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Updated: Jun 4, 2025

Combining Transcranial Magnetic Stimulation and fMRI to Examine the Default Mode Network
Published on: December 28, 2010
Therapeutic DBS for OCD Suppresses the Default Mode Network
Natalya Slepneva1,2, Genevieve Basich-Pease1,2, Lee Reid2,3
1Weill Institute for Neurosciences, University of California, San Francisco, California, USA.
Deep brain stimulation (DBS) for obsessive-compulsive disorder (OCD) may work by suppressing the default mode network (DMN). This circuit-based treatment for OCD may interrupt brain network communication via structural white matter connections.
Area of Science:
- Neuroscience
- Neurosurgery
- Psychiatry
Background:
- Deep brain stimulation (DBS) of the anterior limb of the internal capsule (ALIC) is a circuit-based treatment for severe, refractory obsessive-compulsive disorder (OCD).
- The precise mechanism by which DBS alleviates OCD symptoms is not fully understood, though it is hypothesized to involve modulation of cortico-striato-thalmo-cortical networks.
Purpose of the Study:
- To investigate the network effects of ALIC DBS in patients with severe OCD.
- To explore the relationship between functional brain activity changes and structural connectivity during DBS treatment.
Main Methods:
- Functional MRI (fMRI) with an On/Off cycling paradigm was used in five participants (3 responders, 2 non-responders) undergoing ALIC DBS for OCD.
- Diffusion-weighted imaging (DWI) and tractography were employed to assess structural connectivity between active DBS contacts and brain networks.
Main Results:
- Therapeutic ALIC DBS configurations suppressed BOLD activity in regions including the orbitofrontal cortex, dorsomedial prefrontal cortex, and subthalamic nuclei.
- Many suppressed regions were part of the default mode network (DMN).
- The stimulation field from therapeutic configurations showed significant structural connectivity to core DMN nodes.
Conclusions:
- ALIC DBS for OCD may exert therapeutic effects by suppressing the DMN.
- This suppression is hypothesized to occur through the interruption of communication along structural white matter tracts connected to the DBS electrodes.
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