Why did the white bear return? Obsessive-compulsive symptoms and attributions for unsuccessful thought suppression.
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The current study examined the nature and consequences of attributions about unsuccessful thought suppression. Undergraduate students with either high (n=67) or low (n=59) levels of obsessive-compulsive symptoms rated attributions to explain their unsuccessful thought suppression attempts. We expected that self-blaming attributions and attributions ascribing importance to unwanted thoughts would predict more distress and greater recurrence of thoughts during time spent monitoring or suppressing unwanted thoughts. Further, we expected that these attributions would mediate the relationship between obsessive-compulsive symptom levels and the negative thought suppression outcomes (distress and thought recurrence). Structural equation models largely confirmed the hypotheses, suggesting that attributions may be an important factor in explaining the consequences of thought suppression. Implications are discussed for cognitive theories of obsessive-compulsive disorder and thought suppression. (+info)
Zolpidem and amnestic sleep related eating disorder.
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Nocturnal eating disorders are more common than previously thought. Sleep related eating disorder has been described in association with zolpidem. A review of the literature revealed the presence of 6 previously reported cases. In this presentation, the case of a 46-year-old female who developed sleep related eating disorder when she was treated with zolpidem for insomnia is reported. The patient recovered totally when zolpidem was stopped. Drug-induced sleep related eating disorders should be considered when evaluating patients with nocturnal eating. (+info)
Repeated N-acetylcysteine administration alters plasticity-dependent effects of cocaine.
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Cocaine produces a persistent reduction in cystine-glutamate exchange via system x(c)- in the nucleus accumbens that may contribute to pathological glutamate signaling linked to addiction. System x(c)- influences glutamate neurotransmission by maintaining basal, extracellular glutamate in the nucleus accumbens, which, in turn, shapes synaptic activity by stimulating group II metabotropic glutamate autoreceptors. In the present study, we tested the hypothesis that a long-term reduction in system x(c)- activity is part of the plasticity produced by repeated cocaine that results in the establishment of compulsive drug seeking. To test this, the cysteine prodrug N-acetylcysteine was administered before daily cocaine to determine the impact of increased cystine-glutamate exchange on the development of plasticity-dependent cocaine seeking. Although N-acetylcysteine administered before cocaine did not alter the acute effects of cocaine on self-administration or locomotor activity, it prevented behaviors produced by repeated cocaine including escalation of drug intake, behavioral sensitization, and cocaine-primed reinstatement. Because sensitization or reinstatement was not evident even 2-3 weeks after the last injection of N-acetylcysteine, we examined whether N-acetylcysteine administered before daily cocaine also prevented the persistent reduction in system x(c)- activity produced by repeated cocaine. Interestingly, N-acetylcysteine pretreatment prevented cocaine-induced changes in [35S]cystine transport via system x(c)-, basal glutamate, and cocaine-evoked glutamate in the nucleus accumbens when assessed at least 3 weeks after the last N-acetylcysteine pretreatment. These findings indicate that N-acetylcysteine selectively alters plasticity-dependent behaviors and that normal system x(c)- activity prevents pathological changes in extracellular glutamate that may be necessary for compulsive drug seeking. (+info)
Family burden of compulsive hoarding: results of an internet survey.
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