eMedicine Specialties > Radiology > Brain/Spine

Cysticercosis, CNS

Anil Khosla, MBBS, Assistant Professor, Department of Radiology, Section of Neuroradiology, Mallinckrodt Institute of Radiology, Washington University School of Medicine, Veterans Affairs Medical Center of St Louis

Updated: Sep 9, 2008

Introduction

Background

Cysticercosis is the most common parasitic infestation affecting the central nervous system (CNS). CNS involvement is seen in approximately 90% of patients with cysticercosis; when cysticercosis involves the CNS, it is called neurocysticercosis (NCC). NCC is recognized as a common cause of neurologic disease in developing countries, and it is also seen in developed countries, including the United States. NCC is a chronic disease associated with substantial morbidity and high social and economic costs. A minimal estimate of annual treatment costs in the United States (a country in which NCC is not endemic) is $9 million; in Mexico and Brazil, costs are estimated to be nearly $90 million per year.

The pathogenesis and clinical presentation vary with the site of infection and the host immune response. NCC poses a complex diagnostic and treatment dilemma because of its varied presentation. Factors determining treatment include whether symptoms are present, the location of the cysts, and whether there is a host immune response.^1,2,3,4

Pathophysiology

Infectious organism

Cysticercosis of the CNS (neurocysticercosis, NCC) may be associated with poor sanitation; the disease is acquired after the consumption of infected food or food contaminated with infected feces (ie, fecal-oral transmission). More commonly, transmission occurs through the consumption of fruit and vegetables grown in soil fertilized with contaminated pig or human waste. Less commonly, it occurs after the ingestion of infected pork.

The larval form of the pork tapeworm, Taenia solium, causes NCC. T solium is the only tapeworm for which humans may be both the intermediate host (harboring the larval form) and the definitive host (harboring the adult form). The ingested larvae (ie, embryos or oncospheres) from contaminated food, drink, or soil are absorbed through the intestinal blood vessels into the venous circulation. They pass through the pulmonary circulation and systemically lodge in the skeletal muscle, eyes, and CNS.

In the CNS, the larvae may lodge in the subarachnoid space or in the brain parenchyma, commonly at the junction of gray and white matter. In tissues, oncospheres develop into cysticerci. The encapsulated larval forms contain clear fluid and a viable scolex. If humans ingest infected meat that contains cysticerci, the cysticerci may attach themselves to the intestinal mucosa and develop into mature tapeworms.

Adult worms are composed of hundreds of proglottids, each of which contains oncospheres that repeat the cycle when the proglottid is shed in feces. Cerebral lesions evolve from an active form to a transitional form and then to an inactive form.

The interval from infection to the onset of symptoms is probably lengthy. In a case series of British soldiers infected in Asia, the median time until the first appearance of symptoms was estimated to be 4 years. The proportion of infected persons who develop symptomatic disease is unknown. In various clinical trials, the spontaneous disappearance of all or some of the cysts has been described in a substantial number of patients. Antihelminths have been found to hasten the disappearance of active parenchymal lesions.

Types of NCC

CNS cysts are encountered in 4 types in NCC: (1) meningeal (racemose variety), (2) parenchymal (solitary or multiple cysts), (3) ventricular (usually solitary), and (4) mixed.

Meningeal cysts form mostly in the basal meninges, sometimes causing stroke and hydrocephalus. Parenchymal cysts are usually found in the cerebral cortex, including the cortical-subcortical junction. The white matter is rarely involved. Ventricular cysts are seen in 15% of patients with NCC; in 50% of cases, they are located in the fourth ventricle.⁵ They may cause intermittent hydrocephalus. In approximately 20% of cases, parenchymal cysts are found concomitantly with intraventricular cysts.

When cysticerci become inflamed, the granular ependymitis and accompanying fibrillary astrocytosis cause the cysticerci to adhere to the walls of the ventricles. The racemose form is characterized by proliferative lobulated cysts without a scolex; such cysts are usually found in the ventricular system and the subarachnoid space. Although infrequent, this is the most serious manifestation of NCC.

Spinal cord cysts are rare (1-3% of cases). Intramedullary NCC occurs from either hematogenous or ventriculoependymal spread. In two thirds of patients, the thoracic cord is affected.^6,7

Ocular involvement is seen in approximately 5% of patients; it may be diagnosed by means of fundus examination or ultrasonography (US). Cysts may float freely in the anterior/vitreous chamber of the eye or adhere to retinal and subretinal tissues. Subretinal cysts produce vasculitis and retinal edema. If located in the vitreous, cysts result in chorioretinitis and vitreous detachment; they rarely occur in the eyelids or lacrimal glands.

Stages of NCC

The host may tolerate the worm as long as the embryo is alive. Viable cysticerci are associated with minimal inflammation (vesicular stage). The worm usually dies 2-6 years after infection, and the disintegration of the parasite triggers a vigorous tissue reaction. An inflammatory response to the degenerating cyst results in severe symptoms. As the cysticerci lose the ability to control the host's immune response, the cyst wall becomes infiltrated and is surrounded by predominantly mononuclear cells. Inflammatory cells enter the cyst fluid (colloid stage). As the host's immune response progresses, fibrosis encompasses the cysticercus, with concomitant collapse of the cyst cavity (granular-nodular stage). The dead parasite decays into eosinophilic desiccated material.

The final stage is a calcified nodule, which presumably forms as a result of dystrophic calcification of the necrotic larva (calcific stage). The various pathologic states that may be seen in NCC include the following: (1) meningoencephalitis, (2) granulomatous meningitis, (3) focal granuloma, (4) focal or diffuse multiple cysts, (5) hydrocephalus, (6) intraventricular cysts, (7) ependymitis, and (8) arteritis.

In India, NCC is characterized by small, multiple, diffuse parenchymatous involvement. In Latin America, NCC is characterized by solitary or few large parenchymal cysts, meningeal racemose, and the ventricular involvement.

Frequency

United States

Cysticercosis of the CNS (neurocysticercosis, NCC) is found mostly in immigrant populations; an estimated 1000 new cases are diagnosed each year.

International

Cysticercosis of the CNS (neurocysticercosis, NCC) has a worldwide distribution. NCC is endemic in most of Central America, South America, and Asia. In endemic areas, 25-50% of patients with adult-onset epilepsy have associated NCC. The average prevalence of seropositive findings in patients in endemic areas is 6-10%; 4-5 epilepsy cases per 1000 result from NCC. In Latin America, approximately 400,000 individuals have symptomatic disease. In Mexico, NCC is diagnosed in 13-33% of all patients with intracranial space-occupying lesions.⁸

Mortality/Morbidity

Results of postmortem studies in areas endemic for neurocysticercosis (NCC) suggest that approximately 80% of infections are asymptomatic.

• In Mexico, NCC is the cause of death in 2-3% of patients examined after death.
• In Latin America, where NCC is endemic, 400,000 people are estimated to have symptomatic disease. In endemic areas, 4-5 epilepsy cases per 1000 are presumed to be caused by NCC.

Race

• Multiple lesions are less common in India than in Latin American countries. Neurocysticercosis (NCC) with concomitant intracranial hypertension, as well as the meningeal form of NCC, is uncommon in India.
• Subcutaneous cysticercosis is more common in China than in Latin America and India.
• Differences in the human leukocyte antigen may determine the risk of intracranial infection or symptomatic parenchymal disease in a population infected with cysticercosis.⁹

Sex

• The male-to-female ratio of neurocysticercosis (NCC) is 1:1.
• Cysticercal encephalitis, a rare presentation of NCC, is more common in young girls than in others.

Age

• Rates of seropositive results tend to increase with age; seizures resulting from neurocysticercosis (NCC) typically begin in early adulthood (usually, in patients older than 15 y).
• The incidence of NCC is low in children because of the long incubation period; children probably account for 0.8-27.8% of patients with NCC.

Presentation

The clinical presentation of cysticercosis of the CNS (neurocysticercosis, NCC) is variable. NCC may manifest as any neurologic or psychiatric syndrome. Seizures are the most common clinical manifestation of intraparenchymal NCC at all stages. It is likely that NCC is the most common cause of symptomatic epilepsy worldwide; moreover, it is possible that NCC contributes to the relatively higher epilepsy rate in developing countries. Most patients with seizures have parenchymal cysticerci with associated edema or enhancement (colloid or granular-nodular stage).^10,11,12

Headaches are common with the parenchymal, ventricular, and cisternal types of NCC. Headache and focal symptoms are more common during the active and transitional stages of the cysts. Meningeal and intraventricular cysts may appear as obstructive or communicating hydrocephalus. Symptoms usually result from a host inflammatory response to the parasite or the space occupation. The racemose form commonly seen in Latin America results in chronic meningitis, arachnoiditis, and hydrocephalus. Occasionally, patients with NCC present with progressive dementia, behavioral disturbances, or pseudohypertrophy of the calf muscles.

In general, the clinical presentation depends on the host immune response; on the number of lesions; and on the form (active or inactive), location, and duration of the disease. Clinical findings may be summarized as follows:

• Increased intracranial pressure
  • Pseudotumor (diffuse parenchymal involvement)
  • Obstructive hydrocephalus (intraventricular cysts, racemose meningeal cysts)
• Seizures (focal or multifocal, possibly intractable)
• Intracranial space occupation (parenchymal cysts)
  • Meningoencephalitis
  • Basal arachnoiditis
  • Psychiatric disorders, including dementia

Hydrocephalus occurs less frequently in children with parenchymal disease than in adults with parenchymal disease. Cysticercus encephalitis occurs more often in children and young females than in others. Isolated non-neurologic manifestations, such as ocular or dermal cysts, occur in less than 5% of symptomatic cases.

Preferred Examination

The diagnosis of cysticercosis of the CNS (neurocysticercosis, NCC) is complex; no diagnostic test identifies all cases of cysticercosis. The diagnosis depends on a constellation of the clinical history, exposure history, laboratory results, and imaging findings.

CT scanning or MRI after the intravenous administration of contrast material is the imaging test of choice.¹³

Enzyme-linked immunotransfer blotting (EITB) is the most accurate serologic test and is the most practical screening tool. Its sensitivity for multiple intracranial cysticerci is 90-100%.

Limitations of Techniques

A negative serologic result does not exclude cysticercosis. When inflammation is absent, enzyme-linked immunotransfer blotting (EITB) results are negative in 60-80% of patients. Results are probably negative in more than 80% of cases of neurocysticercosis (NCC) involving only a single lesion. The sensitivity of serologic testing also considerably decreases late in the course of the disease and in patients with calcified lesions. Conversely, asymptomatic patients commonly have seropositive EITB results.

In most patients, neuroimaging findings are not pathognomonic for NCC. If an eccentric scolex is seen within the cyst, NCC may be diagnosed confidently. Neither CT scans nor MRI images are practical for screening a large population for NCC, particularly in developing countries.

Differential Diagnoses

Brain, Abscess
Tuberculosis, CNS

Radiography

Findings

On radiographs, calcified cysticerci appear as multiple elongated lesions shaped like cigars or grains of rice. These lesions are arranged in the direction of the muscle fibers in affected skeletal muscle. Calcified cysticerci are easily visualized on soft tissue images. Calcified intracranial cysts are occasionally seen on skull images.

Radiographs have been used as part of the evaluation during ventriculography for the diagnosis of intraventricular neurocysticercosis (NCC) and during myelography for the diagnosis of intraspinal NCC.

Degree of Confidence

CT is more sensitive than plain radiography in detecting intracerebral calcification.

False Positives/Negatives

The presence in the skeletal muscles of multifocal calcifications resembling grains of rice is suggestive of cysticercosis, particularly in patients from endemic areas. A solitary calcification is nonspecific and is of no diagnostic significance.

Computed Tomography

Findings

An inactive lesion represents a dead organism. Such lesions are densely calcified, with no enhancement. CT reveals 1 or more sites of calcification, typically 2-10 mm in diameter (see Image 1).

Active parenchymal neurocysticercosis (NCC) is the most common form of disease. The viable cyst appears as a thin-walled fluid-filled cyst with a mural nodule (live scolex); the cyst causes no inflammatory reaction or edema, and it does not enhance (see Image 2). Symptomatic infection develops when the cysticercus loses the ability to control the host's inflammatory and immune responses.

In the colloid stage, the cyst is encapsulated; it contains a high-protein fluid, and it demonstrates ring enhancement. Often, associated edema or enhancement is noted in the brain parenchyma (see Image 3). As the cysticercus becomes fibrotic or collapses, a focal area of enhancement suggestive of granuloma is seen (granular-nodular stage) (see Image 4). Finally, a focal area of calcification appears. At any stage, solitary or multiple lesions may exist. Multiple cysts are found in 80% of patients (see Image 5). Cysticercal encephalitis results from infection with a large number of cysticerci that induce an intense inflammatory response in the brain parenchyma. Its appearance is that of diffuse cerebral edema with small, slitlike ventricles.

Intraventricular cysts remain clinically silent until they degenerate. The symptomatic form results in obstructive hydrocephalus. Cysticerci may be seen in any of the ventricles. CT scans may reveal evidence of obstructive hydrocephalus or dilatation or distortion of the involved ventricle. CT scans obtained after the intraventricular administration of contrast material delineate the cyst and the site of the obstruction (see Image 6).

There are 3 subtypes of subarachnoid NCC: 

• In the first subtype, NCC is located in the gyri of the cerebral convexities; in this subtype, the appearance and presentation of cysticerci may resemble that of active parenchymal NCC.
• In the second subtype, cysticerci are found in the fissures (eg, sylvian fissure); they may measure several centimeters in diameter and are termed giant cysticerci (see Image 7). Giant cysticerci may produce a mass effect or parenchymal inflammation. They are readily detected on CT scans, but small cisternal cysticerci may not be seen.
• In the third subtype, cysticercosis involves the basal cisterns. This subtype is characterized by arachnoiditis; it appears as focal or diffuse meningeal enhancement or as vasculitis with stroke. Patients often develop communicating hydrocephalus (see Image 8).

Spinal NCC may be localized to the subarachnoid space or spinal cord. Degenerating cysticerci become fixed at one level and induce inflammation. CT myelography may demonstrate an extramedullary block or filling defects in the intrathecal contrast column.

Ocular involvement may be intravitreal or subretinal. CT may demonstrate cysts in the extraocular muscles (see Image 9).

Degree of Confidence

In most patients, the diagnosis of neurocysticercosis (NCC) may be reliably made on the basis of CT findings; this is particularly true for patients with multifocal parenchymal disease. In the vesicular stage, MRI is more accurate than CT in detecting an eccentric scolex. Intraventricular cysts are more clearly depicted with CT ventriculography or MRI.

False Positives/Negatives

In most cases, CT scans help in the detection of structural disease, but lesions in the brainstem and small cisternal and intraventricular lesions may be missed. If CT is performed without contrast enhancement, isoattenuating lesions may not be detected. In some asymptomatic individuals, CT findings may be suggestive of neurocysticercosis (NCC).

For cases involving small, ring-enhancing lesions in association with vasogenic edema, the differential diagnosis includes metastases, cerebral abscess, parasitic infection, primary neoplasm, and resolving subacute infarction and hematoma.

Magnetic Resonance Imaging

Findings

On MRIs, the contents of live cysts (vesicular stage) are isointense relative to cerebrospinal fluid (CSF) on T1-weighted images (T1WI) and T2-weighted images (T2WI).^14,15

T1WIs clearly show an eccentric, hyperintense, 2- to 5-mm scolex with a pea-in-the-pod appearance (see Image 10). The demonstration of a scolex is pathognomonic of neurocysticercosis (NCC). When the larva begins to die (colloid vesicular stage), the fluid in the cyst becomes more turbid, and it is mildly hyperintense to CSF on both T1WIs and T2WIs. The surrounding edema is hypointense on T1WIs and hyperintense on T2WIs. On T2WIs, the hypointense cyst wall stands out between the hyperintense cyst fluid and edema (see Image 11). The cyst wall may be enhancing in the granular-nodular stage.

Calcified cysts are seen as areas of signal void, especially on gradient-echo images.

All the stages may be seen simultaneously in the same patient.

Cisternal cysts (see Image 12) and intraventricular cysts (see Image 13) are visualized better on MRIs than on CT scans because they stand out in comparison to CSF as a result of the relative T1 shortening. If the cysts induce meningitis, arachnoiditis, or ependymitis, contrast enhancement is clearly noted.

Intraspinal NCC commonly involves the subarachnoid space and, less often, the cord or epidural space.

Contrast-enhanced MRI clearly defines intramedullary and extramedullary cysticerci. Intramedullary NCC usually occurs as a single lesion in the thoracic cord.

Degree of Confidence

MRI is superior to CT in imaging the lesions of neurocysticercosis (NCC), but it is less available than CT in regions of the world where NCC is endemic. MRI is better in detecting cystic lesions in the base of the brain, CSF spaces (eg, ventricular NCC, cisternal NCC), and intramedullary lesions. The scolex may be more readily apparent on MRI than on CT. MRI is superior in demonstrating inflammation around the cyst. The differential diagnosis of spinal intramedullary NCC includes other infectious granulomas and neoplasms.

False Positives/Negatives

A parenchymal cysticercus cyst without a scolex may mimic other cystic lesions. A ring-enhancing lesion with surrounding edema may represent neurocysticercosis (NCC), tuberculosis granuloma, fungal abscess, pyogenic abscess, neoplasm, or resolving hematoma and/or infarct. Rarely, cyst walls are indistinguishable from the CSF in the ventricle or cisterns; in such cases, a preoperative diagnosis may be difficult.

Ultrasonography

Findings

US is useful in the diagnosis of ocular neurocysticercosis (NCC). The cysts are well delineated when they occur in a subretinal location. The cyst wall is well depicted against the vitreous humor, and the cyst elevates the retina.

Degree of Confidence

The degree of confidence in the diagnosis of ocular neurocysticercosis (NCC) depends on expertise of the ultrasonographer. An experienced ultrasonographer can diagnose most NCC lesions of the eyes.

False Positives/Negatives

A cyst without a scolex cannot be differentiated from other cystic lesions of the eye.

Nuclear Imaging

Findings

Nuclear medicine studies are not helpful in the diagnosis of neurocysticercosis (NCC).

Angiography

Findings

Cerebral angiography may be useful in the evaluation of vasculitis resulting from cisternal neurocysticercosis (NCC). Narrowing, occlusion, and the beading of vessels may be seen.

Degree of Confidence

Findings of vasculitis are nonspecific for the diagnosis of neurocysticercosis (NCC).

False Positives/Negatives

Angiographic findings of vasculitis are nonspecific and may be seen in cases of tubercular meningitis, chronic meningitis, and vasculitis related to collagen vascular disease.

Intervention

Interventional imaging techniques have no definitive role in the diagnosis or treatment of neurocysticercosis (NCC).

Multimedia

Media file 1: Nonenhanced CT scan of the brain demonstrates the multiple calcified lesions of inactive parenchymal neurocysticercosis.

Media file 2: Enhanced CT scan of the brain in a patient with neurocysticercosis demonstrates a live cyst with a minimally enhancing wall and an eccentric hyperattenuating scolex.

Media file 3: Nonenhanced (left) and enhanced (right) CT scans of the brain in a patient with neurocysticercosis show multiple ring-enhancing lesions with perifocal edema.

Media file 4: Nonenhanced (left) and enhanced (right) CT images of the brain in a patient with neurocysticercosis show an enhancing disk lesion with perifocal edema suggestive of the granulomatous form of disease (arrow). Multiple ring lesions are also apparent; these are suggestive of the colloid stage of neurocysticercosis.

Media file 5: CT images of the brain in a patient with neurocysticercosis show numerous parenchymal lesions.

Media file 6: Left, CT scan of the brain shows marked dilatation of the right lateral ventricle in a patient with intraventricular neurocysticercosis. Right, Contrast-enhanced ventriculogram shows a fourth ventricular cyst as a filling defect in the contrast-enhanced spinal column.

Media file 7: Nonenhanced CT image of the brain shows large cerebrospinal fluid–attenuating cysts in the suprasellar cisterns in a patient with neurocysticercosis.

Media file 8: Nonenhanced (left) and enhanced (right) CT images of the brain in a patient with neurocysticercosis demonstrate peripheral meningeal enhancement around the cysts in the suprasellar and right sylvian cisterns.

Media file 9: Left, Enhanced CT scan of the orbit shows a calcified neurocysticercosis lesion in the subretinal space of the right globe. Right, Image shows a neurocysticercosis granuloma in the right lateral rectus muscle.

Media file 10: T1-weighted (T1), T2-weighted (T2), and fluid-attenuated inversion recovery (FLAIR) MRIs show a typical cyst with a scolex (arrow) in a patient with neurocysticercosis (NCC).

Media file 11: T1-weighted (T1) and T2-weighted (T2) MRIs show a degenerating cyst with a hypointense wall and hyperintense surrounding edema, which is best depicted on T2-weighted images. The patient has neurocysticercosis (NCC).

Media file 12: MRIs of the brain show multiple, large, cysticercus cysts in the basal cisternal spaces in a patient with neurocysticercosis.

Media file 13: T1-weighted (T1) and T2-weighted (T2) MRIs show a dilated fourth ventricle containing a cyst in a patient with neurocysticercosis (NCC). The cyst wall (straight arrow) and the scolex (curved arrow) are seen clearly depicted. The cyst resulted in obstructive hydrocephalus. A shunt procedure was required.

Media file 14: T2-weighted (T2) and fluid-attenuated inversion recovery (FLAIR) MRIs of the brain clearly demonstrate a small cyst containing a slightly hyperintense eccentric scolex (arrow) and surrounding edema. This is a characteristic finding of a degenerating cysticercus cyst.

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Keywords

CNS cysticercosis, neurocysticercosis, NCC, pork tapeworm, Taenia solium, T solium, CNS parasite, tapeworm, tape worm, cysticercus disease, taeniasis, teniasis, cestode infection, helminthiasis, parasitic disease, meningeal cysts, parenchymal cysts, ventricular cysts

Contributor Information and Disclosures

Author

Anil Khosla, MBBS, Assistant Professor, Department of Radiology, Section of Neuroradiology, Mallinckrodt Institute of Radiology, Washington University School of Medicine, Veterans Affairs Medical Center of St Louis
Anil Khosla, MBBS is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Neuroradiology, North American Spine Society, and Radiological Society of North America
Disclosure: Nothing to disclose.

Medical Editor

Jeffrey L Creasy, MD, Associate Professor, Associate Section Head, Division of Neuroradiology, Director, Neuroradiology Fellowship, Department of Radiology, Vanderbilt University
Jeffrey L Creasy, MD is a member of the following medical societies: American College of Radiology, American Society of Neuroradiology, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

James G Smirniotopoulos, MD, Professor of Radiology, Neurology, and Biomedical Informatics, Chairman, Department of Radiology and Radiological Sciences, Uniformed Services University of the Health Sciences
James G Smirniotopoulos, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Head and Neck Radiology, American Society of Neuroradiology, American Society of Pediatric Neuroradiology, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

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