Current Knowledge and Advances
Wayne X. Shandera, MD, and Joseph S. Kass, MD

Corresponding author
Wayne X. Shandera, MD
Department of Medicine, Section of General Medicine,
2RM-81-001, 1504 Taub Loop, Houston, TX 77030, USA.
Current Neurology and Neuroscience Reports 2006, 6:453 – 459
Current Science Inc. ISSN 1528-4042
Copyright © 2006 by Current Science Inc.

as host immunity. Therefore, a thorough understanding of
this common helminthic infection of the central nervous
system is critical in providing patients a proper standard
of care. In this article we review the epidemiology, basic
science, clinical manifestations, diagnosis, treatment, and
prevention of NCC.

History and Epidemiology
Neurocysticercosis is the most common cause of
acquired seizures worldwide. Most cases of this larval
stage infection of the pork tapeworm Taenia solium
occur in the developing world, although increasing
numbers of cases are being recognized in the United
States, particularly among Hispanic immigrants. The
ability of the pathogen to persist for years within the
host is the subject of immunologic and biochemical investigation. The major presenting symptom is
seizures, although symptoms of obstructive hydrocephalus occur if cysts are located near the ventricles
or in the subarachnoid spaces. Diagnosis is dependent
on clinical, radiologic, and serologic data. Therapy
with antiparasitic agents, especially albendazole, is
effective in large burden disease or disease within
sensitive neuraxis sites (the ventricles, the subarachnoid
spaces). When patients with radiologically enhancing
disease are given cysticidal therapy, there appears
to be a reduction in seizure recurrences. Surgery is
indicated for disease in selected anatomic sites. Longterm prevention requires attention to pork husbandry
and general sanitation, including the potential use of
mass human chemotherapy and porcine vaccination.

Many immigrants residing in the United States come from
countries where the pork tapeworm Taenia solium is
endemic. Hence, physicians in the United States increasingly encounter patients with complications of the larval
stage of T. solium infection, known as neurocysticercosis
(NCC). NCC is the leading cause of seizures in endemic
areas, but other complications may attend infection such
as hydrocephalus and cerebrovascular disease. Treatment
depends on the cyst characteristics and location, as well

Tapeworms were recognized in the time of Hippocrates but
it was German and Dutch investigators who elucidated their
life cycle in the eighteenth and nineteenth centuries. Johann
Goeze (1782) distinguished T. solium from T. saginata
(the beef tapeworm), and Rudolf Leuckart (1856) clarified
the role of transmitting the larval stage of infection from
pig into man [1]. Leuckart worked with Rudolf Virchow
to establish meat inspection laws in Germany in the
nineteenth century. Attention in the early twentieth century
was directed to the disease with the return from India of
British soldiers with a high rate of seizures, often years
after returning [2]. Only with the subsequent advent of
neuroimaging and therapeutics, including anticonvulsants
and cysticidal agents, did advances occur that increased
recognition and improved therapy for NCC.
The current epidemiology of NCC is studied by
assessing either T. solium infections in man (taeniasis) or cysticercal (larval) disease in either pigs or man
(cysticercosis). Serologic data are available from many
parts of the world. Radiologic studies are imperfect
for epidemiology because suspicious lesions may
not always indicate NCC. The best data are clinical
epidemiologic studies that are available from a few
geographic areas, with the strongest being those from
Mexico, Peru, and the United States [3–8]. The US
studies confirm a high prevalence of the disorder
among Hispanic immigrants, document the occasional
autochthonously transmitted case, and attest to a
slightly higher risk of tapeworm carriage among
contacts of US cases. Here we discuss the life cycle
of T. solium and the evolving global epidemiology of
taeniasis and neurocysticercosis.
The life cycle of T. solium is often misunderstood.
Adult tapeworms are the source of Taenia eggs, which are
excreted at a rate of 300,000 per day over a helminth’s

8 cases per 100. we review the nature of the host responses to NCC infection.6 cases per 100. when measures of immunity were studied in NCC patients. and possibly female gender [12]. Another Mexican study reported 500 new cases annually. In Central America.20].000 people between 1994 and 2000.26]. solium to evade the host immune response for long intervals. although most Latin American studies report rates under 3%. This phenomenon explains the occurrence of NCC among a group of Orthodox Jews exposed to a housekeeper from Latin America [14] and among 16 Muslims exposed to a non-Muslim cook in Kuwait [15]. To better understand this interplay between pathogen and host immune response. earthen floors. Risk factors for seropositivity in Peru include origin from highland and coastal villages. In addition. CT-enhancing lesions [25. Subsequently. and INF-γ [23]. a 3500-Dalton RNA-like molecule that decreases the production of IL-2.6%). as well as the overall clinical status of the host. Mexican studies report an increased frequency of human leukocyte antigen (HLA)-A28 (and decreased frequency of HLA-DQW2) among patients with parenchymal disease. the elaboration of parasitic proteins that facilitate infection.7].9]. Higher rates occur among children and middle-aged adults [10. and stage of degeneration. including the host’s immune response [27–29]. The intensity of humoral responses.22]. and HLA-DR B1*13 (and decreased frequency of HLA-A11 and HLA-DR B1*09) among patients with single. with cystine proteases decreasing the expression of CD4 lymphocytes [24].454 Infection 1-year life span in the feces of infected humans. does correlate with the degree of infection in both human and animal models. although results differ by geographic area. The intermediate hosts (either pigs or humans with poor fecal-oral hygiene) ingest the eggs. Most analyses of such predisposition involve human immunogenetic loci. The diversity of responses is reflected in the recognition and use of over 30 antigens in EITB assays [19].2% and 0. lack of sanitary toilets. known as oncospheres. childhood outside Lima. Particular parasitic proteins that facilitate adaptation to the host include metacestode factor. and IL-10.000 people. presumably underestimating the rates among rural populations. Humans are the major final host of Taenia.11]. and a history of taeniasis. number. The ingestion of pork containing cysticerci results in human taeniasis and completes the life cycle [1. Enzyme immunoelectrotransfer blot (EITB) assays are most often used. and the host risk factors for infection. risk factors include a lack of potable water. pig husbandry. Clinical Manifestations The clinical manifestations of NCC reflect the heterogeneity of cysts. Bolivia (22. The destruction of the cysticercal parasites initially requires eosinophils and the eosinophilic mediators eotaxin and IL-5 along with a concomitant Th2 immune response elaborated via interferon (IFN)-γ. Typically. The humoral immune response of man to Taenia antigens is the basis for most diagnostic assays.34 cases per 100. for an incidence of 0. age greater than 20 years. Basic Science Neurocysticercosis is a human pathogen primarily because of the ability of the larval forms of T. Two large Mexican studies. size.6% is reported in rural Peru [10]. and thus transmission may be independent of pork consumption. cysticerci live for years before the parasite dies. which mature in the gastrointestinal tract into globular larval forms. Human host factors predispose to infection. The highest reported seroprevalence rates are from Latin America: Honduras (34%). small. documented by coproscopy for either eggs or antigens or both. granulomas form and fibrosis develops due to a Th1 immune response via elaboration of IL-2 and tumor necrosis factor-α (TNFα) [19. Humoral responses are variable and diverse but this immunity does not prevent development of cysticercal lesions [16–18]. no abnormalities were detected in either humoral or cellular immunity. A prevalence rate of 8. in particular their location. The absence of pork husbandry in Muslim countries accounts for the low prevalence throughout much of Asia. saginata is more common [13]. where eggs are excreted. Serologic estimates of NCC prevalence are also highly variable. where in some areas the beef tapeworm T. and the Mexican Ministry of Health reported an incidence of 3. Seropositivity may merely indicate past exposure to Taenia. The cellular-mediated immune response to Taenia antigens is divergent and important when cysticerci degenerate and die. NCC does occur. yielded prevalence rates of 0. including human leukocyte antigen status [9]. In the United States at least 1000 cases are estimated to occur annually. Taenia also elaborates several immunomodulatory proteases. Human taeniasis. Indian studies from Delhi report an increased frequency of HLA-B63. with over 1000 individuals analyzed in each. The conditions that allow the parasite to perpetuate in the host are a continued subject of study [21. NCC remains the most common cause of .3%. however. Seroreversion after acute infection occurs in up to 40% by 1 to 3 years after initial detection. IL-4. however.000 people [4. with an incidence of 0. occurs variably in the developing world but infrequently in the developed world. Peru (24%). These larval forms invade the body through absorption in the gastrointestinal tract and develop into cysticerci in either muscular or central nervous system tissue. HLV-B58. interleukin (IL)-4. and Guatemala (20%). Mexican seroprevalence rates average 10%. Seizures are the most common clinical manifestation of NCC and occur in over 70% of NCC patients. often decades.

intense headache. do not contrast enhance. chiasmatic syndromes. Intracerebral hemorrhages are reported from mycotic aneurysms that rupture near subarachnoid cysts [27]. Four radiographic stages of degeneration occur with parenchymal cysts. Neuroimaging abnormalities of NCC show a broad differential including brain neoplasms. The gold standard is EITB. and tuberculomas. Such seizures are more prevalent among epileptic patients in NCC-endemic areas. Bruns’ syndrome) may result in episodic vomiting. Whether this reflects the unique immunogenetic profile of this population is not known [37]. In one study of 90 consecutive untreated patients with NCC evaluated at baseline. decreased enhancement and edema. vomiting. the end result of cystic degeneration and the only recognized neuroimaging abnormality in many patients. Vasculitic inflammatory changes in medium. NCC causes seizures in several ways. positional vertigo. Calcified granulomas. nearly one half of such patients will manifest recurrent seizures [31]. with early cyst degeneration. Pseudotumoral forms show lesions indistinguishable from either a brain neoplasm or echinococcal cysts. Degenerating cysts with edema and contrast enhancement on neuroimaging are the typical nidus for seizure activity [27. Acute obstruction of the fourth ventricle from a free-floating intraventricular cyst (ie. the NCC cyst is as bright as CSF. 455 Lesions in the peripheral musculature occur more often among Asian patients with NCC. In the apparent diffusion coefficient (ADC) maps. 15. is followed by a granular-nodular stage with more advanced cyst degeneration. Calcified granulomas periodically undergo vasogenic perilesional edema. the sensitivity and specificity of CT imaging for the diagnosis of parenchymnal NCC is estimated at 95% [38. however. posterior fossa. ophthalmic lesions. A Mexican study comparing the two found that a serum EITB assay was over 92% sensitive for the diagnosis of NCC with multiple cysts. Parenchymal lesions rarely attain a size greater than 10 mm in diameter because of intraparenchymal pressure [33]. Neurocognitive deficits and even frank dementia are under-recognized in NCC patients. Stroke is another cause of acute focal findings in NCC. Early lesions are round and cystic. and lack perilesional edema. Subarachnoid cysts lack this constraint and such cysts. and decreased level of consciousness. Detection of cysticercal . the mortality in subarachnoid cases remains relatively high [27. loss of consciousness. with diameters greater than 10 mm. That sensitivity dropped to about 83% for NCC with a single cyst and 33% for NCC with only calcified lesions. and perilesions edema. however. Mass effect occurs as lesions grow and this accounts for some cases of focal neurologic deterioration [27–29].39]. seizures. Chronic inflammation due to subarachnoid cysticerci may cause fibrosis throughout the ventricular drainage system. In the proper clinical context. perilesional edema.32]. Presenting signs and symptoms may include headache. and the onset of calcification. Even with cerebrospinal fluid shunting (CSF) shunting. An enzyme-linked immunosorbent assay is also available. Two unusual types of parenchymal NCC are the military and pseudotumoral forms. Both intraventricular and subarachnoid cysts can present with either acute or chronic hydrocephalus.Neurocysticercosis Shandera and Kass acquired epilepsy among adults in the developing world [30]. differentiate these entities. The latest stage of involution shows calcified cysts on both CT (small hyperdense lesions) and MRI (small hypointensities on T2 images) [33]. Seizures may also develop from either cerebral infarction due to vasculitis or from thrombosis of penetrating blood vessels by subarachnoid cysts. papilledema. resulting in either communicating or noncommunicating hydrocephalus. neuroimaging. cranial nerve entrapments. and such edema may provoke an increase in epileptogenesis [32]. or vasculitic cerebrovascular complications. Viable cysts that do not elicit a host immune response are usually asymptomatic. subarachnoid. The overall sensitivity for the serum assay was 86%. The lack of hyperperfusion of a suspected NCC lesion on perfusion MRI distinguishes it from brain neoplasms [33]. It is much less sensitive (but less expensive in some countries such as Mexico) than the EITB. Although radiographic tools are the most sensitive and specific tools for diagnosis of NCC. A colloidal state. and enhancement on MRI. Miliary NCC represents a massive infection with multiple small cysts. basal arachnoiditis. or even sudden death brought on by change in head position [34]. serologies based on detecting cysticercal antigens may be used in evaluating suspicious lesions. which yields the highest sensitivity in serum and detects seven glycoprotein bands specific for T.35]. MR perfusion and MR spectroscopy may. are found in the sylvian fissures and basal cisterns [33]. Diffusion-weighted image (DWI) sequence of MRI can often distinguish a NCC cyst and a brain abscess because the scolex of NCC is very bright on a DWI.or smallsized vessels cause cerebral infarctions. Even when disease burden is mild. spinal. solium [36]. Diagnosis The diagnosis of NCC is dependent on the diverse clinical manifestations of disease. other type of abscess. Cerebrovascular disease contributes to morbidity and mortality in patients with subarachnoid disease. CT imaging is much less sensitive than MRI [39].5% met the Diagnostic and Statistical Manual of Mental Disorders (DSM)-IV diagnostic criteria for dementia [36].28. and supporting information from epidemiology and laboratory assays. For ventricular. persist as a cause of continued seizures in patients with neither viable nor degenerating cysts.

and 6) a recent meta-analysis of treatment trials showed that cysticidal treatment resulted in better resolution of colloidal (enhancing) and vesicular (cystic) lesions. which was introduced in 1997 in the United States. For moderate parasitic burden. When possible. Alternatively. and 7) lesions can resolve spontaneously in the absence of antiparasitic therapy [41. 3) in some series seizure control is no better in treated patients than in placebo controls. and the host status. 4) no evidence shows that treated patients develop fewer calcifications. and 3) heavy (> 100 cysts}. primary surgical removal is preferred. For viable cysts and a mild parasitic burden. the most popular option is nontreatment and neuroimaging to follow disease. ventricular cysticerci should be removed neuroendoscopically [34]. A 41% reduction in partial seizures was similarly insignificant (P = 0. placebo-controlled trial showed that the treatment of seizure patients with viable parenchymal cysticerci using first-line antiepileptics with 800 mg/d of albendazole and 6 mg/d of dexamethasone for 10 days reduces the frequency of generalized seizures by a statistically significant amount [45•].30). A well-designed. A bias in this study may have been the heterogeneity of seizure frequency among the placebo group (among which increased frequency was limited to a few individuals) [45•]. 5) treatment is safe as evidenced by only 10 case reports of treatment-related fatalities in the world literature. Both agents effectively destroy parenchymal cysts and are well tolerated. double-blind. patients can undergo CSF shunting followed by antiparasitic treatment. and open surgery. regardless of disease burden. Seizures should be managed with first-line antiepileptic drugs. Hydrocephalus is typically managed neurosurgically. steroids. and reduced the rates of seizures in patients with vesicular lesions [41–43]. 4) inflammation associated with treatment is readily treated with steroids. effects such as seizures and/or hydrocephalus. 6) an exacerbation of symptoms occurs in many patients following therapy. steroids. the overall burden of infestation. . For subarachnoid disease (either giant cysts or chronic meningitis). 3) treated patients manifest fewer seizures and residual calcifications. most specialists favor antiparasitic treatment with steroids. and praziquantel. those treated showed 46% fewer seizures than those given placebo (P = 0. Treatment The treatment of NCC involves the initiation of cysticidal treatment along with the control of secondary effects of the infection. Hydrocephalic patients without cysts on neuroimaging should be offered ventricular shunting without antiparasitic treatment [41]. Opponents of therapy argue the following: 1) faster cyst resolution does not necessarily result in better seizure control. controversy attends their use. which was introduced in 1987. For both spinal disease and ophthalmic disease. and 3) calcified cysticerci. lowered the risk for recurrent seizures in patients with colloidal lesions.456 Infection antigen in the serum suggests the continued presence of viable parasite in the brain. 2) enhancing lesions (degenerating cysts).44]. antiparasitic treatment. The growth of parenchymal lesions is uncommon but may be life threatening. require neither antiparasitic treatment nor steroids because such calcifications represent dead organisms. Consensus guidelines for the treatment of NCC were published in 2002 and were based on US Preventive Task Force levels II-3 evidence (obtained from multiple time series with or without intervention) and III evidence (opinions of respected authorities based on clinical experience). This warrants aggressive treatment with antiparasitic drugs and/or surgical excision [41]. with the choice determined by symptoms and site of disease. steroids alone should be used out of fear that the simultaneous death of many cysts will induce allergic reactions and significant edema [41].40]. Nonetheless. Parenchymal infections The Consensus Group identified three life-cycle categories: 1) viable cysts. although a 67% reduction in generalized seizures was significant (P = 0. Proponents of therapy marshal a number of arguments in support of their claims: 1) treated cysts disappear rapidly. For heavy parasitic burden. The following discussion is based on the Consensus Group opinion as outlined in the published guidelines [41]. For patients with degenerating cysts and a mild to moderate burden of disease. Therapy depends on cyst location and stage of degeneration. With heavier burden of disease (“cysticercotic encephalitis”). At follow-up in 2 to 30 months. including in particular the immune response. Enrolled patients shared statistically similar baseline characteristics in the treatment and control groups. Extraparenchymal disease Extraparenchymal disease requires aggressive intervention because it usually results in hydrocephalus. high-dose steroids and osmotic diuretics (mannitol) without antiparasitic drugs are indicated [41]. Antiparasitic drug treatment The two most effective antiparasitic agents are albendazole. Calcified cysticerci.42. 2) moderate (6–100 cysts). antiparasitic therapy is added to high-dose steroid therapy. and treatment based on this finding may benefit the patient [28. They also identified three infestation categories: 1) mild (1–5 cysts).01). 2) better sanitation and general hygiene probably account for the declining incidence and severity of NCC.44). 2) the incidence of severe cases has fallen in the era of treatment. 5) most pathologic effects of NCC result from host inflammatory responses to dying cysticerci. and ventricular shunting for hydrocephalus are indicated.

unfortunately. Albendazole concentrations. As noted previously. Human vaccination is unlikely to be successful. Such practices. Parenchymal inflammation is treated with corticosteroids (dexamethasone at 4 to 12 mg/d ) for the duration of antiparasitic treatment. Disease manifestations occur usually years. however.5% of the dementia group continued to meet criteria for dementia. Corticosteroid concentrations are actually increased by higher albendazole plasma levels. For parenchymal disease.44]. Supplementing human mass chemotherapy with mass anticysticercal treatment of swine reduced the need for human therapy when the swine received two treatments [49].44]. A double-blind. reduced the incidence of dementia nearly fivefold. and DNA vaccines that also induce humoral immunity. producing obstructive hydrocephalus. extraparenchymal disease). are not universal in the developing world. protective immunity does not appear to be a major defense against disease [9]. solium oncosphere antigens. where transmission occurs with fecal-oral exposure to Taenia-infected contacts. With heavy disease burden. unlike those of praziquantel. T. ultimately modifying NCC manifestations [44]. extinction required 11 interventions at 90-day intervals). Disease is classified by site of involvement. A post-treatment inflammatory reaction representing an exacerbation of neurologic symptoms usually occurs between days 2 and 5 of treatment in 50% to 80% of patients and may necessitate an increase in corticosteroid dosage [42. treatment with albendazole and steroids. Because NCC occurs rarely among either the immunodeficient or the immunosuppressed. are not lowered by phenobarbital. Only 21. including developed nations.35. longer-term corticosteroids are recommended (replacing dexamethasone with prednisone after the acute period) [43]. In the dementia series described previously. Prevention of disease in both pigs and man is the ideal endpoint. after 6 months. Excision of anatomically crucial CNS lesions may be needed. It is less expensive and reduces cyst size and number more effectively than praziquantel [28. The multiplicity of factors affecting both rates of taeniasis and porcine cysticercosis (the endpoints measured in most trials) complicate the data analysis [48]. placebo-controlled study of 1 versus 4 week(s) of albendazole therapy (at 15 mg/kg in two divided doses) in children with mild parenchymal disease burden showed no difference in radiographic resolution of lesions or in seizure control at 2 years [46]. a murine parasite) or T. responded to one treatment cycle [47]. Studies modeling NCC in Peru show that mass treatment of humans is ineffective unless multiple treatments are carried out (in one report. The rationale for this approach is the higher than expected rates of NCC among patients with taeniasis and their contacts. Ventricular disease. Options include a therapeutic vaccine that avoids the issue of vaccinating piglets at a time of life when their immunity is impaired. steroids should be initiated prior to and after the administration of antiparasitic treatment [28]. For ventricular and subarachnoid disease. after exposure and are most serious when crucial anatomic neuraxis areas are impacted. Effective control programs were carried out in trials using praziquantel in Ecuador and Mexico and niclosamide in Guatemala. Adverse effects from albendazole itself are rare. Prevention Because of good sanitation and hygienic pork husbandry practices such as eliminating porcine access to human feces and discarding cysticercus-infested meat.44]. or corticosteroids. NCC is virtually eliminated in the developed world. Neither giant subarachnoid or intraventricular cysts. crassiceps. occurs selectively among patients from Latin America and requires prioritization in therapy. NCC remains the most common cause of adult-onset seizures in much of Latin America. use of recombinant vaccines with either related Taenia (eg. including anticonvulsant . may be amenable to vaccine therapy [50]. even decades. One method used to control disease is mass chemotherapy against taeniasis. Larval disease ensues among the contacted individuals after eggs evolve into oncospheres that are absorbed and form larvae in neurologic and muscular tissues. usually the result of degenerating cysts within the brain parenchyma. The primary manifestations of therapy for such disease are supportive. phenytoin. although some continued to exhibit mild cognitive impairment [36]. albendazole at a dose of 30 mg/kg/d is preferred and in one study reduction from 30 mg/kg/d to 15 mg/kg/d resulted in a worse outcome using cyst reduction on MRI without a change in tolerability. the relationship between NCC and human immunity is to date poorly understood. The most common manifestation of NCC is seizures. Conclusions Neurocysticercosis is increasingly recognized from all parts of the world. although even when vaccines are imperfect in reducing cyst counts they are effective in changing the histopathology of cysts (reducing oncosphere evagination). albendazole is given as 15 mg/kg/d divided every 12 hours for at least 1 week [42. With more chronic inflammation (eg.Neurocysticercosis Shandera and Kass Cysticidal medications Albendazole is now the antiparasitic medication of choice in the treatment of NCC. Porcine disease. however. 457 Praziquantel can potentially induce cerebral inflammation if concomitant cysticercal disease is present whereas niclosamide is more expensive and cannot be used during pregnancy. The two agents used to implement this strategy are praziquantel and niclosamide. and the movement of carriers establishes new sites of disease.

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