The long-term cognitive consequences of calcified neurocysticercosis (NCC) remain poorly understood. This population-based study investigates cognitive trajectories in individuals with calcified NCC in coastal Ecuador. Utilizing repeated Montreal Cognitive Assessment (MoCA) screenings, the study evaluates whether calcified NCC independently contributes to cognitive decline and the role of hippocampal atrophy (HA) in this context. Among 720 community dwellers ages 40 years old and older, 85 (12%) had calcified NCC. The mean interval between baseline and first follow-up MoCA was 3.27 ± 1.07 years and between baseline and second follow-up MoCA was 10.87 ± 1.22 years. Of 720 participants, 617 (86%) completed the first follow-up MoCA, and 464 (75%) of them also had the subsequent follow-up MoCA. Proportions of NCC patients included in follow-ups were consistent with their representation at baseline. Baseline MoCA scores (β: 0.40; 95% CI: −0.48 to 1.29) or rates of MoCA decline at follow-up visits (β: 0.17; 95% CI: −0.67 to 1.0) did not differ significantly between NCC and non-NCC participants after adjusting for relevant covariates. The magnetic resonance imaging substudy showed that 31 of 83 NCC cases and 40 of 283 controls had HA (adjusted odds ratio: 2.63; 95% CI: 1.15–4.11). Additionally, HA was significantly associated with lower MoCA scores at baseline (β: −1.86; 95% CI: −2.98 to −0.74) and follow-up (β: −2.76; 95% CI: −3.83 to −1.69). These results suggest that calcified NCC alone was not associated with cognitive decline over time. However, NCC-associated HA emerged as a major determinant of poor cognitive performance.

Residual brain calcifications that occur after antiparasitic treatment in neurocysticercosis (NCC) can serve as foci of enduring neuroinflammation and associated seizures. Etidronate, a first-generation bisphosphonate, has exhibited efficacy in reducing the formation of ectopic brain calcification. In the present proof-of-concept study, its effects on post-treatment calcifications were evaluated in 12 pigs naturally infected with NCC, confirmed via magnetic resonance imaging. All animals received albendazole plus praziquantel for 5 days, either alone ( n = 6) or with etidronate (20 mg/kg/day for 2 weeks, then 10 mg/kg/day for 8 weeks; n = 6). Eight months post-treatment, the animals were euthanized for ex vivo brain computed tomography, histology, and scanning electron microscopy of calcified lesions. Etidronate reduced the risk of calcification by 21% (risk ratio = 0.79; 95% CI: 0.65–0.90; P = 0.020); however, there was considerable individual variability in the magnitude of this risk reduction, as well as significantly decreased calcium and phosphorus content in granulomas. Etidronate was well tolerated and may serve as an adjunctive therapy to reduce residual calcification after antiparasitic treatment in NCC.

Neurocysticercosis (NCC) remains a major public health problem in endemic countries. Clinical manifestations and therapeutic strategies vary depending on the location of the parasite. While the benefits of cysticidal treatment are well established for parenchymal and subarachnoid NCC, the optimal management of intraventricular NCC (IVNCC) remains controversial. We conducted a retrospective study of 51 patients: 37 (72.54%) received cysticidal treatment as initial therapy and 14 (27.45%) underwent neurosurgical intervention. Although six months after treatment, the proportion of patients with inactive disease was higher in the surgical group, no significant difference was observed after one year. Patients in both groups showed significant improvement in functionality as measured by the Karnofsky Index (KI), with no significant difference between groups. These results are consistent with cysticidal treatment being a valid therapeutic option for IVNCC, with the choice of management largely determined by the available medical infrastructure and the degree of specialization of healthcare personnel.

Differential astrocyte activation by Taenia solium antigens: Specific induction of IL-10 and IL-1β by Excretory/Secretory (ES) products.

Neurocysticercosis (NCC) is a common parasitic infection of the central nervous system and a known cause of focal epilepsy. Its potential role in triggering or contributing to mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) is suggested, but the impact on brain volumetry remains unclear. This study aimed to assess volumetric differences in the brain, with a particular focus on the hippocampus and temporal lobes, in patients with NCC, MTLE, MTLE-HS, and their combinations. This was an observational, cross-sectional, retrospective, single-center exploratory study including five groups: healthy controls; isolated MTLE; isolated NCC; MTLE-HS; and MTLE-HS combined with NCC (MTLE-HS plus NCC). All participants had at least one magnetic resonance imaging (MRI) examination suitable for volumetric post-processing. Volumetric analysis was performed on cerebral cortex regions (frontal, parietal, temporal, and occipital lobes), cerebellum, total and white matter limbic system, amygdala, hippocampus, and thalamus using the T1 MultiAtlas Segmentation tool (Brain GPS©). We also assessed sensitivity by estimating the minimum detectable difference from adjusted models and performed an exploratory analysis of NCC lesion topography with Welch t-tests on lobar/subcortical volumes. After adjusting for age and sex, no significant group differences were found in hippocampal or temporal lobe volumetrics (all p > .10). Effect sizes were small (partial η2 ≤ .10), and MANOVA confirmed the absence of a global effect (Pillai's Trace = .114, p = .623). Adjusted means showed only modest variation with overlapping confidence intervals, indicating that differences likely reflect individual variability rather than systematic group effects. The findings indicate that NCC, whether isolated or combined with MTLE-HS, does not cause significant alterations in brain volume. This suggests the absence of an additive or synergistic effect of NCC on brain morphostructural changes in patients with MTLE-HS. These results contribute to understanding the pathophysiology of epilepsy related to NCC and hippocampal sclerosis, supporting that volumetric brain changes may not underlie their association.

Abstract: Neurocysticercosis (NCC), caused by the larval stage of Taenia solium, is a leading cause of acquired epilepsy, contributing to 30–50% of seizure cases in endemic regions like Latin America and Southeast Asia. Infection occurs via ingestion of T. solium eggs, leading to CNS cyst formation. Symptoms include seizures, headaches, hydrocephalus, and neuropsychiatric disorders, influenced by cyst location and stage. Diagnosis involves neuroimaging (MRI, CT), serological tests (EITB), and molecular methods (PCR). Treatment combines antiparasitic agents (albendazole, praziquantel) with corticosteroids, achieving up to 85% cyst resolution. Antiepileptic drugs and surgical interventions address seizures and complications like hydrocephalus. Preventive strategies, including sanitation, pig farming control, and education, are vital. Emerging therapies, such as immunomodulators and novel antiparasitic drugs, offer potential for overcoming treatment challenges. This review emphasizes advancements in NCC management and the need for integrated global efforts to mitigate its burden.

Identifying viable infections in neurocysticercosis (NCC) is crucial for treatment. Neuroimaging is the primary diagnostic tool, but it is not widely available. Moreover, in many cases, imaging diagnosis is not pathognomonic and requires serological confirmation. The serological assay of choice, enzyme-linked immunoelectrotransfer blot using lentil lectin-purified glycoprotein (LLGP-EITB) Taenia solium antigens to detect specific antibodies, exhibits high predictive values for the presence of viable NCC when the results are positive for multiple (>3) antibody bands; it also exhibits high predictive values for the absence of viable infection when the results are negative or the test reacts to a single antibody band. However, its interpretation in terms of viable infection is limited in cases with two or three positive bands (intermediate results), which occur in one-quarter of patients with NCC. The quantification of specific antibodies could allow for the identification of viable infections. Using a multi-antigen, quantitative multiplex bead assay, antibody levels were measured against Taenia solium proteins rGP50, rT24H, and sTs18var1 in 94 patients with intermediate LLGP-EITB results. The antibody-to-rT24H (25.96 versus 5.49; P = 0.0048) and antibody-to-sTs18var1 ratios (3.62 versus 1.37; P = 0.0083) were higher in subjects with viable cysticerci than in controls. Patients with high antibody levels against the proteins rT24H and sTs18var1 were 5.4 times more likely to have a viable infection than those with low antibody levels. The quantification of antibodies against rT24H and sTs18var1 can help define a viable NCC infection.

ABSTRACTIntroduction:Neurocysticercosis (NCC), caused by the larval stage of Taenia solium, is the leading parasitic disease affecting the central nervous system (CNS), particularly in endemic regions like India. NCC often presents with diverse clinical manifestations, complicating diagnosis. Despite its significant burden, limited data exist on the disease’s epidemiology in Jharkhand, an endemic area. This study aimed to evaluate the demographic, clinical, and radiological profiles of NCC and correlate them with serological findings.Materials and Methods:This cross-sectional study was conducted at the Department of Microbiology, Rajendra Institute of Medical Sciences (RIMS), Ranchi, from September 2018 to August 2019. A total of 69 patients with radiological findings suggestive of NCC were included. Neuroimaging (CT/MRI) findings were categorized as definitive or probable NCC based on revised diagnostic criteria. Serum samples were analyzed using ELISA to detect Taenia solium IgG antibodies. Data were statistically analyzed using SPSS version 20.0.Results:Out of 69 patients, 44 (63.8%) were ELISA positive. Males predominated (77.3%), with most cases in the 11–20 years age group (25.0%). Single lesions were more common (59.1%), with the parietal lobe being the most frequently affected site (50.0%). Seizures were reported in 97.7% of cases, with partial seizures with secondary generalization being the most common type (53.5%). Dietary habits revealed high raw vegetable consumption (95.5%) and non-vegetarian diets (79.5%). Definitive NCC was identified in 6.8% of cases, while 93.2% were classified as probable NCC.Conclusion:This study highlights NCC as a significant health concern in Jharkhand, predominantly affecting males and presenting with seizures. The integration of serological testing, radiographic findings, and clinical data is essential for accurate diagnosis. This first-of-its-kind study emphasizes the need for larger community-based research to understand NCC’s true impact in this region.

Frequency and characteristics of cognitive impairment in individuals with calcified neurocysticercosis.

Taenia solium taeniasis/cysticercosis in humans and pigs remains endemic to Uganda. Although, looking at the lifecycle of the parasite, the risk factors are well known, and many biomedical control options exist – no substantial progress has been made in the eradication of T. solium infections in Uganda to date. Contextual factors including socioeconomic, cultural and infrastructural factors, may influence the adoption of interventions. A community-based study using mixed methods and relying on system effects modelling approach was carried out between March and April 2021 in Kamuli district, Eastern Uganda, and Hoima district, Western Uganda. System effects modelling is a non-linear methodology that captures the varied nature of the unique, individually lived experiences and aggregates them to reflect what is experienced at a population level. The aim of the study was to capture individual stakeholder perceptions on the consequences of T. solium infections and barriers to practice known control options. Overall, 27 factors were identified by 192 participants as consequences of being infected with neurocysticercosis (NCC). For taeniasis, 35 factors were identified with 700 edges/connections made by the participants. Enlargement of stomach, weight loss, diarrhoea, weakness, and stunted growth were the most important consequences. Although porcine cysticercosis (PCC) seemed to be poorly understood by the participants, 14 factors were identified which included poor pig growth, loss of market for pig/pork, and poor pork quality. The study also identified important barriers hindering the adoption of control practices, including lack of knowledge on transmission, sociocultural factors, and resource constraints. For women, lack of knowledge on the mode of transmission and lack of a toilet in the compound ranked highly as important barriers with a weighted degree of 31 and 21, respectively, meaning they were identified by more participants unlike men who ranked lack of a toilet first with a weighted degree of 39, followed by lack of knowledge at 24. Different barriers are associated with the adoption of T. solium control practices among community members, stakeholders, and farmers. Despite efforts to address T. solium infections, misconceptions and limited understanding persist among stakeholders, particularly regarding NCC and its associated consequences. The system effects approach supports developing contextualized interventions to help in the control of the diseases associated with this parasite.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12917-025-05026-x.

A bstract Neurocysticercosis (NCC), the most common parasitic infection of the central nervous system, primarily affects children and young adults in endemic regions. Here, we report a case of an 11-year-old female presenting with unprovoked generalized tonic, clonic seizure. Contrast-enhanced magnetic resonance imaging brain demonstrated a well-defined single, ring-enhanced lesion with scolex in the left frontal lobe. The serological test was positive which supports the diagnosis of NCC. A diagnosis of acute symptomatic seizure due to the intraparenchymal NCC was made. This is among the youngest documented cases of NCC from India. The patient responded well to standard anti-parasitic and anti-epileptic therapy. This case underscores the importance of including NCC in the differential diagnosis of infantile unprovoked seizures, especially in endemic regions.

Taeniasis and neurocysticercosis (NCC), caused by Taenia solium, are significant public health concerns recognised by the World Health Organization (WHO) in developing countries across the Americas, Asia, and Africa. Taeniasis occurs in humans after consuming undercooked pork containing the larval stage (Cysticerci), which matures into the adult reproductive form in the intestine, releasing eggs through faeces. Accidental ingestion of these eggs by humans is the primary cause of NCC, a principal contributor to acquired epilepsy in endemic regions. Interrupting this transmission cycle is crucial to reducing the incidence of human NCC and porcine cysticercosis, thereby underscoring the need for accurate diagnosis and timely treatment of taeniasis. Current diagnostic tests for taeniasis, including microscopy, serology, copro-DNA, and coproantigen assays, exhibit variability in sensitivity, reproducibility, cross-reactivity, and accessibility. To overcome these limitations, bioinformatics tools were integrated with recombinant DNA technology to identify protein sequences with immunological potential. These sequences were evaluated in silico and used to construct an expression system. Subsequently, the antigens were expressed in a eukaryotic system, yielding two purified recombinant protein variants of 21 and 30 kDa. Their purification validated via Western blotting of the molecular tag, paves the way for the development of a direct immunological assay for the specific detection of Taenia solium carriers.

Nanosuspensions of fenbendazole and ivermectin induce parasite death and low inflammatory response in experimental neurocysticercosis.

Up to date, the pharmacological treatment for active neurocysticercosis (NCC) includes only two drugs, praziquantel and albendazole; however, the clinical response is not always successful, due to its low bioavailability; therefore, new approaches are needed. The aim of the present study was to evaluate the pharmacological interaction between praziquantel (PZQ) and oxfendazole (OXF) in vitro; also, the drug-drug interaction between PZQ and OXF or fenbendazole (FBZ) in vivo using Taenia crassiceps metacestode was assessed. For the in vitro study, the surface of synergistic interaction (SSI) analysis was used to determine the kind of drug interaction between PZQ and OXF. Additionally, morphological and ultrastructural effects were investigated using transmission scanning electron microscopy. For the in vivo study, different doses of PZQ and FBZ or OXF were combined, and the cysticidal effect was determined. In vitro, results showed that 12 combinations exhibited synergism, and four exhibited additive effects. The 1:5 ratio of PZQ and OXF exhibited the highest synergistic effect, with an 11-fold increase in comparison to their theoretical sum. Microscopic observations revealed damage to the tegument and germinal layer; microtriches, flame cells, and muscular fibers were also affected. In vivo, results showed that PZQ + FBZ and PZQ + OXF (ratios 1:4 and 1:1, respectively) exhibited a synergistic reduction of the parasites. The findings of the present study show the potential of these combinations as a pharmacological alternative for cysticercosis treatment. Complementary studies are needed to determine their benefits in the clinical field.

Neurocysticercosis (NCC) and central nervous system tuberculosis (CNS TB) are two of the most common causes of ring-enhancing lesions in the brain in endemic regions. Their overlapping clinical and radiological features often pose diagnostic dilemmas and challenges, which can delay appropriate treatment. We report the case of a 55-year-old female from Uttarakhand, India, who initially presented with low-grade fever and holocranial headache. Initial CE-MRI suggested NCC, and she was started on albendazole and corticosteroids with partial relief. Two months later, she developed a worsening headache with altered sensorium. Repeat imaging revealed hydrocephalus, and CSF analysis showed elevated protein, hypoglycorrhachia, and lymphocytic pleocytosis. Confirmatory testing with CBNAAT of CSF and endotracheal aspirate detected Mycobacterium tuberculosis, establishing the diagnosis of disseminated TB. She was started on ATT and dexamethasone, which led to gradual improvement in sensorium and resolution of fever. This case highlights diagnostic complexity in differentiating NCC from CNS TB solely based on imaging. It underscores the importance of integrating microbiological investigations like CBNAAT in patients with atypical progression or poor response to antiparasitic therapy, especially in tuberculosis-endemic areas.

ObjectivesTo describe the neuroimaging findings of patients after successful antiparasitic treatment for subarachnoid and intraventricular neurocysticercosis (NCC).MethodsIn this retrospective case series, we reviewed brain MRIs for 6 patients cared for between 2015 and 2021 with confirmed subarachnoid or intraventricular NCC who were successfully treated, defined as a negative Taenia solium antigen and quantitative PCR from CSF.ResultsOn post-treatment MRIs obtained between 0 months and over 4 years after completion of therapy, all patients had persistently abnormal neuroimaging findings, including residual enhancing cysts and leptomeningeal and vascular enhancement, despite continued clinical improvement.DiscussionPersistent post-treatment MRI abnormalities are common in patients with NCC and do not necessarily warrant additional antiparasitic therapy. Although MRI remains a valuable tool for assessing overall treatment response, complete normalization of neuroimaging findings is uncommon in subarachnoid and intraventricular NCC.

Background and objectivesSubarachnoid neurocysticercosis (SANCC) is the most severe manifestation of neurocysticercosis. Most complications (communicating hydrocephalus, ischemic stroke, aneurysm, and subarachnoid hemorrhage) are due to inflammation localized to the central nervous system (CNS). The role of eosinophils in the inflammation associated with SANCC has not been previously studied. MethodsCryopreserved CSF collected as part of a clinical trial for neurocysticercosis (NCC) were assessed for analytes associated with eosinophil activation and recruitment using multiplex bead assays in both subjects with SANCC (n = 28) and in NCC-negative controls (n = 26). The SANCC patients underwent chart review for extraction of clinical variables as well as grouping by disease severity to identify analytes that may be associated with the development of more severe symptoms of SANCC. ResultsEosinophil granule proteins (EGPs – ECP, EDN, and EPO), markers of eosinophil activation, were elevated in the CSF of SANCC patients compared to controls. Moreover, the eosinophil-associated cytokines/chemokines IL-5, IL-13, IL-18, CCL24/eotaxin-2, and CCL26/eotaxin-3 were also significantly elevated in the CSF of SANCC patients compared to controls. In those for whom there were paired specimens (n = 13) from baseline and following cure, there was a significant reduction in these cytokines/chemokines (except CCL26/eotaxin-3). The percentage of CSF white blood cells that were eosinophils was positively correlated with EDN, EPO, IL-5, IL-13, CCL24, CCL26, CCL8, CCL13, and CCL5/RANTES, as well as the time it took to achieve biomarker cure. When SANCC patients were subdivided between those with severe disease and those with non-severe disease, the levels of eosinophil cationic protein (ECP), the CCR3 ligands (CCL7 and CCL5), CCL4, IL-18, and IL-1RA discriminated clearly between these 2 groups. DiscussionThese data provide evidence for eosinophil recruitment and activation in the subarachnoid space in patients with SANCC, as well as for a potential role of eosinophils in driving inflammation-associated complications.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12974-025-03540-1.

IntroductionIn human neurocysticercosis (NCC), the cellular and molecular mechanisms of host-parasite interactions triggering brain inflammation and epileptic seizures in Sub-Saharan Africa are poorly understood. Emerging evidence indicates that the viability of the cyst of the pork tapeworm Taenia solium determines brain inflammation and, thus, symptom development and disease severity. We have previously shown that while viable cyst-released molecules promote immune regulation and often asymptomatic disease, the fluid from degenerating cysts causes inflammation in microglia and peripheral immune cells, potentially driving immune-mediated pathology. This study aims to elucidate the apoptotic signaling pathways underlying this process and their relevance for symptomatic disease in NCC patients.Materials and methodsHuman and porcine peripheral immune cells, as well as murine microglia, were exposed to T. solium cyst vesicular fluid (CVF). Apoptosis signaling pathways were analysed using flow cytometric FLICA (fluorochrome-labeled inhibitors of caspases) caspase 8 and 9 assays, while mitochondrial dysfunction was assessed via TMRE and MitoTracker Deep Red and Green fluorescent probes. Apoptosis-inducing CVF molecules were identified by differential mass spectrometry and functionally tested using specific inhibitors. Caspase activity and soluble mediators (FasL, ROS, TNFα) were measured in NCC asymptomatic and symptomatic patients’ sera, and inflammatory T cell infiltrates expressing caspases near viable and degenerating cysts in naturally infected pig brain slices were examined via immunohistology.ResultsWe found that vesicular fluid derived from cysts primarily induced apoptosis and caspase 3 and 9 activity, and only minimal necrosis, in a dose-dependent manner across central and peripheral immune cells. This effect was prominent in CD16+ monocytes, microglia, and in CD3+ T cell-expressing caspase 3 near degenerating brain cysts. Apoptotic signaling was predominantly mediated by a dynamic remodeling of caspase 9 pathway, accompanied by a significant loss of mitochondrial potential and a sharp decrease in Bid and Bcl2 transcription, favoring the intrinsic over the FasL-dependent extrinsic pathway and mechanisms. This process is primarily mediated by small molecules (< 30 kDa), and remained unaffected by heat and proteinase treatment. Notably, symptomatic NCC patients exhibited elevated FasL levels correlating with increased caspase activity, underscoring the potential contribution of apoptosis to disease pathogenesis.ConclusionsThis study identifies caspase 9-mediated apoptosis as a mechanism of helminth-induced brain inflammation and implicates FasL in symptomatic disease progression. These insights enhance our understanding of NCC immunopathogenesis and may inform future therapeutic strategies targeting apoptotic pathways.

Neurocysticercosis (NCC) is a parasitic infection of the central nervous system caused by the ingestion of Taenia solium eggs, typically through the consumption of undercooked pork or contaminated water. Recognized as a leading preventable cause of epilepsy, NCC poses a significant public health challenge, particularly in developing nations such as India. This retrospective observational study aimed to investigate the clinical manifestations, radiological characteristics, diagnostic approaches, therapeutic interventions, and follow-up outcomes of pediatric patients diagnosed with NCC. To evaluate the clinical and radiological profiles, diagnosis, treatment, and outcomes of NCC in children through a retrospective analysis of medical records. This retrospective study included patients aged 0-12years with a confirmed NCC diagnosis on basis of clinical features, computed tomography (CT)/magnetic resonance imaging (MRI) scans etc. Patients with incomplete medical records or those who did not receive appropriate treatment were excluded. The extracted data included demographic details, clinical symptoms, radiological findings, diagnostic tests, treatment regimens, and follow-up information. Statistical analyses were performed using descriptive and inferential statistics, with a p-value of < 0.05 considered statistically significant. The study included 18 participants with a male-to-female ratio of 1:2.6 and an average age of 7.9years. Convulsions were the most common symptom (94.44%), followed by headache (16.66%), vomiting (22.22%), and fever (11.11%). Among the patients, 44.44% followed a nonvegetarian diet, whereas 55.56% were vegetarians. The most commonly prescribed antiepileptic medications were phenytoin, levetiracetam, and valproate. the most frequently affected brain regions were the frontal (33.33%) and parietal (27.78%) lobes, followed by the temporal and occipital regions. Statistical analyses revealed a significant association (p < 0.05) between generalized seizures and multiple lesions. This study highlights convulsions as the predominant symptom of NCC in pediatric patients. Given its high prevalence in endemic areas, early diagnosis and appropriate management are essential for improving patient outcomes. Further research with larger cohorts is recommended to validate these findings and enhance treatment strategies.

Background: Neurocysticercosis (NCC) and HIV co-infection frequently occur in sub-Saharan Africa, yet the accuracy of available serological tests for NCC in immunosuppressed patients is uncertain. Methodology: We performed a cross-sectional diagnostic study on 101 people living with HIV from two endemic districts in Tanzania. Participants provided serum for cysticercosis antigen ELISA and Western Blot IgG; any positive result prompted neuroimaging investigation with cerebral computed tomography. NCC was diagnosed according to the 2017 revised Del Brutto criteria based on cCT according to Del Brutto criteria modified to exclude serology. Sensitivity, specificity, and area under the receiver–operating–characteristic curve (AUC) were calculated and adjusted for CD4 count and HIV stage. Two algorithms were compared: parallel testing (“either-test-positive”) and sequential screening (Ag ELISA screen, western blot IgG confirm). Results: NCC prevalence was 23%. Western Blot IgG outperformed Ag ELISA (sensitivity 57% vs. 30%; specificity 87% vs. 86%; AUC 0.73 vs. 0.57). Western blot IgG sensitivity declined to 54% when CD4 < 500 cells µL−1, while Ag ELISA remained low. Western blot IgG positivity independently predicted NCC (adjusted odds ratio 4.1, 95% CI 1.4–11.9); Ag ELISA did not. When we counted a positive if either test was positive (parallel rule), sensitivity rose to 78% and NPV to 87%. When we ran Ag ELISA only if IgG was negative (sequential rule), we saved 70% of IgG strips, kept specificity at 95%, and PPV at 69%, but sensitivity fell to 39%. Conclusions: Western blot IgG is the most reliable single serological test for NCC in PLHIV. Parallel testing increased sensitivity and NPV and may suit better primary-level facilities without routine imaging. Sequential testing achieved high specificity, PPV, and conserved test kits, making it ideal for centers with limited reagents or scanner access. Tiered use of these assays can streamline NCC diagnosis in T. solium endemic, resource-limited settings.