Files

T

2025-10-20 21:15:33 +01:00

40 KiB

Raw Permalink Blame History

title, docid, authors, breadcrumbs, category, cmeTopicId, documentVersionId, imageCount, lastUpdated, pageDescription, pageKeywords, pageTitle, enhancedTitle, type, references, breadcrumbs

title

docid

authors

breadcrumbs

KEY FACTS

Terminology
- Neurocysticercosis (NCC): Intracranial parasitic infection caused by pork tapeworm Taenia solium
Imaging
- Best diagnostic clue: Cyst with "dot" inside
- Convexity subarachnoid spaces most common location - Inflammatory response around cyst may seal sulcus, making lesions appear intraaxial
- May involve cisterns > parenchyma > ventricles
- Intraventricular cysts often isolated, 4th > 3rd ventricle
- Racemose (grape-like) NCC: In basal cisterns; no scolex
- Imaging varies with development stage & host response
- Lesions may be at different stages in same patient
- FLAIR & T1 MR helpful to identify scolex & intraventricular lesions
- GRE/SWI helpful in young adults presenting with seizures
- In children, may see "encephalitic cysticercosis": Multiple small, enhancing lesions (starry-sky) & diffuse edema
Top Differential Diagnoses
- Abscess, tuberculosis, neoplasm
- Epidermoid/arachnoid cyst (racemose NCC differential)
- Toxoplasmosis, enlarged perivascular spaces
Pathology
- 4 pathologic stages (2 vesicular & 2 nodular) - Vesicular, colloidal vesicular, granular nodular, & nodular calcified
Clinical Issues
- Seizures, headaches, hydrocephalus common - NCC asymptomatic until larvae degenerate
- Cysticercosis most common parasitic infection worldwide - CNS involved in 60-90% of cysticercosis cases
- Most common cause of epilepsy in endemic areas
- Increased travel, immigration have spread disease
- Diagnosis confirmed by ELISA of serum or CSF
- Oral albendazole (reduces parasitic burden, seizures)
- Steroids often required to decrease edema
- Consider excision or drainage of parenchymal lesions
Diagnostic Checklist
- Cyst with scolex & calcific foci in patients in endemic areas

TERMINOLOGY

Abbreviations
- Neurocysticercosis (NCC)
Synonyms
- Cysticercosis
Definitions
- Intracranial parasitic infection caused by pork tapeworm Taenia solium; 4 pathologic stages: 2 vesicular & 2 nodular - Vesicular, colloidal vesicular, granular nodular, & nodular calcified

IMAGING

General Features

Best diagnostic clue
```
- Cyst with "dot" (scolex) inside
```

Location

- Convexity **subarachnoid spaces** most common
- May involve cisterns > parenchyma > ventricles
- Parenchymal cysts often at gray-white junction
- Intraventricular cysts are often isolated
        - 4th ventricle most common, then 3rd ventricle
        - May migrate; causes ependymitis & hydrocephalus
- Basal cistern cysts may be racemose (grape-like)
- Rare head & neck/CNS locations: Sella, orbit (especially **extraocular muscles**), spinal **cord**
        - Ocular cysticercosis may present at diagnosis or later after commencing cysticidal treatment
- Other sites: Skeletal/heart muscles, subcutaneous tissue

Size

- ~ 1-cm cysts; range: 5-20 mm; scolex (1-4 mm)
- Parenchymal cysts ≤ 1 cm
- Subarachnoid cysts may be larger

Morphology

- Round or ovoid cyst, solitary in 20-50%
- When multiple, usually small number of cysts
- Disseminated form (a.k.a. **miliary NCC**): Rare

Imaging varies with development stage & host response
Lesions may be at different stages in same patient
Inflammatory response around cyst may seal sulcus, making lesions appear intraaxial
In children &, occasionally, adults (usually young females, rarely males), may see "encephalitic cysticercosis" - Multiple small, enhancing lesions (starry-sky appearance) & diffuse edema

CT Findings

NECT

- **Vesicular** stage (viable larva): Smooth, thin-walled cyst, isodense to CSF, no edema
        - Hyperdense "dot" within cyst = protoscolex
- **Colloidal vesicular** stage (degenerating larva): Hyperdense cyst fluid with surrounding edema
- **Granular nodular** stage (healing): Mild edema
- **Nodular calcified** stage (healed): Small, calcified nodule

CECT

- **Vesicular** stage: No (or mild) wall enhancement
- **Colloidal vesicular** stage: Thick, ring-enhancing capsule
- **Granular nodular**stage: Involuting, enhancing nodule
- **Nodular calcified**stage: Shrunken, Ca⁺⁺ nodule

Intraventricular cysts not well seen on CT
Subarachnoid NCC: Multiple isodense cysts without scolex; may cause meningitis, vasculitis, or hydrocephalus

MR Findings

T1WI

- **Vesicular** stage: Cystic lesion isointense to CSF
        - May see discrete, eccentric scolex (hyperintense)
- **Colloidal vesicular** stage: Cyst mildly hyperintense
- **Granular nodular** stage: Thickened, retracted cyst wall; edema ↓
- **Nodular calcified** stage: Shrunken, Ca⁺⁺ lesion
- Useful to detect intraventricular cysts

T2WI

- **Vesicular** stage: Cystic lesion isointense to CSF
        - May see discrete, eccentric scolex
        - No surrounding edema
- **Colloidal vesicular** stage: Cyst hyperintense
        - Surrounding edema, mild to marked
- **Granular nodular**stage: Thickened, retracted cyst wall; edema ↓
- **Nodular calcified** stage: Shrunken, Ca⁺⁺ lesion

FLAIR

- **Vesicular**stage: Cystic lesion isointense to CSF
        - May see discrete, eccentric scolex (hyperintense to CSF); no edema
- **Colloidal vesicular** stage: Cyst hyperintense
        - Surrounding edema, mild to marked
- Useful to detect intraventricular cysts (hyperintense)
- 100% inspired **oxygen ↑**conspicuity
- **Postcontrast FLAIR** best to detect abnormal meningeal enhancement

T2* GRE

- Useful to demonstrate calcified scolex; SWI better
- May show multiple black dots appearance

DWI

- Cystic lesion typically isointense to CSF
- Scolex detectable as hyperintense nodule

PWI

- Ring-enhancing NCC wall shows lower mean rCBV (1.3) compared with tuberculoma wall
        - Tuberculoma: Mild ↑ mean rCBV (2-3.3)
- Cutoff value of wall rCBV 1.965 for tuberculoma: 90% sensitivity & 100% specificity
- Core of both tuberculoma & NCC lower rCBV than normal white matter

T1WI C+

- **Vesicular** stage: No enhancement typical, may see mild enhancement/eccentric scolex enhancement
- **Colloidal vesicular** stage: Thick cyst wall enhances
        - Enhancing marginal nodule (scolex)
- **Granular nodular** stage: Thickened, retracted cyst wall; may have nodular or ring-like enhancement
- **Nodular calcified** stage: Small calcified lesion, rare minimal enhancement

MRS

- ↑ lactate, alanine, succinate, choline; ↓ NAA & Cr

Steady-state sequences (CISS) for intraventricular cysts
Cisternal NCC may appear racemose (multilobulated, grape-like), typically lacks scolex - Complications: Meningitis, hydrocephalus, vasculitis

Imaging Recommendations

Best imaging tool

- MR most sensitive; SWI MR & CT for calcifications
        - Helpful to identify extraparenchymal NCC (intraventricular, subarachnoid)
- Calcified lesions may be better seen on CT

Protocol advice

- MR with T1, T2, FLAIR, GRE/SWI, contrast
- Thin slices (< 3 mm) to identify scolex

DIFFERENTIAL DIAGNOSIS

Abscess
- Typically T2-hypointense rim & DWI-restricting core
- Multiple lesions may occur related to septic emboli
Tuberculosis
- Tuberculomas often occur with meningitis
- Nodular stages of NCC mimic tuberculoma
Neoplasm
- Primary or metastatic (primary often known)
- Thick, irregular margin enhancement typical
- May have cyst & mural nodule (e.g., pilocytic astrocytoma, hemangioblastoma)
- Metastasis wall show more elevated mean rCBV (5.43) - Cut-off value of ≥ 3.745 for differentiating ring-enhancing metastases from tuberculomas
Arachnoid Cyst & Epidermoid Cyst
- Solitary lesion with CSF density/intensity & no enhancement; racemose NCC differential
- Arachnoid cyst: CSF intensity on T2, FLAIR, & DWI
- Epidermoid: CSF intensity on T2, "dirty" on FLAIR, & shows diffusion restriction on DWI
- Racemose NCC: CSF intensity with septa on T2, "dirty" on FLAIR, but no diffusion restriction on DWI
Enlarged Perivascular Spaces
- Follow CSF on all MR sequences, no enhancement
Other Parasitic Infection
- Toxoplasmosis ring-enhancing cyst with enhancing eccentric target sign of nodule mimicking NCC scolex - Usually in immunocompromised (e.g., AIDS); differential lymphoma in these patients - Basal ganglia common; other multiple lesions can occur
- Other parasitic cysts, but no scolex seen

PATHOLOGY

General Features

Etiology

- Caused by larval form of pork tapeworm*T. solium*
- Humans **intermediate hosts** in life cycle of tapeworm
        - **Fecal-oral**most common route of infection
        - **Ingestion** of **eggs** from contaminated water, food
        - From GI tract, primary larvae (**oncospheres**) disseminate into CNS & skeletal muscle
        - Once intracranial, primary develop into secondary larvae, **cysticerci**
- Humans may also be **definitive hosts** (infected with tapeworm): Typically from **undercooked pork**
        - **Viable larvae ingested**, attach in GI tract

Staging, Grading, & Classification
- 4 pathologic stages (2 vesicular & 2 nodular) - Vesicular, colloidal vesicular, granular nodular, & nodular calcified
- Vesicular stage: Larva small with marginal nodule projecting into small cyst with clear fluid - Viable parasite with little or no inflammation - May remain in this stage for years or degenerate
- Colloidal vesicular stage: Larva begins to degenerate - Scolex shows hyaline degeneration, slowly shrinks - Cyst fluid becomes turbid, & capsule thickens - Surrounding edema & inflammation
- Granular nodularstage: Cyst wall thickens & scolex mineralized granule; surrounding edema regresses
- Nodular calcifiedstage: Lesion completely mineralized & small; no edema
Gross Pathologic & Surgical Features
- Usually small translucent cyst with invaginated scolex
Microscopic Features
- Cyst wall has 3 distinct layers: Outer (cuticular), middle cellular (pseudoepithelial), & inner reticular (fibrillary) layers
- Scolex has rostellum with hooklets, muscular suckers
- Variable inflammatory reaction, acute & chronic

CLINICAL ISSUES

Presentation

Most common signs/symptoms

- Seizure, headaches, hydrocephalus
- Varies with organism development stage, host immune response
- NCC asymptomatic until larvae degenerate
- Other signs/symptoms: Syncope, dementia, visual changes, focal neurologic deficits, stroke

Clinical profile

- Diagnosis confirmed by ELISA of serum or CSF
- Serologic tests may cross react with *Echinococcus*
- CSF studies abnormal in 50%, ↑ lymphocytes

Demographics

Epidemiology

- Cysticercosis most common parasitic infection
- CNS infection in 60-90% of cysticercosis cases
- Endemic in many countries (Latin America, parts of Asia, India, Africa, Eastern Europe)
        - USA: Incidence ↑ in CA, AZ, NM, TX
- ↑ travel, immigration have spread disease

Age: Any; commonly young, middle-aged adults
Sex: Slight male predominance
Ethnicity: In USA, Latin American patients common

Natural History & Prognosis
- Most common cause of epilepsy in endemic areas
- Variable time from initial infection until symptoms: 6 months to 30 years; typically 2-5 years
- Variable time to progress through pathologic stages: 1-9 years; mean: 5 years
- Subarachnoid disease may be complicated by meningitis, vasculitis, & hydrocephalus
- Intraventricular NCC has ↑ morbidity & mortality (↑ morbidity related to acute hydrocephalus)
- High association of NCC coinfection with Japanese encephalitis (JE)
- JE lesions asymmetrically more at ipsilateral side of brain with more NCC lesions or NCC cyst with edema
- JE lesions in coinfections more florid, more common in children, & patients show altered immune status
Treatment
- Oral albendazole (reduces parasitic burden, seizures)
- Albendazole along with praziquantel if > 2 viable cysts - Steroids often required to ↓ edema
- Consider excision or drainage of parenchymal lesions
- Consider endoscopic resection of ventricular lesions
- CSF diversion often required to treat hydrocephalus
- Cysticidal agents contraindicated in patients with encephalitic cysticercosis
- Encephalitic cysticercosis in those without prior exposure, newly infected with heavy load T. solium eggs - Host immune system react actively: Acute encephalitis with multiple degenerating cysticerci & swollen brain - Antiparasitic drugs not needed, as most parasites die spontaneously from host response - Drugs can exacerbate inflammatory reaction turning harmful to patients - If antihelminthic drugs used, give under steroid cover

DIAGNOSTIC CHECKLIST

Consider
- Complex parasitic cysts may mimic brain tumor
Image Interpretation Pearls
- Cyst with scolex & calcific foci in patients in endemic areas
- FLAIR & T1WI helpful to identify scolex & intraventricular lesions
- GRE/SWI helpful in young adults presenting with seizures

8b196bce-9146-4120-82e0-0b8ac0372b2c

References

Selected References

Images

Selected Images

Coronal graphic shows subarachnoid & ventricular neurocysticercosis (NCC). Convexity cysts have a scolex and surrounding inflammation. Note that inflammation around the largest cyst "seals" the sulcus , making it appear parenchymal. Racemose cysts are multilocular, nonviable in the basal cisterns & typically lack scolex.

Axial CECT shows bilateral frontoparietal nonenhancing cysts without edema. One left parietal lobe cyst shows hyperdense scolex , suggesting NCC vesicular stage.

Axial CECT in a young male patient with 1st episode of seizure demonstrates a ring-enhancing lesion with an eccentric hyperdense "dot" that denotes scolex. Note the edema surrounding this colloidal vesicular stage of NCC.

Axial postcontrast MR (left) shows a tiny, solidly enhancing nodule in the left cerebellar hemisphere due to granular nodular stage of NCC. Axial SWI MR (right) in the same patient shows a blooming hypointense focus in the left frontal lobe due to nodular calcified stage of NCC.

Axial NECT in a patient with seizures shows multiple scattered, hyperdense, left more than right frontoparietal lobe calcifications. Perilesional gliosis contributes to the epileptogenicity of nodular calcified NCC.

MRS at TR 1500, TE 144 within the cyst cavity of a colloidal vesicular NCC lesion in a patient (not shown) shows peaks of Cho (3.2 ppm), succinate (2.4 ppm), and lactate (1.3 ppm).

Axial T1 C+ MR demonstrates multiple cysts in the suprasellar cistern and left sylvian fissure . There is extensive leptomeningeal enhancement in the basal cisterns and sylvian fissures. Cisternal NCC, also termed racemose (grape-like) if multiple cysts without scolex, may cause meningeal inflammation, communicating hydrocephalus, vasculitis, and infarcts.

Axial T1 C+ MR in an NCC patient shows a ring-enhancing cyst with tiny scolex enhancement in the quadrigeminal cistern posterior to the midbrain.

Axial T1 C+ MR in a patient with hydrocephalus shows rim-enhancing isolated 4th ventricular NCC with enhancing scolex .

Axial T2WI MR (top left) shows a CSF intensity cyst with septa in prepontine cistern/CP angles . Axial postcontrast T1WI MR (top right) shows no enhancement. Axial FLAIR (bottom left) shows a dirty appearance due to incomplete fluid suppression (excluding arachnoid cyst). Axial DWI (bottom right) shows no diffusion restriction (excluding epidermoid). Findings are consistent with racemose NCC.

Additional Images

Gross pathology shows a translucent cyst with a characteristic invaginated white scolex, diagnostic of NCC. This resected lesion came from a seizure patient. (Courtesy B. Cremin, MD.)

Axial T1 C+ MR shows an NCC cyst with an enhancing nodule in the posterior 3rd ventricle. Note the associated acute obstructive hydrocephalus, a common complication of intraventricular cysts. Intraventricular cysts are often isolated with the 4th ventricle most commonly involved. (Courtesy N. Fischbein, MD.)

Axial NECT shows an enlarged 4th ventricle. On this slice, the enlarged temporal horns of the lateral ventricle and anterior recesses of the 3rd ventricle are obvious, but the cause for the hydrocephalus is not. NCC in the 4th ventricle is better seen on MR.

Axial CECT in a patient with seizures and NCC shows a typical colloidal vesicular-stage cyst with peripheral enhancement and surrounding edema. Note the eccentric scolex .

Axial CECT in a patient with headaches and seizures shows a ring-enhancing mass with surrounding edema in the frontal lobe . A ventricular lesion is present but not well seen . Diagnosis was colloidal vesicular-stage NCC.

Axial T1WI MR shows the frontal lesion and the intraventricular cyst. Note the cyst wall and the hyperintense scolex . T1WI and FLAIR MR help identify ventricular lesions.

Axial CECT shows a right external capsule cyst with a central "dot" representing a scolex. No edema or enhancement is seen in this patient with vesicular-stage NCC. Note the calcified left putamen nodule, calcified nodular stage .

Axial T2WI MR shows cysts in the subarachnoid spaces filling the sylvian fissure and causing mild mass effect on the cerebral peduncle of midbrain with mild edema here. Note the lack of a scolex, typical of cisternal racemose NCC.

Axial T1WI MR shows innumerable cysts , each with a hyperintense scolex in this patient from Mexico. This disseminated form of NCC is rare and is seen in patients from endemic areas. Multiple NCC lesions with a starry-sky appearance may also be seen in the extremely rare encephalitic cysticercosis usually in immunocompetent children and young women without prior exposure, who are newly infected with a heavy load Taenia solium eggs. Significant brain edema will be seen in the encephalitic form.

Axial FLAIR MR shows a right frontal "mass" in a young adult with new focal seizures. The NCC cyst follows CSF signal . Note the surrounding hyperintense edema .

Axial T1 C+ MR in the same patient shows peripheral enhancement of the cyst wall with a central "dot" representing the scolex . The surrounding inflammation has caused the overlying sulcus to seal, making the lesion appear intraaxial. Occasionally, linear enhancement may be seen extending from the lesion, representing inflammation along the pial surface of the sulcus.

Coronal T1 C+ MR in the same patient shows peripheral enhancement of the NCC cyst (colloidal vesicular stage) .

Axial CECT shows a ring-enhancing frontal lobe lesion with a central "dot" and surrounding edema in this patient with colloidal vesicular NCC. CT often shows calcified lesions to better advantage than MR.

Axial T2 GRE MR in this seizure patient shows multifocal "black dots" in the sulci, parenchyma, and right frontal horn related to the nodular calcified stage of NCC . It is important to remember that different lesions may be at different stages in the same patient.*

Axial FLAIR MR shows a 4th ventricular lesion related to colloidal vesicular-stage NCC. Note the eccentric scolex . FLAIR and T1 are the best MR sequences to identify intraventricular lesions, which are often complicated by acute hydrocephalus.

Sagittal STIR MR shows multiple hyperintense cysts in the quadrigeminal cistern and basal subarachnoid spaces related to racemose NCC. Note the typical lack of a scolex. (Courtesy E. Bravo, MD.)

Sagittal FIESTA MR shows hydrocephalus due to intraventricular NCC cysts blocking CSF flow from the 3rd ventricle to the aqueduct.

40 KiB Raw Permalink Blame History

KEY FACTS

Terminology

Imaging

Top Differential Diagnoses

Pathology

Clinical Issues

Diagnostic Checklist

TERMINOLOGY

Abbreviations

Synonyms

Definitions

IMAGING

General Features

Best diagnostic clue

Location

Size

Morphology

CT Findings

NECT

CECT

MR Findings

T1WI

T2WI

FLAIR

T2* GRE

DWI

PWI

T1WI C+

MRS

Imaging Recommendations

Best imaging tool

Protocol advice

DIFFERENTIAL DIAGNOSIS

Neoplasm

PATHOLOGY

General Features

Etiology

Staging, Grading, & Classification

Gross Pathologic & Surgical Features

Microscopic Features

CLINICAL ISSUES

Presentation

Most common signs/symptoms

Clinical profile

Demographics

Epidemiology

Natural History & Prognosis

Treatment

DIAGNOSTIC CHECKLIST

Consider

Image Interpretation Pearls

References

Selected References

Images

Selected Images

Additional Images

40 KiB

Raw Permalink Blame History