Cysticercosis in Emergency Medicine

Updated: May 17, 2021
Author: Mityanand Ramnarine, MD, FACEP; Chief Editor: Barry E Brenner, MD, PhD, FACEP 



Cysticercosis is a systemic illness caused by dissemination of the larval form of the pork tapeworm, Taenia solium. Encystment of larvae can occur in almost any tissue. Involvement of the central nervous system (CNS), known as neurocysticercosis (NCC), is the most clinically important manifestation of the disease and may present with dramatic findings. Moreover, neurocysticercosis is the most common helminthic infection of the CNS.[1]  Neurocysticercosis is a major cause of seizure disorder in parts of the developing world, and its incidence is increasing within developed countries.

In impoverished countries and those in which pigs are raised, T solium is a significant etiology of seizures. Although neurocysticercosis is not widespread in the United States, it must be considered during the evaluation of a patient with newly onset seizure. Up to 10% of hospitalized patients in the United States with neurocysticercosis die of this preventable disease.[2]

See the image below.

Nonenhanced (left) and enhanced (right) CT scans o Nonenhanced (left) and enhanced (right) CT scans of the brain in a patient with neurocysticercosis show multiple ring-enhancing lesions with perifocal edema.


Humans are the definitive T solium hosts and can carry an intestinal adult tapeworm (taeniasis), often without symptoms. Intermittent fecal shedding of egg-containing proglottids or free T solium eggs ensues, with the intention that the intermediate host (normally pigs) will ingest the excreted eggs in contaminated food or water. T solium embryos penetrate the GI mucosa of the pig and are hematogenously disseminated to peripheral tissues with resultant formation of larval cysts (cysticerci). When undercooked pork is consumed, an intestinal tapeworm will again be formed, completing the life cycle of the worm.

Human cysticercosis occurs when T solium eggs are ingested via fecal-oral transmission from a tapeworm host. The human then becomes an accidental intermediate host, with development of cysticerci within organs. Cysticerci may be found in almost any tissue. The most frequently reported locations are skin, skeletal muscle, heart, eye, and the central nervous system (CNS). Involvement of the CNS leads to the most important manifestation of the disease, neurocysticercosis (NCC).

Symptomatology of neurocysticercosis (NCC) ranges from completely asymptomatic to severe disease and death. Symptoms largely depend on the presence of pericystic inflammation, the absence of which will usually manifest as asymptomatic disease. Lack of perilesional inflammation is seen with both "active" healthy parasites, which are able to evade host immunity (an adaptive feat that may be abetted by the immune privilege afforded to the CNS), and in "inactive" disease in which the cysticerci have completely involuted. As a corollary, inflammation is restricted to currently live but degenerating cysts whose ability to escape host defenses is faltering. Upon imaging, these inflamed degenerating cysts are typically seen as ring-enhancing lesions, an appearance that may be termed colloidal. Eventually, cysts will involute and either vanish or undergo granulomatous change and exhibit calcific scarring. Cysts in various stages of viability can be seen simultaneously in one host.

In patients with advanced HIV disease and compromised cell-mediated immunity, neurocysticercosis may exist without significant host response and is likely to be asymptomatic. For this reason, in symptomatic patients with CD4 counts under 200 cells/mm3, alternative diagnoses should be considered.[3]

Serious pathologic findings of neurocysticercosis (NCC) can include seizures, encephalopathy, obstructive hydrocephalus, meningoencephalitis, cognitive decline, focal deficits, and vascular accidents. Involvement of brain parenchyma is common and leads to the most frequent presentation of seizure or headache. Clinical expression of NCC depends primarily on the number and location of CNS cysticerci and degree of inflammatory response. As previously mentioned, host immune response and resultant pericystic inflammation are considered largely responsible for parenchymal disease manifestations. However, some evidence indicates that involuted calcific lesions may be epileptogenic as well and thus contribute to significant morbidity.

Extraparenchymal ventricular and subarachnoid cysts also are found. These carry a worse prognosis and often lead to obstructing hydrocephalus requiring surgical intervention. Cysticerci within the basilar cisterns or Sylvian fissures may become quite large. Those within the cisterns may also cause vasculitis and stroke. Spinal NCC is rare.

Ocular cysts are mostly vitreous, but they may be found in subretinal locations. Visualization of cysts via funduscopy may be diagnostic of the disease. Subcutaneous nodules represent cysticerci in the skin. Skeletal muscle encystment usually is asymptomatic but may cause muscular pseudohypertrophy with a heavy parasite burden. Cardiac cysts may lead to conduction system abnormalities.



United States

Incidence in the United States is increasing due to increased immigration from and travel to endemic areas and improved serologic testing and availability of diagnostic imaging. An estimated 1000 new cases are diagnosed per year in the United States. In southern California, with its large population of immigrants, neurocysticercosis (NCC) may account for at least 10% of seizures seen in some emergency departments and more than 2% of neurological or neurosurgical admissions.[4] The diagnosis of NCC should be considered in any patient from an endemic area presenting with new-onset seizures.


Cysticercosis affects an estimated 50 million people worldwide. Endemic areas include Mexico and Latin America, sub-Saharan Africa, India, and East Asia. NCC is a leading cause of adult-onset seizures worldwide.[5, 6, 7]


Morbidity may result from seizures, strokes, or hydrocephalus and from effects of long-term treatment with anticonvulsants, steroids, or cerebrospinal fluid shunts.

Mortality from cysticercosis is generally limited to cases complicated by encephalitis, cerebral edema, hydrocephalus, and stroke.[8]


Hispanic and Asian populations are more commonly affected due to immigration patterns from endemic areas. The disease is prevalent in South Asia as well, where patients more commonly present with a solitary cyst.


People of any age may be affected. Children may be more likely to develop an unusual encephalitis-type variant.




Neurocysticercosis (NCC) is frequently asymptomatic. Symptoms are generally similar to those found with other intracranial mass lesions, which may be consistent with increased ICP. Cysticercosis of other tissues is almost always asymptomatic. The following symptoms can appear years after infection begins:

  • Seizures (focal or generalized) in 70-90% of patients

  • Chronic headache

  • Nausea and vomiting

  • Vision changes

  • Focal neurological complaints

  • Mental status change

  • Cognitive decline


Physical findings include the following:

  • Absence of fever

  • Usually nonfocal neurologic examination findings

  • Papilledema and decreased retinal venous pulsations

  • Meningismus

  • Hyperreflexia

  • Nystagmus or visual deficits

  • Visualization of intraocular larvae by funduscopy may be diagnostic

  • Subcutaneous nodules resembling sebaceous cysts

  • Muscular pseudohypertrophy


Risk factors associated with cysticercosis include the following:

  • Immigration from an endemic area (especially Mexico, Latin America)

  • Family history of parasitic infestation

  • History of travel to an endemic area

  • Household visitors from an endemic area





Laboratory Studies

Laboratory studies are inferior to imaging in diagnosis of cysticercosis but may play an adjunctive role.

Complete blood cell (CBC) count

Peripheral eosinophilia usually is not present, but eosinophils may be 10%-15% of white blood cells (WBCs).


Serology is the most useful of laboratory tests.

Sensitivity of serology is directly linked to number of parasitic lesions and the stage of lesions. Single lesions and calcification are more likely to be associated with a false-negative assay result. False-positive results may be caused by other parasitic infections.

Enzyme-linked immunosorbent assays (ELISAs) have reported 74% sensitivity and are highly specific for the appropriate antigens. Sensitivity may be increased in cases involving multiple cysts or if the assay is performed on cerebral spinal fluid (CSF) rather than serum.

The newer enzyme-linked immunoelectrotransfer blot (EITB) is preferred to ELISA. It carries a better than 95% sensitivity and nearly 100% specificity in patients carrying multiple cysts. However, its performance is poor in those with a single cyst or with only calcific lesions. In contrast to ELISA, EITB is slightly more sensitive using serum than CSF.[9]

Stool for ova and parasites

Stool sampling may be useful since a minority of patients have a simultaneous intestinal tapeworm infestation, the likelihood of which increases with the severity of cysticerci burden.[1] This test is insensitive, as the life cycle of the adult tapeworm may be self-limited before CNS cysts become symptomatic,[10] and, even in active intestinal infections, many samples may be needed over several days.

The test is nonspecific for T solium species, as the eggs appear similar to those of the beef tapeworm.

It is reasonable to screen close contacts of index patients for the presence of an intestinal tapeworm.

Imaging Studies

Also see Cysticercosis, CNS and Neuroimaging in Neurocysticercosis.


Soft tissue radiography may show calcifications of inactive cysts. These may appear as oblong-shaped "cigar" lesions.

Brain CT scan

CT scan is recommended as the first imaging study.

CT scan is more widely available, less expensive, and has a faster imaging time than MRI.

Obtain contrast and noncontrast studies.

Noncontrast study may show cystic lesions, focal areas of edema in the acute phase of disease, or calcifications of inactive disease (which is the most common disease form at presentation). Mass effect or hydrocephalus may be seen. Ventricular cysts may be isodense with CSF and manifest only as distortion of surrounding tissue. Percutaneous CSF contrast administration may be helpful to delineate these lesions. CT scan is also insensitive for lesions near bone or within the posterior fossa.[11]

Intravenous contrast-enhanced CT may depict nonenhancing cystic lesions with or without edema or ring enhancement, signifying inflammation surrounding an involuting living cysticercus.

See the images below.

Nonenhanced CT scan of the brain demonstrates the Nonenhanced CT scan of the brain demonstrates the multiple calcified lesions of inactive parenchymal neurocysticercosis.
Enhanced CT scan of the brain in a patient with ne Enhanced CT scan of the brain in a patient with neurocysticercosis demonstrates a live cyst with a minimally enhancing wall and an eccentric hyperattenuating scolex.

Brain MRI

MRI is recommended as an adjunct to CT scan. It may aid in cases where previous CT scan was nondiagnostic.

MRI may show a mural nodule within the cyst which represents the larval scolex. This finding is pathognomonic for cysticercosis.

MRI may show cysticerci within the ventricular system, which are often missed on CT scan due to the similar appearance of cerebrospinal and cystic fluids.

MRI is the preferred imaging modality to identify brainstem cysts or those over the cerebral convexities.[12]

Other Tests

Several authors have proposed tiered diagnostic criteria. These utilize clinical, radiologic, histologic, and serologic features along with epidemiologic factors and response to therapy to formulate diagnostic certainty. Detailed explanation of these scoring systems can be found in other references.


Lumbar puncture

It may be necessary to obtain an imaging study prior to lumbar puncture to exclude intracranial mass effect.

CSF testing is neither sensitive nor specific for the diagnosis of cysticercosis. Nonetheless, CSF testing may be essential to rule out other potential causes of meningitis or encephalitis.

CSF is normal in many cases. In the presence of significant inflammation, CSF may show lymphocytosis, increased protein, and/or decreased glucose levels. The finding of pleocytosis is more common in cases of subarachnoid neurocysticercosis (NCC).

Special Wright or Giemsa stains

Special Wright or Giemsa stains are needed to show CSF eosinophilia, a common but nonspecific finding.


Subcutaneous nodules may be biopsied. Demonstration of organisms within nodular tissue is diagnostic of cysticercosis.



Prehospital Care

Patients present with seizure activity, altered mental status, headache, or other neurologic complaints. Prehospital treatment involves standard supportive care including ensuring that adequate airway support, oxygenation, ventilation, and perfusion are maintained. Administration of anticonvulsants may be necessary for prolonged or repeated seizure activity. Empiric naloxone may be given for coma. Hypoglycemia should be corrected.

Emergency Department Care

Secure airway, oxygenation, circulation, adequate glucose delivery, and proper monitoring.

Administer supportive care for those presenting with seizure activity.

Correct metabolic abnormalities.

Anticonvulsants are reliably effective in controlling seizures secondary to cysticercosis. Most patients will respond to first-line agents.

Steroids, osmotic agents, and/or diuretics are indicated with evidence of increased ICP.

Analgesics may be administered for pain control.

Initiate diagnostic procedures, including blood work and imaging.

Consult appropriate specialists.


Consultations may include neurosurgery, neurology, infectious diseases, and ophthalmology. Neurosurgical procedures are frequently required to relieve intracranial pressure extraparenchymal NCC or cysticercotic encephalitis. Biopsy or surgical removal of lesions may be necessary.



Medication Summary

Antihelminthic agents are the mainstay of definitive treatment. Controversy exists as to whether antiparasitic treatment of cysticercosis is necessary in most cases. Some authors claim that patients do well without antiparasitic therapy since symptomatology is produced by pericystic inflammation, which portends imminent involution of the parasite. This suggests that the presence of clinical symptoms is predictive of a subsequent self-limited disease course.

In addition, the calcific lesions of "inactive" disease may not be clinically silent but rather epileptogenic and can thereby confer significant morbidity. A randomized controlled study of 300 patients with neurocysticercosis over several years found that those treated with a course of albendazole plus corticosteroids and anticonvulsants developed significantly more lesional calcification on follow-up imaging than those treated with anticonvulsants alone.[13] During the first year, this treatment group also had a significantly higher incidence of seizures and thereafter displayed a trend toward such. These investigators concluded that antihelminthic treatment may result in more long-term seizure activity since complete resolution of lesions may be more likely when cysts are allowed to spontaneously resolve. They therefore recommend treatment with anticonvulsants alone, with careful clinical and radiologic follow up.

Despite lively controversy surrounding the matter, a preponderance of the literature positively supports treatment with antihelminthics.[14, 15] Several randomized controlled trials have demonstrated benefit of antihelminthic therapy, particularly in reducing the number of active cysts. Benefit seems to be greatest during the first weeks of therapy. As mentioned previously, treatment with antihelminthic medication will initially worsen clinical symptoms as faltering parasite defenses lead to increasing perilesional inflammation. Therefore, in nearly all trials, antiparasitic medication has been combined with steroid therapy. In addition, patients are usually maintained on concomitant anticonvulsant therapy for an indefinite period of time.

Caution is particularly warranted in patients with significant pretreatment encephalitis, hydrocephalus, or vasculitis, since treatment may cause increasing inflammation as cysts involute, leading to worsening clinical states. CSF shunting may be indicated before medical treatment begins since intracranial hypertension may worsen upon administration of antiparasitics.


Class Summary

Parasite biochemical pathways differ sufficiently from those of the human host so as to allow selective interference by chemotherapeutic agents in relatively small doses. Many patients may require more than one course of treatment to entirely eliminate active cysts.

The more effective agent, albendazole, has upstaged praziquantel as the traditional therapeutic agent. Subarachnoid and intraventricular neurocysticercosis (NCC) may be relatively more resistant to treatment. In these cases, repeat courses of medication are usually needed, and there is limited evidence that higher-dose albendazole treatment (30 mg/kg/d) may be beneficial.[16]

Praziquantel (Biltricide)

Increases cell membrane permeability in susceptible worms, resulting in a loss of intracellular calcium, massive contractions, and paralysis of their musculature. In addition, produces vacuolization and disintegration of the schistosome tegument. This is followed by attachment of phagocytes to the parasite and death.

Albendazole (Albenza)

Broad-spectrum anthelmintic that decreases ATP production by the worm causing energy depletion, immobilization, and finally, death.


Class Summary

A temporary increase in pericystic inflammation often is observed during treatment of NCC, as the dying parasite no longer can escape host defenses. For this reason, it is often recommended that corticosteroids be administered in combination with, or instead of, antihelminthics. This practice is controversial and should be tailored to the individual patient according to the number and location of cysticerci. Steroids are more likely indicated in cases involving extraparenchymal cysts.

Prednisone (Orasone, Meticorten, Deltasone)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Dexamethasone (Decadron, Dexone)

For various allergic and inflammatory diseases. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.


Class Summary

Anticonvulsant therapy should proceed as in other epileptiform states. Benzodiazepines are first-line agents for active prolonged or repeated seizures. They should generally be followed by a more definitive anticonvulsant such as phenytoin. Barbiturates may be needed in more refractory cases.

Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life. By increasing the action of gamma-aminobutyric acid (GABA), which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation. Important to monitor blood pressure after administering dose. Adjust as necessary.

Phenytoin (Dilantin)

May act in motor cortex, where it may inhibit spread of seizure activity. Activity of brainstem centers responsible for tonic phase of grand mal seizures may also be inhibited. Dose to be administered should be individualized. Administer larger dose before retiring if dose cannot be divided equally.

Phenobarbital (Solfoton, Luminal, Barbita)

Elevates seizure threshold, limits the spread of seizure activity, sedative.



Further Outpatient Care

Prescribe a follow-up CT scan or MRI to assess response to treatment.

Long-term anticonvulsant therapy is usually necessary in patients with persistent CNS calcifications. Selected patients who demonstrate radiographic cure and display no seizures over prolonged periods may discontinue anticonvulsant medication.

Further Inpatient Care

Inpatient treatment is recommended for those receiving antiparasitic therapy since transient worsening of condition may ensue.

Neurosurgical intervention often is required in cases of obstructive hydrocephalus, ventricular cysticerci, and in cases refractory to medical treatment.

Ophthalmologic surgery is recommended in all cases of ocular cysticercosis since the inflammatory reaction associated with medical therapy may threaten vision.

Only standard isolation is required for patients who are hospitalized.


Patients should be transferred to a facility with neurosurgical capability in cases of extraparenchymal disease and in those involving increased ICP, hydrocephalus, mass effect, or herniation.

Status epilepticus may require neurological intensive care.


Screen family members for parasitic disease. Prophylaxis may be indicated.

Educate patients regarding personal hygiene and handling of food.

Those traveling to endemic countries should be educated in preventative habits such as proper cooking of meat and avoidance of fecal-oral transmission routes.

Endemic areas require inspection for and proper disposal of tainted meat, as well as efforts at proper management of sewage.

Mass treatment of large populations has been historically effective in controlling disease.

Effective human and/or animal vaccines may be deployed in the near future.


Complications of cysticercosis may include the following:

  • Intracranial herniation

  • Stroke

  • Status epilepticus

  • Long-term anticonvulsant use

  • Intraventricular shunt complications


Prognosis for patients with cysticercosis is excellent in almost all cases.

Patient Education

Patients and their families should be familiar with basic first aid for seizures.

Education should be provided on use of prescribed medications and the expected course of disease.

Provide instruction on indications to seek medical care, including signs of increasing ICP or focal neurologic complaints.

Patients prone to seizures should not drive or perform other dangerous activities.