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Neurocysticercosis: A Review

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Original Article Nepal Journal of Neuroscience 3:80-84, 2007

Neurocysticercosis: A Review
Amit Agarawal, MCh
Department of Surgery Neurocysticercosis (NCC) is the most common parasitic
B.P.Koirala Institute of Health Sciences disease of the central nervous system and is a major cause
Dharan, Nepal of epilepsy and neurological morbidity in endemic areas of
Guru Prasad Khanal, MS the world. International travel and immigration are bringing
Department of Orthopedics neuro-cysticercosis to areas where it is not endemic and
B.P.Koirala Institute of Health Sciences incidence of NCC is increasing in the developed countries
Dharan, Nepal also. The diagnosis of neurocysticercosis is difficult because
clinical manifestations are nonspeciûc, most neuroimaging
Address for correspodence:
Amit ASgrawal, MS ûndings are not pathognomonic, and some serologic tests
Department of Surgery have low sensitivity and speciûcity. The treatment of
B.P.Koirala Institute of Health Sciences neurocysticercosis is controversial and depends on the
Dharan, Nepal clinical and neuroimaging features, as well as the extent
Email: dramit@gmail.com and severity of the associated inflammatory reaction.
Received, October 10, 2006 Albendazole and praziquantel are the principal antiparasitic
Accepted, November 25, 2006 drugs used to treat neurocysticercosis. However, better
understanding of the mechanisms of neurocysticercosis; the
life cycle of T. solium, and better sanitation habits of the
population are needed to develop appropriate intervention
and prevention programs. In this article we review the
current concepts in the management of neurocysticercosis.
Key Words: Cysticercosis, Neurocysticercosis, Taenia
solium

N
eurocysticercosis (NCC) is the most common
parasitic disease of the central nervous system.
NCC is a major cause of epilepsy and neurological
morbidity in endemic areas of the world. 1,2,3 It is rare in
non-endemic areas, so a high degree of awareness is
necessary for diagnosis. It is often benign and lesions can
resolve within months. 2 However in less developed
countries the diagnosis of neurocysticercosis is frequently
difficult because several other prevalent neurological
disorders can present with a similar clinical and
neuroimaging picture. 1 The preva-lence of
neurocysticercosis in some of these developing coun-tries
exceeds 10%, 4,5 where it accounts for up to 50% of cases of
late-onset epilepsy. 6 International travel and immigration
are bringing neuro-cysticercosis to areas where it is not
endemic. In this article we review the current concepts in
the management of neurocysticercosis.
Etio-pathology
Taenia solium is a two-host zoonotic cestode. The adult
stage is a 2-to 4-m-long tapeworm that lives in the small
intestine of humans. No other ûnal hosts are known for T.
solium tape-worms in nature. As in all cestodes, the gravid
proglottids at the terminal end of the worm are full of eggs
that are the source of infection with the larval stage, or
cysticercosis. The natural intermediate host is the pig,
harboring larval cysts anywhere in its body. Humans
become infected with cysts by accidental ingestion of T.
solium infective eggs by fecal-oral contamination. After
ingestion of Taenia eggs containing infective onco-spheres,
the parasites become established in the tissues as larval
cysts and reach their mature size in about 3 months. 7,8
Oncospheres cross the gastrointestinal tract and migrate
via the vascular system to the brain, muscle, eyes, and
other structures. Once in the brain, the larval cysts
(cysticerci) initially generate a minimal immune response
and may remain in the brain as viable cysts for years. 9 The
infection burden varies from a single lesion to several
hundreds, and lesions may range in size from a few
millimeters to several centimeters. 10, 11, 12 Laboratory studies
and information from other cestodes suggest that viable
cysts ac-tively modulate the host’s immune system to evade
destruction by it. 13, 14 Prevalence of cysticercosis and
taeniasis may be related with gender, age, residential area
as well as pork consumption and contact with the people
who infected with the adult worm. In addition, higher levels
of human infection are closely associated to porcine
cysticercosis and inadequate sanitary infrastructure. 15

80 Nepal Journal of Neuroscience, Volume 4, Number 1, 2007


Epileptogenesis in Neurocysticercosis
The pathophysiology of the seizures due to NCC is not
completely understood yet. In active and transitional forms,
seizures may be the consequence of compression or
inflammatory reaction. In inactive form, perilesional gliosis
is probably the cause of the seizures. Chronic inflam-matory
reaction sometimes takes several years to di-sappear and it
may have an important role in the pathophysiology of focal
epilepsy in NCC. 16,17 Generally, patients with
neurocysticercosis have partial-onset seizures with or
without secondary generalization. 6 At the time of a ûrst
seizure, most patients have an active cyst—either a
vesicular cyst or a colloidal cyst. 17 New-onset seizures are
commonly associated with active cysts rather than calciûed
granulomas. 17, 18 Chronic epilepsy is usually associated
with calciûed granulomas. 6, 17,18,19,20 Cysts that are active
and undergoing degeneration (colloidal cysts) are the most
epileptogenic. Cysts degenerate fastest within 6 to 12
months after initial presentation. 18 Seizure-recurrence rates
also increase during the same period, because of the
conversion from vesicular cysts to colloidal cysts. 18
Clinical Features
In most patients, neurocysticercosis seems to produce
symp-toms years after the initial invasion of the nervous
system by the parasite, by either inûammation around the
parasite, mass effect, or residual scarring. 21,22 There is a
clear associa-tion between inûammation around one or more
cysts and de-velopment of symptoms, especially with
regard to seizures. 14 Symptomatic disease results almost
exclusively from the in-vasion of the nervous system
(neurocysticercosis) and the eye and is clearly different in
parenchymal neurocysticercosis and extraparenchymal
neurocysticercosis.
Parenchymal Neurocysticercosis
Clinical manifestation of the disease is highly
pleiomorphic and non-specific according to the number
and location of worms infected in the CNS as well as the
stage of the infection. 23 The usual presentation of
parenchymal neurocysticercosis is with seizures, which can
be controlled with antiepileptic drug therapy. Occasionally,
the cysts may grow and produce a mass effect. 24,25,26 Viable
cysts are 10 to 20 mm in diameter, thin-walled sacks ûlled
with clear cyst ûuid. On imaging studies, the wall is not
visible and the ûuid is isodense with the cerebrospinal
ûuid. There is little or no evidence of perilesional
inûammation, and they do not en-hance with contrast media
on neuroimaging. As the parasite loses the ability to control
the host immune response, an inûammatory process begins.
Initially, the cysts show slight pericystic contrast
enhancement. Later they become markedly inûamed and
edematous and appear as ring-like or nodular areas of
enhancement after the injection of contrast. This phase
has been called “granulomatous cysticer-cosis, “cysticerci
in encephalitic phase,” or “enhancing le-sions.” Finally,
the cyst is processed by the cellular response, and its
remnants either are not detectable by imaging or be-come
calciûed lesions. “Giant” cysts, measuring more than 50
mm in diameter, are occasionally found, located pri-marily
Nepal Journal of Neuroscience, Volume 4, Number 1, 2007
Neurocysticercosis
in the Sylvian ûssure. Cysticercotic encephalitis is a rare
form of the disease in which patients have numerous
inûamed cysticerci, leading to diffuse, severe cerebral
edema. 26,27 Headache usually indicates the presence of
hy-drocephalus, meningitis, or increased intracranial
pressure. When hydrocephalus is present, the use of
antiparasitic drugs is relatively contraindicated, unless a
shunt is placed before ad-ministration. The mortality rate
of patients with hydrocephalus or increased intracranial
pressure is higher than the mortality rate of patients with
seizures. 28
Extraparenchymal Neurocysticercosis
Extraparenchymal infection may cause hydrocephalus by
mechanical obstruction of the ventricles or the basal
cisterns, either by the cysts them-selves or by an
inûammatory reaction (ependymitis and/or arachnoiditis).
The so-called racemose variety occurs in the ventricles or
basal cisterns and is characterized by abnormal growth of
cystic membranes with degeneration of the parasite’s head
(scolex). 26,27 Extraparenchymal neurocysticercosis includes
cysticerci in the ventricles and basal cisterns (racemose
cysticercosis. Since the cyst membrane is thin and the ûuid
is isodense with the cerebrospinal ûuid, uninûamed
extraparenchymal cys-ticerci are usually not visible on CT
and may only reveal subtle, indirect ûndings on MRI. Scans
may reveal hydrocephalus without noticeable cysts,
ependymitis, distorted basal cisterns, or basal meningitis.
29,30,31
Diagnosis
The diagnosis of neurocysticercosis is difûcult because
clin-ical manifestations are nonspeciûc, most neuroimaging
ûnd-ings are not pathognomonic, and some serologic tests
have low sensitivity and speciûcity. 32,33 NCC is diagnosed
largely by characteristic neuroimaging findings such as
computerized tomography (CT) and magnetic resonance
(MR). Since the number, size and location of the infected
cysts and stage of infections are variable in many patients,
however, imaging diagnosis is often confusing and
inconclusive in some extents. In such cases, detection of
specific antibodies circulated in the sera or cerebrospinal
fluids (CSF) by enzyme linked immunosorbent assay
(ELISA) or by immunoblot is helpful to confirm or to exclude
the diagnosis. In addition, serological test is useful for
epidemiological survey in a large scale in endemic areas
due to its easy applicability and high reproducibility. 25
Cystic hydatid disease almost always appears on CT/MRI
as a single, large, spherical, and nonenhancing intracranial
cyst. This is a very rare form of presentation of T. solium
cysticercosis. Also, the current assay of choice,
immunoblot, does not cross-react with echinococco-sis.
Other condition that may resemble T. solium cysticercosis
from the clinical and neuroimaging points of view is
coenuro-sis, an extremely rare condition caused by the
cestode Multi-ceps multiceps. 32,33
Neuroimaging has attained enormous progress du-ring
last decade. Despite that, CT is very helpful in NC because
it is a safe, precise and noninvasive method with more than
95% accuracy to define number, localization and
81
Agrawal & Khanal
evolutionary stage of the parasite, especially in the
parenchymal form of the disease. 34 In developing countries
where MRI machines are not always available, and
considering the fact that calcifications are the main
radiological finding in NC, CT is still the most performed
and useful examination.
Management
The treatment of neurocysticercosis is controversial and
depends on the clinical and neuroimaging features, as
well as the extent and severity of the associated
inflammatory reaction. 35 Albendazole and praziquantel are
the principal antipara-sitic drugs used to treat
neurocysticercosis. 18,36,37,38,39 Whether and when
antiparasitic drugs should be administered is
controversial. Data from open-label trials suggest that
prazi-quantel and albendazole reduce the number of cysts
and fre-quency of seizures. 38,40,41,42 In a seminal study,
Vasquez and Sotelo found that seizure-free rates at 3 years,
for those offered antiparasitic therapy, were signiûcantly
higher than those of a nonrandomized control group (94%
seizure free). 42 This ûnding is supported by data from Del
Brutto et al., who found that 83% of those individuals
who received antiparasitic treatment became seizure free,
com-pared with only 26% of those patients who did not
receive treatment. 17 Some authors suggest that
antiparasitic treatment might be counterproductive and
expose patients to increased risk. 37 The risks of
antiparasitic therapy include gastrointestinal side effects,
acute seizures, increased intracranial pressure, and rarely,
death. 28,36,37,39 Side effects, although usually mild, include
nausea, headache, seizures, and occasionally, cerebral
edema. 39 Deaths associated with antiparasitic treatment
are rare (1% to 4%) and occur primarily in patients with
hydrocephalus, increased intracranial pressure, and heavy
cyst burden (i.e., more than 20 cysts). 28 In the ûrst
randomized comparison of al-bendazole, praziquantel, and
steroids for the treatment of active cysts, Carpio found
no signiûcant difference in seizure-free rates among the
three treatment groups. Recently, however, the
Cysticercosis Working Group in Peru compared the
efûcacy and safety of albendazole (400 mg twice a day)
with placebo for the treatment of active cysts as-sociated
with seizures. 43 However, patients randomized to
albendazole experienced a signiûcant (67%) reduction in
generalized tonic–clonic seizures compared with the
control group. 43
Surgery
Prior to the advent of antiparasitic drugs, surgery was
the primary therapy for neurocysticercosis, mainly open
surgery for excision of large cysts or cysts in the
ventricles. The role of surgical therapy in the management
of neurocysticer-cosis has signiûcantly decreased over
time and is now mainly restricted to placement of
ventricular shunts for hydrocephalus secondary to
neurocysticercosis. The main problem in these cases is
the high prevalence of shunt dysfunction; indeed, it is
common for patients with hydrocephalus secondary to
neuro-cysticercosis to have two or three shunt revisions.
82 Nepal Journal of Neuroscience, Volume 4, Number 1, 2007
Prognosis
In adults and children ûrst seen with new-onset
seizures and active cysts, seizure recurrence rates at 4
years are as high as 49%. 18 After a second seizure, the
estimated risk of recur-rence is 68% at 6 years. 18 Prognosis
is best for those patients in whom imaging studies
normalize. The recurrence rate for those patients with
persisting, active cysts (61%) is more than double the
rate of patients with normal imaging (22%). 18 Seizure
recurrence is reduced in patients who initially have
calciûcations rather than active cysts. 17,19,20 Del Brutto et
al. found that patients ûrst seen with new-onset seizures
and calciûcations fared better than those with active cysts:
100% with calciûcations were seizure free at 2 years,
compared with 83% with active cysts. 17 Dur´on et al.
similarly found that among 25 patients initially seen with
calciûcations, seizures remitted in 62.8%. 19 Basal
subarachnoidal cysticercosis and racemose disease of
sylvian fissure may behave aggressively producing
intracranial hypertension, obstructive hydrocephalus,
chronic arachnoiditis, vasculitis, and cerebral infarctions.
44
Subarachnoidal cysticercosis may have a chronic course
and a poor prognosis, and is still treated surgically. 45 Pre-
treatment with corticosteroids reduces the risk of
complications secondary to destruction of cysticerci. 44,46
Prevention Strategies
Cysticercosis is placed in the middle of sociocultural
studies related to poverty and ignorance. 47 Wandering
pigs are a common sight in destitute communities. In
contrast to other flocks, pigs can be fed human faeces,
are resistant to many adverse environmental conditions,
reach a large body size early in life, and are easily
domesticated. Additionally, the fact that these pigs are
fed human waste and the problem of wandering pigs,
which constitute the link in the life cycle of taenia-sis and
cysticercosis in humans is not as easy to break by simple
measures such as confiscating infected meat,
recommending the use of appropriate, but costly, pork
food, and sheltering of animals. 48 The most cost effective
perspective for eradication of cysticercosis, as with many
other diseases, is by edu-cation and public awareness of
the real source of infection. The ingestion of undercooked
pork infected with cysticerci is the exclusive path to the
development of intestinal taenia, which closes the life
cycle of the parasite. This misinformation poses obstacles
for cost effective preventive measures. 48 Public education
and sanitary measures are the essential factors for the
elimination. 48, 49
Conclusions
Neurocysticercosis is a leading cause of epilepsy in
the devel-oping world and is increasingly prevalent in the
developed countries also. Treatment with albendazole has
signiûcantly improved the outcome in patients with
neurocysticercosis. However better understand-ing of the
mechanisms of neurocysticercosis; the life cy-cle of T.
solium and life style and sanitation habits of the
population is needed to develop appropriate intervention
and prevention programs.

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