The disease is primarily transmitted through direct contact with human feces, often through the consumption of food or water containing Taenia solium eggs.

While some people may have no symptoms, others may experience seizures, increased pressure in the skull, cognitive impairment, or specific neurological problems.

Neurocysticercosis is common in developing regions, such as Latin America, China, Nepal, Africa, India, and Southeast Asia.

Neurocysticercosis has a wide range of signs and symptoms, which relate to the location, number of lesions, and immune system's response to the infection.

Sensory impairments, parkinsonian rigidity, involuntary movements, language disturbances, and signs of brain-stem dysfunction can also occur.

Cysticercosis of the spinal cord often causes radicular pain, weakness, and sensory impairments due to localized mass effects or inflammation in the subarachnoid space.

[18] Intracranial hypertension can present as episodic loss of consciousness when moving the head, known as Bruns syndrome; [5] it may be subacute or chronic.

[10] Cysticercotic encephalitis, which is a severe type of neurocysticercosis usually affecting younger women and children, can also cause intracranial hypertension.

[9] Cysticercotic encephalitis is characterized by seizures, intracranial hypertension, clouding of consciousness, optic disc swelling, headache, reduction of visual acuity, and vomiting.

The cysts can cause inflammation of the vitreous membrane, uveitis, and endophthalmitis, which is the most serious complication of ocular cysticercosis and can result in eye shrinkage.

[23][24] Neurocysticercosis, caused by the larvae of Taenia solium is different from taeniasis, which results from infection with the adult tapeworm.

The larvae are cystic, fluid-filled sacs containing a tapeworm head (scolex) with four suckers and a double row of hooks, along with a narrow neck and a body made up of hundreds of segments called proglottids.

When a person eats pork infected with cysts, the scolex (the head of the tapeworm) evaginates and clings to the intestinal wall using its suckers and hooks.

Although the cysts can form in any tissue, they are most commonly found in the central nervous system, skeletal muscle, skin, and eyes.

[27] Cysticerci enter the central nervous system as live parasites (vesicular stage) with a transparent membrane, clear fluid, and a scolex (head) tucked inside.

[31] The lentil lectin purified glycoprotein (LLGP) enzyme-linked immunoelectrotransfer blot (EITB) assay, is the most reliable test for detecting T. solium antibodies in the blood.

[29] The ELISA test for detecting anticysticercal antibodies in cerebrospinal fluid (CSF) is 89% sensitive and 93% specific for active neurocysticercosis infections.

The number of people with positive stool tests for Taenia solium eggs in neurocysticercosis varies and seems to depend on how severe the infection is.

[19] CT scans and magnetic resonance imaging (MRI) give objective information about the number and pattern of lesions, the stage of healing, and how the immune system is responding to the parasites.

[19] MRIs are better for evaluating different spatial planes and provides clearer images, which helps in identifying small lesions at the back of the brain or near the skull that may be missed on CT scans.

[41] Some factors that make T. solium potentially eradicable are humans being the only definitive host, the intermediate host being an animal whose exposure to ova can be controlled, well-developed diagnostic testing allowing infected individuals to be identified, effective treatments available, and the availability of pig vaccines.

[44] To prevent neurocysticercosis, interventions such as increasing education, improving sanitary conditions, and strict animal husbandry and meat inspection procedures are needed.

A program involving human and porcine mass chemotherapy, pig vaccines, and stool coproantigen case confirmation eliminated transmission in 105 out of 107 villages.

The disease has to be characterized in terms of cyst viability, the degree of the host's immunological response to the parasite, and the location and number of lesions to provide proper treatment.

[50] Steroid administration is an important step in the modulation of neurocysticercosis-related inflammation in the central nervous system, since it controls the acute inflammatory response that occurs following the destruction of live cysts.

[57] Antiparasitic medication may be ineffective in cases of severe infection due to the hazards associated with mass inflammation, but these forms of neurocysticercosis carry a high risk of consequences if left untreated.

Reports of neurocysticercosis are growing from several wealthy nations, including the USA and the UK, as a result of increased globalization and worldwide travel.

[65] In endemic regions, CNS infection is extremely common; in many of these groups, the frequency of certain serum antibodies is more than 10%, and residual intraparenchymal brain calcifications on CT scans are seen in 10–20% of the general population.

Friedrich Küchenmeister showed that the consumption of cysticercus from pork caused human intestinal taeniasis by feeding a prisoner food that included cysticerci gathered from a recently killed pig.

[63][66] In the second part of the 19th century, research showed that feeding Taenia eggs from infected humans to pigs caused cysticercosis.