The neural networks of inhibitory control in posttraumatic stress disorder

• Published in: Journal of psychiatry & neuroscience 2008-09, Vol.33 (5), p.413-422
• Main Authors: Falconer, Erin, MSc, Bryant, Richard, PhD, Felmingham, Kim L., PhD, Kemp, Andrew H., PhD, Gordon, Evian, PhD, Peduto, Anthony, MD, Olivieri, Gloria, AssDip (MedRad), Williams, Leanne M., PhD
• Format: Article
• Language: English
• Subjects: Adult; Adult and adolescent clinical studies; Aged; Anxiety disorders. Neuroses; Biological and medical sciences; Clinical trials; Diagnostic and Statistical Manual of Mental Disorders; Female; Fundamental and applied biological sciences. Psychology; Human information processing; Humans; Magnetic Resonance Imaging; Male; Medical Education; Medical imaging; Medical sciences; Methods; Middle Aged; Nerve Net - physiology; Neural Inhibition - physiology; Neural networks; Physiological aspects; Post traumatic stress disorder; Psychiatry; Psychoanalysis; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Psychopathology. Psychiatry; Research Paper; Stress Disorders, Post-Traumatic - physiopathology; Stress Disorders, Post-Traumatic - psychology; Studies; Young Adult
• ISSN: 1180-4882; 1488-2434

Objective Posttraumatic stress disorder (PTSD) involves deficits in information processing that may reflect hypervigilence and deficient inhibitory control. To date, however, no PTSD neuroimaging study has directly examined PTSD-related changes in executive inhibition. Our objective was to investigate the hypothesis that executive inhibitory control networks are compromised in PTSD. Methods Functional magnetic resonance imaging (fMRI) was used during a Go/No-Go inhibition task completed by a sample of patients with PTSD ( n = 23), a matched sample of healthy (i.e. without trauma exposure) control participants ( n = 23) and a sample of control participants with trauma exposure who did not meet criteria for PTSD ( n = 17). Results Participants with PTSD showed more inhibition-related errors than did individuals without trauma exposure. During inhibition, control participants activated a right-lateralized cortical inhibitory network, whereas patients with PTSD activated only the left lateral frontal cortex. PTSD was associated with a reduction in right cortical activation and increased activation of striatal and somatosensory regions. Conclusion The increased inhibitory error and reduced right frontal cortical activation are consistent with compromised inhibitory control in PTSD, while the increased activation of brain regions associated with sensory processing and a greater demand on inhibitory control may reflect enhanced stimulus processing in PTSD, which may undermine cortical control mechanisms.