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Cysticercosis, widely endemic in most developing countries, is now beginning to appear with some frequency in industrialised countries as a result of both increasing travel and globalisation. Fortunately, advances in diagnostic methods, clinical knowledge, and the epidemiology of taeniasis and neurocysticercosis have enriched our understanding of the evolution of this infection and the resulting disease. Modern neuroimaging can now demonstrate milder cases than hitherto, and epidemiological studies using computed tomography (CT) in endemic settings have revealed asymptomatic brain calcifications in 10–20% of the general population.1–3 Neurologically symptomatic individuals attending health centres clearly represent only the tip of a sizable iceberg of infection.4 This article will summarise basic information that should allow neurologists to make the diagnosis and manage human neurocysticercosis.
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As the result of poor socioeconomic development and domestic pig raising, cysticercosis is highly endemic in most developing countries around the world (fig 1). Even in Europe, transmission (albeit at very low rates) still seems to occur in Portugal and Northern Spain.5 6 And in the USA and most of Europe, neurocysticercosis is increasingly recognised as a cause of seizures,7 primarily in immigrants and individuals who have travelled to endemic areas where transmission is common and where serological evidence of exposure to the parasite can be found in 10–25% of the general population.
Clinically, the magnitude of the disease burden associated with neurocysticercosis in endemic countries is enormous; it is the most common cause of acquired epilepsy, and in nearly 30% of patients with seizures the cause is neurocysticercosis.1–3 An estimated 75 million individuals in Latin America alone …
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