Neurocysticercosis:

Current Knowledge and Advances

Wayne X. Shandera, MD, and Joseph S. Kass, MD

Corresponding author
Wayne X. Shandera, MD
Department of Medicine, Section of General Medicine,
2RM-81-001, 1504 Taub Loop, Houston, TX 77030, USA.
E-mail: shandera@bcm.tmc.edu
Current Neurology and Neuroscience Reports 2006, 6:453 459
Current Science Inc. ISSN 1528-4042
Copyright 2006 by Current Science Inc.

as host immunity. Therefore, a thorough understanding of

this common helminthic infection of the central nervous
system is critical in providing patients a proper standard
of care. In this article we review the epidemiology, basic
science, clinical manifestations, diagnosis, treatment, and
prevention of NCC.

History and Epidemiology

Neurocysticercosis is the most common cause of
acquired seizures worldwide. Most cases of this larval
stage infection of the pork tapeworm Taenia solium
occur in the developing world, although increasing
numbers of cases are being recognized in the United
States, particularly among Hispanic immigrants. The
ability of the pathogen to persist for years within the
host is the subject of immunologic and biochemical investigation. The major presenting symptom is
seizures, although symptoms of obstructive hydrocephalus occur if cysts are located near the ventricles
or in the subarachnoid spaces. Diagnosis is dependent
on clinical, radiologic, and serologic data. Therapy
with antiparasitic agents, especially albendazole, is
effective in large burden disease or disease within
sensitive neuraxis sites (the ventricles, the subarachnoid
spaces). When patients with radiologically enhancing
disease are given cysticidal therapy, there appears
to be a reduction in seizure recurrences. Surgery is
indicated for disease in selected anatomic sites. Longterm prevention requires attention to pork husbandry
and general sanitation, including the potential use of
mass human chemotherapy and porcine vaccination.

Introduction
Many immigrants residing in the United States come from
countries where the pork tapeworm Taenia solium is
endemic. Hence, physicians in the United States increasingly encounter patients with complications of the larval
stage of T. solium infection, known as neurocysticercosis
(NCC). NCC is the leading cause of seizures in endemic
areas, but other complications may attend infection such
as hydrocephalus and cerebrovascular disease. Treatment
depends on the cyst characteristics and location, as well

Tapeworms were recognized in the time of Hippocrates but

it was German and Dutch investigators who elucidated their
life cycle in the eighteenth and nineteenth centuries. Johann
Goeze (1782) distinguished T. solium from T. saginata
(the beef tapeworm), and Rudolf Leuckart (1856) claried
the role of transmitting the larval stage of infection from
pig into man [1]. Leuckart worked with Rudolf Virchow
to establish meat inspection laws in Germany in the
nineteenth century. Attention in the early twentieth century
was directed to the disease with the return from India of
British soldiers with a high rate of seizures, often years
after returning [2]. Only with the subsequent advent of
neuroimaging and therapeutics, including anticonvulsants
and cysticidal agents, did advances occur that increased
recognition and improved therapy for NCC.
The current epidemiology of NCC is studied by
assessing either T. solium infections in man (taeniasis) or cysticercal (larval) disease in either pigs or man
(cysticercosis). Serologic data are available from many
parts of the world. Radiologic studies are imperfect
for epidemiology because suspicious lesions may
not always indicate NCC. The best data are clinical
epidemiologic studies that are available from a few
geographic areas, with the strongest being those from
Mexico, Peru, and the United States [38]. The US
studies confirm a high prevalence of the disorder
among Hispanic immigrants, document the occasional
autochthonously transmitted case, and attest to a
slightly higher risk of tapeworm carriage among
contacts of US cases. Here we discuss the life cycle
of T. solium and the evolving global epidemiology of
taeniasis and neurocysticercosis.
The life cycle of T. solium is often misunderstood.
Adult tapeworms are the source of Taenia eggs, which are
excreted at a rate of 300,000 per day over a helminths

454

Infection

1-year life span in the feces of infected humans. Humans

are the major nal host of Taenia. The intermediate hosts
(either pigs or humans with poor fecal-oral hygiene)
ingest the eggs, which mature in the gastrointestinal tract
into globular larval forms, known as oncospheres. These
larval forms invade the body through absorption in the
gastrointestinal tract and develop into cysticerci in either
muscular or central nervous system tissue. The ingestion
of pork containing cysticerci results in human taeniasis
and completes the life cycle [1,9].
Human taeniasis, documented by coproscopy for
either eggs or antigens or both, occurs variably in the
developing world but infrequently in the developed world.
A prevalence rate of 8.6% is reported in rural Peru [10],
although most Latin American studies report rates under
3%. Two large Mexican studies, with over 1000 individuals analyzed in each, yielded prevalence rates of 0.2%
and 0.3%, and the Mexican Ministry of Health reported
an incidence of 3.8 cases per 100,000 people between
1994 and 2000. Higher rates occur among children and
middle-aged adults [10,11]. Another Mexican study
reported 500 new cases annually, with an incidence of 0.6
cases per 100,000 people, presumably underestimating
the rates among rural populations. In the United States at
least 1000 cases are estimated to occur annually, for an
incidence of 0.34 cases per 100,000 people [4,7].
Serologic estimates of NCC prevalence are also highly
variable. Enzyme immunoelectrotransfer blot (EITB)
assays are most often used. Seropositivity may merely
indicate past exposure to Taenia. Seroreversion after
acute infection occurs in up to 40% by 1 to 3 years after
initial detection. The highest reported seroprevalence
rates are from Latin America: Honduras (34%), Peru
(24%), Bolivia (22.6%), and Guatemala (20%). Mexican
seroprevalence rates average 10%. Risk factors for
seropositivity in Peru include origin from highland and
coastal villages, childhood outside Lima, pig husbandry,
age greater than 20 years, and a history of taeniasis. In
Central America, risk factors include a lack of potable
water, earthen oors, lack of sanitary toilets, and possibly
female gender [12].
The absence of pork husbandry in Muslim countries
accounts for the low prevalence throughout much of Asia,
where in some areas the beef tapeworm T. saginata is more
common [13]. NCC does occur, however, where eggs are
excreted, and thus transmission may be independent of pork
consumption. This phenomenon explains the occurrence of
NCC among a group of Orthodox Jews exposed to a housekeeper from Latin America [14] and among 16 Muslims
exposed to a non-Muslim cook in Kuwait [15].

Basic Science
Neurocysticercosis is a human pathogen primarily because
of the ability of the larval forms of T. solium to evade the
host immune response for long intervals, often decades.

To better understand this interplay between pathogen and

host immune response, we review the nature of the host
responses to NCC infection, the elaboration of parasitic
proteins that facilitate infection, and the host risk factors
for infection, including human leukocyte antigen status [9].
The humoral immune response of man to Taenia
antigens is the basis for most diagnostic assays. Humoral
responses are variable and diverse but this immunity does
not prevent development of cysticercal lesions [1618].
In addition, when measures of immunity were studied in
NCC patients, no abnormalities were detected in either
humoral or cellular immunity. The intensity of humoral
responses, however, does correlate with the degree of
infection in both human and animal models. The diversity
of responses is reected in the recognition and use of over
30 antigens in EITB assays [19].
The cellular-mediated immune response to Taenia
antigens is divergent and important when cysticerci degenerate and die. The destruction of the cysticercal parasites
initially requires eosinophils and the eosinophilic mediators eotaxin and IL-5 along with a concomitant Th2
immune response elaborated via interferon (IFN)-, interleukin (IL)-4, and IL-10. Subsequently, granulomas form
and brosis develops due to a Th1 immune response via
elaboration of IL-2 and tumor necrosis factor- (TNF) [19,20]. Typically, cysticerci live for years before the
parasite dies. The conditions that allow the parasite to
perpetuate in the host are a continued subject of study
[21,22].
Particular parasitic proteins that facilitate adaptation
to the host include metacestode factor, a 3500-Dalton
RNA-like molecule that decreases the production of IL-2,
IL-4, and INF- [23]. Taenia also elaborates several immunomodulatory proteases, with cystine proteases decreasing
the expression of CD4 lymphocytes [24].
Human host factors predispose to infection. Most
analyses of such predisposition involve human immunogenetic loci, although results differ by geographic area.
Mexican studies report an increased frequency of human
leukocyte antigen (HLA)-A28 (and decreased frequency
of HLA-DQW2) among patients with parenchymal
disease. Indian studies from Delhi report an increased
frequency of HLA-B63, HLV-B58, and HLA-DR B1*13
(and decreased frequency of HLA-A11 and HLA-DR
B1*09) among patients with single, small, CT-enhancing
lesions [25,26].

Clinical Manifestations
The clinical manifestations of NCC reect the heterogeneity of cysts, in particular their location, size,
number, and stage of degeneration, as well as the overall
clinical status of the host, including the hosts immune
response [2729]. Seizures are the most common clinical manifestation of NCC and occur in over 70% of
NCC patients. NCC remains the most common cause of

Neurocysticercosis Shandera and Kass

acquired epilepsy among adults in the developing world

[30]. Even when disease burden is mild, nearly one half
of such patients will manifest recurrent seizures [31].
NCC causes seizures in several ways. Viable cysts that
do not elicit a host immune response are usually asymptomatic. Degenerating cysts with edema and contrast
enhancement on neuroimaging are the typical nidus for
seizure activity [27,28,32]. Seizures may also develop from
either cerebral infarction due to vasculitis or from thrombosis of penetrating blood vessels by subarachnoid cysts.
Calcied granulomas, the end result of cystic degeneration
and the only recognized neuroimaging abnormality in
many patients, persist as a cause of continued seizures in
patients with neither viable nor degenerating cysts. Such
seizures are more prevalent among epileptic patients in
NCC-endemic areas. Calcied granulomas periodically
undergo vasogenic perilesional edema, and such edema
may provoke an increase in epileptogenesis [32].
Mass effect occurs as lesions grow and this accounts
for some cases of focal neurologic deterioration [2729].
Parenchymal lesions rarely attain a size greater than
10 mm in diameter because of intraparenchymal pressure
[33]. Subarachnoid cysts lack this constraint and such
cysts, with diameters greater than 10 mm, are found in
the sylvian ssures and basal cisterns [33].
Both intraventricular and subarachnoid cysts can
present with either acute or chronic hydrocephalus.
Presenting signs and symptoms may include headache,
vomiting, seizures, papilledema, and decreased level
of consciousness. Acute obstruction of the fourth
ventricle from a free-oating intraventricular cyst (ie,
Bruns syndrome) may result in episodic vomiting,
intense headache, positional vertigo, loss of consciousness, or even sudden death brought on by change in
head position [34]. Chronic inammation due to subarachnoid cysticerci may cause brosis throughout the
ventricular drainage system, resulting in either communicating or noncommunicating hydrocephalus, basal
arachnoiditis, cranial nerve entrapments, chiasmatic
syndromes, or vasculitic cerebrovascular complications.
Even with cerebrospinal uid shunting (CSF) shunting,
the mortality in subarachnoid cases remains relatively
high [27,35].
Stroke is another cause of acute focal ndings in
NCC. Cerebrovascular disease contributes to morbidity
and mortality in patients with subarachnoid disease.
Vasculitic inammatory changes in medium- or smallsized vessels cause cerebral infarctions. Intracerebral
hemorrhages are reported from mycotic aneurysms that
rupture near subarachnoid cysts [27].
Neurocognitive decits and even frank dementia
are under-recognized in NCC patients. In one study of
90 consecutive untreated patients with NCC evaluated
at baseline, 15.5% met the Diagnostic and Statistical
Manual of Mental Disorders (DSM)-IV diagnostic criteria
for dementia [36].

455

Lesions in the peripheral musculature occur more

often among Asian patients with NCC. Whether
this reects the unique immunogenetic prole of this
population is not known [37].

Diagnosis
The diagnosis of NCC is dependent on the diverse clinical
manifestations of disease, neuroimaging, and supporting
information from epidemiology and laboratory assays.
Neuroimaging abnormalities of NCC show a broad
differential including brain neoplasms, other type of
abscess, and tuberculomas. In the proper clinical context,
however, the sensitivity and specicity of CT imaging for
the diagnosis of parenchymnal NCC is estimated at 95%
[38,39]. For ventricular, subarachnoid, posterior fossa,
spinal, ophthalmic lesions, and perilesions edema, CT
imaging is much less sensitive than MRI [39].
Four radiographic stages of degeneration occur with
parenchymal cysts. Early lesions are round and cystic,
do not contrast enhance, and lack perilesional edema. A
colloidal state, with early cyst degeneration, perilesional
edema, and enhancement on MRI, is followed by a
granular-nodular stage with more advanced cyst degeneration, decreased enhancement and edema, and the
onset of calcication. The latest stage of involution shows
calcied cysts on both CT (small hyperdense lesions) and
MRI (small hypointensities on T2 images) [33].
Two unusual types of parenchymal NCC are the military and pseudotumoral forms. Miliary NCC represents a
massive infection with multiple small cysts. Pseudotumoral
forms show lesions indistinguishable from either a brain
neoplasm or echinococcal cysts. MR perfusion and MR
spectroscopy may, however, differentiate these entities.
Diffusion-weighted image (DWI) sequence of MRI can
often distinguish a NCC cyst and a brain abscess because
the scolex of NCC is very bright on a DWI. In the apparent diffusion coefcient (ADC) maps, the NCC cyst is as
bright as CSF. The lack of hyperperfusion of a suspected
NCC lesion on perfusion MRI distinguishes it from brain
neoplasms [33].
Although radiographic tools are the most sensitive
and specic tools for diagnosis of NCC, serologies
based on detecting cysticercal antigens may be used
in evaluating suspicious lesions. The gold standard is
EITB, which yields the highest sensitivity in serum and
detects seven glycoprotein bands specic for T. solium
[36]. An enzyme-linked immunosorbent assay is also
available. It is much less sensitive (but less expensive
in some countries such as Mexico) than the EITB. A
Mexican study comparing the two found that a serum
EITB assay was over 92% sensitive for the diagnosis
of NCC with multiple cysts. That sensitivity dropped
to about 83% for NCC with a single cyst and 33% for
NCC with only calcied lesions. The overall sensitivity
for the serum assay was 86%. Detection of cysticercal

456

Infection

antigen in the serum suggests the continued presence

of viable parasite in the brain, and treatment based on
this nding may benet the patient [28,40].

Treatment
The treatment of NCC involves the initiation of cysticidal
treatment along with the control of secondary effects of the
infection, effects such as seizures and/or hydrocephalus.
Therapy depends on cyst location and stage of degeneration, the overall burden of infestation, and the host status,
including in particular the immune response. Seizures
should be managed with rst-line antiepileptic drugs, with
the choice determined by symptoms and site of disease.
Hydrocephalus is typically managed neurosurgically.

Antiparasitic drug treatment

The two most effective antiparasitic agents are albendazole,
which was introduced in 1997 in the United States, and
praziquantel, which was introduced in 1987. Both agents
effectively destroy parenchymal cysts and are well tolerated.
Nonetheless, controversy attends their use. Proponents of
therapy marshal a number of arguments in support of their
claims: 1) treated cysts disappear rapidly; 2) the incidence
of severe cases has fallen in the era of treatment; 3) treated
patients manifest fewer seizures and residual calcications; 4) inammation associated with treatment is readily
treated with steroids; 5) treatment is safe as evidenced by
only 10 case reports of treatment-related fatalities in the
world literature; and 6) a recent meta-analysis of treatment
trials showed that cysticidal treatment resulted in better
resolution of colloidal (enhancing) and vesicular (cystic)
lesions, lowered the risk for recurrent seizures in patients
with colloidal lesions, and reduced the rates of seizures in
patients with vesicular lesions [4143].
Opponents of therapy argue the following: 1) faster
cyst resolution does not necessarily result in better seizure
control; 2) better sanitation and general hygiene probably
account for the declining incidence and severity of NCC;
3) in some series seizure control is no better in treated
patients than in placebo controls; 4) no evidence shows
that treated patients develop fewer calcications; 5) most
pathologic effects of NCC result from host inammatory responses to dying cysticerci; 6) an exacerbation of
symptoms occurs in many patients following therapy; and
7) lesions can resolve spontaneously in the absence of
antiparasitic therapy [41,42,44].
Consensus guidelines for the treatment of NCC were
published in 2002 and were based on US Preventive Task
Force levels II-3 evidence (obtained from multiple time
series with or without intervention) and III evidence
(opinions of respected authorities based on clinical
experience). The following discussion is based on the
Consensus Group opinion as outlined in the published
guidelines [41].

Parenchymal infections
The Consensus Group identied three life-cycle categories:
1) viable cysts, 2) enhancing lesions (degenerating cysts), and
3) calcied cysticerci. They also identied three infestation
categories: 1) mild (15 cysts), 2) moderate (6100 cysts),
and 3) heavy (> 100 cysts}.
For viable cysts and a mild parasitic burden, most
specialists favor antiparasitic treatment with steroids.
For moderate parasitic burden, antiparasitic therapy is
added to high-dose steroid therapy. For heavy parasitic
burden, steroids alone should be used out of fear that
the simultaneous death of many cysts will induce allergic
reactions and signicant edema [41].
For patients with degenerating cysts and a mild to
moderate burden of disease, the most popular option is
nontreatment and neuroimaging to follow disease. With
heavier burden of disease (cysticercotic encephalitis),
high-dose steroids and osmotic diuretics (mannitol) without
antiparasitic drugs are indicated [41]. Calcied cysticerci,
regardless of disease burden, require neither antiparasitic
treatment nor steroids because such calcications represent
dead organisms.
A well-designed, double-blind, placebo-controlled trial
showed that the treatment of seizure patients with viable
parenchymal cysticerci using rst-line antiepileptics with
800 mg/d of albendazole and 6 mg/d of dexamethasone
for 10 days reduces the frequency of generalized seizures
by a statistically signicant amount [45]. Enrolled
patients shared statistically similar baseline characteristics in the treatment and control groups. At follow-up in
2 to 30 months, those treated showed 46% fewer seizures
than those given placebo (P = 0.30). A 41% reduction
in partial seizures was similarly insignicant (P = 0.44),
although a 67% reduction in generalized seizures was
signicant (P = 0.01). A bias in this study may have been
the heterogeneity of seizure frequency among the placebo
group (among which increased frequency was limited to a
few individuals) [45].
The growth of parenchymal lesions is uncommon but
may be life threatening. This warrants aggressive treatment
with antiparasitic drugs and/or surgical excision [41].
Extraparenchymal disease
Extraparenchymal disease requires aggressive intervention
because it usually results in hydrocephalus. When possible,
ventricular cysticerci should be removed neuroendoscopically [34]. Alternatively, patients can undergo CSF shunting
followed by antiparasitic treatment, steroids, and open
surgery. For subarachnoid disease (either giant cysts or
chronic meningitis), antiparasitic treatment, steroids, and
ventricular shunting for hydrocephalus are indicated. For
both spinal disease and ophthalmic disease, primary surgical
removal is preferred. Hydrocephalic patients without cysts
on neuroimaging should be offered ventricular shunting
without antiparasitic treatment [41].

Neurocysticercosis Shandera and Kass

Cysticidal medications
Albendazole is now the antiparasitic medication of
choice in the treatment of NCC. It is less expensive
and reduces cyst size and number more effectively
than praziquantel [28,35,44]. Albendazole concentrations, unlike those of praziquantel, are not lowered by
phenobarbital, phenytoin, or corticosteroids. Corticosteroid concentrations are actually increased by higher
albendazole plasma levels. Adverse effects from albendazole itself are rare. A post-treatment inammatory
reaction representing an exacerbation of neurologic
symptoms usually occurs between days 2 and 5 of treatment in 50% to 80% of patients and may necessitate an
increase in corticosteroid dosage [42,44].
For parenchymal disease, albendazole is given as
15 mg/kg/d divided every 12 hours for at least 1 week
[42,44]. A double-blind, placebo-controlled study of 1
versus 4 week(s) of albendazole therapy (at 15 mg/kg in
two divided doses) in children with mild parenchymal
disease burden showed no difference in radiographic
resolution of lesions or in seizure control at 2 years [46].
For ventricular and subarachnoid disease, albendazole
at a dose of 30 mg/kg/d is preferred and in one study reduction from 30 mg/kg/d to 15 mg/kg/d resulted in a worse
outcome using cyst reduction on MRI without a change in
tolerability. Neither giant subarachnoid or intraventricular
cysts, however, responded to one treatment cycle [47].
Parenchymal inammation is treated with corticosteroids (dexamethasone at 4 to 12 mg/d ) for the duration of
antiparasitic treatment. With more chronic inammation
(eg, extraparenchymal disease), longer-term corticosteroids are recommended (replacing dexamethasone with
prednisone after the acute period) [43]. With heavy disease
burden, steroids should be initiated prior to and after the
administration of antiparasitic treatment [28].
In the dementia series described previously, treatment with albendazole and steroids, after 6 months,
reduced the incidence of dementia nearly vefold. Only
21.5% of the dementia group continued to meet criteria
for dementia, although some continued to exhibit mild
cognitive impairment [36].

Prevention
Because of good sanitation and hygienic pork husbandry
practices such as eliminating porcine access to human
feces and discarding cysticercus-infested meat, NCC
is virtually eliminated in the developed world. Such
practices, unfortunately, are not universal in the developing world, and the movement of carriers establishes new
sites of disease.
One method used to control disease is mass chemotherapy against taeniasis. The rationale for this approach
is the higher than expected rates of NCC among patients
with taeniasis and their contacts. The two agents used to
implement this strategy are praziquantel and niclosamide.

457

Praziquantel can potentially induce cerebral inammation if concomitant cysticercal disease is present whereas
niclosamide is more expensive and cannot be used during
pregnancy. Effective control programs were carried out
in trials using praziquantel in Ecuador and Mexico and
niclosamide in Guatemala. The multiplicity of factors
affecting both rates of taeniasis and porcine cysticercosis
(the endpoints measured in most trials) complicate the
data analysis [48].
Studies modeling NCC in Peru show that mass treatment of humans is ineffective unless multiple treatments
are carried out (in one report, extinction required 11
interventions at 90-day intervals). Supplementing human
mass chemotherapy with mass anticysticercal treatment
of swine reduced the need for human therapy when the
swine received two treatments [49].
Human vaccination is unlikely to be successful.
Because NCC occurs rarely among either the immunodecient or the immunosuppressed, protective immunity
does not appear to be a major defense against disease [9].
As noted previously, the relationship between NCC and
human immunity is to date poorly understood. Porcine
disease, however, may be amenable to vaccine therapy
[50]. Options include a therapeutic vaccine that avoids
the issue of vaccinating piglets at a time of life when their
immunity is impaired, use of recombinant vaccines with
either related Taenia (eg, T. crassiceps, a murine parasite)
or T. solium oncosphere antigens, and DNA vaccines that
also induce humoral immunity. Prevention of disease in
both pigs and man is the ideal endpoint, although even
when vaccines are imperfect in reducing cyst counts they
are effective in changing the histopathology of cysts
(reducing oncosphere evagination), ultimately modifying
NCC manifestations [44].

Conclusions
Neurocysticercosis is increasingly recognized from all parts
of the world, including developed nations, where transmission occurs with fecal-oral exposure to Taenia-infected
contacts. Larval disease ensues among the contacted
individuals after eggs evolve into oncospheres that are
absorbed and form larvae in neurologic and muscular
tissues. Disease manifestations occur usually years, even
decades, after exposure and are most serious when crucial
anatomic neuraxis areas are impacted. NCC remains the
most common cause of adult-onset seizures in much of
Latin America. Disease is classied by site of involvement.
Ventricular disease, producing obstructive hydrocephalus,
occurs selectively among patients from Latin America and
requires prioritization in therapy. Excision of anatomically
crucial CNS lesions may be needed.
The most common manifestation of NCC is seizures,
usually the result of degenerating cysts within the brain
parenchyma. The primary manifestations of therapy for
such disease are supportive, including anticonvulsant

458

Infection

therapy. When disease is detected either during cyst

degeneration or when it involves crucial elements of the
neuraxis, a trial of albenadazole is benecial in reducing
seizure frequency. Ultimate control of NCC will require
improved pork husbandry, water sanitation, and the
development of a more effective public health infrastructure, particularly in developing nations so that new cases
can more effectively be managed. Geographic foci (hot
spots) in need of better prevention programs should be
identied. A vaccine for porcine disease using diverse
Taenia species and antigens, combined with mass chemotherapeutic trials using praziquantel or niclosamide,
may ultimately result in signicant reductions in porcine
disease, human taeniasis, and eventually NCC.

12.

13.
14.
15.
16.

17.

References and Recommended Reading

Papers of particular interest, published recently,
have been highlighted as:

Of importance

Of major importance
1.
2.
3.
4.
5.

6.

7.

8.

9.
10.

11.

Beaver PC, Jung RC, Wayne E: Cyclophyllidean tapeworms,

In Clinical Parasitology, edn 9. Philadelphia: Lea and
Febiger; 1984:513.
MacArthur WP: Cysticercosis as seen in the British army,
with special reference to the production of epilepsy.
Transaction R Soc Trop Med Hyg 1934, 27:343357.
Richards FO Jr, Schantz PM, Ruiz-Tiben E, Sorvillo
FJ: Cysticercosis in Los Angeles County. JAMA 1985,
254:34443448.
Shandera WX, White AC Jr, Chen JC, et al.: Neurocysticercosis in Houston, Texas. A report of 112 cases.
Medicine (Baltimore) 1994, 73:3752.
Sorvillo FJ, Waterman SH, Richards FO, Schantz PM:
Cysticercosis surveillance: locally acquired and travel-related
infections and detection of intestinal tapeworm carriers in
Los Angeles County. Am J Trop Med Hyg 1992, 47:365371.
Garcia-Garcia ML, Torres M, Correa D, et al.: Prevalence
and risk of cysticercosis and taeniasis in an urban population
of soldiers and their relatives. Am J Trop Med Hyg 1999,
61:386389.
Garca HH, Gilman RH, Gonzales AE: Epidemiologia de
la cysticercosis en el Per. In Taeniasis/Cisticercosis por
T. solium. Edited by Garca HH, Martinez SM. Lima,
Peru: Editorial Universo SA; 1984:313326.
Schantz PM: Taenia solium cysticercosis: an overview of
global distribution and transmission. In Taenia solium
Cysticercosis; from Basic to Clinical Science. Edited by
Singh G, Prabhakar S. Wallingford Oxon, United Kingdom:
CABI Publishing; 2002:6373.
Singh G, Prabhakar S: Taenia solium Cysticercosis; from
Basic to Clinical Science. Wallingford Oxon, United
Kingdom: CABI Publishing; 2002.
Garcia HH, Gilman RH, Gonzalez AE, et al.: What have
we learnt from epidemiological studies of Taenia solium
cysticercosis in Peru? In Taenia solium Cysticercosis; from
Basic to Clinical Science. Edited by Singh G, Prabhakar
S. Wallingford Oxon, United Kingdom: CABI Publishing;
2002:7678.
Sarti E: Epidemiology of Taenia solium taeniasis and
cysticercosis in Mexico. In Taenia solium Cysticercosis;
from Basic to Clinical Science. Edited by Singh G, Prabhakar
S. Wallingford Oxon, United Kingdom: CABI Publishing;
2002:87.

18.

19.

20.
21.
22.

23.
24.

25.

26.

27.
28.
29.
30.

Garcia-Noval J, Sanchez AL, Allan JC: Taenia solium

taeniasis and cysticercosis in Central America. In Taenia
solium Cysticercosis; from Basic to Clinical Science.
Edited by Singh G, Prabhakar S. Wallingford Oxon, United
Kingdom: CABI Publishing; 2002:9495.
Fan PC, Chung WC, Soh CT, et al.: Eating habits of East
Asian people and transmission of taeniasis. Acta Tropica
1992, 50:305315.
Hira PR, Francis I, Abdella NA, Gupta R, et al.: Cysticercosis:
imported and autochthonous infections in Kuwait. Trans R
Soc Trop Med Hyg 2004, 98:233239.
Schantz PM, Moore AC, Muoz JL, et al.: Neurocysticercosis
in an Orthodox Jewish community in New York City. N Engl
J Med 1992, 327:692695.
Restrepo BI, Aguilar MI, Melby PC, Teale JM: Analysis
of the peripheral immune response in patients with
neurocysticercosis: evidence for T cell reactivity to parasite
glycoprotein and vesicular uid antigens. Am J Trop Med
Hyg 2001, 65:366370.
Meza-Lucas A, Carmona-Miranda L, Garcia-Jeronimo
RC, et al.: Short report: limited and short-lasting humoral
response in Taenia solium: seropositive households
compared with patients with neurocysticercosis. Am J
Trop Med Hyg 2003, 69:223227.
Garcia HH, Gonzalez AE, Gilman RH, et al.: Cysticercosis
Working Group in Peru: Short report: transient antibody
response in Taenia solium infection in eld conditionsa
major contributor to high seroprevalence. Am J Trop Med Hyg
2001, 65:3132.
Flisser A, Correa A, Evans CA: Taenia solium cysticercosis:
new and revisited immunological aspects. In Taenia solium
Cysticercosis; from Basic to Clinical Science. Edited by
Singh G, Prabhakar S. Wallingford Oxon, United Kingdom:
CABI Publishing; 2002:16.
Grewal JS, Kaur S, Bhatti G, et al.: Cellular immune
responses in human neurocysticercosis. Parasitol Res 2000,
86:500503.
Robinson P, Altamar R, Lewis D, et al.: Brain granulomas
in murine cysticercosis. Infect Immun 1997, 89:6472.
Robinson P, White AC, Lewis DE, et al.: Sequential expression
of the neuropeptides substance P and somatostatin in granulomas associated with murine cysticercosis. Infect Immun 2002,
70:45344538.
Restrepo BI, Alvarez JI, Castano JA, et al.: Brain granulomas in neurocysticercosis patients are associated with a Th1
and Th2 prole. Infect Immunol 2001, 69:45544560.
Mlinari JL, Tato P: Molecular determinants of host-parasite
interactions: focus on parasite. In Taenia solium Cysticercosis;
from Basic to Clinical Science. Edited by Singh G, Prabhakar
S. Wallingford Oxon, United Kingdom: CABI Publishing;
2002:2832.
Padma V, Jain S, Srivastava A, et al.: Hereditary factors in
neurocysticercosis with emphasis on single, small enhancing
CT lesions. In Taenia solium Cysticercosis; from Basic to
Clinical Science. Edited by Singh G, Prabhakar S. Wallingford Oxon, United Kingdom: CABI Publishing; 2002:5859.
Del Brutto OH, Granados G, Talamas O, et al.: Genetic
pattern of the HLA system: HLA A, B, C, DR, and DQ
antigens in Mexican patients with parenchymal brain
cysticercosis. Hum Biol 1991, 63:8593.
Garcia HH, Del Brutto OH, Nash TE, et al.: New concepts
in the diagnosis and management of neurocysticercosis
(Taenia solium). Am J Trop Med Hyg 2005, 72:39.
Garcia HH, Del Brutto OH, for the Cysticercosis Working
Group in Peru: Neurocysticercosis: updated concepts about
an old disease. Lancet Neurol 2005, 4:653661.
Del Brutto OH: Neurocysticercosis. Sem Neurol 2005,
25:243251.
Del Brutto OH, Santibanez, CA, Noboa CA, et al.: Epilepsy
due to neurocysticercosis: analysis of 203 patients. Neurology
1992, 42:389392.

Neurocysticercosis Shandera and Kass

31.
32.
33.

34.

35.
36.
37.

38.
39.
40.

41.

Carpio A, Hauser WA: Prognosis for seizure recurrence in

patients with newly diagnosed neurocysticercosis. Neurology
2002, 59:17301734.
Nash TE, Del Brutto OH, Butman JA, et al.: Calcic
neurocysticercosis and epileptogenesis. Neurology 2004,
62:19341938.
Do Amaral LL, Ferreira RM, da Rocha AJ, et al.: Neurocysticercosis: evaluation with advanced magnetic resonance
techniques and atypical forms. Top Magn Reson Imaging
2005, 16:127144.
Torres-Corzo, J, Rodriguez-della Vecchia R, Rangel-Castilla
L: Bruns syndrome caused by intraventricular neurocysticercosis treated using exible endoscopy. J Neurosurg 2006,
104:746748.
Takayanagui OM, Odashima NS: Clinical aspects of
neurocysticercosis. Parasitol Int 2006, 55:S111S115.
Ramirez-Bermudez J, Higuera J, Sosa AL, et al.: Is dementia
reversible in patients with neurocysticercosis? J Neurol
Neurosurg Psychiatry 2005, 76:11641166.
Ito A, Nakao M, Okamoto M, et al.: Mitochondrial DNA of
Taenia solium: from basic to applied science. In Taenia solium
Cysticercosis; from Basic to Clinical Science. Edited by Singh
G, Prabhakar S. Wallingford Oxon, United Kingdom: CABI
Publishing; 2002:51.
Nash TE, Neva FA: Recent advances in the diagnosis and
treatment of cerebral cysticercosis. N Engl J Med 1984,
311:14921496.
Dua T, Aneja S: Neurocysticercosis: management issues.
Indian Pediatr 2006, 42:227235.
Proano-Narvaez JV, Meza-Lucas A, Mata-Ruiz O, et al.:
Laboratory diagnosis of human neurocysticercosis: doubleblind comparison of enzyme-linked immunosorbent assay
and electroimmunotransfer blot assay. J Clin Microbiol
2002, 40:21152118.
Garcia HH, Evans CA, Nash TE, et al.: Current consensus
guidelines for treatment of neurocysticercosis. Clin Microbiol
Rev 2002, 15:747756.

459

Riley T, White AC Jr: Management of neurocysticercosis.

CNS Drugs 2003, 17:577591.
43.
Del Brutto OH, Roos KL, Coffey CS, Garcia HH:
Meta-analysis: cysticidal drugs for neurocysticercosis:
albendazole and praziquantel. Ann Intern Med 2006,
145:4351.
44.
Takayanagui OM: Therapy for neurocysticercosis:
Expert Rev Neurotherapeutics 2004, 4:129139.
45. Garcia HH, Pretell EJ, Gilman RH, et al.: A trial of
antiparasitic treatment to reduce the rate of seizures due to
cerebral cyticercosis. N Eng J Med 2004, 350:249258.
Important reference.
46.
Singhi P, Dayal D, Khandelwal N: One week versus four
weeks of albendazole therapy for neurocysticercosis in
children: a randomized, placebo-controlled double blind
trial. Pediatr Infect Dis J 2003, 22:268272.
47.
Gongora-Rivera F, Soto-Hernandez JL, Gonzalez Esquivel
MS, et al.: Albendazole trial at 15 or 30 mg/kg/day for
subarachnoid and intraventricular cysticercosis. Neurology
2006, 66:436438.
48.
Allan JC, Craig PS, Pawlowski ZS: Control of Taenia
solium with emphasis on treatment of taeniasis. In Taenia
solium Cysticercosis; from Basic to Clinical Science.
Edited by Singh G, Prabhakar S. Wallingford Oxon United
Kingdom: CABI Publishing; 2002:416417.
49.
Gonzalez AE, Gilman RH, Garcia HH, Lopez T: Use of a
simulation model to evaluate control programmes against
Taenia solium cysticercosis. In Taenia solium cysticercosis;
from Basic to Clinical Science. Edited by Singh G, Prabhakar
S. Wallingford Oxon, United Kingdom: CABI Publishing;
2002:444.
50.
Gonzalez AE, Gauci CG, Barber D, et al.: Vaccination of
pigs to control human neurocysticercosis. Am J Trop Med
Hyg 2005, 72:837839.
42.