REVIEW

C URRENT
OPINION Neurocysticercosis: an update on diagnosis,
treatment, and prevention
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Roberto Pineda-Reyes and A. Clinton White Jr

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Neurocysticercosis (NCC) is an important cause of neurological disease worldwide, including imported

cases in nonendemic countries.
Purpose of review
The purpose of this review is to update information on diagnosis, management, and prevention of
neurocysticercosis
Recent findings
WHO and Infectious Diseases Society of America/American Society of Tropical Medicine and Hygiene
guidelines emphasize the importance of corticosteroids and antiparasitic drugs for viable parenchymal
disease and single enhancing lesions. Subarachnoid NCC is associated with a high fatality rate unless
optimally treated. Advances in subarachnoid NCC include use of prolonged antiparasitic and anti-
inflammatory courses and the increasing use of antigen-detection and quantitative PCR assays in diagnosis
and follow-up. Emerging data support the safety and efficacy of minimally invasive surgery in ventricular
cases. Calcified neurocysticercosis continues to be associated with a high burden of disease. Field studies
are demonstrating the feasibility of eradication using a combination of mass chemotherapy for human
tapeworms and vaccination/treatment of porcine cysticercosis.
Summary
NCC remains an important and challenging cause of neurological disease with significant morbidity
despite advances in treatment and prevention.
Keywords
albendazole, neurocysticercosis, neurosurgery, seizures, Taenia solium

INTRODUCTION [1,4]. Parenchymal NCC is the most common form

Neurocysticercosis (NCC) is the central nervous sys-
tem infection by the metacestode larval stage of the
&
pork tapeworm Taenia solium [1,2 ]. NCC represents a
public health challenge for many low- and middle-
income countries, and for immigrant populations in
the United States. Endemic areas include Central and
South America, sub-Saharan Africa and parts of Asia.
In higher-income nonendemic locations, most cases
are immigrants, but occasionally patients with travel-
associated or locally acquired NCC may seek medical
attention. A study from Kuwait, where pig farming is
prohibited and pork is not consumed, demonstrates
the presence of autochthonous cases via interaction
with infected foreign nationals from endemic coun-
tries living in the same households [3].
CLINICAL PRESENTATION
NCC is classified as parenchymal or extraparenchy-
mal with different presentations within each (Fig. 1)
and represents over 60% cases. It includes patients
with single enhancing lesions, multiple viable cys-
ticerci, and calcified lesions. Extraparenchymal
NCC comprises ventricular, subarachnoid, spinal,
and ocular NCC.
Parenchymal neurocysticercosis
Seizures are the most common presentation of paren-
chymal NCC and are often focal or secondarily gen-
eralized-focal seizures. Some studies have suggested
Division of Infectious Diseases, Department of Internal Medicine, Uni-
versity of Texas Medical Branch, Galveston, Texas, USA
Correspondence to A. Clinton White Jr, MD, Infectious Disease Division,
Department of Internal Medicine, University of Texas Medical Branch,
301 University Blvd, Galveston, TX 77555-0435, USA.
E-mail: acwhite@utmb.edu
Curr Opin Infect Dis 2022, 35:246–254
DOI:10.1097/QCO.0000000000000831

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 Neurocysticercosis: an update on diagnosis, treatment, and prevention Pineda-Reyes and White
KEY POINTS
 An emerging consensus on diagnosis and management
of neurocysticercosis (NCC) is reflected in recent WHO
and Infectious Diseases Society of America/American
Society of Tropical Medicine and Hygiene guidelines
 Parenchymal cystic and enhancing NCC should be
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treated with symptomatic therapy (antiseizure
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medications), corticosteroids, and antiparasitic drugs
 Subarachnoid NCC carries a high risk for fatality, but
this may be lessened by symptomatic treatment of
hydrocephalus along with chronic anti-inflammatory
and antiparasitic therapy guided by antigen or
qPCR assays
 Ventricular NCC can often be treated with minimally
invasive removal of the cysticerci, which is more
successful if patients are not first treated with
cerebrospinal fluid diversion or antiparasitic drugs
 Calcified neurocysticercosis is associated with chronic
epilepsy, which may be refractory when accompanied
with hippocampal atrophy.
an association between frontal lobe location of cysts
and focal seizures, and secondary generalization with
temporal lobe involvement [5].
A single enhancing lesion is the most common
presentation in India and the United States, whereas
multiple viable cysticerci are more frequently
described in hospitalized patients in Latin America.
Single enhancing lesions typically present with one
or a few seizures or with headaches. The seizures are
often controlled with a single antiseizure medica-
tion (ASM). Viable parenchymal cysticerci often
present after multiple seizures.
Calcified parenchymal NCC is the most com-
mon form of disease among individuals living in
endemic villages [6,7]. Chronic epilepsy or head-
aches are the main clinical manifestation of calcified
NCC. Seizures are more frequent in those with per-
ilesional edema [8,9]. In a prospective study of epi-
lepsy in a village in Ecuador, there was a >1%
incidence of epilepsy and 35% of cases were asso-
ciated with calcified NCC [7]. Chronic epilepsy is
associated with calcified NCC and control is poorer
when accompanied by hippocampal atrophy on
magnetic resonance imaging (MRI) [10].
Extraparenchymal neurocysticercosis
Ventricular NCC occurs when cysts within the ven-
tricular cavities cause obstructive hydrocephalus.
Affected individuals typically present with chronic
headaches. Headaches may be intermittent or
0951-7375 Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.
chronic and can be accompanied by nausea, vomit-
ing, decreased visual acuity, and papilledema, some-
times exacerbated by head movements. Some
present with sudden onset altered mentation
(Bruns’ syndrome). In some, onset is gradual
or intermittent.
Subarachnoid NCC is considered the most
severe form of disease and carries the highest mortal-
&&
ity rates [11,12 ]. Enlarging cysts can cause mass
effect and focal deficits. Communicating hydroce-
phalus may develop from chronic arachnoiditis and
obstructive hydrocephalus from concomitant ven-
tricular disease or outflow tract obstruction by
inflammation. Chronic arachnoiditis may present
as cerebrovascular events or chronic meningitis.
Spinal cord involvement occurs in nearly 1%
cases, and it is usually accompanied by radiculop-
athy and paresthesia. Orbital NCC mainly involves
the orbital muscles [13]. Uncommonly, intraocular,
vitreous, anterior chamber, and retinal involvement
may occur. Clinical presentations vary, and include
diplopia, decreased visual acuity, eye pain, chorior-
etinitis, and retinal detachment.
DIAGNOSIS
The symptoms of neurocysticercosis are nonspe-
cific, as are routine laboratory tests.
Expert-developed diagnostic criteria by Del
Brutto et al. [15] were revised and updated in 2017
[14]. The revised criteria have been validated for
ventricular lesions. The revised criteria emphasize
the importance of neuroimaging for establishing a
definitive diagnosis. Patients with suspected NCC
should be ideally evaluated with both computed
&
tomography (CT) and MRI of the brain [1,2 ]. Cys-
ticerci appear as round, fluid filled cysts (Fig. 1). In
the brain parenchyma, cysticerci are typically 1–
2 cm in diameter, but can be larger, especially if
located in the Sylvian Fissure or subarachnoid space.
In viable cysticerci, the center of the parasite is
liquid (dark on CT or T1 MRI, bright on T2 MRI).
Visualization of a scolex, which appears as a nodule
or elongated lesion of 1–2 mm in diameter, attached
to the wall of the cysticerci, is considered patho-
gnomonic. The host response to the cysticerci may
include pericystic edema, contrast enhancement,
and, eventually, collapse of the cystic component.
Many cases go on to form calcified granulomas.
These are solid calcifications, typically 1–5 mm in
diameter. Cysticerci in the ventricles may only dem-
onstrate evidence of hydrocephalus on CT. On MRI,
ventricular cysticerci may appear as thin-walled
structures with or without a visible scolex. The
appearance of cysticerci in subarachnoid NCC is
variable. CT may only demonstrate distortion of
www.co-infectiousdiseases.com 247
 CNS infections
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FIGURE 1. Stages of human neurocysticercosis. Parenchymal viable cysts (upper left, FLAIR MRI sequence and center,
postcontrast T1 MRI sequence); single enhancing lesion (upper right, postcontrast T1 MRI sequence); extensive basal
subarachnoid neurocysticercosis in the anterior fossa (bottom left, FLAIR MRI sequence); viable cyst in the IV ventricle (bottom
center, FLAIR MRI sequence), and intraparenchymal brain calcifications (noncontrasted computed tomography scan). Lesions
are marked with arrowheads. FLAIR, fluid-attenuated inversion recovery. Originally published in White AC Jr, Garcia HH.
Updates on the management of neurocysticercosis. Curr Opin Infect Dis. 2018 Oct;31(5):377--382.

the shape of the subarachnoid space. In addition to
typical appearing cysticerci, subarachnoid NCC may
appear as large cystic structures (giant cysticerci),
grape-like clusters of small cystic lesions (so called
racemose cysticercosis), or diffuse meningeal
enhancement without discrete lesions.
Compared to MRI, CT scans are fast, cheaper and
more accessible. They are better at detecting calci-
&
fied lesions [2 ,16]. MRI is the test of choice to detect
&
extraparenchymal NCC [2 ,4]. MRI is more sensitive
for small lesions, degenerative changes, and identi-
fication of scolices even within calcified lesions
[6,17]. Advanced MRI techniques such as fast imag-
ing employing steady-state acquisition (FIESTA) and
three-dimensional constructive interference in
steady state (3D CISS) improve sensitivity for sub-
arachnoid and intraventricular parasites [18,19].
Clinicians should also consider evidence of Tae-
nia solium infection. Epidemiologic evidence to sup-
port the diagnosis could include exposure to a
tapeworm carrier or prolonged residence in an
endemic region.
Antibody detection assays are often used to
confirm T. solium infection. The preferred antibody
test is the enzyme-linked immunoelectrotransfer
blot (EITB) [1]. EITB specificity approaches 100%
for T. solium infection. This allows use of serum
samples instead of cerebrospinal fluid (CSF), which
have higher antibody titers. The sensitivity is excel-
lent in those with more than one viable cysticerci.
However, false negative tests are frequent with sin-
gle cysticerci or calcified lesions. Unfortunately,
there have been problems with the availability of
EITB. Enzyme-linked immunosorbent assays (ELISA)

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 Neurocysticercosis: an update on diagnosis, treatment, and prevention Pineda-Reyes and White
for antibodies to T. solium are widely available but
not recommended due to unreliable sensitivity and
specificity [20,21]. Assays with recombinant anti-
gens are in development.
Monoclonal antibody-based antigen detection
assays are being increasingly used for diagnosis.
These assays are commercially available in Europe,
but not in the United States. The assays are more
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sensitive using CSF than with serum and better at
detecting subarachnoid and ventricular NCC than
parenchymal disease. The positive predictive value
of antigen detection is high, but false negatives are
common with parenchymal disease. Antigen-ELISA
urine assays may provide a promising tool for
screening of heavy cysticerci burden in populations
at risk [22].
Molecular methods are increasingly used in
NCC diagnosis. A quantitative real-time polymerase
chain reaction (qPCR) assay by O’Connell et al.
showed 100% clinical sensitivity in CSF and 81%
sensitivity in plasma for subarachnoid and ventric-
&&
ular NCC [23 ]. Studies in subjects with parenchy-
mal NCC are not available. Metagenomic next-
generation sequencing has been reported as a useful
additional diagnostic tool in some difficult cases
[24,25].
TREATMENT APPROACH
NCC exhibits a varied spectrum of disease, and the
therapeutic management must be tailored to the
specific clinical presentation. The initial treatment
of neurocysticercosis should focus on symptomatic
therapy addressing seizures and elevated intracra-
nial pressure.
Seizures
All patients presenting with seizures should be
treated with ASM. Even if it is a single seizure epi-
sode, cysticerci constitute epileptogenic foci and
ASM should be started. Monotherapy with pheny-
toin, carbamazepine, and newer ASM with more
favorable adverse effect profiles such as levetirace-
tam, are commonly used. An open-label random-
ized trial by Santhosh et al. showed relatively better
seizure control with carbamazepine in comparison
with levetiracetam [26,27]. However, more side
effects were noted in the carbamazepine arm. Pro-
spective studies suggest that low risk patients with
single enhancing cysticerci may safely stop ASM
after 6 months. Risk factors for recurrent seizures
include breakthrough seizures, residual lesions,
and development of calcifications [1,27–29]. Opti-
mal duration of ASM in cases with multiple paren-
chymal cysticerci is less clear. However, experts
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generally recommend at least 2 years of ASM after
the last seizure. Calcified lesions are a risk factor
for recurrent seizures, particularly when associated
with perilesional edema or hippocampal atrophy
[9,10,30].
Hydrocephalus
In ventricular NCC, hydrocephalus is due to
mechanical obstruction of one of the ventricular
outflow tracks by cysticerci. This typically occurs
at the foramina of Monro, Luschka, or Magendie or
at the aqueduct of Sylvius. Definitive treatment
requires removal of the obstructing cysticerci,
ideally by minimally invasive surgery. Konar et al.
&&
[31 ] from the National Institute of Mental Health
and Neurosciences, Bengaluru, India, reported 61
cases of ventricular NCC managed by neuroendo-
scopy. Forty-three of 61 were successfully retrieved.
Preoperative placement of a ventriculoperitoneal
shunt, turbid CSF, and bleeding were associated
with failed retrieval. Only 2 required subsequent
shunt surgery. Preoperative antiparasitic drugs
should be avoided since they may make endoscopic
removal more difficult. Aggarwal and colleagues
reported 26 cases from India showed 100% success
rate with endoscopic cyst removal from third and
lateral ventricles and 62% in fourth ventricular cysts
&
[32 ]. Other centers noted success with an open
surgical approach, particularly in removal via sub-
occipital craniotomy for fourth ventricular NCC
[33]. Stereotactic removal in fourth ventricular cysts
has also been described [34].
In subarachnoid NCC, hydrocephalus is often
due to inflammation causing CSF outflow obstruc-
tion (communicating hydrocephalus). However, it
may also be due to obstructive hydrocephalus from
concomitant ventricular NCC. Although anti-
inflammatory medications may lead to resolution
in some patients, most cases require neurosurgical
interventions such as placement of a ventriculoper-
itoneal shunt or removal of ventricular cysts.
Antiparasitic drugs
Antiparasitic drugs play an important role in the
management of some forms of NCC. However, there
are important caveats to their safe use. First, anti-
parasitic therapy is never an emergency and should
only be done under the cover of corticosteroid anti-
inflammatory drugs. Second, antiparasitic drugs,
when they kill the parasites, induce an inflamma-
tory response that can worsen symptoms in the
short term. Thus, they should never be given in
the context of uncontrolled increased intracranial
pressure. Third, antiparasitic drugs do not abate
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 CNS infections
symptoms quickly. Thus, they should not take the
place of effective symptomatic therapy with ASM
and treatment of hydrocephalus. Fourth, antipara-
sitic drugs have no role when there are no viable
parasites (e.g., calcified NCC). Fifth, prior to anti-
parasitic treatment, all patients should undergo a
detailed fundoscopic examination, since it can lead
to ocular inflammation and decreased visual acuity.
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Finally, the optimal antiparasitic regimen varies
considerably by the form of neurocysticercosis. In
parenchymal disease, the goal is to prevent further
seizure activity with ASM and to eradicate the viable
cysticerci while reducing the inflammatory
response, minimizing the chances of seizure recur-
rence, morbidity and disability. Prior to initiation of
treatment, patients should be screened for latent
tuberculosis and strongyloidiasis, given the poten-
tial need for a prolonged course of corticosteroids
[1].
Single enhancing lesions
A single enhancing lesion is the most common form
of NCC in the United States and India. Guidelines
recommend treatment with 1–2 weeks of albenda-
zole 15 mg/kg/day in twice daily doses along with
&
adjunctive corticosteroids [1,2 ]. A recent systematic
review supports the use of adjunctive corticosteroids
with ASM, showing a significant benefit in seizure
reduction and resolution of cystic lesions [28]. The
role of antiparasitic drugs is less clear. However,
antiparasitic treatment is associated with more rapid
resolution of the cystic lesions and fewer recurrent
seizures in the medium term [28,35].
Suthar et al. [29] conducted a prospective study
of children with single enhancing CT lesions for
development of calcified lesions. Overall, 32.5%
of lesions calcified, with increased risk for larger
lesions, increased density of the scolex at baseline,
and baseline diffusion restriction.
Viable parenchymal neurocysticercosis
Antiparasitic drugs are generally recommended for
patients with viable parenchymal neurocysticerco-
&
sis [1,2 ]. This recommendation is based on obser-
vations from two carefully designed placebo-
controlled trials demonstrating more rapid radio-
logic resolution and fewer recurrent generalized
seizures in patients treated with antiparasitic drugs
[36,37]. A recent Cochrane review raised questions
about the safety and efficacy of antiparasitic drugs in
parenchymal NCC. However, this conclusion was
largely driven by a poorly designed trial conducted
from India with major methodological problems
[38]. Unfortunately, about 38% of parenchymal
250 www.co-infectiousdiseases.com
lesions turn into calcifications after antiparasitic
treatment, which is associated with seizure recur-
rence [6,9]. Bustos et al. [6,29] compared the rate of
calcifications among patients from four random-
ized controlled trials. Risk factors associated with
calcifications include chronic seizures, cysts with
edema at baseline, larger cyst size, use of higher
doses of albendazole, lower doses of corticosteroids,
and failure to retreat patients with persistent
lesions.
For patients with 1–2 viable cysticerci, experts
recommend also albendazole treatment at a dose of
&
15 mg/kg/day in divided doses for 8–14 days [1,2 ].
For patients with more than two viable cystic
lesions, two clinical trials by Garcia et al. demon-
strated a significant benefit of adding praziquantel
(50 mg/kg/day in three doses) to albendazole in
terms of higher rates of cysticerci eradication with-
out increased side effects [39]. When antiparasitic
drugs kill the cysticerci, they induce an inflamma-
tory response that can worsen symptoms. Cortico-
steroids are generally used along with the
antiparasitic drugs (see below).
Patients with heavy parasite burdens
Controlled trials of antiparasitic drugs for paren-
chymal NCC excluded patients with more than 20
cysticerci. Del Brutto and Garcia [40] noted that
patients with such heavy parasite burdens fall into
four different groups. Some have a marked inflam-
matory reaction to the parasites and diffuse cerebral
edema (so called cysticercal encephalitis). They
usually present with headaches and altered mental
status. Treatment focuses on relieving the elevated
pressures with corticosteroids and, in some cases,
osmotic diuretics or even surgical decompression.
Antiparasitic drugs are contraindicated acutely and
often not necessary. Some have a CT appearance
described as ‘starry sky’. In these cases, the scolices
may appear as hyperdense and the cystic compo-
nent may not be obvious. Treatment of these cases
should also focus on anti-inflammatory drugs.
Another group of patients are described as having
‘heavy nonencephalitic neurocysticercosis’ or ‘dis-
seminated cysticercosis’. These cases have numer-
ous cystic lesions, but not the diffuse cerebral
edema seen with cysticercal encephalitis. The clin-
ical presentation is similar to parenchymal NCC
with fewer organisms. While there are limited data,
several reports suggest that these patients may
benefit from corticosteroids and treatment with
albendazole alone [41,42]. A fourth group of
patients with massive infection have just calcified
lesions and should be managed as other patients
with calcifications.
Volume 35  Number 3  June 2022
 Neurocysticercosis: an update on diagnosis, treatment, and prevention Pineda-Reyes and White
Calcified neurocysticercosis
Patients with calcified parenchymal cysticerci can
often be treated with symptomatic therapy, typi-
cally with ASM. Seizure control can often be
achieved with a single agent or, in the minority of
cases, multiple drugs. However, a subgroup of
patients may develop refractory epilepsy.
Many of the symptomatic patients with calcified
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neurocysticercosis have perilesional edema or
enhancement on MRI [9]. This group of patients
is more likely to suffer from recurrent seizures and
chronic epilepsy. Some cases have been treated with
corticosteroids, methotrexate, and/or anti-TNF ther-
apy. In the short run, this has been associated with
improvement in symptoms. Steroid withdrawal has
been associated with precipitation of symptoms,
and chronic steroid therapy poses risk for serious
adverse events including osteopenia, fractures, and
superinfections [43]. Thus, at present there is not
enough evidence of benefit to justify the risks of
anti-inflammatory therapy in general.
Increasing evidence is pointing to calcified neu-
rocysticercosis as a cause of hippocampal atrophy/
sclerosis and associated refractory epilepsy
[30,44,45]. There are increasing numbers of calcified
NCC cases with refractory epilepsy that have
improved or resolved with surgical removal of the
epileptiform focus [46].
Extraparenchymal neurocysticercosis
For ventricular NCC, surgical removal is the treat-
ment of choice for hydrocephalus (see above). If the
cyst is completely removed and there is no addi-
tional site of infection, there is no need for antipar-
asitic therapy [33]. Sometimes, the ventricular cysts
cannot be removed surgically, due to adherence to
the ventricular wall or bleeding. CSF diversion with
ventriculoperitoneal shunting is recommended in
these cases. There is frequent shunt failure. Retro-
spective data suggests lower rates of shunt failure if
patients are treated with corticosteroids and anti-
parasitic drugs [1].
Subarachnoid NCC represents the most lethal
form of NCC. In a study of 840 NCC patients seen at
the National Institute of Neurological Sciences in
Peru, Abanto et al. [11] identified 42 deaths. Most
deaths were among the minority with subarachnoid
NCC (32/193, 16.6% of subarachnoid cases). All-
cause mortality rate was 15-fold higher than in
parenchymal NCC. By contrast, recent series of
subarachnoid NCC cases from the United States
&&
did not include any fatalities [12 ,47]. The low
mortality is thought to have resulted from intensive
therapy including shunting for hydrocephalus, anti-
parasitic drugs, and anti-inflammatory treatment.
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Subjects with basilar subarachnoid NCC should
have an MRI of the spine performed to rule out
concomitant spinal involvement, given the high fre-
quency of asymptomatic cases [1,48]. There are no
well controlled trials of antiparasitic drugs in subar-
achnoid NCC. However, there is a strong expert con-
sensus that they should be used in all patients [1].
Patients respond poorly to regimens used for paren-
chymal NCC. Proposed alternative regimens include
prolonged courses of albendazole, cycles of standard
dose or higher dose albendazole (30 mg/kg/day), and
combination of albendazole and praziquantel with
&&
no data comparing regimens [12 ,49,50]. The asso-
ciation of higher dose albendazole with increased rate
of calcification in parenchymal disease suggests that
it is not the preferred option [6].
The optimal duration of therapy for subarach-
noid NCC is unclear. Some experts have proposed
treating until there is resolution on neuroimaging.
However, some lesions may persist on neuroimag-
ing even when there are no longer viable parasites.
The NIH series followed CSF antigen levels. Of those
in whom antigen tests normalized, there did not
&&
seem to be any relapses [12 ]. The use of qPCR in
CSF may play a role in the follow-up and monitoring
&&
response to therapy [23 ]. CSF qPCR seems to nor-
malize more rapidly than antigen assays and may be
more accurate at predicting residual viable parasites.
Anti-inflammatory therapy
Most of the symptoms in NCC are due to the host
inflammatory response. Thus, anti-inflammatory
treatment is critically important in management
of NCC. For single enhancing lesions or viable
parenchymal NCC, typical steroid doses are predni-
sone 1 mg/kg/day and dexamethasone 0.1 mg/kg/
day in divided doses during antiparasitic therapy.
A trial of higher doses of dexamethasone (8 mg/day
for 4 weeks followed by a taper) was associated with a
trend towards fewer recurrent seizures. Recent data
suggests that the higher doses may also lead to fewer
calcifications [6]. In the case of subarachnoid NCC,
treatment courses are typically longer, requiring
more prolonged anti-inflammatory therapy. Metho-
trexate (typical doses of 7.5–20 mg/week) and tumor
necrosis factor (TNF) inhibitors have been used as
&&
steroid-sparing agents [12 ,51,52].
CONTROL AND PREVENTION
T. solium has been recognized as an eradicable
pathogen, with several potential targets in the trans-
&&
mission for strategy implementation [53 ]. Tradi-
tional efforts for disease prevention included
improved sanitation and pig farming practices,
health education, and inspection of pork. However,
www.co-infectiousdiseases.com 251
 CNS infections
these measures were largely unsuccessful in highly
endemic villages [4] Mass chemotherapy for human
taeniasis has been implemented in Ecuador, Guate-
mala, Mexico, Peru, Tanzania, and Madagascar with
praziquantel or niclosamide, although there was
&&
significant heterogeneity among studies [53 ,54–
56]. For example, a recent study in Madagascar
studied praziquantel for mass chemotherapy of tae-
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niasis. No serious adverse events were noted. Para-
site prevalence was temporarily decreased but had
returned to pretreatment levels by one year [57].
Integrated interventions targeting humans, pigs,
and health education are more likely to achieve
better results in transmission interruption and elim-
&&
ination of T. solium [53 ,58]. Garcia et al. [59] in
Peru compared different control strategies and con-
cluded that a combination of mass chemotherapy
with niclosamide to eliminate tapeworm carriers
combined with oxfendazole treatment and immu-
nization for cysticercosis of pigs was required for
effective eradication. Gabriël et al. [60] were able to
eliminate porcine cysticercosis in Zambia using a
combined strategy of mass human chemotherapy
(mainly praziquantel) and immunization/oxfenda-
zole treatment of pigs. A similar program was
administered in a village in Laos [61]. A pilot study
demonstrated marked reduction in porcine cysticer-
cosis by only immunization and treatment of pigs
with oxfendazole [62]. Based on these data, math-
ematical models suggest that T. solium might be
eradicated using the combined approach of human
chemotherapy for tapeworms along with antipara-
sitic treatment and vaccination for porcine cysticer-
&&
cosis [53 ,58].
PAHO/WHO recently issued guidelines on anti-
parasitic drugs for taeniasis in control programs [56].
Niclosamide 2 g as a single dose (adjusted for chil-
dren) was used in a large-scale deworming study in
Peru with few adverse events [59]. Low dose prazi-
quantel (5–10 mg/kg in a single dose) is also recom-
mended. However, neurological inflammation in
individuals with occult NCC is a concern. Measures
to avoid this might include either screening for T.
solium antibody or antigen and avoiding treatment
in those with neurological symptoms. The PAHO/
WHO guidelines strongly recommend having an
established plan for surveillance and management
of neurological adverse events. Albendazole is listed
as an alternative only if niclosamide or praziquantel
are unavailable. The dose of albendazole recom-
mended is close to the doses used to treat neuro-
cysticercosis. Administration without steroids poses
risks of severe neurological side effects. Thus, mass use
should include systems for managing and reporting
neurological adverse effects [56]. Newer evidence
from a clustered randomized trial comparing a ring
252 www.co-infectiousdiseases.com
treatment strategy versus mass drug administration
showed no difference in the reduction of transmis-
sion; however, geographically-targeted approaches
are logistically cumbersome [63].
CONCLUSION
NCC remains a major cause of neurological disease
worldwide, including many cases in immigrants to
nonendemic countries. The WHO and IDSA/ASTMH
guidelines emphasize the importance of corticoste-
roids and antiparasitic drugs for viable parenchymal
disease and single enhancing lesions. Retreatment of
those with persistent lesions and higher doses of
corticosteroids seem to decrease development of cal-
cifications. Subarachnoid NCC is associated with a
high fatality rate unless optimally treated. Advances
in subarachnoid NCC include use of prolonged anti-
parasitic and anti-inflammatory courses and the
increasing use of antigen-detection and qPCR assays
in diagnosis and follow-up. More data support the
safety and efficacy of minimally invasive surgery in
ventricular cases and emphasize improved outcomes
in those not previously treated with CSF diversion.
Calcified NCC continues to be associated with a high
burden of disease, with some cases requiring epilepsy
surgery. Finally, studies are demonstrating the feasi-
bility of eradication using a combination of mass
chemotherapy for human tapeworms and vaccina-
tion/treatment of porcine cysticercosis.
Acknowledgements
We thank Dr Hector Hugo Garcia for the images included
in the figure.
Financial support and sponsorship
No specific funding was obtained or used for this work.
Conflicts of interest
There are no conflicts of interests.
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