AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

INTRODUCTION

Section 2 of 10  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

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.

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. 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 racemose form of NCC, which appears macroscopically as groups of cysticerci, often in clusters that resemble bunches of grapes (see Image 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.

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.

Age

• Peak incidence is between ages 30 and 40 years.
• Although it appears to be the most frequent cause of seizures in children 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

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

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 and is also a complication of the disease.
    • 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 migraine-type headaches, as well as the ones associated with intracranial hypertension, can be a manifestation of NCC.
  • Intracranial hypertension
    • Most often, it is due to obstruction of cerebrospinal fluid (CSF) circulation caused by basal or ventricular cysticercosis. It may be due to large cysts displacing midline structures, 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.
  • Strokes
    • Ischemic cerebrovascular complications of NCC include lacunar infarcts 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: This causes endocrinologic disturbances.
  • 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 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.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

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

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Lab 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 big 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 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

• Skull and soft-tissue radiographs: These can be very helpful in detecting calcification in NCC; however, CT has become the most useful diagnostic procedure.
• CT scan of the brain
• • Findings depend on the location as well as on the stage of development of the parasites. In parenchymal NCC, the various stages are as follows:
  • Vesicular stage is characterized by a small, rounded, low-density area in the brain parenchyma, without edema or enhancement with contrast. Sometimes the scolex can be seen as a hyperdense dot inside the hypodensity. The vesicular form is a viable parasite.
  • Colloidal stage is characterized by a hypodense or isodense lesion with edema and a ring-enhancing pattern after administration of contrast. This is the "acute encephalitic form," manifested as a reaction by the host.
  • Calcified stage is characterized by a dead cysticercus. However, perilesional inflammation and edema may occur around already calcified cysts (see Image 2) and seems to be related to symptom relapse.
  • Transitional stages between these stages also can be seen; the pattern on CT scan is a combination of 2 stages.
  • A condition called "cysticercotic encephalitis" is characterized by intense edema, collapse of the ventricles, and multiple small lesions, usually in a degenerated state.
  • In subarachnoid and ventricular NCC, cysticerci are difficult to visualize, although complications of these forms of NCC can be seen; obstructive hydrocephalus is the most common. Some patients have large cysts visible in the Sylvian fissure, cerebellopontine cistern, and prepontine cisterns, as well as in different compartments of the ventricular system. In such cases, ventriculography or cisternography would be helpful to delineate the parasite.
• MRI
• • If the cysts are intraventricular or too small to be detected by CT scan, MRI may be helpful.
  • It is very helpful for evaluation of the surrounding edema, which can be seen with the use of a paramagnetic contrast material such as gadolinium (see Images 3-4).
  • Contrast MRI also can show changes in the meninges related to arachnoiditis or inflammation.
  • MRI is useful for the diagnosis of spinal cysticercosis when intramedullary or extramedullary disease, as well as leptomeningeal cysts, are present.
• 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.
  • Racemose 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" [Gracia and Martinez, 1999] 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

Section 6 of 10  

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• Differentials
• Workup
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• Medication
• Follow-up
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• References

Medical Care

Treatment 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 treatment 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

Section 7 of 10  

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

Drug Category: Anticysticercal medications

Two medications are currently available, praziquantel (PZQ) and albendazole. 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 cysts 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.

Drug Category: 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.

Drug Category: Glucocorticoids

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

Drug Category: 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.

Drug Category: Anti-taeniasis

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

FOLLOW-UP

Section 8 of 10  

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• Introduction
• Clinical
• Differentials
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• Treatment
• Medication
• Follow-up
• Multimedia
• References

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 NCC. 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

• NCC 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

Section 9 of 10  

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• Differentials
• Workup
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• Medication
• Follow-up
• Multimedia
• References

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

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.
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Media type:  CT

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.
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Media type:  MRI

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.
	View Full Size Image
Media type:  MRI

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

• Barinagarrementeria F, Cantu C. Neurocysticercosis as a cause of stroke. Stroke. Aug 1992;23(8):1180-1. [Medline].
• Barinagarrementeria F, Del Brutto OH. Lacunar syndrome due to neurocysticercosis. Arch Neurol. Apr 1989;46(4):415-7. [Medline].
• Bickerstaff ER, Cloake PC, Hughes B, Smith WT. The racemose form of cerebral cysticercosis. Brain. Mar 1952;75(1):1-18. [Medline].
• Bittencourt PR, Gracia CM, Martins R, et al. Phenytoin and carbamazepine decreased oral bioavailability of praziquantel. Neurology. Mar 1992;42(3 Pt 1):492-6. [Medline].
• Boecher-Schwarz HG, Hey O, Higer HP, Perneczky A. Intrasellar cysticercosis mimicking a pituitary adenoma. Br J Neurosurg. 1991;5(4):405-7. [Medline].
• Cardenas F, Quiroz H, Plancarte A, et al. Taenia solium ocular cysticercosis: findings in 30 cases. Ann Ophthalmol. Jan 1992;24(1):25-8. [Medline].
• Carpio A, Placencia M, Santillan F, Escobar A. A proposal for classification of neurocysticercosis. Can J Neurol Sci. Feb 1994;21(1):43-7. [Medline].
• Case records of the Massachusetts General Hospital. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 26-1994. A 20-year-old Philippine woman with a soft-tissue mass in the forearm. N Engl J Med. Jun 30 1994;330(26):1887-93. [Medline].
• Del Brutto OH, Sotelo J, Roman GC. Neurocysticercosis: A Clinical Handbook. Vol 1. Lisse: Swets & Zeitlinger;1988.
• 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].
• 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].
• Del Brutto OH. [Neurocisticercosis]. 1998;[Full Text].
• Del Brutto OH, Roos KL, Coffey CS, Garcia HH. Meta-analysis: Cysticidal drugs for neurocysticercosis: albendazole and praziquantel. Ann Intern Med. Jul 4 2006;145(1):43-51. [Medline].
• 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].
• Garcia HH, Gilman RH, Gonzales AE. Epidemiology of Tenia solium infection in Peru. Cysticercosis Working Group Peru. In: Garcia HH, Martinez SM. Taenia Solium Taeniasis/Cysticercosis. 2nd ed. 1999:297-305.
• Garcia HH, Martinez SM. Taenia solium/cysticercosis. Lima: Editorial Universo. 1999.
• Garcia HH, Gilman R, Martinez M, et al. Cysticercosis as a major cause of epilepsy in Peru. The Cysticercosis Working Group in Peru (CWG). Lancet. Jan 23 1993;341(8839):197-200. [Medline].
• Garcia HH, Del Brutto OH. Heavy nonencephalitic cerebral cysticercosis in tapeworm carriers. The Cysticercosis Working Group in PerĂº. Neurology. Oct 22 1999;53(7):1582-4. [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].
• Garg RK. Neurocysticercosis. Postgrad Med J. Jun 1998;74(872):321-6. [Medline].
• Garg RK. Medical management of neurocysticercosis. Neurol India. Dec 2001;49(4):329-37. [Medline].
• Gemmel M, Matyas Z, Pawlosky Z. Guidelines for surveillance, prevention and control of taeniasis/cysticercosis. Geneva: WHO. 1983.
• Grisolia JS, Wiederholt WC. CNS cysticercosis. Arch Neurol. Sep 1982;39(9):540-4. [Medline].
• Isidro-Llorens A, Dachs F, Vidal J, Sarrias M. Spinal cysticercosis. Case report and review. Paraplegia. Feb 1993;31(2):128-30. [Medline].
• Lopez-Hernandez A, Garaizar C. Childhood cerebral cysticercosis: clinical features and computed tomographic findings in 89 Mexican children. Can J Neurol Sci. Nov 1982;9(4):401-7. [Medline].
• Miller BL, Staugaitis SM, Tourtellotte WW, et al. Intra-blood-brain barrier IgG synthesis in cerebral cysticercosis. Arch Neurol. Aug 1985;42(8):782-4. [Medline].
• Monteiro L, Coelho T, Stocker A. Neurocysticercosis--a review of 231 cases. Infection. Mar-Apr 1992;20(2):61-5. [Medline].
• Proano JV, Madrazo I, Avelar F, et al. Medical treatment for neurocysticercosis characterized by giant subarachnoid cysts. N Engl J Med. Sep 20 2001;345(12):879-85. [Medline].
• Puri V, Chowdhury V, Gulati P. Myoclonus: a manifestation of neurocysticercosis. Postgrad Med J. Jan 1991;67(783):68-9. [Medline].
• Sotelo J, Guerrero V, Rubio F. Neurocysticercosis: a new classification based on active and inactive forms. A study of 753 cases. Arch Intern Med. Mar 1985;145(3):442-5. [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].
• Soto-Hernandez JL, Gomez-Llata Andrade S, Rojas-Echeverri LA, et al. Subarachnoid hemorrhage secondary to a ruptured inflammatory aneurysm: a possible manifestation of neurocysticercosis: case report. Neurosurgery. Jan 1996;38(1):197-9; discussion 199-200. [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].
• White AC. Neurocysticercosis: a major cause of neurological disease worldwide. Clin Infect Dis. Feb 1997;24(2):101-13; quiz 114-5. [Medline].
• del Brutto OH. [Neurocysticercosis]. Rev Neurol. Sep 1-15 1999;29(5):456-66. [Medline].

Article Last Updated: Oct 2, 2006