¹Albert Einstein College of Medicine, Psychiatry, New York, United States

Background: Conventional repetitive transcranial magnetic stimulation (rTMS) requires daily sessions over several weeks, limiting accessibility and delaying clinical improvement. Accelerated TMS (aTMS), delivering multiple daily sessions in condensed timeframes, offers a strategy to increase treatment efficiency and achieve faster therapeutic effects. However, the mechanistic basis and optimal dosing parameters of accelerated protocols remain under investigation.

Aims & Objectives: The aim of this work is to elucidate the translational mechanisms underlying accelerated TMS (aTMS) and to evaluate its clinical applicability across psychiatric disorders.
The specific objectives are:

1. To examine neurobiological processes involved in aTMS, including synaptic plasticity, metaplasticity, network modulation, and anti-inflammatory effects.
2. To integrate preclinical and clinical evidence supporting accelerated dosing paradigms.
3. To identify potential moderators of treatment response, including age, circuit architecture, neurocognitive phenotype, and inflammatory profile.
4. To outline future directions for biomarker-guided personalization of aTMS within precision psychiatry.

Method: This presentation integrates data from neuroanatomy, functional connectivity, animal models, and early-phase clinical trials. Mechanisms related to synaptic plasticity, metaplasticity, cumulative dosing, network-level modulation, and immunological effects were reviewed alongside outcomes from high-dose sequential stimulation and SAINT-like accelerated paradigms.

Results: Preclinical and neuroimaging studies show that repeated high-frequency stimulation delivered at short intervals induces cumulative plasticity across cortical–subcortical circuits. Accelerated schedules enhance modulation of fronto-limbic and cortico-striatal networks, supporting rapid symptom improvement.
Growing evidence also highlights a significant anti-inflammatory effect of TMS, including reductions in peripheral inflammatory markers (e.g., IL-6, TNF-α) and modulation of microglial activity in animal studies. These immunomodulatory actions may contribute to the accelerated therapeutic response, particularly in disorders characterized by neuroinflammation such as depression and OCD.
Clinically, aTMS has shown rapid and robust antidepressant effects in treatment-resistant depression, often achieving remission within days. Emerging evidence supports its applicability in obsessive–compulsive disorder, addiction, and impulse-control disorders. Moderators such as age, brain network architecture, baseline connectivity, and inflammatory status appear to influence treatment outcomes

Discussion & Conclusions: Accelerated TMS represents an important advancement in neuromodulation, offering faster clinical improvement and broader psychiatric applications. Its therapeutic effects likely arise from synergistic mechanisms involving enhanced neuroplasticity and meaningful anti-inflammatory modulation. Translational evidence supports the development of individualized dosing strategies informed by neural and inflammatory biomarkers. Future work should refine stimulation schedules, optimize target selection, and integrate aTMS into precision psychiatry frameworks.