Quantitative meta-analysis of neural activity in posttraumatic stress disorder
ABSTRACT In recent years, neuroimaging techniques such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) have played a significant role in elucidating the neural underpinnings of posttraumatic stress disorder (PTSD). However, a detailed understanding of the neural regions implicated in the disorder remains incomplete because of considerable variability in findings across studies. The aim of this meta-analysis was to identify consistent patterns of neural activity across neuroimaging study designs in PTSD to improve understanding of the neurocircuitry of PTSD.
We conducted a literature search for PET and fMRI studies of PTSD that were published before February 2011. The article search resulted in 79 functional neuroimaging PTSD studies. Data from 26 PTSD peer-reviewed neuroimaging articles reporting results from 342 adult patients and 342 adult controls were included. Peak activation coordinates from selected articles were used to generate activation likelihood estimate maps separately for symptom provocation and cognitive-emotional studies of PTSD. A separate meta-analysis examined the coupling between ventromedial prefrontal cortex and amygdala activity in patients.
Results demonstrated that the regions most consistently hyperactivated in PTSD patients included mid- and dorsal anterior cingulate cortex, and when ROI studies were included, bilateral amygdala. By contrast, widespread hypoactivity was observed in PTSD including the ventromedial prefrontal cortex and the inferior frontal gyrus. Furthermore, decreased ventromedial prefrontal cortex activity was associated with increased amygdala activity.
These results provide evidence for a neurocircuitry model of PTSD that emphasizes alteration in neural networks important for salience detection and emotion regulation.
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ABSTRACT: Complex posttraumatic stress disorder (PTSD) presents with clinical features of full or partial PTSD (re-experiencing a traumatic event, avoiding reminders of the event, and a state of hyperarousal) together with symptoms from three additional clusters (problems in emotional regulation, negative self-concept, and problems in interpersonal relations). Complex PTSD is proposed as a new diagnostic entity in ICD-11 and typically occurs after prolonged and complex trauma. Here we shortly review current knowledge regarding the biological correlates of complex PTSD and compare it to the relevant findings in PTSD. Recent studies provide support to the validity of complex PTSD as a separate diagnostic entity; however, data regarding the biological basis of the disorder are still very limited at this time. Further studies focused on complex PTSD biological correlates and replication of the initial findings are needed, including neuroimaging, neurobiochemical, genetic, and epigenetic investigations. Identification of altered biological pathways in complex PTSD may be critical to further understand the pathophysiology and optimize treatment strategies.European Journal of Psychotraumatology 04/2015; 6:25913. DOI:10.3402/ejpt.v6.25913 · 2.40 Impact Factor
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ABSTRACT: There have been few direct examinations of the volitional control of emotional responses to provocative stimuli in PTSD. To address this gap, an emotion regulation task was administered to 27 Operation Enduring Freedom/Operation Iraqi Freedom combat veterans and 23 healthy controls. Neutral and aversive photographs were presented to participants who did or did not employ emotion regulation strategies. Objective indices included corrugator electromyogram, the late positive potential, and the electrocardiogram. On uninstructed trials, participants with PTSD exhibited blunted cardiac reactivity rather than the exaggerated cardioacceleratory responses seen in trauma cue reactivity studies. On interleaved regulation trials, no measure evidenced group differences in voluntary emotion regulation. Persons with PTSD may not differ from normals in their capacity to voluntarily regulate normative emotional responses to provocative stimuli in the laboratory, though they may nevertheless respond differentially on uninstructed trials and endorse symptoms of dyscontrol pathognomonic of the disorder outside of the laboratory. Published 2014. This article is a U.S. Government work and is in the public domain in the USA.Psychophysiology 12/2014; DOI:10.1111/psyp.12392 · 3.18 Impact Factor
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ABSTRACT: Post-traumatic stress disorder (PTSD) is a debilitating psychiatric disorder. An important diagnostic feature of PTSD is anhedonia, which may result from deficits in reward functioning. This has however never been studied systematically in PTSD. To determine if PTSD is associated with reward impairments, we conducted a systematic review of studies in which reward functioning was compared between PTSD patients and healthy control participants, or investigated in relation to PTSD symptom severity. A total of 29 studies were included, covering reward anticipation and approach (‘wanting’), and hedonic responses to reward (‘liking’). Overall, results were mixed, although decreased reward anticipation and approach and reduced hedonic responses were repeatedly observed in PTSD patients compared to healthy controls. Decreased reward functioning was seen more often in female than in male PTSD samples and most often in response to social positive stimuli. Though more research is needed, these findings are a first step in understanding the possible mechanisms underlying anhedonia in PTSD.Neuroscience & Biobehavioral Reviews 01/2015; DOI:10.1016/j.neubiorev.2015.01.019 · 10.28 Impact Factor