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The pathological findings of cysticercosis within the brain differ from those elsewhere in the body. The cysticercus develops to form a small, firmly encapsulated cyst. Several pathological forms are found: the cyst may develop in the brain parenchyma or it may be mobile, lying in the ventricles or in the aqueduct. Alternatively, there may be a racemose cyst, a large delicate, thin-walled, translucent, ramifying body (usually sterile) lying in the ventricular system, cisterna magna, or cerebellopontine angle. It may even extend through the foramen magnum into the upper cervical region. In other patients, neither of these forms may exist; instead there may be a basal arachnoiditis without any obvious cysticercus in immediate relationship.

In the brain, the cysticercus becomes surrounded by neuroglia; degeneration leads to a walled-off and discolored ring of glial tissue. Inflammation does not develop until the cysticercus dies and degenerating cysticerci stimulate infiltration of neutrophils, eosinophils, and macrophages. A granulomatous reaction eventually ensues, characterized by foamy macrophages with occasional epithelioid cells and foreign body giant cells. The lesions subsequently become fibrotic and may calcify.

Five types of neurocysticercosis are recognized according to their location: (1) parenchymal, (2) arachnoidal, (3) ventricular, (4) spinal, and (5) mixed.

Parenchymal cysticercal larvae undergo degeneration, and various stages can be identified: (a) vesicular stage, viable cysticerci with immune tolerance by the host; (b) colloidal stage, nonviable cysticerci with the host's immune system reacting against the degeneration of the parasite; (c) granular nodular stage, nonviable cysticerci with immune response and deposition of mineral salt; and (d) calcified stage, the sequelae of nonviable nodular granulomas. The lesions may also be found simultaneously in different stages in the same individual. Another pattern of parenchymal cysticercosis is the miliary or encephalitic type, where numerous small lesions produce severe acute or chronic inflammatory reaction with diffuse brain edema and symmetrical compression of the ventricles.

Arachnoiditis, vasculitis with infarcts, cranial nerve involvement, and impairment of CSF circulation with obstructive communicating hydrocephalus result with involvement of the basal cisterns. Obstruction of the ventricular system may occur from intraventricular lesions and reactive ependymitis.

Involvement of the spinal canal is rare and may give rise to myelopathies when the spinal cord is affected and radiculopathies when the subarachnoid space and leptomeninges are involved by space-occupying lesions or arachnoiditis.

Laboratory Diagnosis

Because of the wide range of nonspecific clinical findings in neurocysticercosis, the diagnosis can be confirmed only with imaging and CSF studies. Both of these methods have dramatically improved diagnostic accuracy because they provide evidence of the location and stage of the cysticerci and the degree of host inflammatory reaction.

False-positive results in immune tests are sometimes seen in individuals from endemic areas because of contact with the parasite without development of the disease. False-negative results in serum can occur because of local production of antibodies without a parallel increase in peripheral blood, and also in HIV-positive patients. In CSF, there is objective evidence of a host reaction against cysticerci within the subarachnoid space, with the degree of inflammation manifested by elevated cells and/or proteins, and a positive immunological reaction to cysticercal antigens in ELISA or complement fixation tests, both of which may have 80% sensitivity and 96% specificity values. These tests are reliable and specific in meningeal cysticercosis and somewhat less useful in cases of parenchymal and ventricular neurocysticercosis, particularly in noninflammatory cerebrospinal fluid.

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Copyright: Palmer and Reeder

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