| Neurocysticercosis | |
|---|---|
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| Magnetic resonance image of a patient with neurocysticercosis demonstrating multiple cysticerci within the brain. | |
| Specialty | Infectious diseases  |
Neurocysticercosis (NCC) is a parasitic infection of the central nervous system caused by Taenia solium. Neurocysticercosis is often caused by improperly cooked infected food or contaminated water. When consumed, cysticerci are released into the small intestine, where they attach to the intestinal wall and grow into a tapeworm. This tapeworm can travel to the brain, muscles, eyes, and skin. Neurocysticercosis presents various signs and symptoms, influenced by the location, number of lesions, and immune response, ranging from asymptomatic to fatal, with common symptoms including seizures, intracranial hypertension, cognitive impairment, and focal deficits.
Neurocysticercosis diagnosis relies on neuroimaging and serology, with diagnostic criteria including the lentil lectin purified glycoprotein (LLGP) enzyme-linked immunoelectrotransfer blot (EITB) assay, CT and MRI. Neurocysticercosis can be categorized as either parenchymal or extraparenchymal. Neurocysticercosis can be prevented through improved sanitation, education, awareness, de-worming and TSOL18 vaccines for endemic areas.
Neurocysticercosis requires a tailored treatment approach based on cyst viability, host's immune response, and the location and number of lesions. Symptoms of neurocysticercosis are treated with antiepileptic, antiedema, analgesic, or anti-inflammatory drugs, such as carbamazepine for seizures, surgery, acetazolamide, steroids, or mannitol for intracranial hypertension. Antiparasitic drugs should not be used in cases with a preexisting risk of developing hydrocephalus, such as sub-arachnoid neurocysticercosis or encephalitic neurocysticercosis, as the inflammation after treatment can raise intracranial pressure and potentially cause death. Common antiparasitic medications include albendazole and praziquantel, which are only suitable for treating vesicular viable cysts or early colloidal phases, and are ineffective against calcified cysts. Steroid administration is crucial in managing neurocysticercosis-related inflammation in the central nervous system. Prednisolone and dexamethasone are often used alongside antiparasitic therapy. In severe cases, antiparasitic medication may be ineffective due to mass inflammation risks. Surgical treatments, such as ventricle-peritoneal shunts and cyst excision, may be necessary for aggressive treatment. Parenchymal and single lesion neurocysticercosis generally has a favorable prognosis, while extraparenchymal neurocysticercosis can lead to obstructive hydrocephalus, sudden death, or slow death.
Neurocysticercosis is endemic in developing countries, particularly in poorer regions with poor sanitation and clean water, such as Latin America, China, Nepal, Africa, India, and Southeast Asia. Although rare in Europe and the US, immigration has increased its prevalence in these areas. Taenia solium has been described since 1500 BC and has been found in ancient Egyptian mummies. The first recorded cases of neurocysticercosis were likely in 1558. In 1792, a Peruvian physician reported simultaneous taeniasis and cysticercosis in the same individual. In the 19th century, German pathologists found similarities between T. solium and cysticercus scolex, and discovered that consumption of cysticercus from pork caused human intestinal taeniasis.