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Intraventricular neurocysticercosis: Presentation, diagnosis andmanagement
作者:天天论文网 日期:2016/8/25 9:12:06 点击:

1. Introduction

Neurocysticercosis is the most important helminthic centralnervous system (CNS) infection worldwide and increasing travel andmigration has led to a growing number of patients being diagnosedin non-endemic countries[1]. The majority of the published literaturerelates to the parenchymal form of the disease, and there is a paucityof epidemiological studies and high quality evidence to guide themanagement of the intraventricular variant.Cysticercosis occurs when eggs from Taenia solium (T. solium),the pork tapeworm, are ingested by humans who become dead-endintermediate hosts. Oncospheres migrate to various tissues, mostcommonly the CNS, eyes, muscles and subcutaneous tissues, andonce fully developed as viable cysts, go through three consecutivedistinct stages in the process of degeneration: colloidal, granularand calcified forms[2]. In intraventricular neurocysticercosis, thelarvae reach the cerebral ventricles via the choroid plexus andcause symptoms either from obstructing CSF flow, ependymitis orboth[3,4].No recent population based prospective data is available onthe frequency and pattern of intraventricular involvement inneurocysticercosis. Several studies, including the largest seriesavailable, were done prior to the introduction of MRI and CTscanning, and most were from non-endemic countries. The majorityof recent publications are from neurosurgical journals, so significantreferral bias can be expected since parenchymal neurocysticercosisis mainly managed medically and is less likely to involve surgicalconsultation. Intraventricular disease has been reported to occurin between 7.3% and 61.3% of cases of neurocysticercosis[3,5,6].Cysts are most often found in the fourth ventricle (range 43%-70%)followed by the lateral (11%-43%) and third (1%-29%) ventricleswith a minority in the Sylvean aqueduct (7%-9%)[3,5,7-9]. Comparedto parenchymal neurocysticercosis, patients with intraventriculardisease have a worse overall outcome and most deaths occur in thissubgroup[10]. We report two cases of intraventricular neurocysticercosis thatillustrate the natural history, diagnostic and management issues.

2. Case report 1

A 30 year old Indonesian female presented in 2004 with acuteheadache, fever and confusion. On examination she had neckstiffness with no focal motor or sensory deficits. She had aleucocytosis of 18×109 white cells per litre, of which 17×109 wereneutrophils, and blood tests including HIV serology were otherwiseunremarkable. A CT scan showed moderate dilatation of lateral andthird ventricles, a normal sized fourth ventricle and effacement of allcerebral sulci (Figure 1a).Figure 1. Findings on imaging and histopathology in two cases ofneurocysticercosis.a: CT scan of brain (Case 1) demonstrating dilated lateral and thirdventricles as well as effaced cerebral sulci; b: Histopathological examination,haematoxylin and eosin stain at magnification×100 (Case 1) showing threedistinct layers consistent with a T. solium cyst: a cuticular layer with hair-likemicrotrichia, a middle cellular layer and an inner reticular layer with focalcalcification; c: MRI brain (Case 2) identifying a bilobed cyst in the foramenof Monro and severe obstructive hydrocephalus; d: CT scan of brain (Case 2)after relief of hydrocephalus showing multiple tiny calcifications throughoutboth hemispheres.Empiric treatment for bacterial meningitis was started andemergency external ventricular drains were inserted into bothlateral ventricles. CSF collected at the time of drain insertioncontained 6×106 white cells per litre of which 5×106 werepolymorphonuclear cells and no organisms were identified on Gramstain or standard bacterial culture. The CSF levels of glucose andprotein were 4.4 mmol/L and 0.09 g/L respectively.The patient’s symptoms improved after drain insertion and asubsequent MRI scan showed mild residual dilatation of the lateralventricles but the third and fourth ventricles were normal in size andCSF flow studies were normal. A post-operative lumbar punctureshowed a mild pleocytosis of 33×106 white cells per litre, with 78%lymphocytes. The glucose concentration was normal at 3.6 mmol/Land protein was normalising at 0.44 g/L. Culture for bacteria, fungiand mycobacteria were all negative.On endoscopic third ventriculostomy a large cyst with a whitemembranous wall was found protruding through the foramen ofMonro. Histopathological examination of the cyst was consistentwith cysticercosis (Figure 1b). Serum testing for cysticercosis IgGwith an enzyme-linked immunosorbent assay (ELISA) was negative(Diagnostic Automation Inc., California, USA).

3. Case report 2

A 50 year old female from Punjab, India was admitted in 2013 withtwo days of headache, nausea, irritability and confusion. She wasafebrile without focal neurological deficits and blood tests includingfull blood count, liver and renal functions were normal.The patient had been living in Australia for 30 years with frequenttrips to India to visit family. Twenty years previously she had beendiagnosed with parenchymal cysticercosis and had a viable cyst inthe right biceps muscle which was removed. She had a brief periodof dysphasia and left arm weakness at the time of diagnosis, butthese symptoms resolved.At the time of the recent presentation a MRI scan revealed a16 mm×18 mm bilobed cystic lesion in the foramen of Monro,with minimal surrounding enhancement and severe obstructivehydrocephalus. No scolex was seen (Figure 1c). The cyst wasremoved endoscopically, an external ventricular drain was insertedand her symptoms resolved. Cerebrospinal fluid sampled at the timeof surgery contained no white cells. Histopathological examinationshowed three distinct layers consistent with cysticercosis. Noserological tests were performed on serum or cerebrospinal fluid asa conclusive histopathological diagnosis was made. A post-operativeCT scan demonstrated resolution of the hydrocephalus and multipletiny calcifications scattered throughout cerebral and cerebellarhemispheres bilaterally consistent with calcified cysts (Figure 1d).

4. Discussion

Management of intraventricular neurocysticercosis is distinctfrom the parenchymal form for which most evidence has beenpublished[11,12]. Guidelines have not been validated in this subgroupof patients and as a consequence, management is mostly based onsmaller case series and expert opinion.As exemplified by our cases, intraventricular neurocysticercosiscommonly presents with acute obstructive hydrocephalus secondaryto either cyst entrapment in narrow foramina or ependymitis[3,4].Headache is reported in nearly all patients and other commonpresentations include nausea, vomiting, decreased visual acuity,altered mental status and cranial nerve palsies[3,5,7-9]. The diagnosis of intraventricular neurocysticercosis is mostoften made radiologically and MRI is considered the most usefulmodality although no direct comparison has been made with othertechniques. Increased T1 and T2 signal of the cyst wall is usuallyseen, although cysts are sometimes missed as seen in Case 1[3,7].The visualisation of a scolex is diagnostic[12]. Enhancement withgadolinium and increased intensity of cyst content on a T1-weightedsequence indicates cyst involution in either the colloidal or granularstage which is often associated with ependymitis[3]. A disadvantageof MRI scanning is that its sensitivity for calcified lesions is poorcompared to CT as seen in Case 2 where these were only apparent ona CT scan after removal of the intraventricular cyst. In the absence ofa visualised scolex, intraventricular cysticercosis can be mistaken fora benign colloid cyst as was the case in Case 2. If a MRI scan doesnot reveal a cyst and there is suspicion of neurocysticercosis, CTventriculography or neuroendoscopic exploration may be warranted.This was illustrated in Case 1, where the cyst only became apparentduring endoscopy.The inflammatory process in neurocysticercosis varies markedlywith parasite location[13]. The interpretation of biochemical andserological tests on blood and CSF in intraventricular disease istherefore problematic since most evidence for their use come fromstudies in patients with parenchymal lesions.The current antibody test of choice is an immunoblot assay usingT. solium antigens on serum or CSF samples[14]. The performanceof this test in patients with intraventricular disease has not beenadequately studied, although the sensitivity is likely around 80%based on the analysis of small subgroups of patients in the originalstudies[15]. It is unclear if the test performs differently on serum andCSF samples and a major drawback of antibody tests is the inabilityto distinguish between active or past infection in patients whotypically come from high-prevalence regions[14].Direct detection of T. solium antigen has the advantage of beingassociated with active infection (viable, colloid and granular stages)and disease severity, and the best studied method is an ELISA usinga monoclonal antibody against the Taenia saginata (beef tapeworm)HP10 antigen[14]. Studies on both serum and CSF have shown ahigh specificity for viable cysts although some have reported a lowersensitivity (21.4%-94.1%) compared to antibody assays[16,17]. Inaddition, antigenaemia predicts the presence of viable cysts in patientswho only have calcified lesions on CT making it useful in settingswhere MRI is not available[18]. In intraventricular neurocysticercosisthe antigen levels are often higher, specificity is close to 100% andserial monitoring with the HP10 assay is a useful way of confirmingthe disappearance of viable cysts with treatment[17]. Applyingthe antigen detection assay to CSF is unlikely to result in bettersensitivity and specificity than when used on serum[17].Detection of T. solium specific DNA in CSF by polymerasechain reaction has been studied in a small number of patients withintraventricular neurocysticercosis where it had variable sensitivity(71%-97%) using different primers[14,16]. Larger studies are stillneeded to confirm its use in intraventricular disease, and its use islimited by cost in most endemic areas.A CSF pleocytosis, which is absent in up to one third of cases,is usually below 500×106 cells per litre and consists mainly oflymphocytes and infrequently eosinophils[5]. These changes havebeen found to be more marked when measured by lumbar puncturecompared to sampling directly from ventricles.Histopathological demonstration of T. solium cysts is an absolutediagnostic criterion in parenchymal neurocysticercosis and althoughthese criteria are not validated for intraventricular disease, this washow the diagnosis was confirmed in both our cases[12]. If only themembranous structures are found, they include an outer eosinophiliclayer, a middle cellular layer with between one and three rows oflymphocyte-like cells and finally an inner reticular layer. Becausethe scolex and membrane lose their distinct features during thedegeneration process, a histopathological diagnosis is limited to theviable stage.The treatment of neurocysticercosis includes antihelmintic drugsand surgical resection of lesions as well as symptomatic treatmentwith analgesia, anti-inflammatory drugs and anti-epileptics.Surgical intervention is usually warranted acutely in intraventricularneurocysticercosis to relieve pressure and remove cysts[4].Traditionally, treatment comprised of emergency shunt placementand cyst removal by open craniotomy allowing for antihelmintictreatment, which generally has poor efficacy. Neuroendoscopiccyst resection with ventriculostomy with or without placementof an external ventricular drain or permanent shunt has nowbecome the surgical treatment of choice, resulting in lesscomplications and higher cure rates and this may be curative withoutantihelmintics[5,6,8,9]. Ventriculostomy at the time of procedure isoften enough to relieve hydrocephalus without external drainagewhich carries a risk of bacterial infection, although it is still neededin patients with extensive disease and ependymitis. When a shuntis placed there is a high risk of shunt failure by blockage andadministration of antihelmintic therapy reduces this.No trials or guidelines are available on the antihelmintic treatmentof the intraventricular form of neurocysticercosis and it has not beendetermined if its use improves outcome when added to surgery.Although medical therapy alone has been reported to lead toresolution of mild cases without significant hydrocephalus, repeatcourses are often necessary. Most clinicians follow the guidelinesfor parenchymal neurocysticercosis from the American Academyof Neurology which recommends albendazole (15 mg/kg/d for 8 d)and either dexamethasone or prednisolone[11]. Praziquantel 50 mg/kg/d for 15 d is an alternative. Although prolonged treatment withalbendazole has not been shown to improve efficacy, increasingthe dose to 30 mg/kg/d was safe and more effective in a smallrandomised trial in patients with extraparenchymal disease but theseresults need confirmation in larger studies[19]. Treatment with antihelmintics may lead to a paradoxical worseningof symptoms or unmask previously undiagnosed neurocysticercosisif treatment is given for another helminthic infection. Treatmentshould therefore be given under observation in hospital withconcomitant corticosteroid administration and in this setting it isthought to be safe[20]. Moderate doses of either dexamethasone(0.1 mg/kg/d) or prednisolone (1 mg/kg/d) are usually given forthe duration of antihelmintic treatment but the dose and durationmay have to be increased in cases with marked symptoms or a largenumber of viable cysts. Corticosteroids have been shown to reducethe plasma level of praziquantel supporting the preferential use ofalbendazole.

5. Conclusions

Intraventricular disease occurs in a significant minority ofpatients with neurocysticercosis, which is no longer an infectionthat is restricted geographically to resource-poor regions. Thepresentation is with features of raised intracranial pressure and theuntreated the mortality is high. The diagnosis is based on imagingwith MRI, but serological tests, PCR, histopathology and directsurgical visualisation are important supplementary diagnostic tools.Treatment is mainly surgical, preferably using a neuroendoscopictechnique, but patients should receive antihelmintic treatment withconcomitant corticosteroids to reduce incidence of shunt failure if aventricular shunt is inserted and to treat undiagnosed viable lesionselsewhere.

Conflict of interest statement

We declare that we have no conflict of interest.

References

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[3] Cuetter AC, Andrews RJ. Intraventricular neurocysticercosis: 18consecutive patients and review of the literature. Neurosurg Focus 2002;12: e5.

[4] Sinha S, Sharma BS. Intraventricular neurocysticercosis: a review ofcurrent status and management issues. Br J Neurosurg 2011; 26: 305-309.

[5] Cuetter AC, Garcia-Bobadilla J, Guerra LG, Martinez FM, Kaim B.Neurocysticercosis: focus on intraventricular disease. Clin Infect Dis 1997;24: 157-164.

[6] Rangel-Castilla L, Serpa JA, Gopinath SP, Graviss EA, Diaz-Marchan P,White AC. Contemporary neurosurgical approaches to neurocysticercosis.Am J Trop Med Hyg 2009; 80: 373-378.

[7] Citow JS, Johnson JP, McBride DQ, Ammirati M. Imaging features andsurgery-related outcomes in intraventricular neurocysticercosis. NeurosurgFocus 2002; 12: e6.

[8] Goel RK, Ahmad FU, Vellimana AK, Suri A, Chandra PS, Kumar R, etal. Endoscopic management of intraventricular neurocysticercosis. J ClinNeurosci 2008; 15: 1096-1101.

[9] Husain M, Jha DK, Rastogi M, Husain N, Gupta RK. Neuro-endoscopicmanagement of intraventricular neurocysticercosis (NCC). Acta Neurochir2007; 149: 341-346

.[10] DeGiorgio CM, Houston I, Oviedo S, Sorvillo F. Deaths associated withcysticercosis. Report of three cases and review of the literature. NeurosurgFocus 2002; 12: e2.

[11] Baird RA, Wiebe S, Zunt JR, Halperin JJ, Gronseth G, Roos KL.Evidence-based guideline: Treatment of parenchymal neurocysticercosis:report of the guideline development subcommittee of the AmericanAcademy of Neurology. Neurology 2013; 80: 1424-1429.

[12] Del Brutto OH. Diagnostic criteria for neurocysticercosis, revisited.Pathog Glob Health 2012; 106: 299-304.

[13] Fleury A, Escobar A, Fragoso G, Sciutto E, Larralde C. Clinicalheterogeneity of human neurocysticercosis results from complexinteractions among parasite, host and environmental factors. Trans R SocTrop Med Hyg 2010; 104: 243-250.

[14] Rodriguez S, Wilkins P, Dorny P. Immunological and moleculardiagnosis of cysticercosis. Pathog Glob Health 2012; 106: 286-98.

[15] Proaño-Narvaez JV, Meza-Lucas A, Mata-Ruiz O, García-JerónimoRC, Correa D. Laboratory diagnosis of human neurocysticercosis:double-blind comparison of enzyme-linked immunosorbent assay andelectroimmunotransfer blot assay. J Clin Microbiol 2002; 40: 2115-2118.

[16] Michelet L, Fleury A, Sciutto E, Kendjo E, Fragoso G, Paris L, et al.Human neurocysticercosis: comparison of different diagnostic tests usingcerebrospinal fluid. J Clin Microbiol 2011; 49: 195-200.

[17] Rodriguez S, Dorny P, Tsang VCW, Pretell EJ, Brandt J, Lescano AG,et al. Detection of Taenia solium antigens and anti-T. solium antibodiesin paired serum and cerebrospinal fluid samples from patients withintraparenchymal or extraparenchymal neurocysticercosis. J Infect Dis2009; 199: 1345-1352.

[18] Zea-Vera A, Cordova EG, Rodriguez S, Gonzales I, Pretell EJ, CastilloY, et al. Parasite antigen in serum predicts the presence of viable brainparasites in patients with apparently calcified cysticercosis only. ClinInfect Dis 2013; 57: e154-e159.

[19] Gongora-Rivera F, Soto-Hernandez JL, Gonzalez Esquivel D, CookHJ, Marquez-Caraveo C, Hernandez Davila R, et al. Albendazole trialat 15 or 30 mg/kg/d for subarachnoid and intraventricular cysticercosis.Neurology 2006; 66(3): 436-438.

[20] Nash TE, Mahanty S, Garcia HH. Corticosteroid use inneurocysticercosis. Expert Rev Neurother 2011; 11: 1175-1183.



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