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Table of Contents    
Year : 2017  |  Volume : 65  |  Issue : 4  |  Page : 885-887

Commentary: Neurocysticercosis: Evolution of our understanding

Department of Neurosurgery, Madurai Medical College, Madurai, Tamil Nadu, India

Date of Web Publication5-Jul-2017

Correspondence Address:
Natarajan Muthukumar
Muruganagam, 138, Anna Nagar, Madurai - 625 020, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/neuroindia.NI_288_17

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How to cite this article:
Muthukumar N. Commentary: Neurocysticercosis: Evolution of our understanding. Neurol India 2017;65:885-7

How to cite this URL:
Muthukumar N. Commentary: Neurocysticercosis: Evolution of our understanding. Neurol India [serial online] 2017 [cited 2020 Jan 25];65:885-7. Available from:

“Mind sees only what it chooses to see”

Dan Brown – The Da Vinci Code [1]

Case reports are often used as opportunities to report the rarity of a particular facet of a disease. However, when analyzed properly, they can be a source of great deal of information if the opportunity is appropriately used to enhance our understanding of the disease.

In this issue of the journal, Sharma et al.,[2] report a patient presenting with back and leg pain, who on imaging, was found to have a multifocal, cystic lesion with peripheral contrast enhancement, with clumping of the roots of the cauda equina. The authors had made a pre-operative diagnosis of an epidermoid cyst. However, on exploration, the lesion turned out to be neurocysticercosis. The authors' treatment and approach to the patient are appropriate. However, there are many hidden pearls within this case report, which can enhance our understanding of neurocysticercosis (NCC), if one chooses to glean the necessary information from the literature.

Cysticercosis is a major public health problem in several Asian and Latin American countries.[3] Neurocysticercosis causes neurological morbidity and thereby imposes considerable economic hardship on already impoverished populations.[3]

Geography determines the clinical as well as radiological features and the outcome of NCC

NCC can affect any region of the CNS - the parenchymal and subarachnoid spaces being the most frequently affected.[4] The incidence of spinal cysticercosis varies from 1.2% to 5.8%.[4] They can be intramedullary, extramedullary- intradural, extradural or rarely even within the vertebral body.[5] It is interesting to note that there is a geographical variation in the incidence of spinal NCC (SC). Recently, Cardenas et al., compared the clinical, radiological and prognostic features of Latin American and Indian patients with NCC, especially those with SC, in a large study that involved two major centres, one in Mexico and the other in India.[4] Their study throws some interesting insights into the geographical differences in NCC. In the Mexican cohort, the incidence of the spinal form of NCC was 2.8%; it was 0.5% in the Indian cohort. In the Mexican cohort, around 30% of patients were known to harbor NCC in the cranial subarachnoid spaces/ventricles, whereas in the Indian cohort, there was no antecedent history of cranial NCC. In Mexican patients, the location of spinal NCC is more likely to be intradural-extramedullary, where as it was more likely to intramedullary in the Indian cohort. The above two findings imply that the spinal form of NCC in Mexican patients is more likely due to seeding of the cysts from the cranial subarachnoid spaces, whereas in the Indian patients, it is more likely to be hematogenous. The other major difference occurred in the pathological stage of the cyst in Mexican and Indian patients; Mexican patients were more likely to have cysts in the vesicular stage, whereas the Indian patients were more likely to have the degenerative stages (vesicular-colloidal or colloidal forms). Multiple, extramedullary cysts were more likely in Mexican than in Indian patients. More importantly, there was significant difference in the clinical outcome between the two groups: only two-thirds of the Mexican patients improved and among the remaining one-third who did not improve, there was one mortality. In the Indian cohort, there was no mortality; however, other clinical outcome measures could not be obtained in Indian patients as the patients were referred back to their local hospitals for further treatment.[4]

Relationship between cranial NCC and spinal NCC and its implications

An analysis of the literature by Cardenas et al., showed that among a series of 133 patients with NCC, in patients with the spinal form of the disease, brain cysticerci were found in 13% patients,[4] which implies that every patient with spinal cysticercosis should undergo brain imaging, as was done in the index case being reported. The same review also found a significant difference in the spinal form between Latin American and Indian patients: the parasites were extramedullary in 82% of Latin American patients whereas they were intramedullary in 62% of Indian patients.[4] This could be explained by the more frequent occurrence of subarachnoid location of the cysticerci in Latin American patients vis-à -vis the more frequent intraparenchymal location in Indian patients implying that extramedullary lesions were due to seeding from the cranial compartment whereas the intramedullary lesions were hematogenous in origin. Interestingly, the first reports of intramedullary cysticercosis to be reported in the literature were from India.[6],[7]

The relationship between cysticercosis of the basal subarachnoid spaces and spinal NCC deserves special mention. In a recent study from Peru, Callacondo et al., showed that patients with basal cisternal NCC have a 60% chance of having spinal NCC whereas patients with intraparenchymal NCC have around 3.7% chance of having spinal NCC [8] and all patients with cisternal NCC had intradural-extramedullary lesions and none had intramedullary or extradural lesions, once again reiterating that spinal subarachnoid disease in NCC is due to seeding from the basal cisterns. Interestingly, this study also showed that 80% of patients with spinal NCC were found during routine MRI screening of the spine and these patients were not symptomatic. This raises the important point that every patient with basal cisternal NCC should undergo screening of the spine to identify asymptomatic spinal dissemination, and vice- versa. This has implications for treatment, as patients with both basal cisternal and spinal subarachnoid forms of the disease have a higher chance of hydrocephalus and a less favourable outcome when compared to those with isolated cranial intraparenchymal disease.[8]

Why should the same parasitic infestation present in such diverse ways in different geographic locations and in different individuals with the same radiological finding?

This difference in presentation in different geographical locations and in individual patients might be because of any one or more of the following:

  • Genotypes of T. Solium from different parts of the world have been found to be different.[9],[10] By phylogenetic analysis of mitochondrial deoxyribonucleic acid (mtDNA) sequences, T. Solium can be divided into two genotypes: Asian and African/Latin American.[10] By analyzing the cytochromeCoxidase 1 (Cox1) of the mtDNA of the pathogen, it is possible to identify from which region of the world the infestation was acquired.[9],[10] This has implications in view of the rapidly increasing travel of people across multiple continents. It is now possible to identify by molecular profiling of the parasite recovered from the patient where the infection was acquired by the patient, and if it is from a non-endemic area, then public health authorities should be alerted to the existence of this disease to prevent its further spread. Moreover, it is also possible that the infectivity of the T. Solium may be different in different regions of the world thereby accounting for the differences in presentation and the response to treatment
  • Susceptibility of individual patients to the same infestation may be different. Thus, the host response to the infestation might be responsible for the differences noted between different geographical areas and between patients in the same geographical area with similar radiological findings. A recent study by Gupta et al., has shown the polymorphism of matrix metalloproteinase-9 to be related to the symptomatology of calcified NCC. Thus, it different in patients presenting with and without seizures.[11] Similarly Qavi and colleagues have shown that Indian patients with Toll-like receptor-4 gene polymorphisms have increased risk of disseminated cysticercosis than those without these polymorphisms.[12]

Summarizing these findings, Latin American patients have a tendency to have cisternal/ventricular forms of NCC with a greater chance of spinal dissemination especially into the spinal subarachnoid spaces with a suboptimal outcome when compared to Indian patients who tend to have more intraparenchymal forms of disease cranially with less chance of spinal NCC. If and when spinal NCC occurs in the Indian patient, it is more often intramedullary than intradural-extramedullary. A review of the literature also reveals that the overall outcome is slightly better in Indian patients than in Latin American patients. Every patient with cysticercus anywhere in the nervous system should undergo a thorough craniospinal imaging to identify asymptomatic disease in other parts of the nervous system.

As suggested by Nash et al., further studies are required to understand the basic pathophysiologic mechanisms that underlie the survival, growth and degeneration of the parasite, the nature and character of the host inflammatory response and its relationship to symptomatology and the mechanisms of actions of antihelminthic medications on the parasite and the host.[13] This is especially important as a study in South India in 2006[14] estimated a disease burden of 1 million patients in India with active epilepsy attributable to NCC. The burden caused by the spinal form of the disease on the society remains to be studied. Needless to emphasize that the ultimate answer to eliminating this disease lies not in diagnosing or treating it but in preventing this disease by appropriate health education practices in endemic areas, as has been shown by the Alexander et al.[15]

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Conflicts of interest

There are no conflicts of interest.

  References Top

Brown D. The Da Vinci Code. London; Corgi Books, 2004.  Back to cited text no. 1
Sharma S, Garg K, Agarwal D, Garg A, Sharma MC, Sharma BS, et al. Isolated primary intradural extramedullary spinal cysticercosis. Neurol India 2017;65:882-4.  Back to cited text no. 2
  [Full text]  
Rajshekar V, Joshi DD, Doanh NQ, van De N, Xiaonong Z. Taenia solium taeniosis/cysticercosis in Asia: Epidemiology, impact and issues. Acta Trop 2003:87:53-60.  Back to cited text no. 3
Cárdenas G, Guevara-Silva E, Romero F, Ugalde Y, Bonnet C, Fleury A, et al. Spinal Taenia solium cysticercosis in Mexican and Indian patients: A comparison of 30-year experience in two neurological referral centers and review of literature. Eur Spine J 2016;25:1073-81.  Back to cited text no. 4
Furtado SV, Dadlani R, Ghosal N, Rao AS.: Solitary thoracic vertebral body cysticercosis presenting with progressive compressive myelopathy. J Neurosurg Spine. 2013;18:394-7.  Back to cited text no. 5
Natarajan M, Ramasubramanian KR, Muthu AK. Intramedullary cysticercosis of the spinal cord. Surg Neurol 1976:3:157-8.  Back to cited text no. 6
Mehta DS, Malik GB, Dar J. Intramedullary cysticercosis. Neurol India 1971;19:92-4.  Back to cited text no. 7
Callacondo D, Garcia HH, Gonzales I, Escalante De, Nash TE. Cysticercosis working group in Peru: High frequency of spinal involvement in patients with basal subarachnoid neurocysticercosis. Neurology 2012;78:1394-1400  Back to cited text no. 8
Yanagida T, Yuzawa I, Joshi DD, Sako Y, Nakao M, Nakaya K, et al. Neurocysticercosis: Assessing where the infection was acquired from. J Travel Med 2010;17:206-8.  Back to cited text no. 9
Nakao M, Okamoto M, Sako Y, Yamasaki H, Nakaya K, Ito A. A phylogenetic hypothesis for the distribution of two genotypes of the pig tapeworm Taenia solium worldwide. Parasitology. 2002;124(Pt 6):657-62.  Back to cited text no. 10
Gupta RK, Awasthi R, Rathore RK, Verma A, Sahoo P, Paliwal VK, et al. Understanding epileptogenesis in calcified neurocysticercosis with perfusion MRI. Neurology 2012;78:618-25.  Back to cited text no. 11
Qavi A, Garg RK, Malhotra HS, Jain A, Kumar N, Malhotra KP, et al. Disseminated cysticercosis: Clinical spectrum, Toll-like receptor-4 gene polymorphisms and role of albendazole: A prospective follow up of 60 cases with review of 56 published cases. Medicine (Baltimore): 2016:95:e4882.  Back to cited text no. 12
Nash TE, Singh G, White AC, Rajshekar V, Loeb JA, Proaño JV, et al. Treatment of neurocysticercosis: Current status and future research needs. Neurology 2006;67:1120-27.  Back to cited text no. 13
Rajshekar V, Raghava MV, Prabakaran V, Oommen A, Muliyil J. Active epilepsy as an index of burden of neurocysticercosis in Vellore district, India. Neurology 2006:67:2135-39.  Back to cited text no. 14
Alexander AM, Mohan VR, Muliyil J, Dorny P, Rajshekar V. Changes in knowledge and practices related to taeniasis/cysticercosis after health education in a South Indian community. Int Health 2012:4:164-9.  Back to cited text no. 15


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