**PTSD, Neuroimaging and Psychotherapy: A Fruitful Encounter**

Julio F.P. Peres, PsyD, PhD.

*Radiology Clinic – Universidade Federal de São Paulo, SP, Psychotraumatology Clinic - Hospital Perola Byington, SP, Brazil* 

#### **1. Introduction**

394 Neuroimaging for Clinicians – Combining Research and Practice

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Most of us have dealt with a traumatic event of some kind such as loss, accident, or illness, or will be dealing with one at some point in our lives. Psychological trauma is closely related to the development of posttraumatic stress disorder (PTSD), involving three sets of symptoms: (i) reliving trauma (traumatic memories, nightmares, intrusive thoughts); (ii) emotional avoidance/numbness (affective distance, emotional anaesthesia); and (iii) increased arousal (irritability, insomnia and hypervigilance) (American Psychiatric Association, 1994). Lifetime prevalence of PTSD-triggering traumatic events may be as much as 50–90%, and actual prevalence in the general population is about 8% (Kessler et al., 1995; Vieweg et al., 2006), while partial PTSD (pPTSD) in an at-risk groups have been estimated at approximately 30% (Weiss et al., 1992). After noting that individuals who do not meet the full set of diagnostic criteria for PTSD may suffer from clinically significant symptoms of PTSD (Weiss et al., 1992), the concept of pPTSD or subthreshold PTSD was introduced to describe subsyndromal forms of PTSD (Blanchard et al., 1995; Stein et al. 1997). Thus, exposure to traumatic stressors and psychological trauma is widespread, with a wide range of cognitive and behavioral responses/outcomes among trauma survivors (Peres et al., 2009; 2011).

One of the main psychological sequelae of traumatic experiences is conditioning of specific fears. In addition to PTSD, traumatic events can significantly influence major depression, somatoform disorders, panic and anxiety disorders, obsessive-compulsive disorders, phobic disorders, and substance abuse (Peres et al., 2009). Although traumatic events are associated with PTSD in the literature, traumatized people do not meet DSM-IV (Diagnostic and Statistical Manual of Mental Disorders, 4th Edition) criteria for PTSD in many cases and often present a range of psychoform or somatoform symptoms. Considerable overlap in symptoms and disease comorbidity has been noted for medically unexplained symptoms in the primary care setting, such as chronic fatigue syndrome, low back pain, irritable bowel syndrome, primary headaches, fibromyalgia, temporomandibular joint disorder, major depression, panic attacks, and PTSD (Peres et al., 2009). Epidemiologic surveys increasingly point to a relation between exposure to traumatic events and more health care utilization, adverse health outcomes, onset of specific diseases, and premature death (Corrigan et al., 2005; Keane et al., 2006). Certain characteristics of traumas, particularly peritraumatic cognitive response and related cognitions, appear to heighten the risk for PTSD (Peres et al.,

PTSD, Neuroimaging and Psychotherapy: A Fruitful Encounter 397

of interpersonal violence during childhood than in combat soldiers and accident victims

In a situation of unknown risk, heart and visceral alterations point to autonomous nervous system hyperactivity, whereas a subjective state of arousal potentiates an immediate search for syntheses and parameters for generating behavior. Peripheral and metabolic alterations (eg, tachycardia, mydriasis) reflect hyperactivity of the sympathetic nervous system and the hypothalamus-hypophysis-adrenal (HPA) axis leading to an immediate self-preservation response (Peres et al., 2007). Neurofunctional studies with hyperarousal PTSD patients using symptom provocation paradigms (in most cases, the retrieval of traumatic memories) suggest that the difficulty of synthesizing, classifying, and integrating a traumatic memory in narrative form may be related to the decreased activity of the prefrontal cortex involved in reducing negative feedback from the activity of the amygdala (Shin et al., 2004). Studies have implicated the HPA and the sympathetic-adrenal-medullar stress axes as key components of this pathogenic process (Boscarino et al., 2006). The relationship between anxiety level and performance is no longer advantageous after a certain point. Selfgenerated information flooding into sensory pathways affects the perceptual processing of data from surroundings, thus hampering the ability to formulate new hypotheses and

Trauma-related studies involving epinephrine (E), norepinephrine (NE), and serotonin (5- HT) suggested that alterations in NE, E, and 5-HT may have relevance for symptoms commonly seen in survivors with PTSD, including hypervigilance, exaggerated startle, irritability, impulsivity, aggression, and intrusive memories (Southwick et al., 1999). Studies related to the role of NE in arousal, orienting to novel stimuli, selective attention, and vigilance demonstrated heightened noradrenergic neuronal reactivity, increased -2 receptor sensitivity and exaggerated arousal in organisms that have been exposed to chronic uncontrollable stress. The way an individual cognitively processes a traumatic event may

Tonic immobility (TI) is a possible component of the fear response characterized by freezing or immobility in situations involving extreme fear coupled with physical restraint, and is observed in 30% to 40% of rape victims (Kaplow et al., 2005). A study of TI in victims of childhood sexual abuse (CSA)—female undergraduates (*n* = 39) and female psychiatric inpatients (*n* = 41)—showed that more than 52% of all participants reported TI in response to CSA. TI reports were associated with greater current psychological impairment (Heidt et al., 2005) and may be typical not only of rape and sexual abuse victims, but other kinds of

Emotional factors play a role in many reflex TI manifestations referred to as *feigning death*. Whether orienting and defense responses provide a valid model in humans has yet to be proven, but the dissociative response in certain trauma cases resembles animal TI. Bovin and colleagues (2008) asked whether TI mediates relations between perceived inescapability, peritraumatic fear, and PTSD symptom severity among sexual assault survivors. Their findings indicated that TI fully mediated relations between perceived inescapability and overall PTSD symptom severity, as well as re-experiencing and

(who do not present hyperarousal symptoms).

trigger an anxious/arousal or a dissociative reaction.

directly experienced traumas as well (Bados et al., 2008).

**2.1 Subtype I** 

syntheses.

**2.2 Subtype II** 

2009). How people process stressors may be critical in determining whether or not trauma will be experienced, as well as the different constellation of symptoms if traumatization is characterized.

A single traumatic event can be processed in very different ways by individuals who experienced the same traumatic episode (Peres et al., 2005; 2011). The psychopathological signs of trauma are not static over time, nor is the form of the expression of traumatic memories. This fluidity is a consequence of the sensitization that is driven by reminders of the traumatic event and the vulnerability of memory to being modified with repeated recall (Peres et al., 2008; 2011). The sensitization of neural pathways involved in this reactivity is central to understanding the neurobiology of PTSD. The purpose of this chapter is to attempt to integrate both neuroimaging and psychotherapeutic findings in relation to PTSD, so that integration might bring greater efficacy to the treatment of psychologically traumatized patients.
