Neurocysticercosis  is a specific form of the infectious parasitic disease cysticercosis that is caused by the infection with Taenia solium, a tapeworm found in pigs. Neurocysticercosis occurs when cysts formed by the infection take hold within the brain, causing neurologic syndromes such as epileptic seizures. It is a common cause of seizures worldwide. It has been called a "hidden epidemic" and "arguably the most common parasitic disease of the human nervous system". Common symptoms of neurocysticercosis include seizures, headaches, blindness, meningitis and dementia. Pathophysiology
Neurocysticercosis most commonly involves the cerebral cortex followed by the cerebellum. The pituitary gland is very rarely involved in neurocysticercosis. The cysts may rarely coalesce and form a tree-like pattern which is known as racemose neurocysticercosis, which when involving the pituitary gland may result in multiple pituitary hormone deficiency. Diagnosis
Neurocysticerosis is diagnosed by computed tomography (CT) scan. Diagnosis may be confirmed by detection of antibodies against cysticerci in CSF or serum through ELISA or immunoblotting techniques. Treatment
Treatment of neurocysticerosis includes epileptic therapy and a long-course medication of praziquantel (PZQ) and/or albendazole. Steroid therapy may be necessary to minimize the inflammatory reaction to dying cysticerci. Surgical removal of brain cysts may be necessary, e.g. in cases of large parenchymal cysts, intraventricular cysts or hydrocephalus.Albendazole has been shown to reduce seizure recurrence in those with a single non-viable intraparenchymal cyst.
This lasts for about three months. Dementia, during which the person becomes unresponsive or mute over the course of six months, is the final stage of the disease, after which death follows.Other symptoms include: profuse sweating, miosis (pinpoint pupils), sudden entrance into menopause or  impotence, neck stiffness, and elevation of blood pressure and heart rate. The sporadic form of the disease often presents with double vision. Constipation is common as well. As the disease progresses, the person becomes stuck in a state of pre-sleep limbo, or hypnagogia, which is the state just before sleep in healthy individuals. During these stages, people commonly and repeatedly move their limbs as if dreaming.The age of onset is variable, ranging from 13 to 60 years, with an average of 50. The disease can be detected prior to onset by genetic testing. Death usually occurs between 6–36 months from onset. The presentation of the disease varies considerably from person to person, even among people within the same family; in the sporadic form, for example, sleep problems are not commonly reported and early symptoms are ataxia, cognitive impairment, and double vision. Cause
The gene PRNP that provides instructions for making the prion protein PrPC is located on the short (p) arm of chromosome 20 at position p13. Both people with FFI and those with familial Creutzfeldt–Jakob disease (fCJD) carry a mutation at codon 178 of the prion protein gene.