Neurocysticercosis


Pathophysiology:
  • CNS infection with the larval stage of the tapeworm Taenia solium.
  • It is the most common cause of secondary epilepsy in the developing world.
  • The most common form of disease is parasitic invasion of brain parenchymal tissue with the establishment of cysts, which may remain asymptomatic for several years.
    • Host response eventually causes localized edema and inflammation.
    • Over 1 to 2 years, the cyst degenerates and becomes fibrotic, leaving a focal area of scarring and calcification.
    • Seizures are the most common clinical manifestation of neurocysticercosis.
    • Extraparenchymal cysticercosis can cause obstructive hydrocephalus, resulting in:
      • Headache or signs of increased intracranial pressure, such as nausea or vomiting, altered mental status, or vision changes.

Diagnosis:

  • In most cases, neuroimaging in neurocysticercosis is not diagnostic.
  • CT scan or MRI
    • May demonstrate a 1- to 2-cm cystic lesion with thin walls and a 1- to 3-mm mural nodule (the parasite), a localized area of ring-like enhancement with edema, a calcified lesion, or hydrocephalus.
  • Definitive diagnosis relies on a combination of the patient's clinical picture, exposure history, serologic testing, and neuroimaging.

Treatment:

  • Seizures in neurocysticercosis are typically controlled by antiepileptic monotherapy.
  • Definitive treatment of neurocysticercosis is controversial and highly variable, depending on the number, location, and viability of the parasites within the CNS.
  • Antiparasitics (praziquantel and albendazole) and steroids are best initiated in consultation with an infectious disease specialist or neurologist.
  • Patients with hydrocephalus need neurosurgical consultation for ventriculoperitoneal shunting