Helminthic Infections Neurocysticercosis

Neurocysticercosis caused by the tapeworm, Taenia solium, has a high incidence in Mexico, Africa, South and Central America, and India. In the United States, it is common in California.

Cysticercosis is acquired by the fecal-oral route through the ingestion of food contaminated by ova excreted in the feces of Taenia carriers. From the gastrointestinal tract, the ova are carried via bloodstream to the visceral organs, the muscles, and the brain, where they mature and become encysted. The cysts—single, multiple or racemose—measure 0.5 to 2 cm and vary greatly in location. Common sites are the cerebral and spinal subarachnoid space, the brain parenchyma, and the ventricles.

Clinically, the cysts manifest in a number of ways: Focal cerebral deficits, signs of spinal cord compression, psychiatric symptoms, and cognitive decline occur in various combinations. Seizures are common. Raised intracranial pressure due to obstructive hydrocephalus,

Calcification Foramen Monro

FIGURE 6.30

Cerebral cysticercosis. CT scan of the head shows multiple calcified cysticercus cysts in a 24-year-old woman who developed an acute hydrocephalus necessitating placement of a ventriculoperitoneal shunt. Note the presence of a calcified cyst at the foramen Monro. A cavum septum pellucidum is also present.

FIGURE 6.30

Cerebral cysticercosis. CT scan of the head shows multiple calcified cysticercus cysts in a 24-year-old woman who developed an acute hydrocephalus necessitating placement of a ventriculoperitoneal shunt. Note the presence of a calcified cyst at the foramen Monro. A cavum septum pellucidum is also present.

and circulatory insufficiency due to arteritis may develop during the course of the disease. On CT scan, the cysts appear as hypodense, ring-enhancing lesions or calcified nodules (Fig. 6.30). MRI demonstrates the nonenhanc-ing viable cysts and also the disintegrated cysts, which display ring or nodular enhancement with contrast material. The diagnosis is confirmed using ELISA or enzyme-limited immunoelectrotransfer blot (EITB).

Pathologically, the cyst wall consists of a hyaline-cuticular layer. Within the cyst, the larvae may remain viable for months or years and may provoke a leptomen-ingitis or encephalitis with plasma cells and eosinophils, and an ependymitis and arteritis. Dead larvae are embedded in granulation tissue or calcify (Fig. 6.31).

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