Trends in prevalence and predictors of anemia among school-aged children in Tanzania: analysis of 2019-2023 cross-sectional surveys using a multilevel logistic regression model.

Vagus nerve stimulation (VNS) is an established treatment for refractory epilepsy, achieving a ≥50% reduction in seizure frequency in approximately half of patients. However, reliable predictors of treatment response have not been fully established. The thalamus is implicated in the therapeutic mechanisms of VNS. Functional neuroimaging studies have demonstrated that thalamic activation is associated with favorable VNS treatment outcomes, and that functional connectivity between the thalamus and cortical regions such as the anterior cingulate cortex, insula, or hippocampus correlates with VNS efficacy. Notably, VNS is delivered via left cervical vagus nerve stimulation in clinical practice, and some functional imaging studies have reported left-predominant thalamic activation or perfusion changes, although the extent of lateralization may vary. Anatomically, vagal afferents terminate in the nucleus tractus solitarius and relay via the parabrachial nucleus to widespread forebrain structures, including thalamic nuclei, providing a plausible pathway for thalamic neuromodulation. Epilepsy also induces structural changes in the thalamus. Thalamic atrophy has been documented across diverse epilepsy syndromes and is thought to reflect the chronic involvement of thalamic nuclei within epileptogenic networks. These structural alterations may compromise the thalamus's capacity to serve as a relay for therapeutic neuromodulation.