= NEUROCYSTICERCOSIS

Organism: Taenia solium = larva of pork tapeworm; frequently involving CNS, eyes, muscle, heart, fat tissue, skin

Incidence: most common parasitic infection involving CNS in developing countries (in up to 90%)

Endemic to: Mexico, South America, Africa, eastern Europe, Asia, Indonesia

Associated with: poverty

Route of infection:

1. Cysticercosis = ingestion of ova by fecal-oral route via contaminated food / water or autoinfection; embryophore is dissolved by gastric acid and enzymes + oncosphere is liberated
2. Taeniasis
   following ingestion of cysticercus by definitive host a tapeworm develops within intestinal tract

Life cycle:

• embryos invade intestinal wall → cross mucosa and move into capillary system → enter circulation disseminating in brain, muscles, and various other parts of body; embryo develops into a cysticercus (= complex wall surrounding a cavity containing vesicular fluid + scolex) usually within <3 months

Location: meninges (39%) esp. in basal cisterns, parenchyma (20%), intraventricular (17%), mixed (23%), intraspinal (1%)

Seeding: through subarachnoid space + ventricles

Site in brain: gray-white matter junction, basal ganglia, cerebellum, brainstem

1. STAGE OF LARVAL TISSUE INVASION
   • asymptomatic
   • localized focus of edema on T2WI
   • nodular tissue enhancement
2. VESICULAR STAGE
   = antigenetically inert, therefore without inflammatory reaction / circumferential edema; parasite protected by cyst wall rich in glycoproteins as an effective barrier toward surrounding tissue
   • asymptomatic
   • single / multiple thin-walled nonenhancing 4–20 mm spherical cysts:
     • center with clear fluid of CSF intensity
     • “target” or “dot in a hole” appearance = 2–3 mm mural nodule (= scolex) of soft-tissue attenuation and signal intensity similar to brain parenchyma
   • NO surrounding edema
3. COLLOIDAL VESICULAR STAGE
   = death of scolex from natural processes / from effects of therapy associated with disruption of cyst wall; unprotected decaying parasite and its metabolic breakdown (colloidal suspension) causes an intense inflammatory reaction → focal meningoencephalitis with breakdown of blood-brain barrier
   • focal seizures (50–70%; in endemic countries most common cause of adult-onset epilepsy
   • markedly hyperintense lesion on FLAIR ← proteinaceous cyst fluid with gelatinous debris
   • center hypointense to white matter and hyperintense to CSF on T1WI
   • hypointense mural nodule on T2WI with strong homogeneous enhancement
   • surrounded by typically extensive white matter edema (DDx: metastasis without edema)
   • avidly ring-enhancing capsule on postcontrast T1WI
4. NODULAR-GRANULAR STAGE
   = degeneration of cysticercus = cyst retraction + formation of granulomatous nodule → surrounding gliosis and mineralization
   • gradually subsiding perilesional edema
   • shrinkage of cyst with thick retracted cyst wall becoming isointense with brain on T1WI + hypointense on T2WI
   • hypointense on all pulse sequences ← completely calcified
   • isoattenuating lesion with enhancement of thick nodular ring on CT
5. CALCIFIED (nonactive) STAGE
   = complete involution of lesion with continued mineralization
   • asymptomatic / posttreatment seizures
   • small focal calcifications; may appear within 8 months to 10 years after acute infection
   • “ricelike” muscle calcifications rarely visible
   • calcified scolex on GRE sequence

Radiographic types:

1. Parenchymal type
   • multiple / solitary cystic lesions up to 6 cm in size:
   • large cysts are usually multiloculated
   • calcified granulomata (larvae not dead unless completely calcified)
   • diffuse encephalitic form more common in young females, children, patients receiving antihelmintic therapy
   • progressive midbrain syndrome = multiple areas of ischemic injury
     Cause: occlusion of vessels traversing cisterns
     Location: midbrain, thalamus
   
   Cx: arachnoiditis, meningitis, cranial nerve palsies, lacunar infarctions
2. Subarachnoid / racemose neurocysticercosis
   = infiltration of basal cisterns + sylvian fissures associated with local meningeal inflammation / fibrosis
   • lucent cystic lesions up to several cm in basal cisterns (= racemose cysts) with variable enhancement, usually located in cerebellopontine angle / suprasellar cistern
   
   Cx: hydrocephalus; scattered infarctions ← vasculitis of basal perforating vessels
3. Intraventricular neurocysticercosis
   • symptoms related to hydrocephalus (30%)
   • papilledema, loss of consciousness (Bruns syndrome)
   • obstructive hydrocephalus ← blockage within various portions of ventricular system from solitary / multiple cysts (OCCULT on CT!)
4. Mixed type (frequently different stages in same patient)

Rx: antihelmintic therapy (usually albendazole, praziquantel)