Review

Neurocysticercosis: updated concepts about an old disease

Hector H Garcia, Oscar H Del Brutto, for The Cysticercosis Working Group in Peru

Neurocysticercosis, the infection of the human brain by the larvae of Taenia solium, is a major cause of acquired Lancet Neurol 2005; 4: 653–61
epilepsy in most low-income countries. Cases of neurocysticercosis are becoming more common in high-income Cysticercosis Unit, Institute of
countries because of increased migration and travel. Diagnosis by neuroimaging and serological assessment has Neurological Sciences, Lima,
and Department of
greatly improved over the past decade, and the natural progression of the disease and response to antiparasitic drugs
Microbiology, Universidad
is now much better understood. Neurocysticercosis is potentially eradicable, and control interventions are underway Peruana Cayetano Heredia,
to eliminate this infection. Meanwhile, updated information on diagnosis and management of neurocysticercosis is Lima, Peru (H H Garcia MD);
required, especially for clinicians who are unfamiliar with its wide array of clinical presentations. Department of Clinical
Neurosciences, Hospital-Clinica
Kennedy, Guayaquil, Ecuador
Introduction contaminated with human faeces and thus T solium (O H Del Brutto MD)
Neurocysticercosis is an old disease. Known in ancient eggs. However, recent epidemiological evidence Correspondence to:
Greece as a disease of swine and since the 17th century suggests that the most common source of infective eggs Dr Hector H Garcia, Cysticercosis
as a human ailment, neurocysticercosis was not is a symptom-free tapeworm carrier in the household.8,9 Unit, Instituto de Ciencias
Neurológicas, Jr Ancash 1271,
considered a public health problem until the second half Therefore, cysticercosis should be seen as a disease
Barrios Altos, Lima 1, Peru
of the 20th century, when British investigators mostly transmitted from person to person, whereas the hgarcia@jhsph.edu
recognised the disease among soldiers returning from role of infected pigs is to perpetuate the infection. In the
India. Since then, hundreds of studies have described usual cycle of transmission of T solium, pigs have access
the epidemiological characteristics and the clinical to contaminated human stools by their coexistence with
manifestations of neurocysticercosis.1,2 During the past human beings in the domestic setting and the lack of
three decades, the introduction of modern diagnostic household sewage or sanitary facilities. Pig-to-pig
tools and potent cysticidal drugs has allowed accurate transmission has been recently described,10 but its effect
diagnosis and improved the prognosis for many on transmission pressure is not yet known.
patients.1,3 Figure 1 shows the larval cysts in the meat of an
Despite these advances in diagnosis and therapy, infected pig. The cyst consists of a scolex, or head, of the
neurocysticercosis remains endemic in most low- future tapeworm surrounded by a vesicle formed by the
income countries, where it represents one of the most extension of the parasite’s tegument (vesicular wall).11
common causes of acquired epilepsy.1 WHO has T solium is a 2–4 m flatworm that lives in the human
calculated that over 50 000 deaths are due to upper small intestine, most often without noticeable
neurocysticercosis each year, and many times this symptoms. It excretes eggs and proglottids irregularly,
number of people have active epilepsy, with all the social which if ingested cause cysticercosis. After ingestion,
and economic consequences that this implies.4 eggs hatch and liberate the embryos or oncospheres into
Neurocysticercosis is being diagnosed with increasing the intestine. Oncospheres actively cross the intestinal
frequency in high-income countries because of
increased migration of people with the disease5 or
tapeworm carriers,5,6 and because of tourism and travel
to endemic areas. It is also one of a few conditions
included in a list of potentially eradicable infectious
diseases of public-health importance,7 and control or
eradication programmes are urgently needed to reduce
its effect.

Life cycle of Taenia solium

Although the pig is the usual intermediate host of the
tapeworm Taenia solium, human cysticercosis occurs
when the eggs, which are excreted in the faeces of an
individual carrying the parasite, are ingested. A common
misconception is that one can acquire neurocysticercosis
by eating pork. However, ingestion of infected pork only
causes adult tapeworm infestation (taeniasis), because
infected pork contains the larval cysts that develop into
adult worms in human intestine, and does not contain
the eggs that cause cysticercosis. Transmission was
previously thought to be by indirect means, such as by
the ingestion of vegetables irrigated with water Figure 1: Infected pork showing multiple viable cysticerci

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 Review
wall, enter the bloodstream, and are carried into the
tissues of the host where they develop into larval cysts.
These cysts are rapidly destroyed by the host’s immune
system in most circumstances, except for those located
in immunologically privileged sites such as the eye and
the nervous system.12
Natural history
There is little information on the natural history of
human cysticercosis or neurocysticercosis. Data from
pigs show that cysts reach their maximum size in
2–3 months,13 and that while alive they trigger little
perilesional inflammation.14 However, most pigs are
slaughtered at about 9 months of age and thus this
model only reflects the early stages of the infection.15 In
human beings, the initial perspective of neuro-
cysticercosis (based on the few cases diagnosed by
radiography, and a series of cases attending surgery or
with the disease detected only at necropsy) was that of a
lethal, aggressive disease, mostly causing intractable
epilepsy and progressive intracranial hypertension.16
Two natural epidemiological scenarios helped to
understand the dynamics of infection and disease, at
least in part. Early in the 20th century, British troops
were sent on duty to India for defined periods of time.
Many (up to 450) of them or their direct relatives had
seizures and were studied by a special unit of the British
Army, which was able to find evidence of neuro-
cysticercosis in up to 75% of those with seizures.16,17
More importantly, the onset of neurological symptoms
was recorded according to the date of return to the UK (a
Figure 2: Diverse presentations of neurocysticercosis
Multiple viable cysts (vesicular stage; A); single enhancing lesion (degenerating cysts; B); multiple intraparenchymal calcifications (C); intraventricular cyst (D); basal
subarachnoid cysticercosis (extraparenchymal neurocysticercosis; E); cysticercotic encephalitis (extraparenchymal neurocysticercosis; F); ocular cysticercosis (G); and
muscle cysticercosis (H).
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cysticercosis-free country), and most individuals had
their initial seizure 2–5 years after their return,
suggesting a long latent stage. In a second, unrelated
episode in 1968, the King of Bali sent pigs as a pre-
electoral gift to the peasants of Papua New Guinea, an
island that was free of cysticercosis. 2 years later, a
sudden epidemic of burns was caused by people falling
into their bonfires because of seizures that occurred
while sleeping close to the fire. Necropsy studies of some
of these people confirmed neurocysticercosis as the
cause of the seizure disorder.18 These bouts of
neurocysticercosis, in cases for which the date of
infection could be traced, were evidence against
symptoms appearing at the time of initial exposure.
The introduction of CT and MRI unveiled a whole
spectrum of mild infections in symptom-free individuals
or in patients with sporadic seizures, which changed the
definition of neurocysticercosis from a fatal or severe
disease, to a less aggressive one. For example, in India,
most individuals with neurocysticercosis present with a
single degenerating cysticercus, whereas in Latin
America and China a substantial proportion of infected
individuals present with a few viable brain cysts.19
Recently, several studies with CT in endemic villages of
Latin America have found that 10–20% of symptom-free
villagers have one or more intraparenchymal brain
calcifications.20–24 We have hypothesised that in most mild
exposures the parasite dies in its early stages by action of
the host’s immune system, whereas a small subgroup of
infections (probably those with heavier egg challenges)
become established and survive as viable cysts.9
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General features of neurocysticercosis
Clinical description
Although neurocysticercosis can cause almost any
neurological symptom, late-onset epilepsy and
intracranial hypertension are its most common clinical
manifestations.25,26 Symptomatic neurocysticercosis
results from a combination of factors, including the
number, stage, and localisation of the parasites within
the nervous system, as well as the severity of the host’s
immune response against the parasites (figure 2).
Seizures occur in up to 70% of patients.26 Patients may
also present with intracranial hypertension that can be
associated with seizures, dementia, or focal signs.
Hydrocephalus, related to arachnoiditis, granular
ependymitis, or ventricular cysts, is the most common
cause of this syndrome.27 Intracranial hypertension also
occurs in patients with giant cysts and in those with the
rare form of cysticercotic encephalitis (resulting from
infection with many cysticerci inducing a severe
immune response from the host).28 Various focal
neurological findings may also occur in patients with
neurocysticercosis. Whereas focal signs usually follow a
subacute or chronic course, some patients present with
acute focal signs due to the occurrence of a
cerebrovascular event.29 Patients are likely to have
transient and fleeting focal neurological deficits that may
either be postictal or are elicited by acute inflammatory
responses to parasites.
Diagnosis
Diagnosis of neurocysticercosis is typically made on the
basis of neuroimaging studies and confirmatory
serological analysis. The most common neuroimaging
examination done in endemic areas is CT. The latest
generation of CT machines have fairly good diagnostic
sensitivity, although some small lesions, especially
those in the posterior fossa, close to the bone, or those
inside the ventricles or basal cisterns, may be missed.30
MRI has better accuracy, although it may miss some
small calcifications, and has the important pitfall of
being much more expensive and less available in areas
where the disease is endemic. Several serological assays
to detect specific antibodies have been used for decades
with different and somewhat conflicting results.31,32
Currently, most centres use an enzyme-linked
immunoelectrotransfer blot (EITB) with purified
glycoprotein antigens (western blot),33 which can be
done in serum samples or in CSF or use ELISAs in CSF
samples. An advantage of EITB is that its sensitivity in
serum samples is equal to or better than that in CSF
samples.34 Although EITB has 100% specificity and an
overall sensitivity of 98%, a major problem is that
approximately 30% of patients with a single brain
parasite may test negative.35 An interesting new
development is the introduction of antigen-detection
ELISA, although no concrete data on sensitivity and
specificity are yet available.36
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Review
Panel: Proposed diagnostic criteria for neurocysticercosis
Absolute
1 Histological demonstration of the parasite from biopsy of a brain or spinal-cord lesion
2 Cystic lesions showing the scolex on CT or MRI
3 Direct visualisation of subretinal parasites by funduscopic examination
Major
1 Lesions highly suggestive of neurocysticercosis on neuroimaging studies (ie, CT or MRI
showing cystic lesions without scolex, enhancing lesions, or typical parenchymal brain
calcifications)
2 Positive serum EITB (with purified extracts of T solium antigens) for the detection of
anticysticercal antibodies (assay developed by the Centers for Disease Control and
Prevention, Atlanta, GA, USA)
3 Resolution of intracranial cystic lesions after therapy with albendazole or praziquantel
4 Spontaneous resolution of small single enhancing lesions (ie, solitary ring-enhancing
lesions measuring less than 20 mm in diameter in patients presenting with seizures, a
normal neurological examination, and no evidence of an active systemic disease)
Minor
1 Lesions compatible with neurocysticercosis on neuroimaging studies (ie, CT or MRI
showing hydrocephalus or abnormal enhancement of the leptomeninges, and
myelograms showing multiple filling defects in the column of contrast medium)
2 Clinical manifestations suggestive of neurocysticercosis (ie, seizures, focal neurological
signs, intracranial hypertension, and dementia)
3 Positive CSF ELISA for detection of anticysticercal antibodies or cysticercal antigens
4 Cysticercosis outside the CNS (ie, histologically confirmed subcutaneous or muscular
cysticercosis, plain radiographic films showing cigar-shaped soft-tissue calcifications,
or direct visualisation of cysticerci in the anterior chamber of the eye)
Epidemiological
1 Evidence of a household contact with T solium infection
2 Individuals coming from or living in an area where cysticercosis is endemic
3 History of frequent travel to disease-endemic areas
Reproduced with permission from Lippincott Williams and Wilkins.37
A set of diagnostic criteria has recently been proposed
to help clinicians and health workers with the diagnosis
of neurocysticercosis.37 Proper interpretation of these
criteria permit two degrees of diagnostic certainty,
definitive or probable (panel).
Treatment
Treatment should be tailored according to the type of
neurocysticercosis (table).38 Physicians in charge of
patients with neurocysticercosis should always
remember that therapy includes a combination of
symptomatic and antiparasitic measures, including
analgesics, antiepileptic drugs (AEDs), cysticidal drugs,
surgical resection of lesions, and placement of
ventricular shunts.
The main point of controversy has been over the use of
cysticidal drugs, used since 1979.39–41 Praziquantel is most
often used at doses of 50 mg/kg/day for 15 days, but the
drug has been given in regimens of 10–100 mg/kg for
3–21 days,42 or even as a single-day regimen (based on
exposing cysticerci to very high concentrations of
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Treatment
Parenchymal neurocysticercosis
Vesicular cysts
Single Albendazole 15 mg/kg/day for 1 week, steroids used only if side-effects
occur; or praziquantel 100 mg/kg in three equal doses
Moderate infections Albendazole 15 mg/kg/day for 1 week, with simultaneous use of steroids.
Heavy infections (100 or more cysts) Albendazole 15 mg/kg/day for 1 week with high doses of steroids
Degenerating (colloidal) cysts
Single lesions Albendazole 15 mg/kg/day for 1 week, steroids used only if side-effects
occur; or no antiparasitic treatment
Moderate infections Albendazole 15 mg/kg/day for 1 week with steroids
Heavy infections (encephalitis) No antiparasitic treatment, high doses of steroids, osmotic diuretics
(mannitol)
Calcifications
Single or multiple No antiparasitic treatment
Extraparenchymal neurocysticercosis
Subarachnoid neurocysticercosis
Giant cyst (usually in Sylvian fissure) Albendazole 15 mg/kg/day for !1 month, with high doses of steroids;
or surgical excision
Basal subarachnoid (racemose) Albendazole 15 mg/kg/day for !1 month, with high doses of steroids.
Ventricular cysts Endoscopic aspiration or surgical resection, use of antiparasitic drugs is
controversial
Hydrocephalus No antiparasitic treatment, ventricular shunt
Arachnoiditis, angiitis No antiparasitic treatment, high doses of steroids for !1 month
Ependymitis No antiparasitic treatment, ventricular shunt if indicated, high doses of
steroids
Other forms of neurocysticercosis
Spinal cysts Surgical resection, albendazole may be used
Ocular cysts Surgical resection
Table: Treatment guidelines for the diverse forms of neurocysticercosis
praziquantel, by giving three doses of 25–30 mg/kg at 2 h
intervals).43 As a drawback, serum concentrations of
praziquantel decrease when steroids are also used.44
Albendazole was initially given at doses of 15 mg/kg/day
for 1 month.40 Further studies showed that at similar
doses, the length of therapy could be shortened to 1 week
without lessening the effectiveness of the drug.45,46 In
general, albendazole has higher parasiticidal effect than
does praziquantel.40 Cysticidal drug therapy has been
harshly criticised by some clinicians because treatment-
associated parasite death leads to an acute, severe
inflammatory reaction in the surrounding brain tissue,
increasing intracranial hypertension and potentially
leading to the death of the patient.47 Another major
argument against the use of cysticidal drugs has been that
there was no evidence that killing the parasites would lead
to fewer seizures during follow-up.48 However, as noted
below, current evidence favours their use in patients with
viable intraparenchymal or extraparenchymal parasites.49,50
The administration of a single first-line AED results
in seizure control in most patients with
neurocysticercosis-related epilepsy.26 However, the
optimum duration of antiepileptic drug therapy in these
patients has not been settled. Up to 50% of those
patients who remain seizure free for 2 years while on
AEDs will have relapses after AED withdrawal,
suggesting that intracranial cysticerci are permanent
substrates for seizures and may be reactivated when the
inhibitory influences of AEDs are absent.51 Prognostic
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factors associated with seizure recurrence include the
development of parenchymal brain calcifications, and
the presence of recurrent seizures and multiple brain
cysts before the institution of therapy.52 Although some
clinicians have proposed that AEDs could be
discontinued after 3 months of resolution of a single
brain-enhancing lesion,53 controlled data supporting
this affirmation are still required.53–55
Corticosteroids are the main form of therapy for
cysticercotic encephalitis, angiitis, and chronic meningitis
that causes progressive entrapment of cranial nerves56
(particularly for extraparenchymal neurocysticercosis).
Simultaneous administration of corticosteroids
ameliorates the secondary effects of headache and
vomiting that may occur during cysticidal drug therapy.
Such manifestations are not associated with the toxic
effects of the drugs but to the destruction of parasites
within the brain, and are reliable indicators of drug
efficacy. In patients with giant subarachnoid cysticerci,
ventricular cysts, spinal cysts, and multiple parenchymal
brain cysts, corticosteroids must be given before, during,
and even some days after the course of cysticidal drugs to
avoid the risk of cerebral infarcts, acute hydrocephalus,
spinal-cord swelling, or massive brain oedema.56
The most common surgical indication in
neurocysticercosis is ventricular shunting to resolve
hydrocephalus.57 Hydrocephalus secondary to neurocys-
ticercosis is associated with high rates of shunt
dysfunction; indeed, it is common for these patients to
have protracted courses of disease and high mortality,
correlated with the number of surgical interventions to
revise the shunt.58 Twice weekly prednisone treatment
reduces the risk of shunt dysfunction.59 Other surgical
indications include the excision of giant cysts or
intraventricular cysts.
Location of neurocysticercosis
One of the main problems in analysing the abundant
literature on neurocysticercosis is the generalisation of
concepts while ignoring the differences between the
disease types. Mixing different types of neuro-
cysticercosis leads to confusing assessments of accuracy
of diagnostic tests, therapeutic approaches, and
prognosis. To avoid the risks of unwarranted
generalisation, we have categorised the main clinical
presentations of neurocysticercosis, and describe their
associated clinical manifestations and specifics of
diagnosis, therapy, and prognosis. A major factor is
whether parasites are in the brain parenchyma or in
extraparenchymal structures.
Intraparenchymal cysts
Pathophysiology
Once established, the larval cysts actively evade the
host’s immune response through several mechanisms,
including inhibition of complement, cytokine release,
and masking with host immunoglobulins.60,61 Thus, only
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scarce inflammatory changes are seen in the
surrounding tissues. In this vesicular stage, parasites
look healthy and have a clear vesicular fluid (figure 2).
Viable cysticerci may remain alive for years, and a
substantial proportion of even those lesions with signs
of inflammation do not die for several months. At some
point, the host’s immune system and the inflammatory
response overcome the immune evasion mechanisms,
resulting in the death of the parasite.60,61
The first stage of involution of cysticerci is the colloidal
stage, in which the vesicular fluid becomes turbid, and
the scolex shows early signs of degeneration. Colloidal
cysticerci are surrounded by a thick collagen capsule and
the surrounding brain parenchyma shows astrocytic
gliosis and diffuse oedema.62 Thereafter, the wall of the
cyst thickens and the scolex is transformed into coarse
mineralised granules; this is called the granular stage. A
single brain cyst in the colloidal or granular stage
compose the so-called single enhancing lesions,
common in Indian patients.63,64 Finally, in the calcified
stage parasite remnants appear as a mineralised nodule.
When parasites enter the granular and calcified stages,
the oedema subsides, but astrocytic changes in the
vicinity of the lesions become more intense than in the
preceding stages.11,65
Imaging
On CT, viable cysts appear as hypodense, rounded, cystic
lesions. Some may enhance after administration of
contrast. The scolex can be occasionally seen as a
hyperintense dot in the interior of the cyst. On MRI, the
cysts are hypointense in T1 and FLAIR sequences, but
hyperintense in T2 sequences. MRI is better than CT to
show small cysts or those close to the skull or in the
posterior fossae. Degenerating cysts appear as contrast-
enhancing rings or nodules surrounded by areas of
brain oedema (figure 2). The scolex is not usually seen
using CT or MRI, creating some diagnostic confusion
with other infections or even with intracranial
neoplasms. FLAIR or diffusion-weighted MRI may allow
the visualisation of the scolex in some degenerating
cysts, facilitating the correct diagnosis in these cases
(figure 3). One of the most important (and difficult)
differential diagnoses of a single degenerating
cysticercus is a tuberculoma. Rajshekhar and Chandy66
have suggested that lesions measuring 20 mm or less
without a shift of the midline structures due to the
surrounding oedema are most probably due to
cysticercosis. Magnetic resonance spectroscopy seems to
detect a peak of lipids in tuberculomas67 not present in
degenerating cysticerci. Calcified cysts appear as
punctate hyperdense dots on CT, or as areas of
subtracted signal on MRI. Because of this, old MRI
methods had poor sensitivity to detect calcified
neurocysticercosis. At the time of a symptomatic relapse,
a third to a half of patients with calcified lesions only
may show oedema around at least one calcified lesion.68,69
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Review
Figure 3: New MRI techniques that may improve diagnostic accuracy for cysticercosis
FLAIR (left) and MRI with inversion recovery (right).
Because most cases of neurocysticercosis are already
calcified or will eventually resolve and become calcified,
this mechanism may be the main reason for morbidity
in neurocysticercosis.
Treatment
A single course of albendazole or praziquantel kills
60–85% of viable brain cysts.40,45,46,50 A recent
randomised, blinded, controlled trial with albendazole
showed the clinical benefit of decreased numbers of
seizures and enhanced resolution of cysts after
treatment, providing evidence for the use of cysticidal
drugs in patients with viable intracranial cysts.50 Several
randomised trials in Indian patients with single
enhancing lesions70–74 showed a non-significant but
consistent trend towards fast radiological resolution of
lesions and decreased likelihood of seizure relapse
(figure 4). Fast radiological resolution after cysticidal
treatment may be helpful in the management of
patients with single enhancing lesions, thus avoiding
diagnostic pitfalls.75 However, in most patients with
single enhancing lesions, the lesions disappear
spontaneously.76 Patients with cysticercotic encephalitis
should not receive cysticidal drugs because they may
exacerbate the intracranial hypertension observed in
this form of the disease.38 Finally, patients with
calcifications alone should not receive cysticidal drugs
because these lesions represent dead parasites (table).
Extraparenchymal neurocysticercosis
Extraparenchymal disease varies in its symptoms or
prognosis according to whether the parasites are located
in the convexity of the cerebral hemispheres, in the basal
subarachnoid space, in the sylvian fissure, or in the
ventricles. Intracranial hypertension is a common
manifestation of extraparenchymal neurocysticercosis
and may be due to mass effect, distortion of the normal
anatomy of CSF pathways, direct obstruction of the
ventricular system by a cyst, or inflammatory reaction in
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with a severe local inflammatory response with high

protein concentrations and cell counts in the CSF.78
Padma70 Other less common manifestations include basal
meningitis, ventriculitis, angiitis, or hydrocephalus with
no discernible cysts (commonly associated with
Baranwal71 inflammatory CSF and strong seropositivity). These
conditions seem to correspond to residual pathology
from old, resolved infections, although the reason for
Kalra72* the chronic inflammatory CSF response is unclear.
MRI is more accurate than CT for the diagnosis of
most cases of extraparenchymal neurocysticercosis.30
Gogia73† Coronal and sagittal sections allow better assessment of
areas infected by the parasites. Lesions may first appear
as multilobed cysts occupying the full space of the CSF
Singhi74
cistern. With further growth, the anatomy of that cistern
is disturbed and adjacent parenchymal structures get
0 2 4 6 8 10 compressed (figure 2). Cerebral infarctions may also be
Odds ratio imaged by either CT or MRI in patients with
cysticercotic arachnoiditis when an artery at the base of
the brain is occluded as the result of the inflammatory
Baranwal71 reaction surrounding the parasites.79
Subarachnoid or sylvian neurocysticercosis will progress
if not treated with cysticidal drugs. However, physicians
Kalra72* should be aware that the management of intracranial
hypertension, when present, is the priority. In patients
with both hydrocephalus and intracranial cysts, cysticidal
Gogia73† drugs should be used only after a ventricular shunt has
been placed to avoid further increases of the intracranial
pressure as a result of drug therapy. Cysticidal drugs must
Singhi74 be used with caution in patients with giant subarachnoid
cysts because the inflammatory reaction developed by the
host in response to the destruction of parasites may
0 1 2 3 4
occlude leptomeningeal vessels surrounding the cyst.80 In
Odds ratio
such cases, treatment with steroids is mandatory to avoid
the hazard of a cerebral infarct.
Figure 4: Treatment of neurocysticercosis with ABZ
Odds ratios for lesion disappearance (top) and seizure relapse (bottom) in randomised trials in patients with single
enhancing lesions treated with ABZ compared to placebo (three trials) or prednisone (three trials, one had both
Ventricular cysticercosis
types of controls). *Included some patients with two enhancing lesions; †data for patients with a single enhancing The manifestation of intraventricular cysts depends on
lesion only. the involved ventricle, and is more severe if the fourth
ventricle is occupied.81 Contrast-enhanced MRI is the
the meninges leading to arachnoiditis.27,77 Cysts in the examination of choice to rule out the existence of live
convexity of the cerebral hemispheres behave as cysts in the ventricles or basal cisterns. Hydrocephalus
intraparenchymal cysts. The other locations are can develop when CSF transit is blocked by parasitic
discussed separately below. membranes.30 In patients with ventricular cysts, the
therapeutic approach with cysticidal drugs should be
Basal subarachnoid neurocysticercosis or cysticercosis of the personalised. Although albendazole successfully
sylvian fissure destroys many ventricular cysts, the inflammatory
When cysts are located outside the brain parenchyma reaction surrounding those cysts may cause acute
they tend to grow irregularly and trigger a more severe hydrocephalus.81 Neuroendoscopic excision is a
inflammatory response. Giant cysts typically develop in promising alternative in cysticercosis of the lateral or
areas where more space is available, like the sylvian third ventricles,82–84 although it is used less in fourth
fissure or the CSF cisterns at the base of the brain, and ventricle cysts, for which microsurgery or antiparasitic
mostly behave as benign tumours due to their persisting treatment are still used in most centres. In the absence
growth.49 By far the worst prognosis is associated with of ependymitis, ventricular shunts are not needed after
basal subarachnoid neurocysticercosis, in which vesicles removal of a ventricular cyst in most cases. By contrast,
in CSF cisterns grow in a very disorganised way, shunt placement should follow or even precede the
infiltrate neighbouring structures, and are associated excision of ventricular cysts associated with ependymitis.

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Other locations
Patients with intrasellar cysticerci present with
ophthalmic and endocrinological disturbances similar to
those produced by pituitary tumours.85 Spinal
cysticercosis, mostly extramedullary, presents with root
pain or motor and sensory deficits that vary according to
the level of the lesion,86 and is most common in the
cervical segments.87–89 Ophthalmic cysticercosis is not
rare in endemic countries and is found in any of the eye
chambers (most commonly the retina or vitreous),
causing a decrease of visual acuity or visual field
defects.90,91 Massive cysticercal infection of striated
muscles may produce generalised weakness associated
with progressive muscle enlargement.1,92
Epidemiology and control
Despite occasional scepticism,93 most clinicians agree
that neurocysticercosis is the main cause of acquired
epilepsy in low-income countries and probably in the
world.94–96 The prevalence of epilepsy in endemic
countries is clearly higher than in North America or
Europe, although this could be due to other factors
including prenatal and delivery care, or other
infections.94 Recently, several articles from different
countries in South and Central America consistently
showed an association between around 30% of all
seizures and cysticercosis.23,24,97
Neurocysticercosis is potentially eradicable, and
several attempts to control it in field conditions have
been tried.15,98–103 Farmers use the examination of the
tongue of the pigs, a time-honoured technique that
detects most animals with heavy infections, to take them
to clandestine meat commercialisation circuits
(bypassing formal slaughterhouse systems).15 Mass
human chemotherapy to eliminate the tapeworm stage
has been tried in Ecuador, Mexico, Guatemala,
Honduras, Peru, and other countries.99–103 Most of these
programmes achieved only a temporal decrease in the
prevalence of cysticercosis (measured in the pig
population, which is the most sensitive and practical
indicator),15 and returned to preintervention levels soon
after the control pressure was interrupted. A wide-based
programme to eliminate cysticercosis in a province of
Peru is underway, funded by the Bill and Melinda Gates
Foundation. Major obstacles include the lack of basic
sanitary facilities in endemic areas, the extent of
domestic pig raising, the costs of the interventions, and
most importantly, their cultural acceptability.
Conclusions
Cysticercosis is a major cause of epileptic seizures in
most developing countries. Although there is little
information on its natural history, most types and
presentations of neurocysticercosis (depending on the
stage, number, location and size of the parasites, as well
as on the immune response of the host) are well defined.
For example, on the Indian subcontinent, most patients
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Search strategy and selection criteria
References for this review were identified by searches of
MEDLINE between 1969 and 2005, Old-MEDLINE since
1949, and references from relevant articles; numerous articles
were also identified through searches of the extensive files of
the authors. The search terms “cysticercosis”,
“neurocysticercosis”, “Taenia solium”, “albendazole”,
“praziquantel”, and “epilepsy” were used. Papers published in
English, Spanish, or Portuguese were reviewed. The final
reference list was generated on the basis of originality and
relevance to the topics covered in the review.
have a single degenerating cysticercus, whereas in Latin
America multiple viable cysts are common. To define
and to recognise these main clinical presentations is
central to the understanding of results of serological
tests and to appropriate medical and surgical treatment.
Appropriate management of intracraneal hypertension
or epileptic syndromes is the main aim of management
of patients with neurocysticercosis. Current evidence
favours the use of antiparasitic drugs in most patients
with viable or degenerating lesions, although in patients
with cysticercotic encephalitis this approach is counter-
indicated and in those with calcified lesions it is
unnecessary. In rural endemic communities, neuro-
cysticercosis seems to be symptomatic in only a few
cases, but the disease is an important cause of seizures
because the prevalence of infection is so high.
Neurocysticercosis is potentially eradicable, and control
or eradication programmes are urgently needed to
reduce the burden of this disease.
Acknowledgments
Research grants P01 AI51976, U01 AI35894, and TW05562 from the
US National Institutes of Health, 01107 from the US Food and Drug
Administration, 063109 from The Wellcome Trust, UK, and 23981 from
The Bill and Melinda Gates Foundation, USA, funded other
cysticercosis research by one of the authors (HHG). The sponsors had
no role in the design or writing of this manuscript. Figure 1 was kindly
provided by Dr A E Gonzalez.
Authors’ contribution
Both authors contributed equally.
Conflicts of interest
We have no conflicts of interest.
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