To the Editor: A 73-year-old man, visiting the United Statesfrom Nepal, presented to our institution with multiple tonic–clonicseizures. In order to control the seizures, the patient wasintubated, admitted to our intensive care unit, and treatedwith intravenous benzodiazepines and anticonvulsant drugs. Computedtomography (CT) of the head showed a 1-cm enhancing lesion withsurrounding vasogenic edema in the left frontal lobe and a focusof increased attenuation within the lesion suggestive of petechialhemorrhage or calcification. Magnetic resonance imaging (MRI)of the brain confirmed these findings and was diagnostic ofa neoplastic lesion. A neurosurgical consultation was sought,and on day 5 of the hospitalization, an excisional biopsy wasperformed. Examination of the biopsy specimen established thediagnosis of neurocysticercosis (Figure 1). Treatment with albendazoleand dexamethasone was started on day 7 of the hospital stay.Fortunately, no recurrent seizures were observed, and the patientwas discharged home on day 11.
Periodic acid–Schiff staining shows inflamed brain parenchyma with gliosis surrounding an inflamed cyst. The cyst contains a Taenia solium cysticercus with the scolex (S) and a fluid-filled bladder (B).
Neurocysticercosis is the major cause of adult-onset epilepsyin the developing world1 and is caused by infection of the centralnervous system by the larvae of Taenia solium. Although humansare the only definitive hosts, cysticercosis develops when humansbecome intermediate hosts by ingesting the embryonated eggsof the tapeworm, which release oncospheres that penetrate theintestinal wall, enter the bloodstream, and develop into cysticerciin tissues, with the brain being a high-impact target organ.These eggs may come from the environment (heteroinoculation),may be regurgitated from proglottids into the stomach (internalautoinoculation), or may be transferred from the fingers ofan infected person (external autoinoculation).
The diagnosis of neurocysticercosis is confirmed by means ofneuroimaging (CT and MRI) and serologic analysis. The enzyme-linkedimmunoelectrotransfer blot has a sensitivity and specificityof more than 98% and is the serologic assay of choice for thedetection of cysticercosis.2 Detection of the parasite in abiopsy specimen of skin nodules may also aid in the diagnosis.Cysticidal treatment is complicated by the fact that it initiatesan inflammatory response that may precipitate seizures.3 However,a recent randomized, placebo-controlled trial showed a reductionin the rate of generalized seizures among the patients treatedwith albendazole.4 Corticosteroids are the primary form of therapyfor cysticercotic encephalitis, angiitis, and arachnoiditis.5Although corticosteroids are recommended in conjunction withanthelmintic treatment to prevent an inflammatory response,the dose, duration, form, and — most important —timing of this treatment still remain controversial.
The diagnosis of neurocysticercosis should be suspected in allvisitors and immigrants from Asia, South America, and CentralAmerica who have adult-onset epilepsy. In the case of nativeAmericans with this form of epilepsy, asking whether they havea household worker from a country where the infection is endemicmay provide a clue.
Igor Mamkin, M.D. Nitesh Sood, M.D. Sundaram V. Ramanan, M.D. University of Connecticut Health Center Farmington, CT 06030 igor_mamkin{at}yahoo.com
Scheel CM, Khan A, Hancock K, et al. Serodiagnosis of neurocysticercosis using synthetic 8-kD proteins: comparison of assay formats. Am J Trop Med Hyg 2005;73:771-776. [Free Full Text]
Garcia HH, Pretell EJ, Gilman RH, et al. A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. N Engl J Med 2004;350:249-258. [Free Full Text]
Garcia HH, Evans CAW, Nash TE, et al. Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev 2002;15:747-756. [Free Full Text]
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