Worldwide distribution is higher in areas with poor sanitation. Neurocysticercosis is highly endemic in Central and South America, sub-Saharan Africa, India, and Asia. Hispanic race has more prevalence of neurocysticercosis due to countries of origin. Neurocysticercosis is the leading cause of foodborne disease and it is estimated by the World Health Organization estimates that 50 million people are infected with 2.8 million disability-adjusted life years worldwide. Because immigration rates have continued to increase in the United States along with increasing international adoption, the incidence of this disease is on the rise in the United States. Neurocysticercosis is currently one of the most common parasitic diseases of the central nervous system in the United States and a leading cause of epilepsy among Hispanic children living in US metropolitan areas along the Mexican border (Gershon et al. 2004).

Taenia solium is the parasite responsible for neurocysticercosis. Parasite infections result when the adult pork tapeworm ingestion occurs from eating undercooked pork contaminated with the organism called Taenia solium (Leonard et al. 2006; Ndimubanzi et al. 2010). The pig is the intermediate host, where ingested larvae cysts embed themselves in the pig’s muscle. Transmission can occur by ingesting eggs of the pork tapeworm or via the fecal-oral route (Wallin and Kurtzke 2004).

Incubation period from time of infection to presenting symptoms can be years. This has nursing implications as many born in developing countries do not know they are infected and can present with symptoms once settled in the United States (Wallin and Kurtzke 2004). Due to the long incubation period, age does not seem to predispose a person, although it is rare to see a child under the age of 2 years diagnosed with neurocysticercosis.

Upon reaching the human GI tract, the egg’s thin outer membrane will dissolve, releasing the inner oncosphere or larvae. Oncospheres are released into the intestines and then migrate through the blood and lymphatic system before being distributed into tissues where they form cysts (Wallin and Kurtzke 2004). The oncospheres readily cross the intestinal lining but are usually destroyed by the immune system. They will escape the defenses of the host if they reach immunologically privileged sites, such as the central nervous system or eyes. In the CNS, the larvae tend to lodge in the small arterioles at the gray-white interface of the cerebral hemispheres and at the leptomeninges (Albright et al. 1999; Choux et al. 1999). However, the larvae can invade any part of the central nervous system, and once they invade, they will each mature into a cysticercus with a life span of approximately 18 months. The cysticercus is characterized by a head, body, four suckers, and some 20 pairs of hooks arranged as a crown (Choux et al. 1999).

The immunological response to the cysticercus lays the foundation for what is known as neurocysticercosis and manifests pathological changes like gliosis, necrosis, vasculitis, blockage of CSF drainage, meningitis, intracranial hypertension, and demyelination. Specifically with neurocysticercosis, the cysts form in the central nervous system. The types of infestation can be categorized according to location. These are parenchymal, meningeal, intraventricular, spinal, or mixed. Even once the cysticercus has died, inflammatory reactions can continue to occur for years (Fig. 15.3).

The most common presenting symptoms are seizures, headache, and intracranial hypertension. Parenchymal forms manifest as convulsive disorders, motor or sensory deficit, or deterioration of consciousness. Meningeal involvement presents with photophobia, headache, nausea, vomiting, nuchal rigidity, and cranial nerve palsies (particularly II, V, VI, VII). Intraventricular infestation may manifest as intermittent acute hydrocephalus, which may result in loss of consciousness with position changes as the cyst blocks the flow of spinal fluid. Hydrocephalus with increased intracranial pressure is associated with a higher mortality rate. Spinal involvement has not been documented in children but presents in adults as motor or sensory deficit, with a combination of upper and lower motor neuron pathology.

Diagnosing is made with neuroimaging with CT or MRI (Saenz et al. 2006). Imaging can reveal active cysts with or without calcified granulomas that represent nonviable cysts. In active disease, a ring-enhancing cyst is noted on CT or MRI, which may have surrounding edema. On these images, the larvae can sometimes be seen within the walls of the cyst (Fig. 12.3).

Confirmation can be obtained on serum and cerebral spinal fluid (CSF) with the enzyme-linked immunotransfer blot (EITB) assay that is used to detect the antibody to T. solium (Mody et al. 2005). This type of testing has a sensitivity of 98 % and specificity of 100 %, but in patients with only a single brain lesion, up to 30 % test negative (Garcia et al. 1991; Richards and Schantz 1991). CSF enzyme-linked immunosorbent assay (ELISA) for detection of antibodies or antigens to T. solium is also available and has a sensitivity of 87 % and specificity of 95 % (Rosas et al. 1986).

Treatment is controversial and is based on the number of viable cysts seen on imaging. Symptomatic management is a mainstay with seizure control and reducing intracranial pressure a priority. Treatment with antiparasitic drugs can cause an inflammatory host response, and, therefore, if antiparasitic therapy is initiated, it should be done in combination with steroid therapy (Marconi et al. 2006). Antiparasitic agents that are used for treatment include albendazole (15 mg/kg/day) and praziquantel (50–100 mg/kg/day) and should only be considered when multiple viable cysts are seen (Sotelo 2004). The risks and benefits must be weighed before initiation of therapy. Patients without evidence of active disease, as evident by only calcified granulomas, do not require treatment and should receive supportive care with anticonvulsant therapy. In cases of encephalitis and intracranial hypertension, antiparasitic therapy is contraindicated because treatment may cause exacerbation of cerebral swelling and edema, leading to herniation and death (Gershon et al. 2004). Other medical management focuses on antiepileptic drugs (AEDs), steroids, analgesics, and osmotic agents. As stated, steroids have a significant role with the initiation of antiparasitic therapy, since the destruction of the cysticerci may lead to significant and devastating inflammatory responses, resulting in increased intracranial pressure and even death.

Surgical therapy is indicated for the removal of space-occupying lesions causing significant mass effect and for the removal of seizure foci that are refractory to AEDs. Endoscopic removal is an option for ventricular lesions, and CSF diversion is often needed to treat communicating or obstructive hydrocephalus. In the case of obstructive hydrocephalus due to intraventricular neurocysticercosis, an attempt should be made to remove the lesion before shunting.

Nursing care is essential during the administration of antiparasitic agents. Analgesics will play a major role, since many will experience headaches during antiparasitic therapy. One must also be on guard for signs of increased intracranial pressure, such as lethargy, vomiting, increasing headache, and unresponsiveness. Steroid administration should be initiated prior to antiparasitic therapy. Seizure precautions should be enforced to protect the child from injury.

Neurocysticercosis can cause rapid deterioration, which can ultimately result in death. During discharge education, this needs to be emphasized, and the family should be instructed to seek immediate medical attention for any change in neurological status. Education should also focus on medications, since the child may be discharged on an AED, an antiparasitic agent or steroids.

Since a large proportion of pediatric patients inflicted with neurocysticercosis may be of Hispanic descent or from a part of the world other than the United States, an interpreter may be needed to help overcome the communication barrier. In addition, cultural issues may need to be addressed, and special help may be sought from the hospital or community to help bridge any gaps. The family members should be screened for disease, especially if the family comes from an endemic part of the world. Also, the patient and family should be taught how the disease is transmitted. Education should focus on frequent handwashing and sanitary handling of food. If the family and patient plan to travel to endemic areas or areas with poor sanitation, caution should be undertaken in the consumption of foods from unsanitary restaurants or street vendors.

Morbidity and mortality are based on whether the disease process is complicated or not. Most cysts are benign and resolve in 2–3 months. Children with a single cyst that can be controlled symptomatically have a favorable prognosis. If neurocysticercosis is treated properly, a cure rate of 90 % can be achieved in children. The real cure will not come from the treatment of the disease but only with the eradication of the parasite. Complications include increased intracranial pressure and difficulty controlling seizures, resulting in hydrocephalus, papilledema, and headaches; therefore, symptomatic management is crucial. Although complications are on the rare end of the spectrum, prognosis is less favorable when they are present.