eMedicine Specialties > Infectious Diseases > CNS Infections

Cysticercosis

Mossammat M Mansur, MD, Infectious Disease Fellow, Louisiana State University
Martin Montes, MD, Fellow, Department of Medicine, Section of Infectious Disease, Baylor College of Medicine; Research Associate, Instituto de Medicina Tropical ‘Alexander von Humboldt', Universidad Peruana Cayetano Heredia, Perú; Linda S Yancey, MD, Consulting Staff, West Houston Infectious Diseases

Updated: Jul 25, 2008

Introduction

Background

Cysticercosis (ie, tapeworm infection) is an increasingly common medical problem in the United States, especially in the Southwest and other areas where large populations migrated from endemic areas and among populations that often travel to these areas.

Cysticercosis is caused by the metacestode, or larval, stage of Taenia solium, the pork tapeworm. The Clinical syndromes caused by T solium are categorized as either neurocysticercosis (NCC) or extraneural cysticercosis (intestinal tapeworm infection). 

Neurocysticercosis refers to CNS infection of the CNS with T solium. Neurocysticercosis, which is probably the most common parasitic infestation of the CNS, has gained increased recognition in the last two decades because of the development of MRI and CT scanning in the United States and in countries where neuro cysticercosis is endemic.

Neurocysticercosis is further divided into parenchymal and extraparenchymal disease. Parenchymal disease is characterized by infection with cysticerci within the brain parenchyma. Extraparenchymal disease develops when cysticerci migrate to the CSF of the ventricles, cisterns, and subarachnoid space or within the eyes or spinal cord.

Pathophysiology

When humans ingest undercooked pork that contains cysticerci of T solium, the scolex evaginates from the cyst and develops into an intestinal tapeworm. The tapeworm grows to a length of up to 10 meters and has hundreds of proglottids. Mature proglottids contain approximately 50,000 eggs each. Free eggs or whole proglottids are released periodically into the stool of the carrier and can survive in the environment for many months.

When pigs ingest the proglottids or eggs, the eggs hatch, penetrate the pigs' intestinal wall, and spread to skeletal muscle, especially the neck, tongue, and trunk. There, the larvae mature into encysted cysticerci over 2-3 months. The cysticerci suppress the host inflammatory response and survive in tissues for months to years. The life cycle is completed when humans ingest inadequately cooked pork that contains viable cysticerci or ingest eggs. Humans are end hosts of the larval stage and develop cysticercosis similar to that in pigs. Ingestion of encysted pork does not directly cause cysticercosis; rather, it produces an intestinal infection of the adult tapeworm and a carrier state for the T solium eggs that, when ingested by humans, produce the clinical syndrome of cysticercosis.

Humans can be infected with eggs through fecal-oral transmission or possibly through autoinfection. Fecal-oral contamination usually occurs via infected food handlers who do not appropriately wash their hands before working or via ingestion of fruit and vegetables fertilized with contaminated human waste. The eggs are sticky and can often be found under the fingers of tapeworm carriers. Thus, even populations who do not eat pork can develop cysticercosis. The egg-containing feces can contaminate water supplies in endemic areas. If the water is used to irrigate fruits and vegetables, eggs are ingested with the contaminated food. Thus, people who have never visited endemic countries can also develop infection. Autoinfection involves the retrograde transmission of proglottids from the intestines into the stomach with subsequent release of T solium eggs into the gut.

Human neurocysticercosis can result after ingestion of food contaminated with T solium eggs. The cystic larval stage that normally occurs in pigs develops in the human host and spreads to the skeletal muscle and brain. In this situation, the human becomes the end intermediate host.

Cysticerci are able to survive in the human brain by disarming host defenses. The cysticercus secretes prostaglandins and other compounds (paramyosin, taeniastatin, sulfated polysaccharides) that inhibit or divert complement activation and cytokine production, resulting in only minimal host inflammation around the viable cysticercus. In addition, humoral antibodies do not kill the mature metacestode. Taeniastatin and other poorly defined factors may also interfere with lymphocyte proliferation and macrophage function, inhibiting normal cellular immune defenses. The clinical manifestations commonly result when an inflammatory response develops around a degenerating cysticercus.

Over a period of years, the parasite may lose its ability to control the host defenses. Consequently, an inflammatory response leads to degeneration of the cysticercus. An inflammatory response that occurs in the CNS parenchyma causes seizures typical of parenchymal neurocysticercosis. As the degeneration continues, the parasite becomes encased in a granuloma, which either resolves or leads to scarring and calcification. In rare cases, patients with numerous parenchymal cysticerci develop a diffuse cerebral edema termed cysticercal encephalitis. Pathologically, cysticercal encephalitis may progress to meningoencephalitis, granulomatous meningitis, focal granulomas or abscess, hydrocephalus, ependymitis, or arteritis.

Approximately 10-20% of patients with neurocysticercosis present with extraparenchymal disease, often with concomitant parenchymal disease. Subarachnoid neurocysticercosis may form in the gyri of the cerebral convexities or in the fissures of the brain, especially the sylvian fissures. These forms of neurocysticercosis are associated with parenchymal inflammation and resemble parenchymal disease in manifestations and pathogenesis.

In severe cases, cysticerci in the sylvian fissures may enlarge to several centimeters in diameter and cause mass effects. Cysticerci can form in the ventricles of the brain, where they can cause hydrocephalus by blocking the outflow of CSF. Obstructive hydrocephalus may also be caused by associated ependymitis. If cysticerci form in the basal cisterns, they can cause basilar arachnoiditis. Arachnoiditis may result in communicating hydrocephalus or vasculitis. Involvement of the arteries may lead to lacunar infarctions or, occasionally, large-vessel strokes.

Cysticerci may be located in the spinal subarachnoid space and the spinal cord medulla. Medullary cysticerci may cause cord compression or other symptoms related to their location. Ocular cysticercosis is generally intravitreal or subretinal. Skeletal muscle cysticerci are common but usually cause only minor local symptoms unless they are present in overwhelming numbers. Subcutaneous cysticerci manifest as painless, palpable, cystic lesions. CNS parenchymal cysticerci may be present in patients with suspected extraparenchymal or extra-CNS disease.

Frequency

United States

Approximately 1,000 new cases of cysticercosis are reported annually in the United States. Most occur among Latin American immigrants in locations such as California (particularly Los Angeles), Phoenix, and Albuquerque. Less frequently, cysticercosis is observed in immigrants from other areas, including Asia and Africa. A small number of cases of cysticercosis develop in people born in the United States who have traveled to areas in which the infection is endemic. These travelers are often the children of immigrants. Locally acquired infection is rare and is associated with contact with a tapeworm carrier. All tapeworm carriers acquire infection from areas of endemic disease.

In a mortality study using data from the NationalCenter for Health Statistics from 1990 to 2002; 62% of patients with cysticercosis had emigrated from Mexico.¹

International

An estimated 50-100 million people are infected with cysticercosis worldwide. This is probably an underestimate since many infections go undiagnosed. Neurocysticercosis is one of the leading causes of adult-onset seizures worldwide. CT scanning and MRI of the brain have greatly improved the diagnosis of neurocysticercosis.

Areas of endemic disease include Central and South America, India, China, Southeast Asia, and sub-Saharan Africa. Studies in Latin America and India have noted adult-onset seizures in approximately 2% of the population, with as many as half due to neurocysticercosis. In Latin America, the seroprevalence rate ranges from 4.9-24%. In India, the estimated prevalence is similar. Rural China and Korea have lower infection rates. The seroprevalence in certain rural South American communities is as high as 10-25%.²

Mortality/Morbidity

• Neurocysticercosis is one of the leading causes of adult-onset seizures and is estimated to cause as many as 50% of adult-onset seizure cases in developing countries where T solium is endemic. Neurocysticercosis was found to be responsible for 10% of newly onset seizures in one Los Angeles, California, emergency department.³ Overall, among patients who presented to emergency departments with newly onset seizure, neurocysticercosis was found to be responsible for 2.1-5.7% of cases.⁴
• A total of 221 deaths were attributed to cysticercosis in the United States from 1990-2002.¹
• Although some patients die of status epilepticus in areas with poor access to medical care, mortality due to parenchymal disease is rare. With modern medical and surgical care, mortality due to extraparenchymal disease is also unusual. However, without aggressive surgical management, hydrocephalus is potentially life-threatening. Even with shunting procedures, subarachnoid cysticercosis is associated with a high 10-year fatality rate.

Race

Immigrants from countries where T solium is endemic are more likely to be infected. While most of these immigrants are Hispanic and some are Asian, prevalence rates appear to be related more to exposure than to genetic predisposition.

Sex

• Cysticercal encephalitis, a severe form of cysticercosis, is more common in children and young females. The cause is unknown.
• No other sex predisposition has been noted.

Age

Patients with cysticercosis are typically aged 10-40 years. However, cases have been described in every age group.

Clinical

History

Postmortem studies in endemic areas suggest that 80% of neurocysticercal infections are asymptomatic.⁵ Consequently, many cases are never diagnosed or are found incidentally during imaging procedures.

The peak severity of neurocysticercosis has been estimated to occur 3-5 years after initial infection, but it can be delayed for more than 30 years. After a variable period of degeneration, cysts can become calcified and may then become inactive. Once they are calcified, they may cease to cause symptoms or may serve as a focus for epileptic activity. The symptoms of neurocysticercosis depend on the stage, site, and number of cysticerci. Cysts frequently develop in multiple locations, and a combination of active and inactive cysts in the same patient is not uncommon.

Symptoms of cysticercosis may include seizures, elevated intracranial pressure (ICP), meningoencephalitis, psychiatric disorder, stroke, and/or radiculopathy or myelopathy, if the spinal cord is involved.

The symptoms are mainly due to mass effect, an inflammatory response, or obstruction of the foramina and ventricular system of the brain. The most common symptoms include seizures, focal neurologic signs, and intracranial hypertension.

Generally, the patient’s history includes exposure to an area where the parasite is endemic and an adolescent- or adult-onset seizure disorder. Symptoms of hydrocephalus should raise concerns about extraparenchymal disease.

• Parenchymal CNS disease
  • Seizures may be focal, focal with secondary generalization, or generalized.
  • Headaches are common and may be migrainelike or tension-type.
  • Neurocognitive deficits may include learning disabilities, depression, or even psychosis.
• Extraparenchymal disease
  • Most patients present with headaches or symptoms of hydrocephalus.
  • Symptoms of increased ICP may include headache, nausea or vomiting, altered mental status, dizziness, and decreased visual acuity due to papilledema.
  • Patients with numerous cysticerci in the basilar cisterns may present with communicating hydrocephalus, meningismus (without fever), symptoms of lacunar infarcts due to small-vessel vasculitis, or symptoms of large-vessel infarcts due to cysticercal erosion into major arteries or severe inflammation of those arteries.
  • Patients with spinal cysticerci typically present with radicular symptoms, but rarely with motor or sensory deficits traceable to a spinal level.
  • Patients with ocular cysticerci report visual changes.
• Spinal cord involvement
  • Radiculopathy
  • Myelopathy
• Other
  • Meningoencephalitis
  • Stroke (in young adults)
  • Subcutaneous nodules
  • Ocular cysts

Physical

Meningoencephalitis may manifest as pyrexia, altered senses, seizures, increased ICP, multiple cranial nerve involvement, or even brainstem or cerebellar involvement.

Both parenchymal and extraparenchymal disease can cause elevated ICP. Signs include hyperreflexia, papilledema (a late sign), and the Cushing reflex (a preterminal event).

• Parenchymal disease
  • Physical examination findings are usually normal.
  • Patients who have had seizures may have typical manifestations of the postictal state, with somnolence, an altered level of consciousness, and poor memory.
  • Focal neurologic deficits are unusual and suggest alternative diagnoses, such as tuberculoma, tumor, or, rarely, extraparenchymal neurocysticercosis.
• Extraparenchymal disease
  • Ocular cysticerci are visible upon ophthalmologic examination.
  • Rare spinal cysticerci manifest as sensory or motor deficits or back tenderness.
  • Patients with neurocysticercosis of the cisterns may present with lacunar infarcts or large-vessel infarction with associated upper motor neuron signs.
  • Subcutaneous cysts may be palpable as fluid-filled nodules that resemble sebaceous cysts.

Causes

• Extraneural cysticercosis: Extraneural infection with T solium typically involves the eye, muscle, or subcutaneous tissue. It is not known whether oncospheres actively migrate to those organs or passively enter tissues during high blood flow. 
• Neurocysticercosis: Infection of the CNS with T solium and associated host inflammation.

Differential Diagnoses

Brain Abscess
Vasculitis

Other Problems to Be Considered

Tuberculoma
CNS tumor
Idiopathic epilepsy
Scar from old disseminated tuberculosis
Scar from old disseminated histoplasmosis
Scar from other old glaucomatous disease
Scar from old trauma

Workup

Laboratory Studies

The diagnosis of cysticercosis is often based on clinical presentation, abnormal findings on neuroimaging, and serology. Occasionally, more invasive procedures (eg, brain biopsy) are required.

Del Brutto et al defined the diagnostic categories of definite neurocysticercosis and probable neurocysticercosis, basing their determinations on the following proposed absolute, major, minor, and epidemiologic criteria. These criteria were modified in 2001.⁶

• Absolute criteria include the following:
  • Histologic demonstration of the parasite on a biopsy sample from the brain or spinal cord lesion
  • Direct visualization of subretinal parasites via funduscopic examination
  • Cystic lesions showing the scolex on CT scans or MRIs
• Major criteria include the following:
  • Lesions highly suggestive of neurocysticercosis on neuroimaging studies (CT scan or MRI showing cystic lesions without scolex, enhancing lesions, or typical parenchymal brain calcifications)
  • Serum anticysticercal antibodies demonstrated by immunoblot assay
  • Resolution of intracranial cystic lesions after therapy with albendazole or praziquantel
  • Spontaneous resolution of small, single, enhancing lesions (single ring-enhancing lesions <20 mm in diameter in patients with seizures, normal neurologic examination findings, no evidence of active systemic disease)
• Minor criteria include the following:
  • Lesions compatible with neurocysticercosis on neuroimaging studies
  • Clinical manifestations suggestive of neurocysticercosis (eg, epilepsy, focal neurologic signs, intracranial hypertension, dementia)
  • Positive findings from CSF enzyme-linked immunosorbent assay (ELISA) for detection of anticysticercal antibodies or cysticercal antigens
  • Cysticercosis outside the CNS
• Epidemiologic criteria include the following:
  • Evidence of a household contact with T solium infection
  • Individuals coming from or living in an area where cysticercosis is endemic
  • Household contact with an individual infected with T solium
• The diagnostic categories that follow pertain to the criteria outlined in the model developed by Del Brutto et al:
  • Definite neurocysticercosis (1 of the following)
    • One absolute criterion
    • Two major criteria plus 1 minor criterion and 1 epidemiologic criterion
  • Probable neurocysticercosis (1 of the following)
    • One major criterion plus 2 minor criteria
    • One major criterion plus 1 minor criterion plus 1 epidemiologic criterion
    • Three minor criteria plus 1 epidemiologic criterion

Findings from laboratory studies such as routine CBC counts and liver function tests are not specific. The WBC count is usually within the reference range, and most patients do not have eosinophilia unless a cyst is leaking, in which case the eosinophilia may be pronounced.

Serologic studies can be helpful in the diagnosis of cysticercosis.

• An enzyme-linked immunoblot transfer blot (EITB) assay can demonstrate serum or CSF anticysticercal antibodies. The findings in the serum are more sensitive than those in the CSF. The assay is highly specific for exposure to T solium. The sensitivity is high (94%) in patients with multiple lesions or extraparenchymal infection but may be as low as 28% in patients with a single parenchymal lesion. EITB assay findings may revert to negative after the cysticercus dies and are often negative in patients with only calcified lesions.
• ELISAs that use unfractionated antigen are fraught with problems regarding sensitivity and specificity, and they are reliably diagnostic only when performed on CSF.
• The observed cross-reactivity of infected sera with antigens of other parasites has limited the accuracy of serologic techniques such as ELISA. The western blot kit (QualiCode) offers qualitative detection of immunoglobulin G (IgG) antibodies to T solium with a sensitivity of 95% and a specificity of 100%. It yields rapid results (<90 min).
• The sensitivity of ELISA using CSF is approximately 80%. False positive results may occur in patients with hydatid cysts, filariasis, tuberculous meningitis, or viral encephalitis. An active inflammatory response is likely to cause high titers; intraventricular cysts cause a low titer.
• An assay using monoclonal antibody HP10 to detect parasite secretory/excretory antigens performed well in CSF samples, with results similar to those from the EITB assay.⁷
• No polymerase chain reaction (PCR) tests are available.

Stool examination for ova and parasites can occasionally be used to diagnose intestinal infection with T solium. However, most people diagnosed with cysticercosis do not have viable T solium tapeworm in their intestine, so eggs are not typically found.

• Because eggs are shed intermittently, most cases of cysticercosis cannot be detected with a single stool test.
• Furthermore, egg morphology is the same for T solium and Taenia saginata.
• Antigen detection tests for stool and serologic tests for tapeworms are being studied; none is available for use in clinical practice.
• Identifying tapeworm carriers does not usually help in diagnosing neurocysticercosis, but it may be useful in detecting the source of infection in cases among US residents who have not traveled.

Imaging Studies

Neuroimaging with contrast-enhanced CT scanning or MRI is the mainstay of diagnosis.

• MRI is better for detecting intraventricular types and extraparenchymal disease and visualizing the scolex within the cysticercus (as high intensity inside a cyst).
• CT scanning is better for detecting intracerebral calcifications.
• Both modalities can reveal hydrocephalus and active intraparenchymal lesions.
• The ventricles may be narrowed with extensive low attenuated areas in the parenchyma, sparing the cortex.
• A ring enhancing active lesion with surrounding edema is the second-most-common finding.
• A homogenously enhancing lesion represents a dying larva.
• Calcified lesions are also common on CT scans.
• The racemose type resembles a bunch of grapes  
• With MRI or CT scanning, the following 4 stages of parenchymal disease can be differentiated:
  • The initial invasion appears as focal areas of edema or enhancement.
  • Viable cysts appear as 0.5- to 2-cm cystic lesions without associated edema. The image density of the cyst fluid is similar to that of CSF. The cyst wall is thin, isodense with brain parenchyma, and not visible.
  • Early degenerating cysts appear as cystic lesions with associated edema, and cysts that degenerate later lose their cystic fluid and resemble a granuloma, with associated edema.
  • The residual phase appears as calcified nodules that are 0.2-1 cm in diameter. No live cysticerci are present at this stage, although parasite antigen may still be present. This phase represents inactive disease.
• Extraparenchymal disease imaging may involve the following:
  • Ventricular, cisternal, and subarachnoid cysticerci have thin walls and may be isodense with CSF, so that hydrocephalus is the only visible abnormality on the CT scan.
  • The cyst wall is usually visible on an MRI.
  • Alternatively, cysts within the subarachnoid space may be better detected by using CT scanning with metrizamide contrast within the subarachnoid space or by using myelography.
  • Advanced MRI techniques such as fluid-attenuated inversion recovery have improved the diagnostic accuracy of ventricular and subarachnoid neurocysticercosis by increasing the CSF signal after 100% oxygen administration.
  • Radiographs of soft tissue may reveal typical cigar-shaped calcifications within the muscles, which correspond to scarring from prior muscular cysticerci. These are highly suggestive of exposure.

Other Tests

• EEGs are frequently obtained in patients who have experienced seizures. The EEG is abnormal in up to 50% of cases, demonstrating various findings (diffuse slowing, focal paroxysmal activity, generalized spike waves) depending on lesion number, size, and location.
  • No pattern is diagnostic for neurocysticercosis.
  • Focal abnormalities may be present in persons with active disease.
  • Seizures may also be caused by inactive disease (calcified nodules of the residual phase), but, in these cases, the EEG does not usually reveal focal abnormalities.

Procedures

• Lumbar puncture: Lumber puncture for a CSF study is usually unnecessary in the diagnosis of neurocysticercosis. This procedure is also contraindicated upon suspicion of increased ICP. If a lumber puncture is performed, examination of CSF shows a normal glucose concentration and protein levels and WBC counts that are usually only mildly elevated. CSF studies in individuals who have a leaking cyst that communicates with the CSF may reveal prominent CSF eosinophilia.
• Biopsy: Biopsy may be required in patients with suspected neurocysticercosis who have a single brain lesion with no characteristic scolex and negative serology findings. Biopsy specimens may be taken from subcutaneous nodules or a muscle lesion. Biopsy of CNS lesions is rarely necessary.

Histologic Findings

Occasionally, CNS lesions are mistakenly identified as tumors and are diagnosed only at surgery. Upon gross examination, the cysticerci appear as 5- to 10-mm semiopaque cysts with a 1- to 2-mm mural nodule containing the scolex.

Histopathologic examination reveals a superficial tegument layer covered with microtriches, a cellular layer below that containing the cell nuclei and musculature, and a loose reticular layer characterized by canaliculi. When the parasites are viable, little surrounding inflammation is observed. Degenerating parasites, on the other hand, are invaded with an inflammatory infiltrate including lymphocytes, macrophages, plasma cells, neutrophils, and eosinophils.

Histologic studies have shown that viable cysticerci in humans and pigs have little or no surrounding inflammation.⁸

Cysticerci can persist in the human host for long periods, often years, without eliciting a surrounding inflammatory reaction.

In contrast, the immune-mediated inflammation around one or more degenerating cysts may precipitate symptomatic disease.

When the parasite begins to involute, either naturally or after treatment with anticysticercal drugs, granulomatous inflammation develops around the cysticerci. The predominant components of this inflammatory response include plasma cells, lymphocytes, eosinophils, and macrophages. The latter engulf parasite remnants, eventually leaving a gliotic scar with calcifications.

Early granulomas in cysticercosis are predominantly associated with a Th1 response, whereas later granulomas, in which parasite destruction is complete, have a mixture of Th1 and interleukin-4 (IL-4). The Th1 response appears to play an important role both in the pathogenesis of disease and in the clearing of the parasites, with IL-4 involved in downregulation of the initial response.

Treatment

Medical Care

• Asymptomatic cysticercosis: As mentioned above, more than 80% of patients with cysticercosis are asymptomatic. No evidence has shown that administering antiparasitic therapy for asymptomatic nonviable cysticercal lesions found incidentally in the brain is beneficial.
• Patients who are found to have cysticerci only in subcutaneous or intramuscular sites generally do not require specific therapy.
• If a single extracranial lesion is found, excision can be considered after neurocysticercosis is excluded with brain imaging.
• Patients with ocular cysticercosis who have extraocular muscle involvement may present with diplopia and recurrent eye pain. Treatment with albendazole and corticosteroids has proven to be beneficial. Some patients may require surgical excision. In patients with intraocular cysticercosis, vitreoretinal surgery (either transscleral or transvitreal) can be performed to remove the cysticerci.
• Patients with subcutaneous or intramuscular cysticercosis who develop symptoms due to inflammation can be treated with cysticerci excision or anti-inflammatory agents. Excision is the treatment of choice for a solitary symptomatic lesion.
• Symptomatic therapy is the mainstay of treatment for neurocysticercosis.
  • Anticonvulsants are prescribed to patients with seizures.
  • Specific anthelminthic therapy with albendazole or praziquantel is prescribed, usually accompanied by corticosteroids.
  • Corticosteroids are used in patients with cerebral edema or vasculitis.
  • CSF diversion is instituted in patients with obstructive hydrocephalus.
• Parenchymal disease should be treated medically.
  • The primary focus is symptomatic therapy for seizures.
  • A postictal patient should initially receive supportive care that includes a safe environment.
  • Anticonvulsants should be administered early but may be tapered when seizures are controlled if findings from neuroimaging studies revert to normal (see Medication).
  • If significant intracranial edema is demonstrated, corticosteroids should be administered before antiparasitic therapy is considered. Some authorities recommend routine use of corticosteroids in all cases of active neurocysticercosis.
  • If viable cysticerci are suspected, antiparasitic drugs (ie, praziquantel and albendazole) may be used to hasten the death of the parasite. However, the decision to use antiparasitic therapy should be individualized to each patient.
  • A prospective randomized study compared the use of antiparasitic agents with placebo in patients with active parenchymal lesions. Results showed no significant difference in the number of subjects with recurrent seizures. However, the number of generalized seizures was significantly reduced with the combination of steroids and antiparasitic drugs. The beneficial effect was seen in a subgroup of subjects with numerous recurrent seizures.⁹
  • Patients with only calcifications (ie, residual phase) with or without edema do not need antiparasitic therapy.
  • Patients with cerebral edema or uncontrolled hydrocephalus should not be treated with antiparasitic therapy until these conditions are resolved.
  • Patients with multiple cysticerci, especially in the basilar cisterns, or with giant cysticerci of the sylvian fissures, should receive both corticosteroids and antiparasitic therapy.
  • Generally, ventricular disease should be treated surgically, preferably via an endoscopic approach. However, if the surgery is being performed only to place a shunt and not to remove the cysts, antiparasitic therapy should be administered after the shunting procedure.
  • Neuroendoscopy provides a safe and minimally invasive procedure for the removal of symptomatic cysts, minimizing morbidity and mortality relating to the natural history of the disease, as well as possibly avoiding a more extensive standard open craniotomy. The endoscopic approach can be made via transventricular corridor, perforating overlying structures such as the septum pellucidum. In some cases, burr holes may be required.

Surgical Care

• Surgical procedures are required in some patients based on complicating factors, such as hydrocephalus or giant cysts (>10 cm) in the setting of intracranial hypertension.
• Surgical intervention should also be considered if a cyst is found in the fourth ventricle, is attached to the middle cerebral artery (MCA), or is compressing the optic chiasma. 
• Extraparenchymal disease was once treated surgically by placing a shunt because most symptoms are due to hydrocephalus.  
• Surgical resection of ventricular neurocysticercosis is associated with a low long-term risk of postoperative morbidity.
• Some studies suggest that endoscopic removal may be able to replace open surgery for removal of cysticerci in most cases.
• Ventriculoperitoneal (VP) shunting is now commonly used for the treatment of hydrocephalus. Case series have shown that the cysticerci are usually ruptured during removal, but no adverse consequences have been noted.
  • In patients with viable cysticerci, the use of VP shunt alone results in treatment failure in almost 75% of cases.¹⁰ The use of antiparasitic drugs and corticosteroids in conjunction with VP shunt placement improve the outcome.
  • Although recurrent blockage of shunts is very common, it is unclear whether antiparasitic therapy or long-term corticosteroid treatment decreases the risk of shunt blockage and malfunction.
  • Recent descriptions of valveless shunts noted lower rates of recurrent hydrocephalus, but these shunts were associated with a higher rate of inadequate drainage.
• Patients with inactive disease may present with hydrocephalus due to scar tissue in the cisterns or ventricular space, without evidence of cystic lesions.
  • VP shunting is necessary in these cases.
  • Antiparasitic drugs and corticosteroids are not needed because the cysticerci have already degenerated and shunt failure is rare.
• Neurocysticercosis of the basilar cisterns should be treated with corticosteroids, prolonged courses (eg, months) of antiparasitic drugs, and VP shunting if hydrocephalus is present.
• Giant subarachnoid cysticerci can cause significant mass effect as associated edema. The edema may respond to steroids, but the mass effect may remain.
  • Surgical drainage may be necessary.
  • Antiparasitic drugs may be beneficial, but only after steroids are given.
• Generally, ocular and spinal medullary cysticerci should be removed surgically.
  • However, cures of spinal medullary disease have been reported with medical treatment including corticosteroids and antiparasitic drugs.
  • Antiparasitic treatment in patients with retinal cysticerci may cause irreversible retinal damage.
• Spinal subarachnoid disease can often be treated medically.

Consultations

• Consultation with a neurosurgeon is essential in patients with hydrocephalus, significant mass effect, or extraparenchymal CNS disease.
• Consultation with a neurologist is needed if protracted or refractory seizures occur.
• Consultation with an infectious disease specialist is recommended if active disease is suspected.
• An ophthalmologist should be consulted for patients with ocular neurocysticercosis. At a minimum, a funduscopic examination should be performed before the initiation of antiparasitic drug therapy.

Diet

• No specific diet restriction is recommended.
• Patients should avoid reinfection and reingestion of ova from original sources by observing the following guidelines:
  • Inspection of pork for cysticerci, which are visible in raw meat ("measly meat")
  • Freezing or adequately cooking meat to destroy cysticerci (Pickling and salting are inadequate.)
  • Administering antiparasitic agents to pigs
  • Good personal hygiene and hand-washing prior to food preparation

Activity

• No activities are restricted if the patient is otherwise asymptomatic.
• All patients who present with seizures should take seizure precautions. Patients with a history of seizures may have state-required restrictions on driving motor vehicles. Physicians may be responsible for informing patients about these restrictions.
• Patients with hydrocephalus may have ataxia and may be at risk for falls.

Medication

Anticonvulsant and anti-inflammatory (steroid) medications are the basis of medical therapy in symptomatic patients. Antiparasitic drugs have not been shown to provide a consistent long-term benefit in patients with parenchymal disease and seizures.

Anticonvulsants

Anticonvulsants should be used in patients with seizures or who are at high risk for recurrent seizures. Patients with parenchymal calcifications carry a high risk of seizure recurrence if anticonvulsants are tapered; therefore, these patients usually remain on anticonvulsants indefinitely. In contrast, patients with active cysticerci in whom lesions resolve without developing calcification should be treated with anticonvulsants until they are free from seizures for at least one year and results of neuroimaging studies show normalization. Anticonvulsants may then be tapered. Patients with recurrent seizures should be maintained on long-term anticonvulsant therapy.

A double-blind, placebo-controlled study in 2004 compared two groups of patients with viable parenchymal cysts, with seizures being treated with anticonvulsants, to see whether anticysticercal drugs improved seizure control. During 30 months of follow-up, the proportion of patients having partial seizures was similar for the group who took albendazole and dexamethasone and those who took placebos, but the treatment group had significantly fewer seizures with generalization, and more of their intracranial lesions resolved. Except for abdominal pain, adverse effects did not differ significantly.¹¹

Phenytoin, carbamazepine, and phenobarbital induce metabolism of praziquantel.

Phenytoin (Dilantin)

Widely available and inexpensive. Has significant drug interactions, and dosage should be adjusted based on therapeutic effect and serum levels. Fosphenytoin may be considered for IV administration if available because it is better tolerated than IV phenytoin, but it is considerably more expensive than phenytoin.

Dosing

Adult

Nonemergent situations: 100 mg PO tid; then adjust based on therapeutic effect and serum level
Emergent situations: 1 g IV loading dose (not to exceed 50 mg/min) or PO in 3 divided doses q2h
Therapeutic: 10-20 mcg/mL or 1-2 mcg/mL for free phenytoin

Pediatric

Nonemergent situations: 5 mg/kg PO qd or divided bid/tid; then adjust by therapeutic effect and serum level
Emergent situations: 10-15 mg/kg IV loading dose
Therapeutic: 10-20 mcg/mL

Interactions

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase toxicity
Barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and sucralfate may decrease effects
May decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, oral contraceptives, and valproic acid

Contraindications

Documented hypersensitivity; sinoatrial block; second- and third-degree AV block; sinus bradycardia; Adams-Stokes syndrome

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Perform CBC counts and urinalyses when therapy is begun and at monthly intervals for several months thereafter to monitor for blood dyscrasias; discontinue use if rash appears, and do not resume use if rash is exfoliative, bullous, or purpuric; rapid IV infusion may result in death from cardiac arrest, marked by QRS widening; caution in acute intermittent porphyria and diabetes (may elevate blood glucose; discontinue use if hepatic dysfunction occurs

Carbamazepine (Tegretol)

Use if phenytoin unavailable, ineffective, or contraindicated. Anticonvulsant therapy should be used for one year after resolution of the active parasitic infection followed by a trial of treatment discontinuation if the patient remains seizure-free.

Dosing

Adult

Nonemergent situations: 200 mg PO bid, increase by 200 mg/d; not to exceed 1600 mg/d (usual dose 400-1200 mg/d)
Therapeutic: 4-12 mcg/mL

Pediatric

Nonemergent situations: 10 mg/kg/d PO divided bid up to 200 mg bid; increase by 100-200 mg q7d; not to exceed 1200 mg/d

Interactions

Serum levels may increase significantly within 30 d of danazol coadministration (avoid whenever possible); do not coadminister with MAOIs; cimetidine may increase toxicity, especially if taken in first 4 wk of therapy; may decrease primidone and phenobarbital levels (coadministration may increase carbamazepine levels)

Contraindications

Documented hypersensitivity; history of bone marrow depression; MAOIs within last 14 d

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Do not use to relieve minor aches or pains; caution with increased intraocular pressure; aplastic anemia and agranulocytosis reported in association with Tegretol; obtain CBC counts and serum iron baseline prior to treatment, during first 2 months, and yearly or every other year thereafter; can cause drowsiness, dizziness, and blurred vision; caution while driving or performing other tasks requiring alertness; toxic epidermal necrolysis and Stevens-Johnson syndrome reported during Tegretol use

Phenobarbital (Barbital, Luminal, Solfoton)

Use if phenytoin unavailable, ineffective, or contraindicated. Interferes with transmission of impulses from thalamus to cortex of brain. Used as sedative.

Dosing

Adult

Nonemergent situations: 60 mg PO bid/tid
Emergent situations: 10-20 mg/kg IV

Pediatric

5 mg/kg PO or IV qd or divided bid

Interactions

May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients stabilized on anticoagulants may require dosage adjustments if added to or withdrawn from their regimen); coadministration with alcohol may produce additive CNS effects and death; chloramphenicol, valproic acid, and MAOIs may increase toxicity; rifampin may decrease effects; induction of microsomal enzymes may result in decreased effects of oral contraceptives in women (must use additional contraceptive methods to prevent unwanted pregnancy; menstrual irregularities may also occur)

Contraindications

Documented hypersensitivity; severe respiratory disease; marked impairment of liver function; nephritis
porphyria; or patients with severe respiratory disease such as severe asthma or severe chronic obstructive pulmonary disorder (COPD).

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

In prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; caution in fever, hyperthyroidism, diabetes mellitus, and severe anemia because adverse reactions can occur; caution in myasthenia gravis and myxedema

Corticosteroids

These agents should be used immediately in patients with significant cerebral edema, mass effect, or vasculitis associated with neurocysticercosis. High doses (approximately 1 mg/kg/d of prednisone) should be used. High-dose dexamethasone (30 mg/d) should be used initially to treat cysticercal encephalitis. If cerebral edema resolves, patients may be treated with antiparasitic drugs later. Long-term courses of corticosteroids should be used in patients with subarachnoid neurocysticercosis who have meningitis, stroke, or communicating hydrocephalus and should be tapered as soon as possible based on lumbar puncture and neuroimaging results.

Long-term course of corticosteroids may also prevent shunt failure in patients with VP shunt and active disease. Patients with intramedullary spinal neurocysticercosis should be treated with steroids until resolution of cord edema. Patients receiving long-term corticosteroids should be given calcium supplementation to help counterbalance osteoporotic effects of corticosteroids.

Prednisone (Deltasone, Meticorten, Orasone)

Inexpensive, widely available, and effective. Use in patients with significant edema, mass effect, or vasculitis.

Dosing

Adult

1 mg/kg/d IV/PO qd or divided doses

Pediatric

Administer as in adults; divided doses may decrease GI tract upset

Interactions

Estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Contraindications

Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective-tissue infections; fungal or tubercular skin infections; GI tract disease

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Abrupt discontinuation may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur

Dexamethasone (Decadron, AK-Dex)

Use in patients with cysticercal encephalitis or in patients with severe mass effect, edema, or vasculitis if preferred over prednisone.

Dosing

Adult

4-6 mg IV q4-6h for total dose of approximately 30 mg/d

Pediatric

Not established

Interactions

Effects decrease with coadministration of barbiturates, phenytoin, or rifampin; decreases effect of salicylates and vaccines used for immunization

Contraindications

Documented hypersensitivity; active bacterial or fungal infection

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering; abrupt discontinuation may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications

Antiparasitics/anthelminthic

Albendazole and praziquantel are antiparasitic drugs used to treat neurocysticercosis. They have been used for more than 20 years, but data by which to judge their therapeutic role are still controversial. Albendazole is preferred over praziquantel because of its favorable pharmacokinetics profile and efficacy. Both agents are cysticidal. These drugs are always administered with corticosteroids.

When praziquantel is administered with cimetidine to increase its bioavailability, praziquantel is probably as effective as albendazole in killing viable cysticerci.

Antiparasitic drugs are contraindicated in cysticercal encephalitis (characterized by diffuse cerebral edema), uncontrolled elevated ICP, ocular disease, and subarachnoid neurocysticercosis in close proximity to blood vessels. In all of these cases, steroids should be administered early so that the inflammatory reaction is quelled. Antiparasitic drugs, which may cause release of more antigens and stimulate more inflammation, can then be considered on a case-by-case basis.

Albendazole (Albenza)

Has no interactions with steroids or anticonvulsants. It is preferred over praziquantel because of its pharmacokinetic profile and efficacy. Parenchymal disease responds to short courses, but longer duration of therapy (months) may be needed in extraparenchymal disease.

Dosing

Adult

15 mg/kg/d (usually 800 mg/d in two divided doses) PO divided bid with meals for 15 d
Shorter course of therapy for 8 d demonstrated higher failure rate

Pediatric

Administer as in adults

Interactions

Coadministration with carbamazepine may decrease efficacy; dexamethasone, cimetidine, and praziquantel may increase toxicity

Contraindications

Documented hypersensitivity; neurocysticercosis resulting in cerebral edema; uncorrected hydrocephalus; cysticerci near cerebral vessels; ocular disease

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use with retinal cysticercosis may cause irreparable damage; discontinue use if LFT values increase significantly (resume when levels decrease to pretest values); abdominal pain, nausea, vomiting, diarrhea, dizziness, vertigo, fever, increased ICP, and alopecia granulocytopenia, anemia, and/or pancytopenia may occur; albendazole may increase theophylline level, so level should be monitored for theophylline toxicity

Praziquantel (Biltricide)

Increases cell membrane permeability in susceptible worms, resulting in loss of intracellular calcium, massive contractions, and paralysis of musculature. Also produces vacuolization and disintegration of schistosome tegument. This is followed by attachment of phagocytes to parasite and death. It does not cross blood-brain barrier well, only 20% of plasma levels.
Tabs should be swallowed whole with some liquid during meals. Keeping tabs in mouth may release bitter taste that can produce nausea or vomiting. The efficacy appears to be lower than that of albendazole. It works better when taken with cimetidine. Its metabolism can be induced by cytochrome P-450 (corticosteroids, phenytoin, phenobarbital). The serum level of praziquantel is lowered when any of these drugs is coadministered. It is usually considered as a second-line therapy.

Dosing

Adult

50 mg/kg/d PO divided tid for 15 days (with cimetidine at 300 mg PO qid if patient also taking steroids or anticonvulsants)
Longer courses (months) may be needed for extraparenchymal infections
Preliminary studies suggest alternative dosage regimen of 75 mg/kg given in single day (25 mg/kg q2h for total of 3 doses) may have similar efficacy

Pediatric

Administer as in adults

Interactions

Significant first-pass metabolism when coadministered with corticosteroids, carbamazepine, phenytoin, or, probably, phenobarbital; levels decrease by approximately one half compared with praziquantel alone; cimetidine coadministration significantly inhibits metabolism and should be used to counterbalance effect of concurrent steroids or anticonvulsants

Contraindications

Documented hypersensitivity; ocular cysticercosis; neurocysticercosis resulting in cerebral edema; uncorrected hydrocephalus; cysticerci near cerebral vessels; ocular disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Destruction of parasite within eyes can cause irreparable lesions (ocular cysticercosis should not be treated with praziquantel); caution while driving or performing other tasks requiring alertness on day of and following treatment; minimal increases in liver enzymes reported; when schistosomiasis or fluke infection associated with cerebral cysticercosis, hospitalize patient for duration of treatment
Nursing mothers should stop breastfeeding when beginning treatment with praziquantel; breastfeeding should not be resumed until 72 h after treatment is completed; during this time, the breast milk should be expressed and discarded

Follow-up

Further Inpatient Care

• ICU monitoring is necessary in patients with uncontrolled seizures, elevated ICP, or severe extraparenchymal disease.
• If antiparasitic therapy is provided, patients should be hospitalized and monitored during the initial phase.
  • As cysticerci die, neurologic symptoms may worsen because of an increased inflammatory response.
  • Most symptoms associated with antiparasitic therapy develop within 3-5 days of beginning therapy.
  • Antiparasitic therapy may then be completed in an outpatient setting.
• Prior initiation of therapy with antiparasitic medications or corticosteroids, the following steps should be taken:
  • Apply a purified protein derivative (PPD) skin test. Patients in whom the PPD result is positive should be treated with isoniazid along with pyridoxine (vitamin B6) for the duration of their steroid treatment.
  • Because many patients with cysticercosis also have risk factors for strongyloidiasis, these patients should be treated with ivermectin (200 μg/kg administered in two single doses two weeks apart before steroids are initiated.
  • An ophthalmologist should perform an eye examination to exclude ocular cysticercosis.

Further Outpatient Care

• The initial brain reimaging should be performed two months after therapy completion.
• Parasite antigen levels typically fall by 3 months after successful treatment. 
• For patient monitoring, the imaging should be performed on a biannual basis to monitor the cysts.
• If the cysts are growing in the absence of therapy, antiparasitic therapy should be considered.
• In patients with seizures due to neurocysticercosis without calcification, perform imaging studies every 3-6 months. If calcification develops, lifelong anticonvulsant therapy is indicated, and further imaging studies can be performed as needed.
• If results of imaging studies show normalization and seizures are under control after 2 years of therapy, anticonvulsants may be tapered, and further imaging can be performed as needed.
• Patients with calcified lesions and a seizure disorder should be maintained on anticonvulsants indefinitely, and they should undergo imaging studies only as needed.
• Monitor anticonvulsant serum levels to prevent toxicity.

Inpatient & Outpatient Medications

• Discharge medications may include steroids, anticonvulsants, antiparasitics, and cimetidine.
• The anticonvulsants carbamazepine and phenytoin are first-choice treatments.
• Antihelminthic agents: Antihelminthic medications are controversial. Reserve such treatment for select cases. When antihelminthics are used, albendazole is preferable to praziquantel.

Transfer

• Patients with extraparenchymal neurocysticercosis should be treated at hospitals with active neurosurgical and neurological services because emergency procedures such as shunt placement or ventriculostomy may be required in patients with worsening hydrocephalus.
• Arrange transfer if the facility is unable to provide neurologic or neurosurgical care.

Deterrence/Prevention

• Educate patients regarding routes of transmission of cysticerci ova.
• Meat inspection has been effective at preventing transmission of tapeworms in developed countries but has been uniformly unsuccessful in developing countries.
• In areas of endemic cysticercosis, avoid undercooked pork to reduce the risk of intestinal infection.
• Be vigilant about avoiding potential fecal-oral transmission to reduce the risk of neurocysticercosis while in endemic areas. Individuals traveling to such areas should observe the following guidelines:
  • Eat only fruits and vegetables that you have peeled yourself.
  • Thoroughly wash (with water from a clean source) all food prior to ingestion.
  • Maintain good personal hygiene and wash hands prior to food preparation.
• Mass chemotherapy has been used to interrupt transmission in some areas of endemic infection, but disease usually returns within a few years.
• Mass anthelminthic therapy yields only limited success and may cause adverse neurologic events in individuals with undiagnosed neurocysticercosis who receive these drugs. 
• Consider identifying human carriers of tapeworms, possibly based on a history of proglottid passage, and instituting targeted treatment.
• Serologic screening of the contacts of patients should also be considered in the management of cysticercosis, particularly in nonendemic countries when transmission may have occurred within a household (eg, via food prepared by a household worker from an endemic country). 
• Vaccines for prevention of cysticercosis have proven effective for other Taenia species and are in development for T solium.
• Transmission of cysticercal infections to pigs can be prevented with the following measures:
• Changing pig-raising practices in endemic areas by confining the animals and preventing them from roaming freely to avoid contact with infectious ova excreted in human feces
• Improving sanitary conditions and proper disposal of human stool
• Possibly vaccinating pigs (Preliminary studies suggest this may be feasible.)

Complications

• Parenchymal disease causes seizures but few long-term complications. However, studies suggest that childhood infection may be associated with learning disabilities and cognitive dysfunction.
• Extraparenchymal disease may cause elevated ICP, resulting in herniation and death.
• Vasculitis associated with cisternal neurocysticercosis may cause strokes, communicating hydrocephalus, and death.

Prognosis

• Most patients with parenchymal cysticercosis either remain asymptomatic or develop a self-limited seizure disorder.
• Among patients who develop intracerebral calcifications, most have recurrent seizures unless treated with anticonvulsants. If treated with anticonvulsants, the seizures are generally easily controlled.
• Ventricular neurocysticercosis usually requires shunting.
  • Neurosurgery may be complicated by focal neurologic damage.
  • Shunt revisions are often needed unless patients are treated with corticosteroids or antiparasitic drugs. However, even with treatment, some still require subsequent revision.
  • Prior to the use of corticosteroids and antiparasitic drugs, subarachnoid disease was associated with a 90% 10-year fatality rate, even with shunting. With current management, fatalities appear to be rare.
• Good evidence indicates that, once infected, patients are immune to reinfection.

Patient Education

• Patients and their family members should be educated on how to decrease the source of egg carriers by emphasizing improvement in sanitation, separation of pigs from humans, and food-preparation hygiene in endemic areas.
• Family members should be queried about symptoms suggestive of tapeworm infection, such as passing proglottids. They should be treated if symptoms are present.
• Family members should also be screened.
• Patients with seizures and their families should know proper seizure first-aid.
• Patients who have had seizures should know about possible driving restrictions, which, in the United States, vary from state to state.
• Patients who have received a VP shunt should be educated about the signs and symptoms of elevated ICP (possible shunt failure) and meningitis (secondary infection of indwelling hardware).
• For excellent patient education resources, please see eMedicine's Infections Center and Parasites and Worms Center.

Miscellaneous

Medicolegal Pitfalls

• Failure to consider the diagnosis and to perform appropriate testing (primarily neuroimaging studies)
  • The symptoms of neurocysticercosis are nonspecific, but imaging studies usually confirm the diagnosis.
  • The key to diagnosis is careful evaluation of patients who are at risk.
  • Diagnostic testing in patients with seizures who have not undergone previous studies should include neuroimaging studies (either CT scanning or MRI).
  • If patients have suggestive lesions, obtaining further history of exposure, serologic analyses, or imaging studies that show soft-tissue calcifications can confirm the diagnosis.
• Failure to promptly initiate therapy for elevated ICP
  • As with other conditions, symptomatic increased ICP in neurocysticercosis is an emergency.
  • Patients usually present with headaches, but the headaches may not be significantly different from those due to a wide range of other causes.
  • Patients with headaches who also have symptoms of increased ICP or mass lesion require more emergent evaluation. These symptoms include nausea and vomiting, dizziness, visual changes, or abnormal neurologic examination findings.
  • Obstructive hydrocephalus often requires surgical intervention.

Special Concerns

• Identification of the source of infection and prevention of further exposure is paramount in the care of neurocysticercosis.
• Cases of cysticercosis do not need to be reported to the CDC unless local transmission is suspected. In this case, the Division of Parasitic Diseases at the CDC can be contacted through state and local health departments. More information is available at the CDC Web site.
• In 1997, a study by Del Brutto et al found an association between neurocysticercosis and cerebral gliomas in adults, possibly due to astrocytic gliosis that surrounds the cyst. Further study and evaluation are needed.¹²

References

1. Sorvillo FJ, DeGiorgio C, Waterman SH. Deaths from cysticercosis, United States. Emerg Infect Dis. Feb 2007;13(2):230-5. [Medline].

2. de Bittencourt PR, Adamolekum B, Bharucha N, et al. Epilepsy in the tropics: I. Epidemiology, socioeconomic risk factors, and etiology. Epilepsia. Nov 1996;37(11):1121-7. [Medline].

3. Wallin MT, Kurtzke JF. Neurocysticercosis in the United States: review of an important emerging infection. Neurology. Nov 9 2004;63(9):1559-64. [Medline].

4. Ong S, Talan DA, Moran GJ, et al. Neurocysticercosis in radiographically imaged seizure patients in U.S. emergency departments. Emerg Infect Dis. Jun 2002;8(6):608-13. [Medline].

5. Bern C, Garcia HH, Evans C, et al. Magnitude of the disease burden from neurocysticercosis in a developing country. Clin Infect Dis. Nov 1999;29(5):1203-9. [Medline].

6. Del Brutto OH, Rajshekhar V, White AC Jr, et al. Proposed diagnostic criteria for neurocysticercosis. Neurology. Jul 24 2001;57(2):177-83. [Medline].

7. Fleury A, Hernandez M, Fragoso G, et al. Detection of secreted cysticercal antigen: a useful tool in the diagnosis of inflammatory neurocysticercosis. Trans R Soc Trop Med Hyg. Sep-Oct 2003;97(5):542-6. [Medline].

8. White AC Jr, Robinson P, Kuhn R. Taenia solium cysticercosis: host-parasite interactions and the immune response. Chem Immunol. 1997;66:209-30. [Medline].

9. Garcia HH, Pretell EJ, Gilman RH, Martinez SM, Moulton LH, Del Brutto OH, et al. A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. N Engl J Med. Jan 15 2004;350(3):249-58. [Medline].

10. Kelley R, Duong DH, Locke GE. Characteristics of ventricular shunt malfunctions among patients with neurocysticercosis. Neurosurgery. Apr 2002;50(4):757-61; discussion 761-2. [Medline].

11. Garcia HH, Pretell EJ, Gilman RH, et al. A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. N Engl J Med. Jan 15 2004;350(3):249-58. [Medline].

12. Del Brutto OH, Castillo PR, Mena IX, et al. Neurocysticercosis among patients with cerebral gliomas. Arch Neurol. Sep 1997;54(9):1125-8. [Medline].

13. Del Brutto OH. Neurocysticercosis. Semin Neurol. Sep 2005;25(3):243-51. [Medline].

14. Del Brutto OH, Santibanez R, Noboa CA, et al. Epilepsy due to neurocysticercosis: analysis of 203 patients. Neurology. Feb 1992;42(2):389-92. [Medline].

15. Garcia HH, Gilman RH, Tovar MA, et al. Factors associated with Taenia solium cysticercosis: analysis of nine hundred forty-six Peruvian neurologic patients. Cysticercosis Working Group in Peru (CWG). Am J Trop Med Hyg. Feb 1995;52(2):145-8. [Medline].

16. García HH, Del Brutto OH. Imaging findings in neurocysticercosis. Acta Trop. Jun 2003;87(1):71-8. [Medline].

17. García HH, Evans CA, Nash TE, et al. Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev. Oct 2002;15(4):747-56. [Medline].

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19. Gravori T, Steineke T, Bergsneider M. Endoscopic removal of cisternal neurocysticercal cysts. Technical note. Neurosurg Focus. Jun 15 2002;12(6):e7. [Medline].

20. Immunetics, Inc. Qualicode Cysticecosis Western Blot Kit. Immunetics [serial online]. 1997;Available at Immunetics-Qualicode Cysticecosis Western Blot Test Kit.

21. Kraft R. Cysticercosis: an emerging parasitic disease. Am Fam Physician. Jul 1 2007;76(1):91-6. [Medline].

22. Nainiwal S, Chand M, Verma L, et al. Intraocular live cysticercus larva. Ophthalmic Surg Lasers Imaging. Nov-Dec 2003;34(6):464-6. [Medline].

23. Salinas R, Counsell C, Prasad K, et al. Treating neurocysticercosis medically: a systematic review of randomized, controlled trials. Trop Med Int Health. Nov 1999;4(11):713-8. [Medline].

24. Sharma T, Sinha S, Shah N, et al. Intraocular cysticercosis: clinical characteristics and visual outcome after vitreoretinal surgery. Ophthalmology. May 2003;110(5):996-1004. [Medline].

25. Sotelo J, Escobedo F, Penagos P. Albendazole vs praziquantel for therapy for neurocysticercosis. A controlled trial. Arch Neurol. May 1988;45(5):532-4. [Medline].

26. Sundaram PM, Jayakumar N, Noronha V. Extraocular muscle cysticercosis - a clinical challenge to the ophthalmologists. Orbit. Dec 2004;23(4):255-62. [Medline].

27. White AC Jr. Neurocysticercosis: a major cause of neurological disease worldwide. Clin Infect Dis. Feb 1997;24(2):101-13; quiz 114-5. [Medline].

28. White AC Jr, Robinson P, Kuhn R. Taenia solium cysticercosis: host-parasite interactions and the immune response. Chem Immunol. 1997;66:209-30. [Medline].

Keywords

cysticercosis, tapeworm infection, tapeworms, Taenia solium, T solium, pork tapeworm, tapeworm, neurocysticercosis, extraneural cysticercosis, parenchymal neurocysticercosis, extraparenchymal neurocysticercosis, NCC, intestinal tapeworm, intestinal tapeworm infection, cysticercal encephalitis, cysticercal meningoencephalitis, tapeworm encephalitis, parasitosis, subarachnoid neurocysticercosis, ocular cysticercosis, subcutaneous cysticercosis, intramuscular cysticercosis

Contributor Information and Disclosures

Author

Mossammat M Mansur, MD, Infectious Disease Fellow, Louisiana State University
Mossammat M Mansur, MD is a member of the following medical societies: American College of Physicians, American Medical Association, British Medical Association, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Coauthor(s)

Martin Montes, MD, Fellow, Department of Medicine, Section of Infectious Disease, Baylor College of Medicine; Research Associate, Instituto de Medicina Tropical ‘Alexander von Humboldt', Universidad Peruana Cayetano Heredia, Perú
Disclosure: Nothing to disclose.

Linda S Yancey, MD, Consulting Staff, West Houston Infectious Diseases
Linda S Yancey, MD is a member of the following medical societies: American College of Physicians, American Medical Association, and Infectious Diseases Society of America
Disclosure: Bristol-Myers Squibb Grant/research funds Original research

Medical Editor

David Hall Shepp, MD, Program Director, Fellowship in Infectious Diseases, Department of Medicine, North Shore University Hospital; Associate Professor, New York University School of Medicine
David Hall Shepp, MD is a member of the following medical societies: Infectious Diseases Society of America
Disclosure: Gilead Sciences Salary Management position

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

John W King, MD, Professor of Medicine, Chief, Section of Infectious Diseases, Director, Viral Therapeutics Clinics for Hepatitis, Louisiana State University Health Sciences Center; Consultant in Infectious Diseases, Overton Brooks Veterans Affairs Medical Center
John W King, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Association of Subspecialty Professors, Infectious Diseases Society of America, and Sigma Xi
Disclosure: emedicine $50.00 author of chapter

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

The authors and editors would like to acknowledge Dr. Martin Montes, Dr. Clinton White Jr., and Dr. Thomas P. Giordano, who were the original authors of this article. They would also like to acknowledge the prior contributions of Dr. John W King to the development and writing of this article.

Principles and Practice of Infectious Disease by Mandell, Douglas, and Bennett, sixth edition (2005), pages 3289-90. 

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