Tanja Michael

Posttraumatic stress disorder following assault: the role of cognitive processing, trauma memory, and appraisals

Two studies of assault victims examined the roles of (a) disorganized trauma memories in the development of posttraumatic stress disorder (PTSD), (b) peritraumatic cognitive processing in the development of problematic memories and PTSD, and (c) ongoing dissociation and negative appraisals of memories in maintaining symptomatology. In the cross-sectional study (n = 81), comparisons of current, past, and no-PTSD groups suggested that peritraumatic cognitive processing is related to the development of disorganized memories and PTSD. Ongoing dissociation and negative appraisals served to maintain PTSD symptoms. The prospective study (n = 73) replicated these findings longitudinally. Cognitive and memory assessments completed within 12-weeks postassault predicted 6-month symptoms. Assault severity measures explained 22% of symptom variance; measures of cognitive processing, memory disorganization, and appraisals increased prediction accuracy to 71%.

Intrusive re-experiencing in post-traumatic stress disorder: phenomenology, theory, and therapy.

The article describes features of trauma memories in post‐traumatic stress disorder (PTSD), including characteristics of unintentional re‐experiencing symptoms and intentional recall of trauma narratives. Re‐experiencing symptoms are usually sensory impressions and emotional responses from the trauma that appear to lack a time perspective and a context. The vast majority of intrusive memories can be interpreted as re‐experiencing of warning signals, i.e., stimuli that signalled the onset of the trauma or of moments when the meaning of the event changed for the worse. Triggers of re‐experiencing symptoms include stimuli that have perceptual similarity to cues accompanying the traumatic event. Intentional recall of the trauma in PTSD may be characterised by confusion about temporal order, and difficulty in accessing important details, both of which contribute to problematic appraisals. Recall tends to be disjointed. When patients with PTSD deliberately recall the worst moments of the trauma, they often do not access other relevant (usually subsequent) information that would correct impressions/predictions made at the time. A theoretical analysis of re‐experiencing symptoms and their triggers is offered, and implications for treatment are discussed. These include the need to actively incorporate updating information ( “I know now …”) into the worst moments of the trauma memory, and to train patients to discriminate between the stimuli that were present during the trauma ( “then”) and the innocuous triggers of re‐experiencing symptoms ( “now”).

Autonomic and Respiratory Characteristics of Posttraumatic Stress Disorder and Panic Disorder

Objective: Posttraumatic stress disorder (PTSD) and panic disorder (PD) are two anxiety disorders with prominent psychophysiological symptoms. The PTSD criterion of persistent hyperarousal suggests autonomic dysregulation, and the disorder has been associated with elevated heart rate. In contrast, PD has been associated with respiratory abnormalities such as low end-tidal Pco2. An integrated analysis of automatic and respiratory function in a direct comparison of these anxiety disorders is currently lacking. Methods: Electrodermal, cardiovascular, and respiratory psychophysiology was examined in 23 PTSD patients, 26 PD patients, and 32 healthy individuals at baseline and during threat of shock. Results: At baseline, the PTSD patients, in contrast to the other two groups, were characterized by attenuated parasympathetic and elevated sympathetic control, as evidenced by low respiratory sinus arrhythmia (a measure of cardiac vagal control) and high electrodermal activity. They also displayed elevated heart rate and cardiovascular sympathetic activation in comparison with healthy controls. PD patients exhibited lower Pco2 (hypocapnia) and higher cardiovascular sympathetic activation compared with healthy controls. PTSD patients, but not PD patients, sighed more frequently than controls. During the threat of shock phase, the PTSD group demonstrated blunted electrodermal responses. Conclusions: Persistent hyperarousal symptoms in PTSD seem to be due to high sympathetic activity coupled with low parasympathetic cardiac control. Respiratory abnormalities were also present in PTSD. Several psychophysiological measures exhibited group-comparison effect sizes in the order of 1.0, supporting their potential for enhancing differential diagnosis and possibly suggesting utility as endophenotypes in genetic studies of anxiety disorders. CSI = cardiovascular sympathetic index; CVT = cardiac vagal tone; ESI = electrodermal sympathetic index; HR = heart rate; HP = heart period; RSA = respiratory sinus arrhythmia; NS-SCR = number of nonspecific skin conductance fluctuations; HRV = heart rate variability; SCL = skin conductance level; Pco2 = end-tidal partial pressure of expired CO2; PDS = Posttraumatic Diagnostic Scale; PTSD = posttraumatic stress disorder; PD = panic disorder; STAI = State-Trait Anxiety Inventory; BDI = Beck Depression Inventory; SCRamp = amplitude of nonspecific skin conductance responses; ECG = electrocardiogram; lnHF = high-frequency power of HP variability; lnLF = low-frequency power of HP variability; lnVLF = very low-frequency power of HP variability; MANOVA = multivariate analysis of variance; HC = healthy controls.

Fear conditioning in panic disorder: Enhanced resistance to extinction.

Enhanced conditionability has been proposed as a crucial factor in the etiology and maintenance of panic disorder (PD). To test this assumption, the authors of the current study examined the acquisition and extinction of conditioned responses to aversive stimuli in PD. Thirty-nine PD patients and 33 healthy control participants took part in a differential aversive conditioning experiment. A highly annoying but not painful electrical stimulus served as the unconditioned stimulus (US), and two neutral pictures were used as either the paired conditioned stimulus (CS+) or the unpaired conditioned stimulus (CS-). Results indicate that PD patients do not show larger conditioned responses during acquisition than control participants. However, in contrast to control participants, PD patients exhibited larger skin conductance responses to CS+ stimuli during extinction and maintained a more negative evaluation of them, as indicated by valence ratings obtained several times throughout the experiment. This suggests that PD patients show enhanced conditionability with respect to extinction.

Glucocorticoids enhance extinction-based psychotherapy

Behavioral exposure therapy of anxiety disorders is believed to rely on fear extinction. Because preclinical studies have shown that glucocorticoids can promote extinction processes, we aimed at investigating whether the administration of these hormones might be useful in enhancing exposure therapy. In a randomized, double-blind, placebo-controlled study, 40 patients with specific phobia for heights were treated with three sessions of exposure therapy using virtual reality exposure to heights. Cortisol (20 mg) or placebo was administered orally 1 h before each of the treatment sessions. Subjects returned for a posttreatment assessment 3–5 d after the last treatment session and for a follow-up assessment after 1 mo. Adding cortisol to exposure therapy resulted in a significantly greater reduction in fear of heights as measured with the acrophobia questionnaire (AQ) both at posttreatment and at follow-up, compared with placebo. Furthermore, subjects receiving cortisol showed a significantly greater reduction in acute anxiety during virtual exposure to a phobic situation at posttreatment and a significantly smaller exposure-induced increase in skin conductance level at follow-up. The present findings indicate that the administration of cortisol can enhance extinction-based psychotherapy.

Enhancing exposure therapy for anxiety disorders with glucocorticoids : from basic mechanisms of emotional learning to clinical applications

Current neurophysiological and psychological accounts view exposure therapy as the clinical analog of extinction learning that results in persistent modifications of the fear memory involved in the pathogenesis, symptomatology, and maintenance of anxiety disorders. Evidence from studies in animals and humans indicate that glucocorticoids have the potential to facilitate the processes that underlie extinction learning during exposure therapy. Particularly, glucocorticoids can restrict retrieval of previous aversive learning episodes and enhance consolidation of memory traces relating to non-fearful responding in feared situations. Thus, glucocorticoid treatment especially in combination with exposure therapy might be a promising approach to optimize treatment of anxiety disorders. This review examines the processes involved in aversive conditioning, fear learning and fear extinction, and how glucocorticoids might enhance restructuring of fear memories during therapy.

Enhanced priming for trauma-related material in posttraumatic stress disorder.

Intrusive reexperiencing in posttraumatic stress disorder (PTSD) has been linked to perceptual priming for trauma-related material. A prospective longitudinal study (N = 69) investigated perceptual priming for trauma-related, general threat, and neutral words in assault survivors with and without PTSD, using a new version of the word-stem completion task. Survivors with PTSD showed enhanced priming for trauma-related words. Furthermore, priming for trauma-related words measured soon after the trauma was associated with subsequent PTSD severity at 3, 6, and 9 months. The enhanced priming effect was specific to trauma-related words. Enhanced perceptual priming for traumatic material appears to be one of the cognitive processes operating in PTSD.

Randomized controlled comparison of two cognitive behavioral therapies for obese children : mother versus mother-child cognitive behavioral therapy

Background: Parent-child treatments have been shown to be superior to child-focused treatments of childhood obesity. Yet until now, the comparative effectiveness of parent-only and parent-child approaches has been little studied. Method: Fifty-six obese children and their families were randomly assigned to a 16-session cognitive behavioral therapy (CBT) for the parents only or for a combined treatment of parents and children. Children’s percent overweight, the body mass index of their mothers, and behavioral and psychological problems of children and mothers were assessed. Results: Both treatments reduced children’s percent overweight significantly and equally by 6-month follow-up. Also both treatments provided similar results in reducing general behavior problems (externalizing and internalizing behavior problems), global and social anxiety, and depression. Conclusions: Our results point to a comparable efficacy of the two treatments. Further, psychological well-being of both mothers and children can be improved in a CBT for obese children and their parents. Future studies should focus on finding ways to improve the adherence of families to long-term treatment of obesity in childhood.

Enhanced perceptual priming for neutral stimuli in a traumatic context: A pathway to intrusive memories?

Clinical observations suggest that re-experiencing symptoms are triggered by stimuli that are perceptually similar to those present shortly before the trauma or its worst moments. Two experiments investigated the possible role of perceptual priming in this phenomenon. Volunteers (N = 28, N = 62) watched a series of “traumatic” and neutral picture stories, and completed blurred object identification (priming) and recognition memory tasks. Neutral objects that immediately preceded the “traumatic” stories were more strongly primed, but not better recognised, than objects from neutral stories. Enhanced priming predicted subsequent re-experiencing symptoms. The results support the role of perceptual priming in re-experiencing.

Influence of stress on fear memory processes in an aversive differential conditioning paradigm in humans

It is widely assumed that learning and memory processes play an important role in the pathogenesis, expression, maintenance and therapy of anxiety disorders, such as phobias or post-traumatic stress disorder (PTSD). Memory retrieval is involved in symptom expression and maintenance of these disorders, while memory extinction is believed to be the underlying mechanism of behavioral exposure therapy of anxiety disorders. There is abundant evidence that stress and stress hormones can reduce memory retrieval of emotional information, whereas they enhance memory consolidation of extinction training. In this study we aimed at investigating if stress affects these memory processes in a fear conditioning paradigm in healthy human subjects. On day 1, fear memory was acquired through a standard differential fear conditioning procedure. On day 2 (24h after fear acquisition), participants either underwent a stressful cold pressor test (CPT) or a control condition, 20 min before memory retrieval testing and extinction training. Possible prolonged effects of the stress manipulation were investigated on day 3 (48 h after fear acquisition), when memory retrieval and extinction were tested again. On day 2, men in the stress group showed a robust cortisol response to stress and showed lower unconditioned stimulus (US) expectancy ratings than men in the control group. This reduction in fear memory retrieval was maintained on day 3. In women, who showed a significantly smaller cortisol response to stress than men, no stress effects on fear memory retrieval were observed. No group differences were observed with respect to extinction. In conclusion, the present study provides evidence that stress can reduce memory retrieval of conditioned fear in men. Our findings may contribute to the understanding of the effects of stress and glucocorticoids on fear symptoms in anxiety disorders and suggest that such effects may be sex-specific.