Cysticercosis: Treatment

INTRODUCTION — Cysticercosis is caused by the larval stage (metacestode) of the pork tapeworm Taenia solium. Clinical syndromes related to this parasite include neurocysticercosis (NCC) and extraneural cysticercosis. NCC, in turn, is divided into parenchymal and extraparenchymal forms. Extraparenchymal forms include intraventricular, subarachnoid, spinal, and ocular disease. Treatment must be individualized based on the disease manifestations.

Guidelines on management of neurocysticercosis were published in 2021 by the World Health Organization; guidelines on diagnosis and treatment were published in 2018 by the Infectious Diseases Society of America and the American Society of Tropical Medicine and Hygiene [1,2].

The treatment of cysticercosis will be reviewed here. The epidemiology, transmission, prevention, clinical features, and diagnosis of cysticercosis and the life cycle of T. solium are discussed in detail separately. (See "Cysticercosis: Epidemiology, transmission, and prevention" and "Cysticercosis: Clinical manifestations and diagnosis".)

The approach to treatment of tapeworm infection with T. solium is discussed in detail separately. (See "Tapeworm infections".)

GENERAL PRINCIPLES — Stages of cysticercosis include an initial (viable) phase, a degenerating phase, and a nonviable phase (table 1 and figure 1 and picture 1 and image 1):

●Viable cysticerci are round, hypodense lesions (usually 5 to 20 mm in diameter) on computed tomography (CT). Viable cysticerci do not cause much inflammation in surrounding tissues and typically do not enhance after contrast administration.

●Cysticerci degenerate when attacked by the host immune response. The cyst wall increases in density and is often accompanied by surrounding edema and/or contrast enhancement; such findings reflect the host inflammatory response against the parasite and are frequently associated with seizures. In many cases, enhancing cysticerci retain features of viable cysticerci, such as ring enhancing lesions. When the cyst fluid begins to increase in density, the cysts are thought to no longer be viable.

●Nonviable cysticerci are solid, calcified nodular lesions (usually 2 to 4 mm in diameter; range 1 to 10 mm); they are usually nonenhancing but may be associated with perilesional edema in some cases. They are also associated with seizures.

Cysticerci may be present in more than one anatomic site. In addition, cysticerci at different stages in their natural history may be present simultaneously; for example, at any one time, a patient may have some non-inflamed viable cysts, some enhancing cysts, and/or some calcified cysts.

In general, treatment should focus on the more severe manifestations of disease and/or the manifestations with greatest likelihood response to therapy. For example, if a patient has intraventricular lesions with hydrocephalus as well as intraparenchymal disease, a number of interventions are needed ( endoscopic removal, anti-inflammatory therapy, antiparasitic therapy, antiseizure medication therapy). The initial focus should be on management of obstructive hydrocephalus, which is a contraindication to antiparasitic therapy.

Issues related to radiographic findings are discussed further separately. (See "Cysticercosis: Clinical manifestations and diagnosis", section on 'Radiographic imaging'.)

INITIAL MANAGEMENT — The initial approach to patients with NCC consists of managing acute symptoms if present, such as increased intracranial pressure (via surgical intervention and/or corticosteroids) and seizures (via antiseizure medications). Initiation of antiparasitic therapy is never urgent and should only be a consideration after initial symptomatic therapy. Thereafter, clinical decisions should be tailored to individual patient circumstances, as discussed in the sections below [3-5].

Managing elevated intracranial pressure — Signs and symptoms of elevated intracranial pressure (headache, nausea/vomiting, papilledema, and somnolence) associated with parenchymal disease may occur in the setting of diffuse cerebral edema on neuroimaging. Management of diffuse cerebral edema consists of corticosteroid therapy (dexamethasone 0.2 to 0.4 mg/kg per day) to reduce inflammation. (See 'Disseminated disease with or without encephalitis' below.)

Causes of elevated intracranial pressure associated with extraparenchymal disease include obstructive hydrocephalus (associated with intraventricular disease) and communicating hydrocephalus (associated with subarachnoid disease) [2]:

●Management of obstructive hydrocephalus usually consists of a surgical approach (via removal of an obstructing cysticercus or placement of an external ventricular drain or shunt). (See 'Obstructive hydrocephalus due to intraventricular cyst' below.)

●Management of communicating hydrocephalus consists of cerebrospinal fluid diversion via ventriculoperitoneal shunt or third ventriculostomy. (See 'Communicating hydrocephalus due to subarachnoid disease' below.)

Antiparasitic therapy is contraindicated in patients with signs or symptoms of elevated intracranial pressure, regardless of the cause. Such patients should only be considered for antiparasitic therapy if elevated pressure has resolved.

Antiseizure medication therapy — Patients with seizures should be managed with antiseizure medication therapy. Even in the case of a single seizure, NCC lesion(s) serve a nidus for recurrent seizures (focal epilepsy) [1,2,6].

The choice of antiseizure medication should be guided by local availability, cost, drug interactions, and potential side effects [1,2,6]. Most reports on management of seizures in the setting of NCC describe use of phenytoin or carbamazepine. Newer therapies (such as levetiracetam) are likely better tolerated, with fewer drug-drug interactions [7]. However, one study suggested that seizure control may be better with carbamazepine than with levetiracetam [8]. In a retrospective review of children with seizures from single enhancing lesions, children treated with lacosamide had fewer side effects and similar seizure control compared to children treated with oxcarbazepine [9]. (See "Overview of the management of epilepsy in adults".)

PARENCHYMAL DISEASE

Medical management — The approach to management of parenchymal neurocysticercosis (NCC) should be guided by findings on radiographic imaging (table 2 and table 3). (See 'General principles' above.)

Prior to antiparasitic therapy — Prior to initiation of antiparasitic therapy for cysticercosis, all patients should have an ophthalmologic examination to exclude ocular cysticercosis [1,2]. Inflammation around degenerating cysticerci in the eye (particularly in the setting of antiparasitic therapy) can threaten vision. (See "Cysticercosis: Clinical manifestations and diagnosis", section on 'Orbital and ocular lesions'.)

In addition, patients who are likely to require prolonged corticosteroids should also undergo screening for latent tuberculosis infection as well as screening or empiric therapy for strongyloidiasis. (See "Tuberculosis infection (latent tuberculosis) in adults: Approach to diagnosis (screening)" and "Strongyloidiasis".)

Antiparasitic therapy — The potential benefits of antiparasitic therapy include hastened resolution of active cysts, diminished seizure risk, and reduced likelihood of recurrent hydrocephalus [1-3]. The major potential risk of antiparasitic therapy is exacerbation of neurologic symptoms due to inflammation around the degenerating cyst, particularly in patients with a large number of lesions or elevated intracranial pressure.

Patient selection — Antiparasitic therapy is warranted for patients with viable and/or degenerating cysts on neuroimaging. Antiparasitic therapy should not be administered in the following circumstances:

●Untreated hydrocephalus (see 'Obstructive hydrocephalus due to intraventricular cyst' below and 'Communicating hydrocephalus due to subarachnoid disease' below)

●Diffuse cerebral edema associated with numerous parasites (eg, cysticercal encephalitis) (See 'Disseminated disease with or without encephalitis' below.)

●Presence of calcified lesion(s) only (See 'Patients with calcified nonviable lesion(s)' below.)

Choice of regimen — Antiparasitic regimens for treatment of patients with viable and/or degenerating cysts on neuroimaging include albendazole and combination therapy with albendazole plus praziquantel.

The choice of antiparasitic regimen depends on the burden of disease [1,2,10-13]:

●For patients with one to two cysts, treatment consists of albendazole (15 mg/kg per day in two daily doses up to 1200 mg per day, with food).

●For patients with more than two cysts, treatment consists of albendazole (15 mg/kg per day in two daily doses up to 1200 mg per day, with food) and praziquantel (50 mg/kg per day in three daily doses).

Adjunctive corticosteroids should be administered prior to and during antiparasitic therapy [1,2]. (See 'Adjunctive use with antiparasitic therapy' below.)

The above approach to antiparasitic therapy is supported by a randomized trial including 120 patients in Peru with viable parenchymal neurocysticercosis (VPN) and seizures; patients were treated with antiseizure medications and randomized to treatment with albendazole (800 mg daily for 10 days) plus dexamethasone (6 mg daily for 10 days) or double placebo [13]. The patients were followed for 30 months or until they were seizure free for six months after tapering of antiseizure therapy. The patients in the treatment arm had fewer generalized seizures (22 versus 68; 67 percent reduction), although there was no significant difference in the overall number of seizures or the number of patients with seizures. The patients in the treatment arm were more likely to have radiographic resolution of intracranial cystic lesions during the 30-month follow-up period, but there was no difference in the development of calcifications between the groups. These findings were confirmed by a subsequent trial performed in Ecuador [14].

Evidence for the management of patients with a solitary cyst includes a systematic review and meta-analysis of 15 randomized trials; 10 trials included 765 patients treated with antiseizure medication therapy with or without albendazole, and 5 trials included 457 people treated with antiseizure medication therapy with or without corticosteroids [15]. Treatment with albendazole was associated with higher rates of seizure freedom (odds ratio [OR] 2.45, 95% CI 1.49-4.03) and higher rates of radiographic resolution (OR 2.09, 95% CI 1.41-3.00). Treatment with albendazole did not alter the likelihood of residual calcification, . A network analysis suggested that a regimen of corticosteroids plus albendazole was associated with a decreased risk of seizure recurrence (OR 0.32, 95% CI 0.10-0.93) [10].

The combination of albendazole and praziquantel has been associated with a higher rate of radiographic resolution than albendazole alone [16-19]. In one randomized trial including 124 patients with VPN randomized to treatment with standard-dose albendazole (15 mg/kg/day), high-dose albendazole (22.5 mg/kg/day), or combination therapy with both albendazole (15 mg/kg/day) and praziquantel (50 mg/kg/day), complete radiographic resolution was observed after six months in 68 percent of patients with more than two cystic lesions treated with combination therapy (compared with 5 percent treated with standard-dose albendazole and 25 percent treated with high-dose albendazole) [18]. Similar findings were observed in another trial [19]. In a randomized trial of children with persistent lesions despite prior antiparasitic drugs, those who were retreated with albendazole plus praziquantel had a greater proportion with resolution and larger decrease in cyst volume than those treated with albendazole [20].

Duration of therapy — The duration of antiparasitic therapy for treatment of parenchymal neurocysticercosis is 7 to 14 days in most cases.

Corticosteroids

Adjunctive use with antiparasitic therapy — Corticosteroids should always be administered concomitantly with antiparasitic therapy [1,2]. Use of corticosteroids during antiparasitic therapy is associated with fewer seizures [1,2,10,21]. Administration of antiparasitic therapy may hasten degeneration of viable cysts, thereby increasing inflammation and increasing risk for seizure. In some cases, inflammation associated with antiparasitic therapy can be so severe that it leads to disability or death.

For patients with single enhancing lesions, use of adjunctive corticosteroids has been associated with reduction in the likelihood of seizure recurrence [22]. This was illustrated in a network meta-analysis including 14 randomized trials; among patients treated with combination albendazole and corticosteroids, corticosteroids alone, albendazole alone, or conservative management, combination therapy was the only regimen that significantly reduced the risk of seizure recurrence relative to conservative treatment (OR 0.32, 95% CI 0.10-0.93) [10]. Limitations of this network meta-analysis include high risk of bias and short follow-up duration in most studies.

For patients with multiple viable cysts, administration of antiparasitic therapy without corticosteroids has been associated with increased seizures shortly after initiation of treatment. In open-label studies, use of adjunctive corticosteroids has been shown to abrogate this response [21]. In addition, a trend toward fewer seizures with enhanced steroid dosing was suggested in a randomized trial [23]; however, that trial was underpowered.

Dose and duration — The optimal adjunctive corticosteroid regimen is uncertain; commonly used regimens include prednisone (1 mg/kg per day) or dexamethasone (0.1 mg/kg per day) begun at least one day prior to antiparasitic therapy, continued for the duration of antiparasitic therapy, and followed by a rapid taper over a few days.

More intensive steroid dosing (such as dexamethasone 8 mg/day for 28 days followed by a taper) may be associated with fewer seizures; further study is needed [23]. In parenchymal neurocysticercosis, dexamethasone doses >6.5 mg/day have been associated with less frequent development of calcifications [24].

Symptomatic use — Use of corticosteroids is warranted for management of cysticercal encephalitis (diffuse cerebral edema associated with multiple inflamed cysticerci). (See 'Disseminated disease with or without encephalitis' below.)

Routine use of corticosteroids is not warranted for patients with calcified lesions and perilesional edema. In such cases when corticosteroids are tapered or stopped, rebound edema may occur [2].

Disseminated disease with or without encephalitis — Patients with disseminated disease may be categorized as follows:

●Disseminated parenchymal neurocysticercosis refers to patients with more than 20 lesions within the brain parenchyma. These include cases with cysticercal encephalitis and heavy non-encephalitic cysticercosis [25]. There is limited information on optimal treatment in these cases; some patients have been treated with corticosteroid and antiparasitic therapy [26,27].

●Cysticercal encephalitis refers to disseminated parenchymal neurocysticercosis with diffuse cerebral edema associated from multiple inflamed cysticerci). Cysticercal encephalitis is a contraindication for antiparasitic therapy, since enhanced parasite killing can exacerbate the host inflammatory response, leading to diffuse cerebral edema and potential transtentorial herniation [25]. Most cases of cysticercal encephalitis improve with high-dose corticosteroid therapy (eg, dexamethasone 0.2 to 0.4 mg/kg per day). The duration of therapy should be individualized based on the clinical and radiographic resolution of edema. In most cases, the cysticerci resolve without antiparasitic therapy.

Patients with calcified nonviable lesion(s) — Management of patients with calcified parenchymal neurocysticercosis (CPN; in the absence of viable or enhancing lesions) consists of symptomatic therapy.

Calcified lesions do not contain viable parasites so there is no role for antiparasitic or anti-inflammatory therapy [2]. Routine use of corticosteroids is not warranted for patients with calcified lesions associated with perilesional edema. In such cases when corticosteroids are tapered or stopped, rebound edema can occur.

Patients with seizures warrant antiseizure medication therapy; in such patients, calcified lesions increase the risk of recurrent seizures and chronic epilepsy [6,28]. No antiseizure medication therapy is warranted for asymptomatic patients.

For patients with a single seizure and no recurrence within six months, tapering and discontinuation of antiseizure medication therapy is reasonable [6,28]. A minority of cases of neurocysticercosis go on to develop refractory seizures, especially temporal lobe seizures. These are frequently associated with hippocampal atrophy. Cures have been noted with resection of the anterior temporal lobe [29].

EXTRAPARENCHYMAL DISEASE

Elevated intracranial pressure — Management of elevated intracranial pressure is discussed above. (See 'Managing elevated intracranial pressure' above.)

Obstructive hydrocephalus due to intraventricular cyst — Patients with intraventricular neurocysticercosis (IVN) and hydrocephalus associated with altered mental status or impending herniation may require emergent cerebrospinal fluid (CSF) diversion via ventriculostomy, placement of a ventriculoperitoneal shunt, or neuroendoscopic cyst removal and third ventriculostomy [2,30-32]. Definitive therapy for patients with cyst(s) causing obstruction consists of cyst removal if possible.

Management of patients with mild or intermittent symptoms of hydrocephalus depends on whether the cysticerci are adherent. In general, cysticerci that appear intact and are not inflamed may be regarded as nonadherent:

●For patients with nonadherent IVN in the lateral or third ventricle, cysticerci should be removed endoscopically if feasible [2,30,31]. For patients with nonadherent IVN in the fourth ventricle, cysticerci should be removed endoscopically, via an open approach, or stereotactic removal; the approach depends on the experience of the surgeon and whether there is dilation of the aqueduct of Sylvius [2,31,33,34]. In many cases, the fourth ventricle is more easily accessed via a suboccipital approach. Most cases of isolated nonadherent IVN can be cured by removal and do not require antiparasitic therapy if all cysticerci are removed [32,35]. There is no role for preoperative antiparasitic therapy, which can lead to an inflammatory response and reduce the likelihood of successful cyst removal. For cases in which not all cysticerci are removed, subsequent antiparasitic therapy (albendazole 15 mg/kg per day in two daily doses up 1200 mg per day, with food for 10 to 14 days) and anti-inflammatory therapy with corticosteroids is warranted.

●For patients with adherent IVN, management consists of CSF diversion via ventriculoperitoneal shunt (rather than cyst removal, which is associated with increased risk of complications), followed by antiparasitic therapy (albendazole 15 mg/kg per day in two daily doses up 1200 mg per day, with food for 10 to 14 days) and anti-inflammatory therapy [36] (see 'Antiparasitic therapy' above and 'Corticosteroids' above). Shunt placement prior to antiparasitic therapy is important since precipitation of hydrocephalus with antiparasitic therapy has been described.

Corticosteroids are often administered prior to, during, and following neurosurgical procedures to reduce inflammation and brain edema. There are no high-quality data on the efficacy of this approach for surgical management of IVN, but it is well established for other neurologic diseases.

Communicating hydrocephalus due to subarachnoid disease — Subarachnoid (racemose) NCC can present with communicating hydrocephalus, meningitis, stroke, or focal neurologic findings [2,37,38]. Subarachnoid NCC is associated with a high case fatality rate [39]. Mixed forms also occur. (See "Cysticercosis: Clinical manifestations and diagnosis", section on 'Subarachnoid lesions'.)

In the setting of subarachnoid neurocysticercosis and communicating hydrocephalus, management consists of CSF diversion via ventriculoperitoneal shunt, followed by antiparasitic and anti-inflammatory (corticosteroid) therapy [2,37,38,40].

In the setting of subarachnoid neurocysticercosis and no hydrocephalus, management consists of antiparasitic therapy and anti-inflammatory (corticosteroid) therapy. Endoscopic removal/debulking of subarachnoid cysts via third ventriculostomy or other approaches have been described; however, the role for this intervention is controversial given the risk of bleeding and neurologic complications [2,41-43].

Subarachnoid cysts do not respond to typical durations and doses of antiparasitic therapy used for parenchymal neurocysticercosis [44]. Therapeutic options include prolonged administration of albendazole (15 mg/kg per day), cycles of higher doses of albendazole (30 mg/kg/day) or combination therapy with albendazole (15 mg/kg per day) plus praziquantel (50 mg/kg per day) [2,37,40,45,46]. However, higher doses of albendazole (22.5 mg/kg per day) have been associated with an increased frequency of calcifications, a risk factor for recurrent seizures [24]. For prolonged albendazole therapy, antiparasitic therapy should be continued until there is radiographic resolution of cysticerci; a year or more of treatment may be required. In some cases, the radiologic changes may persist, but negative studies of CSF for parasite antigen and/or quantitative polymerase chain reaction allow discontinuation of therapy [47]. Patients treated with albendazole for >14 days warrant monitoring for hepatotoxicity and leukopenia [2]. Blood counts and liver and liver enzymes should be checked weekly during the initial month of therapy and monthly thereafter. Follow-up neuroimaging should be performed at least every six months to monitor response to therapy.

Concomitant administration of anti-inflammatory treatment such as corticosteroids is essential, as antiparasitic therapy exacerbates inflammation. A reasonable approach is to use prednisone (up to 60 mg per day) or dexamethasone (up to 12 to 24 mg per day), beginning a few days before initiation of antiparasitic therapy. For patients requiring a prolonged course of therapy (more than a couple weeks), methotrexate may be used as a steroid-sparing agent [2,48,49]. Methotrexate doses usually start at 7.5 mg weekly and can be increased, using protocols similar to those used for rheumatoid arthritis (see "Use of methotrexate in the treatment of rheumatoid arthritis"). Tumor necrosis factor inhibitors have also been used as steroids sparing agents, usually in addition to methotrexate.

There are no controlled clinical trials of treatment for subarachnoid neurocysticercosis [37,38,46]. In one case series including 30 patients, treatment with prolonged courses of albendazole (median 0.55 year) and/or praziquantel (median 0.96 year) led to sustained inactive disease in 96 percent of cases [37]. In another series including 31 patients treated with high-dose albendazole (30 mg/kg/day for 10 days) with dexamethasone (0.4 mg/kg/day for 13 days) followed by a prednisone taper a complete response to a single course of therapy was observed in 26 percent of cases [38].

Giant subarachnoid cyst — In the setting of giant subarachnoid cysticerci (>5 cm in diameter, frequently accompanied by cerebral edema and mass effect), management consists of corticosteroids; rarely, surgical decompression is required. Once mass effect is controlled, management is as described above [40].

The above approach to antiparasitic therapy is supported by a series including 33 patients with subarachnoid cysts at least 5 cm in diameter and intracranial hypertension [40]. All patients received albendazole for four weeks; 10 patients subsequently received treatment with praziquantel for four weeks. In addition, 17 patients received a second course of albendazole, 3 received a third course, and 1 received a fourth course. After a median of 59 months of follow-up, all 33 patients had improved and the cysts had disappeared or become calcified. Of the 22 patients with a history of seizures, 11 continued to receive antiseizure medications. (See 'Communicating hydrocephalus due to subarachnoid disease' above.)

Spinal lesions — Management of spinal neurocysticercosis should be individualized based on symptoms, anatomic location of cysticerci, degree of arachnoiditis, and surgical expertise [2]. There are anecdotes of good responses to medical and/or surgical therapy, but there are no good data supporting one approach over the other [50,51].

In the setting of spinal neurocysticercosis with spinal cord compression and myelopathy (paraparesis or incontinence), treatment with high-dose corticosteroids should be considered, either alone or in conjunction with antiparasitic therapy.

Ocular lesions — Management of intraocular cysticercosis consists of surgical removal [2,52,53]. In one series including 45 patients with intraocular cysticercosis, surgical removal was feasible in all cases; reattachment of the retina was accomplished in 87 percent of 22 eyes, and 67 percent recovered ambulatory vision [52].

Management of cysticercal involvement of the extraocular muscles consists of albendazole (15 mg/kg per day in two daily doses up 1200 mg per day, with food for 10 to 14 days) and corticosteroids (prednisone 1 mg/kg per day or dexamethasone 0.1 mg/kg per day) [53].

Cysticercosis outside the central nervous system — In general, management of patients with symptomatic subcutaneous or intramuscular cysticerci consists of nonsteroidal anti-inflammatory medication. Excision is reasonable for symptomatic solitary lesions. Asymptomatic patients do not require specific therapy.

Patients with extraneural cysticercosis should undergo radiographic imaging of the brain to evaluate for neurocysticercosis. (See "Cysticercosis: Clinical manifestations and diagnosis", section on 'Radiographic imaging'.)

FOLLOW-UP AND MONITORING

Repeat neuroimaging — Follow-up imaging should be performed every six months following completion of initial antiparasitic therapy, until there is resolution of the cystic lesion [2]. Patients with persistent viable or enhancing lesions on follow-up imaging warrant a repeat course of antiparasitic therapy [13,14,20].

Duration of antiseizure medication therapy — The optimal duration of antiseizure medication therapy is uncertain; many patients continue to have seizures following antiparasitic treatment [13,14,54,55]. Risk factors for recurrent seizures include residual cystic lesion or calcification on radiographic imaging, breakthrough seizures, and >2 seizures during the course of the disease [1,2,28,56,57]. Other risk factors include perilesional edema around calcified lesions.

In patients with multiple lesions, antiseizure medication therapy should be continued for at least 24 months. Tapering and discontinuation of antiseizure medication therapy is reasonable for patients with few seizures prior to antiparasitic therapy, resolution of the cystic lesion(s) on radiographic imaging studies, and no seizures for 24 consecutive months [1,2,58]. In one study, none of 21 patients with complete radiologic resolution had subsequent seizures with 24 months of follow-up [57]. (See "Overview of the management of epilepsy in adults".)

For patients with a single enhancing lesion, antiseizure medication therapy should be continued for six months or until radiographic resolution of active infection, if longer; after this period, a trial off antiseizure medication therapy is reasonable in patients with no risk factors for recurrent seizures [1,2,22].

Recurrent seizures should prompt reinitiation of chronic antiseizure medication therapy.

ASYMPTOMATIC INFECTION — The optimal approach to management of asymptomatic patients with incidental radiographic findings of cysticercosis is uncertain.

In general, management of asymptomatic patients with enhancing lesions or viable disease (extremely rare) should be individualized based on patient preference. In studies of the natural history of neurocysticercosis, most cystic lesions resolve with development of calcifications, in the absence of symptoms [59]. However, some patients may prefer antiparasitic therapy; in such cases, the approach is as discussed above. (See 'Initial management' above.)

Asymptomatic patients with nonviable disease do not appear to benefit from any further therapy [7].

CHILDREN AND PREGNANT WOMEN — Children with neurocysticercosis may be managed as described in the preceding sections; medication dosing should be weight based.

Pregnant women with elevated intracranial pressure should be managed as described in the preceding sections. Corticosteroids may be used in pregnancy if necessary. The choice of antiseizure medication therapy should take into account potential teratogenicity and pharmacokinetics in pregnancy. Antiparasitic therapy is rarely required emergently and can be deferred until after pregnancy. (See "Management of epilepsy during preconception, pregnancy, and the postpartum period".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cysticercosis".)

SUMMARY AND RECOMMENDATIONS

●General principles - Cysticercosis is caused by the larval stage of the pork tapeworm Taenia solium. Clinical syndromes related to this parasite include neurocysticercosis (NCC) and extraneural cysticercosis. NCC, in turn, is divided into parenchymal and extraparenchymal forms. Stages of cysticercosis include an initial (viable) phase, a degenerating (enhancing) phase, and a nonviable (calcified) phase (table 1). Cysticerci may be present in more than one anatomic site, and cysticerci at different stages in their natural history may be present simultaneously. (See 'General principles' above.)

●Initial management - The initial approach to patients with NCC consists of managing acute symptoms, if present, such as increased intracranial pressure (via surgical intervention and/or corticosteroids) and seizures (via antiseizure medication therapy). Thereafter, a determination should be made regarding the approach to management of antiparasitic and anti-inflammatory therapy; clinical decisions should be tailored to individual patient circumstances. (See 'Initial management' above.)

●Prior to antiparasitic therapy - Prior to initiation of antiparasitic therapy for cysticercosis, all patients should have an ophthalmologic examination to exclude ocular cysticercosis. In addition, patients who are likely to require prolonged corticosteroids should also undergo screening for latent tuberculosis infection as well as screening or empiric therapy for strongyloidiasis. (See 'Prior to antiparasitic therapy' above.)

●Antiparasitic therapy

•Patient selection - Antiparasitic therapy is warranted for patients with viable and/or degenerating cysts in the brain parenchyma on neuroimaging. Antiparasitic therapy should not be administered to patients with untreated hydrocephalus, cysticercal encephalitis, or calcified lesions only. (See 'Patient selection' above.)

•Choice of regimen - Administration of antiparasitic therapy depends on the number and characteristics of the cyst(s) on neuroimaging:

-Antiparasitic therapy is not indicated for patients with untreated hydrocephalus, cysticercal encephalitis, or calcified lesions only.

-For patients with one to two parenchymal cysts that are viable and/or degenerating, we suggest treatment with albendazole rather than no antiparasitic therapy (Grade 2A).

-For patients with more than two parenchymal cysts that are viable and/or degenerating, we suggest treatment with albendazole and praziquantel rather than monotherapy (Grade 2C).

•Duration - The duration of antiparasitic therapy is 10 to 14 days in most cases; patients with subarachnoid disease warrant an extended duration of antiparasitic therapy.

●Corticosteroid therapy - We recommend adjunctive administration of corticosteroids with antiparasitic therapy (Grade 1C). The optimal regimen is uncertain; commonly used regimens include prednisone (1 mg/kg per day) or dexamethasone (0.1 mg/kg per day) begun at least one day prior to antiparasitic therapy, continued for the duration of antiparasitic therapy, and followed by a rapid taper. (See 'Adjunctive use with antiparasitic therapy' above.)

●Follow-up and monitoring

•Follow-up neuroimaging should be performed every six months following completion of antiparasitic therapy until radiographic resolution. For patients with persistent lesions on follow-up imaging, we suggest a repeat course of antiparasitic therapy (Grade 2C). (See 'Repeat neuroimaging' above.)

•The optimal duration of antiseizure medication therapy is uncertain; many patients continue to have seizures following antiparasitic treatment. For patients with viable and/or multiple lesions, antiseizure medication therapy should be continued for at least 24 months. For patients with a single enhancing lesion, antiseizure medication therapy should be continued for six months or until radiographic resolution of active infection, if longer. (See 'Duration of antiseizure medication therapy' above.)

●Extraparenchymal disease

•Ventricular cysticercosis - Management of ventricular cysticercosis consists of surgical removal if feasible. Frequently, cysts in the third and lateral ventricles may be removed via a minimally invasive approach; cysts in the fourth ventricle may be removed via minimally invasive surgery or open microdissection. (See 'Obstructive hydrocephalus due to intraventricular cyst' above.)

•Subarachnoid cysticercosis - Management of subarachnoid cysticercosis consists of more intensive antiparasitic and anti-inflammatory regimens than those used for parenchymal disease. Antiparasitic therapy should be continued until there is radiographic resolution of the cystic lesions, which often requires months of therapy. Anti-inflammatory therapy should be continued for the duration of antiparasitic therapy. (See 'Communicating hydrocephalus due to subarachnoid disease' above.)

•Spinal cysticercosis - Management of spinal neurocysticercosis should be individualized based on symptoms, anatomic location of cysticerci, degree of arachnoiditis, and surgical expertise. Management of intraocular cysticercosis consists of surgical removal. Management of patients with symptomatic subcutaneous or intramuscular cysticerci consists of nonsteroidal anti-inflammatory medication. Excision is reasonable for symptomatic solitary lesions. (See 'Spinal lesions' above.)