The pig is an intermediate host, which harbors the larvae after ingesting the ova, while the ultimate hosts are humans. (Dhawan, 2007) Neurocysticercosis is caused by the intake of food contaminated with the waste products of a T. solium tapeworm carrier. The adult T. solium inhabits itself in the small intestine of humans, where it attaches itself to the intestinal wall by its suckers and hooks. A few pregnant proglottids are detached from the distal end of the body of the worm every day and passed with the feces; every proglottid contains thousands of eggs, which are fully embryonated, and resistant to all sorts of harsh environments and infective. (Etiopathogenesis of Neurocysticercosis, 2002) If pig products infected with the larvae are ingested, the intestines are subject to a tapeworm infection; when these eggs are ingested and subjected to gastric acid found inside the human stomach, their protective capsule is dissolved and the eggs turn into larval cysts, called oncospheres. Oncospheres travel through the vascular system to the brain, muscle, eyes, and other organs and body parts. The ingested ova develop into larvae (cysticerci) and lodge in soft tissues, especially skin, muscle, and brain. Cysticerci are fluid-filled oval cysts, approximately 1-2 cm in diameter, with an internal scolex. Once in the brain, the larval cysts (cysticerci) initially generate a minimal immune response and may remain in the brain as functional cysts for years. A live cyst can remain in there undetected for as long as 5 years before dying or causing symptoms in the host and cause minor inflammation in the tissue around it. (Christopher M. DeGiorgio, 2004)
Finally, Neurologic symptoms by the cyst arise when it dies and the human mounts an associated inflammatory response. (Dhawan, 2007) The symptoms include:
Seizures, which are severe involuntary movements of the body, headaches, states of confusion, lack of attention with people around and other things in the surrounding, difficulty with balance, Hydrocephalus or the swelling of the brain in which the cerebral ventricle dilate and lastly, sudden death as a cause of heavy infections.
There are basically four stages of cysts within the parenchyma of the brain: vesicular, colloidal, nodular/granular, and calcified granulomas. In the first stage, the viable cyst larva is known as a vesicular cyst and has a minimum amount of activity which is because of little or no host immune response. As time passes the cyst degenerates, fluid from the larval cyst leaks into the parenchyma, creating a noticeable immune response. An enhancing cyst, without a proper scolex, is called a colloidal cyst. During the colloidal this phase, the parasite begins to demonstrate degenerative changes, the vesicular fluid takes on a gelatinous colloidal form, and the wall thickens. The CT scan shows an annular enhancement bounded by perilesional edema. Performing an MRI, the capsule displays a higher signal than the surrounding brain. As the cyst deteriorates more, it forms a nodule. In the nodular phase, the vesicle usually decreases in size, and its contents turn semisolid, and are slowly replaced by granulomatous tissue. After the parasite dies, a mineralization process takes place that ends up in a calcified nodule that inhibits