Cysticercosis, or neurocysticercosis, is the most common parasitic infestation of the central nervous system worldwide. Humans develop cysticercosis when they ingest eggs or larvae of the tapeworm Taenia solium. The eggs and larvae are usually found in fecally-contaminated water and undercooked pork.

Humans are the definitive host for T. solium, which means that the adult tapeworms are found only in the intestine of humans. It is possible for a human to be infested by T. solium (taeniasis) without having cysticercosis; in this case the tapeworm lives in the jejunum and regularly lays its eggs. These eggs do not have the capacity to invade tissue, and they are excreted with the rest of that person's feces. In areas of poor sanitation, swine (and humans) ingest the eggs, which may contaminate the water supply.

The eggs are capable of hatching once ingested. The larvae of T. solium are able to invade tissue, and enter the bloodstream. From there, they are able to spread to many organs (skeletal muscle, heart, eye, brain, spinal cord) and form cysts in tissue called cysticerci. They cannot grow into adult worms in this state, and remain indefinitely encapsulated in tissue. Cysticerci are commonly found at autopsy in asymptomatic inhabitants of endemic areas.

Humans may ingest the eggs or larvae directly from contact with fecally contaminated food or water (common). In rural areas where cysticercosis is common, pigs ingest the eggs by the same means. When pigs eat the eggs, the larvae hatch and disseminate and form cysticerci in the striated muscle, which can be the infective source of cysticercosis for humans who later consume that pork. This describes why swine are the intermediate host of T. solium: pigs eat the eggs laid by the tapeworms that live in the gut of infested humans.

Humans with taeniasis contract cysticercosis in the same manner; they are also capable of autoinfection by vomiting. In the latter case, eggs laid by their infesting tapeworm are pushed back into the stomach. When these eggs pass back into intestines, the larvae hatch and the infestation proceeds as usual.may also be contagious if open wound is exposed and is fatal.

See also Taenia solium and Taenia saginata.


In muscles, cysts cause painless swelling or create nodules under the skin. If cysts form in the eye, they can impair vision by floating in the eye and can cause blindness by causing swelling and detachment of the retina. Heart lesions can lead to abnormal rhythms or heart failure (rare). The most dangerous symptoms are a result of encystment in the central nervous system.

According to a Centers for Disease Control and Prevention Division of Parasitic Diseases, in neurocysticercosis (cysticercosis of the brain), "seizures, and headaches are the most common symptoms. However, confusion, lack of attention to people and surroundings, difficulty with balance, hydrocephalus (compression of the brain tissue due to obstruction of cerebrospinal fluid flow) may also occur." Often, there are few symptoms until the parasite dies. When the parasite dies, the host's immune system detects the worm's remains and attacks them, causing swelling and scarring. This is what causes most of the symptoms. Spinal cord lesions can lead to partial loss of motor control, weakness, and even paralysis.

When death occurs, it is most often due to involvement of the brain resulting in hydrocephalus, cerebral edema, cerebral compression, or epileptic seizures.


Neurocysticercosis is difficult to diagnose in its early stage and may be apparent only when the first neurological symptoms start, or when a CT scan, or an MRI of the brain is performed for other reasons. Antibody tests or a biopsy of the affected area may be necessary to complete the diagnosis.


The anti-parasitic drugs Praziquantel and Albendazole may be used to treat neurocysticercosis. Steroid anti-inflammatory medication is also often used in conjunction to reduce the swelling (brain edema) that results from immune system attacks on dead worms. It is still controversial whether patients benefit from treatment, because live cysticerci do not provoke seizures; only dead or dying parasites invoke an inflammatory response and seizures. In theory, therefore, treating a patient with drugs that kill living parasites can induce seizures in someone who is otherwise well and seizure-free; likewise, treating someone with seizures may not have any effect on outcome as the parasites are already dead and no improvement can be expected. A meta-analysis of 11 trials suggest that is that there is probably some small benefit to patients who have active lesions, but no benefit to those with only dead or inactive lesions.

If the cyst is in certain locations, such as the eye or the brain, steroids may be started a few days before the antiparasitic, in order to avoid problems caused by swelling. If swelling and immune response are not controlled, the treatment itself can be lethal, so the medication is given in low dosages over several days. Sometimes surgery may be needed to remove the infected area or cysts, but this may be impossible when they are located in areas of difficult or dangerous surgical access. Also, some medications may treat symptoms, such as seizures or irregular heartbeat without affecting the worms.

If the cysticerci have calcified in the brain, or if there is only one lesion, treatment is not considered beneficial.


It is possible to avoid infection with T. solium by avoiding undercooked pork and food and water contaminated with human feces. Extra care should be taken in places with poor hygiene or meat inspection laws. Freezing infested pork for a prolonged period will also kill cysticerci.

If a person is already infected with T. solium, they can avoid cysticercosis by treating the infection in the small intestine early, by not ingesting their own feces, and by not vomiting, as this brings eggs to the stomach so they form cysticerci in the small intestine.

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