Post-traumatic Stress Disorder

Dan J. Stein, Matthew Friedman, Carlos Blanco

• Publisher: Wiley
• Year: 2011
• ISBN:
  9781119971481
• Edition: 1
• Topic: Medizin
• Subtopic: Anatomie

Despite the growing interest in the role of psychological trauma in the genesis of psychiatric disorders, few volumes have addressed these issues from a multidisciplinary and international perspective. Given the complexity of reslience and posttraumatic disorder, and given ongoing trauma and violence in many parts of the world, it is crucial to apply such perspectives to review existing knowledge in the field and provide directions for future research.

This book has a broad scope. A key focus is PTSD, because of its clinical and health importance, its obvious link with trauma, and its interest for many clinicians and researchers. However, the book also examines resilience and a range of mental health consequences of trauma, because it has become increasingly clear that not all individuals react to trauma in the same way. It is important for mental health professionals to be aware of the broad range of potential responses to trauma, as well as of relevant evidence-based treatments.

The book includes chapters that address a wide range of topics on trauma-related disorders, including nosology and classification, epidemiology, neurobiology, pharmacotherapy, and psychotherapy. Each chapter comprises a critical review of the existing literature, aimed at being useful for the practitioner. This is followed by selected commentaries from other authorities on the topic, representing diverse geographical locations and points of view, who refine some of the perspectives offered in the review, provide alternative views, or suggest important areas of future work.

Chapter 1

PTSD and Related Disorders

Matthew J. Friedman

Department of Psychiatry and of Pharmacology & Toxicology,

Dartmouth Medical School; National Center for Posttraumatic Stress Disorder,

US Department of Veterans Affairs, Hanover, NH, USA

Introduction

Of the many diagnoses in the Diagnostic and Statistical Manual IV-TR (DSM-IV-TR) [1], very few invoke an aetiology in their diagnostic criteria: (i) organic mental disorders (e.g. caused by a neurological abnormality); (ii) substance-use disorders (e.g. caused by psychoactive chemical agents); (iii) post-traumatic stress disorder (PTSD); (iv) acute stress disorder (ASD); and (v) adjustment disorders (ADs) [2] – the latter three are all caused by exposure to a stressful environmental event that exceeds the coping capacity of the affected individual. The presumed causal relationship between the stressor and PTSD, ASD and AD is complicated and controversial, as will be discussed below. Controversy notwithstanding, acceptance of this causal relationship, initially in the DSM-III [3], has equipped practitioners and scientists with a conceptual tool that has profoundly influenced clinical practice over the past 30 years.

PTSD is primarily a disorder of reactivity rather than of an altered baseline state as in major depressive disorder or general anxiety disorder. Its psychopathology is characteristically expressed during interactions with the interpersonal or physical environment. People with PTSD are consumed by concerns about personal safety. They persistently scan the environment for threatening stimuli. When in doubt, they are more likely to assume that danger is present and will react accordingly. The avoidance and hyperarousal symptoms described below can be understood within this context. The primacy of traumatic over other memories (e.g. the reexperiencing symptoms) can also be understood as a pathological exaggeration of an adaptive human response to remember as much as possible about dangerous encounters in order to avoid similar threats in the future.

The sustained anxiety about potential threats to life and limb, pervasive and uncontrollable sense of danger, and maladaptive preoccupation with concerns about personal safety and the safety of one's family can be explicated in terms of psychological models such as classic Pavlovian fear conditioning, two-factor theory or emotional processing theory [4–6]. The traumatic (unconditioned) stimulus (the rape, assault, disaster, etc.) automatically evokes the post-traumatic (unconditioned) emotional response (fear, helplessness and/or horror). The intensity of this emotional reaction provokes avoidance or protective behaviours that reduce the emotional impact of the stimulus. Conditioned stimuli, reminders of such traumatic events (e.g. seeing someone who resembles the original assailant, confronting war-zone reminders, exposure to high winds or torrential downpours reminiscent of a hurricane, etc.), evoke similar conditioned responses manifested as fear-induced avoidance and protective behaviours.

Such psychological models can also be explicated within the context of neurocircuitry that mediates the processing of threatening or fearful stimuli. In short, traumatic stimuli activate the amygdala, which in turn produces outputs to the hippocampus, medial prefrontal cortex, locus coeruleus, thalamus, hypothalamus, insula and dorsal/ventral striatum [7–9]. In PTSD, the normal restraint on the amygdala exerted by the medial prefrontal cortex – especially the anterior cingulate gyrus and orbitofrontal cortex – is severely disrupted. Such disinhibition of the amygdala creates an abnormal psychobiological state of hypervigilance in which innocuous or ambiguous stimuli are more likely to be misinterpreted as threatening. To be hypervigilant in a dangerous situation is adaptive. To remain so after the danger has passed is not.

Fear-conditioning models help to explain many PTSD symptoms such as intrusive recollections (e.g. nightmares and psychological/physiological reactions to traumatic reminders), avoidance behaviours and hyperarousal symptoms such as hypervigilence. Emotional numbing, another important manifestation of PTSD, has been explicated in terms of stress-induced analgesia [10]. Such emotional anaesthesia is potentially even more disruptive and disturbing to the affected individual and loved ones than other symptoms because it may produce an insurmountable emotional barrier between the PTSD patient and his or her family. Such individuals are unable to experience loving feelings or to reciprocate those of partners and children. As a result, they isolate themselves and become emotionally inaccessible to loved ones to whom they had previously been very close. They also cut themselves off from friends. Finally, there are PTSD symptoms that jeopardise the capacity to function effectively at work, such as diminished ability to concentrate, irritability and loss of interest in work or school. In short, there is a perceived discontinuity between the pre- and post-traumatic self. People with PTSD see themselves as altered by their traumatic experience. They feel as if they have been drastically and irrevocably changed by this encounter. Others have described this discontinuity as a ‘broken connection’ with the past [11]; or as ‘shattered assumptions’ about oneself and one's world [12].

Historical Antecedents

Before the mid-nineteenth century, the psychological impact of exposure to traumatic stress was recorded by poets, dramatists and novelists. Trimble [13], Shay [14] and others have pointed out that Homer, Shakespeare and Dickens (to name only a few) had sophisticated understanding of the profound impact of traumatic stressors on cognitions, feelings and behaviour. Medicalisation of such invisible wounds, usually (but not always) received in combat, occurred on both sides of the Atlantic during the mid-nineteenth century. Explanatory models pointed to the heart (e.g. soldier's heart, Da Costa's syndrome and neurocirculatory asthenia), the nervous system (e.g. railway spine, shell shock) and the psyche (e.g. nostalgia, traumatic neurosis) as the (invisibly) affected system.

In the 1970s, spurred on by social movements in the USA and around the world, what had previously been contextualised primarily as a problem among military personnel and veterans was broadened to include victims of domestic violence, rape and child abuse. The women's movement emphasised sexual and physical assault on women while child advocacy groups emphasised physical and sexual abuse in children. Thus, new clinical entities took their places alongside combat-related syndromes. These included: rape trauma syndrome, battered woman syndrome, child abuse syndrome and others [15–17].

In other words, by the late 1970s clinicians had a wide variety of post-traumatic diagnostic options from which to choose, although none were recognised in the DSM-II [18]. Indeed, from a PTSD perspective, DSM-II was a step backwards, since DSM-I [19] contained the ill-defined ‘gross stress reaction’, which provided a useful, but temporary, diagnostic niche for military veterans, ex-prisoners of war, rape victims and Nazi Holocaust survivors. (If ‘gross stress reaction’ persisted, the diagnosis had to be changed to ‘neurotic reaction’.) In DSM-II, however, even this diagnostic option was eliminated, so that ‘situational reaction’ was the only available diagnosis for people who exhibited clinically significant reactions to catastrophic experiences. Besides trivialising post-traumatic reactions (since this category included any unpleasant experience), ‘situational reactions’ were also considered temporary.

The DSM-III [3] process recognised that these differently labelled syndromes (e.g. rape trauma, post-Vietnam, war sailor, concentration camp syndromes, etc.) were all characterised by a very similar pattern of symptoms that became embodied within the PTSD diagnostic criteria. Hence, the emphasis shifted from the specific traumatic stressor to the relatively similar pattern of clinical expression that could be observed among survivors of a growing list of different severe stressful experiences. The various stressors were aggregated into Criterion A, while the clinical presentation was explicated by the PTSD symptoms themselves (Criteria B–D).

There have been some alterations of the original DSM-III PTSD criteria. The number of possible symptoms has increased from 12 to 17. The original three symptom clusters (reexperiencing, numbing and miscellaneous) have been rearranged into the present triad of reexperiencing, avoidance/numbing and hyperarousal. Criterion E (duration of symptoms must exceed one month) was included in the DSM-III-R in 1987 and Criterion F (that the symptoms must cause clinically significant distress or functional impairment) was added in the DSM-IV in 1994. Most importantly, the fundamental concept that exposure to overwhelming stress may precede the onset of clinically significant and persistent alterations in cognitions, feelings and behaviour has endured. Epidemiological studies have confirmed the DSM-III perspective and shown that exposure to extreme stress sometimes precedes severe and long-lasting psychopathology [20–24]. Such research has also shown, unfortunately, that exposure to traumatic stress is all too common across the population and that the prevalence of rape, domestic violence, child abuse and so on is unacceptably high. Thus, when it was time for the next revision of the diagnostic criteria for DSM-IV [25] it was clear that it was incorrect to characterise Criterion A, exposure to a traumatic event, as an event that ‘is generally outside the range of usual human experience’.

PTSD: DSM-IV-TR Diagnostic Criteria

Criterion A1

The DSM-IV Criterion A was divided into objective (A1) and subjective (A2) components. Criterion A1 resembled the DSM-III-R [26] Criterion A, except that a greater number of events were included as stressor events. These included: being diagnosed with a life-threatening illness, child sexual abuse (without threatened or actual violence), learning about the sudden unexpected death of a family member or close friend, and learning that one's child has a life-threatening illness. The ‘learning about’ traumatic exposure (injury or death) of a loved one has proven to be one of the most controversial changes to Criterion A (see below). In DSM-IV, however, in addition to exposure to an A1 event, it was necessary that exposed individuals experience an intense (fear-conditioned) emotional reaction (Criterion A2) characterised as ‘fear, helplessness or horror’. Although this had been foreshadowed in DSM-III-R's text description, the subjective response was now made an explicit (A2) criterion [27]. It is also worth noting that the timing of A2 was unclear and later subject to different interpretations, with some saying it might happen some time after the event rather than being strictly peritraumatic.

As we consider DSM-IV Criterion A1, there are several questions that must be addressed: (i) Should exposure to a potentially traumatic event be considered aetiologically or temporally significant with regard to the later development of PTSD? (ii) Can we really distinguish ‘traumatic’ from ‘nontraumatic’ stressors? (iii) Should Criterion A1 be eliminated from DSM-5?

Does Traumatic Exposure ‘Cause’ PTSD?

DSM-III and DSM-IV are unclear about the aetiological significance of the Criterion A event [27, 28]. On the one hand, they both suggest that traumatic exposure ‘causes’ PTSD (e.g. ‘evokes’ the characteristic PTSD symptoms). On the other, they both suggest that the traumatic event constitutes a watershed experience that temporally precedes the expression of PTSD symptoms.

We have learned a number of things since 1980 that have a direct bearing on this question. First, we know that people differ with regard to resilience and vulnerability, so that most people exposed to traumatic events do not develop PTSD. Epidemiological research has identified a number of risk and protective factors that differentially affect the susceptibility of different individuals to develop PTSD following exposure. Resilience is a complicated attribute that includes genetic, psychobiological, cognitive, emotional, behavioural, cultural and social components [7, 29]. Second, we must also recognise that events differ with regard to the conditional probability that PTSD will follow exposure. For example, the conditional probability of PTSD following rape is much higher than that for exposure to natural disasters. In other words, there is a complex interaction between individual susceptibility and the toxicity of a given stressful event. Therefore, while we acknowledge that no ...

Table of contents

• Series Page
• Title Page
• Copyright
• Preface
• List of Contributors
• Chapter 1: PTSD and Related Disorders
• Chapter 2: Epidemiology of PTSD
• Chapter 3: Neurobiology of PTSD
• Chapter 4: Pharmacotherapy of PTSD
• Chapter 5: Psychological Interventions for Trauma Exposure and PTSD
• Chapter 6: (Disaster) Public Mental Health
• Index