Neural circuitry of PTSD with or without mild traumatic brain injury: A meta-analysis
Veteran Affairs, San Diego, CA 92161, USA. Neuropharmacology
(Impact Factor: 5.11).
03/2011; 62(2):598-606. DOI: 10.1016/j.neuropharm.2011.03.016
Posttraumatic Stress Disorder (PTSD) and mild traumatic brain injury (mTBI) often occur together. Parsing out the unique and overlapping effects of these conditions on the brain, can inform the selection of appropriate treatments. Although recent studies indicate that warfighters in Operations Enduring and Iraqi Freedom are at a high risk for PTSD and mTBI, there is a dearth of research directly comparing their neural correlates. In this paper, we briefly discuss these conditions and supply two meta-analyses of the relevant functional magnetic resonance imaging studies conducted to date. By looking at the overlap in these analyses, we suggest that the middle frontal gyrus may be an appropriate area for future investigations aimed at disentangling PTSD and mTBI. This article is part of a Special Issue entitled 'Post-Traumatic Stress Disorder'.
Available from: Eileen Martin
- "In the present study, probable PTSD showed the strongest association with psychomotor speed (d=0.29) which is congruent with Scott et al. (2015); albeit our effect size was much smaller and T-scores were in the normal range, thus these associations may be statistically rather than clinically significant. In HIV− individuals with PTSD, functional abnormalities in the prefrontal cortex (Sartory et al. 2013; Simmons and Matthews 2012) are linked to processing speed impairments (Aupperle et al. 2012). Specifically, in a sample of women with PTSD related to intimate partner violence, hypoactivation in the dorsal lateral prefrontal cortex (DLPFC) was associated with impairments in a standardized measure of processing speed (Aupperle et al. 2012). "
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ABSTRACT: The prevalence of post-traumatic stress disorder (PTSD) is higher among HIV-infected (HIV+) women compared with HIV-uninfected (HIV-) women, and deficits in episodic memory are a common feature of both PTSD and HIV infection. We investigated the association between a probable PTSD diagnosis using the PTSD Checklist-Civilian (PCL-C) version and verbal learning and memory using the Hopkins Verbal Learning Test in 1004 HIV+ and 496 at-risk HIV- women. HIV infection was not associated with a probable PTSD diagnosis (17 % HIV+, 16 % HIV-; p = 0.49) but was associated with lower verbal learning (p < 0.01) and memory scores (p < 0.01). Irrespective of HIV status, a probable PTSD diagnosis was associated with poorer performance in verbal learning (p < 0.01) and memory (p < 0.01) and psychomotor speed (p < 0.001). The particular pattern of cognitive correlates of probable PTSD varied depending on exposure to sexual abuse and/or violence, with exposure to either being associated with a greater number of cognitive domains and a worse cognitive profile. A statistical interaction between HIV serostatus and PTSD was observed on the fine motor skills domain (p = 0.03). Among women with probable PTSD, HIV- women performed worse than HIV+ women on fine motor skills (p = 0.01), but among women without probable PTSD, there was no significant difference in performance between the groups (p = 0.59). These findings underscore the importance of considering mental health factors as correlates to cognitive deficits in women with HIV.
Journal of NeuroVirology 09/2015; DOI:10.1007/s13365-015-0380-9 · 2.60 Impact Factor
Available from: Leonardo Baldaçara
- "In turn, abnormal function of the medial prefrontal cortex impairs the inhibition of fear circuitry in PTSD (abnormal topdown regulation) (Rauch et al., 2006; Liberzon and Sripada, 2008). The insula is also affected, thus reflecting an abnormal integration between bodily function and emotions (Simmons and Matthews, 2012). The hippocampus may also be affected, which reflects declarative memory impairment and impaired regulation of the HPA axis (Rauch et al., 2006). "
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To evaluate differences in limbic structure volume of subjects exposed to urban violence during adulthood, between those who developed posttraumatic stress disorder (with PTSD) and resilient matched controls (without PTSD).
Limbic volumetric measures of 32 subjects with PTSD and 32 subjects without PTSD who underwent brain MRI were analyzed in an epidemiological study in the city of Sao Paulo. The hippocampus, amygdala, cingulate, and parahipocampal gyri volumes were estimated using FreeSurfer software. We also investigated the association between limbic volumetric measurements, symptom´s severity, and early life stress history (measure by Early Trauma Inventory – ETI).
Subjects with PTSD presented reduced volume of the right rostral part of the anterior cingulate, compared to subjects without PTSD, after controlling for intracranial volume, ETI, and depressive symptoms. Subjects with PTSD presented larger bilateral hippocampus and right amygdala, but secondary to the higher ETI. In PTSD group there was a positive correlation between ETI with bilateral hippocampus, bilateral amygdala, and left parahippocampus.
First, the cross-sectional study design precludes causal interpretation of limbic structure reduction in PTSD, consequence of PTSD, or other life events. Finally, since the sample size was not sufficiently large, we could not observe whether or not limbic structure volume could be related to the type of trauma.
The present study provides evidence of a reduced anterior cingulate volume in subjects with PTSD than in resilient subjects exposed to urban violence. Enlargement of hippocampus and amygdala volume was observed in subjects with PTSD, however secondary to early trauma experience.
Journal of Affective Disorders 10/2014; 168:13–20. DOI:10.1016/j.jad.2014.06.036 · 3.38 Impact Factor
Available from: scan.oxfordjournals.org
- "Research also suggests that anxiety may be associated with abnormalities in prefrontal regulatory regions (Etkin and Wager, 2007; Aupperle and Paulus, 2010; Etkin, 2010). Although evidence regarding the direction and specific location of PFC dysfunction in anxiety differs across experimental paradigms (Etkin and Wager, 2007; Simmons and Matthews, 2012), attenuated activity is often revealed in medial and dorsolateral PFC regions under conditions requiring attentional or inhibitory control (Bishop et al., 2004; Bishop, 2009; Goldin et al., 2009). This corpus of evidence has been taken to suggest that anxiety is associated with a diminished propensity to recruit top–down PFC control regions to regulate limbic-generated emotional responses (Aupperle and Paulus, 2010; Etkin, 2010). "
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ABSTRACT: Computerized attention modification is a relatively new and empirically validated treatment approach for different types of
anxiety disorders. However, its neural basis and processes involved are poorly understood. This study examined the effect
of a one-time application of an attention modification program (AMP) on neural substrates underlying emotion processing in
individuals with high social anxiety. Fourteen individuals with elevated social anxiety symptoms completed an emotional face
processing task during functional magnetic resonance imaging before and after AMP, and were subsequently exposed to a laboratory
stressor. Results revealed the following: First, there was attenuated activation from pre- to post-AMP in the bilateral amygdala,
bilateral insula and subgenual anterior cingulate cortex. Second, post-AMP, individuals exhibited increased activation in
several regions of the prefrontal cortex (PFC). Third, those individuals with greater enhancement of ventromedial PFC activation
after AMP showed diminished attentional allocation for threat and attenuated anxiety reactivity to the stressor. We conclude
that AMP exerts effects that are similar to those previously reported for standard anxiolytics; however, it also appears to
foster deployment of top–down brain processes aimed to regulate anxiety.
Social Cognitive and Affective Neuroscience 08/2013; 9(9). DOI:10.1093/scan/nst128 · 7.37 Impact Factor
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