|Year : 2016 | Volume
| Issue : 3 | Page : 319-326
Neurocysticercosis: Diagnostic problems & current therapeutic strategies
Department of Neurological Sciences, Christian Medical College & Hospital, Vellore, India
|Date of Submission||18-Jan-2016|
|Date of Web Publication||20-Jan-2017|
Department of Neurological Sciences, Christian Medical College & Hospital, Vellore 632 004, Tamil Nadu
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Neurocysticercosis (NCC) is the most common single cause of seizures/epilepsy in India and several other endemic countries throughout the world. It is also the most common parasitic disease of the brain caused by the cestode Taenia solium or pork tapeworm. The diagnosis of NCC and the tapeworm carrier (taeniasis) can be relatively inaccessible and expensive for most of the patients. In spite of the introduction of several new immunological tests, neuroimaging remains the main diagnostic test for NCC. The treatment of NCC is also mired in controversy although, there is emerging evidence that albendazole (a cysticidal drug) may be beneficial for patients by reducing the number of seizures and hastening the resolution of live cysts. Currently, there are several diagnostic and management issues which remain unresolved. This review will highlight some of these issues.
Keywords: Brain - cysticercosis - diagnosis - epilepsy - taeniasis
|How to cite this article:|
Rajshekhar V. Neurocysticercosis: Diagnostic problems & current therapeutic strategies. Indian J Med Res 2016;144:319-26
| Introduction|| |
Neurocysticercosis (NCC) is the most common parasitic disease affecting the brain and is also the common identifiable cause of new-onset seizures in several regions of the world including India. In a community-based survey involving over 50,000 individuals in a district in Tamil Nadu in southern India, NCC was found to be the cause of active epilepsy (at least one seizure in the five years before the survey) in at least a third of the patients . Based on the results of this large survey, the prevalence of NCC as a cause of active epilepsy in India was calculated to be one per 1000 population. Thus, at least 1.2 million persons in India are suffering from active epilepsy due to NCC. The most common form of the disease in India was the solitary cysticercus granuloma (SCG) ( first identified in 1989) which was seen in up to 60 per cent of patients with NCC ,.
NCC, caused by the larval form of the cestode Taenia solium, is associated with lack of sanitation, poor hygiene and free roaming pigs. Local transmission of the disease is, however, only possible in the presence of an adult Taenia carrier in the gut. Taeniasis is caused only by the consumption of pork infected with cysticercosis, but NCC can also occur in vegetarians and non-pork eaters.
Although the disease can potentially be controlled if not eliminated, there are several socio-economic and healthcare-related issues that constitute barriers to this goal. The problems being faced by clinicians and researchers dealing with NCC include those related to the diagnosis of NCC and taeniasis and their management. This review will address issues related to these problems.
| Diagnostic problems|| |
Since a Taenia carrier is central to the local transmission of the disease, identifying such carriers is also crucial to any control programme. Taenia carriers are typically asymptomatic and, therefore, do not seek medical help. Moreover, the passage of gravid proglottids (the egg-bearing segments of the worm) in the stools of the carriers is intermittent and unpredictable. Unlike Taenia saginata carriers, T. solium carriers do not expel proglottids independent of defecation.
The methods available for diagnosing taeniasis are listed in the [Table 1]. The tests have variable sensitivity being low for stool microscopy and high for the coproantigen assay. In one study, microscopy detected 38 per cent of Taenia carriers whereas coproantigen test detected 98 per cent . However, none of these tests except the species-specific enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (coproPCR) distinguish between infection with T. solium and T. saginata (the latter, beef tapeworm, does not cause NCC).
Confirmation of a positive coproantigen test is obtained by the retrieval of the worm following therapy with niclosamide (single dose of 2 g orally) and a purge . One of the major problems with the coproantigen test has been the issue of false positivity. In the initial field trials of the coproantigen test, 12 of the 79 positive individuals did not expel the worm after treatment and were classified as being false positive . In a study on taeniasis conducted in Vellore district, we found that only two of 10 coproantigen-positive persons expelled the worm following treatment . Explanations for these false positive results include the presence of immature worms in the gut and reactivity to other unknown antigens . Efforts at developing more sensitive and specific tests for taeniasis include a species-specific coproantigen test, a serum antibody test and a coproPCR test ,,. However, none of these have been validated in large field trials. Since none of the advanced tests including the coproantigen test is commercially available, the low sensitivity microscopy remains the most readily accessible test for the diagnosis of taeniasis.
Clinical features: NCC can cause non-specific symptoms such as seizures, headache and focal neurological deficits which can be caused by a number of other pathologies. Hence, there are no specific symptoms or signs that are diagnostic of NCC. Only a rare finding of a live cysticercal cyst seen on fundoscopy in the retina or vitreous of patient with suspected NCC can be considered diagnostic. All patients presenting with new-onset seizures, especially if the seizures are focal with or without secondary generalization should be suspected to have NCC. A search should be performed for any subcutaneous nodules which could indicate subcutaneous cysts, although this finding is rare in those with a single granuloma. Thus, a diagnosis of NCC will require other tests.
Neuroimaging: The mainstay of diagnosis of NCC is neuroimaging using contrast enhanced computerized tomography (CECT) or magnetic resonance imaging (MRI). Both these imaging techniques are expensive, relatively inaccessible to several people in endemic regions and require the use of contrast agents which might have side effects. CT scan is preferred for identifying parenchymal calcifications while MRI is the preferred modality for parenchymal lesions which are in the temporal lobe and frontal lobe close to the skull base, intraventricular cysts and subarachnoid cysts. For patients with SCG, a well performed thin slice CECT scan is as good as an MRI in the detection of the granuloma .
While CT and MRI will almost invariably identify the NCC lesions, there may be diagnostic difficulties in differentiating NCC from other lesions of the brain such as tuberculomas, other parasitic cysts such as hydatid cysts, neoplastic lesions such as gliomas and metastatic lesions. The diagnosis of NCC on imaging is considered to be secure when there is a cystic lesion with an eccentric 'dot' representing the scolex. In CT, the scolex is usually hyperdense, and on T2-weighted MR images, it appears hypointense (dark). Most patients with multiple NCC lesions in the brain parenchyma will show lesions at different stages of involution. Therefore, there will be live cysts, granulomas and calcific lesions, all seen in the same brain. Intraventricular cysts are usually live cysts with a thin wall and can be notoriously difficult to image on CT scan as the density of the cyst fluid is identical to that of the surrounding cerebrospinal fluid (CSF). Since the cyst wall is thin and does not usually enhance with contrast injection, the cyst does not stand out from the surrounding CSF. On MRI using heavily T2 weighted sequences (constructive interference in a steady state or driven equilibrium), intraventricular cysts are easier to identify especially if the scolex is visible [Figure 1]. These special MR sequences utilize the subtle differences in the intensity of the CSF and the cyst fluid to show up the cyst .
|Figure 1: A driven equilibrium sequence axial magnetic resonance image showing a fourth ventricular cysticercal cyst with the scolex seen as a hypointense (dark) dot (arrow).|
Click here to view
There are similar problems in imaging of subarachnoid cysts on CT scans where small cysts will not be distinguishable from the normal subarachnoid cisterns such as sylvian, cerebellopontine angle, suprasellar and prepontine cisterns . Larger subarachnoid cysts can be suspected by asymmetric enlargement of these cisterns, but the cysts themselves are difficult to visualize on the CT scan. Special MR sequences used to identify the intraventricular cysts most often are useful in identifying the subarachnoid cysts. As mentioned above, MRI might miss small parenchymal calcifications unless susceptibility weighted imaging is used.
Immunological tests: Serum is usually tested for the diagnosis of NCC both because of the relative ease of obtaining the sample and also because of some methodological issues; some tests such as the enzyme linked immunotransfer blot (EITB) perform better with serum than with CSF . As of now, EITB is the best serological test available for the diagnosis of NCC. This assay tests for antibodies to seven larval specific antigens. It has a sensitivity of 98 per cent and specificity of 100 per cent in patients with more than one live cyst or subarachnoid disease . However, it only detects the presence of antibodies to the larval antigen and does not necessarily indicate the presence of active disease. Hence, it may be positive in persons with exposure to the parasite antigen (seropositive), those with past treated disease (antibodies may persist up to one year after successful treatment) and those with disease outside the brain . There will be a large number of asymptomatic persons in endemic regions who are seropositive with the EITB but do not have the disease. In a study performed by our group, the seroprevalence (those with positive EITB) was over 15 per cent in a large sample of asymptomatic persons residing in Vellore district . EITB is, however, very specific and does not cross-react with other parasites . In individual patients suspected to have NCC on neuroimaging, a positive EITB can be considered to confirm the diagnosis especially if the individual resides in a non-endemic region. EITB is almost always positive in patients with multiple non-calcified parenchymal lesions, intraventricular and subarachnoid NCC but has a low sensitivity in patients with SCG (around 60%) and is frequently negative in patients with solitary calcific parenchymal lesions ,,. The sensitivity of EITB was enhanced in patients with SCG by nearly 50 per cent by modifying the T. solium glycoproteins using urea .
The antigen ELISA (Ag-ELISA) detects the presence of circulating larval antigens in serum and hence, more likely to be associated with the presence of active disease in a person ,. It is almost always positive in patients with subarachnoid disease but like the EITB, is likely to be negative in those with calcific lesions and with one or two parenchymal lesions. Even in those with more parenchymal lesions, its sensitivity is poor and ranges between 72 and 86 per cent . However, the Ag-ELISA could be used to monitor the effects of therapy as its levels fall rapidly following successful therapy . Asymptomatic persons can also test positive for the Ag-ELISA and on long term follow up remain asymptomatic .
Urine antigen detection ELISA has been used by some workers to avoid the discomfort of obtaining a serum sample in field studies ,. The sensitivity was around 90 per cent in patients with more than one cyst in the brain.
One of the major problems in using immunological tests in clinical practice is that the tests are not easily available commercially and when available are expensive costing around ' 15,000 - 20,000 per patient for the commercial EITB test . The performance of the commercial kits can also be variable as the larval antigens used in the kits are not indigenous.
Diagnostic criteria: Since no single test can definitively diagnose NCC, except by brain biopsy, diagnostic criteria are necessary. In 1993, diagnostic criteria were proposed for the diagnosis of SCG and were validated in a prospective study in 1997, involving 401 patients presenting with seizures and a solitary brain mass on the CT scan (215 with SCG),. SCG diagnostic criteria have sensitivity of 99.5 per cent, specificity of 98.9 per cent, positive predictive value of 99 per cent, negative predictive value of 99.5 per cent and likelihood ratios for the positive and negative tests of 92.99 and 0.005. The high likelihood ratios ensure that the criteria will perform well even in regions of the world where the disease is not endemic, and therefore, the prevalence rates are low.
In 2001, an international experts group proposed diagnostic criteria for NCC in general with a set of absolute, major, minor and epidemiological criteria based on which a patient suspected to have NCC could be diagnosed with definitive or probable NCC . The criteria rely on histological evidence, clinical features, neuroimaging findings, results of immunological tests and exposure to the disease. The diagnostic criteria for SCG have been incorporated in the NCC diagnostic criteria as major criteria. However, the NCC diagnostic criteria have not been validated and have faced some criticism ,. Notwithstanding the criticism, these diagnostic criteria remain the best available resource to clinicians worldwide when confronted with a patient with suspected NCC .
Diagnostic problem: special situations: One of the common clinical situations in our country when the diagnosis is difficult is a patient who presents with seizures and raised intracranial pressure with neuroimaging showing multiple small enhancing granulomas all over the brain with associated oedema [Figure 2]. The images do not reveal calcifications, live cysts, intraventricular or subarachnoid cysts. In this situation, the differential diagnosis includes NCC and tuberculomas. Usually, EITB will be positive in the serum, but in an endemic country like India, EITB can be positive due to exposure to the larval antigen and not due to established disease. Therefore, a positive EITB in this situation may not necessarily indicate a definitive diagnosis of NCC. A brain biopsy may sometimes be necessary to establish a definitive diagnosis.
|Figure 2: Multiple small ring enhancing lesions in a patient presenting with headache and seizures. Enzyme linked immunotransfer blot for cysticercal antibodies in serum was positive. As only granulomas were seen without any of the other stages of the cysts (live and calcific), the patient was treated with anti-tuberculous therapy with resolution of the granulomas. A brain biopsy would be the only method to confirm the diagnosis.|
Click here to view
| Current therapeutic strategies|| |
The mainstay of treatment of a patient with NCC involves symptomatic therapy. Since most patients with NCC present with seizures, antiepileptic drugs (AEDs) are to be used. Steroid therapy may be needed to control oedema associated with the lesions. Dexamethasone or prednisolone is commonly used for short periods of a few days or weeks. As NCC presents with varied symptoms depending on the location of the cyst and the stage of degeneration, the treatment also varies. For an overview of the suggested management of different forms of NCC, a consensus statement of a group of international experts is available . In a later paper, some of the issues pertaining to the treatment of NCC and research needs arising thereof have been dealt with . In the present review, the discussion will be limited to a few specific issues and does not cover the therapeutic strategies for the entire spectrum of NCC. An attempt has been made to provide information obtained from randomized controlled trials (RCTs).
Debate over benefits of cysticidal drugs
Ever since cysticidal drugs were introduced for NCC in the late 1970s (praziquantel) and 1980s (albendazole), it has been a matter of debate as to whether hastening the destruction of the cysts in the brain is symptomatically beneficial to the host or not. While intuitively it might seem that destroying the parasite should benefit the host, it should be recognized that the symptoms of NCC arise from the spontaneous involution or destruction of the parasite . The host inflammatory reaction that accompanies the parasite's death appears acutely in the form of brain oedema around the parasite and release of inflammatory cytokines and chronically in the formation of a gliotic scar. These events, acute and chronic, could lead to symptoms such as those of raised intracranial pressure (due to oedema), seizures (due to the release of cytokines and other neurotoxic agents) and a chronic epileptic scar. This is the basis for the argument against administration of cysticidal drugs .
In recent years, several RCTs and meta-analysis have attempted to provide a definitive answer to the question: Does cysticidal drug therapy benefit the patient? However, a final, conclusive answer continues to evade us.
Cysticidal drugs and steroids in patients with solitary cysticercus granuloma
Since the early studies showing a possible benefit of the use of albendazole in hastening the resolution of persistent SCG , there have been several RCTs ,,,, and one pseudo randomized control trial  evaluating the effect of albendazole in patients with SCG. The effects of albendazole (15 mg/kg/day for 7-14 days) and steroids on seizure outcome and lesion resolution in patients with SCG were usually studied. Unfortunately, most of the RCTs have methodological flaws and all of them report outcomes at a relatively short follow up of less than 12 or 18 months. Meta-analyses based on these RCTs have concluded that there is modest evidence that seizure outcome is better in patients prescribed albendazole ,. Lesion resolution also might be faster with the administration of albendazole, but this effect is not clear. Steroids alone did not seem to offer the benefits that were seen with albendazole therapy. However, steroids are usually administered with albendazole to reduce the side effects associated with cysticidal drug therapy. It has also been reported that albendazole therapy does not reduce the calcification rate of around 20 per cent in patients with SCG ,. Thus, it is likely that long-term seizure recurrence rates might not benefit with albendazole as calcification is a major risk factor for seizure recurrence. The only possible downside to routine administration of albendazole to all patients with SCG is the occurrence of side effects in a substantial proportion of patients . As there is modest evidence of benefit, albendazole is recommended for patients with SCG at initial presentation .
Cysticidal drugs for patients with multilesional neurocysticercosis
One trial reported a 50 per cent reduction in generalized seizures but not all seizures in patients with multilesional NCC [patients with 1-20 viable cysts (live and degenerating) in the brain] treated with albendazole . However, there was no significant reduction in the total number of seizures in the treated group. Another RCT did not find a reduction in seizure numbers or enhanced cyst resolution in the treated group . Similar to the case with SCG, albendazole does not seem to reduce the incidence of calcification in patients with multilesional NCC. Most studies using albendazole have, however, reported a higher rate of lesion resolution when compared to placebo. Therefore, while albendazole appears to destroy larvae, it does not have a profound beneficial effect on seizure outcome and seizure recurrence.
In a recent RCT, 10 days combined therapy with albendazole (15 mg/kg/day) and praziquantel (50 mg/kg/day) was found to be superior to either albendazole alone or high dose albendazole (22 mg/kg/day) in clearing cysts from the brain . Cyst resolution, at six months after treatment, was noted in 64 per cent of patients in the combined therapy group versus 39 per cent in the standard albendazole therapy group. Furthermore, there was no difference in the side effects in the three groups. Thus, combined therapy seems to be good option in patients with multilesional NCC.
Duration of antiepileptic drugs
Most patients with SCG present with a few seizures which are easily controlled with a single AED. AEDs should be continued till the granuloma has resolved on follow up imaging. Once the granuloma has resolved, AEDs can be withdrawn gradually provided the patient has not had a seizure in the past three months. The risk of recurrent seizures after withdrawal of AEDs in patients with a resolved SCG has been studied in a large cohort of patients followed up for 2-10 yr (mean follow up 76.2 months). Recurrent seizures occurred in 15 per cent of patients with most seizures occurring in the first three months after withdrawal of AEDs. Risk factors for recurrence were found to be >2 seizures during the disease, breakthrough seizures (seizures occurring after starting AEDs) and most importantly the presence of a calcific residue on the follow up CT scan. Patients with any of these risk factors or more than one risk factor should be advised to continue AEDs for a longer duration (1-2 years). However, for patients with multilesional NCC, AEDs are needed for several years in over 50 per cent of patients as most of these patients are prone to recurrence of seizures following withdrawal of AEDs ,. Like for SCG, calcification is a major risk factor for recurrence of seizures ,.
Endoscopic surgery for intraventricular cysts
Intraventricular cysts are one of a few surgical indications in patients with NCC . In the last two decades, endoscopic excision of intraventricular cysts has become the procedure of choice as opposed to the open craniotomy and microsurgical excision that was used earlier ,. Endoscopic surgery is minimally invasive being achieved through a single burr hole. It can often be curative if there is a single cyst in the ventricle. The side effects of the surgery are minimal when performed by experienced surgeons. Although there was concern regarding possible anaphylactic reactions to the rupture of a cyst during surgery, these have been proven to be misplaced as no such reactions have been reported in spite of cysts being routinely ruptured during excision.
| Conclusions|| |
Highly sensitive, specific and cost-effective tools for the diagnosis of taeniasis and NCC are lacking although progress has been made in the development of immunological tests for both in the last two decades. Expensive neuroimaging is still central to the diagnosis of NCC. The management of NCC is debated especially with respect to the use of cysticidal drugs as their benefits have not been conclusively proven. There are several other management issues awaiting resolution.
| Acknowledgment|| |
Authors thank Dr Pierre Dorny for his helpful discussions regarding the immunological diagnosis of NCC and taeniasis.
Conflicts of Interest: None.
| References|| |
Rajshekhar V, Raghava MV, Prabhakaran V, Oommen A, Muliyil J. Active epilepsy as an index of burden of neurocysticercosis in Vellore district, India. Neurology
Chandy MJ, Rajshekhar V, Prakash S, Ghosh S, Joseph T, Abraham J, et al.
Cysticercosis causing single, small CT lesions in Indian patients with seizures. Lancet
Rajshekhar V. Etiology and management of single small CT lesions in patients with seizures: understanding a controversy. Acta Neurol Scand
Allan JC, Velasquez-Tohom M, Torres-Alvarez R, Yurrita P, Garcia-Noval J. Field trial of the coproantigen-based diagnosis of Taenia solium
taeniasis by enzyme-linked immunosorbent assay. Am J Trop Med Hyg
Mohan VR, Jayaraman T, Babu P, Dorny P, Vercruysse J, Rajshekhar V. Prevalence and risk factors for Taenia solium
taeniasis in Kaniyambadi block, Tamil Nadu, South India. Indian J Public Health
Lightowlers MW, Garcia HH, Gauci CG, Donadeu M, Abela-Ridder B. Monitoring the outcomes of interventions against Taenia solium
: options and suggestions. Parasite Immunol
Guezala MC, Rodriguez S, Zamora H, Garcia HH, Gonzalez AE, Tembo A, et al.
Development of a species-specific coproantigen ELISA for human Taenia solium
taeniasis. Am J Trop Med Hyg
Wilkins PP, Allan JC, Verastegui M, Acosta M, Eason AG, Garcia HH, et al.
Development of a serologic assay to detect Taenia solium
taeniasis. Am J Trop Med Hyg
Mayta H, Gilman RH, Prendergast E, Castillo JP, Tinoco YO, Garcia HH, et al.
Nested PCR for specific diagnosis of Taenia solium
taeniasis. J Clin Microbiol
Rajshekhar V, Chandy MJ. Comparative study of CT and MRI in patients with seizures and a solitary cerebral cysticercus granuloma. Neuroradiology
Govindappa SS, Narayanan JP, Krishnamoorthy VM, Shastry CH, Balasubramaniam A, Krishna SS. Improved detection of intraventricular cysticercal cysts with the use of three-dimensional constructive interference in steady state MR sequences. AJNR Am J Neuroradiol
Bannur U, Rajshekhar V. Cisternal cysticercosis: a diagnostic problem – a short report. Neurol India
Tsang VCW, Brand JA, Boyer AE. An enzyme-linked immunoelectrotransfer blot assay and glycoprotein antigens for diagnosing human cysticercosis (Taenia solium
). J Infect Dis
Garcia HH, Nash TE, Del Brutto OH. Clinical symptoms, diagnosis, and treatment of neurocysticercosis. Lancet Neurol
Prabhakaran V, Raghava MV, Rajshekhar V, Muliyil J, Oommen A. Seroprevalence of Taenia solium
antibodies in Vellore district, South India. Trans R Soc Trop Med Hyg
Rajshekhar V, Wilson M, Schantz PM. Cysticercus immunoblot assay in Indian patients with single small enhancing CT lesions. J Neurol Neurosurg Psychiatry
Rajshekhar V, Oommen A. Serological studies using ELISA and EITB in patients with solitary cysticercus granuloma and seizures. Neurol Infect Epidemiol
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
Prabhakaran V, Rajshekhar V, Murrell KD, Oommen A. Conformation-sensitive immunoassays improve the serodiagnosis of solitary cysticercus granuloma in Indian patients. Trans R Soc Trop Med Hyg
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
Erhart A, Dorny P, Van De N, Vien HV, Thach DC, Toan ND, et al. Taenia solium
cysticercosis in a village in Northern Viet Nam: seroprevalence study using an ELISA for detecting circulating antigen. Trans R Soc Trop Med Hyg
Zamora H, Castillo Y, Garcia HH, Pretell J, Rodriguez S, Dorny P, et al
. Drop in antigen levels following successful treatment of subarachnoid neurocysticercosis. Am J Trop Med Hyg
Alexander AM, Prabhakaran V, Rajshekhar V, Muliyil J, Dorny P. Long-term clinical evaluation of asymptomatic subjects positive for circulating Taenia solium
antigens. Trans R Soc Trop Med Hyg
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
Mwape KE, Praet N, Benitez-Ortiz W, Muma JB, Zulu G, Celi-Erazo M, et al.
Field evaluation of urine antigen detection for diagnosis of Taenia solium
cysticercosis. Trans R Soc Trop Med Hyg
Rajshekhar V, Haran RP, Prakash GS, Chandy MJ. Differentiating solitary small cysticercus granulomas and tuberculomas in patients with epilepsy. Clinical and computerized tomographic criteria. J Neurosurg
Rajshekhar V, Chandy MJ. Validation of diagnostic criteria for solitary cerebral cysticercus granuloma in patients presenting with seizures. Acta Neurol Scand
Del Brutto OH, Rajshekhar V, White AC Jr., Tsang VC, Nash TE, Takayanagui OM, et al.
Proposed diagnostic criteria for neurocysticercosis. Neurology
Garg RK. Diagnostic criteria for neurocysticercosis: some modifications are needed for Indian patients. Neurol India
Prasad S, MacGregor RR, Tebas P, Rodriguez LB, Bustos JA, White AC Jr. Management of potential neurocysticercosis in patients with HIV infection. Clin Infect Dis
Del Brutto OH. Diagnostic criteria for neurocysticercosis, revisited. Pathog Glob Health
García HH, Evans CAW, Nash TE, Takayanagui OM, White AC Jr., Botero D, et al.
Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev
Nash TE, Singh G, White AC, Rajshekhar V, Loeb JA, Proaño JV, et al.
Treatment of neurocysticercosis: current status and future research needs. Neurology
Carpio A, Santillán F, León P, Flores C, Hauser WA. Is the course of neurocysticercosis modified by treatment with antihelminthic agents? Arch Intern Med
Rajshekhar V. Albendazole therapy for persistent, solitary cysticercus granulomas in patients with seizures. Neurology
Padma MV, Behari M, Misra NK, Ahuja GK. Albendazole in single CT ring lesions in epilepsy. Neurology
Baranwal AK, Singhi PD, Khandelwal N, Singhi SC. Albendazole therapy in children with focal seizures and single small enhancing computerized tomographic lesions: a randomized, placebo-controlled, double blind trial. Pediatr Infect Dis J
Gogia S, Talukdar B, Choudhury V, Arora BS. Neurocysticercosis in children: clinical findings and response to albendazole therapy in a randomized, double-blind, placebo-controlled trial in newly diagnosed cases. Trans R Soc Trop Med Hyg
Kalra V, Dua T, Kumar V. Efficacy of albendazole and short-course dexamethasone treatment in children with 1 or 2 ring-enhancing lesions of neurocysticercosis: a randomized controlled trial. J Pediatr
Singhi P, Jain V, Khandelwal N. Corticosteroids versus albendazole for treatment of single small enhancing computed tomographic lesions in children with neurocysticercosis. J Child Neurol
Thussu A, Chattopadhyay A, Sawhney IMS, Khandelwal N. Albendazole therapy for single small enhancing CT lesions (SSECTL) in the brain in epilepsy. J Neurol Neurosurg Psychiatry
Del Brutto OH, Roos KL, Coffey CS, García HH. Meta-analysis: cysticidal drugs for neurocysticercosis: albendazole and praziquantel. Ann Intern Med
Otte WM, Singla M, Sander JW, Singh G. Drug therapy for solitary cysticercus granuloma: a systematic review and meta-analysis. Neurology
Rajshekhar V. Incidence and significance of adverse effects of albendazole therapy in patients with a persistent solitary cysticercus granuloma. Acta Neurol Scand
Singh G, Rajshekhar V, Murthy JM, Prabhakar S, Modi M, Khandelwal N, et al.
A diagnostic and therapeutic scheme for a solitary cysticercus granuloma. Neurology
Garcia HH, Pretell EJ, Gilman RH, Martinez SM, Moulton LH, Del Brutto OH, et al.
A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. N Engl J Med
Carpio A, Kelvin EA, Bagiella E, Leslie D, Leon P, Andrews H, et al
. The effects of albendazole treatment on neurocysticercosis: a randomized controlled trial. J Neurol Neurosurg Psychiatry
: < slug-pages >1050-5.
Garcia HH, Gonzales I, Lescano AG, Bustos JA, Zimic M, Escalante D, et al.
Efficacy of combined antiparasitic therapy with praziquantel and albendazole for neurocysticercosis: a double-blind, randomised controlled trial. Lancet Infect Dis
Rajshekhar V, Jeyaseelan L. Seizure outcome in patients with a solitary cerebral cysticercus granuloma. Neurology
Carpio A, Hauser WA. Prognosis for seizure recurrence in patients with newly diagnosed neurocysticercosis. Neurology
Del Brutto OH. Prognostic factors for seizure recurrence after withdrawal of antiepileptic drugs in patients with neurocysticercosis. Neurology
Rajshekhar V. Surgical management of neurocysticercosis. Int J Surg
Neal JH. An endoscopic approach to cysticercosis cysts of the posterior third ventricle. Neurosurgery
Bergsneider M, Holly LT, Lee JH, King WA, Frazee JG. Endoscopic management of cysticercal cysts within the lateral and third ventricles. J Neurosurg
[Figure 1], [Figure 2]
|This article has been cited by|
||Targeted burr hole surgery for Sylvian cistern subarachnoid neurocysticercosis
| ||William Lines,Carlos Vasquez,Diana Rivas,Joham Choque-Velasquez |
| ||Interdisciplinary Neurosurgery. 2021; 23: 100996 |
|[Pubmed] | [DOI]|
||Neurocysticercosis Presenting With a New-Onset Seizure: A Case Report
| ||William Lim,Muhammed Atere,Bryan Nugent,Swann Tin,Ambreen Khalil |
| ||Cureus. 2021; |
|[Pubmed] | [DOI]|
||Acute dorsal myelopathy resulting from intramedullary cysticercus: a case report
| ||Durjoy Lahiri,Abhishek Chowdhury,Souvik Dubey,Biman Kanti Ray |
| ||Journal of Medical Case Reports. 2021; 15(1) |
|[Pubmed] | [DOI]|
||Neurocysticercosis in a 14-year-old Nigerian: A case report and review of the literature
| ||SS Soyemi,CO Akinbo,Mgbehoma AI,FE Emiogun,OO Adegboyega,JO Obafunwa |
| ||Annals of Tropical Pathology. 2020; 11(1): 72 |
|[Pubmed] | [DOI]|
||Distinguishing patients with idiopathic epilepsy from solitary cysticercus granuloma epilepsy and biochemical phenotype assessment using a serum biomolecule profiling platform
| ||Jay S. Hanas,James Randolph Sanders Hocker,Betcy Evangeline,Vasudevan Prabhakaran,Anna Oommen,Vedantam Rajshekhar,Douglas A. Drevets,Hélène Carabin,Ugo de Grazia |
| ||PLOS ONE. 2020; 15(8): e0237064 |
|[Pubmed] | [DOI]|
||Endoscopic intervention for intraventricular neurocysticercal cyst: Challenges and outcome analysis from a single institute experience
| ||Subhas Konar,Sandeep Kandregula,Abhinith Sashidhar,A.R. Prabhuraj,Jitender Saini,Dhaval Shukla,Dwarakanath Srinivas,B Indira Devi,Sampath Somanna,Arivazhagan Arimappamagan |
| ||Clinical Neurology and Neurosurgery. 2020; 198: 106179 |
|[Pubmed] | [DOI]|
||Taenia solium proteins: A beautiful Kaleidoscope of pro and anti-inflammatory antigens
| ||Naina Arora,Amit Prasad |
| ||Expert Review of Proteomics. 2020; |
|[Pubmed] | [DOI]|
||Assessing the burden and spatial distribution of Taenia solium human neurocysticercosis in Ecuador (2013–2017)
| ||Marco Coral-Almeida,Aquiles R. Henriquez-Trujillo,Sofia Asanza,Celia Erazo,Michelle Paucar,Manuel Calvopiña,Mar Siles-Lucas |
| ||PLOS Neglected Tropical Diseases. 2020; 14(6): e0008384 |
|[Pubmed] | [DOI]|
||Sorting out difficulties in immunological diagnosis of neurocysticercosis: Development and assessment of real time loop mediated isothermal amplification of cysticercal DNA in blood
| ||Gunjan Goyal,Anil Chandra Phukan,Masaraf Hussain,Vivek Lal,Manish Modi,Manoj Kumar Goyal,Rakesh Sehgal |
| ||Journal of the Neurological Sciences. 2019; : 116544 |
|[Pubmed] | [DOI]|
||Nonspecific dizziness as an unusual presentation of neurocysticercosis
| ||Huiying Li,Jing Sun,Guangxian Nan |
| ||Medicine. 2019; 98(30): e16647 |
|[Pubmed] | [DOI]|
||NEUROCYSTICERCOSIS AS A RARE CAUSE OF POST PARTUM CONVULSIONS
| ||Divya H. S,Ramesh B,Manasa G. V,Rashmi G. B,Renuka Ramaiah,Karthik S,Sreelatha Sreelatha |
| ||Journal of Evidence Based Medicine and Healthcare. 2019; 6(3): 199 |
|[Pubmed] | [DOI]|
||Clinical characteristics of migraine in patients with calcified neurocysticercosis
| ||Sunil Pradhan,Animesh Das,Sucharita Anand,Anirudh Rao Deshmukh |
| ||Transactions of The Royal Society of Tropical Medicine and Hygiene. 2019; |
|[Pubmed] | [DOI]|
||Predictors of seizure in Wilson disease: A clinico-radiological and biomarkers study
| ||Jayantee Kalita,Usha K. Misra,Vijay Kumar,Vasudev Parashar |
| ||NeuroToxicology. 2019; 71: 87 |
|[Pubmed] | [DOI]|
||Neurocysticercosis and epilepsy in sub-Saharan Africa
| ||Athanase Millogo,Alfred Kongnyu Njamnshi,Mesu’a Kabwa-PierreLuabeya |
| ||Brain Research Bulletin. 2018; |
|[Pubmed] | [DOI]|
||A gel-free proteomic analysis of Taenia solium and Taenia crassiceps cysticerci vesicular extracts
| ||Giovani Carlo Veríssimo da Costa,Regina Helena Saramago Peralta,Dário Eluan Kalume,Ana Larissa Gama Martins Alves,José Mauro Peralta |
| ||Parasitology Research. 2018; |
|[Pubmed] | [DOI]|
||Neurocysticercosis in Children with Seizures: A Cross-Sectional Study
| ||Murli Manohar Gupta,Nagendra Chaudhary,Santosh Pathak,Nikhil Agrawal,Jaydev Yadav,Sandeep Shrestha,Om Prakash Kurmi,Baldev Bhatia,Kailash Nath Agarwal |
| ||International Journal of Pediatrics. 2018; 2018: 1 |
|[Pubmed] | [DOI]|
||Antibody Banding Patterns of the Enzyme-Linked Immunoelectrotransfer Blot and Brain Imaging Findings in Patients With Neurocysticercosis
| ||Gianfranco Arroyo,Silvia Rodriguez,Andres G Lescano,Karen A Alroy,Javier A Bustos,Saul Santivañez,Isidro Gonzales,Herbert Saavedra,E Javier Pretell,Armando E Gonzalez,Robert H Gilman,Victor C W Tsang,Hector H Garcia,Hector H Garcia,Robert H Gilman,Armando E Gonzalez,Victor C W Tsang,Silvia Rodriguez,Isidro Gonzalez,Herbert Saavedra,Manuel Martinez,Manuel Alvarado,Manuela Verastegui,Mirko Zimic,Javier Bustos,Holger Mayta,Cristina Guerra,Yesenia Castillo,Yagahira Castro,Maria T Lopez,Cesar M Gavidia,Luis Gomez,Luz M Moyano,Ricardo Gamboa,Claudio Muro,Percy Vilchez,Theodore E Nash,Siddhartha Mahanty,John Noh,Sukwan Handali,Jon Friedland |
| ||Clinical Infectious Diseases. 2018; 66(2): 282 |
|[Pubmed] | [DOI]|
||Solitary Cysticercal Cyst Inside the Blakeæs Pouch Remnant of Mega Cisterna Magna with Associated Aqueductal Stenosis: Clinical and Management Implications
| ||Kuntal Kanti Das,Jaskaran Singh Gosal,Suyash Singh,Anant Mehrotra,Awadhesh Jaiswal,Sushila Jaiswal,Raj Kumar |
| ||World Neurosurgery. 2017; 102: 693.e1 |
|[Pubmed] | [DOI]|
||Target product profiles for the diagnosis of Taenia solium taeniasis, neurocysticercosis and porcine cysticercosis
| ||Meritxell Donadeu,Anna S. Fahrion,Piero L. Olliaro,Bernadette Abela-Ridder,Hector H. Garcia |
| ||PLOS Neglected Tropical Diseases. 2017; 11(9): e0005875 |
|[Pubmed] | [DOI]|