Cysticercosis Clinical Presentation

Updated: Oct 05, 2015
  • Author: Mossammat M Mansur, MD, MBBS; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
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Presentation

History

Postmortem studies in endemic areas suggest that 80% of neurocysticercal infections are asymptomatic. [7] Consequently, many cases are never diagnosed or are found incidentally during imaging procedures.

The peak severity of neurocysticercosis has been estimated to occur 3-5 years after initial infection, but it can be delayed for more than 30 years. After a variable period of degeneration, cysts can become calcified and may then become inactive. Once they are calcified, they may cease to cause symptoms or may serve as a focus for epileptic activity. The symptoms of neurocysticercosis depend on the stage, site, and number of cysticerci. Cysts frequently develop in multiple locations, and a combination of active and inactive cysts in the same patient is not uncommon.

Symptoms of cysticercosis may include seizures, elevated intracranial pressure (ICP), meningoencephalitis, psychiatric disorder, stroke, and/or radiculopathy or myelopathy, if the spinal cord is involved.

The symptoms are mainly due to mass effect, an inflammatory response, or obstruction of the foramina and ventricular system of the brain. The most common symptoms include seizures, focal neurologic signs, and intracranial hypertension.

Generally, the patient’s history includes exposure to an area where the parasite is endemic and an adolescent- or adult-onset seizure disorder. Symptoms of hydrocephalus should raise concerns about extraparenchymal disease. [8]

  • Parenchymal CNS disease
    • Seizures may be focal, focal with secondary generalization, or generalized.
    • Headaches are common and may be migrainelike or tension-type.
    • Neurocognitive deficits, while rare, may include learning disabilities, depression, or even psychosis [9] .
  • Extraparenchymal disease
    • Most patients present with headaches or symptoms of hydrocephalus.
    • Symptoms of increased ICP may include headache, nausea or vomiting, altered mental status, dizziness, and decreased visual acuity due to papilledema.
    • Patients with numerous cysticerci in the basilar cisterns may present with communicating hydrocephalus, meningismus (without fever), symptoms of lacunar infarcts due to small-vessel vasculitis, or symptoms of large-vessel infarcts due to cysticercal erosion into major arteries or severe inflammation of those arteries.
    • Patients with spinal cysticerci typically present with radicular symptoms, but rarely with motor or sensory deficits traceable to a spinal level.
    • Patients with ocular cysticerci report visual changes.
  • Spinal cord involvement
    • Radiculopathy
    • Myelopathy
  • Other
    • Meningoencephalitis
    • Stroke (in young adults)
    • Subcutaneous nodules
    • Ocular cysts
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Physical

Meningoencephalitis may manifest as pyrexia, altered senses, seizures, increased ICP, multiple cranial nerve involvement, or even brainstem or cerebellar involvement.

Both parenchymal and extraparenchymal disease can cause elevated ICP. Signs include hyperreflexia, papilledema (a late sign), and the Cushing reflex (a preterminal event).

Parenchymal disease

Physical examination findings are usually normal.

Patients who have had seizures may have typical manifestations of the postictal state, with somnolence, an altered level of consciousness, and poor memory.

Focal neurologic deficits are unusual and suggest alternative diagnoses, such as tuberculoma, tumor, or, rarely, extraparenchymal neurocysticercosis.

Extraparenchymal disease

Ocular cysticerci are visible upon ophthalmologic examination.

Rare spinal cysticerci manifest as sensory or motor deficits or back tenderness.

Patients with neurocysticercosis of the cisterns may present with lacunar infarcts or large-vessel infarction with associated upper motor neuron signs.

Subcutaneous cysts may be palpable as fluid-filled nodules that resemble sebaceous cysts.

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Causes

Extraneural cysticercosis: Extraneural infection with T solium typically involves the eye, muscle, or subcutaneous tissue. It is not known whether oncospheres actively migrate to those organs or passively enter tissues during high blood flow.

Neurocysticercosis: Infection of the CNS with T solium and associated host inflammation.

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