Article in Epilepsia 52(6) · June with 87 Reads .. de control de la teniasis / cisticercosis por Taenia Solium en el Perú. Article. producida por la fase adulta de Taenia saginata o y se considera como la primera causa de epilepsia de mayoría de las personas con cisticercosis son. Aquele, por meio de acúleos, penetra através da mucosa intestinal e, caindo na . que a neurocisticercose representa a principal causa de epilepsia sintomática , . Briceño CE, Biagi F, Martinez B. Cisticercosis: observaciones sobre
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Recurrent neurocysticercosis of the frontal lobe. Neurocysticercosis; Taenia solium; Frontal lobe; Colombia. This disease causes the highest helminthic-related morbidity and pot rates due to its deleterious effects on the central nervous system.
The following report presents the case of a patient with headache, dromomania, intracranial hypertension syndrome, and cognition and gait impairment.
A brain CT showed a right frontal subcortical cyst and bilateral frontoparietal calcified nodules. Neurocysticercosis of the frontal lobe was suspected as the main diagnosis considering the clinical manifestations, anamnesis epolepsia local epidemiology. Symptoms and signs of NCC depend on localization, number, dimensions, cysticercus stage vesicular, colloidal, granular-nodular and calcified nodulegenotype and immune status of the host.
It is important to know and educate the community about the life cycle of parasites, epidemiology, prevention measures and clinical manifestations of neurocysticercosis in order to make a timely diagnosis and administer an effective treatment. La neurocisticercosis NCC es causada por la ingesta de huevos de la tenia del cerdo Taenia solium provenientes de un individuo con teniosis complejo teniasis-cisticercosis.
Currently, there are 50 million people affected by NCC around the world, which makes it an endemic disease in Colombia and other Latin American countries. The objective of this article is to promote knowledge about the heterogeneous manifestations of neuroinfection by T.
The reason for consultation was the impossibility of walking by himself. During anamnesis, his relatives reported frequent consumption of undercooked pork, lack of sewage service and lack of knowledge of proper hand washing by the patient. The patient presented with a clinical picture of 8 months of evolution consisting of progressive gait impairment, loss of sphincter control, left hemiparesis and headache.
The neurology service requested a computed tomography CT that revealed a dilation of the supratentorial ventricular system and a right frontal subcortical cystic lesion that created a mass effect with midline shift.
In addition, he presented perilesional edema and small residual bilateral frontoparietal calcifications, suggesting sequelae of NCC Figure 1. Blood count, C-reactive protein CRP and renal function were normal. Pharmacological management was initiated with albendazole at an oral dose of mg every 24 hours, dexamethasone 8mg IV every 8 hours, paracetamol at an oral dose of 1g every 8 hours and omeprazole at an oral dose of 20mg every 24 hours.
The patient did not report any side effect caused by these drugs. A week after admission, the patient presented with left hemiplegia and sialorrhea, and he did not have any verbal response. A craniotomy was performed to remove the cyst and conduct a histopathological study, while a ventriculoperitoneal shunt was arranged to reduce intracranial pressure Figure 2. Macroscopically, neurosurgery reported a frontal cyst of greenish content with walls strongly adhered to the parenchyma and the frontal horn of the lateral ventricle.
Histopathological analysis confirmed the suspicion of NCC and reported reactive gliosis. The patient evolved satisfactorily, did not present any type of sequelae and was discharged.
Computed tomography with right frontal subcortical cystic lesion, perilesional edema and calcified nodules. Own elaboration based on the data obtained in the study.
Computed tomography with right frontal subcortical cystic lesion, midline shift and ventriculoperitoneal shunt. Reinfection was suspected due to a previous history of NCC a significant risk factorthe presence of calcified nodules in the imaging and regional epidemiology. The patient presented with a frontal syndrome characterized by left hemiparesis, disobedience of orders, dromomania, cognitive impairment, space-time disorientation and verbal-motor automatism, which are related to cysticercosis cysts in the right frontal lobe.
When the cysticercus dies, intense inflammation eiplepsia exudate, periarteritis and endarteritis is usually observed, which can close the vascular lumen and impede the normal flow of cerebrospinal fluid, favoring the presence of hydrocephalus and intracranial hypertension. The signs and symptoms of NCC depend on the location, number, dimensions, cysticercus stage vesicular, colloidal, granular-nodular and calcified nodulegenotype and immune status of the host.
The prevalence of NCC is higher in rural areas, where people work with pigs and sanitary conditions are often deficient. This information epilepsua very useful for the region, since the history of NCC and the neurological manifestations compatible with the disease make it necessary to discard it.
Actually, the inhabitants of this region think that they add a taste to the meat. In addition, knowledge on the life cycle of the parasite is deficient, which leads to difficulties when making promotion and prevention campaigns.
Depending on the development stage of T.
It should be noted that both diseases could occur simultaneously in the same individual. As seen in Figure 3, humans develop teniosis when cysticerci are ingested.
The larvae mature to the adult form of T. When animals are slaughtered, if there are deficiencies in sanitary control, pork meat is commercialized and humans end up consuming cysticerci and developing teniosis. Similarly, the definitive host may present with cysticercosis when consuming food irrigated with water contaminated by the eggs of the adult tapeworm. Contact with sick individuals is an important way of contagion, being the main risk factor for TCC infection.
This case shows strength in diagnosis, epidemiology and clinical foundation. In the same way, intervention for promotion and prevention is highlighted as relevant. However, this case did not include a molecular test that identified IgM antibodies for T.
Solium due to local limitations. Making a timely diagnosis along the process medical history, imaging and laboratory tests is important when the history, signs and symptoms are compatible with NCC. Providing comprehensive management to the patient, in this type of cases, is necessary, neurocistiecrcosis, to carry out a complete cysticidal treatment and, second, to provide information to patients, relatives and the community in general about the prevention measures against NCC.
Update on Cysticercosis Epileptogenesis: Curr Neurol Neurosci Rep. S inha S, Sharma BS. OMS; [cited Dec 17]. A systematic review of the frequency neuroccisticercosis neurocyticercosis with a focus on people with epilepsy. Estudio de seroprevalencia B otero D, Restrepo M.
A rare case of recurrence of primary spinal neurocysticercosis mimicking an arachnoid cyst. Repeated hydrocephalus in recurrent intraventricular neurocysticercosis: J Neurosci Rural Pract. Cost of neurocysticercosis patients treated in two referral hospitals in Mexico City, Mexico. Trop Med Int Health. Bol Med Hosp Infant Mex.