Jürgen Margraf

Selective processing of threat cues in subjects with panic attacks

Abstract Previous research has demonstrated that patients with generalised anxiety disorder, phobias, and obsessive-compulsive disorder show an attentional bias towards threat cues related to their respective disorders. Two studies are presented that used a modified Stroop colour naming task to assess attentional bias in subjects with panic attacks. In Study 1, 24 panic disorder patients and 24 normal controls were presented three cards containing threat words related to physical harm, separation, or social embarrassment. Colour naming times were compared between these cards and control cards containing matched non-threat words. Reaction time differences in the two groups were in opposite directions, patients tending to be slower in colour naming threat words, and controls, faster. In Study 2, 18 non-clinical panickers and 18 controls were presented cards containing physical threat words, neutral control words, or colour words, respectively. Panickers showed greater interference than controls in colour na...

The emotional Stroop effect in anxiety disorders: General emotionality or disorder specificity?

Selective attentional biases, often documented with a modified Stroop task, are considered to play an important role in the etiology and maintenance of anxiety. Two competing explanations for these effects are selectivity for highly emotional words in general vs. selectivity for disorder-specific words. We tested these explanations in 32 patients with generalized anxiety disorder (GAD), 29 patients with social phobia (SP), and 31 non-anxious controls. Stimuli were of four kinds: GAD-related words, SP-related words, words with a neutral valence, and words with a positive valence. Different attentional biases were observed: GAD patients were slowed by all types of emotional words, while SP patients were distracted specifically by speech-related words.

Sodium Lactate Infusions and Panic Attacks: A Review and Critique

&NA; Response to sodium lactate infusions has been proposed as an experimental model and a biologic marker for panic attacks. Several authors have claimed that patients suffering from panic attacks, but not normal controls, “panic” in response to lactate. A careful review of methods and results of 13 studies, however, reveals serious methodologic problems, lack of specificity and sensitivity, and a failure to consider cognitive variables. When baseline differences are ruled out, the responses of patients and controls may not differ. So far, response to lactate cannot be interpreted as a model and marker for panic attacks and does not provide evidence for their underlying biologic distinctness from other types of anxiety. Known biologic mechanisms do not sufficiently explain the effects of lactate. Instead, an interaction of peripheral physiologic changes, past experience, environmental cues, and their appraisal as threatening or dangerous seems to be a more appropriate model.

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 for the treatment of post-traumatic stress disorder and phobias : a novel therapeutic approach

Post-traumatic stress disorder (PTSD) and phobias belong to the most common anxiety disorders and to the most common psychiatric illnesses in general. In both disorders, aversive memories are thought to play an important role in the pathogenesis and symptomatology. Previously, we have reported that elevated glucocorticoid levels inhibit memory retrieval in animals and healthy humans. We therefore hypothesized that the administration of glucocorticoids might also inhibit the retrieval of aversive memory, thereby reducing symptoms in patients with PTSD and phobias. In recent clinical studies, we found first evidence to support this hypothesis. In patients with PTSD, low-dose cortisol treatment for one month reduced symptoms of traumatic memories without causing adverse side effects. Furthermore, we found evidence for a prolonged effect of the cortisol treatment. Persistent retrieval and reconsolidation of traumatic memories is a process that keeps these memories vivid and thereby the disorder alive. By inhibiting memory retrieval, cortisol may weaken the traumatic memory trace, and thus reduce symptoms even beyond the treatment period. In patients with social phobia, we found that a single oral administration of cortisone 1 h before a socio-evaluative stressor significantly reduced self-reported fear during the anticipation-, exposure-, and recovery phase of the stressor. In subjects with spider phobia, repeated oral administration of cortisol 1 h before exposure to a spider photograph induced a progressive reduction of stimulus-induced fear. This effect was maintained when subjects were exposed to the stimulus again two days after the last cortisol administration, indicating that cortisol facilitated the extinction of phobic fear. In conclusion, by a common mechanism of reducing the retrieval of aversive memories, glucocorticoids may be suited for the treatment of PTSD as well as phobias. More studies are needed to further evaluate the therapeutic efficacy of glucocorticoids in the treatment of anxiety disorders and to explore the potential of combining glucocorticoid treatment with psychotherapy.

Anxiety induced by false heart rate feedback in patients with panic disorder

Summary-The psychophysiological model of panic attacks postulates a positive feedback loop between anxiety symptoms and the patient’s anxious reaction to these symptoms. We tested the underlying assumption that the appraisal of bodily change can induce anxiety in this patient group. Twenty-live patients with panic disorder or agoraphobia with panic attacks (DSM-III) and 25 matched normal controls were given false feedback of an abrupt heart rate increase. Self-ratings of anxiety and excitement. heart rate. skin conductance level. and systolic and diastolic blood pressure were taken. On all measures, patients who believed that the feedback was accurate (N = 19) responded differently to the false feedback than controls (.V = 16). Patients showed increases in anxiety and physiological arousal. The preceding true heart rate feedback did not induce changes in anxiety. Patients and controls did not differ in their accuracy of heart rate perception. The results underline the role of appraisal processes and the fear of anxiety symptoms in pamc disorder.

Obesity and mental illness in a representative sample of young women

OBJECTIVE: To investigate the relation between mental disorders and weight, especially obesity.DESIGN: Epidemiological study of mental disorders with a representative sample of young women.SUBJECTS: A total of 2064 women, age 18–25 y, living in Dresden, Germany.MEASUREMENTS: Verbal reports of body mass index, structured clinical interview for psychological disorders.RESULTS: We found an association between psychological disorders and weight. Obese women had the highest rate of mental disorders overall, and they had higher rates of all subgroups of mental disorders, although many differences were not statistically significant. Most importantly, obese women suffered from an anxiety disorder significantly more often than women who were not obese. The observed differences were independent of socioeconomic status.CONCLUSIONS: In young women, obesity is related to increased rates of mental disorders, most notably anxiety disorders. Future longitudinal research will have to determine the causal relationships behind this correlation.

Biological models of panic disorder and agoraphobia--a review.

Abstract Biological models have had major consequences for the therapy and theory of panic disorder and agoraphobia. Authors such as Klein and Sheehan propose a qualitative biological distinction between panic attacks and other types of anxiety. Central arguments for their models include drug specificity, panic induction, family data, spontaneity of panic attacks and separation anxiety. A look at the evidence, however, shows surprisingly little empirical support for these arguments. In spite of the great heuristic value of Kleins and Sheehans models, alternative approaches focusing on an interaction of physiological and psychological factors seem more capable of integrating the relevant findings.

Explicit Memory in Anxiety Disorders

Two experiments were conducted to study selective memory bias favoring anxiety-relevant materials in patients with anxiety disorders. In the 1st experiment, 32 patients with generalized anxiety disorder (GAD), 30 with social phobia (speaking anxiety), and 31 control participants incidentally learned GAD-relevant words, speech anxiety-relevant words, strongly pleasant words, and words with a neutral valence. Participants did not show any explicit memory bias for threatening materials. Thirty patients suffering from panic disorder (PD) with agoraphobia and 30 controls took part in the 2nd experiment. The design was similar to the 1st experiment. This time a highly specific selective memory bias for threatening words was found. Words describing symptoms of anxiety were better recalled by PD patients. Results are consistent with previous findings but are inexplicable by existing theories.

Lactate infusions and panic attacks: Do patients and controls respond differently?

Ten patients with panic disorder or agoraphobia with panic attacks and 10 normal controls received infusions of normal saline (placebo) and sodium lactate in a single-blind design. The time course of changes in the dependent variables was closely monitored, and expectancy biases and demand characteristics were minimized. Lactate increased self-reported anxiety and heart rate equally in patients and controls. The only variables showing statistically different responses between the groups were systolic and diastolic blood pressure. Overall, in both groups, the effects of lactate were quite similar to states of natural panic or anxiety for both self-report measures and heart rate. Patients had a tendency to endorse somatic symptoms indiscriminately. Our data do not support response to lactate as a biological marker of proneness to panic attacks.