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Modulating intrinsic functional connectivity with visual cortex using low‐frequency repetitive transcranial magnetic stimulation

INTRODUCTION: Intrinsic network connectivity becomes altered in pathophysiology. Noninvasive brain stimulation can modulate pathological functional networks in an attempt to restore the inherent response. To determine its usefulness for visual‐related disorders, we developed procedures investigating...

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Detalles Bibliográficos
Autores principales: Rafique, Sara A., Steeves, Jennifer K. E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8865167/
https://www.ncbi.nlm.nih.gov/pubmed/35049143
http://dx.doi.org/10.1002/brb3.2491
Descripción
Sumario:INTRODUCTION: Intrinsic network connectivity becomes altered in pathophysiology. Noninvasive brain stimulation can modulate pathological functional networks in an attempt to restore the inherent response. To determine its usefulness for visual‐related disorders, we developed procedures investigating repetitive transcranial magnetic stimulation (rTMS) protocols targeting the visual cortex on modulating connectivity associated with the visual network and default mode network (DMN). METHODS: We compared two low‐frequency (1 Hz) rTMS protocols to the visual cortex (V1)—a single 20 min session and five successive 20 min sessions (accelerated/within‐session rTMS)—using multi‐echo resting‐state functional magnetic resonance whole‐brain imaging and resting‐state functional connectivity (rsFC). We also explored the relationship between rsFC and rTMS‐induced changes in key inhibitory and excitatory neurotransmitters, γ‐aminobutyric acid (GABA) and glutamate. GABA (GABA+) and glutamate (Glx) concentrations were measured in vivo using magnetic resonance spectroscopy. RESULTS: Acute disruption with a single rTMS session caused widespread connectivity reconfiguration with nodes of interest. Changes were not evident immediately post‐rTMS but were observed at 1 h post‐rTMS. Accelerated sessions resulted in weak alterations in connectivity, producing a relatively homeostatic response. Changes in GABA+ and Glx concentrations with network connectivity were dependent on the rTMS protocol. CONCLUSIONS: This proof‐of‐concept study offers new perspectives to assess stimulation‐induced neural processes involved in intrinsic functional connectivity and the potential for rTMS to modulate nodes interconnected with the visual cortex. The differential effects of single‐session and accelerated rTMS on physiological markers are crucial for furthering the advancement of treatment modalities in visual cortex related disorders.