Evans, C

Friedland, JS

Garcia, HH

Gilman, RH

Emerging Infectious Diseases

PubMed

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403Vol. 3, No. 3, July–September 1997 Emerging Infectious DiseasesCommentariesControversies in the Managementof CysticercosisCysticercosis, an infection caused by larvae ofthe pork tapeworm Taenia solium in human tis-sues, is a common cause of neurologic disease inmost non-Muslim developing countries, where itaccounts for more than one-third of adult-onsetepilepsy cases (1). Cysticercosis is increasinglydiagnosed in patients in industrialized nations;persons who have never left the United States aswell as visitors to disease-endemic regions are atrisk. Traditionally considered an exotic disease,this infection now accounts for up to 2% of neuro-logic/neurosurgical admissions in southern Cali-fornia (2) and more than 1,000 cases per year inthe United States (3). Further away from disease-endemic regions, an outbreak of cysticercosisamong orthodox Jews living in New York Citywas reported after food was contaminated withT. solium  eggs by immigrant cooks infected withthe pork tapeworm (4); these carriers may havebeen completely unaware of their infections.Neurocysticercosis has been reported in AIDSpatients, but immuno-suppression does notappear to increase the incidence of this infection.Once cysticercosis is diagnosed, treatment maybe necessary, but optimal therapy and particularlythe role of cestocidal drugs is controversial. Inthis commentary, we discuss current options inthe treatment of established cysticercosis.The clinical and pathologic features of neuro-cysticercosis vary, depending on the inflam-matoryresponse around cysticerci, their number, size,and location. The presence of viable, living cysti-cerci in the central nervous system usually doesnot cause symptoms (5). In contrast, inflammationaround degenerating cysticerci may have severeconsequences, including focal encephalitis, edema,and vasculitis. The most frequent symptom isepilepsy. However, neurocysticercosis can causea wide variety of clinical syndromes—fromchronic meningitis and cranial nerve palsies tospinal infarction and symptoms due to either amass effect or, particularly in racemose disease,raised intracranial pressure. Such variable clini-cal features necessitate further investigations tomake a diagnosis before treatment.The diagnosis may be made by excision biopsyof subcutaneous cysticerci, which are found in 4%to 25% of patients with neurocysticercosis (thepercentages are higher in Asia than in LatinAmerica). However, radiologic and serologic testsare usually required for diagnosis unless biopsyof a central nervous system lesion is possible.Computed tomography visualizes living cysticercias hypodense lesions not enhanced with intra-venous contrast; a small, hyperdense scolex maybe observed within a living cyst (6). Degeneratingcysticerci which are more often symptomatic areisodense or hyperdense, and edematous inflam-mation around them usually causes ring or nodu-lar enhancement by intravenous contrast (5).Magnetic resonance imaging provides detailedimages of living and degenerating cysticerci, asseen in a heavily infected patient (Figure), butmay not detect calcified, destroyed cysticerci (3).An immunoblot diagnostic test on serum hasbeen shown to have greater than 98% sensitivityand specificity (7). However, in patients with sin-gle ring-enhancing lesions, sensitivity falls to 60%to 80%. Sensitivity is also reduced if cerebrospinalfluid rather than serum immunoblot is used.Figure. Magnetic resonance image of a patient withneurocysticercosis demonstrating multiple cysticerciwithin the brain.The treatment of established neurocys-ticercosis is controversial and probably dependson the associated inflammatory reaction as wellas clinical and pathologic features. Symptomatic404Emerging Infectious Diseases Vol. 3, No. 3, July–September 1997Commentariestherapy with conventional anticonvulsant drugsis indicated to control epilepsy. Symptoms oftenresult from self-limiting inflammation around adegenerating cysticercus (3,5). Raised intracranialpressure caused by this local reaction usuallyresponds to oral corticosteroids. Steroids havebeen given chronically in occasional cases of per-sistent intracranial inflammation. Surgery alsohas a role: a ventriculoperitoneal shunt relievesobstructive hydrocephalus, although shunt blockageis common when the cerebrospinal fluid proteinis elevated. Because inflammation associatedwith medical therapy may threaten vision, sur-gery has been used to excise intraocular cysti-cerci. Asymptomatic subcutaneous or intra-muscular cysticerci do not require treatment.Cestocidal therapy with praziquantel (50 mg/kg/day tid orally for 14 days) or albendazole (15mg/kg orally tid/bid for 8 to 15 days) acceleratesradiologic disappearance of viable intracranialcysticerci. Albendazole may have slightly greaterefficacy and is generally less expensive thanpraziquantel. Cestocidal treatment combined withsymptomatic care is associated with a goodclinical outcome (8,9). However, these nonran-domized trials were not optimally controlled, anda similarly benign clinical course has beendescribed after symptomatic treatment alone inboth adults (5) and children (10). Furthermore,randomized placebo controlled trials withselected patients have shown no clinical (11) orradiologic (12,13) benefit from the addition ofcestocidal therapy to symptomatic care. A prob-lem with cestocidal therapy is that it causesinflux of inflammatory cells around cysticerci,which is often associated with transient clinicaldeterioration (8). Rarely, this may be fatal inheavy infections, despite administration of cor-ticosteroids, a common practice to minimizeadverse effects (6). Although coadministeringcorticosteroids reduces blood levels of praziquanteland increases those of albendazole, these effectsdo not appear to be relevant clinically. Therefore,the immunologic basis has yet to be determinedfor the inflammation around cysts when they dieor are killed by cestocidal treatment (14).Although recommendations cannot yet bedefinitive, available evidence suggests that via-ble, intact cysticerci that cause epilepsy or othersymptoms can be treated with cestocidal therapy,especially if they are causing mass effect. Ifcestocidal treatment is instituted, there is noreason to avoid the use of steroids. These shouldalways be administered before cestocidal therapyis given to patients with multiple viable intra-cranial cysticerci because the sudden and simul-taneous death of these parasites would otherwisecause inflammation, which can be fatal. Incontrast, when untreated patients have neurologicsymptoms and radiologic evidence of inflammationaround a degenerating cysticercus, the parasitehas probably already died, and cestocidal therapy isunlikely to be of benefit. In such cases, an expec-tant policy is reasonable: symptomatic therapyalone for 6 to 12 weeks, unless the patient’scondition worsens. A repeat computed tomographyscan then usually shows reduction in size or dis-appearance of a degenerating cysticercus (12,13,15).If improvement has not occurred, then empiricalcestocidal chemotherapy may be considered, andpossible alternative diagnoses such as tubercu-losis should be entertained. Intracranial calci-fications and lesions that show ring enhancementon neuroimaging are not living parasites andprobably do not warrant cestocidal therapy.This approach to cestocidal therapy is contro-versial, and the results of at least one ongoing,double-blind, randomized placebo-controlled trialare keenly awaited. Even when the value of cesto-cidal therapy is firmly established or refuted,new antiinflammatory treatments will requiretherapeutic approaches to be reevaluated. Agreater understanding of the pathogenesis ofthis condition is a prerequisite to developingeffective therapy to control inflammationaround degenerating cysticerci.AcknowledgmentsThe ongoing collaboration between the authors isfunded in part by the Wellcome Trust of the United Kingdom,STD4 project PL 950004 from the European Commission,and grant number 1-U01 A135894-01 from the NationalInstitutes of Health, USA.Carlton Evans,* Hector H. Garcia,†‡ Robert H.Gilman,‡§ and Jon S. Friedland¶1*University of Cambridge Clinical School,Cambridge, United Kingdom; †Instituto deCiencias Neurologicas, Lima, Peru;‡Universidad Peruana Cayetano Heredia,Lima,Peru; §Johns Hopkins  University School of Hygieneand Public Health, Baltimore, USA; and ¶RoyalPostgraduate Medical School, HammersmithHospital, London, United Kingdom1Corresponding author1Corresponding author405Vol. 3, No. 3, July–September 1997 Emerging Infectious DiseasesCommentariesReferences  1. Garcia HH, Gilman R, Martinez M, Tsang VCW,Pilcher JB, Herrera G et al. Cysticercosis as a majorcause of epilepsy in Peru. Lancet 1993;341:197-200.  2. McCormick GF. Cysticercosis: review of 230 patients.Bulletin of Clinical Neurosciences 1985; 50:76-101.  3. Shandera WX, White AC, Chen JC, Diaz P, ArmstrongR. Neurocysticercosis in Houston, Texas. Medicine1994; 73:37-52.  4. Schantz PM, Moore AC, Munoz JL, Hartman BJ,Schaefer JA, Aron AM, et al. Neurocysticercosis in anorthodox Jewish community in New York City. N EnglJ Med 1992; 327:692-5.  5. Kramer LD, Locke GE, Byrd SE, Daryabagi J. Cerebralcysticercosis: documentation of natural history withCT. Radiology 1989; 171:459-62.  6. Wadia N, Desai S, Bhatt M. Disseminated cysticercosis:new observations, including CT scan findings andexperience with treatment by praziquantel. Brain1988; 111:597-614.  7. Tsang VCW, Garcia HH. Immunoblot diagnostic test(EITB) for Taenia solium cysticercosis and its con-tribution to the definition of this under-recognized butserious public health problem. In: Garcia HH, MartinezSM (editors). Teniasis/ Cisticercosis por T. solium.Lima: Ed. Universo; 1996. p. 259-69.  8. Sotelo J, Escobedo F, Rodriguez J, Torres B, Rubio F.Therapy of parenchymal brain cysticercosis withpraziquantel. N Eng J Med 1984; 310:1001-7.  9. Vasquez V, Sotelo J. The course of seizures aftertreatment for cerebral cysticercosis. N Engl J Med1992; 327:696-702.10. Mitchell WG, Crawford TO. Intraparenchymal cere-bral cysticercosis in children: diagnosis and treatment.Pediatrics 1988; 82:76-82.11. Carpio A, Santillan F, Leon P, Flores C, Hauser A. Isthe course of neurocysticercosis modified by treatmentwith antihelminthic agents? Arch Intern Med 1995;155:1982-8.12. Padma MV, Behari M, Misra NK, Ahuja GK. Albenda-zole in neurocysticercosis. Neurology 1994; 44:1344-6.13. Padma MV, Behari M, Misra NK, Ahuja GK.Albendazole in single CT ring lesions in epilepsy. NatlMed J India 1995; 8:255-8.14. Evans C, Gonzalez AE, Gilman RH, et al. Cysticercosis:immunology and immunotherapy. In: Rose FC (editor).Recent advances in tropical neurology. Amsterdam:Elsevier; 1996. p. 155-64.15. Singhal BS, Ladiwala U. Neurocysticercosis in India.In: Rose FC (editor). Recent advances in tropical neuro-logy. Amsterdam: Elsevier; 1996. p. 99-109.

Controversies in the management of cysticercosis

Carlton Evans

Hector H. Garcia

Robert H. Gilman

Jon S. Friedland

Directory of Open Access Journals

Controversies in the Management of Cysticercosis

Albendazole in neurocysticercosis. Neurology

Albendazole in single CT ring lesions in epilepsy.

Cerebral cysticercosis: documentation of natural history with CT. Radiology

Cysticercosis as a major cause of epilepsy in Peru. Lancet

Cysticercosis: immunology and immunotherapy.

Cysticercosis: review of 230 patients.

Disseminated cysticercosis: new observations, including CT scan findings and experience with treatment by praziquantel. Brain

Immunoblot diagnostic test (EITB) for Taenia solium cysticercosis and its contribution to the definition of this under-recognized but serious public health problem.

Intraparenchymal cerebral cysticercosis in children: diagnosis and treatment. Pediatrics

Is the course of neurocysticercosis modified by treatment with antihelminthic agents? Arch Intern Med

Neurocysticercosis in an orthodox Jewish community in New York City.

Neurocysticercosis in Houston,

Neurocysticercosis in India. In: Rose FC (editor). Recent advances in tropical neurology.

The course of seizures after treatment for cerebral cysticercosis.

Therapy of parenchymal brain cysticercosis with praziquantel.

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