Cysticercosis Workup

Updated: Dec 06, 2018
  • Author: Mossammat M Mansur, MD, MBBS; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
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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. [10]

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, as follows: [11]

  • 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 but are limited in their usefulness in a community setting by general lack of availability, as follows:

  • 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. [12]
  • A 2017 meta-analysis found that ELISA for antibodies and EITB yield a similar diagnostic value. [13]
  • 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 taeniasis 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 (see image below). No live cysticerci are present at this stage, although parasite antigen may still be present. This phase represents inactive disease.

    Nonenhanced CT scan of the brain demonstrates the Nonenhanced CT scan of the brain demonstrates the multiple calcified lesions of inactive parenchymal neurocysticercosis.

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.



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. Cavellani et al used autopsy protocols to study the influence of age and gender on cardiac and encephalic inflammation caused by cysticercosis. They concluded that inflammation decreases with age and depends on the stage of the disease; women have a more intense response during senescence. [14]

Histologic studies have shown that viable cysticerci in humans and pigs have little or no surrounding inflammation. [15]

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.