Cysticercosis - Clinical Manifestations and Diagnosis - UpToDate

20/11/2021 17:53 Cysticercosis: Clinical manifestations and diagnosis - UpToDate
Official reprint from UpToDate®
www.uptodate.com
© 2021 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
Cysticercosis: Clinical manifestations and diagnosis

Author: A Clinton White, Jr, MD, FACP, FIDSA
Section Editor: Peter F Weller, MD, MACP
Deputy Editor: Elinor L Baron, MD, DTMH
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2021. | This topic last updated: Nov 16, 2021.
INTRODUCTION
Cysticercosis is caused by the larval stage (metacestode) of the pork tapeworm Taenia solium.
Clinical syndromes related to this parasite include neurocysticercosis (NCC) and extraneural
cysticercosis. NCC, in turn, is divided into parenchymal and extraparenchymal forms.
Extraparenchymal forms include intraventricular, subarachnoid, spinal, and ocular disease.
Guidelines on diagnosis and treatment of NCC were published in 2018 by the Infectious
Diseases Society of America and the American Society of Tropical Medicine and Hygiene [1].
The World Health Organization published guidelines in 2021 [2].
The natural history, clinical features, and diagnosis of cysticercosis will be reviewed here. The
epidemiology, life cycle, transmission, and treatment of cysticercosis are discussed
separately. (See "Cysticercosis: Epidemiology, transmission, and prevention" and
"Cysticercosis: Treatment" and "Tapeworm infections".)
CLINICAL MANIFESTATIONS
Overview and disease phases — Following ingestion of T. solium eggs (shed in the stool of a
human tapeworm carrier), tissue cysticerci develop at one or more sites over a period of
three to eight weeks.
Phases of cysticercosis include an initial (viable) phase, early inflammatory stage, a

degenerating phase, and a nonviable phase ( table 1):
● The initial phase is usually asymptomatic; viable cysticerci do not cause much
inflammation in surrounding tissues. This stage typically persists for several years. (See
"Cysticercosis: Epidemiology, transmission, and prevention".)
https://www.uptodate.com/contents/cysticercosis-clinical-manifestations-and-diagnosis/print?search=cysticercosis&source=search_result&select… 1/26
A number of mechanisms for parasite evasion of the host immune response have been
postulated. The parasite elaborates a variety of substances that may interfere with
lymphocyte proliferation and macrophage function, thereby inhibiting normal cellular
immune defenses [3-7]. In addition, humoral antibodies are not capable of killing the
parasite.
● The cysticerci eventually lose their ability to evade the host immune response and are
attacked by the host [4-8]. Radiographic appearance of contrast enhancement and/or
edema in the parasite wall and surrounding tissues reflects the initial activity of the
host immune response against the parasite. In the setting of enhancing
intraparenchymal lesions, the inflammatory response is frequently associated with
seizures. The initial inflammatory response may not affect parasite viability as
demonstrated by a liquid center on neuroimaging.
● As the host response progresses, the parasite begins to degenerate [4-8]. The cyst fluid
is infiltrated with host cells (becoming more dense on T1 magnetic resonance imaging
and computed tomography) and eventually collapses (colloid stage).
● Ultimately, the cysticerci resolve or become nonviable calcified granulomas; presence

of intraparenchymal brain calcifications is also associated with seizures.
Seizures associated with calcified lesions may result from inflammation and/or from
intermittent antigen release [9-11]. In some cases, changes in brain plasticity and
scarring may result in epileptogenic foci [12]. Finally, some cases develop hippocampal
damage and mesotemporal sclerosis and/or atrophy that may serve as a further nidus
for seizures [13,14].
Cysticerci may occur simultaneously in more than one anatomic site. In addition, cysticerci at
different stages in their natural history may be present simultaneously; for example, at any
one time, a patient may have some viable cysts, some enhancing cysts, and/or some
calcified cysts.
In India and the United States, most patients with neurocysticercosis (NCC) present with a
single enhancing lesion [1,7,15,16]. In field studies from endemic areas of Latin America,
most patients have one or more calcified lesions [7,14,17-19]. Among hospitalized patients in
Latin America, the most common presentation is multiple viable cysticerci [1,7].
Clinical manifestations of NCC depend upon whether the cysticerci are localized to the brain
parenchyma, the extraparenchymal tissues, or both [1]. In general, intraparenchymal
cysticerci are associated with seizures and/or headache. Extraparenchymal cysticerci are
associated with symptoms of elevated intracranial pressure (eg, headache, nausea, and
vomiting) and may be accompanied by altered mental status. (See 'Intraparenchymal

neurocysticercosis' below and 'Extraparenchymal neurocysticercosis' below.)
Extraneural cysticercosis may involve a range of tissues; the most common forms include
muscle or subcutaneous tissue involvement. (See 'Extraneural cysticercosis' below.)
Intraparenchymal neurocysticercosis — Intraparenchymal NCC is the most common form

of cysticercosis; it occurs in >60 percent of cases [1,7,8,15,16]. Onset of symptomatic
parenchymal NCC usually occurs three to five years following infection but can occur >30
years following infection; in patients with delayed presentation, presence of nonviable
(calcified) lesions is common [16,20,21].
The clinical manifestations of parenchymal NCC depend on the number and location of
cysticerci and the degree of associated inflammatory response [7,8]:
● Seizures are the most common clinical manifestation of parenchymal NCC; they are
usually focal and may be associated with secondary generalization [7,8,15,16,22,23].
Seizures may occur in the setting of cyst degeneration (associated with enhancement
on radiographic imaging) and/or in the setting of nonviable cysticerci (associated with
calcification on radiographic imaging). In many endemic countries, NCC is the most
common cause of adult-onset seizures [7,8,22]. Headaches are also frequent, but
headache alone does not typically prompt patients with NCC to seek medical attention.
● Less common manifestations of parenchymal NCC include altered vision, focal

neurologic signs, and meningitis. Fever is typically absent. In the absence of mass
effect or stroke, neurologic examination usually does not demonstrate focal signs.
● In patients with massive numbers of parenchymal cysticerci, an intense immune

response with diffuse brain edema can cause a clinical picture resembling encephalitis;
clinical manifestations may include seizures, headache, nausea and vomiting, impaired
consciousness, reduced visual acuity, and occasionally fever. Cysticercal encephalitis is
a rare form of NCC that typically presents in children and young women. Cysticercal
encephalitis can occur spontaneously or can be provoked by antiparasitic therapy
(which causes a large number of cysticerci to degenerate simultaneously).
● Many cases of parenchymal NCC are asymptomatic and are identified incidentally via
radiographic imaging performed for other reasons [17,18,24]. In studies of the natural
history of NCC, most cystic lesions resolve with development of calcifications, in the
absence of symptoms [17,18,24].
The prognosis of parenchymal NCC varies with the number of cysticerci and degree of
inflammation [1,7,8]. Patients with single enhancing lesions have a more favorable
prognosis than those with multiple viable cysticerci.
Extraparenchymal neurocysticercosis — Extraparenchymal NCC can occur in the

ventricles, the subarachnoid space, the spine, and/or the eye; these presentations occur
more commonly in adults than in children [7,8,25,26]. Extraparenchymal NCC can coexist
with intraparenchymal disease.
Extraparenchymal cysticerci are associated with symptoms of elevated intracranial pressure

(eg, headache, nausea, and vomiting) and may be accompanied by altered mental status. In
general, extraparenchymal NCC carries a higher risk for complication or death than
parenchymal NCC [27].
Intraventricular lesions — Intraventricular cysticerci (free-floating cysts in the ventricular

cavity or attached to the choroid plexus) occur in 10 to 20 percent of cases.
Typically, symptoms develop when cysticerci become lodged in the ventricular outflow
tracks, with consequent obstructive hydrocephalus and increased intracranial pressure
(gradual or acute onset) [7,8,16,26,28]. Associated symptoms include headache, nausea and
vomiting, altered mental status, and decreased visual acuity with papilledema. Less frequent
symptoms include seizures and focal neurologic signs, usually from coexistent disease in the
parenchyma or subarachnoid space.
Occasionally, mobile cysts in the third or fourth ventricle can cause intermittent obstruction,
leading to episodes of sudden loss of consciousness related to head movements (Bruns'
syndrome) [29].
Subarachnoid lesions — Subarachnoid neurocysticercosis (SAN) in the basilar cisterns is

the most severe form of NCC; it occurs in about 5 percent of hospitalized cases [8,16,30,31].
In some cases of SAN, the cysticerci have lost the scolex and may consistent of a cluster of
proliferating membranes (referred to as racemose cysticercosis). SAN may be associated
with chronic arachnoiditis and/or mass effect due to cyst enlargement ( figure 1 and
image 1). In addition, there is a strong association between SAN and involvement of the
spinal subarachnoid space [32]. (See 'Spinal lesions' below.)
Chronic arachnoiditis may develop as a result of local inflammation; in some cases, it may be
associated with communicating hydrocephalus, vasculitis, meningitis, and stroke
[7,16,31,33]. The radiographic appearance is similar to other causes of basilar meningitis,
unless cysticerci are visible. Obstructive hydrocephalus can occur in the setting of secondary
occlusion of the foramina of Luschka or Magendie. In addition, meningeal inflammation and
leptomeningeal thickening at the base of the brain can lead to visual field defects and cranial
nerve palsies due to entrapment of the cranial nerves arising from the brainstem. Vascular
involvement can lead to proliferative angiitis and vascular obstruction with secondary
cerebral infarcts [7,31,33-35]. Focal neurologic motor signs, ataxia, and sensory dysfunction
can ensue.
Mass effect and focal neurologic defects can develop in patients whose cysticerci enlarge
within in the subarachnoid space, where cysts may grow to 10 cm or larger. This is
commonly observed with cysticerci in the sylvian fissure, where cyst growth is not limited by
pressure from the brain parenchyma [8].
Spinal lesions — Spinal cord involvement occurs in approximately 1 percent of cases [36].
Spinal cysticerci are usually located in the subarachnoid space where they can cause
inflammatory and demyelinating changes in the peripheral nerve roots. Patients typically
present with radicular pain, paresthesias and/or sphincter disturbances. Neurologic deficits
vary with the location of the lesion and may be clinically indistinguishable from other spinal
cord lesions. There is a strong association between spinal subarachnoid cysticerci and basal
subarachnoid involvement [32]. (See 'Subarachnoid lesions' above.)
Less commonly, intramedullary cysticercosis can occur and may be associated with
transverse myelitis.
Orbital and ocular lesions — Cases of orbital and ocular cysticercosis have been observed
almost exclusively from India; this may reflect changes in transmission dynamics [37]. Ocular
cysticercosis occurs in approximately 1 to 3 percent of cases of neurocysticercosis [38-40].
In a review including 556 cases of ocular cysticercosis, the majority presented with orbital
disease, especially involvement of the extraocular muscles (69 percent) and subconjunctiva
(14 percent). Intraocular involvement was noted in 72 cases, including the vitreous cavity (8
percent), anterior chamber (1.4 percent), and subretina (4 percent). Since the retina is neural
tissue, the presence of subretinal cysticerci reflects neurocysticercosis.
Symptoms may include impaired vision, recurrent eye pain, diplopia, and masses.
Inflammation around degenerating intraocular cysticerci can threaten vision by causing
chorioretinitis, retinal detachment, or vasculitis. However, many patients are asymptomatic.
Ocular cysticercosis should be excluded by an ophthalmologic examination in all patients

with NCC prior to initiating antiparasitic therapy [1]. Direct visualization of the parasite by
funduscopic examination is pathognomonic for diagnosis of cysticercosis ( picture 1).
Extraneural cysticercosis — Extraneural cysticercosis may involve a wide range of tissues.
The most common manifestations include muscle or subcutaneous tissue involvement;

these are usually asymptomatic nodules 0.5 to 2.0 cm in diameter but may cause discomfort
when inflamed. Intramuscular cysts often undergo calcification and may be detected
incidentally as "cigar-shaped calcifications" when radiographs are performed for unrelated
reasons [8]. In the setting of extensive muscle involvement, acute myopathy can develop.
Muscle or subcutaneous tissue involvement is more common in patients from Asia and
Africa than from Latin America.
Cardiac cysticerci have also been described. These may be asymptomatic or may be
associated with arrhythmias and/or conduction abnormalities.
Cysticerci in the anterior chamber of the eye has been described. (See 'Orbital and ocular
lesions' above.)
Laboratory findings — Most patients with cysticercosis have no specific diagnostic findings

on routine blood counts or liver function tests. Peripheral eosinophilia is usually absent.
Stool examination is insensitive since most individuals with cysticercosis do not have a viable
intestinal tapeworm at the time of diagnosis.
DIAGNOSIS
Clinical approach — The diagnosis of cysticercosis should be suspected in patients with

seizures and/or manifestations of elevated intracranial pressure and relevant neuroimaging
findings (such as cystic lesions, enhancing lesions, and/or calcifications), in the setting of
relevant epidemiologic exposure (ingestion of T. solium eggs shed in the stool of a tapeworm
carrier either in association with exposure in an endemic area or household exposure to an
asymptomatic carrier). (See "Cysticercosis: Epidemiology, transmission, and prevention".)
The diagnosis of cysticercosis is established based on clinical manifestations, neuroimaging

findings, and epidemiologic exposure ( table 2 and table 3) [1,2,7,41-44]. Revised
diagnostic criteria have been proposed and validated [45,46], replacing older criteria
[41,43,44]. Neuroimaging studies should include both computed tomography (CT) and
magnetic resonance imaging (MRI), when feasible ( table 1).
Serologic testing should be performed for confirmatory evaluation in patients with

suspected cysticercosis [1,47]. Such results are most useful for patients with neuroimaging
findings that are consistent with NCC but not diagnostic. Patients with diagnostic
neuroimaging findings warrant treatment before serologic results are available. (See
'Serology' below.)
In rare cases, if the radiographic appearance is nonspecific and serologic tests are negative,
biopsy may be required to differentiate NCC from other brain lesions (such as abscess or
malignancy). (See 'Differential diagnosis' below.)
Additional evaluation for all patients with cysticercosis prior to the initiation of therapy
should include an ophthalmologic examination to exclude ocular cysticercosis [1]. Direct
visualization of the parasite by funduscopic examination is pathognomonic for diagnosis of
cysticercosis [41]. Although ocular cysticercosis is relatively uncommon and many patients
are asymptomatic, inflammation around degenerating cysticerci can threaten vision,
particularly in the setting of antiparasitic therapy. (See 'Orbital and ocular lesions' above and
"Cysticercosis: Treatment".)
In addition, patients likely to require prolonged corticosteroids should undergo screening

for latent tuberculosis infection as well as screening or empiric therapy for strongyloidiasis.
(See "Approach to diagnosis of latent tuberculosis infection (tuberculosis screening) in
adults" and "Strongyloidiasis".)
For patients who acquired cysticercosis in a nonendemic area, it is reasonable for household
members to be screened for tapeworm carriage.
Primary diagnostic tools
Radiographic imaging
Modalities — Patients with suspected NCC should be evaluated with CT scan and MRI
of the brain ( table 1) [1,2].
CT is useful for identifying calcifications and parenchymal cysticerci. CT is also useful for
diagnosis of cysticercal involvement of the eye and orbits [38,48]. MRI is useful for detecting
relatively small lesions, evaluating degenerative changes, detecting edema around calcified
lesions, and visualizing scolices within calcified lesions [4,49]. Fluid-attenuated inversion
recovery (FLAIR) images on MRI are particularly helpful in identifying cysticerci in the
parenchyma.
MRI is also useful for intraventricular and subarachnoid lesions [4,49,50]. Three-dimensional
MRI sequences such as fast imaging employing steady-state acquisition (FIESTA) and three-
dimensional constructive interference in steady state (3D CISS) improve the sensitivity of MRI
for cysts at these sites and are useful for identifying cysticerci in cerebrospinal fluid (CSF) [49-
52].
Patients with basal subarachnoid involvement should undergo MRI of the spine, given the
strong association between basal subarachnoid involvement and spinal subarachnoid
cysticerci [1,32]. Myelography may also be helpful. (See 'Subarachnoid lesions' above.)
Patients with suspected extraneural cysticercosis (muscle or subcutaneous tissue

involvement) may be evaluated with plain radiography or CT for detection calcified lesions
("cigar-shaped calcifications") in muscle or subcutaneous tissue [53]. (See 'Extraneural
cysticercosis' above.)
Findings — Radiographic manifestations of intraparenchymal NCC include cystic

lesions, enhancing lesions, and calcifications ( table 1 and image 1 and figure 1).
These forms may coexist simultaneously.
Viable cysts are round, nonenhancing hypodense lesions usually 5 to 20 mm in diameter. As

the cyst begins to degenerate, the cyst wall increases in density and is often accompanied by
edema or contrast enhancement. Following collapse of the cyst, a residual calcified
granuloma may be present; calcifications are usually solid, nodular lesions 2 to 4 mm in
diameter (range 1 to 10 mm). Calcified lesions are usually nonenhancing but may be
associated with perilesional edema in some cases.
Identification of a scolex (the anterior end of the tapeworm with suckers and hooks for
attachment) within a cystic lesion is a pathognomonic radiographic finding ( image 1).
Scolices appear as rounded or elongated bright nodules (2 to 4 mm in diameter) within the
cyst cavity. Scolices are not usually detectable within calcified lesions but occasionally this
finding may be observed on MRI.
Less common manifestations of intraparenchymal NCC include involvement of the

brainstem, cerebellum, or basal ganglia, mass effect, diffuse cerebral edema, cerebral
infarction, giant cysts measuring >20 mm, and multiple cysts numbering >50. Displacement
of midline structures is rare.
Radiographic manifestations of extraparenchymal NCC include intraventricular cysts,

subarachnoid cysts, leptomeningeal enhancement, and/or hydrocephalus with ventricular
enlargement.
Resolution of lesions (either spontaneously or after antiparasitic therapy) is strongly

suggestive of neurocysticercosis.
Serology — Serologic testing should be performed for confirmatory evaluation in patients

with suspected cysticercosis [1,47]. Such results are most useful for patients with
neuroimaging findings that are consistent with NCC but not diagnostic. Patients with
diagnostic neuroimaging findings warrant treatment before serologic results are available.
The serologic test of choice is enzyme-linked immunoelectrotransfer blot (EITB) using

parasite glycoproteins performed on serum [1,45,54]. It was developed by the United States
Centers for Disease Control and Prevention, but thus far is not available in the United States.
Some reference laboratories offer alternative immunoblot assays. Commercial enzyme-
linked immunosorbent assays using unfractionated antigens should not be used, as these
have performed poorly in comparative studies (both false-positive and false-negative results)
[1,55,56].
The sensitivity of EITB varies with the form of NCC and the specimen. Testing serum is
generally more sensitive than CSF [54,57]. In patients with multiple parenchymal lesions,
ventricular lesions, or subarachnoid lesions, the sensitivity of serum EITB is nearly 100
percent [54,57,58]. However, in patients with a single parenchymal lesion or calcifications

only, the sensitivity is poor [57].
Monoclonal antibody-based antigen-detection assays can aid in the diagnosis. These tests
are commercially available in Europe; their availability in the United States is limited but they
can be obtained through the NIH [1,44].
Negative serologic test results do not exclude the diagnosis of NCC in patients with
compatible clinical manifestations and radiographic findings. In addition, for individuals
from endemic areas, positive serologic test results may reflect previous infection and/or
extraneural cysticercosis [59].
Molecular tests — Molecular tests are increasingly used for diagnosis of

neurocysticercosis. A quantitative real time polymerase chain reaction (PCR) assay for T.
solium DNA is highly sensitive and specific for active subarachnoid and ventricular
neurocysticercosis; quantitative changes also correlated with response to therapy [60]. The
assay is more sensitive when performed in cerebral spinal fluid than on serum; the
sensitivity for parenchymal disease has not been reported. There are also increasing reports
of using metagenomic next-generation sequencing for diagnosis of subarachnoid
neurocysticercosis [61,62].
Diagnostic tools used in some circumstances
Cerebrospinal fluid analysis — A lumbar puncture for CSF examination is not necessary
for the diagnosis of NCC; in some circumstances, CSF findings can be helpful for excluding
other diagnoses. Lumbar puncture is contraindicated in the setting of increased intracranial
pressure.
In the setting of parenchymal lesions, CSF typically demonstrates a mildly elevated white cell
count with normal glucose and protein concentrations.
In the setting of arachnoiditis or ventriculitis, pleocytosis with markedly elevated protein

concentrations and decreased glucose concentrations may be observed. Cell counts may
demonstrate a predominance of mononuclear cells, but can also demonstrate neutrophils or
eosinophils.
The EITB assay can be performed on CSF, but the sensitivity is usually higher with serum. In
contrast, antigen detection and quantitative PCR are more sensitive on CSF.
Histopathology — Brain biopsy is warranted only in rare cases for which noninvasive

testing is insufficient to establish the diagnosis of cysticercosis. Excisional biopsy of a skin or
muscle lesion can be useful for diagnosis of extraneural cysticercosis.
A viable cysticercus appears as a translucent fluid-filled membrane (about 5 to 10 mm in

diameter) containing a solid larval tapeworm scolex (2 mm in length) ( image 1).
Histopathology typically demonstrates membranous walls filled with fluid. Less often, the
scolex (the anterior end of the tapeworm with suckers and hooks) may also be visualized;
this finding is pathognomonic for the diagnosis of cysticercosis [63]. The degree of
inflammation can be variable. As the parasite degenerates, the cyst cavity collapses and the
parasite walls are gradually engulfed in granulomatous inflammation.
DIFFERENTIAL DIAGNOSIS
Other conditions that can mimic single or multiple ring or nodular enhancing lesions include
tuberculoma, pyogenic brain abscess, mycotic granuloma, and primary or metastatic brain
tumor.
Cystic lesions of the brain include cystic echinococcosis and coenurosis.
Parenchymal brain calcifications on computed tomography may be observed in the setting

of metabolic disorders, vascular malformations, intracranial neoplasms, and congenital
anomalies; these may be distinguished via magnetic resonance imaging.
Arachnoiditis with ventricular enlargement may be seen in the setting of tuberculous and
fungal meningitis and meningeal carcinomatosis.
Other conditions include primary or metastatic tumors, toxoplasmosis, nocardiosis, and

septic emboli.
The differential diagnosis of an eosinophilic cerebrospinal fluid pleocytosis includes

coccidioidomycosis, gnathostomiasis, baylisascariasis, angiostrongyloidiasis, and
noninfectious causes. (See "Eosinophilic meningitis".)
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Cysticercosis".)
SUMMARY
● Cysticercosis is caused by the larval stage of the pork tapeworm Taenia solium. Clinical
syndromes include neurocysticercosis (NCC) and extraneural cysticercosis. NCC is
divided into parenchymal and extraparenchymal forms. Stages of cysticercosis include
an initial (viable) phase, a degenerating (enhancing) phase, and a nonviable (calcified)
https://www.uptodate.com/contents/cysticercosis-clinical-manifestations-and-diagnosis/print?search=cysticercosis&source=search_result&sele… 10/26
phase ( table 1). Cysticerci may be present in more than one anatomic site, and
cysticerci at different stages in their natural history may be present simultaneously.
(See 'Overview and disease phases' above.)
● Intraparenchymal NCC is the most common form of cysticercosis; it occurs in >60

percent of cases. Onset of symptoms usually occurs three to five years following
infection but can occur >30 years following infection. Seizures are the most common
manifestation; less common manifestations include altered vision, focal neurologic
signs, and meningitis. In patients with massive numbers of parenchymal cysts, an
intense immune response with diffuse edema can cause a clinical picture resembling
encephalitis; manifestations may include seizures, headache, nausea and vomiting,
impaired consciousness, reduced visual acuity, and occasionally fever. Many cases of
parenchymal NCC are asymptomatic and are identified incidentally via radiographic
imaging performed for other reasons. (See 'Intraparenchymal neurocysticercosis'
above.)
● Intraventricular NCC (free-floating cysts in the ventricular cavity or attached to the

choroid plexus) occurs in 10 to 20 percent of cases. Typically, symptoms develop when
cysticerci become lodged in the ventricular outflow tracks, with consequent obstructive
hydrocephalus and increased intracranial pressure. Associated symptoms include
headache, nausea and vomiting, altered mental status, and decreased visual acuity
with papilledema. (See 'Intraventricular lesions' above.)
● Subarachnoid neurocysticercosis is the most severe form of NCC; it occurs in about 5

percent of hospitalized cases. Subarachnoid NCC may be associated with chronic
arachnoiditis and/or mass effect due to cyst enlargement. Chronic arachnoiditis may
develop as a result of local inflammation; in some cases, it may be associated with
communicating hydrocephalus, vasculitis, meningitis, and stroke. Mass effect and focal
neurologic defects can develop in patients whose cysticerci enlarge within in the
subarachnoid space, where cysts may grow to 10 cm or larger. (See 'Subarachnoid
lesions' above.)
● Other clinical presentations of NCC include spinal lesions (1 percent of cases) and
ocular lesions (1 to 3 percent of cases). Spinal cysticerci are usually located in the
subarachnoid space where they can cause inflammatory and demyelinating changes in
the peripheral nerve roots. Patients typically present with radicular pain, paresthesias,
and/or sphincter disturbances. Patients with ocular cysticercosis may have involvement
of the subretinal space, vitreous humor, anterior chamber, conjunctiva, or extraocular
muscles. (See 'Spinal lesions' above and 'Orbital and ocular lesions' above.)
● Extraneural cysticercosis may present with muscle or subcutaneous tissue involvement;

these manifestations are usually asymptomatic but may cause discomfort when
inflamed. Intramuscular cysts often undergo calcification and may be detected

radiographically as "cigar-shaped calcifications." (See 'Extraneural cysticercosis' above.)
● The diagnosis of cysticercosis should be suspected in patients with seizures and/or

manifestations of elevated intracranial pressure and relevant neuroimaging findings
(such as cystic lesions, enhancing lesions, and/or calcifications), in the setting of
relevant epidemiologic exposure (ingestion of T. solium eggs shed in the stool of a
tapeworm carrier either in association with exposure in an endemic area or household
exposure to an asymptomatic carrier). Diagnostic criteria for cysticercosis are based on
clinical manifestations, neuroimaging findings, and epidemiologic exposure ( table 2
and table 3). (See 'Clinical approach' above.)
● Patients with suspected NCC should be evaluated with computed tomography (CT) scan
and magnetic resonance imaging (MRI) of the brain. CT is useful for identifying
calcifications and parenchymal cysticerci. MRI is useful for detecting relatively small
lesions, evaluating degenerative changes, detecting edema around calcified lesions,
and visualizing scolices within calcified lesions. (See 'Modalities' above.)
● Radiographic manifestations of intraparenchymal NCC are summarized in the table (

table 1 and figure 1 and image 1). Viable cysts are round, nonenhancing
hypodense lesions usually 5 to 20 mm in diameter. As the cyst begins to degenerate,
the cyst wall increases in density and is often accompanied by edema or contrast
enhancement. Following collapse of the cyst, a residual calcified granuloma may be
present; calcifications are usually solid, nodular lesions 2 to 4 mm in diameter (range 1
to 10 mm). Identification of a scolex (the anterior end of the tapeworm with suckers
and hooks for attachment) within a cystic lesion is a pathognomonic radiographic
finding ( image 1). Scolices appear as rounded or elongated bright nodules (2 to 4
mm in diameter) within the cyst cavity. (See 'Findings' above.)
● Serologic testing should be performed for confirmatory evaluation in patients with

suspected cysticercosis. Such results are most useful for patients with neuroimaging
findings that are consistent with NCC but not diagnostic. Patients with diagnostic
neuroimaging findings warrant treatment before serologic results are available. (See
'Serology' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. White AC Jr, Coyle CM, Rajshekhar V, et al. Diagnosis and Treatment of

Neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society
of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).
Clin Infect Dis 2018; 66:e49.
2. World Health Organization. WHO guidelines on management of Taenia solium neurocys
ticercosis. https://www.who.int/publications/i/item/9789240032231 (Accessed on Nove
mber 03, 2021).
3. White AC, Jr, Robinson P, Kuhn R. Taenia solium cysticercosis: Host-parasite interactions
and the immune response. In: Immunopathogenetic Aspects of Disease Induced by Hel
minth Parasites, Freedman DO (Ed), Karger, Basel 1997. p.209.
4. Lerner A, Shiroishi MS, Zee CS, et al. Imaging of neurocysticercosis. Neuroimaging Clin
N Am 2012; 22:659.
5. Prodjinotho UF, Lema J, Lacorcia M, et al. Host immune responses during Taenia solium
Neurocysticercosis infection and treatment. PLoS Negl Trop Dis 2020; 14:e0008005.
6. Dixon MA, Winskill P, Harrison WE, Basáñez MG. Taenia solium taeniasis/cysticercosis:
From parasite biology and immunology to diagnosis and control. Adv Parasitol 2021;
112:133.
7. Garcia HH, Gonzalez AE, Gilman RH. Taenia solium Cysticercosis and Its Impact in
Neurological Disease. Clin Microbiol Rev 2020; 33.
8. Coyle CM. Neurocysticerosis: An Individualized Approach. Infect Dis Clin North Am 2019;
33:153.
9. Nash TE, Pretell EJ, Lescano AG, et al. Perilesional brain oedema and seizure activity in
patients with calcified neurocysticercosis: a prospective cohort and nested case-control
study. Lancet Neurol 2008; 7:1099.
10. Gupta RK, Awasthi R, Rathore RK, et al. Understanding epileptogenesis in calcified
neurocysticercosis with perfusion MRI. Neurology 2012; 78:618.
11. Nash TE, Bustos JA, Garcia HH, Cysticercosis Working Group in Perú. Disease Centered
Around Calcified Taenia solium Granuloma. Trends Parasitol 2017; 33:65.
12. Bianchin MM, Velasco TR, Wichert-Ana L, et al. Understanding the association of
neurocysticercosis and mesial temporal lobe epilepsy and its impact on the surgical
treatment of patients with drug-resistant epilepsy. Epilepsy Behav 2017; 76:168.
13. Sánchez SS, Bustos JA, Del Brutto OH, et al. Hippocampal Atrophy/Sclerosis Is Associated
with Old, Calcified Parenchymal Brain Neurocysticercosis, But Not with More Recent,
Viable Infections. Am J Trop Med Hyg 2021.
14. Del Brutto OH, Mera RM, Wu S, et al. Epilepsy, interictal EEG abnormalities and
hippocampal atrophy in patients with calcified neurocysticercosis: a population study in
an endemic milieu. Epileptic Disord 2021; 23:357.
15. Singhi P, Ray M, Singhi S, Khandelwal N. Clinical spectrum of 500 children with
neurocysticercosis and response to albendazole therapy. J Child Neurol 2000; 15:207.
16. Serpa JA, Graviss EA, Kass JS, White AC Jr. Neurocysticercosis in Houston, Texas: an
update. Medicine (Baltimore) 2011; 90:81.
17. Montano SM, Villaran MV, Ylquimiche L, et al. Neurocysticercosis: association between
seizures, serology, and brain CT in rural Peru. Neurology 2005; 65:229.
18. Fleury A, Gomez T, Alvarez I, et al. High prevalence of calcified silent neurocysticercosis
in a rural village of Mexico. Neuroepidemiology 2003; 22:139.
19. Moyano LM, O'Neal SE, Ayvar V, et al. High Prevalence of Asymptomatic
Neurocysticercosis in an Endemic Rural Community in Peru. PLoS Negl Trop Dis 2016;
10:e0005130.
20. del la Garza Y, Graviss EA, Daver NG, et al. Epidemiology of neurocysticercosis in
Houston, Texas. Am J Trop Med Hyg 2005; 73:766.
21. Dixon HB, Lipscomb FM. Cysticercosis: An analysis and follow-up of 450 cases, Her Majes
ty's Stationary Service, London 1961.
22. Medina MT, Durón RM, Martínez L, et al. Prevalence, incidence, and etiology of
epilepsies in rural Honduras: the Salamá Study. Epilepsia 2005; 46:124.
23. Herrick JA, Bustos JA, Clapham P, et al. Unique Characteristics of Epilepsy Development
in Neurocysticercosis. Am J Trop Med Hyg 2020; 103:639.
24. Prasad A, Gupta RK, Pradhan S, et al. What triggers seizures in neurocysticercosis? A
MRI-based study in pig farming community from a district of North India. Parasitol Int
2008; 57:166.
25. Sáenz B, Ruíz-Garcia M, Jiménez E, et al. Neurocysticercosis: clinical, radiologic, and

inflammatory differences between children and adults. Pediatr Infect Dis J 2006; 25:801.
26. Rangel-Castilla L, Serpa JA, Gopinath SP, et al. Contemporary neurosurgical approaches
to neurocysticercosis. Am J Trop Med Hyg 2009; 80:373.
27. Abanto J, Blanco D, Saavedra H, et al. Mortality in Parenchymal and Subarachnoid

Neurocysticercosis. Am J Trop Med Hyg 2021; 105:176.
28. Nash TE, Ware JM, Mahanty S. Intraventricular Neurocysticercosis: Experience and Long-
Term Outcome from a Tertiary Referral Center in the United States. Am J Trop Med Hyg
2018; 98:1755.
29. Torres-Corzo J, Rodriguez-della Vecchia R, Rangel-Castilla L. Bruns syndrome caused by
intraventricular neurocysticercosis treated using flexible endoscopy. J Neurosurg 2006;
104:746.
30. Nash TE, O'Connell EM, Hammoud DA, et al. Natural History of Treated Subarachnoid
Neurocysticercosis. Am J Trop Med Hyg 2020; 102:78.
31. Nash TE, O'Connell EM. Subarachnoid neurocysticercosis: emerging concepts and
treatment. Curr Opin Infect Dis 2020; 33:339.
32. Callacondo D, Garcia HH, Gonzales I, et al. High frequency of spinal involvement in
patients with basal subarachnoid neurocysticercosis. Neurology 2012; 78:1394.
33. Viola GM, White AC Jr, Serpa JA. Hemorrhagic cerebrovascular events and
neurocysticercosis: a case report and review of the literature. Am J Trop Med Hyg 2011;
84:402.
34. Barinagarrementeria F, Cantú C. Frequency of cerebral arteritis in subarachnoid
cysticercosis: an angiographic study. Stroke 1998; 29:123.
35. Jha S, Kumar V. Neurocysticercosis presenting as stroke. Neurol India 2000; 48:391.
36. Alsina GA, Johnson JP, McBride DQ, et al. Spinal neurocysticercosis. Neurosurg Focus
2002; 12:e8.
37. Hamamoto Filho PT, Singh G, Winkler AS, et al. Could Differences in Infection Pressure
Be Involved in Cysticercosis Heterogeneity? Trends Parasitol 2020; 36:826.
38. Pushker N, Bajaj MS, Chandra M, Neena . Ocular and orbital cysticercosis. Acta
Ophthalmol Scand 2001; 79:408.
39. Rath S, Honavar SG, Naik M, et al. Orbital cysticercosis: clinical manifestations,
diagnosis, management, and outcome. Ophthalmology 2010; 117:600.
40. Pujari A, Bhaskaran K, Modaboyina S, et al. Cysticercosis in ophthalmology. Surv
Ophthalmol 2021.
41. Del Brutto OH, Rajshekhar V, White AC Jr, et al. Proposed diagnostic criteria for
neurocysticercosis. Neurology 2001; 57:177.
42. Rajshekhar V, Chandy MJ. Validation of diagnostic criteria for solitary cerebral
cysticercus granuloma in patients presenting with seizures. Acta Neurol Scand 1997;
96:76.
43. Carpio A, Fleury A, Romo ML, et al. New diagnostic criteria for neurocysticercosis:
Reliability and validity. Ann Neurol 2016; 80:434.
44. Gabriël S, Blocher J, Dorny P, et al. Added value of antigen ELISA in the diagnosis of
neurocysticercosis in resource poor settings. PLoS Negl Trop Dis 2012; 6:e1851.
45. Del Brutto OH, Nash TE, White AC Jr, et al. Revised diagnostic criteria for
neurocysticercosis. J Neurol Sci 2017; 372:202.
46. Bustos JA, García HH, Del Brutto OH. Reliability of Diagnostic Criteria for
Neurocysticercosis for Patients with Ventricular Cystic Lesions or Granulomas: A
systematic review. Am J Trop Med Hyg 2017; 97:653.
47. Arroyo G, Rodriguez S, Lescano AG, et al. Antibody Banding Patterns of the Enzyme-
Linked Immunoelectrotransfer Blot and Brain Imaging Findings in Patients With
Neurocysticercosis. Clin Infect Dis 2018; 66:282.
48. Sharma T, Sinha S, Shah N, et al. Intraocular cysticercosis: clinical characteristics and
visual outcome after vitreoretinal surgery. Ophthalmology 2003; 110:996.
49. do Amaral LL, Ferreira RM, da Rocha AJ, Ferreira NP. Neurocysticercosis: evaluation with
advanced magnetic resonance techniques and atypical forms. Top Magn Reson Imaging
2005; 16:127.
50. Carrillo Mezo R, Lara García J, Arroyo M, Fleury A. Relevance of 3D magnetic resonance
imaging sequences in diagnosing basal subarachnoid neurocysticercosis. Acta Trop
2015; 152:60.
51. Hernández RD, Durán BB, Lujambio PS. Magnetic resonance imaging in
neurocysticercosis. Top Magn Reson Imaging 2014; 23:191.
52. Batta A, Mahesh KV, Prabhat N, et al. Newer magnetic resonance imaging techniques in
neurocysticercosis. Neuroradiol J 2020; 33:538.
53. Bustos JA, Garcia HH, Dorregaray R, et al. Detection of muscle calcifications by thigh CT
scan in neurocysticercosis patients. Trans R Soc Trop Med Hyg 2005; 99:775.
54. Tsang VC, Brand JA, Boyer AE. An enzyme-linked immunoelectrotransfer blot assay and
glycoprotein antigens for diagnosing human cysticercosis (Taenia solium). J Infect Dis
1989; 159:50.
55. Garcia HH, Castillo Y, Gonzales I, et al. Low sensitivity and frequent cross-reactions in
commercially available antibody detection ELISA assays for Taenia solium cysticercosis.
Trop Med Int Health 2018; 23:101.
56. Carod JF, Randrianarison M, Razafimahefa J, et al. Evaluation of the performance of 5

commercialized enzyme immunoassays for the detection of Taenia solium antibodies
and for the diagnosis of neurocysticercosis. Diagn Microbiol Infect Dis 2012; 72:85.
57. Garcia HH, O'Neal SE, Noh J, et al. Laboratory Diagnosis of Neurocysticercosis (Taenia
solium). J Clin Microbiol 2018; 56.
58. Vasudevan P, Moorthy RK, Rebekah G, et al. Imaging correlates of serum enzyme-linked
immunoelectrotransfer blot (EITB) positivity in patients with parenchymal
neurocysticercosis: results from 521 patients. Trans R Soc Trop Med Hyg 2021.
59. Garcia HH, Gilman RH, Catacora M, et al. Serologic evolution of neurocysticercosis
patients after antiparasitic therapy. Cysticercosis Working Group in Peru. J Infect Dis
1997; 175:486.
60. O'Connell EM, Harrison S, Dahlstrom E, et al. A Novel, Highly Sensitive Quantitative
Polymerase Chain Reaction Assay for the Diagnosis of Subarachnoid and Ventricular
Neurocysticercosis and for Assessing Responses to Treatment. Clin Infect Dis 2020;
70:1875.
61. Fei X, Li C, Zhang Y, et al. Next-generation sequencing of cerebrospinal fluid for the
diagnosis of neurocysticercosis. Clin Neurol Neurosurg 2020; 193:105752.
62. Wilson MR, O'Donovan BD, Gelfand JM, et al. Chronic Meningitis Investigated via
Metagenomic Next-Generation Sequencing. JAMA Neurol 2018; 75:947.
63. Gutierrez Y. Cysticercosis, Coenurosis, and Sparganosis. In: Diagnostic Pathology of Para
sitic Infection with Clinical Correlation, Gutierrez Y (Ed), Oxford University Press, Oxford
2000. p.635.
Topic 5678 Version 25.0
GRAPHICS
Classification of neurocysticercosis based on location and appearance of the

parasite and surrounding host tissue on neuroimaging
Form* Characteristic on neuroimaging Histopathology
Parenchymal¶
Nonviable Nodular calcifications <20 mm in Calcified granuloma with or without

calcified diameter (often 1 to 5 mm) with or surrounding inflammation and/or
without surrounding edema and/or gliosis.
contrast enhancement.
Single, small Cystic or nodular enhancing lesion <2 Single parenchymal parasites in the
enhancing cm in size. process of degeneration with
surrounding inflammation and variable
opacification or absence of the cyst
fluid.
Viable Vesicular lesions often with evidence of Parasites with intact cyst wall, vesicular
parenchymal associated contrast enhancement fluid, and scolex, with variable amounts
and/or surrounding edema. The scolex of inflammation surrounding the
is often visible on high-definition parasite sometimes invading the cyst
imaging. wall.
ExtraparenchymalΔ
Intraventricular Cysticerci within the ventricles, Viable cysticercus cyst within the
obstructive hydrocephalus or loculated ventricle and/or obstructive
hydrocephalus with disproportionate hydrocephalus.
dilatation of the ventricles in CT/MRI
(suggestive of a cysticercus).
Subarachnoid Cysticerci in the Sylvian fissure, in the Cysticerci in the subarachnoid space
basilar cisterns, or interhemispheric often with arachnoiditis, vasculitis. The
spaces. Strokes or meningitis without cysticerci are often in clusters with
discrete cysts. proliferating membranes (racemose)
and may lack a scolex.
Spinal Cysticerci within the spinal Subarachnoid cysticerci often with

subarachnoid space with or without associated arachnoiditis.
evidence of inflammation/diffuse spinal Intramedullary cysticerci similar
arachnoiditis. Intramedullary cysticerci pathologically to parenchymal
within the spinal cord. cysticerci.
CT: computed tomography; MRI: magnetic resonance imaging.
* Patients with more than one form are classified with the form found lower on the chart, with the
exception that single enhancing lesions that are also viable are grouped with single enhancing
lesions. Ocular cysticercosis is classified separately.
¶ Refers to cysticerci in the brain parenchyma. Small cysticerci in the gyri over the cerebral convexity
behave clinically like parenchymal cysticerci and are grouped with parenchymal cysticerci. Rare forms
of neurocysticercosis include multiple inflamed parenchymal cysticerci with diffuse cerebral edema,
termed cysticercal encephalitis, large parenchymal cysticerci (>20 mm).
Δ Refers to cysticerci in the central nervous system outside of the brain parenchyma.
Reproduced from: White AC Jr, Coyle CM, Rajshekhar V, et al. Diagnosis and treatment of neurocysticercosis: 2017 clinical
practice guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and
Hygiene (ASTMH). Clin Infect Dis 2018; 66(8):e49-e75, by permission of Oxford University Press on behalf of IDSA and ASTMH.
Copyright © 2018. Available at: https://www.idsociety.org/practice-guideline/neurocysticercosis/.
Graphic 117224 Version 8.0
Radiographic findings of cysticercosis
(A) Multiple viable cysts.
(B) Single enhancing lesion (degenerating cyst).
(C) Multiple intraparenchymal calcifications.
(D) Intraventricular cysticercosis.
(E) Basal subarachnoid cysticercosis.
(F) Massive parenchymal cysticercosis.
(G) Ocular cysticercosis.
(H) Muscle cysticercosis.
Reproduced from: Garcia HH, Del Brutto OH. Neurocysticercosis: updated concepts about an old disease. Lancet Neurol 2005; 4:653.
Illustration used with the permission of Elsevier Inc. All rights reserved.
MRI imaging of human neurocysticercosis
Contrast used was gadoterate meglumine. Viable cysts in structural MRI (A); and enhancing nodule (B); ma
calcifications visible (C); massive parenchymal neurocysticercosis (D); basal subarachnoid neurocysticercosi
and intraventricular cysticercosis (F).
MRI: magnetic resonance imaging.
Reproduced from: Garcia HH, Nash TE, Del Brutto OH. Clinical symptoms, diagnosis, and treatment of neurocysticercosis. Lancet Neu
13:1202. Illustration used with the permission of Elsevier Inc. All rights reserved.
Ocular cysticercosis
Preoperative photograph of left eye fundus.
Dashed arrow: Probable site of entry of the cysticercosis from the choroid
showing retinal pigment epithelial disturbance.
Arrow: Shows area of serous retinal detachment.
From: Wani VB, Kumar N, Uboweja AK, Kazem MA. A case of submacular cysticercosis treated by pars
plana vitrectomy in Kuwait. Oman J Ophthalmol 2014; 7(3):144-6. DOI: 10.4103/0974-620X.142599.
Copyright © 2014 Oman Ophthalmic Society. Reproduced with permission from Wolters Kluwer -
Medknow. Unauthorized reproduction of this material is prohibited.
Diagnostic criteria for neurocysticercosis – Table A
A definitive diagnosis of neurocysticercosis is established by any of the following:
One absolute criteria, OR
Two major neuroimaging criteria PLUS any clinical/epidemiologic exposure criteria, OR
One major neuroimaging criteria and one confirmative neuroimaging criteria, PLUS any
clinical/epidemiologic exposure criteria, OR
One major neuroimaging criteria PLUS two clinical/epidemiologic exposure criteria (including at
least one major criterion), AND exclusion of other pathologies producing similar neuroimaging
findings
A probable diagnosis of neurocysticercosis is established by any of the following:
One major neuroimaging criteria PLUS any two clinical/epidemiologic exposure criteria, OR
One minor neuroimaging criteria PLUS one major clinical/epidemiologic exposure criteria
Refer to the separate UpToDate table for summary of absolute criteria, neuroimaging criteria, and
clinical/epidemiologic exposure criteria.
Original table modified for this publication. From: Del Brutto OH, Nash TE, White AC Jr, et al. Revised diagnostic criteria for
neurocysticercosis. J Neurol Sci 2017; 15:372. Table used with the permission of Elsevier Inc. All rights reserved.
Diagnostic criteria for neurocysticercosis – Table B
Absolute criteria
Histological demonstration of the parasite from biopsy of a brain or spinal cord lesion
Visualization of subretinal cysticercus
Conclusive demonstration of a scolex within a cystic lesion* on neuroimaging study
Neuroimaging criteria
Major criteria:
Cystic lesion(s)* with no discernible scolex
Enhancing lesion(s)¶
Multilobulated cystic lesion(s) in the subarachnoid space.
Typical parenchymal brain calcification(s)Δ
Confirmation criteria:
Resolution of cystic lesions after cysticidal drug therapy
Spontaneous resolution of single small enhancing lesions◊
Migration of ventricular cysts documented on sequential neuroimaging studies§
Minor criteria:
Obstructive hydrocephalus or abnormal enhancement of basal leptomeninges
Clinical/epidemiologic exposure criteria

Major criteria:
Detection of specific anticysticercal antibodies or cysticercal antigens by well-standardized

immunodiagnostic tests¥
Cysticercosis outside the central nervous system‡
Household contact with Taenia solium infection
Minor criteria:
Clinical manifestations suggestive of neurocysticercosis†
Individuals with prior or current residence in an area where cysticercosis is endemic**
CSF: cerebrospinal fluid; CT: computed tomography; MRI: magnetic resonance imaging.

* Cystic lesions: Rounded, well-defined lesions with liquid contents of signal similar to that of CSF on
CT or MRI.

¶ Enhancing lesion(s): Ring- or nodular-enhancing lesion(s) of 10 to 20 mm in diameter, with or
without surrounding edema; not displacing midline structures.

Δ Typical parenchymal brain calcification(s): Solid lesion(s), most usually <10 mm in diameter.
◊ Use of corticosteroids makes this criterion invalid.

§ Migration of ventricular cyst: Demonstration of a different location of ventricular cystic lesions on
sequential CTs or MRIs.

¥ Well-standardized immunodiagnostic tests: Antibody detection by enzyme-linked immuno-
electrotransfer blot assay using lentil lectin-purified T. solium nantigens and/or detection of cysticercal
antigens by monoclonal antibody-based enzyme-linked immunosorbent assay.

‡ Cysticercosis outside the central nervous system: Demonstration of cysticerci from biopsy of
subcutaneous nodules, X-ray films or CT demonstrating cigar-shape calcifications in soft tissues, or
parasite visualization in the anterior chamber of the eye.

† Suggestive clinical manifestations: Mainly seizures (often starting in individuals aged 20 to 49 years;
the diagnosis of seizures in this context is not excluded if patients are outside of the typical age
range); other manifestations include chronic headaches, focal neurologic deficits, intracranial
hypertension, and cognitive decline.

** Cysticercosis-endemic area: A region where active transmission of cysticercosis has been
documented.
Original table modified for this publication. From: Del Brutto OH, Nash TE, White AC Jr, et al. Revised diagnostic criteria for
neurocysticercosis. J Neurol Sci 2017; 15:372. Table used with the permission of Elsevier Inc. All rights reserved.
Contributor Disclosures
A Clinton White, Jr, MD, FACP, FIDSA No relevant financial relationship(s) with ineligible companies to
disclose. Peter F Weller, MD, MACP Consultant/Advisory Boards: Knopp Biosciences
[Hypereosinophilic syndrome treatment]; GlaxoSmithKline [Eosinophilic diseases]; Genzyme
[Eosinophilia]. Other Financial Interest: AstraZeneca [Hypereosinophilic syndrome]. Elinor L Baron,
MD, DTMH Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

Cysticercosis - Clinical Manifestations and Diagnosis - UpToDate

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Cysticercosis - Clinical Manifestations and Diagnosis - UpToDate

Uploaded by

Copyright:

Available Formats

20/11/2021 17:53 Cysticercosis: Clinical manifestations and diagnosis - UpToDate

Official reprint from UpToDate®

Cysticercosis: Clinical manifestations and diagnosis

Phases of cysticercosis include an initial (viable) phase, early inflammatory stage, a

● Ultimately, the cysticerci resolve or become nonviable calcified granulomas; presence

vomiting) and may be accompanied by altered mental status. (See 'Intraparenchymal

Intraparenchymal neurocysticercosis — Intraparenchymal NCC is the most common form

● Less common manifestations of parenchymal NCC include altered vision, focal

● In patients with massive numbers of parenchymal cysticerci, an intense immune

Extraparenchymal neurocysticercosis — Extraparenchymal NCC can occur in the

Extraparenchymal cysticerci are associated with symptoms of elevated intracranial pressure

Intraventricular lesions — Intraventricular cysticerci (free-floating cysts in the ventricular

Subarachnoid lesions — Subarachnoid neurocysticercosis (SAN) in the basilar cisterns is

Spinal lesions — Spinal cord involvement occurs in approximately 1 percent of cases [36].

Ocular cysticercosis should be excluded by an ophthalmologic examination in all patients

Extraneural cysticercosis — Extraneural cysticercosis may involve a wide range of tissues.

The most common manifestations include muscle or subcutaneous tissue involvement;

Laboratory findings — Most patients with cysticercosis have no specific diagnostic findings

Clinical approach — The diagnosis of cysticercosis should be suspected in patients with

The diagnosis of cysticercosis is established based on clinical manifestations, neuroimaging

Serologic testing should be performed for confirmatory evaluation in patients with

In addition, patients likely to require prolonged corticosteroids should undergo screening

Primary diagnostic tools

Patients with suspected extraneural cysticercosis (muscle or subcutaneous tissue

Findings — Radiographic manifestations of intraparenchymal NCC include cystic

These forms may coexist simultaneously.

Viable cysts are round, nonenhancing hypodense lesions usually 5 to 20 mm in diameter. As

Less common manifestations of intraparenchymal NCC include involvement of the

Radiographic manifestations of extraparenchymal NCC include intraventricular cysts,

Resolution of lesions (either spontaneously or after antiparasitic therapy) is strongly

Serology — Serologic testing should be performed for confirmatory evaluation in patients

The serologic test of choice is enzyme-linked immunoelectrotransfer blot (EITB) using

percent [54,57,58]. However, in patients with a single parenchymal lesion or calcifications

Molecular tests — Molecular tests are increasingly used for diagnosis of

Diagnostic tools used in some circumstances

In the setting of arachnoiditis or ventriculitis, pleocytosis with markedly elevated protein

Histopathology — Brain biopsy is warranted only in rare cases for which noninvasive

A viable cysticercus appears as a translucent fluid-filled membrane (about 5 to 10 mm in

Cystic lesions of the brain include cystic echinococcosis and coenurosis.

Parenchymal brain calcifications on computed tomography may be observed in the setting

Other conditions include primary or metastatic tumors, toxoplasmosis, nocardiosis, and

The differential diagnosis of an eosinophilic cerebrospinal fluid pleocytosis includes

SOCIETY GUIDELINE LINKS

● Intraparenchymal NCC is the most common form of cysticercosis; it occurs in >60

● Intraventricular NCC (free-floating cysts in the ventricular cavity or attached to the

● Subarachnoid neurocysticercosis is the most severe form of NCC; it occurs in about 5

● Extraneural cysticercosis may present with muscle or subcutaneous tissue involvement;

inflamed. Intramuscular cysts often undergo calcification and may be detected

● The diagnosis of cysticercosis should be suspected in patients with seizures and/or

● Radiographic manifestations of intraparenchymal NCC are summarized in the table (

● Serologic testing should be performed for confirmatory evaluation in patients with

Use of UpToDate is subject to the Subscription and License Agreement.

1. White AC Jr, Coyle CM, Rajshekhar V, et al. Diagnosis and Treatment of

25. Sáenz B, Ruíz-Garcia M, Jiménez E, et al. Neurocysticercosis: clinical, radiologic, and

27. Abanto J, Blanco D, Saavedra H, et al. Mortality in Parenchymal and Subarachnoid

56. Carod JF, Randrianarison M, Razafimahefa J, et al. Evaluation of the performance of 5

Classification of neurocysticercosis based on location and appearance of the

Form* Characteristic on neuroimaging Histopathology

Nonviable Nodular calcifications <20 mm in Calcified granuloma with or without

Spinal Cysticerci within the spinal Subarachnoid cysticerci often with

CT: computed tomography; MRI: magnetic resonance imaging.

Graphic 117224 Version 8.0

Radiographic findings of cysticercosis