Curr Neurol Neurosci Rep
DOI 10.1007/s11910-011-0226-7
INFECTION (BURK JUBELT, SECTION EDITOR)
Clinical Manifestations, Diagnosis, and Treatment
of Neurocysticercosis
Julio Sotelo
# Springer Science+Business Media, LLC 2011
Abstract Neurocysticercosis (NCC) is the most frequent
parasitic disease of the human brain. Modern imaging
studies, CT and MRI, have defined the diagnosis and
characterization of the disease. Through these studies the
therapeutic approach for each case may be individualized
with the aid of antihelmintics, steroids, symptomatic
medicines, or surgery. The use of one or various therapeutic
measures largely depends on the peculiar combination of
number, location, and biological stage of lesions as well as
the degree of inflammatory response to the parasites.
Although there is not a typical clinical picture of NCC,
epilepsy is the most frequent manifestation of parenchymal
NCC, whereas hydrocephalus is the most frequent mani-
festation of meningeal NCC. Eradication of cysticercosis is
an attainable goal by public education and sanitary
improvement in endemic areas.
Keywords Cysticercosis . Albendazole . Praziquantel .
Serodiagnosis . Taeniasis . Hydrocephalus . Epilepsy .
Neurocysticercosis
Introduction
Cysticercosis is a millenary disease, still endemic in areas
with deficient sanitary conditions from most developing
countries of America, Africa, and Asia [1, 2], with the
exception of Muslim countries, where livestock of pigs is
absent and the life cycle of taeniasis/cysticercosis cannot be
J. Sotelo (*)
The Neuroimmunology Unit, National Institute of Neurology
and Neurosurgery of Mexico,
Insurgentes Sur 3877,
Mexico City 14269, Mexico
e-mail: jsotelo@unam.mx
completed. For centuries cysticercosis was also endemic in
Europe, until the improvement of sanitary conditions led to
its disappearance at the beginning of the 20th century, long
before the development of sophisticated diagnostic tech-
nology and specific medical treatments. Nevertheless,
within the last decades neurocysticercosis (NCC) has been
increasingly diagnosed in countries from North America
and Europe that were previously free of the disease, mainly
due to massive human migration from endemic to non-
endemic areas [1, 3••, 4, 5, 6••, 7].
Although cysticercosis was originally described in the
ancient Greece [1, 6••] the course of the disease remained
unchanged until two main factors at the end of the last
century changed drastically the medical approach to NCC;
the advent of brain imaging studies in the 1970s and the
discovery of effective cysticidal therapy in the 1980s.
Imaging studies allowed for the first time to document the
site and number of parasites within the brain and to
elaborate a classification for therapeutic purposes. Cysti-
cercosis of the brain is a very complex disease whose
clinical manifestations and prognosis are related to various
independent factors; the biological status of parasites (from
live, active cysticerci to inactive granulomas and calcifica-
tions), the number and location of lesions, and the degree of
inflammatory response from the host to the parasites, which
may range from immune tolerance to an intense inflamma-
tory response [3••]. Therefore, the severity of the disease
might vary from an asymptomatic stage, discovered by
incidental imaging studies, to a severe neurologic disorder
[4, 8]. The advent of brain imaging—first CT and later
MRI—allowed the clinician for the first time to characterize
the disease [9]. Almost at the same time, the discovery of
drugs with strong cysticidal properties, first praziquantel
[10] and later albendazole [11, 12], opened the possibility
for elimination of parasites thus preventing the use of

surgery, which until that time was the only therapeutic
approach, an obviously expensive and risky procedure with
very limited results.
Life Cycle of Taeniasis/Cysticercosis
Contrary to popular belief in endemic areas, cysticercosis is
not acquired by the ingestion of pork meat contaminated by
cysticerci [13]. In the life cycle of Taeniasis/cysticercosis,
humans are the sole host for both stages of the cestode,
whereas pork is only host for cysticerci. When humans
ingest undercooked pork meat infested with cysticerci, the
metacestode evaginates from the cyst and anchors in the
first segments of the intestinal wall. The larva then grows
fast and evolves to the adult cestode Taenia solium; within
3 months the worm reaches a large size of 2 to 3 m long;
then, the distal proglottids, each containing several thou-
sand fertilized eggs, are detached daily from the cestode
and expelled within the feces of the host. These fertilized
eggs may in turn contaminate the soil, vegetables, and food
prepared under deficient sanitary conditions. When either
humans or pigs eat this contaminated food, the taenia eggs
are absorbed in the digestive tract of the new host and lodge
mostly in the brain or in muscle, where they will hatch and
grow as taenia embryos or cysticerci. In this way, the life
cycle of the parasite will be completed.
These peculiar biological paths easily explain why
intestinal taeniasis in humans is so rare whereas cysticer-
cosis in humans and pigs is so frequent; but also explain
why a single carrier of the intestinal adult cestode becomes
a large and continuous source of contamination by
cysticerci within the community, and even in distant sites
due to modern systems for transportation of edibles. This
cycle also explain why cysticercosis can be acquired by
strict vegetarians or by people that never eat pork meat. The
mechanisms of transmission of Taenia and cysticercus point
out various steps in which public health measures can
interrupt the cycle; for instance, search and treatment of
taenia carriers, a potential vaccine for pigs, and freezing of
infested pork meat [13].
Clinical Manifestations
Brain cysticercosis induces a pleomorphic clinical picture
that depends on location, number, and histologic character-
istics of lesions [3••, 6••, 9, 14]. Clinical expression of NCC
might disclose a variable mixture of neurologic and
psychiatric signs, even a chronic, diffuse brain dysfunction
as dementia can be produced by NCC [6, 15]. A single
cysticercus located in the brainstem, or within the eye, or in
the pituitary gland [16] may produce different and more
Curr Neurol Neurosci Rep
severe clinical manifestations than various cysticerci scat-
tered in brain parenchyma but not situated in eloquent
neurologic sites [9]. Also, the intensity of the immune
response from the host varies widely from one patient to
another, some patients develop a severe immune response
to cysticerci whereas others present a remarkable tolerance
to the parasites [17, 18]; in the former cases the
spontaneous disappearance of cysts provoked by the
immune response of the host can be reasonably predicted
by the initial evidence gathered by imaging studies (eg,
parenchymal cysts surrounded by intense inflammatory
halo) [19]; whereas in the later cases the cysts that are not
accompanied by inflammation may survive and grow
undisturbed for long periods, even years, and reach a large
size of 5 to 10 cm in diameter in the form of a single giant
cyst or a clump of cysts; a peculiar feature of these large
cysts is the absence of metacestode on their interior.
A relevant feature for the pathophysiology of NCC is
that cysticerci located in brain parenchyma induce tissue
damage restricted to the perilesional area, whereas cysti-
cerci located in the subarachnoid space usually induce a
relentless inflammatory reaction that is disseminated to
distant sites by the circulation of the cerebrospinal fluid
(CSF), producing widespread damage (eg, arachnoiditis,
vasculitis accompanied by secondary infarctions, and
chronic hydrocephalus due to the inflammatory obstruction
of CSF absorption at the arachnoid villi) [20••, 21]. In
general terms, the prognosis of parenchymal cysticercosis is
benign [14], whereas meningeal cysticercosis often follows
a protracted course [21].
The above characteristics of cysticercosis explain the
variable clinical manifestations of the disease; almost any
neurologic sign or syndrome can be elicited by cysticerco-
sis [3••, 4, 22•]. Nevertheless, some clinical signs define
peculiar forms of the disease: In most cases of parenchymal
cysticercosis, which is the more frequent form of NCC
[3••], the usual clinical manifestation is epilepsy [13, 23,
24], present in a large proportion of cases with parenchymal
cysts or with granulomas or calcifications; the last two
represent inactive sequelae of cysticerci successfully
destroyed by the host immune response or by spontaneous
involution. Parenchymal granulomas or calcifications are a
frequent, unexpected finding on imaging studies practiced
for incidental reasons (eg, vehicular accidents) to subjects
from endemic areas of cysticercosis. In a strict sense,
calcifications do not represent NCC but its inactive,
permanent sequel not amenable to cysticidal therapy;
however, parenchymal calcifications might be the most
frequent finding of NCC in the everyday clinical practice.
In contrast with parenchymal cysticercosis, in cases of
meningeal or ventricular cysticercosis signs of increased or
elevated intracranial pressure are the most frequent clinical
manifestation [3••, 13]. In cases of meningeal cysticercosis
Curr Neurol Neurosci Rep
a frequent complication is vasculitis that may induce brain
infarctions, transient ischemic attacks, and brain hemor-
rhage [6••]; chronic meningitis due to the presence of
parasites in the subarachnoid space also generates hydro-
cephalus. In cases of ventricular cysticercosis the mechan-
ical obstruction of CSF circulation, due to mobile cysts,
usually located in the fourth ventricle, trigger episodes of
acute hydrocephalus related to movements of the head
(Bruns’ syndrome). A third origin of increased or elevated
intracranial pressure in NCC is due to diffuse brain edema
secondary to subacute cysticercotic encephalitis, which is
seen in the rare cases of severe infection by countless
cysticerci scattered in the brain parenchyma.
Epidemiology
There is a notorious absence of comprehensive epidemio-
logic studies that would define the precise prevalence of
taeniasis and cysticercosis [23]. However, indirect data,
mostly from medical institutions, point out the conspicuous
presence of NCC as a cause of disability and disease in
large human groups. For instance, in endemic regions NCC
is the main cause of late-onset epilepsy and of hydroceph-
alus in adults [3••, 6••, 14]. By regional studies from
autopsy material in large medical centers and by inference
analysis through seroepidemiologic surveys, the frequency
of brain cysticercosis has been calculated as high as 1% to
4% of the general population from endemic areas. The
world figure for incidence of cysticercosis has been settled
around 50 million cases. In the developing world NCC is
the most common cause of acquired epilepsy [1, 6••, 14].
Nonetheless, precise ciphers from integral epidemiologic
studies are lacking due mainly to two facts: first, the
incidence of the disease is highly variable, even between
areas from the same region, due to parochial conditions of
cultural, economical, and sanitary development [23, 25];
second, to confirm or discard the diagnosis of NCC
requires, as a gold standard, the practicing of neuroimaging
studies to all subjects participating in the study [9], and this
requirement imposes economical restrictions to epidemio-
logic analysis.
Diagnosis
The absence of a typical clinical picture of NCC and its
pleomorphism [3••, 9, 14, 22•] explain the impossibility for
diagnosis suspected only on clinical grounds; almost any
neurologic patient from endemic areas can be a candidate
for the diagnosis of NCC. Both CT and MRI are
indispensable tools for diagnosis and characterization of
the disease [6••, 9]; CT is superior for diagnosis of brain
granulomas and calcifications, which are the most frequent
finding of NCC [9, 14, 19, 22•], and may be missed by
MRI. Nonetheless, MRI is more useful than CT for
diagnosis of ocular, ventricular, and subarachnoid cysticer-
cosis and for analysis of the inflammatory reaction that
accompanies most cases of active NCC [9]. Serologic
studies have several limitations for diagnosis [3••, 6••];
among them, a large number of subjects with inactive
cysticercosis, mostly in the form of granulomas or
calcifications in brain parenchyma are negative on serologic
tests; in contrast, it is frequent to have a positive response
to serologic analysis in healthy individuals environmentally
exposed to the parasite who did not develop the disease
[3••, 17, 26]. Moreover, it is also frequent to have negative
serologic results of confirmed cases of NCC who show
either immune tolerance to the parasite or who present a
solitary cyst in brain parenchyma that did not induce a
systemic immune response and did not develop detectable
antibodies in serum. Also, cysticerci are highly complex
parasites that share genetic traits with other helmints [27];
the antigens used for NCC diagnosis in serum may cross-
react with antibodies against other parasites and give false-
positive results. Thus, although useful as an epidemiologic
tool to calculate crude exposure to cysticerci, serologic tests
have limited value to determine the precise incidence and
prevalence of NCC [3••]. Also, the large number of false-
negatives and false-positives due to the peculiarities of the
disease, rather than to technical limitations of the serologic
assays, limit the reliability of these tests in the everyday
practice of neurology.
In the daily medical consultation the gold standard for
NCC diagnosis is through neuroimaging studies, CT or
MRI; however, this represents a serious dilemma, their high
cost limits the timely diagnosis of NCC in patients from the
low economical strata, which coincidentally correspond to
the great majority of NCC cases. In contrast with the
limited help of serologic studies for individual diagnosis,
the immunodiagnostic tests are reliable when practiced in
CSF from NCC patients with active forms of the disease
(alive parenchymal cysticercus or cysticercal arachnoiditis)
[9]; the CSF study confirms the diagnosis, helps to define
therapeutic strategies with cysticidals and with anti-
inflammatory drugs, and guides the long-term follow-up
of the inflammatory process. Although the CSF study is
useful for comprehensive diagnosis and therapeutic plans, it
might not be obtainable in many cases, as the patient’s
consent to lumbar puncture is frequently refused and it may
even be contraindicated in patients with increased or
elevated intracranial pressure.
As a general and cost-effective rule, all residents or
immigrants from endemic countries that present with either
late-onset epilepsy or increased or elevated intracranial
pressure are candidates for diagnosis of NCC and imaging

studies must be obtained. When imaging studies show
hydrocephalus in subjects from endemic areas of cysticer-
cosis, the diagnosis of NCC should be suspected even in
the absence of parenchymal cysts or calcifications; in these
cases immunodiagnostic tests for NCC in CSF would
confirm the diagnosis [9].
Treatment
In the late 1970s praziquantel was reported as an effective
drug for porcine cysticercosis. In the early 1980s it was
tested as a potential cysticidal drug in anecdotal cases; soon
afterward controlled studies confirmed its effectiveness in
patients with alive cysticerci in brain parenchyma that were
effectively eliminated, as seen by CT [10]. Later in 1987,
we demonstrated strong cysticidal properties of albendazole
[11]; further studies confirmed the effectiveness of a short
therapeutic course with albendazole [28]. Nowadays,
albendazole has been adopted as the first drug of choice
by most authors after comparative studies showed its
superiority over praziquantel as elective treatment for active
NCC [3••, 6••, 29]. Albendazole is effective in all locations
of cysticerci; even those in the eye or in the ventricular
cavities, which means that cysticidal amounts of albenda-
zole sulfoxide are achieved in the ocular fluids and in the
CSF after its oral intake.
As with most novel advents in medical therapy, drug
therapy with cysticidals was initially challenged by contro-
versies [1, 3••, 30], with three being the most important: 1)
although imaging studies clearly demonstrated the disap-
pearance of viable cysticerci soon after therapy this fact did
not automatically mean that the affected brain function (eg,
epilepsy) would improve or be restored after the elimination
of the parasites [30]; 2) cysticidal therapy is frequently
accompanied by secondary reactions that are due not to
drug toxicity but to the acute destruction of parasites that is
followed by an inflammatory reaction from the host to the
sudden liberation of antigens triggered by the death of the
parasites [31]; and 3) as several cases of parenchymal
cysticercosis had only a mild clinical picture (eg, occasional
seizures) easily controlled by symptomatic therapy, the
need for cysticidal therapy in these cases would be
questionable [1]. More than 25 years of experience has
accumulated since the advent of cysticidals [12], and along
this time countless studies have been performed with
albendazole and with praziquantel and have provided
answers to these three main questions: 1) adverse inflam-
matory reactions secondary to the drug-induced destruction
of parasites are effectively controlled by a brief course of
steroid therapy; 2) long-term studies have shown that the
opportune elimination of parasites is frequently accompa-
nied by improvement of the specific neurologic dysfunc-
Curr Neurol Neurosci Rep
tions caused by the parasites [1, 29, 32, 33]; and, more
important, 3) it seems logical to consider that in NCC, as in
any other infectious disease in which an effective and
convenient therapy exists (in economical cost, drug toxicity,
and length of therapy), there is no reason to leave the
disease to follow its natural course, in patients with mild
forms of the disease, when an effective and safe cure can be
achieved [6••, 34]. Currently, most experts agree with the
use of antihelmintic therapy when viable cysticerci are
encountered [6••, 33].
Therapeutic Schemes of Antihelmintic Drugs
Viable cysticerci are susceptible to cysticidal therapy: alive
cysts are identified by imaging studies (CT or MRI), and
their principal characteristics are a cyst filled with a clear
fluid of consistency similar to that of CSF [3••, 9]. In these
cases an 8-day course of albendazole (15 mg/kg/day)
separated in two daily doses, one every 12 h, eliminates
most active cysticerci located either in the brain parenchy-
ma, ventricular system, or subarachnoid space. Even in
intraocular cysticerci located in the retina, albendazole is
effective. In cases of cysticercus located in the ocular
cavities albendazole kills the cysticercus, but surgical
extirpation of the dead parasite must follow medical
therapy.
An alternative to albendazole, praziquantel in doses of
50 mg/kg/day separated in three doses, one every 8 h is
effective, particularly for parasites located in brain paren-
chyma. Two different praziquantel schemes have been
proposed: the length of treatment at the original, and most
used scheme, is 2 weeks [10]. However, pharmacokinetic
studies have shown that after its oral ingestion praziquantel
is rapidly absorbed in the digestive tract, achieving
maximal plasma levels within 2 h, sharply decreasing
afterward. Thus, a new scheme of a single-day therapy was
designed in which the three doses of praziquantel were
administered, once every 2 h (eg, at 7:00 AM, 9:00 AM, and
11:00 AM) [10, 12, 35]. Comparative studies have shown
that this single-day scheme seems to be as effective as
the traditional one of 2 weeks, greatly reducing the cost
(nearly 90%), the length of therapy, and the total drug
dose. This scheme is convenient for patients living in
distant areas as the whole treatment may be adminis-
tered in 4 h, thus increasing treatment compliance in the
outpatient clinic. Although praziquantel is a good
alternative to albendazole in cases of parenchymal brain
cysticercosis, it is far less effective in ventricular and
subarachnoid cysticercosis due to lower contents of the
drug achieved in these locations. Recent studies have
suggested a potential synergistic therapeutic effect on a
combined therapy with praziquantel and albendazole
[36].
Curr Neurol Neurosci Rep
Treatment of Inflammation
Steroids are very effective against the inflammatory
reaction that frequently accompanies cysticercosis [1, 37].
Different schemes have been tested according to the
location of parasites, the severity of inflammation, and the
selected cysticidal scheme. The simultaneous administra-
tion of steroids with albendazole or with praziquantel
generates contrasting effects. It increases the plasma
contents of albendazole, but lowers the plasma contents of
praziquantel [6••]; consequently, steroids can be adminis-
tered simultaneously to albendazole as a daily single dose
of prednisone 50 to 100 mg, or dexamethasone 10 mg
intramuscularly along the albendazole course. In contrast,
when praziquantel is given, the steroid therapy should be
administered either the day after cysticidal therapy (in the
case of a single-day course) or, in patients treated with the
2-week course, at anytime, when esteemed necessary in
cases of intense secondary reactions (headache, seizures),
triggered by the inflammation that follows the acute
destruction of parasites. In these cases, the development
of neurologic reactions indicates that the cysticidal effect of
praziquantel has already taken place and the use of steroids
would not hamper its therapeutic efficacy.
Steroids are also effective for the long-term treatment of
chronic arachnoiditis. In these cases we have minimized the
development of adverse complications secondary to the
chronic administration of steroids with a scheme of
prednisone administered as a single dose 50 mg three times
a week, on alternate days (eg, Monday, Wednesday and
Friday) [35]. The length of this therapy must be individu-
ally settled by periodic imaging studies and quantification
of cells and proteins in CSF analysis. Steroids are also very
useful in the rare cases of cysticercotic encephalitis, in
which the main pathophysiology is due to severe, diffuse
brain edema secondary to the acute and widespread
infection by countless cysticerci scattered in brain paren-
chyma. In these cases aggressive immunosuppressant
therapy with steroids and cyclophosphamide must precede
cysticidal therapy, which should wait until the resolution of
increased or elevated intracranial pressure, because the
sudden destruction of the parasites with antihelmintic
therapy might exacerbate the increased or elevated intra-
cranial pressure [35].
Surgery
Despite the advances of medical therapy, surgery is still
required in some instances [20••]. Nowadays, surgical
interventions are restricted largely to the treatment of
hydrocephalus by ventriculo-peritoneal shunting [38]. Most
cases of viable cysticerci, even those with giant clumps of
cysts, can be effectively treated by cysticidal therapy. This
conservative approach has been adopted in most neurologic
centers from endemic countries [6••, 12, 14, 33, 39].
However, there is still some controversy in cases of
intraventricular cysts, in which stereotactic guide has also
been used with adequate results [40, 41]. Yet, I consider
that conservative medical therapy is preferable in most
cases leaving surgery only for resistant cases, or for patients
in whom the diagnosis of NCC cannot be confirmed by
imaging and CSF studies or by a therapeutic trial with
cysticidal drugs. Although there is some evidence on the
apparent decrease of incidence of cysticercosis in some
countries [42], other studies mention the permanence of the
disease in the same areas [43]. In contrast, with reports of
immigrants with cysticercosis acquired in their country of
origin, there are occasional reports on the infection
primarily acquired in regions previously exempt of cysti-
cercosis [5, 44, 45]. This is worrisome because it indicates
the local setting of the cycle of taeniasis/cysticercosis with
serious potential implications because the human carriers of
the intestinal cestode are in most cases asymptomatic, but
are daily producers of several hundred thousand fertilized
eggs expelled in their stools, which in turn may cause the
provincial propagation of cysticercosis.
Conclusions
The appropriate use of brain imaging studies for diagnosis,
the effective and convenient drug therapy and, far more
important, the sanitary measures to prevent the propagation
of the complex Teniasis/cysticercosis in humans and of
cysticercosis in pigs [46] have contributed to a far better
picture of NCC than three decades ago. It is important to
stress the fact that NCC is a highly vulnerable disease by a
simple sanitary measure [1, 42]. Its disappearance in vast
regions demonstrates the fact that education and sanitation
are the most effective actions to eliminate cysticercosis [13,
46, 47].
Disclosure No potential conflict of interest relevant to this article
was reported.
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