Clinical symptoms, diagnosis, and treatment of neurocysticercosis

Abstract

The infection of the nervous system by the cystic larvae of Taenia solium (neurocysticercosis) is a frequent cause of seizure disorders. Neurocysticercosis is endemic or presumed to be endemic in many low-income countries. The lifecycle of the worm and the clinical manifestations of neurocysticercosis are well established, and CT and MRI have substantially improved knowledge of the disease course. Improvements in immunodiagnosis have further advanced comprehension of the pathophysiology of this disease. This knowledge has led to individualised treatment approaches that account for the involvement of parenchymal or extraparenchymal spaces, the number and form of parasites, and the extent of degeneration and associated inflammation. Clinical investigations are focused on development of effective treatments and reduction of side-effects induced by treatment, such as seizures, hydrocephalus, infarcts, and neuroinjury.

Experimental neurocysticercosis: absence of IL-4 induces lower encephalitis

“…In the infected animals, the majority of the cysticerci were located inside the lateral ventricles accompanied by a discrete-to-moderate intensity of inflammatory response. This fact was previously reported in studies that showed that the mere presence of the parasite's antigens are responsible for the development of inflammatory alterations and ventriculomegaly, which may lead to cerebrospinal fluid obstruction 22,23 . Zepeda et al 21 showed that T. crassiceps antigens are able to induce inflammation in the brain tissue and apoptosis of hippocampal cells.…”

Validez de tres métodos de inmuno-diagnóstico de neurocisticercosis: revisión sistemática de la literatura con meta-análisis 1960-2014

“…Para establecer el diagnóstico definitivo y el tipo de enfermedad se requiere la tomografía computarizada (TC) y/o la imagen por resonancia magnética (RM); sin embargo, son procedimientos muy costosos, poco disponibles en zonas endémicas y en muchos pacientes no se obtienen resultados claros debido a la ubicación cerebral o al estado de desarrollo del cisticerco. Por esta razón, se utilizan pruebas serológicas como ayudas diagnósticas; no obstante, en muchos ensayos se han reportado datos de sensibilidad y especificidad muy bajas, por lo que actualmente sólo se utiliza de rutina el ensayo inmunoenzimático de electrotransferencia (EITB) para la detección de anticuerpos y el inmunoensayo ligado a enzimas (ELISA) para la detección de antígenos o anticuerpos, que además de presentar alta sensibilidad y especificidad, son menos costosos, más asequibles en zonas endémicas, lo que deriva en un menor tiempo de diagnóstico, tratamiento oportuno y disminución de las secuelas de la enfermedad [15][16][17] .…”

Neurocysticercosis, familial cerebral cavernomas and intracranial calcifications: differential diagnosis for adequate management

“…A recent review on NCC showed that MRI findings are better predictive for the stage of the cysts and diffusion-weighted images and apparent diffusion coefficient maps allowing better demonstration of the cysticerci in their colloidal phase. Calcified cysts were described as not well depicted and there was a suggestion that more sophisticated sequences, as susceptibility-weighted protocols, would be necessary 9 . Cavernous malformations, on the other hand, are not well seen on CT images, where the lesions will range from non-visualization to the mildly enhancing ones, variable format and, very often, with calcification.…”

“…Carpio detected that the proportion of the seropositivity in epileptic NCC patients was the same reported in the general population in the same geographic areas 3 . On the other hand there is a chance of dual disease, like temporal lobe epilepsy with hippocampal sclerosis and NCC, in endemic regions, being involved in the pathogenesis of epilepsy in patients diagnosed with NC and the differential diagnosis will only be reached by means of special neurophysiological testing 9 . Evidence-based data from well designed prospective studies to establish the surrogates for epilepsy due to NCC is scarce 3,10,11,12 , showing the importance of differential diagnosis with other diseases on the determination of NCC as seizures etiology and the risk of overestimation of neurocysticercosis as a prime cause of seizures.…”