Regional Cerebral Blood Flow in the Amygdala and Medial PrefrontalCortex During Traumatic Imagery in Male and Female Vietnam Veterans With PTSD

Shin, Lisa M.; Orr, Scott P.; Carson, Margaret A.; Rauch, Scott L.; Macklin, Michael L.; Lasko, Natasha B.; Peters, Patricia Marzol; Metzger, Linda J.; Dougherty, Darin D.; Cannistraro, Paul A.; Alpert, Nathaniel M.; Fischman, Alan J.; Pitman, Roger K.

doi:10.1001/archpsyc.61.2.168

Cited by 714 publications

(559 citation statements)

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“…The impaired extinction retention in the PTSD subjects in the present study is consistent with studies reporting deficient activation of this brain region in PTSD (Shin et al, 2004;Bremner et al, 2005;Liberzon et al, 2003;Phan et al, 2006;Britton et al, 2005;Shin et al, 2001). Moreover, a recent twin study reported acquired gray matter reduction in an area of vmPFC (rostral anterior cingulate cortex) in PTSD (Kasai et al, 2007).…”

Section: Discussionsupporting

confidence: 92%

Presence and acquired origin of reduced recall for fear extinction in PTSD: Results of a twin study

Milad

Orr

Lasko

et al. 2008

Journal of Psychiatric Research

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Recall of fear extinction, which is thought to aid in recovery from a psychologically traumatic event, is hypothesized to be deficient in post-traumatic stress disorder (PTSD), but this has not yet been demonstrated in the laboratory, nor has its origin been investigated. To address these two issues, 14 pairs of monozygotic twins discordant for combat exposure, in 7 of which the combat-exposed twin had PTSD, underwent a two-day fear conditioning and extinction procedure. On Day 1, subjects viewed colored light conditioned stimuli, some of which were paired with mild electric shock, followed by extinction of the conditioned responses. On Day 2, recall of Day 1 extinction learning (i.e., extinction retention) was assessed. Skin conductance response (SCR) was the dependent measure. There were no group differences during acquisition or extinction learning. However, a significant PTSD Diagnosis (in the exposed twin) x combat Exposure interaction emerged during extinction recall, with the PTSD combat veterans having larger SCRs than their own co-twins, and than the non-PTSD combat veterans and their co-twins. These results indicate that retention of extinction of conditioned fear is deficient in PTSD. Furthermore, they support the conclusion that this deficit is acquired as a result of combat trauma leading to PTSD, rather than being a predisposing factor to developing PTSD upon the stress of combat.

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Section: Discussionsupporting

confidence: 92%

Presence and acquired origin of reduced recall for fear extinction in PTSD: Results of a twin study

Milad

Orr

Lasko

et al. 2008

Journal of Psychiatric Research

Self Cite

457

393

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“…All correlations are reported for po0.05, two-tailed. ANOVAs examining amygdala volume and function were conducted both including and excluding the subjects meeting PTSD, as PTSD has been associated with both increased (Protopopescu et al, 2005;Shin et al, 2004), and decreased amygdala activity (Britton et al, 2005); amygdala volume in PTSD has been shown not to be different from controls (Bremner, 2002;Wignall et al, 2004).…”

Section: Resultsmentioning

confidence: 99%

Amygdala–Prefrontal Disconnection in Borderline Personality Disorder

New

Hazlett

Buchsbaum

et al. 2007

Neuropsychopharmacol

258

160

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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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“…Hyporesponsive PFC, as well as reduced connectivity to the amygdala (Jin et al, 2013;Shin et al, 2004a) may indicate insufficient inhibitory control over exaggerated fear responses. Lastly, abnormal hippocampal function (Corcoran and Maren, 2001) and reduced connectivity to the amygdala (Dolcos et al, 2004;McGaugh, 2004) may underlie impairments in contextual memory processing and the ability to inhibit intrusive memories (Shin et al, 2004a), although findings have been mixed (Hughes and Shin, 2011). A recent resting-state fMRI study showed increased activity in amygdala and reduced spontaneous neural activity in the dorso-lateral PFC (DLPFC) (Yan et al, 2013).…”

Section: Clinicalmentioning

confidence: 99%

The role of biomarkers and MEG-based imaging markers in the diagnosis of post-traumatic stress disorder and blast-induced mild traumatic brain injury

Huang

Risling

Baker

2016

Psychoneuroendocrinology

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SummaryBackground: Pervasive use of improvised explosive devices (IEDs), rocket-propelled grenades, and land mines in the recent conflicts in Iraq and Afghanistan has brought traumatic brain injury (TBI) and its impact on health outcomes into public awareness. Blast injuries have been deemed signature wounds of these wars. War-related TBI is not new, having become prevalent during WWI and remaining medically relevant in WWII and beyond. Medicine's past attempts to accurately diagnose and disentangle the pathophysiology of war-related TBI parallels current lines of inquiry and highlights limitations in methodology and attribution of symptom etiology, be it organic, psychological, or behavioral. New approaches and biomarkers are needed. Preclinical: Serological biomarkers and biomarkers of injury obtained with imaging techniques represent cornerstones in the translation between experimental data and clinical observations. Experimental models for blast related TBI and PTSD can generate critical data on injury threshold, for example for white matter injury from acceleration. Carefully verified and validated models can be evaluated with gene expression arrays and proteomics to identify new candidates for serological biomarkers. Such models can also be analyzed with diffusion MRI and microscopy in order to identify criteria for detection of diffuse white matter injuries, such as DAI (diffuse axonal injury). The experimental models can also be analyzed with focus on injury outcome in brain stem regions, such as locus coeruleus or nucleus raphe magnus that can be involved in response to anxiety changes. * Corresponding author at: UCSD Radiology Imaging Laboratory, San Diego, CA 92121, USA. Tel.: +1 858 534 1254; fax: +1 8585346046. E-mail address: mxhuang@ucsd.edu (M. Huang). Clinical: Mild (and some moderate) TBI can be difficult to diagnose because the injuries are often not detectable on conventional MRI or CT. There is accumulating evidence that injured brain tissues in TBI patients generate abnormal low-frequency magnetic activity (ALFMA, peaked at 1-4 Hz) that can be measured and localized by magnetoencephalography (MEG). MEG imaging detects TBI abnormalities at the rates of 87% for the mild TBI, group (blast-induced plus non-blast causes) and 100% for the moderate group. Among the mild TBI patients, the rates of abnormalities are 96% and 77% for the blast and non-blast TBI groups, respectively. There is emerging evidence based on fMRI and MEG studies showing hyper-activity in the amygdala and hypo-activity in prefrontal cortex in individuals with PTSD. MEG signal may serve as a sensitive imaging marker for mTBI, distinguishable from abnormalities generated in association with PTSD. More work is needed to fully describe physiological mechanisms of post-concussive symptoms.Published by Elsevier Ltd. BackgroundBlast injuries are deemed the signature wounds of the first wars (Afghanistan and Iraq) of the 21st century (Lancet, 2007;Galarneau et al., 2008). According to a recent U.S. Department Veterans Affairs (DVA) ...

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Regional Cerebral Blood Flow in the Amygdala and Medial PrefrontalCortex During Traumatic Imagery in Male and Female Vietnam Veterans With PTSD

Abstract: These results suggest a reciprocal relationship between medial prefrontal cortex and amygdala function in PTSD and opposing associations between activity in these regions and symptom severity consistent with current functional neuroanatomic models of this disorder.

Cited by 714 publications

References 44 publications

Presence and acquired origin of reduced recall for fear extinction in PTSD: Results of a twin study

Presence and acquired origin of reduced recall for fear extinction in PTSD: Results of a twin study

Amygdala–Prefrontal Disconnection in Borderline Personality Disorder

The role of biomarkers and MEG-based imaging markers in the diagnosis of post-traumatic stress disorder and blast-induced mild traumatic brain injury

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