Posttraumatic Stress Disorder Is Associated with α Dysrhythmia across the Visual Cortex and the Default Mode Network
Kevin J Clancy1, Jeremy A Andrzejewski2, Jessica Simon2
1Department of Psychology, Florida State University, Tallahassee, FL 32304 wenli@psy.fsu.edu clancy@psy.fsu.edu.
Posttraumatic stress disorder (PTSD) is linked to reduced alpha (α) brainwave activity in the visual cortex and default mode network (DMN), correlating with hypervigilance. These α deficits may unify DMN and sensory processing anomalies in PTSD.
Area of Science:
- Neuroscience
- Psychiatry
- Brain Oscillations
Background:
- Posttraumatic stress disorder (PTSD) is associated with distinct alterations in brain activity, including the default mode network (DMN) and alpha (α) oscillations.
- Previous research suggests α oscillations play a role in DMN function through synchronization and sensory inhibition, but a unifying pathology in PTSD remains unclear.
Purpose of the Study:
- To investigate a unifying hypothesis of α deficits within the visual cortex-DMN system as a neural underpinning of PTSD.
- To examine the relationship between α activity, DMN function, and hypervigilance symptoms in patients with PTSD compared to generalized anxiety disorder (GAD) and healthy controls (HCs).
Main Methods:
- High-density electroencephalogram (hdEEG) was recorded from 25 PTSD patients, 24 GAD patients, and 20 HCs during eyes-open resting state (S-RS) and a modified resting state (M-RS) with visual stimuli.
- Intracortical α activity (power and Granger causality) was analyzed using exact low-resolution electromagnetic tomography (eLORETA).
- Analyses focused on the visual cortex (VC), posterior cingulate cortex (PCC), and medial prefrontal cortex (mPFC) as key DMN hubs.
Main Results:
- Patients with PTSD exhibited significantly reduced α power in the VC, PCC, and mPFC compared to GAD and HC groups during both resting states.
- Reduced α power in these regions correlated with the severity of hypervigilance symptoms in PTSD patients.
- During M-RS, PTSD patients showed decreased α-frequency directed connectivity from the VC to DMN hubs (PCC, mPFC) and within the DMN (PCC→mPFC), indicating impaired inter-network communication.
Conclusions:
- The findings reveal interrelated α deficits in the visual cortex and DMN in PTSD, supporting a unifying neural pathology.
- These α dysrhythmias contribute to observed DMN hypoactivity, sensory disinhibition, and hypervigilance in PTSD.
- Targeting visual-cortex-DMN α oscillations presents a novel therapeutic avenue for network-based interventions in PTSD.
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