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Few studies comprehensively evaluate which types of life stress are most strongly associated with depressive episode onsets, over and above other forms of stress, and comparisons between acute and chronic stress are particularly lacking. Past research implicates major (moderate to severe) stressful life events (SLEs), and to a lesser extent, interpersonal forms of stress; research conflicts on whether dependent or independent SLEs are more potent, but theory favors dependent SLEs. The present study used 5 years of annual diagnostic and life stress interviews of chronic stress and SLEs from 2 separate samples (Sample 1 N = 432; Sample 2 N = 146) transitioning into emerging adulthood; 1 sample also collected early adversity interviews. Multivariate analyses simultaneously examined multiple forms of life stress to test hypotheses that all major SLEs, then particularly interpersonal forms of stress, and then dependent SLEs would contribute unique variance to major depressive episode (MDE) onsets. Person-month survival analysis consistently implicated chronic interpersonal stress and major interpersonal SLEs as statistically unique predictors of risk for MDE onset. In addition, follow-up analyses demonstrated temporal precedence for chronic stress; tested differences by gender; showed that recent chronic stress mediates the relationship between adolescent adversity and later MDE onsets; and revealed interactions of several forms of stress with socioeconomic status (SES). Specifically, as SES declined, there was an increasing role for noninterpersonal chronic stress and noninterpersonal major SLEs, coupled with a decreasing role for interpersonal chronic stress. Implications for future etiological research were discussed.

This study examined the role of presleep attributions about physiological events during sleep in nocturnal panic attacks. Patients who regularly experienced nocturnal panic were physiologically monitored as audio signals were presented during sleep. They were randomly assigned to 1 of 3 conditions: expected, in which signals of intense physiological changes were expected; unexpected, in which signals of intense physiological changes were not expected; or control, involving distinctly different signals unrelated to physiological responses. The unexpected condition led to substantially more self-reported distress and panic attacks. The experimental conditions did not elicit different autonomic reactions, but those who panicked showed stronger physiological responses than those who did not panic. The findings are consistent with a cognitive model of nocturnal panic attacks.

Expectation about arousal seems to affect the response to signals during sleep in subjects suffering from nocturnal panic (NP) attacks. NP patients told that feedback signals indicate unexpected arousal are more anxious and exhibit more reactions in response to the signals when awakened from sleep in comparison to patients told that the signals are expected and harmless. The response observed in control subjects is not significantly different across the two experimental conditions, although more anxiety is reported in the unexpected-no reassurance condition. The results suggest that cognitive-behavioral treatment may be appropriate for NP attacks.

A considerable relationship exists between the dimension of the Dysfunctional Attitude Scale, calculated by the Perfectionistic Achievement factor, and enhanced depressive symptoms in response to poorer-than-expected performance. The test of cognitive diathesis-stress model of depression, performed on a group of undergraduate students, detected increased depressive symptoms.

An analysis of the effects of predicted and unpredicted attacks in several individuals enables a study of the long term effects exerted by these attacks. There is a decrease in the level of anxiety and worry regarding panic a day after predicted attack, while there is an increase a day after unpredicted attacks. The frequency of panic attack does not influence this anxiety pattern or acute distress indexes. A higher degree of agoraphobic avoidance is seen in patients subjected to predicted panic attacks.

The fourth edition of 'Diagnostic and Statistical Manual of Mental Disorders' provides new conceptual and empirical proof leading to new definitions of panic, which are precise and more empirical than those of the third edition. The design of the new edition is more for clinicians than researchers. Panic definitions are a heterogeneous mix of emotional phenomena. Conservative definition of panic and its relation to limited symptom attacks and nonfearful panic are examined.

Nocturnal panic is defined as a panic attack that occurs while the individual is sleeping. The precise cause of nocturnal panic is not known, but it has been surmised that it is related to respiration and carbon dioxide imbalances, in particular, a build-up of carbon dioxide in the blood (hypercapnia) due to chronic hyperventilation. Therefore, the ventilatory response associated with nocturnal panic was investigated in 34 patients who met the criteria for panic disorder. Sixteen of these patients reported nocturnal panic and 18 individuals had not had a previous episode of nocturnal panic; these two groups were compared. Measurements were taken to detect chronic hyperventilation and hypersensitivity to carbon dioxide. Three intervals were assessed: baseline, forced periods of hyperventilation, and carbon dioxide inhalation phases. Psychophysiological and subjective measurements were also made. No differences between the two groups were observed in their reactions to carbon dioxide or in the frequency of panic attacks induced during the assessment. The same proportion of subjects within each group experienced panic attacks in response to laboratory stimuli (hyperventilation or carbon dioxide inhalation). No support for the theory that carbon dioxide hypersensitivity and chronic hyperventilation cause nocturnal panic attacks was obtained. (Consumer Summary produced by Reliance Medical Information, Inc.)