Neurocysticercosis is the most common helminthic infection of the CNS but its diagnosis remains difficult. Clinical manifestations are nonspecific, most neuroimaging findings are not pathognomonic, and some serologic tests have low sensitivity and specificity. The authors provide diagnostic criteria for neurocysticercosis based on objective clinical, imaging, immunologic, and epidemiologic data. These include four categories of criteria stratified on the basis of their diagnostic strength, including the following: 1) absolute-histologic demonstration of the parasite from biopsy of a brain or spinal cord lesion, cystic lesions showing the scolex on CT or MRI, and direct visualization of subretinal parasites by funduscopic examination; 2) major-lesions highly suggestive of neurocysticercosis on neuroimaging studies, positive serum enzyme-linked immunoelectrotransfer blot for the detection of anticysticercal antibodies, resolution of intracranial cystic lesions after therapy with albendazole or praziquantel, and spontaneous resolution of small single enhancing lesions; 3) minor-lesions compatible with neurocysticercosis on neuroimaging studies, clinical manifestations suggestive of neurocysticercosis, positive CSF enzyme-linked immunosorbent assay for detection of anticysticercal antibodies or cysticercal antigens, and cysticercosis outside the CNS; and 4) epidemiologic-evidence of a household contact with Taenia solium infection, individuals coming from or living in an area where cysticercosis is endemic, and history of frequent travel to disease-endemic areas. Interpretation of these criteria permits two degrees of diagnostic certainty: 1) definitive diagnosis, in patients who have one

The larval stage of the pork tapeworm (Taenia solium) infects the human nervous system, causing neurocysticercosis. This disease is one of the main causes of epileptic seizures in many less developed countries and is also increasingly seen in more developed countries because of immigration from endemic areas. Little information is available on the natural evolution of taeniasis or cysticercosis. Available therapeutic measures include steroids, treatments for symptoms, surgery, and, more controversially, antiparasitic drugs to kill brain parasites. Efforts to control and eliminate this disease are underway through antiparasitic treatment of endemic populations, development of pig vaccines, and other measures.Taenia solium infection and the resulting disease neurocysticercosis are endemic in less developed countries where pigs are raised as a food source. 1 , 2 Neurocysticercosis is common throughout Latin America, most of Asia, sub-Saharan Africa, and parts of Oceania, and is the greatest cause of acquired epilepsy worldwide. 3 It is now increasingly diagnosed in more developed countries owing to immigration of tapeworm carriers from endemic zones. 2 , 4 T solium has a complex two-host life cycle. Human beings are the only definitive host and harbour the adult tapeworm (taeniasis), whereas both people and pigs can act as intermediate hosts and harbour the larvae or cysticerci (figure 1). TaeniasisTaeniasis occurs only in the human host, after ingestion of undercooked pork infected with cysticerci. Although cysticercosis has been known for ages, its relation to the adult tapeworm was not clear until it was shown by Kuchenmaister in 1855; he fed condemned

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Taenia solium neurocysticercosis is a common cause of epileptic seizures and other neurological morbidity in most developing countries. It is also an increasingly common diagnosis in industrialized countries because of immigration from areas where it is endemic. Its clinical manifestations are highly variable and depend on the number, stage, and size of the lesions and the host's immune response. In part due to this variability, major discrepancies exist in the treatment of neurocysticercosis. A panel of experts in taeniasis/cysticercosis discussed the evidence on treatment of neurocysticercosis for each clinical presentation, and we present the panel's consensus and areas of disagreement. Overall, four general recommendations were made: (i) individualize therapeutic decisions, including whether to use antiparasitic drugs, based on the number, location, and viability of the parasites within the nervous system; (ii) actively manage growing cysticerci either with antiparasitic drugs or surgical excision; (iii) prioritize the management of intracranial hypertension secondary to neurocysticercosis before considering any other form of therapy; and (iv) manage seizures as done for seizures due to other causes of secondary seizures (remote symptomatic seizures) because they are due to an organic focus that has been present for a long time

In this hyperendemic area, an important proportion of seizure cases are associated with neurocysticercosis as demonstrated by serology or brain CT.

Neurocysticercosis is responsible for increased rates of seizures and epilepsy in endemic regions. The most common form of the disease, chronic calcific neurocysticercosis, is the end result of the host's inflammatory response to the larval cysticercus of Taenia solium. There is increasing evidence indicating that calcific cysticercosis is not clinically inactive but a cause of seizures or focal symptoms in this population. Perilesional edema is at times also present around implicated calcified foci. A better understanding of the natural history, frequency, epidemiology, and pathophysiology of calcific cysticercosis and associated disease manifestations is needed to define its importance, treatment, and prevention.Neurocysticercosis is a major cause of seizures and other neurologic problems in many less developed countries 1 and a significant health concern in developed countries as well, mostly due to migration of infected persons. 2 Over the last two decades the development of MRI and CT imaging, effective and safe cysticidal drugs, and specific and relatively sensitive serologic tests have given rise to a renaissance in our understanding of the disease and efficacy of treatments. Much of our increased understanding has focused on disease associated with viable or degenerating cysts, broadly referred to as "active" cysticercosis, Copyright © 2004 Life cycleHumans harbor the tapeworm that is acquired by eating poorly cooked pork containing cysticerci of Taenia solium. Ova or proglottids containing ova are excreted in the feces and when ingested by free roaming pigs develop into cysts primarily in the muscles and brain. The usual life cycle is fulfilled after humans ingest undercooked pork. Ova, accidentally ingested by humans, also develop into cysts, mostly in the brain, muscle, and subcutaneous tissues, and this condition is referred to as cysticercosis. 5 Course of infectionAlthough incompletely documented, a reasonable view of the natural history can be ascertained from pathologic, radiologic, and parasitologic studies. Cysticercosis and epilepsyWhile many patients present with single or groups of seizures at various stages of this disease, not all patients develop recurrent seizures, or epilepsy. There are three possibly different scenarios concerning the relationship between cysticercosis and epilepsy: 1) causal relationship, namely, cysticercosis as the cause of focal epilepsies; 2) non causal relationship or simple overlap of two independent and unrelated diseases; and 3) dual pathology. At present there is overwhelming evidence supporting neurocysticercosis as a cause of seizures and epilepsy. Because neurocysticercosis, particularly calcific cysticercosis, is so common in endemic regions (see below), it is likely that two pathologies known to incite seizure activity will be present in some individuals 12 and whether there are interactions or dual pathology between two conditions is speculative. 12 Multiple causes of seizures in cysticercosisThere are multiple ways that cysticercosis can ca...

Background Cysticercosis due to Taenia solium is a leading cause of adult acquired seizures and epilepsy that frequently occurs in patients with only calcified larval cysts. Transient episodes of perilesional brain edema occur around calcified foci but its importance, association with seizures, incidence, and pathophysiology are unknown. Methods One hundred and ten persons with only calcified lesions and a history of seizures or severe headaches were followed prospectively in a cohort design to assess the incidence of seizure relapses. In a nested case-control sub study, perilesional edema was assessed by MRI at the time a seizure occurred in the symptomatic patient and in a matched asymptomatic control, amongst the 110 followed. Results Median follow up was 32.33 months (SD 19.99). Twenty-nine people had an incident seizure with an estimated 5 year seizure incidence of 36%. Twenty-four patients of the 29 with seizure relapse had an MRI evaluation within five days of the event. Perilesional edema was found in 12 (50.0%) compared to 2 of 23 asymptomatic matched controls (8.7%). Conclusions Perilesional edema occurs frequently and is associated with episodic seizure activity in calcified neurocysticercosis. Our findings are likely representative of symptomatic patients in endemic regions and suggest a unique and possibly preventable cause of seizures in this population.