Studies have suggested that the default mode network is active during mind wandering, which is often experienced intermittently during sustained attention tasks. Conversely, an anticorrelated task-positive network is thought to subserve various forms of attentional processing. Understanding how these two systems work together is central for understanding many forms of optimal and sub-optimal task performance. Here we present a basic model of naturalistic cognitive fluctuations between mind wandering and attentional states derived from the practice of focused attention meditation. This model proposes four intervals in a cognitive cycle: mind wandering, awareness of mind wandering, shifting of attention, and sustained attention. People who train in this style of meditation cultivate their abilities to monitor cognitive processes related to attention and distraction, making them well suited to report on these mental events. Fourteen meditation practitioners performed breath-focused meditation while undergoing fMRI scanning. When participants realized their mind had wandered, they pressed a button and returned their focus to the breath. The four intervals above were then constructed around these button presses. We hypothesized that periods of mind wandering would be associated with default mode activity, whereas cognitive processes engaged during awareness of mind wandering, shifting of attention and sustained attention would engage attentional subnetworks. Analyses revealed activity in brain regions associated with the default mode during mind wandering, and in salience network regions during awareness of mind wandering. Elements of the executive network were active during shifting and sustained attention. Furthermore, activations during these cognitive phases were modulated by lifetime meditation experience. These findings support and extend theories about cognitive correlates of distributed brain networks.
Background A central problem in posttraumatic stress disorder (PTSD) is a reduced capacity to suppress fear under safe conditions. Previously, we have shown that combat-related PTSD patients have impaired inhibition of fear-potentiated startle. Given the high comorbidity between PTSD and depression, our goal was to see whether this impairment is specific to PTSD, or a nonspecific symptom associated with both disorders. Methods Fear-potentiated startle (FPS) was assessed in 106 trauma-exposed individuals divided into four groups: a) No diagnosis control, b) PTSD only, c) major depression (MDD) only, and d) comorbid PTSD and MDD. We used a novel conditional discrimination procedure, in which one set of shapes (the danger signal) was paired with aversive airblasts to the throat, and different shapes (the safety signal) were presented without airblasts. The paradigm also included fear inhibition transfer test. Results Subjects with comorbid MDD and PTSD had higher FPS to the safety signal and to the transfer test compared to controls and MDD only subjects. In contrast to the control and MDD groups, the PTSD and comorbid PTSD and MDD groups did not show fear inhibition to safety cues. Conclusions These results suggest that impaired fear inhibition may be a specific biomarker of PTSD symptoms.
Objective To determine the effectiveness of Virtual Reality Exposure (VRE) augmented with D-cycloserine (50mg) or alprazolam (0.25mg), compared to placebo, in reducing PTSD due to military trauma in Iraq and Afghanistan. Method A double-blind, placebo-controlled randomized clinical trial comparing augmentation methods for VRE for subjects (n= 156) with PTSD was conducted. Results PTSD symptoms significantly improved from pre- to post-treatment over the 6-session VRE treatment (p<.001) across all conditions and were maintained at 3, 6, and 12 months follow-up. There were no overall differences between the D-cycloserine group on symptoms at any time-point. The alprazolam and placebo conditions significantly differed on the post-treatment Clinician Administered PTSD scale (p = .006) and the 3-month post-treatment PTSD diagnosis, such that the alprazolam group showed greater rates of PTSD (79.2% alprazolam vs. 47.8% placebo). Between-session extinction learning was a treatment-specific enhancer of outcome for the D-cycloserine group only (p<.005). At post-treatment, the D-cycloserine group was the lowest on cortisol reactivity (p<.05) and startle response during VR scenes (p<.05). Conclusions A small number of VRE sessions were associated with reduced PTSD diagnosis and symptoms in Iraq/Afghanistan veterans, although there was no control condition for the VRE. Overall, there was no advantage of D-cycloserine on PTSD symptoms in primary analyses. In secondary analyses, benzodiazepine use during treatment may impair recovery, and D-cycloserine may enhance VRE in patients who demonstrate within-session learning. D-cycloserine augmentation treatment in PTSD patients may reduce cortisol and startle reactivity compared to the alprazolam and placebo treatment, consistent with the animal literature.
One of the central problems in posttraumatic stress disorder (PTSD) is the inability to suppress fear even under safe conditions. The neural underpinnings of fear is a clinically relevant issue that is poorly understood. This study assessed fear potentiation and fear inhibition using fear-potentiated startle in a conditional discrimination procedure (AX+/BX-). We hypothesized that patients with PTSD would show normal fear potentiation and impaired fear inhibition. 28 healthy volunteers and 27 PTSD patients (14 with low current symptoms, 13 with high current symptoms) were presented with one set of colored lights (AX trials) paired with aversive air blasts to the throat, and a different series of lights (BX trials) presented without air blasts. We then presented A and B together (AB trials) to see whether B would inhibit fear potentiation to A. All groups showed robust fear potentiation in that they had significantly greater startle magnitude on AX trials compared to noise alone trials. However, the high symptom PTSD group did not show fear inhibition: these subjects had significantly greater fear potentiation on the AB trials than both the controls and the low symptom PTSD patients.
Abstract-Our primary aim was to document the rate of comorbidity of physician-diagnosed chronic pain conditions in veterans who were seeking treatment for posttraumatic stress disorder (PTSD). Chronic pain diagnoses (e.g., chronic lowback pain and osteoarthritis) were examined with retrospective chart review. Of the patients with PTSD, 66% had chronic pain diagnoses at pretreatment. These findings are consistent with previous studies that documented the high comorbidity of chronic pain and PTSD using samples of pain patients. Our secondary aim was to examine pain ratings before, during, and after PTSD treatment. Using data that were a part of clinical practice, we found that patients with more pain before treatment reported reductions in pain over the course of PTSD treatment and in the 4 months following treatment. While our results must be interpreted cautiously because of multiple confounding factors and the absence of experimental manipulation, they highlight the importance of PTSD and pain comorbidity.
The purpose of this study was to analyze fear extinction and reinstatement in humans using fear-potentiated startle. Participants were fear conditioned using a simple discrimination procedure with colored lights as the conditioned stimuli (CSs) and an airblast to the throat as the unconditioned stimulus (US). Participants were extinguished 24 h after fear conditioning. Upon presentation of unsignaled USs after extinction, participants displayed significant fear reinstatement. In summary, these procedures produced robust fear-potentiated startle, significant CS+/CS− discrimination, within-session extinction, and significant reinstatement. This is the first demonstration of fear extinction and reinstatement in humans using startle measures.A failure to inhibit fear is believed to underlie the pathophysiology of several anxiety disorders, including post-traumatic stress disorder (PTSD) (Cannistraro and Rauch 2003). One methodology for investigating fear inhibition is extinction, a form of learning in which the frequency and/or intensity of a conditioned response (CR), previously acquired through pairing a conditioned stimulus (CS; e.g., light) with an aversive unconditioned stimulus (US; e.g., shock), is reduced through the repeated presentation of the CS without the US (cf. Myers and Davis 2002). Evidence suggests that fear to a CS is not erased after extinction, but instead suppressed by a competing parallel inhibitory process (cf. Myers and Davis 2002), as demonstrated by the return of fear following extinction under specific conditions. One example of fear return after extinction is reinstatement (Rescorla and Heth 1975;Bouton and Swartzentruber 1991). In a traditional reinstatement procedure, subjects undergo fear acquisition and extinction training, and are then presented with a small number of USs without the CS. In a later test session, the conditioned fear response will reappear upon representation of the CS (Rescorla and Heth 1975;Bouton and Bolles 1979;Richardson et al. 1999b;Myers and Davis 2002), provided that the test occurs in the context in which the unsignaled USs were presented (Westbrook et al. 2002). Unsignaled US presentations are believed to reinstate extinguished CRs through multiple mechanisms, including summation of fear conditioned to the context by the unsignaled USs with subthreshold fear to the extinguished CS (Bouton and Bolles 1979;Bouton and King 1983). The context specificity of reinstatement has been demonstrated in animal and human studies (see Bouton 2004;LaBar and Phelps 2005).Conditioned fear extinction and reinstatement have been widely investigated in animals by observing fear responses such as freezing, avoidance, or fear-potentiated startle (Falls et al. 1992;Gewirtz et al. 1997;Richardson et al. 1999a;Lu et al. 2001;Westbrook et al. 2002;Ledgerwood et al. 2003Ledgerwood et al. , 2004Chhatwal et al. 2005;Myers et al. 2006). In humans, reinstatement has been observed in verbal ratings of fear and US-expectancy (Hermans et al. 2005), reaction time task performance (Dirikx et ...
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