Pediatric Neurocysticercosis Medication

  • Author: Vinod K Dhawan, MD, FACP, FRCP(C); Chief Editor: Russell W Steele, MD   more...
 
Updated: Jul 22, 2011
 

Medication Summary

Anticonvulsants are of universal benefit in stopping seizures and are successful in most cases.

Many children with solitary cysts are found to have calcified or edematous lesions (ie, indicative of cyst death) on imaging studies and have had excellent resolution of their lesions without antihelminthic agents.

Most experts treat children with viable cysts (ie, those that have not calcified or shown signs of edema on imaging studies) and/or multiple cysts. Current options for drug therapy of neurocysticercosis include use of albendazole or praziquantel. No evidence suggests that treatment affects the long-term seizure outcome.

Treating children with severe edema with antihelminthic medications is not recommended because of risk of causing further swelling. Destruction of cysts by antihelminthic agents can cause inflammation that results in neurologic symptoms (eg, headache, vomiting, seizures), which usually occur within 24-48 hours of initiation of therapy. Prophylactic treatment with dexamethasone is beneficial in decreasing the severity of such acute symptoms.

A single dose of praziquantel (5-10 mg/kg) can be administered to individuals found to have T solium tapeworms in their stool.

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Antihelminthics

Class Summary

These agents are used in children with viable or multiple cysts. They are used in patients with T solium tapeworms in their stool. Avoid use of antihelminthics in patients with severe edema. Parasite biochemical pathways are different from the human host; thus, toxicity is directed to the parasite, egg, or larvae. The mechanism of action varies within the drug class. Antiparasitic actions may include the following:

  1. Inhibition of microtubules causing irreversible block of glucose uptake
  2. Tubulin polymerization inhibition
  3. Depolarizing neuromuscular blockade
  4. Cholinesterase inhibition
  5. Increased cell membrane permeability, resulting in intracellular calcium loss
  6. Vacuolization of the schistosome tegument
  7. Increased cell membrane permeability to chloride ions via chloride channels alteration
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Albendazole (Albenza)

 

Is produced by Glaxo Smith Kline and was made available in the United States in June 1996. Mechanism of action is via its inhibitory effect on tubulin polymerization, which results in the loss of cytoplasmic microtubules. Albendazole is available in 200-mg tabs. To avoid inflammatory response in the CNS, the patient must also be started on anticonvulsants and high-dose glucocorticoids.

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Praziquantel (Biltricide)

 

More expensive than albendazole and probably less effective. Available in 600-mg tabs. 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 schistosome tegument. This is followed by attachment of phagocytes to parasite and death.

Tabs should be swallowed whole with some liquid during meals. Keeping tabs in mouth is not advised because of bitter taste, which can produce nausea or vomiting.

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Corticosteroids

Class Summary

These agents are useful in patients with increased intracranial pressure as a result of anthelmintic-induced cyst death and resultant inflammation.

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Dexamethasone (Decadron)

 

Begin therapy in children on the second or third day of antihelminthic therapy if symptoms arise.

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Anticonvulsants

Class Summary

These agents are used to control seizures that result from cysts. Most experts taper doses for children after 1-2 years without further seizures. Others suggest that anticonvulsants can be tapered even sooner (6 mo).

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Carbamazepine (Tegretol)

 

Appears to act by reducing polysynaptic responses and blocking posttetanic potentiation.

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Phenytoin (Dilantin)

 

Primary site of action of hydantoins, such as phenytoin, appears to be the motor cortex, where it may inhibit the spread of seizure activity. May reduce the maximal activity of brainstem centers responsible for the tonic phase of grand mal seizures.

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Contributor Information and Disclosures
Author

Vinod K Dhawan, MD, FACP, FRCP(C)  Professor, Department of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Infectious Diseases, Rancho Los Amigos National Rehabilitation Center, Downey, California.

Vinod K Dhawan, MD, FACP, FRCP(C) is a member of the following medical societies: American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and Royal College of Physicians and Surgeons of Canada

Disclosure: Pfizer Inc Honoraria Speaking and teaching

Coauthor(s)

Eric HW Kossoff, MD  Assistant Professor, Departments of Pediatrics and Neurology, Associate Director of Pediatric Neurology Residency Program, Johns Hopkins School of Medicine

Eric HW Kossoff, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, American Epilepsy Society, and Child Neurology Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Ashir Kumar, MD, MBBS, FAAP  Professor Emeritus, Department of Pediatrics and Human Development, Michigan State University College of Human Medicine

Ashir Kumar, MD, MBBS, FAAP is a member of the following medical societies: American Association of Physicians of Indian Origin and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Leslie L Barton, MD  Professor Emerita of Pediatrics, University of Arizona College of Medicine

Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Sanofi Pasteur Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD  Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

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Case 1: Coronal image MRI of a 6-year-old boy from Peru with single right frontal cyst.
Case 1: Axial image MRI of a 6-year-old boy from Peru with single right frontal cyst.
Case 2: MRI of a 40-year-old patient with a single parietal calcified cyst.
Case 2: CT scan of a 40-year-old patient with a single parietal calcified cyst.
Case 3: MRI of a 47-year-old man with 2 right parietal cysts, one with edema.
Case 3: MRI of a 47-year-old man with 2 right parietal cysts, one with edema, after the larger cyst had involuted.
Case 4: CT scan of 28-year-old woman with occipital headaches and diplopia; imaging reveals a superior cerebellar cyst, mild ventricular dilatation, and old calcifications in the right insular region. Image courtesy of Gholam Motamedi, MD.
Case 4: MRI of 28-year-old woman with occipital headaches and diplopia; MRI discerns prepontine and suprasellar lesions, as well as the superior cerebellar cyst. Image courtesy of Gholam Motamedi, MD.
MRI of multiple cysts. Image courtesy of the Centers for Disease Control and Prevention.
MRI of an 87-year-old patient from Europe with bitemporal lesions found incidentally. Image courtesy of Jon Poling, MD.
Two parietal lesions observed on autopsy specimen.
MRI of a 40-year-old woman with severe epilepsy and a left temporal single cyst.
MRI of a 21-year-old woman with left temporal lobe epilepsy and a single cyst.
 
 
 
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