# Echoes of Dormancy: Anomic Aphasia Unveils Neurocysticercosis Reactivation in a Patient on Semaglutide

## TL;DR

A patient with a dormant parasitic brain infection experienced a rare symptom after starting a new medication, showing how metabolic treatments might reactivate old infections.

## Contribution

This case reveals a potential link between semaglutide use and reactivation of dormant neurocysticercosis, suggesting a novel interaction between metabolic drugs and immune responses.

## Key findings

- Anomic aphasia was identified as a rare manifestation of reactivated neurocysticercosis.
- Semaglutide may have contributed to NCC reactivation by affecting the protective inflammatory response.
- Treatment with antiparasitic agents and corticosteroids improved the patient's condition.

## Abstract

Neurocysticercosis (NCC), a parasitic infection caused by Taenia solium larvae, remains a leading cause of acquired epilepsy worldwide, particularly in regions with inadequate sanitation and healthcare access. We present a case of NCC reactivation in a 64-year-old female who developed anomic aphasia—a rare manifestation of NCC—decades after her initial diagnosis. The patient’s clinical course was complicated by a potential trigger of semaglutide, which potentially attenuated the protective inflammatory response maintained by astrocytes and microglia, leading to the reactivation of dormant cysts. Brain imaging confirmed localized cystic changes, and treatment with antiparasitic agents and corticosteroids led to marked clinical improvement. This case highlights the complexity of NCC reactivation, highlighting the interplay of metabolic, immune, and parasitic factors. It emphasizes the need for vigilance in managing patients with dormant infections and investigating potential risks associated with novel therapeutic agents like GLP-1 receptor agonists. Further research is essential to unravel the mechanisms linking metabolic modulation to parasitic reactivation, offering insights into prevention and treatment strategies.