Understanding Neurocysticercosis: From Parasitic Origins to Clinical Presentations

Neurocysticercosis is a parasitic infection resulting from ingesting eggs from the adult tapeworm, Taenia solium. This central nervous system manifestation of cysticercosis is the most common parasitic brain infection and a leading cause of epilepsy in the developing world.

  • In recent years, neurocysticercosis has become a significant cause of seizures, accounting for up to 10% of emergency room visits for seizures.

Natural History

  • Acquired through consuming contaminated food with the feces of a T. solium tapeworm carrier (fecal-oral contact).
  • Tapeworm eggs, shed in stool, contaminate food through poor hygiene.
  • Ingested eggs transform into larval cysts (oncospheres) in the human stomach.
  • Oncospheres migrate to the brain, muscles, eyes, and other structures via the vascular system.
  • Larval cysts may remain viable in the brain for years.

Epidemiology

  • Endemic in Central and South America, Asia, and Africa.
  • Linked to poor sanitation and hygiene.
  • No gender or race predilection; affects symptomatic patients aged 15-40 years.

Clinical Presentation

  • Seizures: Most common symptom, a leading cause of seizures in young adults in endemic areas.
  • Headaches
  • Hydrocephalus
  • Altered mental status
  • Neurological deficits

Stages of Neurocysticercosis

  1. Vesicular: Viable parasite with intact membrane; no host reaction.
  2. Colloidal Vesicular: Parasite dies within 4-5 years, cyst fluid becomes turbid; most symptomatic stage.
  3. Granular Nodular: Edema decreases, cyst retracts, enhancing persists.
  4. Nodular Calcified: End-stage quiescent calcified cyst remnant; no edema.

Location

  • Cysts can occur intraaxially or extraaxially in the neuraxis.
  • Parenchyma: Most common, usually involving the grey-white matter junction.
  • Subarachnoid space over the cerebral hemispheres: Can be very large.
  • Ventricles
  • Spinal forms: Usually associated with concomitant intracranial involvement.

Imaging Features by Stage

  1. Vesicular Stage
    • Cyst with dot sign.
    • CSF density/intensity.
    • Eccentric hyperintense scolex on T1.
    • No enhancement; no surrounding vasogenic edema.
  2. Colloidal Vesicular Stage
    • Turbid cyst fluid.
    • CT: Hyperattenuating to CSF.
    • MRI T1: Hyperintense to CSF.
    • Surrounding edema; thickened, brightly enhancing cyst wall.
  3. Granular Nodular Stage
    • Edema decreases.
    • Cyst retracts, becoming a small enhancing nodule.
    • Less marked enhancement persists.
  4. Nodular Calcified Stage
    • Quiescent calcified nodule.
    • No edema.
    • No enhancement on CT.
    • Signal drop-out on T2 and T2* sequences.
    • Long-term enhancement may predict ongoing seizures.

Case Report

  • Patient:
    • Age: 34-year-old male.
    • Clinical Presentation: Headache & Seizure.
  • NCCT Brain Findings:
    • Multiple calcified 3-7 mm nodules scattered throughout the bilateral cerebral hemispheres.
    • Some nodules causing minimal surrounding edema, particularly in the left frontal lobe.
    • Indicative of varying stages of healed neurocysticercosis.

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