Several aspects of this disease have no clear, practical guidelines. Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH) published a guideline intended to be applicable and feasible for developed nations (North America) [10]. These recommendations may not be applicable or feasible for developing countries like India, due to limited resources. Thus, there is a need for clear, pragmatic guidelines, summarizing the available evidence, and filling in the gaps in evidence with collated expert advice to manage children with NCC. To this end, the Association of Child Neurology took the initiative to get together experts to look at the evidence and bring forward a practice guideline to aid the management of children with neurocysticercosis.

The guideline aims to provide directions for daily practice for the diagnosis and treatment of neurocysticercosis in children. The guideline not only looks at the up-to-date scientific evidence but also tempers it with expert advice to adapt to the Indian setting.

The writing group formulated six focus areas and several sub-questions, which aimed to cover all clinically relevant areas in diagnosing and managing neurocysticercosis in children. Within the major topics, several questions were shortlisted by the writing group to have further opinions and consensus among a broader range of experts. These included epidemiology, clinical features; Diagnosis: radiological tests, immunological tests, and other methods; antihelminthics: dose, duration, based on lesion load; management of NCC at atypical sites; steroids and anti-seizure drug use; and, statement on follow up, outcomes, and prevention (Web Box I). Web Fig. 1 shows the constitution of the DELPHI group and the process followed.

The expert group and the writing group consisted of twenty-four members with varied expertise. It included 18 pediatric neurologists, four neuroradiologists, and one neurologist and parasitologist each. The 5-step Delphi process is outlined in Web Fig. 1. The writing group members then prepared the manuscript based on the relevant review of the literature and the results of the DELPHI consensus.

Quality of evidence scoring: The literature was selected by the committee members and was graded for quality based on the European Society for Clinical Microbiology and Infectious Diseases (ESCMID) quality-of-evidence system [11]. The quality of articles to substantiate the conclusions by the group is provided with the concluding answer to each question.

Strength of recommendation assessment: On the basis of the selected literature and the online consensus development process, the group reached a consensus on a recommendation. The strength of the recommendation is expressed using the ESCMID strength of recommendation system [11], and many times does not always correlate with the quality of evidence. Hence, high quality of evidence may result in a marginal recommendation for use, while low-quality evidence may result in a strong recommendation for use.

In view of the long incubation period between infection with NCC and the onset of symptoms, many of the tapeworm carriers who originally transmitted the infection may have cleared the intestinal infection or may no longer live near the patient [1,10,12]. Hence, stool examination for ova (which is the only available diagnostic test for tapeworms) is often negative in tapeworm carriers [13]. Even multiple examinations may not detect the tapeworm carrier. Even when ova are found, the morphology of the ova cannot distinguish T. solium from other taenia species. Thus, the yield of microscopy for the identification of tapeworm carriers is generally low, even in cases with apparent transmission outside of endemic areas [10]. Nevertheless, among patients who apparently acquired infection in the United States, tapeworms were documented in close contacts of 22% of NCC cases. Thus, most authorities would recommend screening for cases acquired outside endemic areas. Newer methods such as antigen detection in stool or detection of tapeworm-stage specific antibodies by immunoblot might improve the usefulness of screening, but these are presently only research techniques and not commercially available [10].

Routine screening of family members of children with NCC is not recommended. If at all screening is performed, fecal testing of the family for ova/cyst can be done.

Quality of evidence: 3; Strength of recommendation: D

The serologic antibody test of choice is the enzyme-linked immunoelectrotransfer blot (EITB) using parasite glycoproteins performed on serum. Enzyme-linked immunosorbent assay (ELISA) using crude antigens to detect antibodies are associated with frequent false-positive and false-negative results and should generally be avoided. Although EITB has 100% specificity and a sensitivity of 98% in patients with two or more cerebral lesions, up to 50% of patients with a single brain lesion or with only calcified parasites may test negative [10]. The main problem related to ELISA on serum is the poor specificity, which is reported around 70% or less [14], compared with 86% for EITB [15]. The sensitivity of EITB varies with the form of NCC and specimen. In patients with multiple parenchymal, ventricular or subarachnoid NCC, the sensitivity of serum EITB is close to 100%. However, the sensitivity is poor in patients with a single parenchymal lesion or with only calcifications. Testing of serum is generally more sensitive than CSF using the EITB assay [16].

Antigen-based tests: They are also reported to be less sensitive than EITB. However, positive results correlate with the number of viable cysticerci. Parasite antigens are commonly detected in both serum and CSF in cases with multiple cysticerci such as subarachnoid NCC, and serial measurements may be helpful in the follow-up of complex cases [4].

Molecular tests: T. solium DNA has been detected by PCR or deep genomic sequencing using CSF of patients with subarachnoid NCC. However, there are no reports of its use in parenchymal NCC cases and its use may be even lesser in patients with a single brain lesion where most diagnostic problems arise. Cell-free T. solium DNA has been demonstrated in the urine and serum of patients with NCC, and recent data suggest that monocyte gene expression and serum mass spectrometry profiles could be used to identify NCC cases. To date; however, molecular biology assays are neither practical nor economical for routine case assessments. Techniques promoting amplification of DNA in a simple heating block or water bath may facilitate their application in resource-poor settings and include the loop-mediated isothermal amplification (LAMP) PCR [4].

The use of serological tests for diagnosis and clinical decision-making in children with NCC is not recommended.

Quality of evidence: 2; Strength of recommendation: D

Neuroimaging is established as a modality that can be used as an absolute diagnostic criterion for NCC [17]. The conclusive demonstration of a scolex within a cystic lesion on either computed tomography (CT) or magnetic resonance imaging (MRI) confirms the diagnosis of NCC (Table I). The scolex is seen as a hyperdense dot within a cystic lesion on CT. It appears as hyperintense on T1-weighted images and hypointense on T2-weighted images on MRI. Sometimes other sequences of MRI are required to identify the scolex such as fluid attenuated inversion recovery (FLAIR), diffusion-weighted imaging (DWI), susceptibility-weighted imaging (SWI), or high-resolution heavily T2-weighted thin images including fast imaging employing steady-state acquisition (FIESTA), constructive interference in steady-state (CISS), or driven equilibrium (DRIVE). The typical appearance of the cyst is a less than 2 cm sized lesion with well-defined thin rounded walls located near the grey-white matter junction or basal ganglia. Other uncommon locations include the posterior fossa, subarachnoid spaces, intraventricular space, and spinal cord.

MRI plays a role in better characterization of the lesion by the demonstration of the scolex and internal characteristics. This further helps in differentiating NCC from its other close differentials, tuberculomas, and metastasis. The solid caseating tuberculomas character-istically have a T2 hypointense core which is not seen in any stage of NCC unless it is significantly calcified. It is one of the most helpful features in differentiating the two. Other features, though not specific, favouring a tuberculoma are a larger size (>2 cm), thicker and irregular walls, marked perilesional edema with mass effect, and associated basal meningitis. The presence of two-three conglomerate lesions may be seen in both entities and is not helpful in differentiation. On the other hand, some features suggest NCC over tuberculoma, such as intraventricular or subarachnoid location and multiple stages present simultaneously and pathognomonic features of individual lesions in case of multiple lesions [18].

MR spectroscopy of tuberculomas show elevated lipids and elevated choline/creatinine and choline/NAA ratios whereas these are not seen in NCC. On the other hand, NCC may show elevated acetate/succinate. Mag-netisation transfer (MT) imaging has also been shown to be helpful in differentiating the two. The tuberculomas show a bright cellular component on T1-weighted MT images. The tuberculoma shows a hypointense centre with a hyperintense rim on T1-weighted MT images. The MT ratio of this hyperintense rim is significantly lower for tuberculomas compared to NCC and is due to the high lipid content in them [19,20].

MR also scores over CT for detection of lesions in atypical locations including intraventricular, sub-arachnoid, and intraspinal space. The high resolution heavily T2-weighted sequences are very useful in this. Even the lesions in the posterior fossa and those close to the skull are better delineated on MRI. Conglomerate lesions, subarachnoid or intraventricular lesions, and peripheral T2 hypointense ring with increased perfusion are the atypical neuroimaging of NCC [19].

MRI need not be done following CT in the following situations:

MRI should be considered after CT in the following situations:

If conventional MRI sequences have not been able to conclusively differentiate NCC from its differentials, including tuberculoma, by failing to demonstrate scolex, then additional MR sequences may be acquired like MR spectroscopy and magnetization transfer imaging. However, the results of these may be used as supportive evidence rather than in isolation to differentiate the two.

Quality of evidence: 2; Strength of recommendation: B

Demonstration of scolex either on CT or MRI is the most conclusive evidence to differentiate between the two. In the absence of that, the features favoring NCC include a solitary well defined, thin-walled cystic or ring-enhancing lesion usually <2 cm in size with mild perilesional edema in a typical location of grey-white matter junction or basal ganglia. The presence of a T2 hypointense central core on MRI is strongly suggestive of tuberculoma over NCC in the absence of calcification as evidenced on CT or SWI sequences on MRI. The multicentricity of lesions with lesions showing different stages/features strongly favors NCC. Findings of MRS and MT imaging may be used as supportive evidence.

Quality of evidence: 2; Strength of recommendation: B

If the initial imaging (CT and/or MRI with recommended sequences when indicated) is not conclusive to differentiate NCC from tuberculoma, then a repeat contrast-enhanced MRI may be performed at an interval of 6-8 weeks to look for interval change. The imaging may be performed earlier if indicated by worsening or new clinical symptoms/signs.

Quality of evidence: 3; Strength of recommendation: C

The repeat imaging after treatment of NCC should be done at the interval of 6 months unless guided earlier by any worsening/new clinical symptoms/signs. This applies to both single and multiple NCC. MRI may be the preferred modality keeping into account the risk of radiation exposure with CT. The decision of administration of contrast may be left at the discretion of the radiologist, based on findings on plain MRI. A plain CT scan may sometimes be required after MRI if the presence of calcification is not conclusive on the MRI, and is required for clinical management.

Quality of evidence: 2; Strength of recommendation: B

Albendazole with steroids should be considered for children with neurocysticercosis, to decrease the number of active lesions as well as to reduce seizure frequency. A short-course of albendazole treatment is as efficacious as four weeks treatment course in solitary cysticercus granuloma [24-27]. Monotherapy with albendazole is comparable to combination therapy of albendazole and praziquantel in the single solitary enhancing lesion in CT (SSECTL) [28].

The use of 10-14 days of albendazole therapy for all patients with single viable cyst is recommended.

Quality of evidence: 1; Strength of recommendation: B

Albendazole 15　mg/kg/day (maximum 1200 mg/day) in twice-daily doses should be given with meals. The quality of evidence is strong for use of albendazole but not for the duration of use.

Antihelminthic drugs for multiple viable cysts: Albendazole (ABZ) and praziquantel (PZQ) have different mechanisms of action, which may be beneficial when combined together in treating multiple NCC. Praziquantel is a pyrazinoisoquinoline derivative, of which the main pharmacological effects include muscle contractions, paralysis, and tegumentary damage, whereas albendazole is a benzimidazole, whose main mechanism of action is through selective degeneration of cytoplasmic microtubules resulting in energy depletion, disrupted cell division, and altered glucose intake.

Combination therapy with albendazole and praziquantel has been found to be safe and effective without any increase in adverse events. Increased serum albendazole concentrations were observed in patients receiving combination treatment compared with those receiving albendazole alone. Albendazole serum levels increased by 48% when given in combination with praziquantel [29]. Garcia, et al. [29] reported that combination of albendazole and praziquantel was associated with increased albendazole sulfoxide plasma concentrations. This along with a possible synergistic effect of two drugs may be beneficial for patients. A randomized trial of 32 pateints showed that the combination therapy was more effective in destroying viable brain cysticercosis cysts than ABZ alone [30].

Combined treatment with albendazole and praziquantel was found to be superior in a three-arm randomized double-blinded study. One twenty-four patients (aged 16 to 65 years with 1 to 20 viable cysts) were randomly assigned to three arms (43 received standard dose albendazole; 40 received high dose (22.5 mg/kg/day) albendazole and 41 patients received combination therapy with standard dose albendazole and praziquantel). Complete cyst resolution in MRI brain performed 6 months after initial therapy was seen in 63% of patients who received combination therapy vs 73% and 83% resolution in the standard dose and high dose albendazole, respectively (P=0.141) in patients with one to two viable cysts. However, in patients with three or more then three cysts, complete cyst resolution was seen in 94% of patients who received combination therapy vs 21% and 48% resolution in the standard dose and high dose albendazole, respectively (P<0.001) [31]. Anti-helminthic drugs are not recommended in patients with cysticercal encephalitis or ‘starry sky NCC’ for fear of worsening the intracranial edema.

Albendazole (15 mg/kg/day) combined with praziquantel (50 mg/kg/day) for 10-14 days is recommended for more than two viable cyst.

Quality of evidence: 1; Strength of recommendation: B

Praziquantel dose at 50 mg/kg/day (upto 3600 mg/day), quality of evidence extrapolated from studies done in adult patients.

Treatment of persistent viable cysts: Response to a single course of cysticidal therapy is variable. A persistent cyst is seen in 30-40% of patients with a single viable lesion on follow-up. The persistence of the lesion is associated with seizure recurrence [32,33]. Rajashekar, et al. [32] treated 11 patients with persistent lesions with a repeat course of albendazole for two weeks. A significant reduction in cyst size was observed in two patients and complete resolution in two patients in follow-up CT scans. There are no randomized controlled trials or convincing data to suggest retreatment is better than symptomatic treatment; however, experts recommend retreatment [31]. Options for retreatment include a second course of albendazole or using the combination of albendazole and praziquantel.

There are two options to treat the persistent lesion. One is retreatment with the same dose and duration of albendazole and the second option is the concurrent administration of albendazole and praziquantel as for multiple lesion NCC.

Quality of evidence: 3; Strength of recommendation: C

The long-term management of cysticercal ence-phalitis is challenging, and the clinical course is often punctuated by recurrent episodes of symptomatic raised intracranial pressure and/or seizures.

Pulse intravenous steroids should be used to reduce the acute symptomatic edema in children with cysticercal encephalitis. The steroids suggested are methylpre-dnisolone (10-30 mg/kg for 3-5 days; maximum 1000 mg/day) or dexamethasone (3-6 mg/kg/day for 3-5 days; maximum 16 mg/day).

Quality of evidence: 3; Strength of recommendation: A

Steroids can be used for long-term management of cysticercal encephalitis to prevent episodes of acute symptomatic cerebral edema in children with cysticercal encephalitis. Steroids in minimal doses and for the shortest possible period are suggested. Rapid tapering to the lowest effective dose and use of intermittent dose (e.g., alternate day) and monitoring for steroid side effects is suggested.The group does not support or recommend against the use of steroid-sparing drugs due to lack of evidence.

Quality of evidence: 3; Strength of recommendation: C

Subarachnoid, ventricular and spinal NCC: These varieties of NCC are exceedingly rare in children in the Indian sub-continent. Most of the reports on subarachnoid and ventricular cysticerci are from South-America [36,37]. Due to the rarity of the condition in India, and the availability of recent evidence-based guidelines published by IDSA and ASTMH [10], the group recommended that these guidelines may be adopted for these rarer kinds of NCC.

Local inflammatory reaction surrounding NCC is widely prevalent as evidenced by worsening of clinical symptoms (e.g., headache), presence of perilesional edema and contrast enhancement on neuroimaging [38], and increased pleocytosis and elevated protein on serial CSF studies [39]. Host immune reaction to the degenerating cysts underly the pathophysiology of neuroinflammation in NCC. The resulting perilesional white-matter edema might occasionally produce focal neurological deficits and other devastating consequences due to mass effect and raised intracranial pressure. This is especially true when the cysts are located in the subarachnoid space, within the ventricles, orbit, brain stem, or the spinal cord. Thus, treatment with anti-inflammatory medications, particularly cortico-steroids is routinely considered in children with NCC.

In most observational and randomized controlled trials of NCC, patients were routinely treated with oral corticosteroids with or without the combination of anti-cysticercal treatment. Oral prednisolone has been used in doses ranging from 1-2 mg/kg/day for 3-10 days in most studies [40,41]. One meta-analysis, which included 13 studies with low-quality evidence, suggested that corticosteroids reduced seizure recurrence rate and hastened lesion resolution in the medium term (6-12 months) [42]. A recent meta-analysis found that the combination of albendazole with oral steroids provided superior seizure prevention and lesion resolution outcomes in cases of solitary cysticercus granulomas. But another meta-analysis concluded that corticosteroid treatment did not impact any outcomes significantly [43]. Thus, the available evidence is still conflicting about the effectiveness of a particular corticosteroid drug, dose, or duration of treatment in different stages of NCC.

Neuroimaging showing new-onset localized inflam-mation with perilesional edema and contrast enhance-ment in calcified NCC, years after the initial presentation, are well documented [44-46]. These cases present with seizures recurrences, headaches, or maybe asymptomatic [45]. The role of treatment with steroids in addition to anti-seizure prophylaxis in such cases is unclear. We do not recommend the routine use of steroids in such cases. Steroids might be considered in cases of large perilesional edema causing mass effect, midline shift, or other manifestations of raised ICT.

There is no role for routine use of steroids in cases of contrast-enhancing calcified NCC presenting with recurrence of seizures. Steroid use should be reserved for symptomatic cerebral edema.

Quality of evidence: 3; Strength of recommendation: D

As seizures are the most common presenting symptom, most patients with NCC receive anti-seizure medication (ASM) prophylaxis for varying durations depending on lesion resolution or calcification. Patients with calcified NCC receive long-duration ASM because of seizure recurrences after varying periods of seizure freedom, either on or off ASM. Though there is no high-quality evidence available to indicate the choice, dose, or duration of ASM in different NCC types, monotherapy with phenytoin and carbamazepine has been most commonly used [40], given the focal nature of epilepsy in this population. One pilot study demonstrated the safety, tolerability, and effectiveness of clobazam in NCC, but clobazam treatment was more expensive than phenytoin [47].

In the case of NCC presenting with other symptoms without seizures, there appears to be no role for routine anti-seizure medication prophylaxis.

Quality of evidence: 3; Strength of recommendation: D

Carbamazepine or oxcarbazepine are best suited for seizure prophylaxis in children with NCC in India. Phenytoin and Levetiracetam are other alternatives.

Quality of evidence: 3; Strength of recommendation: B

Residual perilesional gliosis surrounding calcified NCC is thought to be responsible for long-term epilepsy [48]. Though most cases of epilepsy due to calcified NCC are controlled with ASM, a minority end up being drug-resistant. Surgical resection is one of the most effective curative treatment options available in cases of drug-resistant epilepsy due to calcified NCC. The pre-requisites for the surgical resection are that epilepsy should be truly drug-resistant, seizures are frequent and disabling enough, clinical and video-EEG analysis proves that the calcified NCC is responsible for epilepsy and its removal is likely to cause seizure freedom. In endemic countries, calcified NCC’s co-existence with hippocampal sclerosis (dual pathology) is well documented [49-53]. These patients are amenable to surgery, but the surgical strategy should be individualized. Patients with drug-resistant epilepsy should be referred early for consi-deration of epilepsy surgery.

Epilepsy surgery workup should be considered in children with NCC who failed two appropriately chosen ASM tried in optimal doses.

Quality of evidence: 3; Strength of recommendation: B

A review published in October, 2019 in the Cochrane Database of Systematic Reviews found four studies (466 patients) which addressed the question of duration of ASMs in patients with neurocysticercosis [54]. There was no difference in seizure recurrence in patients receiving anti-seizure drugs for 6, 12, or 24 months. The odds of seizure recurrence in six months treatment compared with 12 to 24 months treatment was not statistically significant [OR(95% CI) 1.34 (0.73 to 2.47); three studies, 360 participants, low certainty evidence]. When six to 12 months of therapy was compared with 24 months treatment, this too was not statistically significant [OR (95% CI) 1.36 (0.72 to 2.57); three studies, 385 participants; low certainty evidence].

Can the results of this analysis be extrapolated to children? Of the studies included in the analysis, one analyzed children between 3-14 years, one had only adults, one had both children and adults (age range 4-52 years), and the previous study did not clearly mention the age range [55-58]. All studies were single-center studies conducted in India. Notably, these studies excluded patients with persistent lesions, multiple NCC, and those needing albendazole therapy. The presence of calcified lesions was suggested to correlate with seizure recur-rence and the need for prolonged therapy.

Two of these studies have suggested that the presence of calcification and persistence of the lesion on neuroimaging increases the risk of seizures and may require longer ASMs. A large prospective study of 185 patients (38.4% children <14 years) evaluated factors that predict seizure recurrence in patients with solitary cerebral cysticercosis granuloma when ASMs were withdrawn 3-12 weeks after cyst resolution on neuroimaging. Calcific residue on CT scan, breakthrough seizures, and a history of more than two seizures were found to be risk factors for recurrence on multivariate analysis [59].

For a single ring-enhancing lesion, six months of therapy anti-seizure medications is recommended if the lesion resolves on follow-up. Those with persistent lesions, calcification, or multiple lesions require a longer treatment duration of at least 24 months.

Quality of evidence: 2; Strength of recommendation: B

Anti-seizure medication may be withdrawn after 6 months if there is no calcific residue, there is resolution of cyst on neuroimaging, and the child has had less than three seizures in the past.

Children with evidence of calcification, persistent cyst, or a history of more than two seizures in the past may require a longer duration of therapy.

Quality of evidence: 2; Strength of recommendation: B

These guidelines are intended for pediatricians, neurologists, and family physicians, and reflect our approach to the management of the children with NCC based on the best available evidence in the literature and expert opinions.

Note: Additional material related to this study is available with the online version at www.indianpediatrics.net

Contributors: NS and PS: conceptualized the idea; NS, RAK, MK, LK, AK, GRP, IKS, PS: constituted the writing committee and drafted the manuscript; NS: devised and conducted Delphi process. All authors approved the final version of manuscript, and are accountable for all aspects of the manuscript.

Funding: None; Competing interest: None stated.

Rajni Farmania, New Delhi; Jatinder Singh Goraya, Ludhiana, Punjab; Vineet Bhushan Gupta, New Delhi; Rakesh Gupta, Gurugram, Haryana; Rakesh Jain, Gurugram, Haryana; Prashant Jauhari, New Delhi; Gurpreet Singh Kochar, Ludhiana, Punjab; Rashmi Kumar, Lucknow, Uttar Pradesh; Priyanka Madaan, Chandigarh; Abhishek Mewara, Chandigarh; Anita Sharma, Gurugram, Haryana; Lokesh Saini, Jodhpur, Rajasthan; Jitender Saini, Bangalore, Karnataka; Gangandeep Singh, Ludhiana, Punjab; Nitish Vora, Ahmedabad, Gujarat; Sameer Vyas, Chandigarh.

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