According to a new study published early online and in the December issue of Lancet Neurology, researchers better understand the disease mechanisms behind brain seizures that are due to the tapeworm-derived parasitic infection called neurocysticercosis. Their finding that the seizures are frequently associated with fluid or perlesional oedema (PO) around dead calcified cysticercal granulomas (immune cells) may lead to better possible treatment targets.
Dr Theodore Nash (National Institutes of Health, Bethesda, MD, USA) and Dr. Héctor H. Garcia (Universidad Peruana Cayetano Heredia and the Instituto Nacional de Ciencias Neurologicas, Lima, Peru) explain that most adult acquired seizures and epilepsy cases in many regions of the developing world are due to neurocysticercosis. The tapeworm Taenia solium – which grows in human intestines after being acquired by eating raw or undercooked pork contaminated with cysticerci (cysts) of T. solium – infects the brain in larval form. Free-roaming pigs (or humans) can contract tapeworm eggs that are released into feces. After the eggs hatch, the developing parasites spread throughout the host’s body via the circulatory system where they infect the brain, muscles, and subcutaneous tissues. Eventually the larvae degenerate and turn into calcified granulomas – blocks of dead immune cells – that are frequently located in the same place as the seizure.
This recent research analyzed 110 patients to show that about 50% of patients with both neurocysticercosis and seizures had PO around these calcified granulomas. Although PO is a recently-recognized phenomenon, the results of the research suggest that PO is common and probably accounts for a lot of responsibility in seizure development. This new understanding also means that new therapies and treatments will be tested to treat epilepsy and seizures due to neurocysticercosis.
“Perilesional oedema is common and associated with episodic seizure activity in patients with calcified neurocysticercosis. Our findings are probably representative of symptomatic patients in regions where T. solium neurocysticercosis is endemic and suggest a unique and possibly preventable cause of seizures in this population,” conclude Nash and Garcia. Currently, researchers are planning trials that will test corticosteroids for treatment of PO.
Dr Benoît Marin and Dr Pierre-Marie Preux (Institut d’Epidémiologie et de Neurologie Tropical, Université de Limoges, France) write in an accompanying reflection and reaction that: “Such treatment of perilesional oedema [with corticosteroids] in calcific neurocysticercosis could be a good target in the prevention of seizure recurrence in endemic countries.”
Perilesiona brain oedema and seizure activity in patients with calcified neurocysticercosis: a prospective cohort and nested case-control study
Theodore E Nash, E Javier Pretell, Andres G Lescano, Javier A Bustos, Robert H Gilman, Armando E Gonzalez, Héctor H Garcia, for The Cysticercosis Working Group in Peru
The Lancet Neurology (2008).
DOI:10.1016/S1474-4422(08)70243-6
Written by: Peter M Crosta