eMedicine Specialties > Pediatrics: General Medicine > Parasitology

Neurocysticercosis: Treatment & Medication

Author: Vinod K Dhawan, MD, FACP, FRCP(C), Professor, Department of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Professor of Medicine, Charles Drew University of Medicine and Science; Chief, Division of Infectious Diseases, MLK-Harbor Hospital
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
Contributor Information and Disclosures

Updated: Sep 14, 2009

Treatment

Medical Care

  • Drug therapy for neurocysticercosis is controversial. Several nonrandomized case series have suggested faster resolution of lesions with treatment using both praziquantel and albendazole.16 Other controlled, randomized trials have not shown such a beneficial effect in intraparenchymal CNS cysticerci. Furthermore, anthelmintic therapy may exacerbate obstruction of CSF flow, precipitating hydrocephalus. Inflammatory response associated with drug therapy may impair vision in ocular disease and may increase the risk of paralysis with spinal cord lesions.
  • Drug therapy for intraventricular cysts may prove efficacious and is currently recommended by many experts. A meta-analysis of cysticidal drug therapy with albendazole and praziquantel concluded that drug therapy results in better resolution of colloidal and vesicular cysticerci, lower risk for recurrence of seizures in patients with colloidal cysticerci, and a reduction in the rate of generalized seizures in patients with vesicular cysticerci.3
  • Medical care depends on whether the disease is simple or complicated.
    • Simple neurocysticercosis occurs in children living in nonendemic areas with only a single exposure to cysts. These children tend to have solitary cysts and fewer complications. They often can be treated symptomatically and have a favorable prognosis. In most cases, the cyst has died and cysticidal drugs are not necessary.
    • Complicated neurocysticercosis occurs in children living in endemic areas who are constantly reexposed to ova. These children may have a less favorable prognosis because of complications from increased intracranial pressure and difficulty controlling in seizures.

Surgical Care

  • Reserve neurosurgical intervention for cases of cysts that have failed to resolve with antihelminthic treatment and are causing severe neurologic sequelae. Resolution of lesions with medical management alone is superior and should be attempted first.
  • In general, indications of surgery include cysts that compress the brain and cranial nerves locally, intracranial hypertension or edema refractory to medical treatment, intraventricular cysts, spinal cysts with cord or root compression, and ocular cysts. Recently, endoscopic approaches for ventricular cysts have been developed and are now the treatment of choice for ventricular cysts with hydrocephalus.11
  • Shunting may be indicated if cysts have led to hydrocephalus.

Consultations

  • Consult a neurologist for management of seizures, increased intracranial pressure, and any other neurologic sequelae of this disease.
  • Consult an infectious disease specialist for help with a questionable diagnosis, eradication of the organism, and public health issues.
  • Consult an ophthalmologist to examine the child for any signs of subretinal cysts.
  • Consult a neurosurgeon if a biopsy or resection is called for or if the child requires shunting because of hydrocephalus.

Diet

  • Avoid reinfection and reingestion of ova from the original source.
  • No other specific diet is necessary.

Activity

  • No activity restrictions are necessary.

Medication

Anticonvulsants are of universal benefit in stopping seizures and are successful in most cases. However, the use of antihelminthic medications is quite controversial. 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. However, studies on adults performed in 1992 showed a significant decrease in seizures in those treated. In a 2002 study of 176 cases in India by Talukdar et al, lesions disappeared regardless of albendazole therapy. In a double-blind, placebo-controlled trial of albendazole in 2004, the incidence of seizures was reduced by 46% (not significant), but seizures were reduced 67% with generalization.4 No evidence suggests that treatment affects the long-term seizure outcome.

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. 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.

In a recent study in children, a combination of albendazole and praziquantel was statistically comparable to sole therapy with albendazole in eradicating lesions and preventing seizures.10

Antihelminthics

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.

Adult

400 mg PO bid for 30 d with meals
Alternatively, 3-day to 8-day course in adults with 3 or fewer cysts

Pediatric

15 mg/kg/d PO divided bid for 30 d with meals; not to exceed 800 mg/d
Recent data suggest a 1-wk course is as effective as a 4-wk course in children (Singhi, 2003)

Increase in serum and CSF metabolite concentrations with concomitant corticosteroids; possible increase in metabolism and decrease in efficacy with carbamazepine; possible increase in plasma levels when administered concurrently with dexamethasone and praziquantel

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

Administer with meals; adverse effects include headache, nausea, dizziness, vomiting, and abnormalities in liver functions; possibility of increased intracranial pressure as a result of cyst death; observe children for first 24-48 h for signs; rare adverse effects include alopecia, rash, fever, and pancytopenia; perform biweekly CBC counts and monitoring of LFTs during therapy


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.

Adult

50 mg/kg/d PO divided q6-8h for 15 d
Some evidence suggests that a 1-d course may be just as effective by administering 3 doses of 25 mg/kg at 2-h intervals after an overnight fast (Corona, NEJM, 1996)

Pediatric

<4 years: Not established
>4 years: 50 mg/kg/d PO divided q6-8h for 15 d

Substrate of CYP450; decrease in levels with concomitant corticosteroids, carbamazepine, and phenytoin; cimetidine may increase serum levels

Documented hypersensitivity; ocular cysticercosis

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adverse effects include dose-dependent, mild-to-moderate, and transient dizziness, headache, fatigue, limb pain, abdominal distress, and bloody diarrhea; advise patients not to drive during and 1 day after therapy because of dizziness; administer with meals, swallow whole (ie, do not chew or crush)

Corticosteroids

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.

Adult

4 mg IV q6h for no more than 3-4 d

Pediatric

1-1.5 mg/kg/d IV divided q4-6h for no more than 3-4 d; not to exceed 16 mg/d; tapering unnecessary unless used >4 d

Possible increased level of albendazole and decreased level of praziquantel with coadministration; possible decreased effect with concomitant use of barbiturates, phenytoin, and rifampin

Documented hypersensitivity; uncontrolled diabetes mellitus; systemic fungal infections

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

Possibility of sodium and fluid retention, hypertension, hyperglycemia, peptic ulcer, and headache; caution with hyperthyroidism, cirrhosis, nonspecific ulcerative colitis, osteoporosis, peptic ulcer, diabetes mellitus, and myasthenia gravis

Anticonvulsants

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.

Adult

Initial dose: 200 mg PO bid; increase dose at weekly intervals (by 200 mg/d) until optimal response achieved
Usual dose: 800-1200 mg/d PO divided tid/qid

Pediatric

10-20 mg/kg/d PO divided bid/tid; increase weekly to achieve optimal clinical response, administered tid/qid

Substrate of CYP3A4 and CYP3A4 isoenzyme inducer; CYP3A4 inhibitors (eg, macrolides, loratadine) can increase levels; (CYP3A4 inducers (eg, phenytoin, theophylline) can decrease levels; not for concomitant use with MAOIs; mandatory discontinuation of MAOIs for at least 14 d before carbamazepine administration; possible decreased primidone, phenobarbital, and higher carbamazepine serum concentrations with concomitant use; possible increase in carbamazepine plasma levels and toxicity when administered concurrently with cimetidine, especially in first 4 wk of therapy

Documented hypersensitivity; bone marrow depression; known sensitivity to any tricyclic compounds; MAOIs

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Possible adverse drug reactions include dizziness, drowsiness, and abdominal pain; rarely, rash, agranulocytosis, aplastic anemia, and Stevens-Johnson reaction; regular CBC counts, hepatic function tests, and Tegretol levels needed


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.

Adult

300 mg PO qhs

Pediatric

4-8 mg/kg/d PO divided bid/tid

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, omeprazole, phenacemide, phenylbutazone, succinimides, sulfonamides, trimethoprim, and valproic acid may increase toxicity with coadministration; conversely, possible decreased effects when administered concurrently with barbiturates, carbamazepine, diazoxide, rifampin, theophylline, antacids, and sucralfate; possible decreased effects of acetaminophen, amiodarone, carbamazepine, cardiac glycosides, corticosteroids, haloperidol, methadone, mexiletine, quinidine, theophylline, and valproic acid with coadministration

Documented hypersensitivity; sinoatrial block; sinus bradycardia; second-degree and third-degree AV block; Adams-Stokes syndrome

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Possible adverse reactions include gingival hyperplasia, nausea, and vomiting; rarely, Stevens-Johnson syndrome, nystagmus, slurred speech, and ataxia; check phenytoin levels regularly; discontinue if rash appears and do not resume use with exfoliative, bullous, or purpuric rash; caution with liver dysfunction; discontinue if hepatic dysfunction occurs

More on Neurocysticercosis

Overview: Neurocysticercosis
Differential Diagnoses & Workup: Neurocysticercosis
Treatment & Medication: Neurocysticercosis
Follow-up: Neurocysticercosis
Multimedia: Neurocysticercosis
References

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Further Reading

Keywords

cysticercosis, taeniasis, tapeworm diseases, parasite, parasitic infection, tapeworm, tapeworm infection, larval infection, hydrocephalus, treatment, diagnosis

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; Professor of Medicine, Charles Drew University of Medicine and Science; Chief, Division of Infectious Diseases, MLK-Harbor Hospital
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 None None

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.

Medical Editor

Ashir Kumar, MBBS, MD, FAAP, Professor, Department of Pediatrics and Human Development, College of Human Medicine, Michigan State University; Consulting Staff, Department of Pediatrics, EW Sparrow Hospital
Ashir Kumar, MBBS, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association of Physicians of Indian Origin, American Federation for Clinical Research, American Society for Microbiology, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Leslie L Barton, MD, Professor, Program Director, Department of Pediatrics, University of Arizona School 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.

CME Editor

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

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: None None None

 
 
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