Summary: Neurocysticercosis (NC) remains a major public health problem in developing and some developed countries. Currently, the best procedures for diagnosing NC are neuroimaging studies. Immunoserologic assays, such as enzyme‐linked immunoelectrotransfer blot assay (EITB) or enzyme‐linked immunosorbent assay (ELISA), detect antibodies against Taenia solium, or cysticercus. Consequently, they are useful in identifying a population at risk of contact with the parasite but do not necessarily indicate a systemic active infection. Most seropositive individuals are asymptomatic. No data from prospective studies concern the proportion of these individuals that will develop seizures or other neurologic symptoms. There is a discrepancy between the results of serologic assays and neuroimaging studies: >50% of those individuals with NC diagnosed by computed tomography (CT) scan test EITB negative.Pathophysiologic classification of NC into active, transitional, and inactive forms permits a good correlation between clinical manifestations and neuroimaging procedures and facilitates medical and surgical management and research. The most frequent clinical manifestations of NC are seizures. We assume that NC is the main cause of symptomatic epilepsy in developing countries; however, no case‐control or cohort studies demonstrate this association. Most patients with NC with seizures have a good prognosis; nevertheless, further studies analyzing factors related to recurrence of seizures and possibilities of discontinuation of antiepileptic medications (AEDs) are needed.Regarding treatment of NC with antihelminthic drugs, no controlled clinical trials exist that establish specific indications, definitive doses, and duration of treatment. The most effective approach to taeniasis/cysticercosis infection is prevention. This should be a primary public health focus for developing countries.We critically review the available information regarding the epidemiology and diagnosis of human cysticercosis, the physiopathology and imaging correlation of the parasite in the central nervous system (CNS) of the host, the relation between seizures or epilepsy and NC, and the issues surrounding the treatment and prognosis of NC, including the use of antihelminthic therapy.

Neurocysticercosis is a disease of poverty and underdevelopment. Little is known about the natural history of the infection in humans, but some of the mechanisms whereby the parasite remains silent and evades the host immune response are understood. Symptomatic neurocysticercosis usually results from host inflammatory response after parasite death, and the clinical manifestations can be diverse. There is no evidence that cysticidal treatment does more good than harm in addition to conventional antiepileptic treatment. Population control measures involving immunisation or mass treatment have not shown long term effectiveness. Epilepsy, similarly to neurocysticercosis, is a largely unrecognised but increasing burden on the welfare and economies of developing countries. The technology of drug treatment and psychosocial rehabilitation is well known but requires widespread and effective dissemination at low cost. There is little epidemiological data on risk factors for epilepsy in developing countries on which to base prevention strategies. The public health prioritisation of chronic disorders such as epilepsy remains a challenge for policy and practice in developing countries. For both neurocysticercosis and epilepsy, there is a dilemma about whether limited public resources would better be spent on general economic development, which would be expected to have a broad impact on the health and welfare of communities, or on specific programmes to help individual affected people with neurocysticercosis and epilepsy. Either approach requires detailed economic evaluation.

Aim: The aim of this trial was to evaluate the effects of albendazole (ALB) on cyst disappearance, reduction of the number of cysts and seizure recurrence. Methods: 178 patients with new onset symptoms due to active or transitional neurocysticercosis were randomly assigned to receive either 800 mg of ALB daily or placebo for 8 days. All patients also received prednisone. Imaging studies were done at baseline and at months 1, 6 and 12 of follow-up. Results: Active cysts were identified in 59 of 88 people randomised to ALB and 57 of the 90 in the placebo arm. By 1 month, 31% were free of active cysts in the treatment group compared with 7% in the placebo group (p = 0.001). In addition, the ALB group had a greater reduction in the number of active cysts compared with the placebo group (p = 0.001). After 1 month following treatment there was no additional gain by treatment group in the disappearance or reduction in the number of active cysts. ALB treatment had little effect on cysts in the transitional or calcification stage. We found no difference between the ALB and placebo groups in symptoms during treatment or in seizure recurrence during the 12 months after treatment. Conclusion: Albendazole plus symptomatic treatment leads to the disappearance of active cysts in 31% of patients compared with 7% of those with symptomatic treatment alone. This treatment effect occurs within the first 30 days after treatment. Trial registration number: NCT00283699.

Objective: To determine the risk of seizure recurrence after a first seizure due to neurocysticercosis (NC) and to evaluate risk factors for seizure recurrence, including the influence of antihelminthic treatment. Methods: The authors prospectively followed 77 patients with a first seizure and active or transitional NC for >7 years (median 24 months). Results: Thirty-one patients (40.3%) experienced seizure recurrence. Kaplan–Meier estimated recurrence was 22% at 6 months, 32% at 12 months, 39% at 24 months, and 49% at 48 and 84 months. Treatment with an antihelminthic (albendazole) did not influence recurrence. On multivariable analysis, none of the following predicted recurrence: sex, presenting seizure type, classification of NC, localization of cysts, Todd paralysis, neurologic deficits at presentation, EEG abnormalities. Only change in CT predicted recurrence: 22% in patients in whom cysts disappeared and 56% in patients with persistent cysts (p < 0.05). In this latter group, recurrence was associated with persistence of an active lesion. Of those with two seizures, estimated risk of a third seizure was 68% by 6 years after the second seizure. Conclusions: Seizure recurrence is high after a first acute symptomatic seizure due to NC, but this seems related to persistence of active brain lesions. Recurrence risk is low and in keeping with seizure risk following other brain insults leading to a static encephalopathy in those in whom the NC lesion clears. Patients with NC should receive antiseizure medications until the acute lesion clears on CT. There is no correlation between treatment with antihelminthic agents and seizure recurrence.