neurocyticercosis

8/12/2019 neurocyticercosis

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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. soliumis

shown inFig. 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 2shows 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
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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).
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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 withnormal 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).

Go to:

Conclusion

Neurocysticercosis is a leading cause of epilepsy in the developing world and is increasinglyprevalent 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. soliumis 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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Neurocysticercosis is the result of accidental ingestion of eggs of Taenia solium(ie, pork tapeworm), usuallydue to contamination of food by people with taeniasis. In developing countries, neurocysticercosis is the mostcommon parasitic disease of the nervous system and is the main cause of acquired epilepsy. In the UnitedStates, 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 acorticosteroid for the treatment of parenchymal neurocysticercosis.[1] The guideline, which is also endorsed bythe American Epilepsy Society, recommends treatment with albendazole (400 mg twice daily for adults orweight-based dosing for either adults or children) plus either dexamethasone or prednisolone to decrease thenumber 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, andthe host's immune response.[3] Many patients are asymptomatic. Possible symptomatic presentations includethe following:

Epilepsy: Most common presentation (70%) Headache, dizziness

Stroke

Neuropsychiatric dysfunctionOnset 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 wherethe 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 signsSeeClinical Presentationfor more detail.

Diagnosis

Neurocysticercosis is commonly diagnosed with the routine use of diagnostic methods such as computedtomography (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 andperilesional 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 seenMRI is the imaging modality of choice for neurocysticercosis, especially for evaluation of intraventricular andcisternal/subarachnoidal cysts. Findings on MRI include the following:
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Vesicular stage: Cysts follow the CSF signal; T2 hyperintense scolex may be seen, with no edema andusually 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 ringenhancement is present

Lab studies

CSF analysis for neurocysticercosis is indicated in every patient presenting with new-onset seizures orneurologic deficit in whom neuroimaging shows a solitary lesion but does not offer a definitive diagnosis. CSFis contraindicated in cases of large cysts causing severe edema and displacement of brain structures, as wellas 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 casesSeeWorkupfor more detail.

Management

Treatment of neurocysticercosis depends upon the viability of the cyst and its complications.[5] If the parasite isdead, 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 isrecommended before the use of anticysticercal drugs

Antiparasitic treatment[6] with albendazole is also useful in cysticercosis of the racemose type (ie, multiplecysts 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 beconsidered, 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 surgicalextirpation 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 andsubsequent medical therapy

SeeTreatmentandMedicationfor more detail.
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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 causeof acquired epilepsy in developing countries. It has also been a problem in industrialized countries because ofthe 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 byaccidental ingestion of contaminated food. Cases of auto-ingestion, in which persons with taeniasis may ingestthe eggs of T soliuminto 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 alsoNeuroimaging in Neurocysticercosis.

PathophysiologyNeurocysticercosis is the result of accidental ingestion of eggs of Taenia solium(ie, pork tapeworm), usuallydue to contamination of food by people with taeniasis.T soliumhas a 2-host biologic cycle, with humans as thedefinitive hosts carrying the intestinal tapeworm, and pigs as the normal intermediate hosts harboring thelarvae or cysticerci. This parasite has a head (scolex) with 4 suckers and a double crown of hooks, anunsegmented 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
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the strobila, fertile eggs are excreted into the gravid proglottids. Up to 60,000 eggs may be contained in aproglottid.

Pigs ingest stool contaminated with Taeniaeggs, the embryos actively cross the intestinal wall, get into thebloodstream, and are transported to most tissues, where they reside as cysticerci. Larvae are found mostcommonly in the central nervous system (CNS), but they can also be located in the eye, muscle, orsubcutaneous or other tissues.

Epidemiology

Neurocysticercosis is the most common parasitic infection of the central nervous system (CNS). Approximately2.5 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 thestates of California, Texas, and New Mexico. Neurocysticercosis represents a major cause of morbidity amongthe Hispanic population. Although most of the cases have been diagnosed in persons of Hispanic origin, theincidence is increasing in nonendemic countries because of travel to zones of endemic disease. Native caseshave also been reported, presumably because of ingestion of infected food that was handled by carriers of Tsolium.

The incidence of neurocysticercosis has been steadily increasing in the United States. Although still mostlyprevalent 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 someregions 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 ofMexico), and in Australia, Japan, and New Zealand, as well as in Israel and in the Muslim countries of Africaand Asia.

Cysticercosis can be seen in immigrant populations with a relatively high frequency, as in the US Southwestand South Africa, and subcutaneous cysticercosis is more common in Asian populations than in other peoplesof other areas of endemic disease. It is not clear whether this is due to variations in parasite strain or to those inthe host.

Although neurocysticercosis appears to affect men and women equally, there is some evidence to suggest thatinflammation around the parasites may be more severe in women than in men.[11] In addition, despite the factthat 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 aftertreatment with anticysticercal drugs and, once treated, the seizures are controlled by a first-line antiepilepticagent. Duration of treatment, however, is not defined.

No figures are available for the burden of mortality associated with neurocysticercosis. However, theracemose[13] form of this diseasewhich appears macroscopically as groups of cysticerci, often in clusters thatresemble bunches of grapes located in the subarachnoid spaceis associated with poor prognosis andelevated mortality rate (>20%).

Neurocysticercosis-associated epilepsy is an important cause of neurologic morbidity,[14] and chronic epilepsy isone 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, multiplelesions 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 increasinglyimportant condition in regions in which the disease is not endemic. Comprehensive programs of long-termintervention involve appropriate legislation, health education, modernization of swine husbandry practices,


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improvement of efficiency and coverage of meat inspection, provision of adequate sanitary facilities, andmeasures to detect and treat human tapeworm carriers.

Political and economic realities in many communities where T soliumis endemic today provide little hope thatall these goals can be achieved in the near future. However, short-term approaches can be effective in thelong-term, and these include educational campaigns in personal hygiene and general sanitation within thedisease-endemic area.

Note that the usual restrictions for patients with epilepsy would be applicable for patients withneurocysticercosis presenting with seizures.

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