Abstract

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Introduction
Cysticercosis is a parasitic infection that results from ingestion of eggs from the adult
tapeworm, Taenia solium (T. solium) (1,2). When cysticercosis involves the central nervous system,
it is called neurocysticercosis. Neurocysticercosis is the most common parasitic infection of the brain
and a leading cause of epilepsy in the developing world, especially Latin America, India, Africa, and
China (112).
Once largely the domain of the developing countries, neurocysticercosis is currently a growing public
health problem in the United States (13,14). Because millions of people have immigrated to the
United States from Latin America in recent years, neurocysticercosis has become an increasingly
important cause of seizures in the United States (14). For example, between 1994 and 1998, an
average of 120 patients with cysticercosis were admitted to Los Angeles County/USC Medical Center
per year (15,16), which was a substantial increase from 1983, when 80 cases were identified in all
four Los Angeles County hospitals together (13). Cysticercosis now accounts for up to 10% of
emergency room visits for seizures in the southwestern United States (14).
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Natural History
Neurocysticercosis is acquired through consumption of food contaminated with feces of a T.
soliumtapeworm carrier (i.e., through fecaloral contract) (4,5,12). The life cycle of T. solium is
shown in Fig. 1. Eggs of the tapeworm are shed in stool and contaminate food through poor hygiene.
When these eggs are ingested and exposed to gastric acid in the human stomach, they lose their
protective capsule and turn into larval cysts, called oncospheres. 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.

FIGURE 1
Life cycle of Taenia solium.
Figure 2 shows the four stages of cysts within the parenchyma of the brain: vesicular, colloidal,
nodular/granular, and calcified granulomas. The viable larval cyst is known as a vesicular cyst (Fig.
2A) and has minimal enhancement, which is due to little or no host immune response. At this stage,
the scolex usually is identified as an eccentric nodule within the cyst. As the cyst degenerates, fluid
from the larval cyst leaks into the parenchyma, generating a strong immune response, characterized
by enhancement on contrast computed tomography (CT) and magnetic resonance imaging (MRI).
An enhancing cyst, without a well-defined scolex, is termed a colloidal cyst (Fig. 2B). As the cyst
further deteriorates, it forms a nodule, which continues to demonstrate contrast enhancement (Fig.
2C). Finally the degenerating cyst forms a calcified granuloma, which is recognized as nonenhancing
punctuate calcifications on CT (Fig. 2D). Cysts that lodge in the cisterns or ventricles of the brain
may cause hydrocephalus and frequently do not have a scolex (e.g., racemic cysts).

FIGURE 2
Brain imaging demonstrating the four stages of parenchymal neurocysticercosis. A: Magnetic
resonance imaging (MRI) of a vesicular cyst. Note the well-defined scolex, minimal contrast
enhancement, and mass effect. B: MRI of a colloidal cyst. Note ring...
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Presentation
Neurocysticercosis typically is first seen either with seizures (70% to 90% of acutely symptomatic
patients) or headache (4,5,7,11,12). Headache usually indicates the presence of hydrocephalus,
meningitis, or increased intracranial pressure. When hydrocephalus is present, the use of
antiparasitic drugs is relatively contraindicated, unless a shunt is placed before administration. The
mortality rate of patients with hydrocephalus or increased intracranial pressure is higher than the
mortality rate of patients with seizures (16).
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Epileptogenesis in Neurocysticercosis
Generally, patients with neurocysticercosis have partial-onset seizures with or without secondary
generalization (6). At the time of a first seizure, most patients have an active cysteither a vesicular
cyst (Fig. 2A) or a colloidal cyst (Fig. 2B) (11). New-onset seizures are commonly associated with
active cysts rather than calcified granulomas (11,19). Chronic epilepsy is usually associated with
calcified granulomas (6,11,1719). Cysts that are active and undergoing degeneration (colloidal cysts)
are the most epileptogenic. Cysts degenerate fastest within 6 to 12 months after initial presentation
(19). Seizure-recurrence rates also increase during the same period, because of the conversion from
vesicular cysts to colloidal cysts (19). Animal data support the concept that active or degenerating
cysts (vesicular or colloidal) are the most epileptogenic (20). Products from acute cysts injected into
animal brains are significantly more epileptogenic than are products from chronic granulomas (20).
Epileptogenesis in patients with neurocysticercosis can be attributed to several factors:
inflammation, gliosis, genetics, and predilection for the cysts to travel to the frontal and temporal
lobes (17,18,2023). The host response to degenerating cysts plays an important role in the
associated epileptogenesis (22). In children and young women, a profound host reaction develops to
parasitic infection of the brain, whereas adults have a more variable response. Within-subject
responses also vary. For example, in the same patient, intense inflammation may surround one cyst,
whereas an adjacent cyst may show no inflammation (17,19).
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Treatment
Albendazole and praziquantel are the principal antiparasitic drugs used to treat neurocysticercosis
(1,2,12,19,2227). Whether and when antiparasitic drugs should be administered is controversial.
Data from open-label trials suggest that praziquantel and albendazole reduce the number of cysts
and frequency of seizures (2325,30). In a seminal study, Vasquez and Sotelo (30) found that
seizure-free rates at 3 years, for those offered antiparasitic therapy, were significantly higher than
those of a nonrandomized control group (94% seizure free). This finding is supported by data from
Del Brutto et al. (11), who found that 83% of those individuals who received antiparasitic treatment
became seizure free, compared with only 26% of those patients who did not receive treatment.
Some authors suggest that antiparasitic treatment might be counterproductive and expose patients
to increased risk (12,27). The risks of antiparasitic therapy include gastrointestinal side effects, acute
seizures, increased intracranial pressure, and rarely, death (1,12,16,26). Side effects, although usually
mild, include nausea, headache, seizures, and occasionally, cerebral edema (26,27). 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) (16).
In the first randomized comparison of albendazole, praziquantel, and steroids for the treatment of
active cysts, Carpio (27) found no significant difference in seizure-free rates among the three
treatment groups.
Recently, however, the Cysticercosis Working Group in Peru compared the efficacy and safety of
albendazole (400 mg twice a day) with placebo for the treatment of active cysts associated with
seizures (31). As in the study of Carpio et al., total seizure-recurrence rates at long-term follow-up
were no different for the active and control groups (27,31). However, patients randomized to
albendazole experienced a significant (67%) reduction in generalized tonicclonic seizures compared
with the control group (31). Safety was excellent, and no deaths were reported. The low death rate
may have been due to the relatively small size of the study (n= 120; 60 in each treatment group) and
the exclusion of patients with increased intracranial pressure. This study is a major advance, for it is
the first randomized, placebo-controlled clinical trial to demonstrate that albendazole substantially
reduces generalized tonicclonic seizure recurrence (31).
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Prognosis
In adults and children first seen with new-onset seizures and active cysts, seizure recurrence rates at
4 years are as high as 49% (19). After a second seizure, the estimated risk of recurrence is 68% at 6
years (19). 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%) (19). Seizure recurrence is reduced in patients who initially have calcifications
rather than active cysts (11,17,18). Del Brutto et al. (11) found that patients first seen with new-onset
seizures and calcifications fared better than those with active cysts: 100% with calcifications were
seizure free at 2 years, compared with 83% with active cysts. Durn et al. similarly found that among
25 patients initially seen with calcifications, seizures remitted in 62.8% (17).
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Conclusion
Neurocysticercosis is a leading cause of epilepsy in the developing world and is increasingly
prevalent in the United States. New data from the Cysticercosis Working Group indicate that
treatment with albendazole significantly improves the prognosis for the recurrence of generalized
tonicclonic seizures in highly selected patients. Results of this trial should not be applied to high-
risk patients, such as those with heavy cyst burden or increased intracranial pressure. Better
understanding of the mechanisms of neurocysticercosis and the life cycle of T. solium is needed to
develop appropriate intervention and prevention programs. Global strategies for prevention and
control should be developed and enforced with the aid of international health organizations,
including the World Health Organization.
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References
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1999. pp. 607630. Advances in neurology.
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Neurocysticercosis is the result of accidental ingestion of eggs of Taenia solium(ie, pork tapeworm), usually
due to contamination of food by people with taeniasis. In developing countries, neurocysticercosis is the most
common parasitic disease of the nervous system and is the main cause of acquired epilepsy. In the United
States, neurocysticercosis is mainly a disease of immigrants.
Essential update: The American Academy of Neurology issues a treatment guideline on
parenchymal neurocysticercosis
Guidelines issued in April 2013 by the American Academy of Neurology recommend use of albendazole plus a
corticosteroid for the treatment of parenchymal neurocysticercosis.
[1]
The guideline, which is also endorsed by
the American Epilepsy Society, recommends treatment with albendazole (400 mg twice daily for adults or
weight-based dosing for either adults or children) plus either dexamethasone or prednisolone to decrease the
number of active lesions on brain imaging studies and reduce long-term seizure frequency.
[2]

Signs and symptoms
Clinical manifestations of neurocysticercosis vary with the locations of the lesions, the number of parasites, and
the host's immune response.
[3]
Many patients are asymptomatic. Possible symptomatic presentations include
the following:
Epilepsy: Most common presentation (70%)
Headache, dizziness
Stroke
Neuropsychiatric dysfunction
Onset of most symptoms is usually subacute to chronic, but seizures present acutely
Abnormal physical findings, which occur in 20% or less of patients with neurocysticercosis, depend on where
the cyst is located in the nervous system and include the following:
Cognitive decline
Dysarthria
Extraocular movement palsy or paresis
Hemiparesis or hemiplegia, which may be related to stroke, or Todd paralysis
Hemisensory loss
Movement disorders
Hyper/hyporeflexia
Gait disturbances
Meningeal signs
See Clinical Presentation for more detail.
Diagnosis
Neurocysticercosis is commonly diagnosed with the routine use of diagnostic methods such as computed
tomography (CT) and magnetic resonance imaging (MRI) of the brain.
Imaging studies
CT findings vary as follows, depending on the stage of evolution of the infestation:
Vesicular stage (viable larva): Hypodense, nonenhancing lesions
Colloidal stage (larval degeneration): Hypodense/isodense lesions with peripheral enhancement and
perilesional edema
Nodular-granular stage: Nodular-enhancing lesions
Cysticercotic encephalitis: Diffuse edema, collapsed ventricles, and multiple enhancing parenchymal lesions
Active parenchymal stage: The scolex within a cyst may appear as a hyperdense dot
Calcified stage: When the parasite dies, nodular parenchymal calcifications are seen
MRI is the imaging modality of choice for neurocysticercosis, especially for evaluation of intraventricular and
cisternal/subarachnoidal cysts. Findings on MRI include the following:
Vesicular stage: Cysts follow the CSF signal; T2 hyperintense scolex may be seen, with no edema and
usually no enhancement
Colloidal stage: Cysts are hyperintense to the CSF; there is surrounding edema, and the cyst wall enhances
Nodular-granular stage: The cyst wall thickens and retracts, there is a decrease in edema, and nodular or ring
enhancement is present
Lab studies
CSF analysis for neurocysticercosis is indicated in every patient presenting with new-onset seizures or
neurologic deficit in whom neuroimaging shows a solitary lesion but does not offer a definitive diagnosis. CSF
is contraindicated in cases of large cysts causing severe edema and displacement of brain structures, as well
as in lesions causing obstructive hydrocephalus.
CSF findings include the following:
Mononuclear pleocytosis
Normal or low glucose levels
Elevated protein levels
High IgG index
Oligoclonal bands, in some cases
Eosinophilia (5-500 cells/L); however, this also occurs in neurosyphilis and CNS tuberculosis
[4]

CSF ELISA for neurocysticercosis has a sensitivity of 50% and a specificity of 65%
Other tests are as follows:
Stool examination: 10-15% of neurocysticercosis patients have taeniasis
Brain biopsy: Necessary only in extreme cases
See Workup for more detail.
Management
Treatment of neurocysticercosis depends upon the viability of the cyst and its complications.
[5]
If the parasite is
dead, the approach is as follows:
Treatment is directed primarily against the symptoms
Anticonvulsants are used for management of seizures; monotherapy is usually sufficient
Duration of the treatment remains undefined
If the parasite is viable or active, treatment varies as follows:
Patients with vasculitis, arachnoiditis, or encephalitis: A course of steroids or immunosuppressants is
recommended before the use of anticysticercal drugs
Antiparasitic treatment
[6]
with albendazole is also useful in cysticercosis of the racemose type (ie, multiple
cysts in the basal cisterns)
Patients with parenchymal, subarachnoid, or spinal cysts and without complications (eg, chronic epilepsy,
headaches, neurologic deficits related to strokes, and hydrocephalus): anticysticercal treatment can be
considered, with the concomitant use of steroids
Multiple trials with anticysticercal treatment may be required for giant subarachnoid cysts
Patients with seizures due to viable parenchymal cysts: antiparasitic therapy
[7]

Indications for surgical intervention and recommended procedures are as follows:
Hydrocephalus due to an intraventricular cyst: Placement of a ventricular shunt, followed by surgical
extirpation of the cyst and subsequent medical treatment
[8]

Multiple cysts in the subarachnoid space (ie, the racemose form): Urgent surgical extirpation
Obstruction due to arachnoiditis: Placement of a ventricular shunt followed by administration of steroids and
subsequent medical therapy
See Treatment and Medication for more detail.
Image library
Computed tomographic (CT) scan of the brain in a patient who presented with an episode
of generalized tonic-clonic seizure. Note the calcified lesion in the left parieto-occipital region. Subsequent evaluation confirmed the
diagnosis of neurocysticercosis.
Background
Neurocysticercosis (NCC) is the most common parasitic disease of the nervous system and is the main cause
of acquired epilepsy in developing countries. It has also been a problem in industrialized countries because of
the immigration of tapeworm carriers from areas of endemic disease.
[9, 10]

Neurocysticercosis can be acquired via fecal-oral contact with carriers of the adult tapeworm Taenia solium.
This usually indicates the presence of a tapeworm carrier in the immediate environment (ie, household) or by
accidental ingestion of contaminated food. Cases of auto-ingestion, in which persons with taeniasis may ingest
the eggs of T solium into their intestine, have been reported.
An example of an image of human neurocysticercosis is provided below.
Massive nonencephalitic neurocysticercosis. Photo courtesy of Cysticercosis Working Group in
Peru.
See also Neuroimaging in Neurocysticercosis.
Pathophysiology
Neurocysticercosis is the result of accidental ingestion of eggs of Taenia solium(ie, pork tapeworm), usually
due to contamination of food by people with taeniasis.T solium has a 2-host biologic cycle, with humans as the
definitive hosts carrying the intestinal tapeworm, and pigs as the normal intermediate hosts harboring the
larvae or cysticerci. This parasite has a head (scolex) with 4 suckers and a double crown of hooks, an
unsegmented neck, and a large body with several hundreds of hermaphrodite proglottids.
Cysticerci are ingested by humans through poorly cooked infected pork. Cysts evaginate in the small intestine,
attach to the wall by its suckers and hooks, and develop strobila or chains of proglottids. From the distal end of
the strobila, fertile eggs are excreted into the gravid proglottids. Up to 60,000 eggs may be contained in a
proglottid.
Pigs ingest stool contaminated with Taenia eggs, the embryos actively cross the intestinal wall, get into the
bloodstream, and are transported to most tissues, where they reside as cysticerci. Larvae are found most
commonly in the central nervous system (CNS), but they can also be located in the eye, muscle, or
subcutaneous or other tissues.
Epidemiology
Neurocysticercosis is the most common parasitic infection of the central nervous system (CNS). Approximately
2.5 million people worldwide carry the adult tapeworm, and many more are infected with cysticerci.
In the United States, neurocysticercosis is mainly a disease of immigrants, and the disease is prevalent in the
states of California, Texas, and New Mexico. Neurocysticercosis represents a major cause of morbidity among
the Hispanic population. Although most of the cases have been diagnosed in persons of Hispanic origin, the
incidence is increasing in nonendemic countries because of travel to zones of endemic disease. Native cases
have also been reported, presumably because of ingestion of infected food that was handled by carriers of T
solium.
The incidence of neurocysticercosis has been steadily increasing in the United States. Although still mostly
prevalent in the southwestern United States, imported cases have been reported throughout the country.
Globally, neurocysticercosis is endemic in Central and South America, sub-Saharan Africa, and in some
regions of the Far East, including the Indian subcontinent, Indonesia, and China, reaching an incidence of 3.6%
in some regions. This disease is rare in Eastern and Central Europe, in North America (with the exception of
Mexico), and in Australia, Japan, and New Zealand, as well as in Israel and in the Muslim countries of Africa
and Asia.
Cysticercosis can be seen in immigrant populations with a relatively high frequency, as in the US Southwest
and South Africa, and subcutaneous cysticercosis is more common in Asian populations than in other peoples
of other areas of endemic disease. It is not clear whether this is due to variations in parasite strain or to those in
the host.
Although neurocysticercosis appears to affect men and women equally, there is some evidence to suggest that
inflammation around the parasites may be more severe in women than in men.
[11]
In addition, despite the fact
that neurocysticercosis appears to be the most frequent cause of seizures in children
[12]
and adults (peak
incidence, 30-40 y), the exact incidence in children is not known.
Prognosis
In most patients with neurocysticercosis, the prognosis is good. Associated seizures seem to improve after
treatment with anticysticercal drugs and, once treated, the seizures are controlled by a first-line antiepileptic
agent. Duration of treatment, however, is not defined.
No figures are available for the burden of mortality associated with neurocysticercosis. However, the
racemose
[13]
form of this diseasewhich appears macroscopically as groups of cysticerci, often in clusters that
resemble bunches of grapes located in the subarachnoid spaceis associated with poor prognosis and
elevated mortality rate (>20%).
Neurocysticercosis-associated epilepsy is an important cause of neurologic morbidity,
[14]
and chronic epilepsy is
one of the most frequent complications of neurocysticercosis. Others include headaches, neurologic deficits
related to strokes, and hydrocephalus. Patients with complications such as hydrocephalus, large cysts, multiple
lesions with edema, chronic meningitis, and vasculitis are acutely ill and do not respond very well to treatment.
Frequently, they have complications due to medical and surgical therapy.
Patient Education
Neurocysticercosis is a major public health problem in developing countries and is emerging as an increasingly
important condition in regions in which the disease is not endemic. Comprehensive programs of long-term
intervention involve appropriate legislation, health education, modernization of swine husbandry practices,
improvement of efficiency and coverage of meat inspection, provision of adequate sanitary facilities, and
measures to detect and treat human tapeworm carriers.
Political and economic realities in many communities where T solium is endemic today provide little hope that
all these goals can be achieved in the near future. However, short-term approaches can be effective in the
long-term, and these include educational campaigns in personal hygiene and general sanitation within the
disease-endemic area.
Note that the usual restrictions for patients with epilepsy would be applicable for patients with
neurocysticercosis presenting with seizures.