Survivors of sexual assault are the hidden face of Post-Traumatic Stress Disorder.
December 5th, 2017 | via US News & World Report
The Trauma after the Storm
Following hurricanes and other major disasters comes another wave of trouble: post traumatic stress
November 7th, 2017 | via Scientific American
Amygdala, medial prefrontal cortex, and hippocampal function in PTSD.
Shin, L. M., Rauch, S. L., & Pitman, R. K. (2006).
Annals of the New York Academy of Science, 1071, 67-79.
The last decade of neuroimaging research has yielded important information concerning the structure, neurochemistry, and function of the amygdala, medial prefrontal cortex, and hippocampus in posttraumatic stress disorder (PTSD). Neuroimaging research reviewed in this article reveals heightened amygdala responsivity in PTSD during symptomatic states and during the processing of trauma-unrelated affective information. Importantly, amygdala responsivity is positively associated with symptom severity in PTSD. In contrast, medial prefrontal cortex appears to be volumetrically smaller and is hyporesponsive during symptomatic states and the performance of emotional cognitive tasks in PTSD. Medial prefrontal cortex responsivity is inversely associated with PTSD symptom severity. Lastly, the reviewed research suggests diminished volumes, neuronal integrity, and functional integrity of the hippocampus in PTSD. Remaining research questions and related future directions are presented.
Posttraumatic stress disorder: a sensitization reaction.
Dykman, R. A., Ackerman, P. T., & Newton, J. E. O. (1997).
Integrative Physiological and Behavioral Science, 32(1), 9-18.
This article discusses past research bearing on the question of the etiology of Posttraumatic Stress Disorder (PTSD). It argues that PTSD can be adequately accounted for by a process of emotional sensitization and that this is a more parsimonious explanation than the two-factor learning theory of Mowrer, now postulated by several writers. In brief, the etiology and subsequent development of PTSD is viewed as the result of the sensitization of fear/anxiety which is linked to a variety of to be conditional stimuli by both backward and forward association: these become conditional stimuli (CSi) once paired with the instigating circumstances. It is furthermore assumed that PTSD will not occur in the absence of a genetic susceptibility that may vary from zero to absolute certainty. Thus far, our evidence is limited to a sensitivity to loud sounds, but it is highly probable that touch and other sensory systems are involved (not necessarily in parallel). The fact that abuse often leads to behavioral disorders, including sexually seductive behaviors in children sexually abused, requires a recognition that emotional reactions other than fear may be sensitized. Fear in combination with pleasure or pleasure alone coupled with a loss of self-esteem may explain these acting-out behaviors.
The amygdala, fear, and memory.
Fanselow, M. S. & Gale, G. D. (2003).
Annals of the New York Academy of Science, 985, 125-134.
Lesions of the frontotemporal region of the amygdala, which includes lateral and basal nuclei, cause a loss of conditional fear responses, such as freezing, even when the lesions are made over a year and a half from the original training. These amygdala-damaged animals are not hyperactive and show normal reactivity to strong stimuli such as bright lights. After receiving tone-mild shock pairings rats normally display an appropriately weak response when exposed to the tone. Rats' fear of the tone can be inflated by giving them exposure to strong shocks in the absence of the tone between training and testing. This inflation of fear memory is abolished if the frontotemporal amygdala is inactivated by muscimol only during the inflation treatment with strong shocks. Based on such findings we suggest that the frontotemporal amygdala permanently encodes a memory for the hedonic value of the aversive stimulus used to condition fear.
Stress-induced enhancement of fear learning: An animal model of posttraumatic stress disorder.
Rau, V., De Cola, J. P., & Fanselow, M. S. (2005).
Neuroscience & Biobehavioral Reviews, 29, 1207–1223.
Fear is an adaptive response that initiates defensive behavior to protect animals and humans from danger. However, anxiety disorders, such as Posttraumatic Stress Disorder (PTSD), can occur when fear is inappropriately regulated. Fear conditioning can be used to study aspects of PTSD, and we have developed a model in which pre-exposure to a stressor of repeated footshock enhances conditional fear responding to a single context-shock pairing. The experiments in this chapter address interpretations of this effect including generalization and summation or fear, inflation, and altered pain sensitivity. The results of these experiments lead to the conclusion that pre-exposure to shock sensitizes conditional fear responding to similar less intense stressors. This sensitization effect resists exposure therapy (extinction) and amnestic (NMDA antagonist) treatment. The pattern predicts why in PTSD patients, mild stressors cause reactions more appropriate for the original traumatic stressor and why new fears are so readily formed in these patients. This model can facilitate the study of neurobiological mechanisms underlying sensitization of responses observed in PTSD.
Psychobiological mechanisms of resilience and vulnerability: implications for successful adaptation to extreme stress.
Charney, D. S. (2004).
American Journal of Psychiatry, 161, 195-216.
Most research on the effects of severe psychological stress has focused on stress-related psychopathology. Here, the author develops psychobiological models of resilience to extreme stress.
An integrative model of resilience and vulnerability that encompasses the neurochemical response patterns to acute stress and the neural mechanisms mediating reward, fear conditioning and extinction, and social behavior is proposed.
Eleven possible neurochemical, neuropeptide, and hormonal mediators of the psychobiological response to extreme stress were identified and related to resilience or vulnerability. The neural mechanisms of reward and motivation (hedonia, optimism, and learned helpfulness), fear responsiveness (effective behaviors despite fear), and adaptive social behavior (altruism, bonding, and teamwork) were found to be relevant to the character traits associated with resilience.
The opportunity now exists to bring to bear the full power of advances in our understanding of the neurobiological basis of behavior to facilitate the discoveries needed to predict, prevent, and treat stress-related psychopathology.
Biology of posttraumatic stress disorder.
Yehuda, R. (2001).
Journal of Clinical Psychiatry, 62, 41-46.
Most biological findings in posttraumatic stress disorder (PTSD) are compatible with those of the chronic stress response, such as increased corticotropin-releasing factor (CRF) concentrations, catecholamine depletion within the central nervous system, and reduced hippocampal volume. However, over the last 10 years, biological observations have been made in PTSD that are different from what has been typically associated with chronic stress, notably certain hypothalamic-pituitary-adrenal (HPA) axis findings. In particular, urinary and plasma cortisol levels are considerably lower in PTSD patients than in non-PTSD trauma survivors and normal controls. Furthermore, the circadian pattern of cortisol release from the adrenal glands follows a greater dynamic range in PTSD than in patients with major depression or in normal controls. The reduction in cortisol levels results from an enhanced negative feedback by cortisol, which is secondary to an increased sensitivity of glucocorticoid receptors in target tissues. This HPA axis alteration contrasts with the well-known chronic stress cascade in which CRF release results in erosion of negative feedback and down-regulation of glucocorticoid receptors. Sensitization of the HPA axis is consistent with the clinical picture of hyperreactivity and hyperresponsiveness in PTSD.
Risk factors for the development of psychopathology following trauma.
Charney, D. S. (2004).
American Journal of Psychiatry, 161, 195-216.
Traumatic experiences can lead to a range of mental health problems with posttraumatic stress disorder (PTSD) leading as the most documented disorder following trauma. Epidemiological research has found the rate of exposure to trauma to far outweigh the prevalence of PTSD. Indicating that most people do not develop PTSD following a traumatic event, this phenomenon has led to an interest in evaluating risk factors to determine who develops PTSD. Risk factors for the development of psychopathology following trauma exposure fall into three categories: pre-trauma, peri-trauma and post-trauma factors. Pre-trauma factors can include age, gender, race/ethnicity, education, prior psychopathology, and neurobiological factors. Peri-trauma factors can include the duration/severity of trauma experience and the perception that the trauma has ended. Post-trauma factors can include access to needed resources, social support, specific cognitive patterns, and physical activity. To date, several important risk factors have been found to impact the risk of developing PTSD including gender, age, education, IQ, race and ethnicity, sexual orientation, pre-trauma psychopathology, prior trauma exposure, familial psychiatric history, and neurobiological factors. This article outlines the state of research findings on pretraumatic, peritraumatic, and posttraumatic risk factors for the development of PTSD and associated psychopathology following trauma.