Selectively reduced regional cortical volumes in post-traumatic stress disorder

Rauch, Scott L.; Shin, Lisa M.; Segal, Ethan; Pitman, Roger K.; Carson, Margaret A.; McMullin, Katherine; Whalen, Paul J.; Makris, Nikos

doi:10.1097/01.wnr.0000071767.24455.10

Cited by 152 publications

(79 citation statements)

References 22 publications

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“…The PVTp projection to mPFC targets IL in a highly preferential manner (Moga et al, 1995), warranting consideration of this region in the adaptive adjustments of the axis to chronic stress. From a pathological perspective, neuroimaging studies reveal functional impairment and shrinkage of mPFC in posttraumatic stress disorder (PTSD) (Rauch et al, 2003;Shin et al, 2005) that find a parallel in reports of dendritic atrophy and synapse loss after chronic emotional stress in rodents (Cook and Wellman, 2004;Radley et al, 2004Radley et al, , 2006. PTSD is associated with HPA axis dysregulation that may be variable in nature (for review, see Newport and Nemeroff, 2000;Yehuda, 2001) and consistent increases in cardiovascular reactivity Shalev et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Regional Differentiation of the Medial Prefrontal Cortex in Regulating Adaptive Responses to Acute Emotional Stress

Radley¹,

Arias²,

Sawchenko³

2006

J. Neurosci.

402

279

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The medial prefrontal cortex (mPFC) is an important neural substrate for integrating cognitive-affective information and regulating the hypothalamo-pituitary-adrenal (HPA) axis response to emotional stress. mPFC modulation of stress responses is effected in part via the paraventricular hypothalamic nucleus (PVH), which houses both autonomic (sympathoadrenal) and neuroendocrine (HPA) effector mechanisms. Although the weight of evidence suggests that mPFC influences on stress-related PVH outputs are inhibitory, discordant findings have been reported, and such work has tended to treat this cortical region as a unitary structure. Here we compared the effects of lesions of the dorsal versus ventral aspects of mPFC, centered in the prelimbic and infralimbic fields, respectively, on acute restraint stress-induced activation of PVH cell groups mediating autonomic and neuroendocrine responses. Lesions to the dorsal mPFC enhanced restraint-induced Fos and corticotropin-releasing factor (CRF) mRNA expression in the neurosecretory region of PVH. Ablation of the ventral mPFC decreased stress-induced Fos protein and CRF mRNA expression in this compartment but increased Fos induction in PVH regions involved in central autonomic control. Repetition of the experiments in rats bearing retrograde tracer deposits to label PVHautonomic projections confirmed that ventral mPFC lesions selectively increased stress-induced Fos expression in identified preautonomic neurons. Finally, hormonal indices of HPA activation in response to acute stress were augmented after dorsal mPFC lesions and attenuated after ventral mPFC lesions. These results suggest that dorsal and ventral aspects of the mPFC differentially regulate neuroendocrine and autonomic PVH outputs in response to emotional stress.

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Section: Discussionmentioning

confidence: 99%

Regional Differentiation of the Medial Prefrontal Cortex in Regulating Adaptive Responses to Acute Emotional Stress

Radley¹,

Arias²,

Sawchenko³

2006

J. Neurosci.

402

279

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“…Structural MRI studies have observed reductions in gray matter volume in participants with PTSD, in both rostral (Rauch et al 2003;Woodward et al, 2006;Kasai et al, 2008;Herringa et al 2012) and caudal (Woodward et al, 2006;Chen et al, 2012;Chao et al, 2013) subdivisions of the ACC. In many cases, these volume reductions correlated with PTSD symptom severity.…”

Section: Anterior Cingulate Cortex and Ptsdmentioning

confidence: 99%

“…Thus, an important line of inquiry is whether individuals with PTSD show changes in ERN amplitude. This is particularly salient in light of the structural and functional alterations in MFC observed in this disorder (Hamner et al, 1999;Shin et al, 2001;Rauch et al, 2003;Kim et al, 2005).…”

Section: Introductionmentioning

confidence: 97%

Intact error monitoring in combat Veterans with post-traumatic stress disorder

Swick

Honzel

Turken

2015

Psychiatry Research: Neuroimaging

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The error-related negativity (ERN) is a neuroelectric signature of performance monitoring during speeded response time tasks. Previous studies indicate that individuals with anxiety disorders show ERN enhancements that correlate with the degree of clinical symptomology. Less is known about the error monitoring system in post-traumatic stress disorder (PTSD). PTSD is characterized by impairments in the regulation of fear and other emotional responses, as well as deficits in maintaining cognitive control. Here, combat Veterans with PTSD were compared to control Veterans in two different versions of the flanker task (n=13 or 14 per group). Replicating and extending previous findings, PTSD patients showed an intact ERN in both experiments. In addition, task performance and error compensation behavior were intact. Finally, ERN amplitude showed no relationship with self-reported PTSD, depression, or post-concussive symptoms. These results suggest that error monitoring represents a relative strength in PTSD that can dissociate from cognitive control functions that are impaired, such as response inhibition and sustained attention. A healthy awareness of errors in external actions could be leveraged to improve interoceptive awareness of emotional state. The results could have positive implications for PTSD treatments that rely on self-monitoring abilities, such as neurofeedback and mindfulness training.

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“…More specifically, vmPFC engagement during extinction learning predicts extinction success and is associated with “top‐down” modulation of amygdala‐driven fear expression (Do‐Monte, Manzano‐Nieves, Quiñones‐Laracuente, Ramos‐Medina, & Quirk, 2015; Lebrón, Milad, & Quirk, 2004; Milad et al., 2005, 2007; Phelps, Delgado, Nearing, & LeDoux, 2004; Quirk, Likhtik, Pelletier, & Paré, 2003; Rosenkranz, Moore, & Grace, 2003). Results from studies with PTSD patients revealed deficits in extinction recall (Milad et al., 2008), reduced vmPFC volume, and activation during fear extinction compared to controls (Bremner et al., 2005; Milad et al., 2009; Rauch et al., 2003; Rougemont‐Bücking et al., 2011; Shin, Rauch, & Pitman, 2006). Therefore, facilitating endogenous vmPFC activity using brain stimulation techniques, in the context of extinction learning, may be one method to improve fear extinction and retention (i.e., recall of safety memories; Milad & Quirk, 2002; Milad, Vidal‐Gonzalez, & Quirk, 2004) in those suffering from PTSD.…”

Section: Introductionmentioning

confidence: 99%

Transcranial direct current stimulation may modulate extinction memory in posttraumatic stress disorder

et al. 2017

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BackgroundAbnormalities in fear extinction and recall are core components of posttraumatic stress disorder (PTSD). Data from animal and human studies point to a role of the ventromedial prefrontal cortex (vmPFC) in extinction learning and subsequent retention of extinction memories. Given the increasing interest in developing noninvasive brain stimulation protocols for psychopathology treatment, we piloted whether transcranial direct current stimulation (tDCS) during extinction learning, vs. during consolidation of extinction learning, might improve extinction recall in veterans with warzone‐related PTSD.MethodsTwenty‐eight veterans with PTSD completed a 2‐day Pavlovian fear conditioning, extinction, and recall paradigm. Participants received one 10‐min session of 2 mA anodal tDCS over AF3, intended to target the vmPFC. Fourteen received tDCS that started simultaneously with extinction learning onset, and the remaining 14 participants received tDCS during extinction consolidation. Normalized skin conductance reactivity (SCR) was the primary outcome measure. Linear mixed effects models were used to test for effects of tDCS on late extinction and early extinction recall 24 hr later.ResultsDuring early recall, veterans who received tDCS during extinction consolidation showed slightly lower SCR in response to previously extinguished stimuli as compared to veterans who received tDCS simultaneous with extinction learning (p = .08), generating a medium effect size (Cohen's d = .38). There was no significant effect of tDCS on SCR during late extinction.ConclusionsThese preliminary findings suggest that testing the effects of tDCS during consolidation of fear extinction may have promise as a way of enhancing extinction recall.

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Selectively reduced regional cortical volumes in post-traumatic stress disorder

Cited by 152 publications

References 22 publications

Regional Differentiation of the Medial Prefrontal Cortex in Regulating Adaptive Responses to Acute Emotional Stress

Regional Differentiation of the Medial Prefrontal Cortex in Regulating Adaptive Responses to Acute Emotional Stress

Intact error monitoring in combat Veterans with post-traumatic stress disorder

Transcranial direct current stimulation may modulate extinction memory in posttraumatic stress disorder

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