Neurocysticercosis Treatment — Stage-Dependent Antiparasitic Therapy

Why NCC Treatment Is Complex

Neurocysticercosis (NCC) is infection of the central nervous system by the larval cyst of the pork tapeworm Taenia solium. The 2017 clinical practice guideline of the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH) describes management as depending on careful staging: whether the cysticerci are viable or degenerating parenchymal cysts, calcified lesions, cysts in the ventricles, in the subarachnoid space, in the spine or in the eye. A patient can have cysts in more than one of these locations at once.

The inflammation paradox: The guideline states that antiparasitic drugs can worsen the symptoms of NCC by inducing an inflammatory response around dying cysts. Most side effects of albendazole and praziquantel in NCC come from this parasiticidal activity (headaches, seizures, dizziness), and there is a transient increase in seizures after therapy. In patients with diffuse cerebral edema (cysticercal encephalitis) or untreated hydrocephalus, the guideline reports that antiparasitic drugs can lead to fatal adverse events such as herniation, and it recommends managing the raised intracranial pressure alone rather than giving antiparasitic treatment (strong recommendation, moderate-quality evidence).

Cyst stage and location: Calcified lesions contain no viable parasite. Viable parenchymal cysts and single enhancing lesions are the forms with placebo-controlled antiparasitic trials. Ventricular and subarachnoid cysts are managed differently from parenchymal cysts, often with surgery or much longer drug courses. Stage descriptions are on the NCC brain cysts page.

The 2017 IDSA/ASTMH guideline: The guideline was published as White et al., Clinical Infectious Diseases 2018 (PubMed PMID: 29481580), with an executive summary in the same journal. Its authors note that, because of the limitations of the literature, many recommendations rest on observational studies, anecdotal data or expert opinion rather than randomized trials, that they are written for North American settings, and that clinicians with little experience of the disease benefit from a low threshold for consulting an expert.

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Calcified NCC — No Living Parasite to Treat

Calcified NCC is the end stage of a cysticercus. The guideline states that calcified lesions do not contain viable parasites, so there is no reason to use antiparasitic therapy, and it recommends symptomatic therapy alone instead of antiparasitic drugs for calcified parenchymal lesions (strong, moderate).

Why calcified lesions still cause seizures:

• Some calcified granulomas are foci of seizure activity, according to the guideline's evidence summary.
• Approximately 30–50% of the time, transient episodes of perilesional edema develop around calcified foci that are foci of seizure activation when symptoms first appear. In an urban population in Lima with seizures and only calcifications, 50% of those with recurring seizures had perilesional edema.
• The guideline describes this edema as likely an immune-mediated inflammatory response to antigen remaining in the calcified granuloma. Episodes often recur, sometimes over decades, and perilesional edema regresses without treatment in 3–6 weeks.

How calcified NCC is managed in the guideline: Antiepileptic drugs are used according to existing epilepsy guidelines, including choice of drug and when to stop. In one prospective study at least 36% of patients developed recurrent seizures; the guideline notes that people with few prior seizures and a long seizure-free period (for example 2 years of good control) may be candidates for tapering off antiepileptic drugs. The guideline suggests that corticosteroids not be routinely used for isolated calcified NCC with perilesional edema (weak, low), because case reports describe new or rebound perilesional edema when corticosteroids are lowered or stopped, and there is not enough evidence to judge whether the benefits of corticosteroids or other immunosuppressive drugs outweigh the risks. For refractory epilepsy with calcified NCC, it suggests evaluation for surgical removal of the seizure focus (weak, low).

Imaging appearance: According to the guideline, calcifications are best seen on noncontrast CT, the most sensitive method. They are typically small (for example 1–4 mm), dense and round, though sometimes large and irregular; most patients have 1–2. On MRI calcifications appear as voids (black regions), and perilesional edema is best seen on FLAIR or T2 sequences.

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Viable Vesicular Parenchymal Cysts

Viable (living) cysticerci in the brain parenchyma are the form for which the guideline identifies two high-quality placebo-controlled trials of antiparasitic drugs. In the absence of raised intracranial pressure, the guideline recommends antiparasitic drugs for all patients with viable parenchymal NCC (strong, moderate).

What "viable" means on imaging: The guideline defines a viable cyst by a cystic lesion with a fluid-filled center, hypodense on CT or T1 images or hyperintense on T2 images. Nonviable lesions lack the cystic component.

Regimens the 2017 guideline lists:

• 1–2 viable cysts: albendazole alone for 10–14 days, recommended over no antiparasitic therapy (strong, high) and over combination therapy (weak). The usual dose it gives is 15 mg/kg/day in two daily doses with food, with a maximum of 1200 mg/day. The guideline notes that albendazole is poorly absorbed and that absorption improves with food, especially fatty meals.
• More than 2 viable cysts: albendazole 15 mg/kg/day combined with praziquantel 50 mg/kg/day for 10–14 days, recommended over albendazole alone (strong, moderate).
• Corticosteroids begun before the antiparasitic drugs in all patients receiving antiparasitic therapy (strong, moderate).
• Liver enzymes and blood counts monitored in patients receiving albendazole for more than 14 days (strong, moderate).

Albendazole versus placebo: In a double-blind trial by Garcia and colleagues (N Engl J Med 2004, PubMed PMID: 14724304), 120 patients with living cysts and seizures received albendazole 800 mg/day plus dexamethasone 6 mg/day for 10 days, or two placebos. The 46% reduction in total seizures over months 2–30 was not statistically significant, but seizures with generalization fell significantly (by 67%), and more cystic lesions resolved in the albendazole group.

Combination versus albendazole alone: Garcia et al. (2014, Lancet Infectious Diseases, PubMed PMID: 24999157) randomized 124 patients with viable parenchymal NCC to 10 days of albendazole 15 mg/kg/day plus praziquantel 50 mg/kg/day, standard albendazole (15 mg/kg/day) or increased-dose albendazole (22.5 mg/kg/day), all with dexamethasone. Complete cyst resolution on the 6-month MRI occurred in 25 of 39 patients (64%) given the combination versus 15 of 41 (37%) given standard albendazole (rate ratio 1.75, p=0.014); the increased-dose albendazole group (53%) did not differ significantly from standard albendazole. Adverse events did not differ significantly between groups, and enrolment was stopped after an interim analysis showed parasiticidal superiority of one group. The guideline adds that, among patients with 3 or more cysts in this trial, all viable cysts resolved in 13 of 19 (68%) on the combination versus 1 of 21 (5%) on standard albendazole.

Follow-up and retreatment: The guideline suggests MRI at least every 6 months until the cystic component resolves, a first clinical follow-up at 2–4 weeks, and a CT scan before stopping antiepileptic drugs to see whether calcifications have formed. For cystic lesions persisting 6 months after the end of the first course it suggests retreatment (weak, low); options it lists are a second course of albendazole, switching to praziquantel, or the combination.

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Single Enhancing Granuloma

A single enhancing lesion (SEL), also termed a solitary cysticercus granuloma, is a degenerating cyst showing contrast enhancement. The guideline notes that children are more likely than adults to present with SELs and with cysticercal encephalitis.

Natural history: In a prospective CT study of 210 patients with seizures and a recently diagnosed solitary cysticercus granuloma, Rajshekhar (Neurology 2001, PubMed PMID: 11756620) found complete spontaneous resolution in 18.8% at 3 months, 36.4% at 6 months and 62.5% at 1 year. In the meta-analysis summarized by the guideline (Otte and colleagues), six trials reported radiologic resolution at 6 months in 67% of patients given albendazole versus 48% given placebo, with considerable heterogeneity; at 6 months 90% versus 83% were seizure-free; and there was no significant difference in the frequency of calcification at the end of follow-up.

What the guideline lists: It suggests albendazole rather than no antiparasitic therapy for all patients with SELs (weak, moderate), at 15 mg/kg/day in twice-daily doses with meals for 1–2 weeks; trials comparing 7 with 28 days, 7 with 14 days, and 2 with 15 days found no significant differences, so the panel suggests 7–14 days. It recommends corticosteroids started before the antiparasitic drug (strong, moderate) and antiepileptic drugs for all patients with SELs and seizures (strong, moderate).

Seizure outcomes: In a prospective cohort of 185 patients with SELs cited by the guideline, most did not develop recurrent seizures; 16.2% had a seizure a week or more after the first while on antiepileptic drugs, and 15.1% had recurrence after the drugs were withdrawn (follow-up 24–125 months). Monotherapy with phenytoin or carbamazepine controlled seizures in 86.5%.

Antiepileptic drug duration: At least three trials compared 6 months with 12–24 months of antiepileptic treatment and found no benefit from the longer course when the granuloma had completely resolved; the risk of recurrent seizures stayed high when the lesion left a calcific residue on CT, and in that group longer treatment appeared to offset it. The guideline suggests that tapering and stopping be considered after lesion resolution in patients seizure-free for 6 months without risk factors for recurrence (weak, moderate) — residual cystic lesions or calcifications, breakthrough seizures, or more than 2 seizures.

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Ventricular NCC

In most case series, according to the guideline, 10–20% of patients with NCC have cysticerci in the ventricles. These cysts are typically silent for years and usually present when they obstruct cerebrospinal fluid (CSF) flow and cause hydrocephalus; fourth-ventricle cysts have been associated with acute obstructive hydrocephalus and drop attacks (Bruns syndrome). The guideline describes ventricular disease as prone to a high case-fatality rate.

Antiparasitic drugs before surgery: Untreated hydrocephalus is a contraindication to antiparasitic therapy in the guideline. Most experts it cites recommend that antiparasitic drugs not be given before surgery, because they can disrupt the parasite and provoke an inflammatory response that could prevent successful cyst removal. Where hydrocephalus is present and medical therapy is planned, the guideline states that a shunt is always placed first, because antiparasitic therapy has been reported to precipitate hydrocephalus.

Neuroendoscopic removal: For cysts of the lateral and third ventricles the guideline recommends removal by minimally invasive neuroendoscopy, when possible, over other surgical or medical approaches (strong, moderate). Case series report high cure rates and minimal morbidity. Cyst rupture during endoscopic removal is frequent, and the guideline reports no convincing evidence that it causes adverse outcomes. Inflamed or degenerating cysts that adhere to the ventricular wall are a contraindication to removal by any approach, because of a high risk of hemorrhage and neurologic sequelae. For fourth-ventricle cysts the guideline recommends surgical removal, where possible, over medical therapy and/or shunt surgery (strong, moderate), by endoscopic or microsurgical (suboccipital) approaches depending on the surgeon's experience.

Shunting: When removal is technically difficult, the guideline suggests shunt surgery for the hydrocephalus (weak, low). Shunting alone was complicated by shunt failure in most reported cases — approximately 60% without antiparasitic drugs — and lower failure rates were noted in nonrandomized series of patients who also received antiparasitic drugs and corticosteroids. The guideline therefore suggests antiparasitic drugs with corticosteroids after shunt insertion when the cysts cannot be removed (weak, low).

After successful removal: The guideline suggests that antiparasitic drugs are not needed after successful removal of isolated intraventricular cysts (weak, low), noting that outcomes are excellent without further antiparasitic therapy when follow-up imaging is negative; other coexisting lesions may still have their own indications. Corticosteroids around the time of surgery to reduce brain edema are recommended (not graded), and the guideline mentions anecdotal use of dexamethasone 8–24 mg/day to stabilize patients before surgery.

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Subarachnoid and Racemose NCC

The guideline separates two kinds of subarachnoid NCC. Structurally normal cysts in fissures on the surface of the cerebral convexities follow a benign course similar to parenchymal cysts and are managed similarly. Cysts in the basal cisterns or Sylvian fissure can cause severe disease.

Why basal subarachnoid NCC is difficult:

• Almost all cases involve a host inflammatory response causing meningitis, edema and scarring, which leads to communicating hydrocephalus, focal neurologic signs, nerve entrapment and cerebrovascular complications; strokes occur in 4–12% of patients.
• Other reported manifestations include cognitive dysfunction, psychiatric disease, Parkinson-like syndromes, visual loss from papilledema, and cranial nerve deficits.
• Before antiparasitic drugs were available, one series documented a 50% mortality rate in patients treated with ventriculoperitoneal shunting alone.
• There are no randomized or well-controlled treatment trials. Most experts cited in the guideline conclude that this form responds poorly to the drug doses and durations developed for parenchymal disease.

Antiparasitic therapy in the guideline: It recommends antiparasitic drugs for subarachnoid cysts (strong, low) and suggests continuing them until MRI shows radiologic resolution of viable cysticerci and other evidence of infection has resolved (weak, low); responses often require therapy for more than a year, and successful treatment may take years. Options it lists are prolonged albendazole (15 mg/kg/day for months) or albendazole combined with praziquantel 50 mg/kg/day, the combination being used by some experts without published data. Short courses of high-dose albendazole (30 mg/kg/day) showed better cysticidal activity, but their safety is not well established. In a series of 33 patients with giant cysts, most failed a single course but eventually responded to repeated courses, and no deaths were reported.

Anti-inflammatory therapy: The guideline recommends anti-inflammatory therapy such as high-dose corticosteroids started before antiparasitic drugs (strong, moderate). Doses it describes as generally used are prednisone 1 mg/kg/day or dexamethasone 0.2–0.4 mg/kg/day, given 3–4 days before and during antiparasitic treatment and slowly decreased with careful tapering. It suggests methotrexate as a steroid-sparing agent for prolonged courses (weak, low), describing an initial 7.5 mg weekly increased to a maximum of 20 mg weekly. Before prolonged corticosteroids it suggests screening for latent tuberculosis (weak, low) and screening or empiric therapy for Strongyloides stercoralis (weak, low), since corticosteroids raise the risk of Strongyloides hyperinfection.

Surgery: The guideline recommends shunt surgery in addition to medical therapy for hydrocephalus from subarachnoid NCC (strong, low) and suggests that some patients may benefit from surgical debulking (weak, low); it warns that attempts to remove adherent cysts in the basilar cisterns can be catastrophic. Because basal subarachnoid NCC is strongly associated with silent spinal involvement, the guideline calls for MRI of the spine in all patients with intracranial subarachnoid disease.

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Antiepileptic Drugs (AEDs)

The guideline recommends antiepileptic drugs for all NCC patients with seizures (strong, low). There are no controlled trials, but AEDs appear to control seizures in parenchymal NCC as well as in other seizure disorders, and poor adherence to them is a major risk factor for seizure recurrence.

AED selection: No controlled data compare different AEDs in NCC, and the guideline leaves the choice to local availability, cost, drug interactions and side effects (not graded). Points it makes:

• Phenytoin and carbamazepine are the drugs used most often in T. solium-endemic regions, largely for availability and cost. Both are potent hepatic P450 enzyme inducers; in pharmacokinetic studies they decrease blood levels (area under the curve) of praziquantel and, to a lesser extent, albendazole. The clinical significance of this interaction is unknown.
• Levetiracetam and other newer agents have fewer drug interactions; the guideline says they may be preferable to older agents, and that giving a non-enzyme-inducing AED at least during antiparasitic treatment is one way around the interaction, a strategy not tested in any controlled trial.
• Phenobarbital has high rates of drug interactions with antiparasitic agents and corticosteroids; the guideline states it may be better to avoid it during antiparasitic therapy.
• In pregnancy, the guideline notes that phenobarbital and valproic acid have high rates of teratogenicity.

Duration of AED therapy in the guideline:

• Viable parenchymal cysts: tapering off may be considered in patients with few seizures before treatment, resolution of the cystic lesion, and no seizures for 24 consecutive months (weak, moderate).
• Single enhancing lesion: tapering may be considered after lesion resolution in patients seizure-free for 6 months without risk factors (weak, moderate); a calcific residue raises recurrence risk.
• Calcified NCC: managed according to guidelines for other seizure disorders; those with few prior seizures and about 2 years of good control may be candidates for tapering.
• Risk factors for recurrence the guideline lists include the number of seizures before treatment and development of calcified lesions; recurrence is unusual when the lesion resolves on CT without calcification and there are no seizures for more than 12 months.

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Corticosteroid Role

The guideline recommends adjunctive corticosteroids begun before antiparasitic drugs, rather than no adjunctive therapy, in all patients receiving antiparasitic therapy (strong, moderate). The basis it gives is anecdotal evidence and large case series showing fewer adverse events when antiparasitic drugs are combined with steroids. The effect of corticosteroids on cyst resolution and on later calcification is unknown.

Doses used in trials: The guideline states that the optimal corticosteroid dose has not been defined. Regimens in the trials it summarizes include dexamethasone 6 mg/day for 10 days (Garcia 2004), dexamethasone 0.1 mg/kg/day (Garcia 2014), and prednisone 75 mg/day (a placebo-controlled albendazole trial by Carpio and colleagues); other studies used prednisone 1–1.5 mg/kg/day. A trial of enhanced dexamethasone (8 mg/day for 28 days with a 14-day taper) versus 6 mg/day for 10 days, both with 10 days of albendazole, found significantly fewer partial seizures over the first 21 and first 180 days in the enhanced-dose arm, with no difference in cyst resolution; the study was underpowered because of slow enrolment.

Interaction with praziquantel: According to the guideline, praziquantel undergoes extensive first-pass metabolism that is induced by drugs often given alongside it, including AEDs and corticosteroids. Cimetidine inhibits this metabolism and raises praziquantel levels, but no controlled clinical data show the clinical impact of giving them together.

Adverse effects: Short courses are usually well tolerated; the guideline lists hyperglycemia and gastritis, and, with prolonged therapy, opportunistic infections, osteopenia, Cushing syndrome, aseptic necrosis of joints, mood changes (depression, psychosis) and skin changes. It describes monitoring blood sugar in patients on corticosteroids for more than 2 weeks and screening for latent tuberculosis and Strongyloides before prolonged courses.

Calcified NCC: Here the guideline suggests corticosteroids not be used routinely for perilesional edema (weak, low), because of case reports of rebound edema when steroids are lowered or stopped.

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Surgical Options

Surgery has a role in NCC where drug therapy is insufficient or unsafe. The guideline's positions by indication:

Neuroendoscopic cyst removal: Recommended when possible for cysts of the lateral and third ventricles (strong, moderate). The endoscopic approach often requires enlarged ventricles; most isolated, nonadherent cysts there can be cured by neuroendoscopy without later antiparasitic drugs or a shunt if all cysts are removed. In case series, outcomes were better with endoscopic removal than with open procedures.

Fourth-ventricle cysts: Endoscopic or microsurgical cystectomy, the endoscopic route through the aqueduct being technically demanding and reserved for an experienced neuroendoscopist.

Ventriculoperitoneal (VP) shunting: Used for hydrocephalus when cysts cannot be removed (for example adherent or inflamed cysts) and in subarachnoid NCC. Shunts work acutely, but the guideline reports a very high rate of shunt malfunction in NCC, possibly lower when combined with corticosteroids and antiparasitic treatment.

Spinal NCC: The guideline suggests that both medical (antiparasitic plus anti-inflammatory drugs) and surgical approaches be considered (weak, low), with no good data favoring one; corticosteroids are recommended when there is spinal cord dysfunction (strong, moderate).

Ocular cysticercosis: The guideline suggests surgical removal of intraocular cysticerci rather than antiparasitic drugs (weak, low). Untreated intraocular disease was thought to be a contraindication to cysticidal therapy because the induced inflammation can lead to blindness, and there are not enough data on the safety of medical therapy. For this reason it recommends a funduscopic eye examination in all patients with NCC before antiparasitic therapy (strong, moderate).

Epilepsy surgery: For refractory epilepsy with calcified NCC, evaluation for surgical removal of the seizure focus is suggested (weak, low).

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2017 IDSA/ASTMH Guidelines Summary

The 2017 IDSA/ASTMH clinical practice guideline (White et al., Clin Infect Dis 2018) grades each recommendation by strength (strong or weak) and quality of evidence (high, moderate or low) using the GRADE framework. Its main treatment recommendations, as stated in the guideline:

Raised intracranial pressure (untreated hydrocephalus or diffuse cerebral edema):

• Management of the raised pressure alone, without antiparasitic treatment (strong, moderate)

Viable parenchymal cysts:

• 1–2 cysts: albendazole 15 mg/kg/day (maximum 1200 mg/day) for 10–14 days (strong, high versus no treatment)
• More than 2 cysts: albendazole 15 mg/kg/day plus praziquantel 50 mg/kg/day for 10–14 days (strong, moderate)
• Corticosteroids begun before antiparasitic drugs (strong, moderate)
• Retreatment for cystic lesions persisting 6 months after the first course (weak, low); MRI at least every 6 months until resolution

Single enhancing lesion:

• Albendazole 15 mg/kg/day for 1–2 weeks (weak, moderate), with corticosteroids (strong, moderate)
• Antiepileptic drugs for patients with seizures (strong, moderate)

Calcified-only NCC:

• Symptomatic therapy, no antiparasitic drugs (strong, moderate)
• Corticosteroids not routinely used for perilesional edema (weak, low)

Ventricular NCC:

• Neuroendoscopic removal for lateral and third ventricle cysts when possible (strong, moderate); surgical removal for fourth ventricle cysts when possible (strong, moderate)
• Shunt surgery when removal is technically difficult (weak, low), with antiparasitic drugs and corticosteroids after the shunt (weak, low)
• No antiparasitic drugs after successful removal of isolated intraventricular cysts (weak, low)

Subarachnoid NCC:

• Antiparasitic drugs (strong, low), continued until radiologic resolution (weak, low)
• High-dose corticosteroids begun before antiparasitic drugs (strong, moderate); methotrexate as a steroid-sparing option (weak, low)
• Shunt surgery for hydrocephalus in addition to medical therapy (strong, low)

Special populations: The guideline finds no evidence that children are managed differently from adults with the same form of disease (strong, moderate), with weight-based dosing, and suggests deferring antihelminthic therapy until after pregnancy (weak, low).

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Key Research Papers

1. White AC Jr, Coyle CM, Rajshekhar V, Singh G, Hauser WA, Mohanty A, et al. Diagnosis and Treatment of Neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH) [executive summary]. Clin Infect Dis. 2018;66(8):1159-1163. [PubMed PMID: 29617787]. — Search PubMed
2. White AC Jr, Coyle CM, Rajshekhar V, Singh G, Hauser WA, Mohanty A, et al. Diagnosis and Treatment of Neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH) [full guideline]. Clin Infect Dis. 2018;66(8):e49-e75. PubMed PMID: 29481580
3. Nash TE, Singh G, White AC, Rajshekhar V, et al. Treatment of neurocysticercosis: current status and future research needs. Neurology. 2006;67(7):1120-1127. [PubMed PMID: 17030744]. — Search PubMed
4. 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. 2004;350(3):249-258. [PubMed PMID: 14724304]. — Search PubMed
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. 2014;14(8):687-695. PubMed PMID: 24999157
6. Carpio A et al. Neurocysticercosis: new knowledge, new doubts. Curr Neurol Neurosci Rep. [Search PubMed]. — Search PubMed (editorial note: no record matching this title was found in PubMed or Crossref on 2026-10-14)
7. Garcia HH, Nash TE, Del Brutto OH. Clinical symptoms, diagnosis, and treatment of neurocysticercosis. Lancet Neurol. 2014;13(12):1202-1215. [PubMed PMID: 25453460]. — Search PubMed
8. Bhatt GC et al. Cysticercosis and Neurocysticercosis. Pediatr Clin North Am. [Search PubMed]. — Search PubMed (editorial note: no record matching this title was found in PubMed or Crossref on 2026-10-14)
9. García HH, Gonzalez AE, Evans CA, Gilman RH; Cysticercosis Working Group in Peru. Taenia solium cysticercosis. Lancet. 2003;362(9383):547-556. [PubMed PMID: 12932389]. — Search PubMed
10. Rajshekhar V. Rate of spontaneous resolution of a solitary cysticercus granuloma in patients with seizures. Neurology. 2001;57(12):2315-2317. [PubMed PMID: 11756620]. — Search PubMed
11. Del Brutto OH, Nash TE, White AC Jr, Rajshekhar V, et al. Revised diagnostic criteria for neurocysticercosis. J Neurol Sci. 2017;372:202-210. [PubMed PMID: 28017213]. — Search PubMed
12. Fleury A, Gomez T, Alvarez I, Meza D, Huerta M, Chavarria A, et al. High prevalence of calcified silent neurocysticercosis in a rural village of Mexico. Neuroepidemiology. 2003;22(2):139-145. [PubMed PMID: 12629280]. — Search PubMed

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