Clinical Implications of Neuroscience Research in PTSD (original) (raw)
Clinical implications of neuroscience research for treatment of PTSD
The research showing how exposure to extreme stress affects brain function is making important contributions to understanding the nature of traumatic stress. This includes the notion that traumatized individuals are vulnerable to react to sensory information with subcortically initiated responses that are irrelevant, and often harmful, in the present.
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.
The Neurobiological Basis of Posttraumatic Stress Disorder and Its Treatment
Neuron, 2009
Post-Traumatic Stress Disorder: Basic Science and Clinical Practice is an edited volume on a topic of great interest to the lay public, clinicians, and research scientists. Because many of the readers of Neuron may not be familiar with posttraumatic stress disorder (PTSD), it seems propitious to first describe this all too common psychiatric disorder. PTSD is the only syndrome in the entire Diagnostic and Statistical Manual-IV (DSM-IV), published by the American Psychiatric Association, that occurs as a consequence of exposure to a stressor, namely a traumatic event. The traumatic event that the person experienced or witnessed must have involved actual or threatened death or injury, or threat to physical injury of oneself or others, and the person must have responded with intense fear, helplessness, or horror. In addition, patients experience three additional major symptom clusters including re-experiencing, avoidance or numbing, and increased arousal. Re-experiencing (requires one or more symptoms) includes recurrent intrusive recollections of the traumatic event, nightmares, flashbacks, and both psychological and physiological distress upon exposure to the trauma or related stimuli. Avoidance and numbing (requires three or more symptoms) include avoidance of thoughts, feelings, conversations, activities, places, and people associated with the trauma, as well as amnesia, diminished interest in activities, detachment or estrangement from others, restricted range of affect, and the sense of a limited future. Increased arousal (requires two or more symptoms) includes sleep disturbances, irritability and anger outbursts, difficulty concentrating, hypervigilence, and being easily startled. In order to fulfill DSM-IV criteria for PTSD, patients must exhibit symptoms from each of the aforementioned categories, which cause significant distress or impairment and persist for at least one month. In addition, of all the major psychiatric syndromes, PTSD exhibits the highest rate of comorbidity with other disorders, most notably major depression, other anxiety disorders, substance abuse, and a variety of medical disorders. Although PTSD was first recognized as a consequence of experiences that occurred during military combat, it has now appropriately been expanded to responses to a variety of traumatic events, including natural disasters, rape, automobile and airplane accidents, and terrorism, to name a few. Indeed, although PTSD was once considered a relatively rare condition,
Experimental neurology, 2016
Posttraumatic Stress Disorder (PTSD) is associated with alterations in attention at the behavioral and neural levels. However, there are conflicting findings regarding the specific type of attention impairments present in PTSD, as the commonly used tests of attention do not isolate the mechanisms behind attention abnormalities, and the constructs measured do not map onto the neurocircuits governing attention. Here, we review the literature on attention processing in PTSD and offer directions for future research to clarify these unanswered questions. First, using instruments that allow assessment of behavioral and neurophysiological attention components will be necessary to understand attention deficits in PTSD. Second, focus on intra-individual variability in addition to assessment of central tendency may help clarify some of the mixed findings. Third, longitudinal studies on attentional processes are warranted to determine how attention contributes to the development and maintenanc...
Examining of trauma and post traumatic stress disorder in terms of neuroscience perspective
DergiPark (Istanbul University), 2023
Trauma is an unexpected and terrifying event that has the potential to damage a person's bodily integrity or risk death. After this event, some negative emotional, cognitive and behavioral reactions are observed in people. If it has been one month or more after the event, and if the person shows avoidance behavior in addition to these negative reactions, or experiences the event over and over with flashbacks and has increased arousal, it can be mentioned that the person shows the symptoms of post-traumatic stress disorder (PTSD). Just as every behavior we do during the day has a neurobiological basis, the reactions shown during and after trauma also have a neurobiological basis. The stress at the time of trauma causes various activities in the brain and as a result of these activities, changes occur in the person's feelings, thoughts and behaviors. So we can talk about a two-way interaction. This interaction of different systems helps us understand PTSD. Oner, Y. (2023). Examining of trauma and post traumatic stress disorder in terms of neuroscience perspective. Psychology Research on Education and Social Sciences, 4(3), 117-123. Oner Psychology Research on Education and Social Sciences 4(3) (2023) 117-123 118 distress, avoidance memories, thoughts or feelings associated traumatic event and external reminders such as people or places, negative alterations in cognitions and mood, irritable or self-destructive behavior (APA, 2013a, p.271-272). Criteria of the PTSD are the results of a series of changes that occur in the brain after trauma. The events that take place in the brain during trauma stem from the person's survival instinct. Rather than processing and examining the information received during the event in a long and detailed way, the brain is alerted in faster ways to keep the person alive. This sometimes causes people to act irrationally. Like people jumping out of windows in earthquakes. After such traumatic events, the brain may not easily come out of the alarm state. Changes that occur during trauma may be permanent for a while. Here, we see PTSD symptoms for months or even years in people whose brain cannot fully come out of the alarm state. Having the opportunity to reach social support after trauma is very important for recovery. The fact that the environment in which people are in the acute period is safe, that they can meet their urgent needs, and that they know that they can reach help whenever they want helps people to spend this period better. Still, the effects can last a long time and lead to PTSD. Today, there are proven methods in the treatment of PTSD. If people have not been able to get rid
2014
The following article outlines the possible application of the technologies of neuroscience to improve medical and mental health professionals' understanding of the sequelae and maintenance of symptoms of posttraumatic stress disorder (PTSD). A neurocognitive model of PTSD is presented, incorporating findings of frontal and subcortical dysregulation after exposure to trauma. Suggestions for incorporating more neurologically-based techniques into PTSD treatment, including cognitive rehabilitation and neurofeedback, and speculations regarding the utility of transcranial magnetic stimulation (TMS) and deep brain stimulation (DBS) in the treatment of PTSD are also presented.
Gms Psycho Social Medicine, 2004
Neuroimaging research on the neurobiology of chronic PTSD (posttraumatic stress disorder) has revealed structural and functional alterations primarily affecting areas of the medial temporal lobe (hippocampus, amygdala, and parahippocampal gyrus) and the frontal cortex known to be associated with the disorder. Using functional magnetic resonance imaging (fMRI), the present study studied the functional neuroanatomy of traumatic and non-traumatic emotional memory in two surgical patients who had sustained severe accident trauma. While patient 1 had developed acute PTSD following the traumatic event, patient 2 (control) did not. When confronted with traumatic (relative to negatively valenced non-traumatic) memory, the PTSD patient exhibited evidence for increased neural activity in the right and the left superior temporal lobe, the amygdala, the left angular gyrus, and the medial frontal gyrus, while the non-PTSD patient exposed to identical conditions showed increased activations in frontal and parietal regions. Both patients exhibited identical activation patterns when recalling non-traumatic memories relative to neutral memories. It is concluded that the pronounced activation patterns in the PTSD patient may be considered specific for acute PTSD, involved with the emotional arousal and the vivid visual recollections typical for the acute phase of the disorder. Neuere bildgebende Studien zur Neurobiologie der chronifizierten PTSD lassen vermuten, dass das Störungsbild sowohl mit funktionellen als auch strukturellen Veränderungen in umschriebenen Hirnregionen des medialen Temporallappens (Hippokampus, Amygdala, Parahippokampaler Gyrus) und des frontalen Cortex einhergeht. Die vorliegende fMRT(funktionelle Magnetresonanztomografie)-Studie untersuchte die funktionelle Neuroanatomie traumatischer und nicht-traumatischer Erinnerungen bei zwei chirurgischen Patienten nach schwerer Unfalltraumatisierung. Nur Patient 1 entwickelte eine akute PTSD, während Patient 2 ohne klinisch relevante PTSD-Symptomatik blieb. Konfrontiert mit der Unfallerinnerung (im Vergleich zu negativen, aber nicht traumatischen Erinnerungen) zeigte der PTSD-Patient vermehrte neuronale Aktivitäten im Bereich des rechten und linken superioren Temporallappens, im Bereich der Amygdalae, des linken Gyrus angularis, und des Gyrus frontalis medialis. Der Patient ohne PTSD-Symptome zeigte bei gleichen Untersuchungsbedingungen vermehrte neuronale Aktivitäten in frontalen und parietalen Regionen. Beide Patienten zeigten identische Aktivierungsmuster für den Vergleich negativer, nicht-traumatischer zu neutralen Erinnerungen. Die Untersuchungsergebnisse lassen vermuten, dass die besonderen Aktivierungsmuster bei dem Patienten mit akuter PTSD spezifisch für das Stadium einer akuten PTSD sind, die typischerweise durch sehr lebendige und emotional belastende Wiedererinnerungen der traumatischen Situation charakterisiert ist.
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.
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.
Journal of Affective Disorders, 2010
Background: Cognitive theories of anxiety disorders postulate an increased attentional bias to environmental cues associated with threat that underlies the exaggerated fear response. The role of trauma, which may represent strong competitive advantage for attention, remains unclear. We investigated the influence of trauma exposure and the presence of anxiety/stress disorders on the impact of emotional distractors on cognitive performance. Methods: Fourteen trauma-exposed subjects with PTSD, 12 trauma-exposed subjects with anxiety disorders other than PTSD, 12 trauma-exposed healthy subjects and 19 non-traumaexposed healthy controls participated in this study. The impact of emotion on cognition was determined by the Affective Stroop task that measures the effect of irrelevant emotional distractors on the speed of operant responding. Results: The speed of cognitive performance was significantly reduced in the presence of negative distractors versus neutral or positive distractors in subjects with PTSD, while there was no significant influence of the distractor type on performance in the other diagnostic groups (diagnosis-by-distractor type interaction, p b 0.001). While negative distractors induced the same levels of anxiety and depersonalization in subjects with PTSD and subjects with other anxiety disorders, distractor-induced depersonalization was associated with slowing of cognitive performance in PTSD (p = 0.02) but not in other groups. Limitations: Different types of anxiety disorders in the non-PTSD group might reduce the selectivity of the results; some subjects received medication possibly impacting on their cognitive functioning. Conclusions: The cognitive impairments in the presence of negative distractors specifically found in PTSD call for research into novel psychotherapeutic approaches, e.g. attentional training, for PTSD.