Letters
Infectious diseases
Volume 193 - Issue 4

Seizures related to praziquantel therapy in neurocysticercosis

Authors:  Saliya S Hewagama, Jonathan D Darby, Harsha Sheorey and John R Daffy

Med J Aust 2010; 193 (4): 246-247. || doi: 10.5694/j.1326-5377.2010.tb03885.x
Published online: 16 August 2010
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To the Editor: Seizures can be precipitated by treatment with praziquantel in patients with underlying neurocysticercosis, but this is rare and has not previously been described in Australia. We describe the case of a patient who developed seizures after antischistosomal therapy.

An asymptomatic 23-year-old Burmese man underwent migrant health screening by his local doctor a month after arriving in Australia. His schistosomal serological results were positive (titre, 1:32) and he received three doses of 600 mg praziquantel. Three days later, he experienced several generalised tonic–clonic seizures in short succession, each lasting a few minutes. A magnetic resonance imaging (MRI) scan revealed three ring-enhancing lesions less than 1 cm in diameter, suggestive of neurocysticercosis. He was treated with phenytoin and also received dexamethasone for 1 month. A repeat MRI scan 6 months later showed significant reduction in the size of the lesions, to less than 3 mm. Phenytoin therapy was ceased after 3 months, with no seizures at last review (6 months). In view of the temporal association between the treatment and the seizures in this previously asymptomatic patient, we believe the seizures were precipitated by the praziquantel therapy.

Cysticercosis, which is endemic across the developing world, is caused by the helminth Taenia solium. Clinical disease, including neurocysticercosis, is often asymptomatic. Symptomatic neurocysticercosis often presents as seizures, especially as the cysts degenerate, and is the commonest cause of acquired, late-onset epilepsy in the developing world.1 The benefit of treatment remains controversial, especially when there are only a few cysts.1-3 Praziquantel and albendazole therapy accelerate cyst degeneration, and subsequent inflammation may precipitate seizures, which are sometimes pre-emptively managed with corticosteroids.1 There is conflicting evidence on the benefit of treatment for long-term seizure frequency.2,3

Although screening for some parasitic infections in refugees in Australia is recommended,4 this does not include cysticercosis. Serological tests for T. solium cannot differentiate between active and past infections, have limited sensitivity, are not widely available in Australia, and cannot differentiate between neurocysticercosis and cysticercal disease elsewhere.5 The only reliable method for diagnosis is neuroimaging, which is impractical for mass screening.

Nevertheless, we advocate a high degree of suspicion for neurocysticercosis in migrants from Taenia-endemic areas. Geographical origin alone is insensitive for identifying an at-risk population. A history of seizures, or the presence of subcutaneous nodules, should prompt investigation with serological testing and subsequent neuroimaging before consideration of treatment. In such symptomatic patients, this will allow the need for anthelmintic therapy to be assessed, along with consideration of adjunctive corticosteroid therapy.

Authors

  • Saliya S Hewagama1
  • Jonathan D Darby1
  • Harsha Sheorey1
  • John R Daffy1
  • 1. St Vincent’s Hospital, Melbourne, VIC.

Correspondence: Jonathan.Darby@svhm.org.au

References

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