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Neuromodulation for treatment-resistant depression: Functional network targets contributing to antidepressive outcomes

Non-invasive brain stimulation is designed to target accessible brain regions that underlie many psychiatric disorders. One such method, transcranial magnetic stimulation (TMS), is commonly used in patients with treatment-resistant depression (TRD). However, for non-responders, the choice of an alte...

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Autores principales: Idlett-Ali, Shaquia L., Salazar, Claudia A., Bell, Marcus S., Short, E. Baron, Rowland, Nathan C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10018031/
https://www.ncbi.nlm.nih.gov/pubmed/36936612
http://dx.doi.org/10.3389/fnhum.2023.1125074
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author Idlett-Ali, Shaquia L.
Salazar, Claudia A.
Bell, Marcus S.
Short, E. Baron
Rowland, Nathan C.
author_facet Idlett-Ali, Shaquia L.
Salazar, Claudia A.
Bell, Marcus S.
Short, E. Baron
Rowland, Nathan C.
author_sort Idlett-Ali, Shaquia L.
collection PubMed
description Non-invasive brain stimulation is designed to target accessible brain regions that underlie many psychiatric disorders. One such method, transcranial magnetic stimulation (TMS), is commonly used in patients with treatment-resistant depression (TRD). However, for non-responders, the choice of an alternative therapy is unclear and often decided empirically without detailed knowledge of precise circuit dysfunction. This is also true of invasive therapies, such as deep brain stimulation (DBS), in which responses in TRD patients are linked to circuit activity that varies in each individual. If the functional networks affected by these approaches were better understood, a theoretical basis for selection of interventions could be developed to guide psychiatric treatment pathways. The mechanistic understanding of TMS is that it promotes long-term potentiation of cortical targets, such as dorsolateral prefrontal cortex (DLPFC), which are attenuated in depression. DLPFC is highly interconnected with other networks related to mood and cognition, thus TMS likely alters activity remote from DLPFC, such as in the central executive, salience and default mode networks. When deeper structures such as subcallosal cingulate cortex (SCC) are targeted using DBS for TRD, response efficacy has depended on proximity to white matter pathways that similarly engage emotion regulation and reward. Many have begun to question whether these networks, targeted by different modalities, overlap or are, in fact, the same. A major goal of current functional and structural imaging in patients with TRD is to elucidate neuromodulatory effects on the aforementioned networks so that treatment of intractable psychiatric conditions may become more predictable and targeted using the optimal technique with fewer iterations. Here, we describe several therapeutic approaches to TRD and review clinical studies of functional imaging and tractography that identify the diverse loci of modulation. We discuss differentiating factors associated with responders and non-responders to these stimulation modalities, with a focus on mechanisms of action for non-invasive and intracranial stimulation modalities. We advance the hypothesis that non-invasive and invasive neuromodulation approaches for TRD are likely impacting shared networks and critical nodes important for alleviating symptoms associated with this disorder. We close by describing a therapeutic framework that leverages personalized connectome-guided target identification for a stepwise neuromodulation paradigm.
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spelling pubmed-100180312023-03-17 Neuromodulation for treatment-resistant depression: Functional network targets contributing to antidepressive outcomes Idlett-Ali, Shaquia L. Salazar, Claudia A. Bell, Marcus S. Short, E. Baron Rowland, Nathan C. Front Hum Neurosci Neuroscience Non-invasive brain stimulation is designed to target accessible brain regions that underlie many psychiatric disorders. One such method, transcranial magnetic stimulation (TMS), is commonly used in patients with treatment-resistant depression (TRD). However, for non-responders, the choice of an alternative therapy is unclear and often decided empirically without detailed knowledge of precise circuit dysfunction. This is also true of invasive therapies, such as deep brain stimulation (DBS), in which responses in TRD patients are linked to circuit activity that varies in each individual. If the functional networks affected by these approaches were better understood, a theoretical basis for selection of interventions could be developed to guide psychiatric treatment pathways. The mechanistic understanding of TMS is that it promotes long-term potentiation of cortical targets, such as dorsolateral prefrontal cortex (DLPFC), which are attenuated in depression. DLPFC is highly interconnected with other networks related to mood and cognition, thus TMS likely alters activity remote from DLPFC, such as in the central executive, salience and default mode networks. When deeper structures such as subcallosal cingulate cortex (SCC) are targeted using DBS for TRD, response efficacy has depended on proximity to white matter pathways that similarly engage emotion regulation and reward. Many have begun to question whether these networks, targeted by different modalities, overlap or are, in fact, the same. A major goal of current functional and structural imaging in patients with TRD is to elucidate neuromodulatory effects on the aforementioned networks so that treatment of intractable psychiatric conditions may become more predictable and targeted using the optimal technique with fewer iterations. Here, we describe several therapeutic approaches to TRD and review clinical studies of functional imaging and tractography that identify the diverse loci of modulation. We discuss differentiating factors associated with responders and non-responders to these stimulation modalities, with a focus on mechanisms of action for non-invasive and intracranial stimulation modalities. We advance the hypothesis that non-invasive and invasive neuromodulation approaches for TRD are likely impacting shared networks and critical nodes important for alleviating symptoms associated with this disorder. We close by describing a therapeutic framework that leverages personalized connectome-guided target identification for a stepwise neuromodulation paradigm. Frontiers Media S.A. 2023-03-02 /pmc/articles/PMC10018031/ /pubmed/36936612 http://dx.doi.org/10.3389/fnhum.2023.1125074 Text en Copyright © 2023 Idlett-Ali, Salazar, Bell, Short and Rowland. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Idlett-Ali, Shaquia L.
Salazar, Claudia A.
Bell, Marcus S.
Short, E. Baron
Rowland, Nathan C.
Neuromodulation for treatment-resistant depression: Functional network targets contributing to antidepressive outcomes
title Neuromodulation for treatment-resistant depression: Functional network targets contributing to antidepressive outcomes
title_full Neuromodulation for treatment-resistant depression: Functional network targets contributing to antidepressive outcomes
title_fullStr Neuromodulation for treatment-resistant depression: Functional network targets contributing to antidepressive outcomes
title_full_unstemmed Neuromodulation for treatment-resistant depression: Functional network targets contributing to antidepressive outcomes
title_short Neuromodulation for treatment-resistant depression: Functional network targets contributing to antidepressive outcomes
title_sort neuromodulation for treatment-resistant depression: functional network targets contributing to antidepressive outcomes
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10018031/
https://www.ncbi.nlm.nih.gov/pubmed/36936612
http://dx.doi.org/10.3389/fnhum.2023.1125074
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