Epilepsy is one of the world's oldest diseases. Social stigma, misunderstanding and thus, discrimination have surrounded patients and their families from the beginnings until nowadays. Approximatively up to 80% of epilepsy cases worldwide are found in developing regions. The risk of premature death is two to three times higher than for the general population. There is contradictory evidences concerning the question of whether to inform patients about the possibility of sudden unexpected death in epilepsy (SUDEP). Actual guidelines states that individuals with epilepsy and their families or careers should be given access to information on SUDEP. We have information about how, when and what to say to the patients and families about SUDEP. But it's a delicate subject, and some patients do not want to know that they are at risk for this.
A male from rural area, S.M., aged 77 years, was admitted in our department for discontinuous headache. His medical history was irrelevant. He has been experiencing intermittent right parietal-occipital headaches during the last 3 months. Neurologic exam revealed a slight right limb ataxia. Initial laboratory findings revealed a white blood cell count of 6500/mm3 with 75% polymorphonuclear leukocytes, 15% lymphocytes and 8% monocytes. His serum glucose was 90 mg/dL. Non Gadolinium CT scan shows rounded, inhomogenous spontaneous hyperdense area (40-45 UH) between 5-12 mm diameter, localized frontal, temporal, occipital and cerebellar bilaterally. The question was whether the lesions were metastasis or parasitic infection? Cerebral MRI showed unenhanced,well lesions defined,multiple lesions between3-17 mm, with iso- • Active parenchymal stage: the scolex within acyst hyperintensityT1, T2, and FLAIR, spreadout may appear as a hyperdense dot periventriculary, subcortically, infrontal, temporal, • Calcified stage: when the parasite dies, parietal lobes andsubtentorially, right and left nodularparenchymal calcifications are seen. cerebellum(figure 2). After serological testsfrom blood and CSF the diagnosticof neurocysticercosis was certified(an enzyme-linked immunosorbentassay of the CSF was positivefor immunoglobulin G cysticercosisantibody, with 1.32 optical densityunits (OD) (positive result > 0.50OD); his serum IgG cysticercosis antibodywas positive with 5.12 OD). CT findings are depending on the stageof evolution: • Vesicular stage (viable larva): hypodense, nonenhancinglesions • Colloidal stage (larval degeneration): hypodense/isodense lesions with peripheral enhancementand edema • Nodular-granular stage: nodular-enhancinglesions • Cysticercotic encephalitis: diffuse edema,collapsed ventricles, and multiple enhancingparenchymal Our patient has multiple lesions in differentphases of evolution (active and calcified). DISCUSSIONS Neurocysticercosis is a parasitic brain infection,caused by larval cysts of the tapeworm Taenia soliumby accidental ingestion of eggs. It is the most common parasitic disease of the nervous system and it is themain cause of acquired epilepsy mainly in developingcountries. Once in the human intestine, Taenia eggsevolve to oncospheres 1 Carol Davila Central Emergency Military Hospital, Bucharest 2 Carol Davila University of Medicine and Pharmacy, Faculty of Medicine, Bucharest 40
