Neurocysticercosis: A Review

Abstract

Neuroysticercosis is the most common helminthic infection of the nervous system, and a leading cause of acquired epilepsy worldwide. The disease occurs when humans become intermediate hosts of Taenia solium by ingesting its eggs from contaminated food or, most often, directly from a taenia carrier by the fecal-to-oral route. Cysticerci may be located in brain parenchyma, subarachnoid space, ventricular system, or spinal cord, causing pathological changes that are responsible for the pleomorphism of neurocysticercosis. Seizures are the most common clinical manifestation, but many patients present with focal deficits, intracranial hypertension, or cognitive decline. Accurate diagnosis of neurocysticercosis is possible after interpretation of clinical data together with findings of neuroimaging studies and results of immunological tests. The introduction of cysticidal drugs have changed the prognosis of most patients with neurocysticercosis. These drugs have shown to reduce the burden of infection in the brain and to improve the clinical course of the disease in most patients. Further efforts should be directed to eradicate the disease through the implementation of control programs against all the interrelated steps in the life cycle of T. solium, including human carriers of the adult tapeworm, infected pigs, and eggs in the environment.

Inflammation is a key risk factor for persistent seizures in neurocysticercosis

“…These seizures are thought to be caused by perilesional gliosis, inflammation, and/or neurotoxicity from calcified lesions1, 4, 5, 6, 7 and may lead to epilepsy (a disease of chronic recurrent seizures). NCC is the most common cause of acquired adult epilepsy worldwide 4, 7, 8, 9, 10, 11, 12, 13. Epilepsy due to NCC can lead to severe health consequences as seizures are associated with an increased risk of sudden death14, 15, 16, 17 and 20–30% of NCC patients with epilepsy continue to have seizures despite treatment 9…”

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

“…Aunque la detección de anticuerpos mediante ELISA o EITB, presentan buena sensibilidad y especificidad y ambas tienen alta capacidad discriminante entre sanos y enfermos, estas técnicas no tienen utilidad diagnóstica cuando el cisticerco está calcificado; no obstante, cabe resaltar que la reacción inflamatoria se presenta cuando pasa del estadio vesicular, donde se encuentra viable, al estadio coloidal, donde inicia el proceso de involución [6][7][8][9] , por tanto es en esos estadios donde mayor sintomatología se presenta y es importante el diagnóstico.…”

“…El parásito subsiste en el SNC y presenta pocos cambios inflamatorios. Al iniciar el ciclo de vida del cisticerco se presentan varios estadios: se inicia con el vesicular en el que el cisticerco se encuentra vivo, puede permanecer por décadas y la reacción inflamatoria es escasa; después de una reacción inflamatoria efectiva aparece el estadio coloidal en el cual hay una involución, la membrana del cisticerco se vuelve más gruesa y el escólex muerto se transforma en gránulos mineralizados, dando origen al estadio nodular granular el cual presenta duración variable y posteriormente da origen a la etapa nodular calcificada en la cual sólo se identifica un nódulo calcificado con escasa reacción inflamatoria [6][7][8][9] .…”

Serodiagnosis of human neurocysticercosis using antigenic components of Taenia solium metacestodes derived from the unbound fraction from jacalin affinity chromatography

“…Group 1 was composed of 40 patients who had been diagnosed with definitive NCC based on the presence of clinical symptoms, epidemiological data, positive immunological tests and evidence of the parasite by computerised tomography, as follows: (i) clinical syndrome: all patients presented at least one type of clinical manifestation that was suggestive of NCC, including epilepsy (55%), cephalea (50%), dizziness (27.5%), dementia (12.5%), faintness (10%) and hydrocephalus (2.5%) and no signs or symptoms that were suggestive of the presence of metacestodes in other organs were present; (ii) epidemiological data: all patients came from or lived in an area where cysticercosis is endemic, as previously described (Barcelos et al 2012), in addition to at least two instances of household contact with T. solium infection; (iii) immunological diagnosis: cerebrospinal fluid samples were positive for anti-cysticercal IgG antibodies by ELISA; (iv) cerebral computerised tomographic findings: all patients presented evidence of the parasite by neuroimaging with the following classifications based on Sotelo et al 1985: eight (20%) vesicular, 15 (37.5%) vesicular/ calcified and 17 (42.5%) calcified metacestodes. According to the Del Brutto diagnostic criteria, all patients from Group 1 had a definitive diagnosis; 29 (72.5%) had the absolute criteria and 11 (27.5%) presented two major plus one minor or epidemiologic criteria (Del Brutto 2012). Of the patients who presented with the active form of NCC (n = 23), 16 (70%) had the absolute criteria, whereas of those who presented with calcified lesions (n = 17), 13 (76%) had the absolute criteria.…”