Neuroimaging studies of emotional responses in PTSD (original) (raw)
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Emotion and cognition interactions in PTSD: a review of neurocognitive and neuroimaging studies
Frontiers in Integrative Neuroscience, 2012
Posttraumatic stress disorder (PTSD) is a psychiatric syndrome that develops after exposure to terrifying and life-threatening events including warfare, motor-vehicle accidents, and physical and sexual assault. The emotional experience of psychological trauma can have long-term cognitive effects. The hallmark symptoms of PTSD involve alterations to cognitive processes such as memory, attention, planning, and problem solving, underscoring the detrimental impact that negative emotionality has on cognitive functioning. As such, an important challenge for PTSD researchers and treatment providers is to understand the dynamic interplay between emotion and cognition. Contemporary cognitive models of PTSD theorize that a preponderance of information processing resources are allocated toward threat detection and interpretation of innocuous stimuli as threatening, narrowing one's attentional focus at the expense of other cognitive operations. Decades of research have shown support for these cognitive models of PTSD using a variety of tasks and methodological approaches. The primary goal of this review is to summarize the latest neurocognitive and neuroimaging research of emotion-cognition interactions in PTSD. To directly assess the influence of emotion on cognition and vice versa, the studies reviewed employed challenge tasks that included both cognitive and emotional components. The findings provide evidence for memory and attention deficits in PTSD that are often associated with changes in functional brain activity. The results are reviewed to provide future directions for research that may direct better and more effective treatments for PTSD.
Neural Systems for Cognitive and Emotional Processing in Posttraumatic Stress Disorder
Frontiers in Psychology, 2012
Individuals with posttraumatic stress disorder (PTSD) show altered cognition when traumarelated material is present. PTSD may lead to enhanced processing of trauma-related material, or it may cause impaired processing of trauma-unrelated information. However, other forms of emotional information may also alter cognition in PTSD. In this review, we discuss the behavioral and neural effects of emotion processing on cognition in PTSD, with a focus on neuroimaging results. We propose a model of emotion-cognition interaction based on evidence of two network models of altered brain activation in PTSD. The first is a trauma-disrupted network made up of ventrolateral PFC, dorsal anterior cingulate cortex (ACC), hippocampus, insula, and dorsomedial PFC that are differentially modulated by trauma content relative to emotional trauma-unrelated information. The trauma-disrupted network forms a subnetwork of regions within a larger, widely recognized network organized into ventral and dorsal streams for processing emotional and cognitive information that converge in the medial PFC and cingulate cortex. Models of fear learning, while not a cognitive process in the conventional sense, provide important insights into the maintenance of the core symptom clusters of PTSD such as re-experiencing and hypervigilance. Fear processing takes place within the limbic corticostriatal loop composed of threatalerting and threat-assessing components. Understanding the disruptions in these two networks, and their effect on individuals with PTSD, will lead to an improved knowledge of the etiopathogenesis of PTSD and potential targets for both psychotherapeutic and pharmacotherapeutic interventions.
Preliminary Study of Acute Changes in Emotion Processing in Trauma Survivors with PTSD Symptoms
PloS one, 2016
Accumulating evidence suggests traumatic experience can rapidly alter brain activation associated with emotion processing. However, little is known about acute changes in emotion neurocircuits that underlie PTSD symptom development. To examine acute alterations in emotion circuit activation and structure that may be linked to PTSD symptoms, thirty-eight subjects performed a task of appraisal of emotional faces as their brains were functionally and structurally studied with MRI at both two weeks and three months after motor vehicle collision (MVC). As determined by symptoms reported in the PTSD Checklist at three months, sixteen survivors developed probable PTSD, whereas the remaining 22 did not meet criteria for PTSD diagnosis (non-PTSD). The probable PTSD group had greater activation than the non-PTSD group in dorsal and ventral medial prefrontal cortex (dmPFC and vmPFC) while appraising fearful faces within two weeks after MVC and in left insular cortex (IC) three months after MVC...
Psychiatry Research: Neuroimaging, 2009
Information processing models of posttraumatic stress disorder (PTSD) suggest that PTSD is characterized by preferential allocation of attentional resources to potentially threatening stimuli. However, few studies have examined the neural pattern underlying attention and emotion in association with PTSD symptomatology. In the present study, combat veterans with PTSD symptomatology engaged in an emotional oddball task while undergoing functional magnetic resonance imaging (fMRI). Veterans were classified into a high or low symptomatology group based on their scores on the Davidson Trauma Scale (DTS). Participants discriminated infrequent target stimuli (circles) from frequent standards (squares) while emotional and neutral distractors were presented infrequently and irregularly. Results revealed that participants with greater PTSD symptomatology showed enhanced neural activity in ventral-limbic and dorsal regions for emotional stimuli and attenuated activity in dorsolateral prefrontal and parietal regions for attention targets. In the anterior cingulate gyrus, participants with fewer PTSD symptoms showed equivalent responses to attentional and emotional stimuli while the high symptom group showed greater activation for negative emotional stimuli. Taken together, the results suggest that hyperresponsive ventral-limbic activity coupled with altered dorsal-attention and anterior cingulate function may be a neural marker of attention bias in PTSD.
Posttraumatic Stress Disorder: The Role of Medial Prefrontal Cortex and Amygdala
The Neuroscientist, 2009
Post-traumatic stress disorder (PTSD) is characterized by recurrent distressing memories of an emotionally traumatic event. In this review, we present neuroscientific data highlighting the function of two brain areas-the amygdala and ventromedial prefrontal cortex (vmPFC)-in PTSD and related emotional processes. A convergent body of human and non-human studies suggests that the amygdala mediates the acquisition and expression of conditioned fear and the enhancement of emotional memory, whereas the vmPFC mediates the extinction of conditioned fear and the volitional regulation of negative emotion. It has been theorized that the vmPFC exerts inhibition on the amygdala, and that a defect in this inhibition could account for the symptoms of PTSD. This theory is supported by functional imaging studies of PTSD patients, who exhibit hypoactivity in vmPFC but hyperactivity in amygdala. A recent study of brain-injured and trauma-exposed combat veterans confirms that amygdala damage reduces the likelihood of developing PTSD. But contrary to the prediction of the top-down inhibition model, vmPFC damage also reduces the likelihood of developing PTSD. The putative roles of amygdala and vmPFC in the pathophysiology of PTSD, as well as implications for potential treatments, are discussed in light of these results.
Brain activation in PTSD in response to trauma-related stimuli
Biological Psychiatry, 1999
Background: Repetitive recall of traumatic memories and chronic intermittent hyperarousal are characteristic of posttraumatic stress disorder (PTSD). Hyperarousal and memory dysfunction implicates "limbic" brain regions, including the amygdaloid complex, hippocampal formation, and limbic cortex, such as the orbitofrontal and anterior cingulate areas. To investigate the neurobiologic role of these brain regions in PTSD, we measured regional cerebral blood flow in PTSD with single photon emission computerized tomography (SPECT) during a symptom provocation paradigm. Methods: Fourteen Vietnam veterans with PTSD, 11 combat control subjects, and 14 normal control subjects were studied with [ 99m Tc]HMPAO in two sessions 48 hours apart: one session after exposure to white noise and the other following exposure to combat sounds. Skin conductance, heart rate, and subjective experience were recorded at the time of the studies. Results: Activation for all three groups occurred in the anterior cingulate/middle prefrontal gyrus. Activation in the region of the left amygdala/nucleus accumbens was found in PTSD patients only. Deactivation was found in all three groups in the left retrosplenial region. Conclusions: These findings implicate regions of the "limbic" brain, which may mediate the response to aversive stimuli in healthy individuals and in patients suffering from PTSD. Biol Psychiatry 1999;45:817-826
American Journal of Psychiatry, 2007
Objective: Hypothalamic-pituitary-adrenal axis activity and cortisol release are consequences of central stress system activation, but they may also influence cognitive and emotional processes within the brain. Despite the importance of central stress response systems, little is known about the specific brain circuits through which psychosocial stimuli activate the hypothalamic-pituitary-adrenal axis and through which cortisol feedback modulates central processing. The authors used [ 15 O]H 2 O positron emission tomography (PET) on subjects with posttraumatic stress disorder (PTSD) to study these circuits.
The neurobiology of posttraumatic stress disorder: dysfunction in the prefrontal-amygdala circuit?
Psychology and Neuroscience, 2011
Posttraumatic stress disorder (PTSD) is an anxiety disorder that can develop following exposure to a traumatic event, including terrifying or life-threatening situations such as sexual assault or natural disasters. The disorder is characterized by a reaction of intense fear, helplessness, or horror when the individual experiences, testifies about, or is faced with one or more events that involve death, severe wounds, or a threat to one's own or another's physical integrity. One of the most important symptoms of PTSD is the revival of the traumatic event, which has been interpreted as an inability to downregulate negative emotions. Neuroimaging studies that probed the ability to regulate emotions in healthy volunteers have found a pattern characterized by activation of the prefrontal cortex associated with a reduction in amygdala activity. This suggests an inhibitory prefrontal cortexamygdala circuit that underlies emotional regulation. The hypothesis that increased amygdala activation associated with PTSD results from dysfunction in the inhibitory mechanism exerted by the prefrontal cortex has been the topic of debate. The present review investigates the validity of dysfunction in the prefrontal-amygdala pathway in PTSD. The studies provide evidence that the amygdala and prefrontal cortex exhibit distinct activation patterns in PTSD, thus supporting the model of a dysfunctional circuit. Inconsistencies in the literature may be attributable to distinct PTSD subgroups, different experimental approaches, different contrasts employed in neuroimaging studies, and small sample sizes.