P4 Anxiety disorders and anxiolytics
$532
(33/54, 61.1%) than men (16/47, 34.0%) (p 0.048). The subjects (n 53) who were present at the moment of the explosion were more likely to receive a current diagnosis of PTSD (p 0.023) and less likely to receive no psychiatric diagnosis (p 0.007), in comparison with people not present. On the contrary, there was no difference between the two groups in the rate of GAD and of PTSD in remission. The subjects who had seen dead or injured people (N 29) were more likely to receive a current diagnosis of PTSD (p 0.043) and less likely to receive no psychiatric diagnosis (p 0.000), in comparison with people who had not seen dead or injured people. On the contrary, there was no difference between the two groups in the rate of GAD and of PTSD in remission. History of child mourning or separation, or of previous stress, as well as familiarity for any psychiatric disorder were not related to the rate of ascertained psychiatric diagnoses. Discussion: This study attempts to draw together some of the current questions related to the methodology of exploring the psychological and psychiatric aspects of human response to disaster. It sets out some of the key areas in which research questions might be mounted. In this population, only a minority of subjects received no psychiatric diagnosis, twenty months after the event. DSM-IV-TR PTSD and GAD were the most frequent diagnoses. Women were more likely to present PTSD. Interestingly, some indices of more direct exposure to the event were related to the risk of developing PTSD but not to the risk of developing GAD or to the likelihood of PTSD remission. History of previous trauma or familiarity for psychiatric disorders do not seem play in major role in the development of PTSD.
State-Trait Anxiety Inventory- Trait subscale (STAI-T) and the Retrospective Childhood Inhibition Scale (RCIS) 1 2 weeks prior to the CCK-4 challenge. On the day of the challenge, subjects received a bolus injection of CCK-4. Behavioural response to CCK-4 was assessed with a DSM-IV derived Panic Symptom Scale (PSS) and cardiovascular response was automatically recorded with a Dinamap vital signs monitor. Results: No significant correlations were found between any of the personality measures and the number and sum intensity of CCK-4-induced panic symptoms or the maximum change from baseline in heart rate and blood pressure. However, a significant positive correlation was found between neuroticism and the number of reported response bias items (r 0.33, p < 0.05). Conclusion: Overall, these data indicate that individual differences in anxiety-related personality traits do not significantly influence behavioural and cardiovascular sensitivity to CCK-4 in healthy volunteers
References [1] Swain, J., Koszycki, D., Shlik, J., Bradwejn, J., 2003. Pharmacological challenges in anxiety. In, Anxiety Disorders, D Nutt and J Ballenger (eds), Blackwell Science, Oxford England, pp.26%295. [2] Koszycki, D., Zacharko, R.M., Bradwejn, J., 1996. Influence of personality on behavioral response to cholecystokinin-tetrapeptide in patients with panic disorder. Psychiatry Research 62, 131 138. [3] Koszycki, D., Cox, B., Bradwejn, J., 1993. Anxiety sensitivity and response to CCK-4 in healthy volunteers. Am Journal of Psychiatry 150, 1881 1883.
References
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[1] North CS, Kawasaki A, Spitznagel EL, Hong BA, 2004. The course of PTSD, major depression, substance abuse, and somatizaion after a natural disaster. J NeLw Ment Dis 192, 823 829. [2] Mollica RF, Cardozo BL, Osofsky HJ, Raphael B, Ager A, Salama P, 2004. Mental health in complex emergencies Lancet 364(9450), 2058 2067.
F. Moreira*, F.S. Guimaraes. University of Sdo Paulo, Pharmacology, Ribeirdo Preto, Brazil
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Influence of personality on behavioral and cardiovascular response to cholecystokinintetrapeptide in healthy volunteers
D. Koszycki *, J. Shlik, J. Bradwejn. University of Ottawa htstitute
of Mental Health Research, Psychiatty, Ottawa, Canada Objective: Systemic administration of CCK-tetrapeptide (CCK-4) reliably provokes symptoms of panic-anxiety in healthy subjects. Several studies indicate that the panicogenic effects of CCK-4 are mediated by a complex interactions between CCK and other neurotransmitters. The role of psychological factors in mediating reactivity to CCK-4 has not been extensively studied. Existing data indicate that anxiety sensitivity does not influence CCK-4 sensitivity in either healthy subjects or panic disorder (PD) patients. However, neurotic introversion was found to capture some of the variance in response to CCK-4 in PD patients. In this study, we sought to verify whether individual differences in anxietyrelated personality traits might predict response to low dose CCK-4 (25 mcg) in healthy volunteers. Specifically, we explored the relationship between CCK-4 sensitivity and anxiety sensitivity, neuroticism, extraversion, trait anxiety, and behavioural inhibition in childhood. Method: Forty-nine subjects between the ages of 18 and 45 with no history of psychiatric illness and in good physical health completed the NEO-PI-R, Anxiety Sensitivity Index (ASI), the
Activation of N A D P H - d i a p h o r a s e positive neurons in rats after exposure to a live predator: effects of clomipramine treatments
Purpose of the study: The enzyme nitric oxide synthase (NOS) is expressed in brain regions related fear and anxiety behaviours, such as the dorsolateral periaqueductal gray (dlPAG) and the paraventricular nucleus of the hypothalamus (PVH). While NOS inhibitors injected into the dlPAG induces anxiolytic-like effects, local injection of NO-donors induces escape reactions (Moreira et al, 2004). Exposure of rats to a live cat induces fear reactions which can be prevented by anxiolytic drugs. Moreover, cat exposure activates NO-producing neurons in regions related to fear and anxiety. Activation of NO-producing neurons can be detected by a double-staining procedure employing NADPHdiaphorase histochemistry to indicate the presence of NOS and Fos immunohistochemistry to detect neuronal activation. The aim of this study was to test the hypothesis that the fear reaction and the activation of NO-producing neurons induced by the cat exposure would be prevented by the anxiolytic drug clomipramine. Methods: Male Wistar rats (220 250g; n 6 7/group) were treated with saline and acute or chronic clomipramine (20 mg/kg; 21 days). Thirty min after the last injections they were exposed to a toy cat (control) or to a live cat for 10min in a Plexiglass box ( 8 0 × 2 2 × 5 0 cm). A metal grid wall located in the middle of the box separated the rat compartment from the cat compartment. Two hours later the brains were removed and processed for NADPHd and Fos immunohistochemistry. Double-stained (DS) cells were represented as percentage of NADPHd positive neurons (mean±SEM) and analyzed by ANOVA followed by the Duncan test.