Experimental neurocysticercosis and demyelination

Neurocisticercose experimental e desmielinização

Dear Editor,

We read with great interest the recent article by Moura et al, titled “Demyelination in experimental intraventricular neurocysticercosis”¹. The authors are well-experienced with experimental neurocysticercosis, having previously published papers demonstrating inflammatory features in this model, as well as the effects of anti-parasitic drugs on the energetic metabolism of Taenia crassiceps^2,3,4.

In this article, the authors demonstrated the occurrence of demyelination in periventricular regions, including alterations in the hippocampus’ architecture, accompanying inflammatory patterns throughout the brain. The authors proposed good insights concerning the link between inflammation and neurodegeneration. We would like to add to the discussion the fact that dementia and cognitive impairment have been well documented in patients with neurocysticercosis, including changes in episodic verbal memory, executive functions, naming, verbal fluency, constructive praxis, and visuospatial orientation⁵. Besides that, regardless of the phase of neurocysticercosis (active or inactive), the disease may lead to a broad spectrum of cognitive abnormalities, from impairment in a single domain to dementia.⁶

The authors have achieved a good laboratory system of a commonly observed clinical condition, and this welcome model may help the current knowledge of neurocysticercosis and mesial temporal lobe changes. However, a point should be observed: the ventricle enlargement induced by the presence of cysts resembling the hydrocephalus may also have played a role in the development of demyelination.

This concern is especially important because patients with neurocysticercosis and hydrocephalus may have remission of symptoms after ventricle derivation, including reversible dementia. It is well-recognized that, in experimental models, hydrocephalus itself can cause demyelination and morphological changes in the corpus callosum and hippocampus⁷. Alternatively, the study’s observed demyelination may be a combination of both factors: inflammation and mechanical compression of the periventricular regions.

Finally, the authors referenced five experimental models of neurocysticercosis, but they omitted our model, in which cysts of Taenia crassiceps injected into the subarachnoid space of rats lead to progressive hydrocephalus and enlarged basal cisterns. In this model, the immunopositivity of aquaporin-4 is increased to compensate for cerebrospinal fluid absorption^8,9.

In both models, understanding the role of inflammation in the development of demyelination and hydrocephalus provides a roadmap for further elucidation of neurocysticercosis, a neglected but still relevant disease.

References

• ¹
  Moura VBL, Milhomem AC, Lima SB, Matos-Silva H, Sugita DM, Vinaud MC, Lino-Júnior RS. Demyelination in experimental intraventricular neurocysticercosis. Arq Neuropsiquiatr. 2020 Feb;78(2):103-11. https://doi.org/10.1590/0004-282X20190155
  » https://doi.org/https://doi.org/10.1590/0004-282X20190155
• ²
  Matos-Silva H, Reciputti BP, Paula EC, Oliveira AL, Moura VB, Vinaud MC, et al. Experimental encephalitis caused by Taenia crassiceps cysticerci in mice. Arq Neuropsiquiatr. 2012 Mar;70(4):287-92. https://doi.org/10.1590/S0004-282X2012005000010
  » https://doi.org/https://doi.org/10.1590/S0004-282X2012005000010
• ³
  Moura VBL, Lima SB, Matos-Silva H, Vinaud MC, Loyola PRAN, Lino RS. Cellular immune response in intraventricular experimental neurocysticercosis. Parasitology. 2016 Mar;143(3):334-42. https://doi.org/10.1017/S0031182015001572
  » https://doi.org/https://doi.org/10.1017/S0031182015001572
• ⁴
  Vinaud MC, Ferreira CS, Lino-Junior RS, Bezerra JCB. Taenia crassiceps: energetic and respiratory metabolism from cysticerci exposed to praziquantel and albendazole in vitro. Exp Parasitol. 2008 Nov;120(3):221-6. https://doi.org/10.1016/j.exppara.2008.07.008
  » https://doi.org/https://doi.org/10.1016/j.exppara.2008.07.008
• ⁵
  Ciampi de Andrade D, Rodrigues CL, Abraham R, Castro LH, Livramento JA, Machado LR, Leite CC, Caramelli P. Cognitive impairment and dementia in neurocysticercosis: a cross-sectional controlled study. Neurology. 2010 Apr;74(16):1288-95. https://doi.org/10.1212/WNL.0b013e3181d9eda6
  » https://doi.org/https://doi.org/10.1212/WNL.0b013e3181d9eda6
• ⁶
  Rodrigues CL, Andrade DC, Livramento JA, Machado LR, Abraham R, Massaroppe L, et al. Spectrum of cognitive impairment in neurocysticercosis: differences according to disease phase. Neurology. 2012 Mar;78(12):861-6. https://doi.org/10.1212/WNL.0b013e31824c46d1
  » https://doi.org/https://doi.org/10.1212/WNL.0b013e31824c46d1
• ⁷
  Del Bigio R, Wilson MJ, Enno T. Chronic hydrocephalus in rats and humans: white matter loss and behavior changes. Ann Neurol. 2003 Mar;53(3):337-46. https://doi.org/10.1002/ana.10453
  » https://doi.org/https://doi.org/10.1002/ana.10453
• ⁸
  Hamamoto Filho PT, Fabro AT, Rodrigues MV, Bazan R, Vulcano LC, Biondi GF, et al. Taenia crassiceps injection into the subarachnoid space of rats simulates radiological and morphological features of racemose neurocysticercosis. Childs Nerv Syst. 2017 Jan;33(1):119-23. https://doi.org/10.1007/s00381-016-3239-3
  » https://doi.org/https://doi.org/10.1007/s00381-016-3239-3
• ⁹
  Hamamoto Filho PT, Fogaroli MO, Oliveira MAC, Oliveira CC, Batah SS, Fabro AT, et al. A rat model of neurocysticercosis-induced hydrocephalus: Chronic progressive hydrocephalus with mild clinical impairment. World Neurosurg. 2019 Dec;132:e535-44. https://doi.org/10.1016/j.wneu.2019.08.085
  » https://doi.org/https://doi.org/10.1016/j.wneu.2019.08.085

Publication Dates

• Publication in this collection
  27 July 2020
• Date of issue
  Aug 2020

History

• Reviewed
  12 Feb 2020
• Received
  01 Mar 2020
• Accepted
  11 Mar 2020