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Neuroimaging in Neurocysticercosis


Taeniasis and cysticercosis remain a global public health problem in both the developing and developed countries. Infection is becoming increasingly common in the latter because of the increasing immigration and more frequent travel to regions of endemic disease. These parasitic diseases are related to poverty and poor sanitary infrastructure. Therefore, cysticercosis has been designated as a biological marker of the social and economic development of a community.

Neurocysticercosis (NC) commonly is associated with clinical manifestations such as seizures, headache, and focal neurological deficits, and may lead to long-term neurological sequelae such as epilepsy, hydrocephalus, and dementia. The pleomorphism of NC makes its diagnosis impossible on clinical grounds alone. An accurate diagnosis is possible only after suspicion on epidemiologic grounds, proper interpretation of clinical data, and synthesis of findings on neuroimaging studies specific immunologic tests on the cerebrospinal fluid (CSF).


Humans are the only known host to harbor the adult cestode parasite, Taenia solium, in the intestine. Infection is acquired by ingesting undercooked pork infected with Taenia larvae (ie, cysticerci). The cysticerci evaginate into the intestines where they mature into adult worms. The worms consist of a scolex, which attaches itself to the intestinal wall, and numerous proglottids (ie, segments). Proglottids and eggs are shed intermittently into the stool.

The intermediate host, typically the pig, is infected by ingesting parasite eggs or proglottids containing eggs (ie, porcine cysticercosis). The oncospheres escape from the eggs, penetrate the intestinal mucosa, migrate through the bloodstream, and lodge in the tissues. Over weeks to months, they evolve into larvae that enlarge and mature into cysticerci. The life cycle is completed when humans ingest pork contaminated with the cysts.

Human cysticercosis is acquired after eating food contaminated with fertilized eggs excreted in the feces of Taenia carriers. In humans, the most common routes of infection are ingestion of T solium eggs from contaminated food and rarely from fecal-oral autoinfestation from patients harboring the adult parasite in their intestines. While the cysts can develop in any human tissue, they have a predilection for the central nervous system (CNS), skeletal muscle, subcutaneous tissue, and eyes.

Immune response

In humans and pigs, the cysticerci may live within the host tissue without causing inflammation or disease. The immune response is unpredictable and may vary from a complete tolerance to an intense immune response. A single patient may show an intense inflammation around a cyst at any stage of the degeneration process, together with viable cysts with lack of inflammation and several calcifications scattered in the brain. Autopsies of victims of warfare and road/traffic accidents have revealed that a large proportion of NC infection is asymptomatic and discovered incidentally at necropsy. Individuals who undergo computed tomography (CT) of the head for unrelated reasons (eg, head injury) may demonstrate multiple parenchymal calcifications.

Several studies have analyzed the mechanisms of the immune response elicited against T solium cysticercus, such as the heterogeneity of the humoral immune response, the existence of immune evasive mechanisms, and the fact that the immune response can both protect and harm the host.

The humoral immune response to antigens of T solium cysticerci is evident from the number of immunodiagnostic assays that have been developed using different types of antigens. Several immunoglobulin (Ig) classes are produced as specific antibodies against the parasite. The most frequent is immunoglobulin G (IgG), which can be detected in serum, CSF, and saliva and suggests that infection is of long duration. The immune response against T solium cysticerci appears to have components of both T helper type 1 cells (Th1) and T helper type 2 cells (Th2), although the underlying mechanisms are yet to be clarified. The parasite is probably killed by eosinophils, which are attracted to the site by lymphoid cells. It is assumed that this specific response is mediated by Th2 cytokines.

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