Review Article

Neurocysticercosis
Address correspondence to
Dr Oscar H. Del Brutto, Air
Center 3542, PO Box 522970,
Miami, FL 33152-2970,
oscardelbrutto@hotmail.com.
Relationship Disclosure:
Dr Del Brutto has received
travel expenses for serving
on the Safe Implementation
of Treatment of Stroke
steering committee.
Unlabeled Use of
Products/Investigational
Use Disclosure: Dr Del Brutto
reports no disclosure.
* 2012, American Academy
of Neurology.
Oscar H. Del Brutto, MD, FAAN
ABSTRACT
Purpose of Review: Neurocysticercosis occurs when humans become intermediate
hosts in the life cycle of Taenia solium by ingesting its eggs directly from a taenia
carrier or, less often, by contaminated food. Within the nervous system, cysticerci may
lodge in the brain parenchyma, subarachnoid space, ventricular system, or spinal cord,
causing a number of pathologic changes that are responsible for the pleomorphism of
neurocysticercosis. This article discusses the clinical manifestations, diagnosis, and treat-
ment of neurocysticercosis.
Recent Findings: Formerly endemic in the developing world, mass immigration of
people from disease-endemic to nonendemic areas has caused a recent increase in the
prevalence of neurocysticercosis in developed countries, where this condition should no
longer be considered exotic. Recent advances in neuroimaging and immune diagnostic
methods, and the introduction of a set of diagnostic criteria, have enhanced the
diagnostic accuracy for neurocysticercosis. Likewise, introduction of potent cysticidal
drugs has radically changed its prognosis.
Summary: Neurocysticercosis is the most common helminthic infection of the CNS and
a major cause of acquired epilepsy worldwide. Diagnosis of neurocysticercosis is possible
after interpretation of clinical data together with findings of neuroimaging studies and
results of immunologic tests in a proper epidemiologic context. The use of cysticidal drugs
reduces the burden of infection in the brain and improves the clinical course of most
patients. Further efforts must be directed to eradicate the disease through the imple-
mentation of control programs against all interrelated steps in the life cycle of T. solium,
including human carriers of the adult tapeworm, infected pigs, and eggs in the environment.

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INTRODUCTION cysticercosis with emphasis on recent

Neurocysticercosis, defined as infection
of the CNS by the larval stage of the pork
tapeworm Taenia solium, is currently
considered the most common helmin-
thic disease of the CNS in humans and
a major public health challenge for
most of the developing world. In rural
areas of endemic countries, almost all
conditions favoring the transmission
of the disease, including warm climate,
poverty, and illiteracy, are combined.
The complex and unpredictable
nature of the immunologic reaction
of the host against cysticerci, as well as
the myriad pathologic lesions that
parasites may induce in the CNS, make
neurocysticercosis a fascinating dis-
ease. Basic and clinical aspects of neuro-
1392 www.aan.com/continuum
advances on diagnosis and therapy will
be discussed in this review.
EPIDEMIOLOGY
The exact prevalence of neurocysticer-
cosis is unknown; however, it is esti-
mated that millions of people living in
the developing world are infected by
the larval form of T. solium, and that
many of them will experience the clin-
ical consequences of this infection at
any point of their lives.1 In broad terms,
neurocysticercosis is endemic in most
Latin American countries, sub-Saharan
Africa, and some regions of Asia, includ-
ing the Indian subcontinent, Indonesia,
Vietnam, Korea, and China. Cysticerco-
sis is rare in Northern Europe, Canada,
December 2012

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 KEY POINTS
Australia, Japan, and New Zealand, A similar scenario has been observed in h In broad terms,
except among immigrants, and is only Spain, where mass immigration of peo- neurocysticercosis is
occasionally reported from Israel and ple from South America has caused a endemic in most Latin
Muslim countries of Africa and Asia recent increase in the prevalence of American countries,
(Figure 8-1). Neurocysticercosis was this parasitic disease.4 These and other sub-Saharan Africa,
rare in the United States and Western major cysticercosis outbreaks have re- and some regions
European countries up to 30 years ago. sulted from mass movement of people of Asia, including the
With the growing number of immigrants (or infected swine) from endemic to non- Indian subcontinent,
from endemic areas, an increased num- endemic areas (Figure 8-2). Indonesia, Vietnam,
ber of patients in these countries are While neurocysticercosis is still an Korea, and China.
estimated to have neurocysticercosis. important cause of admission to neuro- h In the United States,
These outbreaks, followed by an endemic logic hospitals and a major cause of ac- most cases of
nature of cysticercosis in the affected quired epilepsy, some recent evidence neurocysticercosis have
region, together with the appearance suggests that its prevalence is decreas- been reported from
ing in developing countries, not only the southwestern
of indigenous cases, are examples of
states, where more
the difficulties that exist to control a in urban centers but also at the rural
than 20 million Mexican
zoonotic disease once it has been estab- level. It has been considered that wide-
Americans live. Almost
lished. In the United States, most cases spread use of cysticidal drugs, im- 90% of patients with
have been reported from the south- proved sanitation, and increased neurocysticercosis
western states, where more than 20 mil- public awareness of the disease may diagnosed in the
lion Mexican Americans live. Almost be responsible for the recently recog- United States are
90% of patients with neurocysticercosis nized drop in the number of patients with immigrants from Mexico
diagnosed in the United States are immi- symptomatic neurocysticercosis in or South America.
grants from Mexico or South America.2,3 endemic areas.5,6

FIGURE 8-1 World map showing regions where neurocysticercosis is endemic.

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 Neurocysticercosis

KEY POINT
h The life cycle of Taenia
solium involves two
hosts: humans and pigs.
Humans are the only
definitive hosts for the
adult cestode, whereas
both pigs and humans
may act as intermediate
hosts for the larval form
called cysticercus.

FIGURE 8-2 World map showing major outbreaks of human cysticercosis related to mass
movement of people or infected swine from endemic to nonendemic areas. (1)
Return of British soldiers from India to England; (2) gift of infected swine from
Bali to Irian Jaya; (3) mass return of Portuguese living in African colonies after wars in Angola
and Mozambique; (4) migratory movements of people from Mexico and South America to the
United States (mainly to the southwestern and the New York City areas); (5) mass migration of
people from Ecuador, Perú, and Bolivia to Spain; (6) migration of people from India to countries
of the Arabian Peninsula (mainly Kuwait, Saudi Arabia, and Qatar).

ETIOPATHOGENESIS the only definitive hosts for the adult ces-

Life Cycle of Taenia Solium tode, whereas both pigs and humans may
The life cycle of T. solium involves two act as intermediate hosts for the larval
hosts: humans and pigs. Humans are form called cysticercus (Figure 8-3).

FIGURE 8-3 Diagram of major steps in the life cycle of Taenia solium.

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 FIGURE 8-4 Pigs roaming free in rural villages of
developing countries. In this way, pigs have
access to human feces, become infected with
Taenia solium eggs, and develop cysticercosis.

The head (scolex) of the adult solium is completed when humans

T. solium consists of four suckers and consume improperly stored and
a double crown of hooks, a narrow cooked pork meat infected with cys-
neck, and a body formed by hundreds ticerci (Figure 8-5). This process results
of proglottids. The adult parasite is in release of cysticerci in the small in-
attached to the intestinal wall by its testine where, by the action of digestive
potent suckers and hooks. Every few enzymes, scolices evaginate and attach
days, some gravid proglottids are to the intestinal wall, and proglottids
detached from the distal end of the
worm and passed with the feces. Each
proglottid liberates thousands of fertile
eggs that are resistant to the environ-
ment. In places with deficient disposal
of human feces, free-roaming pigs have
access to human feces containing T.
solium eggs (Figure 8-4). Once in the
intestinal tract of the pig, the eggs
liberate embryos (oncospheres), which
cross the intestinal wall, enter the
bloodstream, and are carried to the
tissues, where they evolve to form
metacestodes, which, in turn, evolve
into larvae (cysticerci). The larvae are
small vesicles that consist of two parts,
the vesicular wall and the scolex.7
Under these circumstances, pigs FIGURE 8-5 Consumption of undercooked pork meat
under poor sanitary conditions is a threat to
develop cysticercosis and become thousands of people living in rural villages of developing
intermediate hosts in the life cycle of countries.
T. solium. The normal life cycle of T.
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 Neurocysticercosis
FIGURE 8-6
membranes surrounded by dense mononuclear inflammatory
reaction. C, Dense exudate surrounding the brainstem and
the engulfing basilar artery.
KEY POINTS
h Human cysticercosis
should now be
considered as a disease
mostly transmitted from
person to person; the
role of infected pigs is
to perpetuate the
infection.
h It is common to find
cysticerci in different
involutive stages in the
same person. It is
unknown whether this
represents cysts of
different ages from
recurrent infections
or a single infection
in which only some
parasites have been
attacked by the host’s
immune system.
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Anatomopathologic findings in
neurocysticercosis. A, Vesicular cysts in brain
parenchyma. B, Subarachnoid parasitic
begin to multiply and become mature
approximately 4 months after the
infection.
Humans can also act as intermediate
hosts for T. solium after ingesting its
eggs, thereby allowing human cysticer-
cosis to develop. The mechanisms by
which eggs cross the intestinal wall and
lodge in human tissues are the same as
those described in the pig. Humans
most often acquire cysticercosis by the
fecal-oral route from a close contact har-
boring the adult parasite in the intestine.
Recent epidemiologic data showing
clustering of people with cysticercosis
around taeniasic individuals have changed
previous concepts crediting the environ-
ment as the main source of human con-
tamination with T. solium eggs.8 Human
cysticercosis should now be considered
as a disease mostly transmitted from
person to person; the role of infected
pigs is to perpetuate the infection.
Morphology and Stages
of Involution of Cysticerci
After entering the CNS, cysticerci are in
a vesicular (viable) stage in which the
parasites have a transparent membrane,
a clear vesicular fluid, and a normal in-
vaginated scolex (Figure 8-6A). Cysti-
cerci may remain viable for years or, as
the result of the host’s immunologic attack,
enter into a process of degeneration
that ends with their transformation into
inert nodules. It is also possible that the
immune attack can occur even before
the transformation of metacestodes into
vesicular cysticerci. Independently, if the
metacestode or the vesicular cyst
undergoes the immunologic attack
from the host, the first stage of involu-
tion of cysticerci is the colloidal stage, in
which the vesicular fluid becomes tur-
bid and the scolex shows signs of
hyaline degeneration. Thereafter, the
wall of the cyst thickens and the scolex
is transformed into mineralized gran-
ules; this stage, in which the cysticercus
is no longer viable, is called the granular
stage. Finally, the parasite remnants
appear as a calcified nodule. It is com-
mon to find cysticerci in different
involutive stages in the same individual.
It is unknown whether this represents
cysts of different ages from recurrent
infections or a single infection in which
only some parasites have been attacked
by the host’s immune system.
In some cysticercus, the scolex can-
not be identified. These parasites are
composed of several membranes at-
tached to each other that tend to group
in clusters resembling a bunch of grapes.
This form is called the racemose form of
cysticerci, and is usually observed in par-
asites located within the CSF cisterns at
the base of the brain, where they may
attain a large size.9 While the mecha-
nisms responsible for the transformation
of cysticerci from single vesicles to the
racemose form are not totally under-
stood, it is likely that scolices disappear
December 2012
and parasites grow as the result of a de-
generative process called hydropic de-
generation, caused by the continuous
entrance of CSF into the vesicles.
Tissue Reaction
Around Cysticerci
Parenchymal brain cysticerci in the
vesicular stage elicit a scarce perile-
sional inflammatory reaction that is
mainly composed of plasma cells, lym-
phocytes, and eosinophils. Colloidal cys-
ticerci are surrounded by a thick collagen
capsule and a mononuclear inflamma-
tory reaction that usually includes the
parasite itself. The surrounding brain
parenchyma shows an astrocytic gliosis
associated with microglial proliferation,
edema, neuronal degenerative changes,
and perivascular cuffing of lymphocytes.
When parasites enter into the granular
and calcified stages, the edema subsides
but the astrocytic changes in the vicinity
of the lesions may become more in-
tense, and epithelioid cells appear and
coalesce to form multinucleated giant
cells (Table 8-1).
Meningeal cysticerci usually elicit a
severe inflammatory reaction in the sub-
arachnoid space with formation of an
exudate composed of collagen fibers,
lymphocytes, multinucleated giant cells,
eosinophils, and hyalinized parasitic mem-
branes leading to abnormal thickening
of the leptomeninges (Figure 8-6B).
This inflammation may be dissemi-
nated, inducing damage in structures
distant to the site where the parasites
lodge. The optic chiasm and cranial
nerves arising from the brainstem are
encased in this leptomeningeal thick-
ening. The foramina of Luschka and
Magendie may also be occluded by the
thickened leptomeninges and parasitic
membranes, with the subsequent de-
velopment of obstructive hydrocephalus.
Intracranial vessels may also be
affected by the subarachnoid inflam-
matory reaction (Figure 8-6C) and cause
occlusion of the lumen of the vessel

TABLE 8-1 Correlation Between Appearance of Parasites and

Pathologic Changes in CNS According to Stage of
Involution of Parenchymal Brain Cysticerci

Stage of Pathologic Changes in

Involution Appearance of the Parasite the Brain Parenchyma
Vesicular Translucent vesicular wall Scarce inflammatory reaction
stage
Transparent vesicular fluid Formation of a thin collagen
capsule around the parasite
Viable invaginated scolex
Colloidal Thick vesicular wall Intense inflammatory reaction
stage that includes the parasite
Turbid vesicular fluid
Thick collagen capsule around
Scolex showing signs of
the parasite
hyaline degeneration
Granular Thick vesicular wall Astrocytic gliosis around the cyst
stage
Degenerated scolex Microglial proliferation
Calcified Transformation of the parasite Intense gliosis
stage in coarse calcified nodules
Multinucleated giant cells

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 Neurocysticercosis

KEY POINT
h Defining a typical
syndrome of
neurocysticercosis is
unrealistic. In endemic
areas this parasitic
disease has traditionally
been considered the
‘‘great imitator,’’ as it
may mimic almost any
neurologic disorder.
with the subsequent development of a
cerebral infarction.10
Ventricular cysticerci may also elicit
an inflammatory reaction if they are
attached to the choroid plexus or to the
ventricular wall. The ependymal lining
is disrupted, and proliferating subepen-
dymal glial cells protrude toward the
ventricular cavities, blocking the transit
of CSF, particularly when the site of
protrusion is at or near the foramina of
Monro or the cerebral aqueduct.9
Immune Response
Against Cysticerci
Some cysticercal antigens play a role in
the evasion of the immune surveillance
against the parasite. One of them, an-
tigen B, is a paramyosin with affinity for
collagen that may bind to C1q, inhibit-
ing the classic pathway of complement
activation. Since destruction of cysticerci
seems to be mediated by activation of
the complement cascade, antigen B
could play a role in the protection of
cysticerci against the host’s immuno-
logic attack. Host immunoglobulins have
been found around living intracranial
cysts, suggesting that cysticerci use these
molecules as a screen to avoid recogni-
tion from the immune system.
Some reports suggest the occur-
rence of cellular immune dysfunction
in patients with neurocysticercosis. This
impairment results from an increase in
the subpopulations of CD8 T lympho-
cytes, impaired proliferation of lympho-
cytes, and abnormal concentration of
cytokines. The depressed cellular immu-
nity may be responsible for the associa-
tion of neurocysticercosis with conditions
resulting from immunodeficiency states
and glial tumors. In the latter, the in-
tense glial proliferation around the para-
sites, along with the suppression of the
cellular immune responses, may cause
inhibition of the immunologic surveil-
lance against cancer, leading to malig-
nant transformation of astrocytes.11
CLINICAL MANIFESTATIONS
Neurocysticercosis may produce no
clinical manifestations at all or may be
severe enough to cause the death of the
patient. This pleomorphism is related
to individual differences in the num-
ber and location of the lesions as well
as in the severity of the host’s immune
response to the parasite. Therefore, defin-
ing a typical syndrome of neurocysticer-
cosis is unrealistic. In endemic areas this
parasitic disease has traditionally been con-
sidered the ‘‘great imitator,’’ as it may
mimic almost any neurologic disorder.12
A recent systematic review showed that
recurrent seizures occur in approximately
80% of symptomatic neurocysticercosis
cases, confirming previous findings that
epilepsy is the most common clinical man-
ifestation of the disease.13 Other man-
ifestations of neurocysticercosis include
focal neurologic deficits (16%), increased
intracranial pressure (12%), and cognitive
decline (5%). Cysticercosis outside the
CNS is not associated with clinical man-
ifestations, with the exception of ocular
cysticercosis and some cases with mas-
sive muscular involvement.12
Cysticercosis affects males and females
equally from infancy to old age, with a
peak incidence among middle-aged
adults. The course of the disease is some-
what different in infants and children
compared to adults, and neurocysticerco-
sis tends to be more severe in women.
The reasons for these findings are incom-
pletely understood; however, it is possi-
ble that the interaction of several factors,
including increased reactivity of the
immune system in children and women,
could be responsible for the age- and
gender-related observed differences in
the pattern of disease expression.
Geographic differences in the clinical
spectrum of the disease have also been
noted. For unclear reasons, subcutaneous
and muscular cysticercosis is observed
far more frequently in Asia and Africa
than in the Americas. Moreover, almost

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all reported patients with massive and
symptomatic infection of skeletal mus-
cles came from China and the Indian
subcontinent.14 Such geographic dif-
ferences have led to the suggestion of
possible strain differences of cysticerci;
however, other factors such as a more
severe burden of infection due to en-
vironmental, cultural, dietary, and nutri-
tional differences, as well as genetic
variations between populations, could
more suitably explain clinical differences
among African, Asian, and American pa-
tients with the disease.
Seizures/Epilepsy
Recurrent seizures usually represent
the primary or sole manifestation of
parenchymal brain cysticercosis.1,15 Neu-
rocysticercosis is a leading cause of
acquired epilepsy in endemic areas and
partly responsible for the increased
prevalence of epilepsy in the devel-
oping world.16Y18 While some series
have shown that most patients with
neurocysticercosis-related epilepsy
have generalized seizures, it is most
likely that those patients actually had
partial seizures with rapid secondary
generalization. Epileptogenesis in
neurocysticercosis has been a subject
of debate. While it has been suggested
that seizures occur when the parasites
begin to degenerate, large series have
shown that seizures may also occur in
patients who only have vesicular (viable)
cysts at the time of diagnosis.15 There
has also been debate about the risk of
recurrent seizures in patients with calci-
fied parenchymal brain cysticerci.19 While
calcifications have been considered inert
lesions, recent data suggest that calcified
cysticerci may cause recurrent seizures
when parasitic antigens trapped in the
calcium matrix are exposed to the host
immune system because of a process
of calcification remodeling, inducing in-
flammatory changes in the brain paren-
chyma.20,21 Recurrent seizures may
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KEY POINTS
also be the cause of hippocampal h Neurocysticercosis is
sclerosis, thus perpetuating the risk of a leading cause of
seizures.22 acquired epilepsy in
endemic areas and is
Focal Neurologic Deficits partly responsible for
Neurocysticercosis has been associated the increased
with almost any known focal deficit of prevalence of epilepsy
central origin, including motor and sen- in the developing world.
sory deficits, language disturbances, invol- h While calcifications have
untary movements, parkinsonian rigidity, been considered inert
gait disturbances, incoordination, and lesions, recent data
signs of brainstem dysfunction.13 Such suggest that calcified
deficits may be related to strategically cysticerci may cause
located parenchymal brain cysts or, most recurrent seizures
when parasitic antigens
often, to compressive effects of large sub-
trapped in the calcium
arachnoid cysticerci. Other patients pres-
matrix are exposed to
ent with focal signs of acute onset related the host immune system
to the occurrence of a cerebral infarct because of a process of
due to cysticercotic angiitis. Ischemic ce- calcification remodeling,
rebrovascular complications of neuro- inducing inflammatory
cysticercosis include lacunar infarcts and changes in the brain
large cerebral infarcts. Lacunar infarcts parenchyma.
occur as the result of inflammatory oc-
clusion of small perforating arteries at
the base of the brain and may be lo-
cated at the posterior limb of the inter-
nal capsule, the corona radiata, or the
brainstem; they produce typical lacu-
nar syndromes, clinically indistinguish-
able from those caused by hypertensive
arteriolopathy. Large cerebral infarcts
may be caused by occlusion of major
intracranial arteries; patients present
with profound focal neurologic deficits
secondary to an infarct involving basal
ganglia and cerebral cortex, or may de-
velop subacute dementia when both
anterior cerebral arteries are occluded.10
Cysticercotic arachnoiditis may also cause
entrapment of cranial nerves arising from
the ventral aspect of the brainstem. This
may cause extraocular muscle paralysis
due to damage of oculomotor nerves,
as well as sensorineural hearing loss,
facial palsy, or even trigeminal neuralgia
due to involvement of lower cranial
nerves. Neurocysticercosis of the spinal
canal also occurs with focal neurologic
signs, including weakness and sensory
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 Neurocysticercosis
KEY POINT
h The frequency of
positive stool
examinations for
T. solium eggs has
varied from one series
to another and seems
to be related to the
severity of infection.
Patients with heavy
infections have a
greater chance of also
having taeniasis.
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disturbances below the level of the
lesion that may be associated with
radicular pain when cysts are located
in the spinal subarachnoid space.23
Intracranial Hypertension
Various mechanisms explain the occur-
rence of increased intracranial pressure
in patients with neurocysticercosis.
The most common is hydrocephalus,
which, in turn, is most often related to
inflammatory occlusion of the Luschka
and Magendie foramina, although some
patients develop hydrocephalus be-
cause of blockage of CSF circulation by
ventricular cysts or ependymitis occlud-
ing Monro foramina or the cerebral
aqueduct.24 The clinical course of in-
creased intracranial hypertension in
patients with hydrocephalus due to
basal arachnoiditis is subacute or
chronic, while that of patients with
hydrocephalus related to fourth ven-
tricle cysts may be punctuated by
episodes of sudden loss of conscious-
ness related to movements of the head
(Bruns syndrome), and that of cerebral
aqueduct stenosis may be associated
with paroxysmal headache and Pari-
naud syndrome (Case 8-1).
Irrespective of their pathogenetic
mechanism, hydrocephalus is an omi-
nous sign associated with high mortality
rates.
Intracranial hypertension may also
be related to the occurrence of the so-
called cysticercotic encephalitis, which
is a severe form of parenchymal neuro-
cysticercosis that usually affects children
and young women (Case 8-2). Patients
with cysticercotic encephalitis present
with cloudiness of consciousness of acute
or subacute onset associated with sei-
zures, decreased visual acuity, headache,
vomiting, and papilledema.12
Cognitive Decline
Cognitive decline, ranging from poor
performance on neuropsychological
testing to severe dementia, may occur
in some patients with neurocysticercosis,
particularly in those with chronic normal
pressure hydrocephalus.12 Before the
introduction of CT, these patients were
admitted to psychiatric hospitals for
years until the correct diagnosis was
suspected because of the occurrence
of seizures or focal neurologic signs.
Some patients with parenchymal brain
lesions develop psychotic episodes char-
acterized by confusion, paranoid idea-
tion, psychomotor agitation, violent
behavior, and visual hallucinations;
some of these episodes could repre-
sent attacks of psychomotor epilepsy
or postictal psychosis.
DIAGNOSIS
Peripheral eosinophilia is a common,
albeit nonspecific, hematologic abnor-
mality in patients with neurocysticerco-
sis. The frequency of positive stool
examinations for T. solium eggs among
these patients has varied from one
series to another and seems to be re-
lated to the severity of infection. Pa-
tients with heavy infections have a
greater chance of also having taenia-
sis.25,26 Recognition of Taenia eggs is
not easy, and many patients may es-
cape detection when coproparasitologic
studies are performed. Specific coproan-
tigen detection by ELISA and PCR has
improved the screening for T. solium
carriers.27
Nonspecific abnormalities in the
cytochemical composition of CSF are
common in patients with neurocysti-
cercosis. These abnormalities directly
correlate with the activity of the disease
and with whether or not the parasites
are located in the subarachnoid space.
The most common finding is a moder-
ate mononuclear pleocytosis, with cell
counts rarely exceeding 300/2L. Mild
increase in CSF protein counts, usually
in the range of 50 mg/dL to 300 mg/dL,
is also common. CSF glucose levels are
December 2012
 Case 8-1
A 60-year-old woman was evaluated because of progressive headache and
vomiting. She had been admitted 2 months before at another hospital
because of hydrocephalus with asymmetric dilatation of the lateral ventricles,
as well as dilatation of the third and fourth ventricles. A right ventricular
shunt was placed with isolated reduction in the size of the right lateral
ventricle, and 15 days later, she underwent the placement of another
ventricular shunt, this time on the left side, with reduction in the size of left
lateral and third ventricles. However, because the fourth ventricle remained
dilated she was transferred to the present institution for further evaluation.
On admission, neurologic examination revealed abnormal downward gaze
and generalized increased muscle stretch reflexes with bilateral Babinski
signs. CT of the head showed collapse of both lateral ventricles resulting from
shunt placement and an abnormally dilated fourth ventricle (Figure 8-7). MRI
showed no evidence of a cystic lesion in the fourth ventricle. A serum
immunoblot test for the detection of anticysticercal antibodies was positive.
She underwent the placement of another shunt device for drainage of
the fourth ventricle, with progressive clinical improvement and further
reduction in the size of that ventricle.
Comment. This
woman had double
compartment
hydrocephalus
related to
simultaneous
occlusion of the
cerebral aqueduct
and the Luschka and
Magendie foramina.
She also had
ependymitis at the
FIGURE 8-7 CT scans of a patient with double
compartment hydrocephalus due to
level of the right
simultaneous occurrence of aqueductal stenosis and occlusion Monro foramen,
of Luschka and Magendie foramina. which explains the
fact that the first
ventricular shunt
only reduced the size of the right lateral ventricle, and it was only after
the second derivative procedure that the size of the left lateral and third
ventricle returned to normal. Double compartment hydrocephalus in
neurocysticercosis may also be related to a fourth ventricle cyst occluding
the CSF transit at both the cerebral aqueduct and the Luschka and Magendie
foramina levels. In this patient, the absence of a fourth ventricle cyst on
MRI and the finding of an incomplete Parinaud syndrome favored the
diagnosis of aqueductal stenosis, since fourth ventricle cysts have rarely, if
ever, been associated with Parinaud syndrome. Differential diagnosis between
these two pathogenetic mechanisms causing an isolated fourth ventricle in
patients with neurocysticercosis is important, as the therapeutic approaches
are completely different. For patients with a fourth ventricle cyst, endoscopic
resection of the lesion is advised. In contrast, multiple shunts are needed for
patients with segmental occlusion of the CSF transit at different levels because
of the simultaneous occurrence of ependymitis and basal arachnoiditis.

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 Neurocysticercosis

Case 8-2
A 20-year-old woman presented with a 1-week history of progressive headache, vomiting, and
somnolence. On admission, neurologic examination showed obtundation, bilateral papilledema
(Figure 8-8), increased muscle stretch reflexes, and bilateral Babinski signs. MRI showed diffuse brain
swelling with collapse of the ventricular system, and multiple small cysticerci disseminated through the
brain parenchyma with predominance of the cerebral cortex.
Lesions showed a ringlike pattern of enhancement after
contrast medium administration (Figure 8-9). Serum
immunoblot for the detection of anticysticercal antibodies was
strongly positive. ELISA and Western blot for the detection
of antibodies against HIV were negative. High doses of
dexamethasone (8 mg IV every 8 hours) and mannitol
(100 mL of a 20% solution every 6 hours) were started.
Standard doses of sodium phenytoin were also added to
the regimen. The patient improved over the next few days.
Mannitol was discontinued after 3 days, and IV
dexamethasone was switched to oral prednisone after 1 week.
She was discharged asymptomatic 2 weeks after admission.
Comment. This young woman had cysticercotic encephalitis,
FIGURE 8-8 Funduscopic examination a severe form of neurocysticercosis related to an intense
showing papilledema. inflammatory reaction from the host in response to massive
cysticerci infestation of the brain parenchyma. Diagnosis is
suspected on clinical and imaging grounds and must be confirmed by the practice of a serum immunoblot
test. It is also prudent to evaluate the HIV status of the patient, since Toxoplasma encephalitis or other
HIV-related opportunistic infections of the nervous system may occur with similar clinical and
neuroimaging
findings. Cysticidal
drugs are formally
contraindicated
in patients with
cysticercotic
encephalitis, as
therapy may
exacerbate the
inflammatory
reaction within the
brain parenchyma,
causing further FIGURE 8-9 MRI of patient with cysticercotic encephalitis. A, T1-weighted imaging showing
diffuse brain edema with collapse of the ventricular system. B, T2-weighted
increase in the imaging showing multiple colloidal parenchymal brain cysts surrounded by edema. C, After contrast
intracranial pressure administration, cysticerci appear as ring-enhancing lesions.
and death. In
contrast, prompt administration of corticosteroid and osmotic diuretics usually result in marked clinical
improvement. Decompressive craniotomies have been suggested for patients who do not respond to this
initial therapeutic approach. Patients who survive recover without sequelae, and further neuroimaging
studies from 3 to 6 months after the acute episode usually show complete resolution of lesions.

usually normal despite active meningeal Immunologic Diagnosis

disease. Hypoglycorrhachia, observed Immune diagnostic tests have been used
in a few patients, is associated with a to assess the prevalence of cysticercosis
poor prognosis. in populations and to exclude or confirm

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the diagnosis of neurocysticercosis in
neurologic patients with inconclusive
neuroimaging findings. The comple-
ment fixation test and the serum ELISA
are time-honored tests used for deca-
des to diagnose cysticercosis. These tests,
however, have been faced with prob-
lems related to poor sensitivity or
specificity. False-negative results are
due to local production of antibodies
within the CNS, without a parallel
increase of antibodies in peripheral
blood, or to immune tolerance to the
parasite without production of anticysti-
cercal antibodies at all. False-positive
results are due to previous contact
with the adult T. solium or to cross-
reactivity with other helminths.28
Enzyme-linked immunoelectro-
transfer blot assay for detection of
antibodies to T. solium glycoprotein
antigen in serum. The only reliable
serologic test for the detection of anti-
bodies specific for T. solium antigens is
the enzyme-linked immunoelectrotrans-
fer blot (EITB) using partially purified
antigenic extracts. The EITB has been ex-
tensively evaluated in different hospital-
based and population-based studies. This
assay has a documented specificity ap-
proaching 100% and a sensitivity of up
to 98% for patients with two or more
parasites in the nervous system. A major
weakness of the EITB is the high rate
of false-negative results (up to 50%) ob-
served in patients with a single intra-
cranial cysticercus.29 Sensitivity of the
EITB is also poor in patients with cal-
cified cysticerci. Since antibody assays
reflect cysticercus infection in any tis-
sue, not only patients with neurocysti-
cercosis but also those with muscular
or subcutaneous cysticercosis may test
positive. Consequently, results of the
EITB must be evaluated with caution,
since extraneural cysticercosis or even
exposure without infection may result
in antibody development. Paradoxically,
the sensitivity and specificity of antibody
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KEY POINTS
detection by EITB performed in CSF is h The only reliable
lower than that performed in serum, serologic test for the
even in patients with evidence of CNS detection of antibodies
involvement. specific for T. solium
ELISA for detection of anticysticer- antigens is the
cal antibodies or cysticercal antigens enzyme-linked
in CSF. Detection of anticysticercal anti- immunoelectrotransfer
bodies by ELISA using CSF is 87% sen- blot using partially
sitive and 95% specific, and remains a purified antigenic
relatively useful tool for the diagnosis extracts.
of neurocysticercosis in areas with h A major weakness of
limited access to the EITB assay. ELISA the enzyme-linked
may be falsely negative in patients with immunoelectrotransfer
only parenchymal brain lesions or in blot is the high rate of
false-negative results
those with inactive disease, and it may
(up to 50%) observed in
be falsely positive in patients with other
patients with a single
helminthic infections.28 intracranial cysticercus.
Detection of cysticercal antigens. Sensitivity of the
Detection of circulating parasitic anti- enzyme-linked
gens using monoclonal antibodies is immunoelectrotransfer
another immune diagnostic technique blot is also poor in
that has been used in some field studies. patients with calcified
However, detection of circulating anti- cysticerci.
gens is possible only in patients with
active disease. While the sensitivity of
this test as a screening tool for the di-
agnosis of neurocysticercosis is poor,
it may be of value to monitor the
response to cysticidal drug therapy.27
Some studies have also suggested that
this test may be useful for the demon-
stration of excretory-secretory cysticer-
cal antigens in CSF, as it has sensitivity
ranging from 72% to 86%, with false-
negative cases restricted to patients
with a single intracranial cysticercus
and inactive disease. However, the
specificity of this assay has not been
assessed in patients with other infec-
tions of the CNS.
Neuroimaging
The advent of modern neuroimaging
techniques has drastically improved
diagnostic accuracy for neurocysticer-
cosis. Both CT and MRI provide objec-
tive evidence on the topography of
lesions, the burden of infection, the
stage of involution of cysticerci, and the
www.aan.com/continuum 1403
 Neurocysticercosis

KEY POINTS
h CT remains the best
screening neuroimaging
procedure for patients
with suspected
neurocysticercosis,
since many patients
have parenchymal
brain calcifications as
the sole evidence of
the disease, and many
of these lesions may
escape detection if only Imaging findings in parenchymal brain cysticercosis. A, T1-weighted MRI of
FIGURE 8-10
an MRI is performed. vesicular cysticerci showing scolices. B, Contrast-enhanced MRI showing single
colloidal cysticercus. C, Plain CT showing parenchymal brain calcifications.
h Many vesicular cysts
have in their interior an
eccentric hyperdense
severity of the host’s inflammatory (Figure 8-10). Vesicular cysticerci ap-
nodule representing the
reaction against the parasites. While pear as small and rounded cystic lesions
scolex, giving the lesions
a pathognomonic
MRI is the preferred method for evalu- that are well demarcated from the sur-
‘‘hole-with-dot’’ ating patients with cystic lesions located rounding brain parenchyma. Imaging
appearance. in the ventricular system, the brain- shows little or no perilesional edema
stem, and the subarachnoid space, CT and no abnormal enhancement after
remains the best screening neuroimag- contrast-medium administration. Many
ing procedure for patients with sus- vesicular cysts have in their interior
pected neurocysticercosis, since many an eccentric hyperdense nodule repre-
patients have parenchymal brain calcifi- senting the scolex, giving the lesions
cations as the sole evidence of the a pathognomonic ‘‘hole-with-dot’’
disease, and many of these lesions appearance. When the infection is
may escape detection if only an MRI is massive, as in the so-called heavy non-
performed.30 encephalitic form of neurocysticerco-
Parenchymal neurocysticercosis. sis,25 the brain looks like a ‘‘Swiss
The stage of involution of parenchy- cheese,’’ another imaging finding that
mal brain cysticerci determines their is pathognomonic of neurocysticercosis
appearance on neuroimaging studies (Figure 8-11).

FIGURE 8-11 A, B, C, Contrast CT of patient with heavy nonencephalitic parenchymal brain

cysticercosis showing more than 100 vesicular cysts with no evidence of
abnormal enhancement or perilesional edema.

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 Colloidal cysticerci appear as ill-
defined lesions surrounded by edema,
and most of them show an abnor-
mal ring pattern of enhancement after
contrast medium administration. Since
the scolex is rarely visualized in colloi-
dal cysticerci using CT or conventional
MRI sequences, the presence of one
or two ring-enhancing lesions in the
brain parenchyma has generated much
debate in the literature and may repre-
sent a diagnostic challenge, as other
conditionsVtuberculomas, Toxoplasma
brain abscesses, primary or metastatic
brain tumorsVmay course with similar
neuroimaging findings.29 In doubtful
cases, the practice of diffusion-weighted
images and apparent diffusion coeffi-
cient maps facilitates the diagnosis by
allowing the recognition of the scolex
(Figure 8-12).31 Another particular
neuroimaging pattern of parenchymal
neurocysticercosis in the colloidal
stage is observed in patients with
cysticercotic encephalitis (Case 8-2).
In this severe form of the disease, both
CT and MRI show diffuse or multifocal
brain edema and collapse of the ven-
tricular system without midline shift.
After contrast administration, multi-
ple small nodular or ring-enhancing
lesions appear disseminated through
the brain parenchyma.
Parenchymal brain cysticerci may
also appear on CT as discretely hyper-
dense nodular-enhancing lesions sur-
rounded or not by edema. This pattern
corresponds to the granular stage of
cysticerci, which on MRI are often vi-
sualized as areas of signal void on both
T1- and T2-weighted images, surrounded
by hyperintense rims representing gli-
osis. Calcified cysticerci appear on CT
as small, hyperdense nodules without
perilesional edema or abnormal enhance-
ment after contrast-medium administra-
tion. As noted before, the sensitivity of
conventional MRI sequences for the de-
tection of calcified lesions is poor. Recent
evidence, however, suggests that the
use of susceptibility-weighted images
may enhance the identification of cal-
cifications by MRI.32
Subarachnoid neurocysticercosis.
Subarachnoid cysts are most often
small when located within cortical sulci
and may present with similar neuro-
imaging findings to those described for
parenchymal brain cysts, ie, cystic lesions
showing the scolex, ring-enhancing le-
sions, or calcifications. On the other
hand, cystic lesions located within the
sylvian fissures or at the CSF cisterns at
the base of the brain usually attain
a large size and have a multilobulated
appearance (the racemose form of

FIGURE 8-12 A, Contrast-enhanced imaging; B, diffusion-weighted imaging; and

C, apparent diffusion coefficient map of patient with colloidal parenchymal
cysticerci. Scolices are visualized only on the last two sequences.

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 Neurocysticercosis
KEY POINTS
h Cystic lesions located
within the sylvian
fissures or at the CSF
cisterns at the base of
the brain usually attain
a large size and have
a multilobulated
appearance (the
racemose form of
neurocysticercosis),
displacing neighboring
structures and behaving
as space-occupying
mass lesions.
h Cyst mobility within
the ventricular cavities
in response to
movements of the
head, the ventricular
migration sign,
facilitates the diagnosis
of ventricular
cysticercosis in
some cases.
FIGURE 8-14
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FIGURE 8-13 Imaging findings in subarachnoid cysticercosis. A, Contrast-enhanced CT
showing large cyst in sylvian fissure. B, Contrast-enhanced CT showing
hydrocephalus associated with cysts in CSF cisterns. C, T1-weighted MRI showing huge cyst
compressing brainstem.
neurocysticercosis), displacing neigh-
boring structures and behaving as space-
occupying mass lesions (Figure 8-13).
Another common finding in patients
with subarachnoid neurocysticercosis is
hydrocephalus caused by inflammatory
occlusion of the Luschka and Magen-
die foramina. The fibrous arachnoidi-
tis responsible for the development of
hydrocephalus is seen on CT or MRI as
areas of abnormal leptomeningeal en-
hancement at the base of the brain.24,30
Cerebrovascular complications of neu-
rocysticercosis are well visualized with
CT or MRI. In patients with cysticercosis-
Cysticercotic angiitis. A, Plain CT showing
infarct in territory of left anterior cerebral
artery. B, Angiogram showing segmental
narrowing of A1 segment of left anterior
cerebral artery.
related infarcts, the association of sub-
arachnoid cystic lesions (particularly at
the suprasellar cistern) or abnormal en-
hancement of basal leptomeninges sug-
gests the correct diagnosis.10 Angiographic
findings in subarachnoid neurocysticerco-
sis include segmental narrowing or oc-
clusion of the major intracranial arteries
in patients with infarcts (Figure 8-14)
or even in those lacking clinical or neu-
roimaging evidence of a cerebral infarct.
Magnetic resonance angiography is a
valuable noninvasive imaging modality
to demonstrate narrowing or occlusion
of intracranial arteries in patients with
subarachnoid neurocysticercosis.
Ventricular neurocysticercosis. Ven-
tricular cysticerci appear on CT as
hypodense lesions that distort the ven-
tricular system, causing asymmetric ob-
structive hydrocephalus. Ventricular
cysts are isodense with CSF; there-
fore, they cannot be directly visual-
ized (Figure 8-15). In contrast, most
ventricular cysts are readily visualized
on MRI because the signal properties
of the cystic fluid or the scolex dif-
fer from those of the CSF.30 Cyst mo-
bility within the ventricular cavities in
response to movements of the head,
the ventricular migration sign, facili-
tates the diagnosis of ventricular cysti-
cercosis in some cases. In other patients,
December 2012
 is not identified, however, it may be
difficult to differentiate this condi-
tion from spinal tumors. Leptomenin-
geal cysts are easily identified with MRI
(Figure 8-16). These lesions may be
freely mobile within the spinal subar-
achnoid space and change their posi-
tion during the examination according
to movements of the patient on the
exploration table.

Unification of
Diagnostic Criteria
Despite the introduction of the above-
FIGURE 8-15 Plain CT showing described immune diagnostic tests and
ventricular
cysticercus causing asymmetric
neuroimaging methods, the diagnosis of
dilatation of right lateral ventricle. neurocysticercosis can still be a challenge
because clinical manifestations are non-
specific, neuroimaging findings are often
not pathognomonic, and immune diag-
parasitic membranes or ventriculitis nostic tests are faced with problems
occlude the Monro foramina. In such related to poor sensitivity or specificity.
cases, it is common to observe Moreover, histologic demonstration of
asymmetric internal hydrocephalus, the parasite is not possible in most cases.
most often noticed after the placement During the second half of the 20th
of a ventricular shunt, as the lateral century, it was common in field studies
ventricle contralateral to the shunt to diagnose neurocysticercosis in pa-
remains dilated after the derivative tients presenting with seizures and
procedure. A particular finding in ven- a positive immunologic test for the
tricular cysticercosis is the so-called detection of anticysticercal antibodies
double compartment hydrocephalus,
in which the fourth ventricle is isolated
from the rest of ventricular cavities
because of simultaneous occlusion of
the cerebral aqueduct and the foramina
of Luschka and Magendie (Case 8-1).
Spinal cord neurocysticercosis.
While myelography and CT were used
for years for the diagnosis of spinal
cysticercosis, they are now of historical
significance since MRI has become the
imaging modality of choice for the
evaluation of patients with suspected
cysticercosis of the spinal cord or the
spinal subarachnoid space. On MRI, T1-weighted gadolinium
FIGURE 8-16
intramedullary cysticerci appear as contrast-enhanced MRI
of patient with spinal
rounded or septated lesions that may cysticercosis showing multiple hypointense
have an eccentric hyperintense nodule cystic lesions in the spinal canal.
representing the scolex.30 If the scolex
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 Neurocysticercosis
KEY POINTS
h Revised criteria for
the diagnosis of
neurocysticercosis include
four categoriesVabsolute,
major, minor, and
epidemiologicVstratified
on the basis of their
individual diagnostic
strength. Absolute criteria
allow unequivocal
diagnosis; major criteria
strongly suggest the
diagnosis but cannot be
used alone to confirm the
diagnosis; minor criteria
are frequent but
nonspecific manifestations
of the disease; and
epidemiologic criteria
refer to circumstantial
evidence favoring the
diagnosis.
h Accurate characterization
of neurocysticercosis in
terms of viability of cysts,
degree of the host’s
immune response to the
parasites, and location
of the lesions is important
for a rational therapy.
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in serum. Such practice could have
resulted in the inclusion of many pa-
tients who actually had cryptogenic
epilepsy and false-positive results on
immunologic testing. On the other
hand, some infected persons escaped
detection just because they had neg-
ative immunologic study results. In the
hospital setting, diagnosis of neurocys-
ticercosis usually rested only on neuro-
imaging findings. Using this approach,
neurocysticercosis could be overdiag-
nosed in endemic areas. In contrast, this
disease used to be overlooked in other
regions of the world simply because it
was rare. Such diagnostic pitfalls could
lead either to the progression of other
diseases requiring urgent therapy or to
the practice of unnecessary and inva-
sive diagnostic procedures.
In 1996, the first attempt to settle a
chart of diagnostic criteria for human
cysticercosis was published, based on
the objective evaluation of clinical,
radiologic, immunologic, and epide-
miologic data of patients.33 After some
years of experience, the same group of
investigators considered that chart to
be somewhat confusing and complex,
since it was developed for the diag-
nosis of patients with neurocysticerco-
sis as well as those with systemic
cysticercosis. With few exceptions, cys-
ticercosis outside the CNS is not clinically
relevant. Therefore, it was considered
that a more accurate and stringent set of
diagnostic criteria exclusively devoted to
the diagnosis of neurocysticercosis would
be more comprehensible than those
initially identified.34 As in the 1996
publication, revised criteria included four
categoriesVabsolute, major, minor, and
epidemiologicVstratified on the basis
of their individual diagnostic strength.
Absolute criteria allowed unequivocal
diagnosis of neurocysticercosis; major
criteria strongly suggested the diagno-
sis but could not be used alone to
confirm the diagnosis; minor criteria
were frequent but nonspecific manifes-
tations of the disease; and epidemio-
logic criteria referred to circumstantial
evidence favoring the diagnosis. Inter-
pretation of these criteria permitted
two degrees of diagnostic certainty: (1)
definitive diagnosis in patients who
had one absolute criterion or in those
who had two major plus one minor
and one epidemiologic criteria; and (2)
probable diagnosis in patients who
had one major plus two minor criteria,
in those who had one major plus one
minor and one epidemiologic criteria,
and in those who had three minor plus
one epidemiologic criteria (Table 8-2).34
This set of diagnostic criteria was
promptly adopted by the medical com-
munity and is now considered by many
as the gold standard for the diagnosis
of neurocysticercosis.
Advances in neuroimaging from the
time of that publication should be incor-
porated in the subheading of ‘‘highly
suggestive lesions’’ to enhance the di-
agnostic accuracy of MRI. These include
the use of diffusion-weighted imaging
to visualize the scolex in doubtful cases,
the use of susceptibility-weighted images
to enhance the identification of calcifica-
tions, and the practice of spectroscopy to
differentiate neurocysticercosis from
neurotuberculosis in selected cases.30Y32
THERAPY
Accurate characterization of neurocysti-
cercosis in terms of viability of cysts,
degree of the host’s immune response
to the parasites, and location of the
lesions is important for a rational ther-
apy.35 Therapeutic approaches may
include a combination of symptomatic
therapy, cysticidal drugs, surgical resec-
tion of lesions, and placement of ven-
tricular shunts. General strategies of
therapy described in Table 8-3 may
need some adjustment in the individual
patient, particularly in those who have
mixed forms of the disease.
December 2012
TABLE 8-2 Diagnostic Criteria for Neurocysticercosisa

b Diagnostic Criteria

& Absolute Criteria

Histologic demonstration of the parasite from biopsy of a brain or spinal
cord lesion

Evidence of cystic lesions showing the scolex on neuroimaging studies

Direct visualization of subretinal parasites by funduscopic examination

& Major Criteria

Evidence of lesions highly suggestive of neurocysticercosis on neuroimaging studies
Positive serum immunoblot for the detection of anticysticercal antibodies
Resolution of intracranial cystic lesions after therapy with albendazole or
praziquantel

Spontaneous resolution of small single-enhancing lesions

& Minor Criteria

Evidence of lesions suggestive of neurocysticercosis on neuroimaging studies
Presence of clinical manifestations suggestive of neurocysticercosis

Positive CSF ELISA for detection of anticysticercal antibodies or cysticercal antigens

Evidence of cysticercosis outside the CNS

& Epidemiologic Criteria

Individuals coming from or living in an area where cysticercosis is endemic
History of frequent travel to disease-endemic areas
Evidence of a household contact with Taenia solium infection

b Degrees of Diagnostic Certainty

& Definitive Diagnosis

Presence of one absolute criterion

Presence of two major plus one minor or one epidemiologic criteria

& Probable Diagnosis

Presence of one major plus two minor criteria

Presence of one major plus one minor and one epidemiologic criteria
Presence of three minor plus one epidemiologic criteria
a
Reprinted from Del Brutto OH, et al, Neurology.34 B 2001, with permission from American Academy of
Neurology. www.ncbi.nlm.nih.gov/pmc/articles/PMC2912527/.

Parenchymal Neurocysticercosis ous infections and should not be treated

Parenchymal brain calcifications. Cal- with cysticidal drugs. In cysticercosis-
cifications represent sequelae of previ- endemic areas, parenchymal brain

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 Neurocysticercosis

TABLE 8-3 General Guidelines for Therapy of Neurocysticercosisa

b Parenchymal Neurocysticercosis

& Vesicular Cysts

Single cyst: Use albendazole 15 mg/kg/d for 3 days or praziquantel 30 mg/kg in three divided
doses every 2 hours. Corticosteroids are rarely needed. Use antiepileptic drugs (AEDs) for seizures.

Mild to moderate infections: Use albendazole 15 mg/kg/d for 1 week or praziquantel

50 mg/kg/d for 15 days. Corticosteroids may be used when necessary. Use AEDs for seizures.
Heavy infections: Use albendazole 15 mg/kg/d for 1 week (repeated cycles of albendazole may be
needed). Corticosteroids are mandatory before, during, and after therapy. Use AEDs for seizures.

& Colloidal Cysts

Single cyst: Use albendazole 15 mg/kg/d for 3 days or praziquantel 30 mg/kg in three divided doses
every 2 hours. Corticosteroids may be used when necessary. Use AEDs for seizures.
Mild to moderate infections: Use albendazole 15 mg/kg/d for 1 week. Corticosteroids are usually
needed before and during therapy. Use AEDs for seizures.

Cysticercotic encephalitis: Cysticidal drugs are contraindicated. Use corticosteroids and osmotic diuretics to
reduce brain swelling. Use AEDs for seizures. Perform decompressive craniotomies in refractory cases.

& Granular and Calcified Cysticerci

Single or multiple: Cysticidal drug therapy is unnecessary. Use AEDs for seizures. Use corticosteroids in
patients with recurrent seizures and perilesional edema surrounding calcifications.
b Extraparenchymal Neurocysticercosis

& Small Cysts Over Convexity of Cerebral Hemispheres

Single or multiple: Use albendazole 15 mg/kg/d for 1 week. Corticosteroids may be used when
necessary. Use AEDs for seizures.

& Large Cysts in Sylvian Fissures or Basal CSF Cisterns

Racemose cysticercus: Use albendazole 15 mg/kg/d to 30 mg/kg/d for 15 to 30 days (repeated cycles
of albendazole may be needed). Corticosteroids are mandatory before, during, and after therapy.

& Other Forms of Extraparenchymal Neurocysticercosis

Hydrocephalus: Cysticidal drug therapy is unnecessary. Insert a ventricular shunt. Continual
corticosteroid administration (50 mg 3 times a week for up to 2 years) may be needed to reduce the
rate of shunt dysfunction.
Ventricular cysts: Perform endoscopic resection of cysts. Albendazole may be used only in small lesions
located in lateral ventricles. Ventricular shunt only needed in patients with associated ependymitis.
Angiitis, chronic arachnoiditis: Cysticidal drug therapy is unnecessary. Corticosteroids are mandatory.

Cysticercosis of the spine: Perform surgical resection of lesions. Anecdotal use of albendazole with
good results has been reported.
a
Level 1 evidence favors the use of cysticidal drugs in patients with parenchymal brain vesicular and colloidal cysts. For other forms
of the disease, guidelines are based on Level 2 and Level 3 evidence.

calcifications may be an incidental tients is unknown, prophylactic anti-

finding on neuroimaging studies. Since epileptic drug (AED) therapy is not
the actual risk of epilepsy in these pa- justified in such cases. In contrast,
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treatment with AEDs is advised when
parenchymal brain calcifications are
associated with seizures. In these cases,
the administration of a single AED
usually produces adequate seizure con-
trol.15 Length of AED therapy in
patients with epilepsy due to paren-
chymal brain calcifications remains
undefined as some studies have shown
that the risk of seizure recurrence after
AED withdrawal is high, even in patients
who had been seizure-free for 2 years.36
Neuroimaging studies performed imme-
diately after seizure relapse have shown
focal edema and abnormal contrast en-
hancement around previously inert cal-
cifications.19,20,36 As previously noted,
these observations suggest that paren-
chymal brain calcifications represent
permanent epileptogenic foci suscep-
tible to reactivation when the host im-
mune system is exposed to antigenic
material located in the interior of the
lesion.19 While epilepsy due to paren-
chymal brain calcifications is easily con-
trolled with AEDs, a seizure-free state
without medication seems to be diffi-
cult to achieve in many patients. These
patients should receive corticosteroids to
relieve the inflammatory reaction that is
causing recurrent seizures.19
Viable parenchymal brain (vesicular)
cysts. Vesicular cysts have reached a state
of immune tolerance with the host and
may remain for years in the brain
parenchyma. Therefore, the only way to
destroy these cysts is by the use of a
cysticidal drug (Figure 8-17). Level 1
evidence favors the use of cysticidal
drugs in such cases, as this approach
provides clinical improvement and res-
olution of lesions in most patients when
compared with placebo or no ther-
apy.37,38 The optimal therapeutic regimen
in such patients, however, is somewhat
uncertain.39 Current evidence seems
to favor the use of albendazole over
praziquantel; however, the latter is also
a potent drug that may be needed in
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KEY POINTS
some cases, particularly in albendazole h Calcifications represent
failures. The initial regimen of therapy for sequelae of previous
patients with parenchyma brain vesicu- infections and should
lar cysts mainly depends on the burden not be treated with
of infection. Levels 2 and 3 evidence cysticidal drugs.
favor the use of albendazole for 3 days or h While epilepsy due to
a single-day course of praziquantel ther- parenchymal brain
apy for patients with a single cyst, calcifications is easily
albendazole for 1 week or praziquan- controlled with
tel for 15 days for patients with mild to antiepileptic drugs, a
moderate infections, and albendazole seizure-free state
for 1 week for patients with heavy without medication
infections (Table 8-3). Repeated courses seems to be difficult
of therapy may be needed as control neu- to achieve in many
patients.
roimaging studies, performed 3 months
after the trial, showed persistence of h Vesicular cysts have
some lesions. In such cases, it is advised reached a state of
to give a different cysticidal drug than immune tolerance
with the host and
the one used in the first attempt.12
may remain for years
During the trial with cysticidal drugs,
in the brain parenchyma.
some patients develop headache, vomit- Therefore, the only
ing, or seizures. These manifestations way to destroy these
are related to the inflammatory reaction cysts is by the use of a
developed by the host in response to cysticidal drug.
destruction of the parasites and may
be anticipated in patients with more
than a few cysts in the brain paren-
chyma. Simultaneous use of corticoste-
roids usually results in control of these
adverse reactions.35 Likewise, patients
with epilepsy due to vesicular cysts
Contrast-enhanced CT of patient with
FIGURE 8-17
heavy infection of the brain parenchyma by
multiple vesicular cysticerci, before (A) and
3 months after (B) a trial with albendazole. Note the resolution
of most lesions as a result of therapy.
www.aan.com/continuum 1411
 Neurocysticercosis
KEY POINTS
h The use of albendazole
results not only in a
more expedited
resolution of colloidal
cysticerci, but also in a
reduction of the risk of
seizure recurrence in
most patients.
h Cysticidal drugs must
not be used in patients
with cysticercotic
encephalitis, since these
drugs may exacerbate
the inflammatory
response within the
brain parenchyma that
occurs in this severe
form of parenchymal
neurocysticercosis.
h Higher doses of
albendazole, more
prolonged courses of
therapy, or even repeated
cycles may be needed
for patients with
racemose cysticercus.
h Routine corticosteroid
administration is
mandatory when
treating patients with
large subarachnoid cysts
with albendazole, in
order to avoid the
hazard of a cerebral
infarct.
1412 www.aan.com/continuum
Copyright @ American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
must be treated with AEDs regardless
of the specific cysticidal drug used. The
length of AED therapy will depend on
whether the lesions disappear or are
transformed into calcifications as the
result of therapy.36
Dying parenchymal brain (colloidal)
cysts. Colloidal cysts are degenerating
parasites that result from the host’s im-
munologic attack, so the natural history
of most of these lesions would be to
vanish or end up as a calcified nod-
ule.29 While some of these lesions may
disappear without therapy, Level 1 evi-
dence also favors the use of cysticidal
drugs in these patients.38 According to
a number of double-blind trials, the use
of albendazole results not only in a
more expedited resolution of colloi-
dal cysticerci, but also in a reduction
of the risk of seizure recurrence in
most patients.40Y42 As described for pa-
tients with vesicular cysts, many patients
with colloidal cysts also experience ad-
verse reactions during the trial of cystici-
dal drugs. In such cases, simultaneous
administration of corticosteroids usu-
ally results in prompt relief of symp-
toms. The length of AED therapy will
also be related to whether colloidal cysts
vanished or were transformed into calci-
fied nodules as the result of therapy, as it
is generally accepted that in the latter
case, the risk of seizure recurrences
after AED withdrawal is high.29
Cysticidal drugs must not be used in
patients with cysticercotic encephalitis,
since these drugs may exacerbate the
inflammatory response within the brain
parenchyma that occurs in this severe
form of parenchymal neurocysticerco-
sis. High doses of corticosteroids and
osmotic diuretics are advised as the first
therapeutic measures in order to reduce
the severity of brain edema (Case 8-2).
This therapeutic approach should be
prolonged for 2 to 3 weeks until the
edema subsides. Refractory cases
should undergo decompressive cra-
niotomies to avoid the life-threatening
risk of intracranial hypertension.
Extraparenchymal
Neurocysticercosis
Subarachnoid cysts. Medical treatment
of small subarachnoid cysts over the
convexity of cerebral hemispheres is
similar to that described for parenchy-
mal brain cysts; the only difference is
that albendazole is the preferred drug
because it penetrates the subarachnoid
space better and reaches higher con-
centrations in the CSF than praziquan-
tel. Clinical experience with this form
of the disease is limited, but Level 2 evi-
dence suggests that the percentage of
small subarachnoid cysts disappearing
after albendazole treatment is similar
to that reported for parenchymal cysts.43
Treatment of giant cysts located in-
side CSF cisterns is controversial (Level 3
evidence). While some authors recom-
mend surgical resection of these le-
sions, it has been suggested that medical
therapy with albendazole may be an
equally effective albeit less aggressive
approach. Higher doses of albenda-
zole, more prolonged courses of ther-
apy, or even repeated cycles may be
needed for patients with racemose
cysticercus (Table 8-3).24,44,45 In addi-
tion to the dramatic improvement in-
duced by albendazole on neuroimaging
studies, reports have shown marked
improvement in the neurologic mani-
festations, mainly in focal neurologic
deficits, after therapy. Because of the
vicinity of blood vessels arising from
the circle of Willis, it is possible that the
inflammatory reaction that follows
destruction of the cysts enhances a
process of endarteritis resulting in a
cerebral infarct. Routine corticosteroid
administration is mandatory when
treating patients with large subarach-
noid cysts with albendazole to avoid
the hazard of a cerebral infarct. Corti-
costeroids must be given before the
December 2012

TABLE 8-4 Strategies for Elimination of Taeniasis and Cysticercosis
b Community Level
Improving living conditions
Health education and awareness of mechanisms of disease acquisition
Mass human chemotherapy (useless without education)
b Infected Pigs
Improved husbandry (pig corralling)
Slaughterhouse control
Control of illegal markets for infected pigs
Freezing of pork meat before human consumption
Mass chemotherapy of pigs
Pig vaccination
start of albendazole therapy, and their
use must be prolonged for several days
after the trial has been completed.24,44,45
Hydrocephalus. Patients with hydro-
cephalus due to cysticercotic arachnoidi-
tis require a ventricular shunt before other
therapeutic measures are attempted.35
In contrast, not all patients with hydro-
cephalus due to ventricular cysts need
a derivative procedure. In the latter, the
need for a ventricular shunt depends
on the location of the cyst and the co-
existence of granular ependymitis.
Patients with hydrocephalus due to cys-
ticercotic arachnoiditis usually have a
protracted course and a poor progno-
sis. The main problem in these cases is
the high frequency of shunt dysfunc-
tion. Mortality, which can be as high as
50% at 2 years, has been directly re-
lated to the number of surgical interven-
tions to change the shunt.24 Continuous
administration of prednisone may re-
duce the risk of shunt dysfunction (Level
3 evidence).
Ventricular cysts and ependymitis.
Depending on its size and location,
ventricular cysticercosis may be treated
by surgical resection or by cysticidal
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KEY POINTS
h Patients with
hydrocephalus due to
cysticercotic arachnoiditis
usually have a protracted
course and a poor
prognosis. The main
problem in these cases
is the high frequency of
shunt dysfunction.
Mortality, which can
be as high as 50% at
2 years, has been directly
related to the number
of surgical interventions
to change the shunt.
h The surgeon must
always consider the
possibility of cyst
migration within the
ventricular cavities from
the time of diagnosis
drugs. While some reports suggest that to the moment of
albendazole therapy destroys ventricu- surgery.
lar cysts, consensus guidelines, based on
Level 3 evidence, have favored surgical
resection of most of these lesions, with
the possible exception of small cysts lo-
cated in the lateral ventricle (a site where
the inflammatory reaction secondary to
destruction of the cyst is not danger-
ous).35 Surgical approaches include direct
excision of the cyst or endoscopic aspira-
tion using a flexible ventriculoscope.
The surgeon must always consider the
possibility of cyst migration within the
ventricular cavities from the time of di-
agnosis to the moment of surgery; there-
fore, it must be a routine practice to
obtain a control neuroimaging study im-
mediately before surgery to avoid an un-
necessary surgical procedure.
In patients without associated epen-
dymitis, permanent shunting procedures
are unnecessary after the excision of a
ventricular cyst. In contrast, placement
of a ventricular shunt must follow or
even precede excision of the cyst in
patients who also have granular epen-
dymitis. Surgical excision of a ventricular
cysticercus associated with ependymitis
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 Neurocysticercosis
KEY POINT
h Neurocysticercosis
eradication programs
must be directed to all
the targets for control,
particularly human
carriers of the adult
tapeworm, infected
pigs, and eggs in the
environment.
1414 www.aan.com/continuum
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is more difficult than excision of a freely
floating cyst, and it has been suggested
that the efforts of therapy must be
primarily directed to the resolution of
hydrocephalus by a ventricular shunt
and not to cyst removal. A peculiar form
of ventricular neurocysticercosis is dou-
ble compartment hydrocephalus, caused
by the dual effect of granular ependymitis
of the cerebral aqueduct and arachnoidi-
tis occluding the foramina of Luschka
and Magendie. In these patients, two
independent shunt devices may be
needed, with one draining the supra-
tentorial ventricular system and the
other draining the isolated fourth
ventricle (Case 8-1).
Spinal cysticercosis. Current accep-
ted therapy for intramedullary cysts
and cysts in the spinal subarachnoid
space is surgical resection of the lesion
(Level 3 evidence).12,35 Possible migra-
tion of spinal subarachnoid cysts be-
tween the time of diagnosis and the
laminectomy must be ruled out by re-
peating neuroimaging studies immedi-
ately before surgery. The prognosis after
surgery is usually good unless prolonged
compression of spinal nerve roots oc-
curred before diagnosis. Albendazole has
been used with good results in anecdotal
cases. Further experience with medical
treatment is needed before a clear rec-
ommendation can be made for either a
surgical or medical approach to this
form of the disease.
CONTROL MEASURES
As previously noted, neurocysticercosis
is common in areas where conditions
favoring the transmission of T. solium
are found, including warm climate, pov-
erty, deficient disposal of human feces,
low levels of education, slaughtering of
pigs without veterinary control, and
presence of free-roaming pigs around
households. Neurocysticercosis is a po-
tentially eradicable disease as was dem-
onstrated in European countries by the
end of the 19th century. To be effective,
however, eradication programs must be
directed to all the targets for control,
particularly human carriers of the adult
tapeworm, infected pigs, and eggs in the
environment (Table 8-4). Since these
targets represent interrelated steps in
the life cycle of T. solium, inadequate
coverage of one of them may result in a
rebound in the prevalence of taeniasis/
cysticercosis after the program has been
completed.5,46,47
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