OBJECTIVE: To discuss the possible mechanisms underlying a dual pathology combining neurocysticercosis and hippocampal atrophy, illustrated by the observation of four patients with epilepsy. CASE REPORTS: The first patient presented at the age of four years with a first episode of status epilepticus, presumably due to an inflamed, calcified, parenchymal cysticercus granuloma. Thereafter, he had occasional seizures. Routine MRI undertaken several years later revealed unilateral hippocampal atrophy and sclerosis. Two other patients with initial imaging evidence of active neurocysticercosis located close to the hippocampus, and occasional seizures, developed ipsilateral hippocampal sclerosis. The seizure disorder of our fourth patient, with medically intractable epilepsy, was initially attributed to a calcified cysticercus granuloma. Clinical description, video-EEG telemetry and imaging work-up suggested a diagnosis of mesial temporal lobe epilepsy due to hippocampal sclerosis. CONCLUSIONS: Definitive conclusions as to the underlying mechanisms cannot be derived from the present, retrospective series of only four patients. However, the following suggestions can be made: 1) seizures due to neurocysticercosis may constitute the initial precipitating illness for the development of hippocampal sclerosis, 2) the hippocampus may be involved in host brain inflammation and gliosis in response to a nearby, degenerating cysticercus, 3) the seizure focus formed by the degenerating cysticercus, engenders epileptogenic changes in the hippocampus through kindling, and 4) the two conditions may coexist purely by chance. Systematic and prospective, serial MRI evaluations of hippocampal structures in patients with neurocysticercosis should contribute to further clarify the underlying mechanisms.
OBJECTIVE: To discuss the possible mechanisms underlying a dual pathology combining neurocysticercosis and hippocampal atrophy, illustrated by the observation of four patients with epilepsy. CASE REPORTS: The first patient presented at the age of four years with a first episode of status epilepticus, presumably due to an inflamed, calcified, parenchymal cysticercus granuloma. Thereafter, he had occasional seizures. Routine MRI undertaken several years later revealed unilateral hippocampal atrophy and sclerosis. Two other patients with initial imaging evidence of active neurocysticercosis located close to the hippocampus, and occasional seizures, developed ipsilateral hippocampal sclerosis. The seizure disorder of our fourth patient, with medically intractable epilepsy, was initially attributed to a calcified cysticercus granuloma. Clinical description, video-EEG telemetry and imaging work-up suggested a diagnosis of mesial temporal lobe epilepsy due to hippocampal sclerosis. CONCLUSIONS: Definitive conclusions as to the underlying mechanisms cannot be derived from the present, retrospective series of only four patients. However, the following suggestions can be made: 1) seizures due to neurocysticercosis may constitute the initial precipitating illness for the development of hippocampal sclerosis, 2) the hippocampus may be involved in host brain inflammation and gliosis in response to a nearby, degenerating cysticercus, 3) the seizure focus formed by the degenerating cysticercus, engenders epileptogenic changes in the hippocampus through kindling, and 4) the two conditions may coexist purely by chance. Systematic and prospective, serial MRI evaluations of hippocampal structures in patients with neurocysticercosis should contribute to further clarify the underlying mechanisms.
Authors: Oscar H Del Brutto; Perla Salgado; Julio Lama; Victor J Del Brutto; Xavier Campos; Mauricio Zambrano; Héctor H García Journal: Am J Trop Med Hyg Date: 2014-10-27 Impact factor: 2.345
Authors: Mateus de Oliveira Taveira; Marcia Elisabete Morita; Clarissa Lin Yasuda; Ana Carolina Coan; Rodrigo Secolin; Alberto Luiz Cunha da Costa; Fernando Cendes Journal: PLoS One Date: 2015-07-01 Impact factor: 3.240