Helminthic Brain Infections
(See also Introduction to Brain Infections.)
Parasitic helminthic worms infect the CNS of millions of people in developing countries. Infected people who visit or immigrate to nonendemic areas, including the US, may present there. Worms may cause meningitis, encephalitis, cerebral masses, hydrocephalus, stroke, and myelopathy.
Among about 20 helminths that can cause neurologic disorders, the pork tapeworm Taenia solium causes by far the most cases in the Western Hemisphere. The resulting disorder is neurocysticercosis. After a person eats food contaminated with the worm’s eggs, larvae migrate to tissues, including the brain, spinal cord, and CSF pathways, and form cysts. Cyst diameter rarely exceeds 1 cm in neural parenchyma but may exceed 5 cm in CSF spaces.
Brain parenchymal cysts cause few symptoms until death of the worms triggers local inflammation, gliosis, and edema, causing seizures (most commonly), cognitive or focal neurologic deficits, or personality changes. Larger cysts in CSF pathways may cause obstructive hydrocephalus. Cysts may rupture into CSF, inducing acute or subacute eosinophilic meningitis. Mortality rate for symptomatic neurocysticercosis is up to 50%.
Neurocysticercosis is suspected in patients who live in or have come from developing countries and who have eosinophilic meningitis or unexplained seizures, cognitive or focal deficits, or personality changes. It is suggested by multiple calcified cystic lesions seen on CT or MRI; a contrast agent may enhance the lesions. Diagnosis requires serum and CSF serologic tests and occasionally cyst biopsy.
Albendazole (7.5 mg/kg po q 12 h for 8 to 30 days; maximum daily dose, 800 mg) is the antihelminthic drug of choice. Alternatively, praziquantel 20 to 33 mg/kg po tid may be given for 30 days. Dexamethasone 8 mg once/day IV or po for the first 2 to 4 days may lessen the acute inflammatory response as the worms die. Antihelminthic therapy can cause serious morbidity in patients with a large number of cysts and may not help patients with a single cyst. Treatment must be carefully individualized.
Short- or long-term anticonvulsant treatment may be required. Surgical excision of cysts and ventricular shunts may also be required.
In schistosomiasis, necrotizing eosinophilic granulomas develop in the brain, causing seizures, increased intracranial pressure, and diffuse and focal neurologic deficits.
Large, solitary echinococcal cysts can cause focal deficits and, occasionally, seizures.
Coenurosis, caused by tapeworm larvae, usually produces grapelike cysts that may obstruct CSF outflow in the 4th ventricle. Symptoms require several years to develop and, if the brain is involved, include increased intracranial pressure, seizures, loss of consciousness, and focal neurologic deficits.
Gnathostomiasis, a rare infection by larvae of the nematode Gnathostoma sp, results in necrotic tracts surrounded by inflammation along the nerve roots, spinal cord, and brain or in subarachnoid hemorrhage, causing low-grade fever, stiff neck, photophobia, headache, migratory neurologic deficits (occasionally affecting the 6th or 7th cranial nerve), and paralysis.
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