Article

Clarifying the origin of biological abnormalities in PTSD through the study of identical twins discordant for combat exposure

Harvard University, Cambridge, Massachusetts, United States
Annals of the New York Academy of Sciences (Impact Factor: 4.31). 08/2006; 1071:242-54. DOI: 10.1196/annals.1364.019
Source: PubMed

ABSTRACT A biological abnormality found to be associated with posttraumatic stress disorder (PTSD) may be, among other things, a pretrauma vulnerability factor, that is, it may have been present prior to the event's occurrence and increased the individual's likelihood of developing PTSD upon traumatic exposure. Alternately, it may be an acquired PTSD sign, that is, it may have developed after the traumatic exposure, along with the PTSD. We have studied pairs of Vietnam combat veterans and their noncombat-exposed, identical twins in an effort to resolve these competing origins. Combat veterans were diagnosed as current PTSD or non-PTSD (i.e., never had). Average heart rate responses (HRRs) to a series of sudden, loud-tone presentations were larger in Vietnam combat veteran twins with PTSD, but these larger responses were not shared by their noncombat-exposed cotwins, whose responses were similar to those of the non-PTSD combat veterans and their noncombat-exposed cotwins. These results suggest that larger HRRs to sudden, loud tones represent an acquired sign of PTSD. In contrast, increased neurological soft signs (NSSs), diminished hippocampal volume, and presence of abnormal cavum septum pellucidum (CSP) were found in Vietnam combat veteran twins with PTSD and their "high-risk," unexposed cotwins compared to Vietnam combat veteran twins without PTSD and their "low-risk," unexposed cotwins. These results support the conclusion that the latter abnormalities represent antecedent, familial vulnerability factors for developing chronic PTSD upon exposure to a traumatic event.

Download full-text

Full-text

Available from: Scott P Orr, Jun 17, 2015
0 Followers
 · 
98 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Retrospective and prospective studies consistently show that individuals exposed to human-generated traumatic events carry a higher risk of developing Posttraumatic Stress Disorder (PTSD) than those exposed to other kinds of events. These studies also consistently identify perceptions of social support both before and after a traumatic event as an important factor in the determining vulnerability to the development of PTSD. We review the literature on interpersonal traumas, social support and risk for PTSD and integrate findings with recent advances in developmental psychopathology, attachment theory and social neuroscience. We propose and gather evidence for what we term the social ecology of PTSD, a conceptual framework for understanding how both PTSD risk and recovery are highly dependent on social phenomena. We explore clinical implications of this conceptual framework.
    Annual Review of Psychology 02/2008; 59:301-28. DOI:10.1146/annurev.psych.58.110405.085650 · 20.53 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Exposure to traumatic stress is a requirement for the development of posttraumatic stress disorder (PTSD). However, because the majority of trauma-exposed persons do not develop PTSD, examination of the typical effects of a stressor will not identify the critical components of PTSD risk or pathogenesis. Rather, PTSD represents a specific phenotype associated with a failure to recover from the normal effects of trauma. Thus, research must focus on identifying pre- and posttraumatic risk factors that explain the development of the disorder and the failure to reinstate physiological homeostasis. In this review, we summarize what is known about the clinical and biological characteristics of PTSD and articulate some of the gaps in knowledge that can be addressed by basic neuroscience research. We emphasize how knowledge about individual differences related to genetic and epigenetic factors in behavioral and brain responses to stress offers the hope of a deeper understanding of PTSD.
    Neuron 11/2007; 56(1):19-32. DOI:10.1016/j.neuron.2007.09.006 · 15.98 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: In lower animals and humans, stress/anxiety can enhance dorsal striatal-dependent habit memory,at the expense of hippocampal-dependent cognitive memory. The present review considers the potential for this 'stress/anxiety-induced habit bias' to explain some aspects of post-traumatic stress disorder (PTSD). In rats,anxiety induced by peripheral or intra-amygdala infusions of anxiogenic drugs can enhance habit memory and impair cognitive memory. In tasks in which both habit and cognitive memory processes may provide a learned solution, stress and drug-induced anxiety favors the use of habit memory. The effect of stress and anxiety on the use of multiple memory systems in rats depends on the functional integrity of the basolateral amygdala. Thus,under robust emotional arousal, amygdala activation can modulate the relative use of memory systems in a manner that favors habit memory. We propose a similar mechanism may underlie the development and persistence of some PTSD symptoms. The traumatic memories of PTSD patients can be deficient in hippocampus-dependent contextual or autobiographical aspects, and enhanced in responding to trauma-related cues, which we suggest may reflect increased involvement of the dorsal striatum.We briefly consider the potential role of a stress/anxiety induced habit bias with regard to other psychopathologies,including obsessive-compulsive disorder and drug addiction.
    Reviews in the neurosciences 11/2012; 23(5-6):627-643. DOI:10.1515/revneuro-2012-0049 · 3.31 Impact Factor