|Year : 2022 | Volume
| Issue : 1 | Page : 15-20
High prevalence of neurocysticercosis among patients with epilepsy in a tertiary care hospital of Assam, India
K Rekha Devi1, Debasish Borbora2, Narayan Upadhyay3, Dibyajyoti Goswami1, SK Rajguru1, Kanwar Narain1
1 ICMR, Regional Medical Research Centre, Dibrugarh, Assam, India
2 ICMR, Regional Medical Research Centre, Dibrugarh; Department of Biotechnology, Gauhati University, Guwahati, Assam, India
3 Department of Neurology, Assam Medical College and Hospital, Dibrugarh, Assam, India
|Date of Submission||28-Jun-2020|
|Date of Decision||19-Aug-2020|
|Date of Acceptance||18-Sep-2020|
|Date of Web Publication||26-Jun-2022|
ICMR, Regional Medical Research Centre, N. E. Region, Dibrugarh - 786 001, Assam
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background: Neurocysticercosis (NCC) is a parasitic disease of the central nervous system, which is caused by the metacestode of the pork tapeworm, Taenia solium. The present unicentric, hospital-based, cross-sectional study was undertaken to assess the contribution of NCC as a cause of active epilepsy among patients attending a tertiary health care center in Assam, India.
Materials and Methods: Over a period of 2 years, 152 active epilepsy patients were investigated based on clinical, epidemiological, neuroimaging (contrast-enhanced computerized tomography), and immunological techniques to establish the diagnosis of NCC. A precoded questionnaire was administered to patients and/or guardians to collect detailed medical history.
Results: Ninety-three cases (61.2%) fulfilled either definitive or probable diagnostic criteria for NCC. Anti-cysticercus immunoglobulin G antibodies were detected by ELISA and enzyme electro-immune transfer blot in 69 (45.4%) active epilepsy patients. Seroprevalence was higher in males, 46.6% (54/116); than in females, 41.7% (15/36), and increased significantly with age; peaking in the 20–39 years age group (36/76; χ2 = 5.64; P = 0.02). Among the seropositive cases, 54 (78.3%) were diagnosed with NCC. A significantly higher number of seropositive individuals were diagnosed with NCC in the 20–39 years age group as compared to the 40 years and above age group (χ2 = 6.28; P = 0.01). The association between seropositivity for NCC, and the number of lesions in the brain was statistically significant (χ2 = −8.33; P = 0.003).
Conclusions: This study indicates that NCC is a major cause of active epilepsy in Assam. A high prevalence of pediatric NCC is also a major concern.
Keywords: Epilepsy, hospital-based, India, Northeast, pediatric neurocysticercosis
|How to cite this article:|
Devi K R, Borbora D, Upadhyay N, Goswami D, Rajguru S K, Narain K. High prevalence of neurocysticercosis among patients with epilepsy in a tertiary care hospital of Assam, India. Trop Parasitol 2022;12:15-20
|How to cite this URL:|
Devi K R, Borbora D, Upadhyay N, Goswami D, Rajguru S K, Narain K. High prevalence of neurocysticercosis among patients with epilepsy in a tertiary care hospital of Assam, India. Trop Parasitol [serial online] 2022 [cited 2023 Mar 28];12:15-20. Available from: https://www.tropicalparasitology.org/text.asp?2022/12/1/15/348308
| Introduction|| |
Epilepsy is a neurological disorder that affects >10 million patients in India. It is also a major public health concern in the tea garden communities of Assam, Northeast India. One of the main causes of community-acquired epilepsy in resource-poor endemic regions (Asia, Sub-Saharan Africa, and Latin America) is neurocysticercosis (NCC), which is caused by the metacestode (larva) of the pork tapeworm, Taenia solium., Humans (only definitive host), suffer from taeniasis when the adult tapeworms reside in the intestine, while both humans and pigs (intermediate hosts) suffer from cysticercosis as the larvae infect various soft tissues., NCC is the most severe form of cysticercosis wherein cysts develop in the central nervous system (CNS), leading to pathological symptoms, including epileptic seizures, headaches, and hydrocephalus. It can be acquired under any cultural and socioeconomic conditions where there is close contact with a taeniasis carrier, but its management becomes problematic in resource-poor settings where sanitation, hygiene, and pig management practices are poor.
NCC has been reported from different parts of India, but reports about its prevalence and association as a definable risk factor of epilepsy are largely lacking from Northeast India. Hence in light of the above, the current hospital-based study is aimed to determine the incidence of NCC among people with active epilepsy at a tertiary health-care facility in Assam, India.
| Materials and Methods|| |
The present study was approved by the ethics committee, and all the experiments were carried out in accordance with that approval. Written informed consent was obtained from all patients and/or their guardians (in the case of minors) before including them for this study.
This hospital-based study was conducted at Assam Medical College and Hospital in Dibrugarh-a major tertiary health care center in the study area. The sample size was calculated, assuming that the occurrence of NCC related seizures among people with epilepsy (p) would be 10% (based on data from prior clinical studies conducted in endemic regions). Other assumptions made during the sample size calculation were a 95% confidence interval (CI) with a 5% margin of error (d). This yields a sample size of 138. Assuming 10% nonresponse, we planned to enroll 152 active epilepsy patients. All patients older than 5 years, who reported seizures, were evaluated by a neurologist. Patients with a history of any other chronic disease or with a history of head injury and females with underlying pregnancy were excluded from the present study. At the end of 2 years, a total of 152 patients with active epilepsy were recruited.
A precoded questionnaire was administered to patients and/or guardians in the local language to collect detailed medical history, including the history of seizure as well as other known risk factors leading to epilepsy such as head trauma, alcohol consumption, and diseases like tuberculosis.
Diagnostic criteria for active epilepsy
A prevalent case of active epilepsy was defined as two or more afebrile seizures unrelated to the withdrawal of alcohol or drugs or to acute metabolic disorders within 5-year period of the interview. Epileptic seizures and syndromes were grouped according to a classification suggested for developing countries, which conforms to the International League Against Epilepsy guidelines.,
Diagnostic criteria for neurocysticercosis
The diagnosis of NCC was based on the modified diagnostic criteria suggested by Del Brutto and guidelines specific to the Indian context by Garg., These guidelines are intended to help differentiate between cysticercus granuloma and tuberculoma as we have previously reported a high incidence of pulmonary tuberculosis in the tea garden community of Assam. Based on the objective evaluation of clinical, radiological, immunological, and epidemiological data, a set of defined criteria were used to establish cases into either definitive or probable NCC.
Computed tomography scan of the brain
Contrast-enhanced computed tomography (CT) imaging of the brain was done for all cases. Neuroimaging studies were carried out to identify cystic lesions, which are pathognomonic for cysticercosis. Cysticerci in the brain parenchyma were initially classified into three groups according to definitions proposed by Carpio et al. These cysticerci were then classified into four histopathological stages : Active (vascular), transitional (colloidal vascular and granular vascular), and inactive/calcified (nodular calcified); based on suggestions made by Escobar and Salgado et al.,, Scolex within a parenchymal cysticercus cyst was considered absolute and diagnostic of NCC. Brain imaging observations, including cystic lesion without a visible scolex, parenchymal brain calcifications, and single or multiple rings or nodular enhancing lesions; were considered highly suggestive of NCC. A diagnosis of hydrocephalus or abnormal leptomeningeal enhancement was considered compatible with NCC. Solitary calcifications were considered compatible only after other forms of granulomatous diseases, mainly tuberculosis, were clinically ruled out.
Enzyme electro-immune transfer blot analysis
For the immunoblot assay, we used cystic fluid obtained from cysticerci collected from locally available infected pigs. Immunoblotting was carried out by a slight modification of the method described earlier. A sample was considered positive if one or more bands <50 kDa were detected.
Seroprevalence of immunoglobulin G antibodies against Taenia solium metacestode
A total of 152 serum samples were available for the detection of specific immunoglobulin G (IgG) antibodies against T. solium metacestode. These samples were tested using an in-house ELISA method, and absorbance measurements were taken at 492 nm using a microplate reader. The sensitivity, specificity, positive, and negative predictive values of the IgG-ELISA test was determined using sera samples from confirmed NCC cases and sera from patients infected with other parasitic diseases. During our internal testing, the IgG-ELISA test had a 100% sensitivity for the diagnosis of NCC in patients with multiple (active and mixed) cysts in the brain parenchyma (unpublished data).
Data were compiled and subjected to analysis using IBM SPSS version 16.0 (SPSS Inc., Chicago, IL, USA). The outcomes for continuous variables are expressed as median (interquartile range). Categorical data values are presented as numbers. For analyses, study participants of different ages were segregated by age into four groups (≤10, 11–19, 20–39, ≥40 years). The Chi-square test was performed for testing the differences between proportions across select categorical variables (https://www. medcalc.org/calc/comparison_of_proportions. php, last accessed on 22.06.2020). All statistical tests were two-tailed. A probability (P) value of < 0.05 was used as the level of significance.
| Results|| |
The study made 93 (61.2%) diagnoses of NCC among the active epilepsy cases with a male, 75/116 (64.7%); to female, 18/36 (50.0%); ratio of 4.17:1 (χ2 = −2.48; P = 0.115). The age range of the male cases was 5–74 years (median age = 30 years) and that of female cases was from 8 to 65 years (median age = 27.0 years). All of these cases had parasitic lesions suggestive of NCC on CT imaging. Solitary lesions were more predominant (61/93; 65.6%) than multiple lesions (32/93; 34.4%) [Table 1] [Figure 1]. Among individuals with a solitary lesion, the active ring-enhancing lesion is the most frequent presentation (39/93).
|Table 1: Computed tomography scan features of active epilepsy patients with neurocysticercosis (n=93)|
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|Figure 1: Contrast-enhanced computed tomography scan showing (a) solitary, and (b) multiple ring enhancing lesions with surrounding edema|
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Of the 152 active epilepsy patients tested, 61 (40.1% overall) had IgG antibodies for T. solium cysticercosis by ELISA [Table 2]. Interestingly, 15 patients who tested positive had no apparent brain lesions on CT. Further, the association between seropositivity for NCC, and the number of lesions in the brain was found to be statistically significant (χ2 = 8.33; P = 0.003). Patient samples that tested negative during IgG-ELISA were further evaluated by enzyme-linked electro-immune transfer blot (EITB) assay. Overall, anti-cysticercus IgG antibodies were detected in 69 (45.4%) active epilepsy patients; the majority of whom presented solitary active lesion (29.0%) followed by multiple degenerative lesions (18.8%), multiple active lesions (13.0%), solitary calcified lesion (11.6%), and multiple calcified lesions (5.8%).
|Table 2: Results of anti-cysticercus immunoglobulin G-ELISA (n=152) in active epilepsy patients with respect to type of lesions detected in brain by computed tomography|
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Seroprevalence (as determined by EITB or IgG-ELISA) was higher in males, 46.6% (54/116); than in females, 41.7% (15/36), and increased significantly with age; peaking in the 20–39 years age group (36/76; Overall trend χ2 = 5.64; P = 0.02) [Table 3]. In this study group, involuntary muscle movements were the most common clinical presentation (39.7%), followed by unconsciousness (36.0%) and headaches (35.3%). Most of these active epilepsy patients (83.8%) had a history of pork consumption, which significantly increased their risk of acquiring NCC (odds ratio [OR], 2.73; 95% CI, 1.1–6.7; P = 0.03).
|Table 3: Gender and age-associated changes in neurocysticercosis seropositivity in active epilepsy patients|
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| Discussion|| |
NCC has been identified as a major cause of epilepsy in the developing world. However, in spite of India being in the endemic belt, the proportion of epilepsy due to NCC is not well documented.
In the present study, a high prevalence of NCC was recorded among active epilepsy patients attending a tertiary care center in Dibrugarh, Assam. Ninety-three cases (61.2%) fulfilled either definitive or probable diagnostic criteria for NCC; which is greater than those reported by previous hospital-based studies from NCC endemic areas in South Africa (61.1%), Bhutan (25.4%), Rwanda (23.3%), Nepal (16.0%), Tanzania (2.0%–13.7%), Peru (12.0%), and rest of India including Odisha (43.7%), and Andhra Pradesh (27.5%) suggesting that NCC is a larger public health problem in this region.,,,,,,,,
Solitary lesions were the predominant finding in 65.6% of patients. This observation is in agreement with prior clinical and community studies from India, wherein NCC presents itself as solitary cysts but unlike reports from Latin America and China where most cases present more than one viable lesion.,,,,,, In this study, all the cases presented parenchymal NCC. Parenchymal NCC is more common in the Indian subcontinent, while extraparenchymal NCC is frequent in Latin America. This variability could be related to a complex range of host-parasite and environmental interactions.
Seroprevalence against T. solium was also evaluated using both ELISA and EITB. While EITB is the preferred method over ELISA, studies have described that ELISA based on cystic fluid/vesicular fluid of T. solium cysticerci is highly dependable for immunodiagnosis of NCC. As determined by ELISA, 40.1% (61/152) active epilepsy patients and 49.5% (46/93) NCC patients were seropositive. The seronegativity observed during ELISA may be partly associated with the fact that the average time between acquisition of parasite and development of symptomatic infection is about 7 years, and the fact that a sizable number of calcified lesions (solitary, 22/61 and multiple, 10/32) were recorded among NCC patients, which are known to illicit minimal immune response.,
In our case-series, specific serology with EITB method is shown to be better sensitive, especially in cases with “calcified” lesions. The EITB assay detected circulating anti–T. solium antibodies in eight ELISA negative, CT-positive cases (8/47; calcified 62.5% vs. active 37.5%). ELISA negative individuals, with no evidence of cysticercosis of the CNS (NCC) were not considered for EITB. These results are consistent with previous findings that the diagnostic performance of EITB (sensitivity and specificity) when performed using serum is better than that of ELISA., Furthermore, detection of antibody in the serum of patients who presented only calcified NCC lesions does not necessarily imply the existence of undetected viable brain cysts as circulating antibodies may persist over a period of several months or years after the parasites have died.
Seropositivity rate was significantly higher among patients with late-onset epilepsy (after age 20) than in those with earlier onset epilepsy (χ2 = −2.31; P = 0.04). Within this cohort, seroprevalence was higher in males, 46.6% (54/116); than in females, 41.7% (15/36), and increased significantly with age; peaking in the 20–39 years age group (36/76; overall trend χ2 = −5.64; P = 0.02) [Table 3]. Although statistically insignificant, data generated during a regression analysis suggest that individuals in the 20–39 years age group were 2.7-fold more likely to suffer from epilepsy due to NCC (OR, 2.72;95% CI, 0.6–13.1). There is also a significant difference in the number of seropositive individuals diagnosed with NCC in the older age groups (χ2 = −6.28; P = 0.01)-88.9% in the 20–39 years age group versus 60.9% in the 40 years and above age group. Such age-dependent difference in the manifestation of NCC has been reported previously and draws us toward concluding that individuals aged 40 years and above may have developed immunity against T. solium NCC.
Interestingly, in the pediatric age group (all patients aged 1–16 years, n = 23), 4 out of 5 (80.0%) of the seropositive cases and 8 out of 18 (44.4%) of the seronegative cases were diagnosed with NCC (12/23, 52.2%). Although the sample was relatively small and validation requires further research, these rates are greater than those reported by previous hospital-based studies from Nepal (overall frequency 43.0%), Italy (0.4%), Madagascar (17.6%), and rest of India, including Andhra Pradesh (37.7%), and Puducherry (22.8%).,,,, The prevalence, however, is less than that reported from Haryana (54.4%). NCC is less frequently among children (52.2% vs. 62.8%), probably due to age-based differences on the mode of disease acquisition and differences in immune reactivity against the parasite (seropositivity, 21.7% vs. 49.6%).
| Conclusions|| |
Our study identified NCC as a major cause of epilepsy in this region. A high prevalence of pediatric NCC is of major concern and warrants further investigation.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Trinka E, Kwan P, Lee B, Dash A. Epilepsy in Asia: Disease burden, management barriers, and challenges. Epilepsia 2019;60 Suppl 1:7-21.
Medhi GK, Hazarika NC, Shah B, Mahanta J. Study of health problems and nutritional status of tea garden population of Assam. Indian J Med Sci 2006;60:496-505.
] [Full text]
Debacq G, Moyano LM, Garcia HH, Boumediene F, Marin B, Ngoungou EB, et al
. Systematic review and meta-analysis estimating association of cysticercosis and neurocysticercosis with epilepsy. PLoS Negl Trop Dis 2017;11:e0005153.
Ahmad R, Khan T, Ahmad B, Misra A, Balapure AK. Neurocysticercosis: A review on status in India, management, and current therapeutic interventions. Parasitol Res 2017;116:21-33.
Prasad KN, Singh SK. Taeniasis and neurocysticercosis: Emerging public health problems. In: Singh PP, editor. Infectious Diseases and Your Health. Singapore: Springer Singapore; 2018, p. 113-34.
Del Brutto OH. Neurocysticercosis: A review. Sci World J 2012;2012:159821.
Senanayake N, Román GC. Epidemiology of epilepsy in developing countries. Bull World Health Organ 1993;71:247-58.
Winkler AS, Schaffert M, Schmutzhard E. Epilepsy in resource poor countries-Suggestion of an adjusted classification. Epilepsia 2007;48:1029-30.
Guidelines for epidemiologic studies on epilepsy. Commission on Epidemiology and Prognosis, International League Against Epilepsy. Epilepsia 1993;34:592-6.
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.
Garg RK. Diagnostic criteria for neurocysticercosis: Some modifications are needed for Indian patients. Neurol India 2004;52:171-7.
] [Full text]
Chelleng PK, Devi KR, Borbora D, Chetia M, Saikia A, Mahanta J, et al
. Risk factors of pulmonary tuberculosis in tea garden communities of Assam, India. Indian J Med Res 2014;140:138-41.
] [Full text]
Carpio A, Escobar A, Hauser WA. Cysticercosis and epilepsy: A critical review. Epilepsia 1998;39:1025-40.
Escobar A. The pathology of neurocysticercosis. In: Palacios E, Rodríguez-Carbajal J, Taveras JM, editors. Cysticercosis of the Central Nervous System. Springfield, IL: Charles C Thomas Pub Limited; 1983. p. 27-54.
Carpio A, Placencia M, Santillán F, Escobar A. A proposal for classification of neurocysticercosis. Can J Neurol Sci 1994;21:43-7.
Salgado P, Rojas R, Sotelo J. Cysticercosis. Clinical classification based on imaging studies. Arch Intern Med 1997;157:1991-7.
Del Brutto OH. Neurocysticercosis: Up-dating in diagnosis and treatment. Neurologia 2005;20:412-8.
Yang HJ, Chung JY, Yun D, Kong Y, Ito A, Ma L, et al
. Immunoblot analysis of a 10 kDa antigen in cyst fluid of Taenia solium
metacestodes. Parasite Immunol 1998;20:483-8.
Ocana GS, Sablon JC, Tamayo IO, Arena LA, Ocana LM, Govender SJ. Neurocysticercosis in patients presenting with epilepsy at St Elizabeth's Hospital, Lusikisiki. S Afr Med J 2009;99:588-91.
Brizzi K, Pelden S, Tshokey T, Nirola DK, Diamond MB, Klein JP, et al
. Neurocysticercosis in Bhutan: A cross-sectional study in people with epilepsy. Trans R Soc Trop Med Hyg 2016;110:517-26.
Rottbeck R, Nshimiyimana JF, Tugirimana P, Düll UE, Sattler J, Hategekimana JC, et al
. High prevalence of cysticercosis in people with epilepsy in southern Rwanda. PLoS Negl Trop Dis 2013;7:e2558.
Ojha R, Shah D, Shrestha A, Koirala S, Dahal A, Adhikari K, et al
. Neurocysticercosis in Nepal: A retrospective clinical analysis. Neuroimmunol Neuroinflammation 2015;2:167. [Full text]
Schmidt V, O'Hara MC, Ngowi B, Herbinger KH, Noh J, Wilkins PP, et al
. Taenia solium
cysticercosis and taeniasis in urban settings: Epidemiological evidence from a health-center based study among people with epilepsy in Dares Salaam, Tanzania. PLoS Negl Trop Dis 2019;13: e0007751.
Winkler AS, Blocher J, Auer H, Gotwald T, Matuja W, Schmutzhard E. Epilepsy and neurocysticercosis in rural Tanzania-An imaging study. Epilepsia 2009;50:987-93.
Garcia HH, Gilman R, Martinez M, Tsang VC, Pilcher JB, Herrera G, et al
. Cysticercosis as a major cause of epilepsy in Peru. The Lancet 1993;341:197-200.
Sahu PS, Patro S, Jena PK, Swain SK, Das BK. Imaging and serological-evidence of neurocysticercosis among patients with seizures in Odisha, an unexplored eastern coastal province in India. J Clin Diagn Res 2015;9:DC06-10.
Pappala BC, Indugula JP, Talabhatula SK, Kolli RS, Shrivastava AK, Sahu PS. Diagnosis of neurocysticercosis among patients with seizures in northern coastal districts of Andhra Pradesh, India. Asian Pacific Journal of Tropical Biomedicine 2016;6:903-8.
Singh G, Singh P, Singh I, Rani A, Kaushal S, Avasthi G. Epidemiologic classification of seizures associated with neurocysticercosis: Observations from a sample of seizure disorders in neurologic care in India. Acta Neurologica Scandinavica 2006;113:233-40.
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.
Raina SK, Razdan S, Pandita KK, Sharma R, Gupta VP, Razdan S. Active epilepsy as indicator of neurocysticercosis in rural Northwest India. Epilepsy Res Treat 2012;2012:802747.
Singh G. Neurocysticercosos in South-Central America and the Indian subcontinent. A comparative evaluation. Arq Neuropsiquiatr 1997;55:349-56.
Prasad KN, Verma A, Srivastava S, Gupta RK, Pandey CM, Paliwal VK. An epidemiological study of asymptomatic neurocysticercosis in a pig farming community in Northern India. Trans R Soc Trop Med Hyg 2011;105:531-6.
Singhi P. Neurocysticercosis. Ther Adv Neurol Disord 2011;4:67-81.
Suzuki LA, Rossi CL. Evaluation of two Taenia solium
cysticercal antigenic preparations (vesicular fluid and a glycoprotein fraction with affinity for lentil lectin) for the immunodiagnosis of neurocysticercosis by enzyme-linked immunosorbent assay (ELISA). Arq Neuropsiquiatr 2011;69:470-4.
Brunetti E. Cystic Echinococcosis. In: Schwartz E, editor. Tropical Diseases in Travelers. Hoboken, New Jersey: John Wiley & Sons; 2009. p. 264-74.
Garcia HH, O'Neal SE, Noh J, Handali S; Cysticercosis Working Group in Peru. Laboratory diagnosis of neurocysticercosis (Taenia solium
). J Clin Microbiol 2018;56: e00424-18.
Gupta MM, Chaudhary N, Pathak S, Agrawal N, Yadav J, Shrestha S, et al
. Neurocysticercosis in children with seizures: A cross-sectional Study. Int J Pediatr 2018;2018:1030878.
Zammarchi L, Angheben A, Fantoni T, Chiappini E, Mantella A, Galli L, et al
. Screening for neurocysticercosis in internationally adopted children: Yield, cost and performance of serological tests, Italy, 2001 to 2016. Euro Surveill 2018;23:1700709.
Grill J, Rakotomalala W, Andriantsimahavandy A, Boisier P, Guyon P, Roux J, et al
. High prevalence of serological markers of cysticercosis among epileptic Malagasy children. Ann Trop Paediatr 1996;16:185-91.
Sahu PS, Seepana J, Padela S, Sahu AK, Subbarayudu S, Barua A. Neurocysticercosis in children presenting with afebrile seizure: Clinical profile, imaging and serodiagnosis. Rev Inst Med Trop Sao Paulo 2014;56:253-8.
Thamilselvan P, Muthuraman KR, Mandal J, Parija SC. Rising trends of neurocysticercosis: A serological report from tertiary-care hospital in South India. Trop Parasitol 2016;6:141-6.
] [Full text]
Mital AK, Choudhary P, Jain RB. Prevalence and risk factors for neurocysticercosis in children with a first-onset seizure in rural North India. Paediatr Int Child Health 2020;40:158-65.
Zammarchi L, Angheben A, Gobbi F, Zavarise G, Requena-Mendez A, Marchese V, et al
. Profile of adult and pediatric neurocysticercosis cases observed in five Southern European centers. Neurol Sci 2016;37:1349-55.
[Table 1], [Table 2], [Table 3]