Neurocysticercosis, prevalent wherever pigs are raised in the presence of poor sanitation, is the most common identifiable cause of new-onset
epilepsy throughout the developing world. As immigration patterns have changed, children with
neurocysticercosis are seen throughout the United States. Acute
cysticercosis, the most common manifestation in children, reflects the host response to the dying parasite. Children typically present with
seizures and have an excellent prognosis. Neuroimaging demonstrates a single ring or nodular enhancing lesion surrounded by
edema. Short-term
anticonvulsant therapy is indicated, but treatment with
antiparasitic agents is not required. Other forms, such as active
cysts (intact organism), intraventricular or subarachnoid racemous
cysticercosis, and cysticercal
meningoencephalitis, are less common manifestations of
parasitic infection.
Toxoplasmosis, caused by the parasite Toxoplasma gondii, can be acquired by ingestion of infected undercooked meat or from oocytes shed in cat feces. Acquired
cerebral toxoplasmosis, due to primary or reactivated
infections, rarely occurs in immunocompetent children. In children who are immunodeficient as the result of
AIDS,
chemotherapy,
tissue transplantation, or congenital immunodeficiency,
toxoplasmosis may be difficult to distinguish from cerebral
lymphoma. A variety of techniques, including neuroimaging,
Thallium-201 SPECT, polymerase chain reaction analysis of CSF, and special histological methods, may be used to diagnose acquired
toxoplasmosis.
Antiparasitic therapy, using
pyrimethamine and
sulfadiazine, and serial neuroimaging often enable clinicians to differentiate
toxoplasmosis from other central nervous system lesions.
Toxoplasmosis may respond to other antimicrobials, including
macrolide antibiotics,
dapsone, clinidamycin, and
atovaquone. Suppressive treatment is generally required for life in immunodeficient patients. Immunodeficient children with acquired
toxoplasmosis have high rates of mortality and neurological sequelae.