eMedicine Specialties > Infectious Diseases > CNS Infections
Cysticercosis: Treatment & Medication
Updated: Jul 25, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
- Asymptomatic cysticercosis: As mentioned above, more than 80% of patients with cysticercosis are asymptomatic. No evidence has shown that administering antiparasitic therapy for asymptomatic nonviable cysticercal lesions found incidentally in the brain is beneficial.
- Patients who are found to have cysticerci only in subcutaneous or intramuscular sites generally do not require specific therapy.
- If a single extracranial lesion is found, excision can be considered after neurocysticercosis is excluded with brain imaging.
- Patients with ocular cysticercosis who have extraocular muscle involvement may present with diplopia and recurrent eye pain. Treatment with albendazole and corticosteroids has proven to be beneficial. Some patients may require surgical excision. In patients with intraocular cysticercosis, vitreoretinal surgery (either transscleral or transvitreal) can be performed to remove the cysticerci.
- Patients with subcutaneous or intramuscular cysticercosis who develop symptoms due to inflammation can be treated with cysticerci excision or anti-inflammatory agents. Excision is the treatment of choice for a solitary symptomatic lesion.
- Symptomatic therapy is the mainstay of treatment for neurocysticercosis.
- Anticonvulsants are prescribed to patients with seizures.
- Specific anthelminthic therapy with albendazole or praziquantel is prescribed, usually accompanied by corticosteroids.
- Corticosteroids are used in patients with cerebral edema or vasculitis.
- CSF diversion is instituted in patients with obstructive hydrocephalus.
- Parenchymal disease should be treated medically.
- The primary focus is symptomatic therapy for seizures.
- A postictal patient should initially receive supportive care that includes a safe environment.
- Anticonvulsants should be administered early but may be tapered when seizures are controlled if findings from neuroimaging studies revert to normal (see Medication).
- If significant intracranial edema is demonstrated, corticosteroids should be administered before antiparasitic therapy is considered. Some authorities recommend routine use of corticosteroids in all cases of active neurocysticercosis.
- If viable cysticerci are suspected, antiparasitic drugs (ie, praziquantel and albendazole) may be used to hasten the death of the parasite. However, the decision to use antiparasitic therapy should be individualized to each patient.
- A prospective randomized study compared the use of antiparasitic agents with placebo in patients with active parenchymal lesions. Results showed no significant difference in the number of subjects with recurrent seizures. However, the number of generalized seizures was significantly reduced with the combination of steroids and antiparasitic drugs. The beneficial effect was seen in a subgroup of subjects with numerous recurrent seizures.9
- Patients with only calcifications (ie, residual phase) with or without edema do not need antiparasitic therapy.
- Patients with cerebral edema or uncontrolled hydrocephalus should not be treated with antiparasitic therapy until these conditions are resolved.
- Patients with multiple cysticerci, especially in the basilar cisterns, or with giant cysticerci of the sylvian fissures, should receive both corticosteroids and antiparasitic therapy.
- Generally, ventricular disease should be treated surgically, preferably via an endoscopic approach. However, if the surgery is being performed only to place a shunt and not to remove the cysts, antiparasitic therapy should be administered after the shunting procedure.
- Neuroendoscopy provides a safe and minimally invasive procedure for the removal of symptomatic cysts, minimizing morbidity and mortality relating to the natural history of the disease, as well as possibly avoiding a more extensive standard open craniotomy. The endoscopic approach can be made via transventricular corridor, perforating overlying structures such as the septum pellucidum. In some cases, burr holes may be required.
Surgical Care
- Surgical procedures are required in some patients based on complicating factors, such as hydrocephalus or giant cysts (>10 cm) in the setting of intracranial hypertension.
- Surgical intervention should also be considered if a cyst is found in the fourth ventricle, is attached to the middle cerebral artery (MCA), or is compressing the optic chiasma.
- Extraparenchymal disease was once treated surgically by placing a shunt because most symptoms are due to hydrocephalus.
- Surgical resection of ventricular neurocysticercosis is associated with a low long-term risk of postoperative morbidity.
- Some studies suggest that endoscopic removal may be able to replace open surgery for removal of cysticerci in most cases.
- Ventriculoperitoneal (VP) shunting is now commonly used for the treatment of hydrocephalus. Case series have shown that the cysticerci are usually ruptured during removal, but no adverse consequences have been noted.
- In patients with viable cysticerci, the use of VP shunt alone results in treatment failure in almost 75% of cases.10 The use of antiparasitic drugs and corticosteroids in conjunction with VP shunt placement improve the outcome.
- Although recurrent blockage of shunts is very common, it is unclear whether antiparasitic therapy or long-term corticosteroid treatment decreases the risk of shunt blockage and malfunction.
- Recent descriptions of valveless shunts noted lower rates of recurrent hydrocephalus, but these shunts were associated with a higher rate of inadequate drainage.
- Patients with inactive disease may present with hydrocephalus due to scar tissue in the cisterns or ventricular space, without evidence of cystic lesions.
- VP shunting is necessary in these cases.
- Antiparasitic drugs and corticosteroids are not needed because the cysticerci have already degenerated and shunt failure is rare.
- Neurocysticercosis of the basilar cisterns should be treated with corticosteroids, prolonged courses (eg, months) of antiparasitic drugs, and VP shunting if hydrocephalus is present.
- Giant subarachnoid cysticerci can cause significant mass effect as associated edema. The edema may respond to steroids, but the mass effect may remain.
- Surgical drainage may be necessary.
- Antiparasitic drugs may be beneficial, but only after steroids are given.
- Generally, ocular and spinal medullary cysticerci should be removed surgically.
- However, cures of spinal medullary disease have been reported with medical treatment including corticosteroids and antiparasitic drugs.
- Antiparasitic treatment in patients with retinal cysticerci may cause irreversible retinal damage.
- Spinal subarachnoid disease can often be treated medically.
Consultations
- Consultation with a neurosurgeon is essential in patients with hydrocephalus, significant mass effect, or extraparenchymal CNS disease.
- Consultation with a neurologist is needed if protracted or refractory seizures occur.
- Consultation with an infectious disease specialist is recommended if active disease is suspected.
- An ophthalmologist should be consulted for patients with ocular neurocysticercosis. At a minimum, a funduscopic examination should be performed before the initiation of antiparasitic drug therapy.
Diet
- No specific diet restriction is recommended.
- Patients should avoid reinfection and reingestion of ova from original sources by observing the following guidelines:
- Inspection of pork for cysticerci, which are visible in raw meat ("measly meat")
- Freezing or adequately cooking meat to destroy cysticerci (Pickling and salting are inadequate.)
- Administering antiparasitic agents to pigs
- Good personal hygiene and hand-washing prior to food preparation
Activity
- No activities are restricted if the patient is otherwise asymptomatic.
- All patients who present with seizures should take seizure precautions. Patients with a history of seizures may have state-required restrictions on driving motor vehicles. Physicians may be responsible for informing patients about these restrictions.
- Patients with hydrocephalus may have ataxia and may be at risk for falls.
Medication
Anticonvulsant and anti-inflammatory (steroid) medications are the basis of medical therapy in symptomatic patients. Antiparasitic drugs have not been shown to provide a consistent long-term benefit in patients with parenchymal disease and seizures.
Anticonvulsants
Anticonvulsants should be used in patients with seizures or who are at high risk for recurrent seizures. Patients with parenchymal calcifications carry a high risk of seizure recurrence if anticonvulsants are tapered; therefore, these patients usually remain on anticonvulsants indefinitely. In contrast, patients with active cysticerci in whom lesions resolve without developing calcification should be treated with anticonvulsants until they are free from seizures for at least one year and results of neuroimaging studies show normalization. Anticonvulsants may then be tapered. Patients with recurrent seizures should be maintained on long-term anticonvulsant therapy.
A double-blind, placebo-controlled study in 2004 compared two groups of patients with viable parenchymal cysts, with seizures being treated with anticonvulsants, to see whether anticysticercal drugs improved seizure control. During 30 months of follow-up, the proportion of patients having partial seizures was similar for the group who took albendazole and dexamethasone and those who took placebos, but the treatment group had significantly fewer seizures with generalization, and more of their intracranial lesions resolved. Except for abdominal pain, adverse effects did not differ significantly.11
Phenytoin, carbamazepine, and phenobarbital induce metabolism of praziquantel.
Phenytoin (Dilantin)
Widely available and inexpensive. Has significant drug interactions, and dosage should be adjusted based on therapeutic effect and serum levels. Fosphenytoin may be considered for IV administration if available because it is better tolerated than IV phenytoin, but it is considerably more expensive than phenytoin.
Adult
Nonemergent situations: 100 mg PO tid; then adjust based on therapeutic effect and serum level
Emergent situations: 1 g IV loading dose (not to exceed 50 mg/min) or PO in 3 divided doses q2h
Therapeutic: 10-20 mcg/mL or 1-2 mcg/mL for free phenytoin
Pediatric
Nonemergent situations: 5 mg/kg PO qd or divided bid/tid; then adjust by therapeutic effect and serum level
Emergent situations: 10-15 mg/kg IV loading dose
Therapeutic: 10-20 mcg/mL
Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase toxicity
Barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and sucralfate may decrease effects
May decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, oral contraceptives, and valproic acid
Documented hypersensitivity; sinoatrial block; second- and third-degree AV block; sinus bradycardia; Adams-Stokes syndrome
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Perform CBC counts and urinalyses when therapy is begun and at monthly intervals for several months thereafter to monitor for blood dyscrasias; discontinue use if rash appears, and do not resume use if rash is exfoliative, bullous, or purpuric; rapid IV infusion may result in death from cardiac arrest, marked by QRS widening; caution in acute intermittent porphyria and diabetes (may elevate blood glucose; discontinue use if hepatic dysfunction occurs
Carbamazepine (Tegretol)
Use if phenytoin unavailable, ineffective, or contraindicated. Anticonvulsant therapy should be used for one year after resolution of the active parasitic infection followed by a trial of treatment discontinuation if the patient remains seizure-free.
Adult
Nonemergent situations: 200 mg PO bid, increase by 200 mg/d; not to exceed 1600 mg/d (usual dose 400-1200 mg/d)
Therapeutic: 4-12 mcg/mL
Pediatric
Nonemergent situations: 10 mg/kg/d PO divided bid up to 200 mg bid; increase by 100-200 mg q7d; not to exceed 1200 mg/d
Serum levels may increase significantly within 30 d of danazol coadministration (avoid whenever possible); do not coadminister with MAOIs; cimetidine may increase toxicity, especially if taken in first 4 wk of therapy; may decrease primidone and phenobarbital levels (coadministration may increase carbamazepine levels)
Documented hypersensitivity; history of bone marrow depression; MAOIs within last 14 d
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Do not use to relieve minor aches or pains; caution with increased intraocular pressure; aplastic anemia and agranulocytosis reported in association with Tegretol; obtain CBC counts and serum iron baseline prior to treatment, during first 2 months, and yearly or every other year thereafter; can cause drowsiness, dizziness, and blurred vision; caution while driving or performing other tasks requiring alertness; toxic epidermal necrolysis and Stevens-Johnson syndrome reported during Tegretol use
Phenobarbital (Barbital, Luminal, Solfoton)
Use if phenytoin unavailable, ineffective, or contraindicated. Interferes with transmission of impulses from thalamus to cortex of brain. Used as sedative.
Adult
Nonemergent situations: 60 mg PO bid/tid
Emergent situations: 10-20 mg/kg IV
Pediatric
5 mg/kg PO or IV qd or divided bid
May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients stabilized on anticoagulants may require dosage adjustments if added to or withdrawn from their regimen); coadministration with alcohol may produce additive CNS effects and death; chloramphenicol, valproic acid, and MAOIs may increase toxicity; rifampin may decrease effects; induction of microsomal enzymes may result in decreased effects of oral contraceptives in women (must use additional contraceptive methods to prevent unwanted pregnancy; menstrual irregularities may also occur)
Documented hypersensitivity; severe respiratory disease; marked impairment of liver function; nephritis
porphyria; or patients with severe respiratory disease such as severe asthma or severe chronic obstructive pulmonary disorder (COPD).
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
In prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; caution in fever, hyperthyroidism, diabetes mellitus, and severe anemia because adverse reactions can occur; caution in myasthenia gravis and myxedema
Corticosteroids
These agents should be used immediately in patients with significant cerebral edema, mass effect, or vasculitis associated with neurocysticercosis. High doses (approximately 1 mg/kg/d of prednisone) should be used. High-dose dexamethasone (30 mg/d) should be used initially to treat cysticercal encephalitis. If cerebral edema resolves, patients may be treated with antiparasitic drugs later. Long-term courses of corticosteroids should be used in patients with subarachnoid neurocysticercosis who have meningitis, stroke, or communicating hydrocephalus and should be tapered as soon as possible based on lumbar puncture and neuroimaging results.
Long-term course of corticosteroids may also prevent shunt failure in patients with VP shunt and active disease. Patients with intramedullary spinal neurocysticercosis should be treated with steroids until resolution of cord edema. Patients receiving long-term corticosteroids should be given calcium supplementation to help counterbalance osteoporotic effects of corticosteroids.
Prednisone (Deltasone, Meticorten, Orasone)
Inexpensive, widely available, and effective. Use in patients with significant edema, mass effect, or vasculitis.
Adult
1 mg/kg/d IV/PO qd or divided doses
Pediatric
Administer as in adults; divided doses may decrease GI tract upset
Estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective-tissue infections; fungal or tubercular skin infections; GI tract disease
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Abrupt discontinuation may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur
Dexamethasone (Decadron, AK-Dex)
Use in patients with cysticercal encephalitis or in patients with severe mass effect, edema, or vasculitis if preferred over prednisone.
Adult
4-6 mg IV q4-6h for total dose of approximately 30 mg/d
Pediatric
Not established
Effects decrease with coadministration of barbiturates, phenytoin, or rifampin; decreases effect of salicylates and vaccines used for immunization
Documented hypersensitivity; active bacterial or fungal infection
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering; abrupt discontinuation may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications
Antiparasitics/anthelminthic
Albendazole and praziquantel are antiparasitic drugs used to treat neurocysticercosis. They have been used for more than 20 years, but data by which to judge their therapeutic role are still controversial. Albendazole is preferred over praziquantel because of its favorable pharmacokinetics profile and efficacy. Both agents are cysticidal. These drugs are always administered with corticosteroids.
When praziquantel is administered with cimetidine to increase its bioavailability, praziquantel is probably as effective as albendazole in killing viable cysticerci.
Antiparasitic drugs are contraindicated in cysticercal encephalitis (characterized by diffuse cerebral edema), uncontrolled elevated ICP, ocular disease, and subarachnoid neurocysticercosis in close proximity to blood vessels. In all of these cases, steroids should be administered early so that the inflammatory reaction is quelled. Antiparasitic drugs, which may cause release of more antigens and stimulate more inflammation, can then be considered on a case-by-case basis.
Albendazole (Albenza)
Has no interactions with steroids or anticonvulsants. It is preferred over praziquantel because of its pharmacokinetic profile and efficacy. Parenchymal disease responds to short courses, but longer duration of therapy (months) may be needed in extraparenchymal disease.
Adult
15 mg/kg/d (usually 800 mg/d in two divided doses) PO divided bid with meals for 15 d
Shorter course of therapy for 8 d demonstrated higher failure rate
Pediatric
Administer as in adults
Coadministration with carbamazepine may decrease efficacy; dexamethasone, cimetidine, and praziquantel may increase toxicity
Documented hypersensitivity; neurocysticercosis resulting in cerebral edema; uncorrected hydrocephalus; cysticerci near cerebral vessels; ocular disease
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Use with retinal cysticercosis may cause irreparable damage; discontinue use if LFT values increase significantly (resume when levels decrease to pretest values); abdominal pain, nausea, vomiting, diarrhea, dizziness, vertigo, fever, increased ICP, and alopecia granulocytopenia, anemia, and/or pancytopenia may occur; albendazole may increase theophylline level, so level should be monitored for theophylline toxicity
Praziquantel (Biltricide)
Increases cell membrane permeability in susceptible worms, resulting in loss of intracellular calcium, massive contractions, and paralysis of musculature. Also produces vacuolization and disintegration of schistosome tegument. This is followed by attachment of phagocytes to parasite and death. It does not cross blood-brain barrier well, only 20% of plasma levels.
Tabs should be swallowed whole with some liquid during meals. Keeping tabs in mouth may release bitter taste that can produce nausea or vomiting. The efficacy appears to be lower than that of albendazole. It works better when taken with cimetidine. Its metabolism can be induced by cytochrome P-450 (corticosteroids, phenytoin, phenobarbital). The serum level of praziquantel is lowered when any of these drugs is coadministered. It is usually considered as a second-line therapy.
Adult
50 mg/kg/d PO divided tid for 15 days (with cimetidine at 300 mg PO qid if patient also taking steroids or anticonvulsants)
Longer courses (months) may be needed for extraparenchymal infections
Preliminary studies suggest alternative dosage regimen of 75 mg/kg given in single day (25 mg/kg q2h for total of 3 doses) may have similar efficacy
Pediatric
Administer as in adults
Significant first-pass metabolism when coadministered with corticosteroids, carbamazepine, phenytoin, or, probably, phenobarbital; levels decrease by approximately one half compared with praziquantel alone; cimetidine coadministration significantly inhibits metabolism and should be used to counterbalance effect of concurrent steroids or anticonvulsants
Documented hypersensitivity; ocular cysticercosis; neurocysticercosis resulting in cerebral edema; uncorrected hydrocephalus; cysticerci near cerebral vessels; ocular disease
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Destruction of parasite within eyes can cause irreparable lesions (ocular cysticercosis should not be treated with praziquantel); caution while driving or performing other tasks requiring alertness on day of and following treatment; minimal increases in liver enzymes reported; when schistosomiasis or fluke infection associated with cerebral cysticercosis, hospitalize patient for duration of treatment
Nursing mothers should stop breastfeeding when beginning treatment with praziquantel; breastfeeding should not be resumed until 72 h after treatment is completed; during this time, the breast milk should be expressed and discarded
More on Cysticercosis |
| Overview: Cysticercosis |
| Differential Diagnoses & Workup: Cysticercosis |
 Treatment & Medication: Cysticercosis |
| Follow-up: Cysticercosis |
| References |
| Further Reading |
| « Previous Page | Next Page » |
References
Sorvillo FJ, DeGiorgio C, Waterman SH. Deaths from cysticercosis, United States. Emerg Infect Dis. Feb 2007;13(2):230-5. [Medline].
de Bittencourt PR, Adamolekum B, Bharucha N, et al. Epilepsy in the tropics: I. Epidemiology, socioeconomic risk factors, and etiology. Epilepsia. Nov 1996;37(11):1121-7. [Medline].
Wallin MT, Kurtzke JF. Neurocysticercosis in the United States: review of an important emerging infection. Neurology. Nov 9 2004;63(9):1559-64. [Medline].
Ong S, Talan DA, Moran GJ, et al. Neurocysticercosis in radiographically imaged seizure patients in U.S. emergency departments. Emerg Infect Dis. Jun 2002;8(6):608-13. [Medline].
Bern C, Garcia HH, Evans C, et al. Magnitude of the disease burden from neurocysticercosis in a developing country. Clin Infect Dis. Nov 1999;29(5):1203-9. [Medline].
Del Brutto OH, Rajshekhar V, White AC Jr, et al. Proposed diagnostic criteria for neurocysticercosis. Neurology. Jul 24 2001;57(2):177-83. [Medline].
Fleury A, Hernandez M, Fragoso G, et al. Detection of secreted cysticercal antigen: a useful tool in the diagnosis of inflammatory neurocysticercosis. Trans R Soc Trop Med Hyg. Sep-Oct 2003;97(5):542-6. [Medline].
White AC Jr, Robinson P, Kuhn R. Taenia solium cysticercosis: host-parasite interactions and the immune response. Chem Immunol. 1997;66:209-30. [Medline].
Garcia HH, Pretell EJ, Gilman RH, Martinez SM, Moulton LH, Del Brutto OH, et al. A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. N Engl J Med. Jan 15 2004;350(3):249-58. [Medline].
Kelley R, Duong DH, Locke GE. Characteristics of ventricular shunt malfunctions among patients with neurocysticercosis. Neurosurgery. Apr 2002;50(4):757-61; discussion 761-2. [Medline].
Garcia HH, Pretell EJ, Gilman RH, et al. A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. N Engl J Med. Jan 15 2004;350(3):249-58. [Medline].
Del Brutto OH, Castillo PR, Mena IX, et al. Neurocysticercosis among patients with cerebral gliomas. Arch Neurol. Sep 1997;54(9):1125-8. [Medline].
Del Brutto OH. Neurocysticercosis. Semin Neurol. Sep 2005;25(3):243-51. [Medline].
Del Brutto OH, Santibanez R, Noboa CA, et al. Epilepsy due to neurocysticercosis: analysis of 203 patients. Neurology. Feb 1992;42(2):389-92. [Medline].
Garcia HH, Gilman RH, Tovar MA, et al. Factors associated with Taenia solium cysticercosis: analysis of nine hundred forty-six Peruvian neurologic patients. Cysticercosis Working Group in Peru (CWG). Am J Trop Med Hyg. Feb 1995;52(2):145-8. [Medline].
García HH, Del Brutto OH. Imaging findings in neurocysticercosis. Acta Trop. Jun 2003;87(1):71-8. [Medline].
García HH, Evans CA, Nash TE, et al. Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev. Oct 2002;15(4):747-56. [Medline].
Gordon E, Cartwright M, Avasarala J. Ventricular obstruction from neurocysticercosis. Arch Neurol. Jun 2005;62(6):1018. [Medline].
Gravori T, Steineke T, Bergsneider M. Endoscopic removal of cisternal neurocysticercal cysts. Technical note. Neurosurg Focus. Jun 15 2002;12(6):e7. [Medline].
Immunetics, Inc. Qualicode Cysticecosis Western Blot Kit. Immunetics [serial online]. 1997;Available at Immunetics-Qualicode Cysticecosis Western Blot Test Kit.
Kraft R. Cysticercosis: an emerging parasitic disease. Am Fam Physician. Jul 1 2007;76(1):91-6. [Medline].
Nainiwal S, Chand M, Verma L, et al. Intraocular live cysticercus larva. Ophthalmic Surg Lasers Imaging. Nov-Dec 2003;34(6):464-6. [Medline].
Salinas R, Counsell C, Prasad K, et al. Treating neurocysticercosis medically: a systematic review of randomized, controlled trials. Trop Med Int Health. Nov 1999;4(11):713-8. [Medline].
Sharma T, Sinha S, Shah N, et al. Intraocular cysticercosis: clinical characteristics and visual outcome after vitreoretinal surgery. Ophthalmology. May 2003;110(5):996-1004. [Medline].
Sotelo J, Escobedo F, Penagos P. Albendazole vs praziquantel for therapy for neurocysticercosis. A controlled trial. Arch Neurol. May 1988;45(5):532-4. [Medline].
Sundaram PM, Jayakumar N, Noronha V. Extraocular muscle cysticercosis - a clinical challenge to the ophthalmologists. Orbit. Dec 2004;23(4):255-62. [Medline].
White AC Jr. Neurocysticercosis: a major cause of neurological disease worldwide. Clin Infect Dis. Feb 1997;24(2):101-13; quiz 114-5. [Medline].
White AC Jr, Robinson P, Kuhn R. Taenia solium cysticercosis: host-parasite interactions and the immune response. Chem Immunol. 1997;66:209-30. [Medline].
Keywords
cysticercosis, tapeworm infection, tapeworms, Taenia solium, T solium, pork tapeworm, tapeworm, neurocysticercosis, extraneural cysticercosis, parenchymal neurocysticercosis, extraparenchymal neurocysticercosis, NCC, intestinal tapeworm, intestinal tapeworm infection, cysticercal encephalitis, cysticercal meningoencephalitis, tapeworm encephalitis, parasitosis, subarachnoid neurocysticercosis, ocular cysticercosis, subcutaneous cysticercosis, intramuscular cysticercosis
