Asymptomatic neurocysticercosis over 15 years between transitory ischemic attack as initial and epilepsy as second manifestation


Neurocysticercosis(NCC) is a CNS parasitosis, which is non-progressive in case of intra-parenchymal lesions, but progressive in case of extra-parenchymal lesions [1]. Intraparenchymal NCC is frequently associated with epilepsy and extra-parenchymal NCC with intracranial hypertension. Persistence of viable cysts over the years is not rare, but infrequently reported. Here, we present a patient with non-progressive NCC who developed epilepsy 15 years after the diagnosis of NCC. A previously healthy Romanian female experienced recurrent episodes of right-sided hemihypesthesia and headache at age 40 years. Based on the clinical presentation, serological testing, and cerebral MRI which showed an enhancing right parieto-occipital and a left parietal nodular lesion with perilesional edema, NCC was diagnosed. After praziquantel (1,800 mg for 2 weeks), she became symptom free. At age 55 years (15 years later), she experienced a first tonic–clonic seizure followed by transient right-sided hemiparesis. Serum IgG antibodies against Taenia solium were positive on Western blot and 7.12 (n \ 1.1) on an ELISA. Detailed descriptions of the methods used for the ELISA and the Western blot, however, were not provided in the written reports. Carbamazepine (400 mg/day) was given and, since seizure activity was attributed to exacerbation of the parasitololgical infection, she also received albendazol (800 mg/day) for 4 weeks and erythromycin (500 mg/day) 3 day/week for 3 weeks. One month after starting carbamazepine, it was replaced by valproic acid (1,000 mg/day) because of recurrent focal seizures of the right arm. Since focal seizures recurred 2 months later, she received praziquantel (1,800 mg/day) for 3 weeks. One month later, albendazole (800 mg/day) was given for 3 weeks followed by a second cycle 3 months later. Seven months after the first tonic– clonic seizure, she experienced a second one. IgG antibodies against Taenia solium were 3.11 (n \ 1.1) on an ELISA. Cerebral MRI showed multiple supra-tentorial, intra-parenchymatous, calcified lesions, which did not show perilesional edema (Fig. 1). Additionally, two enhancing nodular lesions, one in the right parieto-occipital region and the other in a left high parietal location, were found. Carbamazepine (400 mg/day) was added to valproic acid (1,000 mg/day). Though she did not follow the advice to stepwise increase carbamazepine to 900 mg/day, she remained seizure free during the next 2 years until today. The presented case is interesting for several aspects. First, the patient is from Romania where NCC is endemic and has a higher prevalence than in Western Europe [2]. Whether the lower prevalence in Western Europe is due to a higher standard of hygiene or due to under-diagnosing the condition remains speculative, but with intensified migration the prevalence of NCC will increase also here. Second, NCC initially manifested as headache and transitory ischemic attack (TIA), and remained subclinical during the next 15 years. TIA as the initial manifestation of NCC could be explained with arteritis predominantly occurring with subarachnoid cysts [1]. However, the patient did not show subarachnoid lesions on MRI. Alternatively, TIA occurred independently of NCC due to atherosclerosis (the patient’s risk factors were arterial hypertension and smoking), or was a non-convulsive partial seizure. Though J. Finsterer (&) Krankenanstalt Rudolfstiftung, Postfach 20, 1180 Vienna, Austria e-mail:

DOI: 10.1007/s13760-012-0144-8

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@article{Finsterer2012AsymptomaticNO, title={Asymptomatic neurocysticercosis over 15 years between transitory ischemic attack as initial and epilepsy as second manifestation}, author={Josef Finsterer and Herbert Auer}, journal={Acta Neurologica Belgica}, year={2012}, volume={113}, pages={203-204} }