Brain seizures that are due to neurocysticercosis caused by tapeworm infection are commonly associated with fluid (perlesional oedema/PO) around dead calcified cysticercal granulomas (see below). This phenomenon suggests unique disease mechanisms and a possible treatment target. These are the conclusions of an Article published early Online and in the December edition of Lancet Neurology, written by 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.
Neurocysticercosis is the most common cause of adult acquired seizures and epilepsy in many regions of the developing world. It is caused by brain infection with the larval form of the tapeworm Taenia solium. When humans ingest raw or undercooked pork that is contaminated with the cysticerci (cysts) of T solium, a tapeworm grows in their intestine. Tapeworm eggs are released in the faeces and ingested by free-roaming pigs or accidentally by human beings; when the eggs hatch, the developing parasites are distributed around the host's body, probably by the circulatory system, mostly to the brain, muscles, and subcutaneous tissues.Larvae degenerate and eventually evolve into calcified granulomas that are often the site of seizure location.
This latest report, which studied 110 patients, shows that PO around these calcified granulomas is found in about 50% of patients with neurocysticercosis who had seizures. PO was unrecognized until relatively recently, but this result indicates that PO is common and likely plays an important role in seizures in a large proportion of those afflicted. Epilepsy and seizures due to neurocysticercosis may be amenable to specific and previously unthought of therapies and treatments. Since PO can at times be found in asymptomatic individuals, the study also showed that PO was highly associated with seizures.
The authors conclude: "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." They add that treatment trials for PO using corticosteroids are in the planning stage.
In an accompanying Reflection and Reaction comment, Dr Benoît Marin and Dr Pierre-Marie Preux, Institut d'Epidémiologie et de Neurologie Tropical, Université de Limoges, France, discuss possible treatment of PO with corticosteroids, and say: "Such treatment of perilesional oedema in calcific neurocysticercosis could be a good target in the prevention of seizure recurrence in endemic countries."
For Dr Theodore Nash, National Institutes of Health, Bethesda, MD, USA, please contact Ann Oplinger, communications T) +1 301 402 1663 E) tnash@niaid.nih.gov / aoplinger@niaid.nih.gov
Dr Benoît Marin and Dr Pierre-Marie Preux, Institut d'Epidémiologie et de Neurologie Tropical, Université de Limoges, France T) +33 555435820 E) pierre-marie.preux@unilim.fr
For full Article and Reflection and Reaction, see: http://press.thelancet.com/TLNoedema.pdf
Journal
The Lancet Neurology