# Volumetric MRI study of the brain in patients with neurocysticercosis and mesial temporal lobe epilepsy

## TL;DR

This study examines brain volume differences in patients with neurocysticercosis and mesial temporal lobe epilepsy, finding no significant volumetric changes linked to the condition.

## Contribution

The study provides new evidence that neurocysticercosis does not cause significant brain volume changes in patients with mesial temporal lobe epilepsy.

## Key findings

- No significant group differences were found in hippocampal or temporal lobe volumetrics.
- Effect sizes were small, and adjusted means showed modest variation with overlapping confidence intervals.
- NCC does not appear to cause additive or synergistic morphostructural brain changes in MTLE-HS patients.

## Abstract

Neurocysticercosis (NCC) is a common parasitic infection of the central nervous system and a known cause of focal epilepsy. Its potential role in triggering or contributing to mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE‐HS) is suggested, but the impact on brain volumetry remains unclear. This study aimed to assess volumetric differences in the brain, with a particular focus on the hippocampus and temporal lobes, in patients with NCC, MTLE, MTLE‐HS, and their combinations.

This was an observational, cross‐sectional, retrospective, single‐center exploratory study including five groups: healthy controls; isolated MTLE; isolated NCC; MTLE‐HS; and MTLE‐HS combined with NCC (MTLE‐HS plus NCC). All participants had at least one magnetic resonance imaging (MRI) examination suitable for volumetric post‐processing. Volumetric analysis was performed on cerebral cortex regions (frontal, parietal, temporal, and occipital lobes), cerebellum, total and white matter limbic system, amygdala, hippocampus, and thalamus using the T1 MultiAtlas Segmentation tool (Brain GPS©). We also assessed sensitivity by estimating the minimum detectable difference from adjusted models and performed an exploratory analysis of NCC lesion topography with Welch t‐tests on lobar/subcortical volumes.

After adjusting for age and sex, no significant group differences were found in hippocampal or temporal lobe volumetrics (all p > .10). Effect sizes were small (partial η2 ≤ .10), and MANOVA confirmed the absence of a global effect (Pillai's Trace = .114, p = .623). Adjusted means showed only modest variation with overlapping confidence intervals, indicating that differences likely reflect individual variability rather than systematic group effects.

The findings indicate that NCC, whether isolated or combined with MTLE‐HS, does not cause significant alterations in brain volume. This suggests the absence of an additive or synergistic effect of NCC on brain morphostructural changes in patients with MTLE‐HS. These results contribute to understanding the pathophysiology of epilepsy related to NCC and hippocampal sclerosis, supporting that volumetric brain changes may not underlie their association.