The neural networks of inhibitory control in posttraumatic stress disorder

Brain Dynamics Centre, Westmead Millenium Institute, Westmead Hospital, Westmead, NSW, Australia.
Journal of psychiatry & neuroscience: JPN (Impact Factor: 5.86). 10/2008; 33(5):413-22.
Source: PubMed


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.
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).
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.
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.

Download full-text


Available from: Andrew Haddon Kemp,
50 Reads
  • Source
    • "Furthermore, most affective disorders including depression or PTSD do not result from a single locus. Multiple regions including cortical, limbic and basal ganglia structures can be involved as a network to produce psychopathology [71] [72]. OFC is also seen to be involved in many other dysfunctional behaviors including addiction and pathological gambling, disorders that as yet have no obvious relationship to PNES [73] [74]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Psychogenic nonepileptic seizures (PNES) often mimic epileptic seizures and occur in both people with and without epilepsy. Pathophysiology of conversion disorders such as PNES remains unclear though significant psychological, psychiatric and environmental factors have been correlated with a diagnosis of PNES. Many clinical signs that have been considered typical for PNES can also be found in frontal epileptic seizures. Given the resemblance of seizures and affective changes from Orbitofrontal cortical dysfunction to PNES like events and correlation of psychological and environmental stress to conversion disorders such as PNES, we propose a two-factor model for the pathogenesis of PNES. We hypothesize that patients with PNES could have a higher likelihood of having both Orbitofrontal cortical dysfunction and a history of psychological stressors rather than a higher likelihood of having either one or the other. We further explore the implications of this two-factor model, including possible therapies. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Medical Hypotheses 01/2015; 84(4). DOI:10.1016/j.mehy.2015.01.034 · 1.07 Impact Factor
  • Source
    • "Similarly, others have shown that those with PTSD perform significantly worse than healthy controls on tasks that require inhibitory control (e.g., the stroop test) but not those tasks that assess attention span and working memory capacity (Flaks et al., 2014). Moreover, individuals with PTSD show deficient motor response control as evidenced by high inhibition-related error rates on the Go/No-Go and Stop-Signal tasks (Casada and Roache, 2005; Falconer et al., 2008; Wu et al., 2010; Swick et al., 2012). Because inhibition is often required for adaptive self-regulation, individual differences in inhibitory control should be associated with PTSD severity. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Post-traumatic stress disorder (PTSD) is characterized by deficits in cognitive functioning, particularly cognitive control. Moreover, these deficits are thought to play a critical role in the etiology and maintenance of core PTSD symptoms such as intrusive thoughts and memories. However, the psychophysiological concomitants of cognitive control remain largely unexamined. In this article, we suggest that individual differences in heart rate variability (HRV), a physiological index of self-regulatory capacity, may underlie the association between cognitive control ability and intrusive cognitions in PTSD. We review evidence showing that individual differences in HRV at rest are related to prefrontal cortical activity and performance on a broad range of cognitive control tasks. We highlight the importance of inhibition as a mechanism by which HRV promotes successful cognitive control. In addition, we summarize recent research linking individual differences in HRV to performance on laboratory tasks that assess the ability to control unwanted memories and intrusive thoughts. We conclude by suggesting that future studies should examine the role of low HRV as a risk factor for developing PTSD.
    Frontiers in Psychology 07/2014; 5:758. DOI:10.3389/fpsyg.2014.00758 · 2.80 Impact Factor
  • Source
    • "Understandably, while most neuroimaging research regarding PTSD uses symptom provocation studies, it is also important to determine whether deficits in inhibitory function can be found under nonemotional conditions. The results of the current study suggest more general inhibitory control deficits in PTSD/mTBI individuals, consistent with the findings of Falconer et al., [47] in PTSD individuals. Therefore, future research using standard cognitive tasks may help to determine whether the neural systems affecting these populations are “generally” dysfunctional or whether they exhibit deficits only under certain conditions (e.g., threat/fear stimuli). "
    [Show abstract] [Hide abstract]
    ABSTRACT: A significant portion of previously deployed combat Veterans from Operation Enduring Freedom and Operation Iraqi Freedom/Operation New Dawn (OEF/OIF/OND) are affected by comorbid posttraumatic stress disorder (PTSD) and mild traumatic brain injury (mTBI). Despite this fact, neuroimaging studies investigating the neural correlates of cognitive dysfunction within this population are almost nonexistent, with the exception of research examining the neural correlates of diagnostic PTSD or TBI. The current study used both voxel-based and surface-based morphometry to determine whether comorbid PTSD/mTBI is characterized by altered brain structure in the same regions as observed in singular diagnostic PTSD or TBI. Furthermore, we assessed whether alterations in brain structures in these regions were associated with behavioral measures related to inhibitory control, as assessed by the Go/No-go task, self-reports of impulsivity, and/or PTSD or mTBI symptoms. Results indicate volumetric reductions in the bilateral anterior amygdala in our comorbid PTSD/mTBI sample as compared to a control sample of OEF/OIF Veterans with no history of mTBI and/or PTSD. Moreover, increased volume reduction in the amygdala predicted poorer inhibitory control as measured by performance on the Go/No-go task, increased self-reported impulsivity, and greater symptoms associated with PTSD. These findings suggest that alterations in brain anatomy in OEF/OIF/OND Veterans with comorbid PTSD/mTBI are associated with both cognitive deficits and trauma symptoms related to PTSD.
    03/2014; 2014:691505. DOI:10.1155/2014/691505
Show more