Pediatric Neurocysticercosis Medication

Updated: Mar 03, 2015
  • Author: Vinod K Dhawan, MD, FACP, FRCPC, FIDSA; Chief Editor: Russell W Steele, MD  more...
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Medication

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

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.

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.

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).

Carbamazepine (Tegretol)

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

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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