A Functional Magnetic Resonance Imaging Study of Amygdala and Medial Prefrontal Cortex Responses to Overtly Presented Fearful Faces in Posttraumatic Stress Disorder

Shin, Lisa M.; Wright, Christopher I.; Cannistraro, Paul A.; Wedig, Michelle M.; McMullin, Katherine; Martis, Brian; Macklin, Michael L.; Lasko, Natasha B.; Cavanagh, Sarah R.; Krangel, Terri S.; Orr, Scott P.; Pitman, Roger K.; Whalen, Paul J.; Rauch, Scott L.

doi:10.1001/archpsyc.62.3.273

Cited by 841 publications

(675 citation statements)

References 58 publications

(85 reference statements)

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“…[40][41][42][43][44] Across these studies, however, dysfunctional alterations occurred in different parts of the prefrontal cortex, indicating that failure of prefrontal inhibition in PTSD needs to be clarified in the future. In the present study, a reduction of GABA A -benzodiazepine BP throughout the frontal cortex was found.…”

Section: Discussionmentioning

confidence: 90%

Reduced GABAA benzodiazepine receptor binding in veterans with post-traumatic stress disorder

et al. 2007

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c-Aminobutyric acid (GABA A ) receptors are thought to play an important role in modulating the central nervous system in response to stress. Animal data have shown alterations in the GABA A receptor complex by uncontrollable stressors. SPECT imaging with benzodiazepine ligands showed lower distribution volumes of the benzodiazepine-GABA A receptor in the prefrontal cortex of patients with post-traumatic stress disorder (PTSD) in one, but not in another study. The objective of the present study was to assess differences in the benzodiazepine-GABA A receptor complex in veterans with and without PTSD using [ 11 C]flumazenil and positron emission tomography (PET). Nine drug naive male Dutch veterans with deployment related PTSD and seven male Dutch veterans without PTSD were recruited, and matched for age, region and year of deployment. Each subject received a [ 11 C]flumazenil PET scan and a structural magnetic resonance imaging scan. Dynamic 3D PET scans with a total duration of 60 min were acquired, and binding in template based and manually defined regions of interest (ROI) was quantified using validated plasma input and reference tissue models. In addition, parametric binding potential images were compared on a voxel-by-voxel basis using statistical parametric mapping (SPM2). ROI analyses using both template based and manual ROIs showed significantly reduced [ 11 C]flumazenil binding in PTSD subjects throughout the cortex, hippocampus and thalamus. SPM analysis confirmed these results. The observed global reduction of [ 11 C]flumazenil binding in patients with PTSD provides circumstantial evidence for the role of the benzodiazepine-GABA A receptor in the pathophysiology of PTSD and is consistent with previous animal research and clinical psychopharmacological studies.

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Section: Discussionmentioning

confidence: 90%

Reduced GABAA benzodiazepine receptor binding in veterans with post-traumatic stress disorder

et al. 2007

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“…However, other studies have demonstrated negative correlations between amygdala and medial OFC (Hariri et al, 2000(Hariri et al, , 2003. Previous fMRI studies showing negative correlations between amygdala and OFC have employed event-related designs showing acute reactions to aversive stimuli (Dougherty et al, 2004;Shin et al, 2005). Our study, in contrast, employs 18 FDG-PET, which reflects an average of activity of a 30-min epoch.…”

Section: Implications Of Group Differences In Fronto-amygdala Correlamentioning

confidence: 91%

“…Studies of patients with affective disorder (Drevets et al, 1992) and post-traumatic stress disorder (Shin et al, 2005) have tended to find negative correlations between specifically medial PFC and amygdala in patients but not controls, suggesting coupling only in psychopathology. Recent data suggest a role for serotonin in modulating connectivity between PFC and the amygdala, with subjects carrying the 'short' allele of the serotonin transporter gene (a gene possibly conferring a risk for mood disorders), showing greater fMRI amygdala/medial OFC 'coupling' during an emotional picture viewing task than those with only the 'long' allele (Hariri et al, 2006;Heinz et al, 2005;Pezawas et al, 2005).…”

Section: Introduction the Prefrontal-amygdala Circuitmentioning

confidence: 99%

Amygdala–Prefrontal Disconnection in Borderline Personality Disorder

New

Hazlett

Buchsbaum

et al. 2007

Neuropsychopharmacol

251

158

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Abnormal fronto-amygdala circuitry has been implicated in impulsive aggression, a core symptom of borderline personality disorder (BPD). We examined relative glucose metabolic rate (rGMR) at rest and after m-CPP (meta-chloropiperazine) with 18 fluorodeoxyglucose (FDG) with positron emission tomography (PET) in 26 impulsive aggressive (IED)-BPD patients and 24 controls. Brain edges/amygdala were visually traced on MRI scans co-registered to PET scans; rGMR was obtained for ventral and dorsal regions of the amygdala and Brodmann areas within the prefrontal cortex (PFC). Correlation coefficients were calculated between rGMR for dorsal/ventral amygdala regions and PFC. Additionally, amygdala volumes and rGMR were examined in BPD and controls. Correlations PFC/amygdala Placebo: Controls showed significant positive correlations between right orbitofrontal (OFC) and ventral, but not dorsal, amygdala. Patients showed only weak correlations between amygdala and the anterior PFC, with no distinction between dorsal and ventral amygdala. Correlations PFC/amygdala: m-CPP response: Controls showed positive correlations between OFC and amygdala regions, whereas patients showed positive correlations between dorsolateral PFC and amygdala. Group differences between interregional correlational matrices were highly significant. Amygdala volume/metabolism: No group differences were found for amygdala volume, or metabolism in the placebo condition or in response to meta-chloropiperazine (m-CPP). We demonstrated a tight coupling of metabolic activity between right OFC and ventral amygdala in healthy subjects with dorsoventral differences in amygdala circuitry, not present in IED-BPD. We demonstrated no significant differences in amygdala volumes or metabolism between BPD patients and controls.

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“…This suggests that traumatic life events disrupt the normal pattern of mPFC and amygdala regulation (Williams et al, 2006). In addition, two other studies reported that the severity of PTSD symptoms was negatively correlated with mPFC activity (Shin et al, 2005, Hopper et al, 2007. Moreover, a recent study investigated the relationship between default mode network connectivity and the severity of PTSD symptoms in subjects who had experienced an acute traumatic event 6-12 weeks before.…”

Section: Traumatic Experiences Disrupt Amygdala-prefrontal Connectivitymentioning

confidence: 99%

Traumatic Experiences Disrupt Amygdala – Prefrontal Connectivity

Oh¹

2012

The Amygdala - A Discrete Multitasking Manager

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A Functional Magnetic Resonance Imaging Study of Amygdala and Medial Prefrontal Cortex Responses to Overtly Presented Fearful Faces in Posttraumatic Stress Disorder

Abstract: These results provide evidence for exaggerated amygdala responsivity, diminished medial prefrontal cortex responsivity, and a reciprocal relationship between these 2 regions during passive viewing of overtly presented affective stimuli unrelated to trauma in PTSD.

Cited by 841 publications

References 58 publications

Reduced GABAA benzodiazepine receptor binding in veterans with post-traumatic stress disorder

Reduced GABAA benzodiazepine receptor binding in veterans with post-traumatic stress disorder

Amygdala–Prefrontal Disconnection in Borderline Personality Disorder

Traumatic Experiences Disrupt Amygdala – Prefrontal Connectivity

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