# Bilateral rhythmic stimulation as a possible modulator of meningeal lymphatic flow: a regulatory T cell–centered neuroimmune hypothesis of eye movement desensitization and reprocessing

**Authors:** Ioulia Milovanov

PMC · DOI: 10.3389/fnint.2026.1758529 · Frontiers in Integrative Neuroscience · 2026-02-18

## TL;DR

This paper proposes a new hypothesis about how EMDR therapy works by linking eye movements to changes in brain immune activity and lymphatic flow.

## Contribution

The novel contribution is a neuroimmune hypothesis linking bilateral rhythmic stimulation in EMDR to regulatory T cell activity and meningeal lymphatic dynamics.

## Key findings

- Bilateral rhythmic stimulation in EMDR may modulate autonomic balance and meningeal lymphatic flow.
- Regulatory T cells may influence microglial activation and synaptic stability through neuroimmune interactions.
- The hypothesis offers testable predictions about how behavioral interventions affect neural and behavioral outcomes.

## Abstract

Eye Movement Desensitization and Reprocessing (EMDR) is an established therapeutic intervention for post-traumatic stress disorder and related conditions, yet its neurobiological mechanisms remain incompletely understood. While prevailing models emphasize cognitive processes such as working memory taxation and memory reconsolidation, these accounts may not fully explain the durability and generalization of therapeutic effects. Here, we propose a hypothesis in which bilateral rhythmic stimulation associated with EMDR modulates neuroimmune interactions through state-dependent changes in autonomic balance and meningeal lymphatic dynamics. Within this framework, regulatory T cells are conceptualized as contributors to baseline neuroimmune tone, influencing microglial activation states, synaptic stability, and network-level regulation. By integrating findings from autonomic physiology, lymphatic biology, and neuroimmunology, this hypothesis generates testable predictions linking behavioral interventions to sustained neural and behavioral outcomes. The model is intended to guide future experimental investigation rather than assert definitive causal pathways.

## Linked entities

- **Diseases:** post-traumatic stress disorder (MONDO:0005146)

## Full-text entities

- **Genes:** P2RY12 (purinergic receptor P2Y12) [NCBI Gene 64805] {aka ADPG-R, BDPLT8, HORK3, P2T(AC), P2Y(12)R, P2Y(AC)}, TMEM119 (transmembrane protein 119) [NCBI Gene 338773] {aka OBIF}
- **Diseases:** EMDR (MESH:D015835), post-traumatic stress disorder (MESH:D013313), Autism spectrum disorder (MESH:D000067877), respiratory sinus arrhythmia (MESH:D001146), traumatic (MESH:D014947), inflammation (MESH:D007249), autism (MESH:D001321)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

22 references — full list in the complete paper: https://tomesphere.com/paper/PMC12956776/full.md

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Source: https://tomesphere.com/paper/PMC12956776