Background: Experimental models of neurocysticercosis (NCC) are helpful for an improved understanding of the pathophysiological mechanisms of human diseases and for testing novel therapeutic approaches. Controlling inflammation without reducing the effectiveness of anthelmintics is an important challenge in treating neurocysticercosis. This study investigates the effects of currently used drugs (Albendazole and Dexamethasone) in treating murine extraparenchymal NCC. Methods: Twenty-two rats were inoculated with Taenia crassiceps in the subarachnoid space. The animals underwent magnetic resonance imaging to ascertain the success of infection 3 months after inoculation. The infected animals were randomly assigned to one of the three groups (five rats each): control (no treatment), Albendazole (ABZ), or Albendazole + Dexamethasone (ABZ + DXM) for 14 days. The animals were subsequently euthanised for morphological assessment 2 weeks after the end of treatment. Results: Macroscopically integrated cysts were found in all animals. The ABZ + DXM animals demonstrated lower ventricular sizes, lymphocyte infiltration rates, and immunopositivity for IL-6, with statistical differences in lymphocytes within the arachnoid region. Conclusions: This experimental model, which has previously shown similarities to human infections, is also helpful in reproducing the morphological changes upon treatment with Albendazole and Dexamethasone.

Oxidative stress is associated with several infectious diseases, as well as the severity of inflammatory reactions. The control of inflammation during parasite destruction is a target of neurocysticercosis treatment, as inflammation is strongly related to symptom severity. In this study, we investigated the presence of malondialdehyde and protein carbonyl, two by-products of reactive oxygen species (ROS), in an experimental model of extraparenchymal neurocysticercosis. Twenty male and twenty female rats were inoculated with 50 cysts of Taenia crassiceps in the subarachnoid space of the cisterna magna. Ten animals (five males and five females) were used as controls. Three months after inoculation, their brains were harvested for oxidative stress and histological assessments. Infected animals had higher scores for inflammatory cell infiltrates, malondialdehyde, and protein carbonyl. These results encourage future efforts to monitor oxidative stress status in neurocysticercosis, particularly in the context of controlling inflammation.

Purpose: To retrospectively evaluate magnetic resonance images acquired from rats subjected to a murine model of extraparenchymal neurocysticercosis. Methods: The model consisted of injecting 50 Taenia crassiceps cysticerci into the cisterna magna of Wistar rats. To validate disease induction, magnetic resonance imaging was performed, focusing on the assessment of hydrocephalus and cysts distribution throughout the cerebrospinal fluid compartments. Ventricular dilation was quantified using the frontal horn ratio (FHR), calculated by dividing the maximal width of the frontal horns by the inner-table internal diameter. Results: Intracranial abnormalities were found 63.0% of the animals, predominantly ventricular dilation (> 90%), mainly involving the lateral ventricles. The most affected compartments were the cisterna magna (85.2%) and supratentorial basal cisterns (78.8%). Cysts were identified in the cerebral convexity in 10.6% of cases and in the subcutaneous tissue in 39.2% of infected animals. The mean FHR was 0.62 ± 0.13. Higher FHR values were associated with the presence of cysts in the CSF, but not in the subcutaneous tissue ( p = 0.743). Conclusion: The translational relevance of this extraparenchymal NCC model is underscored by neuroimaging findings that closely resemble the human condition, providing a valuable platform for future mechanistic studies on pathogenesis and treatment development.