Cysticercosis: Clinical manifestations and diagnosis

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".)

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 [3-6,8]. 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 [3-6,8]. 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 and mesial temporal lobe sclerosis and/or atrophy that may serve as a further nidus for seizures [13,14]. (See "Focal epilepsy: Causes and clinical features", section on 'Mesial temporal lobe epilepsy'.)

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 hospitalized patients with neurocysticercosis (NCC) present with a single enhancing lesion [1,6,15,16]. In field studies from endemic areas, most patients have one or more calcified lesions [6,14,17-21]. Among hospitalized patients in Latin America, the most common presentation is multiple viable cysticerci [1,6].

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 [1,6,8,15,16]. 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 [16,22,23].

The clinical manifestations of parenchymal NCC depend on the number and location of cysticerci and the degree of associated inflammatory response [6,8]:

●Seizures are the most common clinical manifestation of parenchymal NCC; they are usually focal and may be associated with secondary generalization [6,8,15,16,24,25]. 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 [6,8,24]. 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.

●Massive numbers of cysticerci may be observed. Some of these patients have limited inflammation and relatively mild symptoms. Cysticercal encephalitis is a rare form of NCC in which massive numbers of parenchymal cysticerci are associated with an intense immune response and diffuse brain edema. Clinical manifestations include impaired consciousness, seizures, headache, nausea and vomiting, reduced visual acuity, and occasionally fever.

●Many cases of parenchymal NCC are asymptomatic and are identified incidentally via radiographic imaging performed for other reasons [17,18,26]. In studies of the natural history of NCC, most cystic lesions resolve with development of calcifications, in the absence of symptoms [17,18,26,27].

The prognosis of parenchymal NCC varies with the number of cysticerci and degree of inflammation [1,6,8]. 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 [6,8,28,29]. 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 [30].

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) [6,8,16,29,31]. 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) [32].

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 [8,16,33,34]. 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 [35]. (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 [6,16,34,36]. The radiographic appearance is similar to other causes of basilar meningitis, unless cysticerci are visible. In contrast with other causes of basilar meningitis, fever is not typically present. 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 [6,34,36-38]. 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 [39].

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 [35]. (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 [40]. Ocular cysticercosis occurs in approximately 1 to 3 percent of cases of neurocysticercosis [41-43].

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.

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) [1,2,6,44-46]. Revised diagnostic criteria have been proposed and validated [47,48], replacing older criteria [44,46]. Neuroimaging studies should include both computed tomography (CT) and magnetic resonance imaging (MRI), when feasible (table 1).

Serologic or molecular testing should be performed for confirmatory evaluation in patients with suspected cysticercosis [1]. 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 [44]. 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 "Tuberculosis infection (latent tuberculosis) in adults: Approach to diagnosis (screening)" 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 [41,49]. MRI is useful for detecting relatively small lesions, evaluating degenerative changes, detecting edema around calcified lesions, and visualizing scolices within calcified lesions [3]. 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 [3,50]. 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 for identifying the scolex and are useful for identifying cysticerci in cerebrospinal fluid (CSF) [50-52].

Patients with basal subarachnoid involvement should undergo MRI of the spine, given the strong association between basal subarachnoid involvement and spinal subarachnoid cysticerci [1,35]. Myelography may also be used as an alternative. (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 parenchymal cysts are usually round hypodense lesions usually 5 to 20 mm in diameter. Cysticerci in the ventricles or Sylvian fissure may be larger. 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]. Antibody tests are most useful for patients with neuroimaging findings that are consistent with NCC but not diagnostic. Patients with diagnostic neuroimaging findings warrant treatment regardless of serologic results. Antigen-detection tests can also be used for follow-up.

The antibody test of choice is enzyme-linked immunoelectrotransfer blot (EITB) using parasite glycoproteins performed on serum [1,47,54]. It was developed by and is available from the United States Centers for Disease Control and Prevention. Some reference laboratories also offer 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 EITB is nearly 100 percent specific for T. solium infection. The sensitivity varies with the form of NCC and the specimen. Testing serum is generally more sensitive than testing 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 are increasingly used for diagnosis and follow-up of neurocysticercosis. These assays are licensed commercially in Europe; however, availability in the United States is limited [1,46]. CSF antigen detection tests are more sensitive than serum assays. Antigen test results normalize with successful treatment (in contrast with antibody tests).

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. Quantitative PCR is available from the NIH and could be implemented in other laboratories. For some cases of unexplained central nervous system lesions, metagenomic next-generation sequencing has successfully identified subarachnoid neurocysticercosis [61,62].

Diagnostic tools used in some circumstances

Cerebrospinal fluid analysis — A lumbar puncture for CSF examination is not usually necessary for the diagnosis of NCC; in some circumstances, CSF findings can be helpful. 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 usually 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 when performed 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

●Overview and disease phases – 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) 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 – 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 and headache 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.)

●Extraparenchymal NCC

•Intraventricular NCC – 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 NCC – 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 manifestations – 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 – 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.)

●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). Diagnostic criteria for cysticercosis are based on clinical manifestations, neuroimaging findings, and epidemiologic exposure (table 2 and table 3). Increasingly, antigen-detection and molecular tests are aiding with the diagnosis. (See 'Clinical approach' above.)

•Radiographic imaging

-Modalities – 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, visualizing the scolex, and identifying lesions within the cerebrospinal fluid. (See 'Modalities' above.)

-Findings – Radiographic manifestations of intraparenchymal NCC are summarized in the table (table 1 and figure 1 and image 1). Viable parenchymal 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.)

•Serology – 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.)