Pediatric Cysticercosis Clinical Presentation

Updated: Oct 17, 2016
  • Author: Delaram Ghadishah, MD; Chief Editor: Russell W Steele, MD  more...
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Presentation

History

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  • The clinical presentation of cysticercosis depends on the number, location, and stage of the lesions present, as well as the host immune response.

  • In general, the diagnosis of neurocysticercosis should be considered in any individual who is from or has traveled to an area where T solium is endemic and who has new-onset partial seizures (with or without secondary generalization), behavioral disturbances, confusion, stupor, cognitive impairment, or signs of increased intracranial pressure (ICP).

  • Seizures are the presenting symptom in more than 70% of cases. The seizures frequently begin as simple or complex partial seizures but become generalized in 80% of cases. [4]

  • Parenchymal disease causes seizures and focal neurologic deficits.

  • Headache, vertigo, vomiting, papilledema, an altered level of consciousness, and gait disturbances may be present in patients with meningeal cysticercosis.
  • Neurocysticercosis can present with nearly any type of focal neurologic deficit. Persons with arachnoiditis can present with stroke syndromes due to occlusion of small and medium size intracranial arteries.  Arachnoiditis can produce entrapment of cranial nerves resulting in extraocular muscle palsies, hearing loss, facial nerve palsy.  Spinal neurocysticercosis can cause spinal cord compression, nerve root pain, focal extremity weakness and sensory deficits, transverse myelitis, or meningitis. [5]

  • Intraventricular neurocysticercosis (5-10% of all cases) is associated with hydrocephalus and acute, subacute, or intermittent signs of increased ICP without localizing signs.

    • The lateral ventricles are less likely to become obstructed, whereas the fourth ventricle most commonly becomes obstructed.

    • Hydrocephalus develops from the intense and widespread immune response in the subarachnoid space.

  • Neurocysticercosis-associated inflammation is more severe in children and women than in adult men. 

  • Children are more likely to have single, enhancing nodules.

  • Cysticercoid encephalitis is seen in children and presents with altered mental status associated with seizures and raised intracranial pressure. These patients usually have hundreds of small, viable, or degenerating cyst with a diffuse inflammatory reaction. 

  • Ocular cysticercosis may decrease visual acuity because of retinal detachment, iridocyclitis, or floating cysticerci in the vitreous. [6]

  • Heavy infections in skeletal or heart muscle may result in myositis or carditis, respectively.

  • Rarely, cysticerci may obstruct small terminal arteries or cause a vasculitis, leading to a cerebral infarction.

  • Children with an acute infection that is massive may present with signs and symptoms of fulminant encephalitis.

  • Intellectual deterioration due to extensive frontal lobe disease may simulate dementia or parkinsonism.

  • Chronic basilar meningitis is associated with many forms of neurocysticercosis. In addition to signs of meningeal irritation, increased ICP due to inflammation, edema, or an obstructing cyst may be present.

  • A study that evaluated 81 cases of neurocysticercosis from 1980-2013 in five centers in Italy and Spain found that when comparing pediatric cases to adult cases, pediatric cases were more likely to have eosinophilia, to have other parasitic infections, and to be asymptomatic. [7]

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Physical

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  • Findings vary depending on the number, location, and local effects of cysticerci, as well as on the host response.

  • In general, neurologic deficits, seizures, and subcutaneous or ocular cysts may be present.

  • Cysts may be palpable under the skin.

  • The features of the history assist in focusing the physical examination.

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Causes

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  • Cysticercosis is caused by the ingestion of T solium eggs. The human is the only definitive host of the adult pork tapeworm, which lives in the human intestinal tract and lays eggs that are shed in human feces. In the normal life cycle of the parasite, eggs shed in human feces are ingested by pigs, which then develop cysticerci in muscle tissue. Human infection with the adult tapeworm develops in people who ingest raw or poorly cooked pork that contains cysticerci. Note that human ingestion of pork does not result in the development of cysticercosis.

  • Contamination of water, fruits, and vegetables by human feces that contain eggs is usually the result of poor sanitation.

  • Untreated, adult T solium worms may cause autoinfection by means of fecal-oral ingestion and reverse peristalsis, but this is believed to be very uncommon.

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