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Neuroimaging in Neurocysticercosis Workup

  • Author: Arturo Carpio, MD; Chief Editor: Niranjan N Singh, MD, DM  more...
 
Updated: Nov 12, 2014
 

Laboratory Studies

Laboratory studies are inferior to imaging in the diagnosis of cysticercosis but may play an adjunctive role.

On complete blood count (CBC), peripheral eosinophilia is usually not present, but eosinophils may comprise 10-15% of white blood cells (WBCs).

Immunoserologic assays may be useful.

Immunoserologic assays, such as EITB or enzyme-linked immunosorbent assay (ELISA) can detect antibodies against T solium or cysticercus and are useful in identifying the population at risk of contact with the parasite.

These assays demonstrate a potential impact of cysticercosis on public health, but clinicians should be aware that the presence of antibodies in the host against both T solium and/or cysticercus does not necessarily indicate that an individual has active neurocysticercosis.

In ELISA, cross-reactions with other helminthic infections may occur.

An EITB using specific glycoprotein antigens was developed for the immunodiagnosis of human cysticercosis, the sensitivity and specificity of which are reported to be high (98% and 100%, respectively). Another study confirmed these results in patients with 2 or more cysts shown by CT scan or MRI (94% sensitivity), but sensitivity was markedly low in patients with single enhancing cysts and calcifications (28%).

ELISA and EITB are performed in many (but certainly not all) laboratories in the United States.

Immunologic techniques for the detection of anticysticercal antibodies in the CSF are more reliable than those performed in serum. However, the accuracy depends on the viability of cysticerci and their location within the CNS.

EITB are used mainly in serum samples. The complement fixation test and the ELISA in the CSF are highly sensitive and specific in cases of subarachnoidal neurocysticercosis.

Sensitivity decreases considerably when the lesions are calcified or when viable parenchymal cysts are not in contact with the subarachnoid space.

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Imaging Studies

The only truly reliable standard for diagnosing neurocysticercosis (NC) is pathologic confirmation through biopsy or autopsy. Nevertheless, even without definitive scientific data, CT scan and MRI are considered the main tools for the diagnosis of NC.[6, 7]

Multiple calcifications disseminated in the parenchyma simultaneously with viable cysts and transitional stage lesions are a typical finding on imaging studies in NC.

The relationship between imaging studies and the anatomopathologic changes has been well described. It can be summarized with the following recommendations:

  • Brain CT scan should be obtained as a first imaging study. CT is more widely available, less expensive, and has a faster imaging time than MRI. Contrast and noncontrast studies should be obtained.
  • Noncontrast studies will show calcification of inactive cysts, which is the most common disease form at presentation.
  • Contrast studies will show ring enhancement, signifying edema surrounding the involuting live cysticercus.

MRI is recommended as an adjunctive diagnostic tool.

Demonstration of viable cystic lesions with a mural nodule (ie, the invaginated scolex) associated with transitional or degenerative cysts and calcifications corresponds to a typical image of cysticercosis (see the image below). However, this typical imaging is not necessarily the most frequent one. Conversely, single enhancing lesions are probably more common, especially in children

Neuroimaging in neurocysticercosis. CT scans showi Neuroimaging in neurocysticercosis. CT scans showing different phases of neurocysticercosis. Top left: CT scan showing many calcifications and active cysts with scolices in both hemispheres. Top right: T1-weighted MRI showing 2 active cysts with the scolex in their interior (vesicular phase). Bottom left: Postcontrast CT scan showing a ring-enhancing cyst (colloidal phase) on left. Bottom right: Proton density-weighted MRI showing a thick capsule with adjacent scolex and perilesional edema (colloidal phase).

MRI is a superior imaging study for intraventricular or subarachnoid cysts, while CT is better for calcification of inactive lesions.

Lesions at different stages are not uncommon. Multiple calcifications disseminated in the parenchyma with viable cysts and transitional stage lesions are actually the rule as opposed to the exception in NC.

Soft tissue x-ray: Plain films may show calcification of inactive cysts.

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Other Tests

See the list below:

  • Electroencephalography: EEG may be normal or may show focal or generalized abnormalities.
  • Stool for ova and parasites: Many patients will have simultaneous intestinal tapeworm infestation. The test is nonspecific for T solium species.
  • Serologic-based assay: An immunoblot assay, EITB-T, has been developed for detection of human taeniasis carriers. It uses coproantigens of adult T solium tapeworms. The results from studies that use coproantigen detection have indicated that these assays are considerably more sensitive than microscopy.
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Procedures

See the list below:

  • Biopsy of a subcutaneous nodule or muscle lesion: Demonstration of the organism is diagnostic of cysticercosis.
  • Brain biopsy: Brain biopsy is not justified in a suspected NC lesion. In addition to the obvious morbidity (and possibly mortality) associated with this procedure, the cysts can reduce spontaneously. Moreover, cysts can resolve in response to anticysticercal therapy. Finally, waiting 1-2 months and repeating the CT scan or MRI can clarify the diagnosis.
  • Lumbar puncture
    • Lumbar puncture should be performed when arachnoiditis is suspected (ie, headache, cranial nerve palsies, cognitive changes).
    • Inflammatory changes in the CSF are largely related to the extraparenchymal location, especially with arachnoiditis. The most consistent finding is moderate mononuclear pleocytosis, usually not exceeding 200-300 cells/mm3. Protein levels are also raised to within the range of 50-200 mg/dL. CSF glucose levels are normal or moderately low. These CSF abnormalities may be difficult to distinguish from those of granulomatous infections such as tuberculosis meningitis.
    • This test is insensitive and nonspecific in the diagnosis of cysticercosis.
  • An imaging study should be done prior to lumbar puncture to exclude an intracranial mass lesion.
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Histologic Findings

Macroscopic and microscopic pathology

Cysticercus cellulosae presents a characteristic rounded and ovoid form of about 4-20 mm in length (see the first image below) covered by a thin membrane surrounding hyaline liquid. It invaginates in some sites of the membrane, giving origin to the scolex (see the second image below), which is constituted by a neck, 4 suckers, and a double crown of hooks.

Neuroimaging in neurocysticercosis. Cysticercus ce Neuroimaging in neurocysticercosis. Cysticercus cellulosae in neurocysticercosis.
Neuroimaging in neurocysticercosis. Cysticercus ce Neuroimaging in neurocysticercosis. Cysticercus cellulosae showing the invaginated scolex in neurocysticercosis.

The cysts usually are located in the gray matter due to the richer vascularization of this tissue, and in the subcortical white matter (see the image below). In severe cases of parenchymal cysticercosis, the number of parasites may reach several hundreds, but commonly only a scattered few are seen. Cysts also may be found in the subarachnoidal location, and less frequently inside the ventricles and in the spinal cord.

Neuroimaging in neurocysticercosis. Subcortical pa Neuroimaging in neurocysticercosis. Subcortical parenchymatous cysticercosis

The parasite produces an inflammatory reaction composed of a conglomerate of round mononuclear lymphocytic and plasma cells. Some of the inflammatory cells are found around the perivascular spaces in the adjacent nervous tissue. A variable number of eosinophils are also present; this eosinophilic reaction is highly variable and occurs in almost every patient (see the image below).

Neuroimaging in neurocysticercosis. Inflammatory r Neuroimaging in neurocysticercosis. Inflammatory reaction in parenchymatous cysticercosis.
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Contributor Information and Disclosures
Author

Arturo Carpio, MD Professor, University of Cuenca School of Medicine, Ecuador; Senior Research Scientist, GH Sergievsky Center, Columbia University

Arturo Carpio, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Coauthor(s)

Nicholas Lorenzo, MD, MHA, CPE Founding Editor-in-Chief, eMedicine Neurology; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc

Nicholas Lorenzo, MD, MHA, CPE is a member of the following medical societies: Alpha Omega Alpha, American Association for Physician Leadership, American Academy of Neurology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Florian P Thomas, MD, PhD, Drmed, MA, MS Director, National MS Society Multiple Sclerosis Center; Professor and Director, Clinical Research Unit, Department of Neurology, Adjunct Professor of Physical Therapy, Associate Professor, Institute for Molecular Virology, St Louis University School of Medicine; Editor-in-Chief, Journal of Spinal Cord Medicine

Florian P Thomas, MD, PhD, Drmed, MA, MS is a member of the following medical societies: Academy of Spinal Cord Injury Professionals, American Academy of Neurology, American Neurological Association, Consortium of Multiple Sclerosis Centers, National Multiple Sclerosis Society, Sigma Xi

Disclosure: Nothing to disclose.

Chief Editor

Niranjan N Singh, MD, DM Associate Professor of Neurology, University of Missouri-Columbia School of Medicine

Niranjan N Singh, MD, DM is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Headache Society

Disclosure: Nothing to disclose.

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Neuroimaging in neurocysticercosis. CT scans showing different phases of neurocysticercosis. Top left: CT scan showing many calcifications and active cysts with scolices in both hemispheres. Top right: T1-weighted MRI showing 2 active cysts with the scolex in their interior (vesicular phase). Bottom left: Postcontrast CT scan showing a ring-enhancing cyst (colloidal phase) on left. Bottom right: Proton density-weighted MRI showing a thick capsule with adjacent scolex and perilesional edema (colloidal phase).
Neuroimaging in neurocysticercosis. Natural history of neurocysticercosis. Top left: This CT scan shows a large occipital active cyst (vesicle phase), many calcifications, and small cortical cysts. Top right: After 18 months, the occipital cyst has been replaced by a calcification and the remaining cysts have disappeared. Bottom left: A single parietal nodular-enhancing lesion (transitional, nodular-granular phase) is shown. Bottom right: Six months later, the lesion has disappeared.
Neuroimaging in neurocysticercosis. Noncontrast and contrast-enhanced CT scan of neurocysticercosis. Left: Normal noncontrast CT scan. Right: After administration of the contrast medium, the CT scan of the same patient shows a single parietal nodular-enhancing lesion (transitional, nodular phase).
Neuroimaging in neurocysticercosis. Cysticercotic encephalitis. Left: Contrast-enhanced CT scan showing multiple, small, nodular, and annular areas of abnormal enhancement in brain parenchyma. Right: Gadolinium-enhanced T1-weighted MRI showing hyperintense lesions.
Neuroimaging in neurocysticercosis. Cysticercus cellulosae in neurocysticercosis.
Treatment of Neurocysticercosis
Neuroimaging in neurocysticercosis. Cysticercus cellulosae showing the invaginated scolex in neurocysticercosis.
Neuroimaging in neurocysticercosis. Subcortical parenchymatous cysticercosis
Neuroimaging in neurocysticercosis. Inflammatory reaction in parenchymatous cysticercosis.
Neuroimaging in neurocysticercosis. Antiepileptic treatment for patients with first seizure due to neurocysticercosis.
Neuroimaging in neurocysticercosis. Probability of seizure recurrence (Kaplan-Meier curve) after a first seizure in patients with NC as function of cysticidal treatment.
 
 
 
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