELISA is highly sensitive and specific for the diagnosis of living cysticerci (vesicular) localized in the subarachnoideal space at the base of the skull. [59],[60] Antigen detection assays also permit monitoring and follow-up of anti-parasitic treatment. [39] Though the antigen detection reflects the presence of viable parasites, but a positive antigen detection test is no definitive indication of active NCC, because cysts can be located outside the CNS. Fleury et al. have shown the detection of secreted cysticercal antigen in CSF a useful tool for the diagnosis of inflammatory NCC. [60] Sensitivity was shown to be higher in cases with inflammation compared to non-inflammatory disease (94% vs. 33%) and in cases of multiple- compared with single-cyst cysticercosis (85% vs. 33%). Thus, antigen positivity is a strong indicator of active, inflammatory, multiple-cyst NCC. [60] Garcia et al. evaluated the utility of circulating parasite antigen in sera of patients with hydrocephalous secondary to NCC. [61] The assay gave positive results in 48% of patients with hydrocephalus, but was consistently negative in patients with calcifications. A study from Peruvian individuals demonstrated the sensitivity of 86% for detection of antigen in CSF by ELISA. [62] Negative results were restricted to patients with only a single live cyst or only enhancing lesions. Thus, though the sensitivity was high in multiple cystic lesions, but it had poor diagnostic value in patients having single cyst.

Most of the immunodiagnostic tests need elaborate standardization and cannot be performed with ease at rural areas and underdeveloped regions where the actual burden of disease is present. This creates a necessity of exploration of simpler tests with/without use of non-invasive samples, which can be utilized for point-of-care service. Such tests have not, though, seen the light of the day to be truly useful for patient care in large scale settings. Simple and rapid latex-based agglutination test for detection of T. solium metacestode antigen in the CSF and serum has been evaluated for diagnosis of NCC exhibiting sensitivity and specificity of 64% and 85% and 52% and 96% in CSF and serum samples, respectively. [63] Non-invasive samples such as urine and saliva have also been evaluated for antigen detection. Parija et al. reported a sensitivity of 62% and specificity of 91% for detection of cysticercus antigen in urine specimens using a polyclonal antibody-based ELISA assay. [64] Castillo et al. reported 92% sensitivity of urine antigen detection for viable parasites, which decreased to 62% in single cyst patients. [65]

Molecular techniques

More recently, methods based on detection of cysticercal deoxyribonucleic acid (DNA) have been increasingly explored. Nucleic acid amplification techniques may provide an answer to the challenge of diagnosis of NCC by virtue of their high sensitivity and specificity, ability to detect parasite load and faster turn-around-time. Both conventional and real-time polymerase chain reaction (PCR) assays have been developed for diagnosis of NCC in CSF samples. In a study, using highly repetitive elements of the parasite as probes, as little as 10 fg of T. solium DNA has been detected by PCR in CSF of 96% patients. [66] A semi-nested PCR based on HDP2 able to detect 0.174 fg of T. solium DNA has been reported. [28],[67] PCR based on pTsol9 amplification detected 90-100% of NCC cases depending on stage and location of the parasite, exhibiting 95% sensitivity and variable specificity (80% or 100%) depending on the controls used. [57] A real-time TaqMan based PCR has been developed targeting pTsol9 gene yielding a sensitivity of 92% and specificity of 100% in CSF samples from patients with definitive NCC. [68] There is a lack of literature regarding the usefulness of molecular diagnosis of NCC in patients with single lesions, in serum samples and whether parasite DNA load in CSF can be used for follow-up of NCC patients. Solitary NCC lesions are often missed by serological methods and laboratory confirmation of such cases is a major challenge. Thus detection of parasite DNA by PCR can aid in diagnosing cases, which are missed by available radiological or immunological tests.


The treatment of NCC is controversial and despite several advances, the various therapies remain either suboptimal or based on empiric observations and subsequent refinements through clinical trials. [69] The treatment depends on anatomic location, stage of evolution, number of cysts, degree of inflammation, severity of disease and life-threatening complications which require emergency treatment. Both praziquantel and albendazole are proven cysticidal agents, though their effectiveness is variable and a single course of anti-parasitic therapy may not eliminate all cysts. A meta-analysis assessing the effect of cysticidal drugs on neuroimaging and clinical outcomes of patients with NCC concluded that with therapy there is better resolution of colloidal and vesicular cysticerci, with lower recurrence of seizures in patients with colloidal cysticerci and a reduction in the rate of generalized seizures in patients with vesicular cysticerci. [70] More randomized controlled studies are required in future studies to evaluate and identify more efficacious and safe anthelmintic agents, better combinations of agents and better regimens. Surgery plays a role in the treatment of complicated disease, in removal of easily approachable symptomatic cysts through neuroendoscopy, removal of large approachable cysts that are likely to lead to long-term exposure to immunosuppressives or anthelmintics by open surgery, or shunt placement for hydrocephalus. [69]


NCC is a preventable and eradicable disease. The transmission of parasite is related to social, cultural and economic factors such as poverty, inadequate sanitation and close association of humans with pigs with access of pigs to areas used for defecation. Hence the control measures, which are certain to be effective are health education, improved socio-economic conditions and life-style changes, mass treatment of carriers, restricted sale of measly pork and full cooking of pork. [23] Another important measure to break the host-parasite transmission cycle is the development of vaccines targeting cysticercosis in pigs which are safe, effective, inexpensive and administrable in edible form. Flisser et al. have evaluated recombinant oncosphere antigens TSOL18 and TSOL45-1A to induce 100% protection in three independent vaccine trials in pigs in Mexico and Cameroon. [71] Gauci et al. evaluated the recombinant antigens TSOL16, TSOL45-1A and TSOL45-1B and found TSOL16 to be capable of inducing high levels of immunity in pigs against a challenge infection. [72] Further studies are thus required for production of effective vaccines, which would aid in control and eradication of NCC.

   Conclusion Top

NCC is an important cause of morbidity and mortality in humans. Being a disease of poor socio-economic strata, the approach toward control of this disease is multi-sectorial; the control requiring not just delivery of practical instruments of diagnosis, treatment and prevention by science, but also commitment at administrative and political level, which is required to improve basic health care infrastructure of endemic nations. A simple measure such as provision of adequate sanitary latrines to prevent indiscriminate defecation can effectively prevent millions of cases of epilepsy. Despite being the most common cause of adult-acquired epilepsy world-wide, the morbidity due to NCC is underappreciated and research is underfunded and hence the study of NCC lags behind most other major infectious diseases. [73] A balanced commitment of resources to develop more effective approaches that could lead to better treatment and control of the disease may be the key to improve the quality-of-life of millions of people.

   References Top

1.Ramesh V. Cysticercosis. Int J Dermatol 1984;23:348-50.  Back to cited text no. 1
2.Nieto D. Historical notes on cysticerocsis. In: Flisser A, Wilms K, Laclette JP, Larralde C, Ridaura C, Beltran F, editors. Cysticercosis. Present State of Knowledge and Perspectives. New York: Academic Press Inc.; 1982. p. 1-7.  Back to cited text no. 2
3.Garcia HH, Del Brutto OH. Taenia solium cysticercosis. Infect Dis Clin North Am 2000;14:97-119, ix.  Back to cited text no. 3
4.Giri S, Parija SC. A review on diagnostic and preventive aspects of cystic echinococcosis and human cysticercosis. Trop Parasitol 2012;2:99-108.  Back to cited text no. 4
  Medknow Journal  
5.Coyle CM, Mahanty S, Zunt JR, Wallin MT, Cantey PT, White AC Jr, et al. Neurocysticercosis: Neglected but not forgotten. PLoS Negl Trop Dis 2012;6:e1500.  Back to cited text no. 5
6.Savioli LS, Daumerie D. First WHO Report on Neglected Tropical Diseases: Working to Overcome the Global Impact of Neglected Tropical Diseases. Geneva: World Health Organisation; 2010. WHO/HTM/NTD/2010.1.  Back to cited text no. 6
7.White AC Jr. Neurocysticercosis: A major cause of neurological disease worldwide. Clin Infect Dis 1997;24:101-13.  Back to cited text no. 7
8.Walker J, Chen S, Packham D, McIntyre P. Five cases of neurocysticercosis diagnosed in Sydney. Southeast Asian J Trop Med Public Health 1991;22:242-4.  Back to cited text no. 8
9.Lustigman S, Prichard RK, Gazzinelli A, Grant WN, Boatin BA, McCarthy JS, et al. A research agenda for helminth diseases of humans: The problem of helminthiases. PLoS Negl Trop Dis 2012;6:e1582.  Back to cited text no. 9
10.Ndimubanzi PC, Carabin H, Budke CM, Nguyen H, Qian YJ, Rainwater E, et al. A systematic review of the frequency of neurocyticercosis with a focus on people with epilepsy. PLoS Negl Trop Dis 2010;4:e870.  Back to cited text no. 10
11.Sanchez AL, Ljungström I, Medina MT. Diagnosis of human neurocysticerocosis in endemic countries: A clinical study in Honduras. Parasitol Int 1999;48:81-9.  Back to cited text no. 11
12.Praet N, Speybroeck N, Manzanedo R, Berkvens D, Nsame Nforninwe D, Zoli A, et al. The disease burden of Taenia solium cysticercosis in Cameroon. PLoS Negl Trop Dis 2009;3:e406.  Back to cited text no. 12
13.Montano SM, Villaran MV, Ylquimiche L, Figueroa JJ, Rodriguez S, Bautista CT, et al. Neurocysticercosis: Association between seizures, serology, and brain CT in rural Peru. Neurology 2005;65:229-33.  Back to cited text no. 13
14.Rajshekhar V, Raghava MV, Prabhakaran V, Oommen A, Muliyil J. Active epilepsy as an index of burden of neurocysticercosis in Vellore district, India. Neurology 2006;67:2135-9.  Back to cited text no. 14
15.Parija SC, Raman GA. Anti-Taenia solium larval stage Ig G antibodies in patients with epileptic seizures. Trop Parasitol 2011;1:20-5.  Back to cited text no. 15
  Medknow Journal  
16.Parija SC, Balamurungan N, Sahu PS, Subbaiah SP. Cysticercus antibodies and antigens in serum from blood donors from Pondicherry, India. Rev Inst Med Trop Sao Paulo 2005;47:227-30.  Back to cited text no. 16
17.Khurana S, Aggarwal A, Malla N. Prevalence of anti-cysticercus antibodies in slum, rural and urban populations in and around Union territory, Chandigarh. Indian J Pathol Microbiol 2006;49:51-3.  Back to cited text no. 17
18.Prasad KN, Prasad A, Gupta RK, Nath K, Pradhan S, Tripathi M, et al. Neurocysticercosis in patients with active epilepsy from the pig farming community of Lucknow district, north India. Trans R Soc Trop Med Hyg 2009;103:144-50.  Back to cited text no. 18
19.García HH, Evans CA, Nash TE, Takayanagui OM, White AC Jr, Botero D, et al. Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev 2002;15:747-56.  Back to cited text no. 19
20.Carlos R, Contreras E, Rivera H, Galvez M. Extracranial head and neck cysticercosis: Report of nine cases with emphasis in serologic analysis and natural history of the disease. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2004;98:196-8.  Back to cited text no. 20
21.Jain S, Kumar S, Joshi D, Kaushal A. Racemose cysticercosis presenting as cystic neck swelling. Trop Parasitol 2012;2:55-7.  Back to cited text no. 21
  Medknow Journal  
22.Bothale KA, Mahore SD, Maimoon SA. A rare case of disseminated cysticercosis. Trop Parasitol 2012;2:138-41.  Back to cited text no. 22
  Medknow Journal  
23.Prasad KN, Prasad A, Verma A, Singh AK. Human cysticercosis and Indian scenario: A review. J Biosci 2008;33:571-82.  Back to cited text no. 23
24.Carabin H, Ndimubanzi PC, Budke CM, Nguyen H, Qian Y, Cowan LD, et al. Clinical manifestations associated with neurocysticercosis: A systematic review. PLoS Negl Trop Dis 2011;5:e1152.  Back to cited text no. 24
25.Bickerstaff ER, Cloake PC, Hughes B, Smith WT. The racemose form of cerebral cysticercosis. Brain 1952;75:1-18.  Back to cited text no. 25
26.Rabiela MT, Rivas A, Flisser A. Morphological types of Taenia solium cysticerci. Parasitol Today 1989;5:357-9.  Back to cited text no. 26
27.Fleury A, Morales J, Bobes RJ, Dumas M, Yánez O, Piña J, et al. An epidemiological study of familial neurocysticercosis in an endemic Mexican community. Trans R Soc Trop Med Hyg 2006;100:551-8.  Back to cited text no. 27
28.Hernández M, Gonzalez LM, Fleury A, Saenz B, Parkhouse RM, Harrison LJ, et al. Neurocysticercosis: Detection of Taenia solium DNA in human cerebrospinal fluid using a semi-nested PCR based on HDP2. Ann Trop Med Parasitol 2008;102:317-23.  Back to cited text no. 28
29.Singh G. Neurocysticercosos in South-Central America and the Indian subcontinent. A comparative evaluation. Arq Neuropsiquiatr 1997;55:349-56.  Back to cited text no. 29
30.Fleury A, Escobar A, Fragoso G, Sciutto E, Larralde C. Clinical heterogeneity of human neurocysticercosis results from complex interactions among parasite, host and environmental factors. Trans R Soc Trop Med Hyg 2010;104:243-50.  Back to cited text no. 30
31.Maravilla P, Gonzalez-Guzman R, Zuñiga G, Peniche A, Dominguez-Alpizar JL, Reyes-Montes R, et al. Genetic polymorphism in Taenia solium cysticerci recovered from experimental infections in pigs. Infect Genet Evol 2008;8:213-6.  Back to cited text no. 31
32.Del Brutto OH, Granados G, Talamas O, Sotelo J, Gorodezky C. Genetic pattern of the HLA system: HLA A, B, C, DR, and DQ antigens in Mexican patients with parenchymal brain cysticercosis. Hum Biol 1991;63:85-93.  Back to cited text no. 32
33.Jain S, Padma MV, Kanga U, Puri A, Mehra NK, Maheshwari MC. Human leukocyte antigen studies in Indian probands with seizures associated with single small enhancing computed tomography lesions and seizure types in their family members. J Epilepsy 1997;10:55-61.  Back to cited text no. 33
34.Jain S, Padma MV, Kanga U, Mehra NK, Puri A, Maheshwari MC. Family studies and human leukocyte antigen class II typing in Indian probands with seizures in association with single small enhancing computed tomography lesions. Epilepsia 1999;40:232-8.  Back to cited text no. 34
35.García HH, Gonzalez AE, Rodriguez S, Tsang VC, Pretell EJ, Gonzales I, et al. Neurocysticercosis: Unraveling the nature of the single cysticercal granuloma. Neurology 2010;75:654-8.  Back to cited text no. 35
36.Rajshekhar V. Etiology and management of single small CT lesions in patients with seizures: Understanding a controversy. Acta Neurol Scand 1991;84:465-70.  Back to cited text no. 36
37.Garcia HH, Del Brutto OH, Nash TE, White AC Jr, Tsang VC, Gilman RH. New concepts in the diagnosis and management of neurocysticercosis (Taenia solium). Am J Trop Med Hyg 2005;72:3-9.  Back to cited text no. 37
38.Osborn AG, Preece MT. Intracranial cysts: Radiologic-pathologic correlation and imaging approach. Radiology 2006;239:650-64.  Back to cited text no. 38
39.Garcia HH, Del Brutto OH, Cysticercosis Working Group in Peru. Neurocysticercosis: Updated concepts about an old disease. Lancet Neurol 2005;4:653-61.  Back to cited text no. 39
40.Garcia HH, Herrera G, Gilman RH, Tsang VC, Pilcher JB, Diaz JF, 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;50:152-7.  Back to cited text no. 40
41.Sciutto E, Fragoso G, Fleury A, Laclette JP, Sotelo J, Aluja A, et al. Taenia solium disease in humans and pigs: An ancient parasitosis disease rooted in developing countries and emerging as a major health problem of global dimensions. Microbes Infect 2000;2:1875-90.  Back to cited text no. 41
42.Del Brutto OH, Rajshekhar V, White AC Jr, Tsang VC, Nash TE, Takayanagui OM, et al. Proposed diagnostic criteria for neurocysticercosis. Neurology 2001;57:177-83.  Back to cited text no. 42
43.Das S, Mahajan RC, Ganguly NK, Sawhney IM, Dhawan V, Malla N. Detection of antigen B of Cysticercus cellulosae in cerebrospinal fluid for the diagnosis of human neurocysticercosis. Trop Med Int Health 2002;7:53-8.  Back to cited text no. 43
44.Flisser A, Woodhouse E, Larralde C. Human cysticercosis: Antigens, antibodies and non-responders. Clin Exp Immunol 1980;39:27-37.  Back to cited text no. 44
45.Kaur M, Ganguly NK, Mahajan RC, Malla N. Identification of antigenic fractions of Cysticercus cellulosae by Western blotting in the serodiagnosis of human neurocysticercosis: Before and after treatment. Immunol Infect Dis 1995;5:67-72.  Back to cited text no. 45
46.Kaur M, Goyal R, Ganguly NK, Mahajan RC, Malla N. Evaluation and characterization of purified antigenic fraction-II of Cysticercus cellulosae by enzyme-linked immunosorbent assay for the diagnosis of neurocysticercosis: Before and after treatment. Immunol Infect Dis 1996;6:25-9.  Back to cited text no. 46
47.Mahajan RC, Chopra JS, Chitkara NL. Comparative evaluation of indirect haemagglutination and complement fixation tests in serodiagnosis of cysticercosis. Indian J Med Res 1975;63:121-5.  Back to cited text no. 47
48.Malla N, Kaur M, Kaur U, Ganguly NK, Mahajan RC. Evaluation of enzyme linked immunosorbent - Assay for the detection of anticysticercus antibodies in cerebrospinal fluid from patients with neurocysticercosis. J Hyg Epidemiol Microbiol Immunol 1992;36:181-90.  Back to cited text no. 48
49.Dorny P, Brandt J, Zoli A, Geerts S. Immunodiagnostic tools for human and porcine cysticercosis. Acta Trop 2003;87:79-86.  Back to cited text no. 49
50.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;159:50-9.  Back to cited text no. 50
51.Prabhakaran V, Rajshekhar V, Murrell KD, Oommen A. Taenia solium metacestode glycoproteins as diagnostic antigens for solitary cysticercus granuloma in Indian patients. Trans R Soc Trop Med Hyg 2004;98:478-84.  Back to cited text no. 51
52.Garcia HH, Gilman RH, Catacora M, Verastegui M, Gonzalez AE, Tsang VC. Serologic evolution of neurocysticercosis patients after antiparasitic therapy. Cysticercosis Working Group in Peru. J Infect Dis 1997;175:486-9.  Back to cited text no. 52
53.Larralde C, Montoya RM, Sciutto E, Diaz ML, Govezensky T, Coltorti E. Deciphering western blots of tapeworm antigens (Taenia solium, Echinococcus granulosus, and Taenia crassiceps) reacting with sera from neurocysticercosis and hydatid disease patients. Am J Trop Med Hyg 1989;40:282-90.  Back to cited text no. 53
54.Atluri VS, Singhi PD, Khandelwal N, Malla N. 2D-PAGE analysis of Taenia solium metacestode 10-30 kDa antigens for the serodiagnosis of neurocysticercosis in children. Acta Trop 2011;118:165-9.  Back to cited text no. 54
55.Tsang VC, Pilcher JA, Zhou W, Boyer AE, Kamango-Sollo EI, Rhoads ML, et al. Efficacy of the immunoblot assay for cysticercosis in pigs and modulated expression of distinct IgM/IgG activities to Taenia solium antigens in experimental infections. Vet Immunol Immunopathol 1991;29:69-78.  Back to cited text no. 55
56.Hancock K, Khan A, Williams FB, Yushak ML, Pattabhi S, Noh J, et al. Characterization of the 8-kilodalton antigens of Taenia solium metacestodes and evaluation of their use in an enzyme-linked immunosorbent assay for serodiagnosis. J Clin Microbiol 2003;41:2577-86.  Back to cited text no. 56
57.Michelet L, Fleury A, Sciutto E, Kendjo E, Fragoso G, Paris L, et al. Human neurocysticercosis: Comparison of different diagnostic tests using cerebrospinal fluid. J Clin Microbiol 2011;49:195-200.  Back to cited text no. 57
58.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;100:39-48.  Back to cited text no. 58
59.Fleury A, Hernández M, Avila M, Cárdenas G, Bobes RJ, Huerta M, et al. Detection of HP10 antigen in serum for diagnosis and follow-up of subarachnoidal and intraventricular human neurocysticercosis. J Neurol Neurosurg Psychiatry 2007;78:970-4.  Back to cited text no. 59
60.Fleury A, Hernández M, Fragoso G, Parkhouse RM, Harrison LJ, Sciutto E. Detection of secreted cysticercal antigen: A useful tool in the diagnosis of inflammatory neurocysticercosis. Trans R Soc Trop Med Hyg 2003;97:542-6.  Back to cited text no. 60
61.Garcia HH, Gonzalez AE, Gilman RH, Bernal T, Rodriguez S, Pretell EJ, et al. Circulating parasite antigen in patients with hydrocephalus secondary to neurocysticercosis. Am J Trop Med Hyg 2002;66:427-30.  Back to cited text no. 61
62.Garcia HH, Harrison LJ, Parkhouse RM, Montenegro T, Martinez SM, Tsang VC, 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;92:411-4.  Back to cited text no. 62
63.Biswas R, Parija SC. A rapid slide agglutination test for the diagnosis of neurocysticercosis in the rural health set up. Trop Parasitol 2011;1:94-8.  Back to cited text no. 63
  Medknow Journal  
64.Parija M, Biswas R, Harish BN, Parija SC. Detection of specific cysticercus antigen in the urine for diagnosis of neurocysticercosis. Acta Trop 2004;92:253-60.  Back to cited text no. 64
65.Castillo Y, Rodriguez S, García HH, Brandt J, Van Hul A, Silva M, et al. Urine antigen detection for the diagnosis of human neurocysticercosis. Am J Trop Med Hyg 2009;80:379-83.  Back to cited text no. 65
66.Almeida CR, Ojopi EP, Nunes CM, Machado LR, Takayanagui OM, Livramento JA, et al. Taenia solium DNA is present in the cerebrospinal fluid of neurocysticercosis patients and can be used for diagnosis. Eur Arch Psychiatry Clin Neurosci 2006;256:307-10.  Back to cited text no. 66
67.Harrison LJ, Delgado J, Parkhouse RM. Differential diagnosis of Taenia saginata and Taenia solium with DNA probes. Parasitology 1990;100 Pt 3:459-61.  Back to cited text no. 67
68.Yera H, Dupont D, Houze S, Ben M'rad M, Pilleux F, Sulahian A, et al. Confirmation and follow-up of neurocysticercosis by real-time PCR in cerebrospinal fluid samples of patients living in France. J Clin Microbiol 2011;49:4338-40.  Back to cited text no. 68
69.Nash TE, Singh G, White AC, Rajshekhar V, Loeb JA, Proaño JV, et al. Treatment of neurocysticercosis: Current status and future research needs. Neurology 2006;67:1120-7.  Back to cited text no. 69
70.Del Brutto OH, Roos KL, Coffey CS, García HH. Meta-analysis: Cysticidal drugs for neurocysticercosis: Albendazole and praziquantel. Ann Intern Med 2006;145:43-51.  Back to cited text no. 70
71.Flisser A, Gauci CG, Zoli A, Martinez-Ocaña J, Garza-Rodriguez A, Dominguez-Alpizar JL, et al. Induction of protection against porcine cysticercosis by vaccination with recombinant oncosphere antigens. Infect Immun 2004;72:5292-7.  Back to cited text no. 71
72.Gauci CG, Jayashi CM, Gonzalez AE, Lackenby J, Lightowlers MW. Protection of pigs against Taenia solium cysticercosis by immunization with novel recombinant antigens. Vaccine 2012;30:3824-8.  Back to cited text no. 72
73.Nash TE, Mahanty S, Garcia HH. Neurocysticercosis-more than a neglected disease. PLoS Negl Trop Dis 2013;7:e1964.  Back to cited text no. 73


  [Table 1]

This article has been cited by
1 Chronic administration of cryptolepine nanoparticle formulation alleviates seizures in a neurocysticercosis model
Priscilla Kolibea Mante,Nana Ofori Adomako,Paulina Antwi,Nana Kofi Kusi-Boadum
Current Research in Pharmacology and Drug Discovery. 2021; 2: 100040
[Pubmed] | [DOI]
2 Climate change and epilepsy: Insights from clinical and basic science studies
Medine I. Gulcebi,Emanuele Bartolini,Omay Lee,Christos Panagiotis Lisgaras,Filiz Onat,Janet Mifsud,Pasquale Striano,Annamaria Vezzani,Michael S. Hildebrand,Diego Jimenez-Jimenez,Larry Junck,David Lewis-Smith,Ingrid E. Scheffer,Roland D. Thijs,Sameer M. Zuberi,Stephen Blenkinsop,Hayley J. Fowler,Aideen Foley,Sanjay M. Sisodiya,Simona Balestrini,Samuel Berkovic,Gianpiero Cavalleri,Daniel José Correa,Helena Martins Custodio,Marian Galovic,Renzo Guerrini,David Henshall,Olga Howard,Kelvin Hughes,Anna Katsarou,Bobby P.C. Koeleman,Roland Krause,Daniel Lowenstein,Despoina Mandelenaki,Carla Marini,Terence J. OćBrien,Adrian Pace,Luca De Palma,Piero Perucca,Asla Pitkänen,Finola Quinn,Kaja Kristine Selmer,Charles A. Steward,Nicola Swanborough,Roland Thijs,Phil Tittensor,Marina Trivisano,Sarah Weckhuysen,Federico Zara
Epilepsy & Behavior. 2021; 116: 107791
[Pubmed] | [DOI]
3 Neurocysticercosis in a Japanese woman with lung cancer who repeatedly visited endemic countries
Tomoya Kinouchi, Yasuyuki Morishima, Shinichi Uyama, Tadashi Miyamoto, Hidehisa Horiguchi, Naomi Fujimoto, Hiromi Ueta
BMC Infectious Diseases. 2021; 21(1)
[Pubmed] | [DOI]
4 Neurocysticercosis and epilepsy in sub-Saharan Africa
Athanase Millogo,Alfred Kongnyu Njamnshi,Mesu’a Kabwa-PierreLuabeya
Brain Research Bulletin. 2018;
[Pubmed] | [DOI]
5 Infectious Diseases of Poverty in Children
Caitlin Hansen,Elijah Paintsil
Pediatric Clinics of North America. 2016; 63(1): 37
[Pubmed] | [DOI]
6 Neglected tropical diseases: progress towards addressing the chronic pandemic
David H Molyneux,Lorenzo Savioli,Dirk Engels
The Lancet. 2016;
[Pubmed] | [DOI]
7 IFN-gamma role in granuloma formation in experimental subcutaneous cysticercosis
Aline A. Freitas,Vânia B.L. Moura,Vicente R.C. Irusta,Marina C. Vinaud,Milton A.P. Oliveira,Ruy S. Lino-Júnior
Experimental Parasitology. 2016;
[Pubmed] | [DOI]
8 Imaging spectrum of neurocysticercosis
Jing-Long Zhao,Alexander Lerner,Zheng Shu,Xing-Jun Gao,Chi-Shing Zee
Radiology of Infectious Diseases. 2015; 1(2): 94
[Pubmed] | [DOI]
9 Relevance of 3D magnetic resonance imaging sequences in diagnosing basal subarachnoid neurocysticercosis
Roger Carrillo Mezo,Javier Lara García,Mariana Arroyo,Agnčs Fleury
Acta Tropica. 2015; 152: 60
[Pubmed] | [DOI]
10 Genome analysis of Excretory/Secretory proteins in Taenia solium reveals their Abundance of Antigenic Regions (AAR)
Sandra Gomez,Laura Adalid-Peralta,Hector Palafox-Fonseca,Vito Adrian Cantu-Robles,Xavier Soberón,Edda Sciutto,Gladis Fragoso,Raúl J. Bobes,Juan P. Laclette,Luis del Pozo Yauner,Adrián Ochoa-Leyva
Scientific Reports. 2015; 5: 9683
[Pubmed] | [DOI]
11 Characterization of a Thioredoxin-1 Gene fromTaenia soliumand Its Encoding Product
Lucía Jiménez,Oscar Rodríguez-Lima,Alicia Ochoa-Sánchez,Abraham Landa
BioMed Research International. 2015; 2015: 1
[Pubmed] | [DOI]
12 Longer epilepsy duration and multiple lobe involvement predict worse seizure outcomes for patients with refractory temporal lobe epilepsy associated with neurocysticercosis
Lucas Crociati Meguins,Rodrigo Antônio Rocha da Cruz Adry,Sebastiăo Carlos da Silva Júnior,Carlos Umberto Pereira,Jean Gonçalves de Oliveira,Dionei Freitas de Morais,Gerardo Maria de Araújo Filho,Lúcia Helena Neves Marques
Arquivos de Neuro-Psiquiatria. 2015; 73(12): 1014
[Pubmed] | [DOI]
13 Culinary delights and travel? A review of zoonotic cestodiases and metacestodiases
Akira Ito,Christine M. Budke
Travel Medicine and Infectious Disease. 2014; 12(6): 582
[Pubmed] | [DOI]
14 Untangling the pathomechanisms of temporal lobe epilepsy—The promise of epileptic biomarkers and novel therapeutic approaches
Tibor Szilágyi,Iringó Száva,Erzsébet-Júlia Metz,István Mihály,Károly Orbán-Kis
Brain Research Bulletin. 2014;
[Pubmed] | [DOI]


    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

  In this article
    Article Tables

 Article Access Statistics
    PDF Downloaded315    
    Comments [Add]    
    Cited by others 14    

Recommend this journal