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Table of Contents    
CORRESPONDENCE
Year : 2017  |  Volume : 65  |  Issue : 4  |  Page : 924-926

Be careful while using albendazole/praziquantel in neurocysticercosis


Department of Neurology, King George Medical University, Lucknow, Uttar Pradesh, India

Date of Web Publication5-Jul-2017

Correspondence Address:
Ravindra Kumar Garg
Department of Neurology, King George Medical University, Lucknow - 226 003, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/neuroindia.NI_424_16

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How to cite this article:
Garg RK, Uniyal R, Malhotra HS. Be careful while using albendazole/praziquantel in neurocysticercosis. Neurol India 2017;65:924-6

How to cite this URL:
Garg RK, Uniyal R, Malhotra HS. Be careful while using albendazole/praziquantel in neurocysticercosis. Neurol India [serial online] 2017 [cited 2019 Aug 23];65:924-6. Available from: http://www.neurologyindia.com/text.asp?2017/65/4/924/209508




Sir,

Chatterjee and co-workers have described a very interesting case of ulnar artery thrombosis following antiparasitic treatment in an epileptic patient with a single cysticercal lesion of the brain. Asymptomatic cysts were discovered near the proximal ulnar artery.[1]

Neurocysticercosis is a common parasitic condition affecting the brain, spinal cord, eye, skin, muscles and other body parts. Neurocysticercosis is caused by the larval form of Taenia solium. In human brain, cysticercus larvae pass through four stages of evolution; each stage has a different amount of perilesional inflammation. These stages are vesicular, colloidal, granular-nodular and calcific. Inflammatory changes are often minimal in vesicular (viable) cysts. Intense inflammation is often associated with colloidal and granulo-nodular (degenerating) stages of cysts. A calcified lesion, though representing a dead parasite, may still produce an intense perilesional inflammation.[2],[3] Perilesional inflammation in and around the cysticerci is often responsible for symptoms.[4] In the brain, perilesional inflammation presents with a sort of focal encephalitis and often manifests as seizures. In other locations, for example, in the spinal cord, the parasitic inflammation causes arachnoiditis; and, in the, eye, inflammatory changes can lead to retinal detachment and blindness. In the brain, perilesional inflammation can produce focal cerebritis, ependymitis and vasculitis. Praziquantel and albendazole are the two antiparasitic drugs that are effectively used in the treatment of symptomatic neurocysticercosis.[2],[3]

Association of neurocysticercosis with cerebral vascular complications is well recognized. Vasculitis of the brain manifests with focal neurological deficits and severe disabilities. Cerebral infarction, transient ischemic attacks, and cerebral hemorrhage may occur in patients with neurocysticercosis.[5] After demise of the cysticercal larvae, massive release of parasite antigens provokes an inflammatory reaction that affects surrounding brain tissues. Vessels in the region of inflammation are also affected (innocent bystander) resulting in arteritis and subsequently stroke. Cerebral infarction is much more frequent with the subarachnoidal and racemose forms of neurocysticercosis. Cystic contents have intense antigenic properties. In a report, the authors noted a severe inflammatory reaction within the ventricular system and basal cisterns after the intraoperative cysticerci ruptured while an endoscopic transventricular removal of cyst was being attempted.[6]

Cysts are known to present in the brain and other body parts without producing symptoms for a long time. These asymptomatic cysts are liable to become symptomatic following treatment with antiparasitic drugs. A cyst may remain asymptomatic for a variable period of time ranging from one year to thirty years. In a study from Northern India, the prevalence of asymptomatic neurocysticercosis, in apparently healthy population, was estimated to be 15% of the population engaged in pig farming.[7] Among family members of symptomatic neurocysticercosis patients, the prevalence of asymptomatic neurocysticercosis was as high as 29%.[7] Significantly higher proportion of the asymptomatic population had vesicular stage of the parasite.[8] There are several reports where even a single dose, taeniacidal use of antiparasitic drugs in patients with intestinal taeniasis unravelled a hidden cyst, making the patient symptomatic. In most of these reports, otherwise asymptomatic individuals developed seizures and/or headache after taking antiparasitic drugs (praziquantel or albendazole) for the purpose of deworming [Table 1].[9],[10],[11],[12],[13]
Table 1: Reports on cases of neurocysticercosis where deworming uncovered a lesion: A review

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The common adverse effects seen in patients with symptomatic neurocysticercosis following antiparasitic therapy include fever, seizures, headache, nausea, vomiting, meningismus, increased intracranial pressure, altered sensorium and stroke. These adverse reactions are probably not due to a toxic effect of the drug but rather due to an inflammatory reaction produced by the host in response to a massive destruction of cysticerci and the release of cysticercal antigens.[14],[15],[16] In isolated instances, even calcified neurocysticercosis lesions triggered severe inflammatory reactions during the antiparasitic therapy.[17]

Subarachnoidal form and racemose form of neurocysticercosis are, in particular, more liable to develop adverse reactions because of their closeness to cerebrospinal fluid spaces. Catastrophic complications, in the form of raised intracranial pressure, hydrocephalus, chronic arachnoiditis and vasculitis, can even be life-threatening. The host's inflammatory reaction in response to an acute destruction of the parasite within the subarachnoid space may occlude the vessels surrounding the cyst. There are several reports available where antiparasitic treatment led to cerebral infarction or other inflammatory complications [Table 2].[18],[19],[20],[21],[22]
Table 2: Vascular complications and myositis in neurocysticercosis following antiparasitic treatment: Review of literature

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Anti-inflammatory drugs, particularly corticosteroids, are used to control paradoxical aggravations of inflammation following antiparasitic therapy in patients with neurocysticercosis. In patients with giant subarachnoid cysticerci, ventricular cysts, spinal cysts, numerous cerebral parenchymal cysts and in patients with disseminated cysticercosis, corticosteroids must be administered before commencement of the course of antiparasitic drugs to avoid disastrous complications.[23]

The case described by Chatterjee et al., also suggests that corticosteroids should always be administered along with antiparasitic therapy.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Chatterjee R, Chatterjee K, Sen C. Proximal ulnar artery thrombosis after cysticidal therapy: A rare complication of neurocysticercosis. Neurol India 2017;65:167-9.  Back to cited text no. 1
[PUBMED]  [Full text]  
2.
Garcia HH, Nash TE, Del Brutto OH. Clinical symptoms, diagnosis, and treatment of neurocysticercosis. Lancet Neurol 2014;13:1202-15.  Back to cited text no. 2
[PUBMED]    
3.
Nash TE, Garcia HH. Diagnosis and treatment of neurocysticercosis. Nat Rev Neurol 2011;7:584-94.  Back to cited text no. 3
[PUBMED]    
4.
Fleury A, Cardenas G, Adalid-Peralta L, Fragoso G, Sciutto E. Immunopathology in Taenia solium neurocysticercosis. Parasite Immunol 2016;38:147-57.  Back to cited text no. 4
[PUBMED]    
5.
Marquez JM, Arauz A. Cerebrovascular complications of neurocysticercosis. Neurologist 2012;18:17-22.  Back to cited text no. 5
[PUBMED]    
6.
Jiménez-Vázquez OH, Nagore N. Endoscopic evidence of ventricular and cisternal inflammatory changes after intraoperative cysticercal rupture during endoscopic third-ventriculostomy removal. Br J Neurosurg 2013;27:137-8.  Back to cited text no. 6
    
7.
Prasad KN, Verma A, Srivastava S, Gupta RK, Pandey CM, Paliwal VK. An epidemiological study of asymptomatic neurocysticercosis in a pig farming community in northern India. Trans R Soc Trop Med Hyg 2011;10:531-6.  Back to cited text no. 7
    
8.
Prasad A, Gupta RK, Pradhan S, Tripathi M, Pandey CM, Prasad KN. What triggers seizures in neurocysticercosis? A MRI-based study in pig farming community from a district of North India. Parasitol Int 2008;55:166-71.  Back to cited text no. 8
    
9.
Torres JR, Noya O, de Noya BA, Mondolfi A. Seizures and praziquantel. A case report. Rev Inst Med Trop Sao Paulo 1988;30:433-6.  Back to cited text no. 9
    
10.
Torres JR. Use of praziquantel in populations at risk of neurocysticercosis. Rev Inst Med Trop Sao Paulo 1989;31:290.  Back to cited text no. 10
    
11.
Flisser A, Madrazo I, Plancarte A, Schantz P, Allan J, Craig P, Sarti E. Neurological symptoms in occult neurocysticercosis after single taeniacidal dose of praziquantel. Lancet 1993;342:748.  Back to cited text no. 11
    
12.
Garcia HH, Gonzalez I, Mija L; Cysticercosis Working Group in Peru. Neurocysticercosis uncovered by single-dose albendazole. N Engl J Med 2007;356:1277-8.  Back to cited text no. 12
    
13.
Ramos-Zúñiga R, Pérez-Gómez HR, Jáuregui-Huerta F, del Sol López-Hernández M, Valera-Lizárraga JE, Paz-Vélez G, et al. Incidental consequences of antihelmintic treatment in the central nervous system. World Neurosurg 2013;79:149-53.  Back to cited text no. 13
    
14.
Verma A, Pauranik A, Maheshwari MC. Adverse reactions during treatment of neurocysticercosis with praziquantel. Neurol India 1987;35:344-52.  Back to cited text no. 14
    
15.
Wadia N, Desai S, Bhatt M. Disseminated cysticercosis: New observations, including CT scan findings and experience with treatment by praziquantel. Brain 1988;111:597-614.  Back to cited text no. 15
    
16.
Fong GC, Cheung RT. Caution with praziquantel in neurocysticercosis. Stroke 1997;28:1648-9.  Back to cited text no. 16
    
17.
Poeschl P, Janzen A, Schuierer G, Winkler J, Bogdahn U, Steinbrecher A. Calcified neurocysticercosis lesions trigger symptomatic inflammation during antiparasitic therapy. AJNR Am J Neuroradiol 2006;27:653-5.  Back to cited text no. 17
    
18.
Bang OY, Heo JH, Choi SA, Kim DI. Large cerebral infarction during praziquantel therapy in neurocysticercosis. Stroke 1997;28:211-3.  Back to cited text no. 18
    
19.
Woo E, Yu YL, Huang CY. Cerebral infarct precipitated by praziquantel in neurocysticercosis - A cautionary note. Trop Geogr Med 1988;40:143-6.  Back to cited text no. 19
    
20.
Arteaga-Rodríguez C1, Naréssi-Munhoz AH, Hernández-Fustes OJ. Extensive cerebral infarction and neurocysticercosis. Rev Neurol 2004;39:583.  Back to cited text no. 20
    
21.
Barinagarrementeria F, del Brutto OH. Lacunar syndrome due to neurocysticercosis. Arch Neurol 1989;46:415-17.  Back to cited text no. 21
    
22.
Takayanagui OM, Chimelli L. Disseminated muscular cysticercosis with myositis induced by praziquantel therapy. Am J Trop Med Hyg 1998;59:1002-3.  Back to cited text no. 22
    
23.
Cuello-García CA, Roldán-Benítez YM, Pérez-Gaxiola G, Villarreal-Careaga J. Corticosteroids for neurocysticercosis: A systematic review and meta-analysis of randomized controlled trials. Int J Infect Dis 2013;17:e583-92.  Back to cited text no. 23
    



 
 
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