eMedicine Specialties > Neurology > Neurological Infections

Neurocysticercosis

Mohammed J Zafar, MD, FAAN, Associate Clinical Professor of Medicine, Kalamazoo Center for Medical Studies, Michigan State University; NeuroImager, Premier Medical Care, PC, Premier Radiology, Kalamazoo Neurologic Institute.

Updated: Jul 1, 2009

Introduction

Background

Neurocysticercosis (NCC) is the most common parasitic disease of the nervous system and is the main cause of acquired epilepsy in developing countries. Lately, it has also been a problem in industrialized countries because of immigration of tapeworm carriers from areas of endemic disease.

See also, eMedicine article Neuroimaging in Neurocysticercosis.

Pathophysiology

NCC is the result of accidental ingestion of eggs of Taenia solium (ie, pork tapeworm), usually due to contamination of food by people with teniasis. T solium has a two-host biological cycle, with man as the definitive host carrying the intestinal tapeworm, and pig as the normal intermediate host harboring the larvae or cysticerci. It has a head (scolex) with 4 suckers and a double crown of hooks, an unsegmented neck, and a large body with several hundreds of hermaphrodite proglottids.

Cysticerci are ingested by humans through poorly cooked infected pork. Cysts evaginate in the small intestine, attach to the wall by its suckers and hooks, and develop strobila or chains of proglottids. From the distal end of the strobila, fertile eggs are excreted into the gravid proglottids. Up to 60,000 eggs may be contained in a proglottid. Pigs ingest stool contaminated with Taenia eggs, the embryos actively cross the intestinal wall, get into the bloodstream, and are transported to most tissues, where they reside as cysticerci. Larvae are found most commonly in the CNS, but they can also be located in the eye, muscle, or subcutaneous or other tissues.

Frequency

United States

NCC is mainly a disease of immigrants in the United States. Currently the disease is prevalent in the states of California, Texas, and New Mexico. It represents a major cause of morbidity among the Hispanic population. Most of the cases have been diagnosed in persons of Hispanic origin; however, because of travel to zones of endemic disease, the incidence is increasing in nonendemic countries. Native cases have been reported, presumably because of ingestion of infected food that was handled by carriers of T solium.

International

NCC is endemic in Central and South America, sub-Saharan Africa, and in some regions of the Far East, including the Indian subcontinent, Indonesia, and China, reaching an incidence of 3.6% in some regions. It is rare in Eastern and Central Europe, in North America (with the exception of Mexico), and in Australia, Japan, and New Zealand, as well as in Israel and in the Muslim countries of Africa and Asia. Cysticercosis can be seen in immigrant populations with a relatively high frequency, as in the southwest of United States and South Africa. NCC is the most common parasitic infection of the CNS. Approximately 2.5 million people worldwide carry the adult tapeworm, and many more are infected with cysticerci.

Mortality/Morbidity

No figures are available for the burden of mortality associated with NCC. However, the racemose¹ form of NCC, which appears macroscopically as groups of cysticerci, often in clusters that resemble bunches of grapes (see Media file 1), located in the subarachnoid space, is associated with poor prognosis and elevated mortality rate (over 20%). NCC-associated epilepsy is an important cause of neurological morbidity.²

Massive nonencephalitic neurocysticercosis. Photo courtesy of Cysticercosis Working Group in Peru.

Race

Subcutaneous cysticercosis is more common in Asian populations than in other peoples of other areas of endemic disease. It is not clear whether this is due to variations in parasite strain or to those in the host.

Sex

• NCC appears to affect men and women equally.
• Some evidence suggests that inflammation around parasites may be more severe in women than in men.³

Age

• Peak incidence is between ages 30 and 40 years.
• Although neurocysticercosis appears to be the most frequent cause of seizures in children⁴ and adults, the exact incidence in children is not known. The disease is increasingly commonly diagnosed with the routine use of diagnostic methods such as computed tomography (CT) and magnetic resonance imaging (MRI) of the brain.

Clinical

History

NCC is a pleomorphic disease, although it sometimes produces no clinical manifestation. This pleomorphism is due to variations in the locations of the lesions, the number of parasites, and the host's immune response.

• Many patients are asymptomatic; others report vague symptoms such as headache or dizziness.
• The onset of symptoms is usually subacute to chronic, with the exception of seizures, which present in an acute fashion. Patients may present with the following:
  • Epilepsy
    • Epilepsy is the most common presentation (70%) and is also a complication of the disease.²
    • NCC is the leading cause of adult-onset epilepsy and is probably one of the most frequent causes of childhood epilepsy in the world.
    • Seizures secondary to NCC may be generalized or partial. Simple and complex partial seizures may be associated with the presence of a single lesion. Generalized seizures are usually tonic-clonic; this is thought to be related to the presence of multiple lesions. However, irritation of focal cortical tissue by one of the lesions most probably leads to focal onset with secondary generalization. Myoclonic seizures also have been described.
  • Headache
    • Chronic headaches associated with nausea and vomiting (simulating migraines) 
    • Headaches associated with intracranial hypertension and indicative of hydrocephalus
    • Headaches due to meningitis
  • Intracranial hypertension
    • Most often, intracranial hypertension is due to obstruction of cerebrospinal fluid (CSF) circulation caused by basal or ventricular cysticercosis. It may also result from large cysts displacing midline structures, granular ependymitis, arachnoiditis, or the so-called cysticercotic encephalitis caused by the inflammatory response to a massive infestation of cerebral parenchyma with cysticerci.
    • These patients may have seizures and deterioration of their mental status, mainly due to the host's inflammatory reaction as an exaggerated response to the massive infestation.
  • Strokes⁵
    • Ischemic cerebrovascular complications of NCC include lacunar infarcts⁶ and large cerebral infarcts due to occlusion or vascular damage.
    • Hemorrhage also can occur, and has been reported as a result of rupture of mycotic aneurysms of the basilar artery.
    • Strokes may be responsible for the following signs and symptoms: paresis or plegias, involuntary movements, gait disturbances, or paresthesias.
  • Neuropsychiatric disturbances
    • These range from poor performance on neuropsychological tests to severe dementia.
    • These symptoms appear to be related more to the presence of intracranial hypertension than to the number or location of parasites in the brain.
  • Diplopia: This is a result of intracranial hypertension or arachnoiditis producing entrapment or compression of cranial nerves III, IV, or VI.
  • Hydrocephalus
    • Ten to thirty percent of patients with NCC develop communicating hydrocephalus due to inflammation and fibrosis of the arachnoid villi or inflammatory reaction to the meninges and subsequent occlusion of the foramina of Luschka and Magendie.
    • Noncommunicating hydrocephalus may be a consequence of intraventricular cysts.
• Other forms of neurocysticercosis
  • Intrasellar neurocysticercosis: Patients present with ophthalmologic and endocrinologic manifestations mimicking those of pituitary tumors.
  • Spinal NCC: This is rare. Spinal NCC may be either intramedullary or extramedullary. The latter is the most frequent and is responsible of symptoms of spinal dysfunction such as radicular pain, weakness, and paresthesias. Intramedullary presentation may cause paraparesis, sensory deficits with a level, and sphincter disturbances.
  • Ocular cysticercosis: This occurs most commonly in the subretinal space. Patients may present with decreased visual acuity, visual field defects, or monocular blindness.
  • Systemic cysticercosis: This is most common in the Asian continent. The parasites may be located in the subcutaneous tissue or muscle. Peripheral nerve involvement as well as involvement of liver or spleen have been reported.

Physical

Twenty percent or less of infected patients have abnormal neurological findings. Physical findings will depend on where the cyst is located in the nervous system and include the following:

• Cognitive decline
• Dysarthria
• Extraocular movement palsy or paresis
• Hemiparesis or hemiplegia, which may be related to stroke, or Todd paralysis
• Hemisensory loss
• Movement disorders
• Hyper/hyporeflexia
• Gait disturbances
• Meningeal signs

Causes

NCC can be acquired via fecal-oral contact with carriers of the adult tapeworm. This usually indicates the presence of a tapeworm carrier in the immediate environment (ie, household) or by accidental ingestion of contaminated food. Cases of autoingestion, in which persons with teniasis may ingest the eggs of T solium into their intestine, have been reported.

Differential Diagnoses

Other Problems to Be Considered

Brain abscess
Cerebral amebiasis
CNS tumors
CNS toxoplasmosis
CNS cryptococcosis
Mycotic granulomas
Tuberculosis of the CNS
Carotid disease and stroke

Workup

Laboratory Studies

• CSF analysis
  • Analysis of the CSF is indicated in every patient presenting with new-onset seizures or neurological deficit in whom neuroimaging shows a solitary lesion but does not offer a definitive diagnosis.
  • It is contraindicated in cases of large cysts causing severe edema and displacement of brain structures, as well as in lesions causing obstructive hydrocephalus.
  • When parasites are located in the brain parenchyma, results of CSF analysis may be normal. It is usually abnormal (50-80%) when parasites are present in the basal cisterns or in the ventricles.
  • CSF findings include mononuclear pleocytosis, normal glucose levels, elevated protein levels, high immunoglobulin G index, and in some cases presence of oligoclonal bands.
  • Eosinophilia in the CSF suggests neurocysticercosis (NCC); however, eosinophils also are elevated in neurosyphilis and tuberculosis of the CNS.
• Stool examination
  • Taeniasis and NCC coexist in 10-15% of patients with NCC. A recent study found that intestinal taeniasis is very common in patients with massive infestation with cysticerci but without cysticercotic encephalitis.
  • Tapeworm carriers may be identified by examining the stool of the relatives of a patient with cysticercosis encephalitis.
• Immunological tests
  • Enzyme-linked immunosorbent assay (ELISA) is the most widely used test of CSF; it has a sensitivity of 50% and a specificity of 65% for NCC.
  • The new enzyme-linked immunoelectrotransfer blot assay in serum is highly sensitive and specific, initially described to be 98% and 100%, respectively.
• Other tests: Peripheral leukocytosis, eosinophilia, and elevated erythrocyte sedimentation rate may be found.

Imaging Studies

• CT scan
  • CT scan is the preferred imaging study for detection of parenchymal calcifications.
  • Depending on the stage of evolution of the infestation, the findings are variable.
  • Vesicular stage (viable larva): Hypodense, nonenhancing lesions are seen.
  • Colloidal stage (larval degeneration): Hypodense/isodense lesion with peripheral enhancement and perilesional edema are seen.
  • Nodular-granular stage: Nodular-enhancing lesions
  • Cysticercotic encephalitis is characterized by diffuse edema, collapsed ventricles, and multiple enhancing parenchymal lesions.
  • During the active parenchymal stage, the scolex within a cyst may appear as a hyperdense dot.
  • Calcified  stage: When the parasite dies, nodular parenchymal calcifications are seen.
    
    

    

    CT scan of the brain in a patient who presented with an episode of generalized tonic-clonic seizure. Note the calcified lesion in the left parieto-occipital region. Subsequent evaluation confirmed the diagnosis of neurocysticercosis.

    
    
• MRI
  • MRI is the imaging modality of choice, especially for evaluation of intraventricular and cisternal/subarachnoidal cysts. Noninvasive MR cisternography or FLAIR sequences before and after inhalation of 100% oxygen may provide better detection, especially of small racemose cisternal cysts. MR is also more helpful in evaluation of cystic degeneration and pericystic inflammatory reaction. 
  • Vesicular stage: Cysts follow CSF signal; T2 hyperintense scolex may be seen. No edema. Usually no enhancement.
  • Colloidal stage: Cysts are hyperintense to CSF; surrounding edema, cyst wall enhances.
  • Nodular-granular stage: Cyst wall thickens and retracts; decrease in edema, nodular or ring enhancement.
    
    

    

    T2-weighted MRI of the brain showing the presence of increased signal as a result of edema in the right frontal region; subsequent studies found a cysticercus in that location.

    
    
    
    

    

    MRI of a patient who presented with an episode of generalized tonic-clonic seizure (also shown in Image 2). Note cyst in the left parieto-occipital region with perilesional edema.

    
    
• MR spectroscopy: Reports have shown a decrease in N -acetyl aspartate (NAA) and creatine levels and elevated lactate and metabolites such as alanine and succinate.
• Other tests: Myelogram and cerebral angiogram, as well as cisternographies and ventriculographies, may be used for the purpose of localization.

Procedures

Only in extreme cases is a brain biopsy necessary. A trial of anticysticercal drugs with follow-up imaging shortly thereafter (ie, 2 months) is recommended before considering biopsy.

Histologic Findings

• Cysticercus is a liquid-filled vesicle with a 3-layer wall and scolex, although the scolex may not be found. The parasite can adopt 3 different presentations in the nervous system—cystic, racemose, and mixed form.
  • Cystic form refers to the presence of cysts anywhere in the brain; cysts are approximately 7 mm in diameter and may be single or multiple. Their most frequent locations are the leptomeninges and the cerebral cortex.
  • Racemose¹ form refers to the presence of multiple cysts in the basal cisterns where the vesicles can have different sizes, and the cysts can be attached to the meninges; they do not have a scolex. Because of their location, they can produce hydrocephalus, which is caused by inflammation of meninges with subsequent fibrosis and obstruction. Sometimes they give the impression of an "infiltrative" aspect (Trelles "canceriform"⁷ presentation).
  • Mixed form refers to the presence of both of these 2 forms.
• While in the nervous system, the parasite goes through different stages of involution, which include the following:
  • Vesicular stage, a viable parasite with a mild inflammatory reaction
  • Colloidal stage, a parasite with a scolex in the process of degeneration and a severe inflammatory reaction around it
  • Granular stage, a parasite with a degenerated scolex and astrocytic gliosis around the cyst
  • Calcified stage, a parasite transformed into a calcified nodule with intense gliosis around the cyst

Treatment

Medical Care

Treatment of neurocysticercosis depends upon the viability of the cyst and its complications. Management includes symptomatic treatment as well as treatment directed against the parasite.

• If the parasite is dead, the treatment is directed primarily against the symptoms (eg, anticonvulsants for management of seizures). Monotherapy is usually sufficient. Duration of the treatment remains undefined, and depends neither on the type of seizure at presentation nor on other risk factors for recurrence, such as age at onset and number of seizures before diagnosis. Calcification remains an epileptogenic focus. Treating patients with viable cysts with a course of anticysticercal drugs in order to achieve better control of seizures is common practice.
• If the parasite is viable or active and the patient has vasculitis, arachnoiditis, or encephalitis, a course of steroids or immunosuppressants is recommended before the use of anticysticercal drugs. Antiparasitic treatment⁸ with albendazole is also useful in cysticercosis of the racemose type. If only parenchymal, subarachnoid, or spinal cysts are present without the complications mentioned, anticysticercal treatment can be considered, with the concomitant use of steroids, even in patients with massive brain infection. Reports indicate that multiple trials with anticysticercal treatment may be required for giant subarachnoid cysts.
• A recent double-blind, placebo-controlled study has shown that in patients with seizures due to viable parenchymal cysts, antiparasitic therapy decreases the burden of parasites and is safe and effective, at least in reducing the number of seizures with generalization.

Surgical Care

• In the presence of hydrocephalus due to intraventricular cyst, placement of a ventricular shunt is recommended, followed by surgical extirpation of the cyst and subsequent medical treatment.
• In cases of multiple cysts in the subarachnoid space (ie, the racemose form), surgical extirpation, on an urgent basis, is recommended.
• If the obstruction is due to arachnoiditis, placement of a ventricular shunt should be followed by administration of steroids and subsequent medical therapy.
• Because of frequent shunt dysfunctions due to entry of inflammatory tissue as well as parasitic debris inside the ventricular cavities, Sotelo designed a device that functions at a constant flow without the valvular mechanism of Pudenz-type shunts.
• Neuroendoscopy is a new tool with great potential for use in the management of ventricular cysticercosis.
• Surgical treatment in the particular case of medically refractory epilepsy due to a single lesion has been reported. Evaluation in an epilepsy center is indicated.

Activity

Usual restrictions for patients with epilepsy would be applicable for patients with NCC presenting with seizures.

Medication

The goals of pharmacotherapy are to reduce morbidity, prevent complications, and eradicate the infestation.

Anticysticercal medications

Two medications are currently available, praziquantel (PZQ) and albendazole.^9,10 Both eliminate the cysticerci or markedly reduce their number. Albendazole appears to be superior to PZQ and also seems to be more effective in giant cysts¹¹ and subarachnoid, intraventricular, or spinal NCC. Drugs such as dexamethasone, phenytoin, or carbamazepine may decrease plasma levels of praziquantel due to the interaction with the cytochrome P-450 microsomal system. This is not seen with albendazole (which is excreted unchanged in the urine). Simultaneous administration of dexamethasone appeared to increase plasma levels of albendazole and decreased its rate of elimination.

Praziquantel (Biltricide)

Isoquinolone that destroys scolex, produces paralysis of parasite musculature, and causes extensive integumental destruction followed by inflammatory reaction.

Dosing

Adult

50 mg/kg/d PO divided tid for 15 d
Time of treatment variable, recent studies supported short treatment period of 1 d

Pediatric

<4 years: Not established
>4 years: 50 mg/kg/d PO divided tid X 15 d

Interactions

Hydantoins may reduce serum concentrations, possibly leading to treatment failures

Contraindications

Documented hypersensitivity; ocular cysticercosis

Precautions

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 PZQ); caution while driving or performing other tasks requiring alertness on day of and following treatment; minimal increases in liver enzymes reported; hospitalization is indicated

Albendazole (Albenza)

Decreases ATP production in worm, as well as inhibits polymerization of component of microtubules, thus preventing their formation. This will cause energy depletion, immobilization, and finally death. To avoid inflammatory response in CNS, patient also must be started on anticonvulsants and high-dose glucocorticoids.

Dosing

Adult

15 mg/kg/d PO divided bid for 8-30 d; not to exceed 800 mg/d
As seen with PZQ, treatment duration varies from study to study; 8-d period advocated by most recent studies

Pediatric

Administer as in adults

Interactions

Carbamazepine may decrease efficacy

Contraindications

Documented hypersensitivity

Precautions

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

Discontinue use if LFTs increase significantly (resume when levels decrease to pretest values); abdominal pain, nausea, vomiting, diarrhea, dizziness, vertigo, fever, increased intracranial pressure, and alopecia may occur

Antiepileptics

In case of seizures with calcification, administration of a first-line antiepileptic drug is the most suitable treatment. In patients with viable cysts, the treatment needs to be combined with anticysticercal drugs. The use of newer antiepileptic medications (eg, valproic acid, lamotrigine, levetiracetam, topiramate, zonisamide) has not been evaluated in this particular condition, but they may be equally effective.

Phenytoin (Dilantin)

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

Dosing

Adult

10-20 mg/kg PO loading dose followed by 5 mg/kg/d PO qd or divided doses as maintenance dose

Pediatric

5 mg/kg/d PO loading dose followed by 5-8 mg/kg/d PO maintenance dose

Interactions

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, valproic acid

Contraindications

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

Precautions

Pregnancy

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

Precautions

Perform blood counts and urinalyses when therapy is begun and at monthly intervals for several months thereafter to monitor for blood dyscrasias; discontinue use if skin 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)

Used for management of partial seizures; blocks sodium channels and inhibits high-frequency repetitive firing. Also acts presynaptically to decrease synaptic transmission.

Dosing

Adult

100-200 mg PO qhs initially for 5-7 d, then increase by 200 mg/d (bid/qid) q5-7d to therapeutic dose; maintenance dose is 400-2400 mg/d (8-20 mg/kg/d) PO bid/qid

Pediatric

10-35 mg/kg/d PO bid/qid

Interactions

Do not coadminister with MAOIs
Danazol within last 30 days may decrease serum levels significantly (avoid whenever possible); cimetidine may increase toxicity especially if taken in first 4 wk of therapy; may decrease primidone and phenobarbital levels (their coadministration may increase carbamazepine levels)

Contraindications

Documented hypersensitivity; history of bone marrow depression; MAOIs within last 14 d

Precautions

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

Do not use to relieve minor aches or pains; caution with increased intraocular pressure; obtain CBCs and serum iron at 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

Phenobarbital (Barbita, Luminal)

Useful in treatment of partial seizures and generalized tonic-clonic seizures; enhances GABA-mediated inhibition and reduces glutamate-mediated excitation.
Elevates seizure threshold and limits spread of seizure activity.

Dosing

Adult

10-20 mg/kg IV loading dose; maintenance dose is 60-240 mg/d (1-3 mg/kg/d) PO qd

Pediatric

<12 years: 3-7 mg/kg/d PO divided bid
>12 years: Administer as in adults

Interactions

May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients with coagulation parameters stabilized on anticoagulants may require dosage adjustments if added to or withdrawn from their regimen); 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 also may occur

Contraindications

Documented hypersensitivity; severe respiratory disease; marked impairment of liver function; nephritis

Precautions

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 since adverse reactions can occur; caution in myasthenia gravis and myxedema

Glucocorticoids

These agents are used for the management of complications due to NCC.

Dexamethasone (Decadron, AK-Dex)

Concomitant medication for management of reactions to anticysticercal treatment in parenchymal, subarachnoid, or spinal cysts and in presence of vasculitis, arachnoiditis, or encephalitis.

Dosing

Adult

First 4 d of anticysticercal treatment: 10 mg IM qd, or 10 mg IM after initial treatment of PZQ; 10 mg IM qd for next 2 d
For cerebral edema: 10 mg IV followed by 4 mg q6h

Pediatric

First 4 d of anticysticercal treatment: 1-1.5 mg/kg IM q4h after initial treatment of PZQ; 1-1.5 mg/kg qd for next 2 d

Interactions

Barbiturates, phenytoin and rifampin decrease effects; decreases effect of salicylates and vaccines used for immunization

Contraindications

Documented hypersensitivity; active bacterial or fungal infection

Precautions

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 drug; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use

Diuretic (osmotic)

These agents may reduce intracranial pressure and cerebral edema by creating an osmotic gradient across an intact blood-brain barrier. As water diffuses from the brain into the intravascular compartment, intracranial pressure decreases.

Mannitol (Osmitrol, Resectisol)

May reduce subarachnoid space pressure by creating osmotic gradient between CSF in arachnoid space and plasma. Not for long-term use.

Dosing

Adult

1.5-2 g/kg/dose IV as 15-20% solution over 30 min, keeping serum osmolality of 310-320 mOsmol/kg

Pediatric

Not established

Interactions

May decrease serum lithium levels

Contraindications

Documented hypersensitivity; anuria; severe pulmonary congestion; progressive renal damage; severe dehydration; active intracranial bleeding; progressive heart failure

Precautions

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

Carefully evaluate cardiovascular status before rapid administration of mannitol, since sudden increase in extracellular fluid may lead to fulminating CHF; avoid pseudoagglutination—when blood given simultaneously, add at least 20 mEq of sodium chloride to each liter of mannitol solution; do not give electrolyte-free mannitol solutions with blood

Anti-taeniasis

Medication for taeniasis is required in patients with a concomitant intestinal infection.

Niclosamide (Niclocide)

This antiparasitic medication not absorbed in GI system. That property allows concomitant use with anticysticercal treatment.
Not available in the United States.

Dosing

Adult

2 g PO once

Pediatric

<11 kg: Not established
11-34 kg: 1 g PO once
>34 kg: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Associated with GI distress, anorexia, drowsiness, dizziness, headache, and rash

Follow-up

Further Outpatient Care

• Intracerebral lesions can cause epilepsy in the future. Administration of antiepileptic medication is the same as in any other epileptic syndrome.
• Follow-up imaging study is recommended after 2-3 months, especially in cases in which anticysticercal medications are used as a diagnostic tool. The use of imaging will guide the requirement of future trials of anticysticercal medication in cases of subarachnoid cysticercosis.

Complications

Chronic epilepsy is one of the most frequent complications of neurocysticercosis. Others include headaches, neurological deficits related to strokes, and hydrocephalus.

Prognosis

• In most patients, the prognosis is good.
• Associated seizures seem to improve after treatment with anticysticercal drugs and, once treated, seizures are controlled by a first-line antiepileptic agent. Duration of treatment, as already mentioned, is not defined.
• Patients with complications such as hydrocephalus, large cysts, multiple lesions with edema, chronic meningitis, and vasculitis are acutely ill and do not respond very well to treatment. Frequently, they have complications due to medical and surgical therapy.

Patient Education

• Neurocysticercosis is a major public health problem in developing countries and is emerging as an increasingly important condition in regions in which the disease is not endemic. Comprehensive programs of long-term intervention involve appropriate legislation, health education, modernization of swine husbandry practices, improvement of efficiency and coverage of meat inspection, provision of adequate sanitary facilities, and measures to detect and treat human tapeworm carriers.
• Political and economic realities in many communities where T solium is endemic today provide little hope that all these goals can be achieved in the near future. However, short-term approaches can be effective in the long-term, and these include educational campaigns in personal hygiene and general sanitation within the disease-endemic area.

Multimedia

Media file 1: Massive nonencephalitic neurocysticercosis. Photo courtesy of Cysticercosis Working Group in Peru.

Media file 2: CT scan of the brain in a patient who presented with an episode of generalized tonic-clonic seizure. Note the calcified lesion in the left parieto-occipital region. Subsequent evaluation confirmed the diagnosis of neurocysticercosis.

Media file 3: T2-weighted MRI of the brain showing the presence of increased signal as a result of edema in the right frontal region; subsequent studies found a cysticercus in that location.

Media file 4: MRI of a patient who presented with an episode of generalized tonic-clonic seizure (also shown in Image 2). Note cyst in the left parieto-occipital region with perilesional edema.

References

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2. 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].

3. Del Brutto OH, Garcia E, Talamas O, Sotelo J. Sex-related severity of inflammation in parenchymal brain cysticercosis. Arch Intern Med. Mar 1988;148(3):544-6. [Medline].

4. Gaffo AL, Guillen-Pinto D, Campos-Olazabal P, Burneo JG. [Cysticercosis as the main cause of partial seizures in children in Peru]. Rev Neurol. Nov 16-30 2004;39(10):924-6. [Medline].

5. Barinagarrementeria F, Cantu C. Neurocysticercosis as a cause of stroke. Stroke. Aug 1992;23(8):1180-1. [Medline].

6. Barinagarrementeria F, Del Brutto OH. Lacunar syndrome due to neurocysticercosis. Arch Neurol. Apr 1989;46(4):415-7. [Medline].

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Keywords

NCC, parasitic disease, cerebral cysticercosis, Taenia solium, taeniasis, tapeworm, teniasis, pork tapeworm, cysticerci, subcutaneous cysticercosis, epilepsy, seizures, subarachnoid cysticercosis

Contributor Information and Disclosures

Author

Mohammed J Zafar, MD, FAAN, Associate Clinical Professor of Medicine, Kalamazoo Center for Medical Studies, Michigan State University; NeuroImager, Premier Medical Care, PC, Premier Radiology, Kalamazoo Neurologic Institute.
Mohammed J Zafar, MD, FAAN is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Society of Neuroimaging, and Michigan State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Amy A Pruitt, MD, Associate Professor of Neurology, University of Pennsylvania; Attending Neurologist, Hospital of the University of Pennsylvania
Amy A Pruitt, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Florian P Thomas, MD, MA, PhD, Drmed, Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University
Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Paraplegia Society, and National Multiple Sclerosis Society
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
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The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Jorge G Burneo, MD, MSPH to the development and writing of this article.

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