Separation anxiety disorder in childhood as a risk factor for future mental illness.

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Separation anxiety disorder in childhood as a risk factor for future mental illness.

Lewinsohn PM, Holm-Denoma JM, Small JW, Seeley JR, Joiner TE Jr.

Oregon Research Institute, Eugene, OR 97403, USA. pete@ori.org

OBJECTIVE: To ascertain the extent to which childhood separation anxiety disorder (SAD) confers risk for the development of psychopathology during young adulthood (ages 19-30). METHOD: A subset of the participants of the Oregon Adolescent Depression Project (n = 816) was used. Subjects provided retrospective reports of lifetime mental illness (including SAD) and concurrent reports of current mental illness at age 16 and were then followed prospectively until age 30. Diagnostic assessments were conducted twice during adolescence and again at ages 24 and 30. Based on diagnosis during childhood/adolescence, the subjects were partitioned into four orthogonal groups: SAD (n = 42), other anxiety disorders (n = 88), a heterogeneous psychiatric disorders control group (n = 389), and a not mentally ill control group (n = 297). Adjusting for demographic variables that were significantly associated with group status and for comorbid disorders prior to age 19, the results were analyzed with hierarchical multiple logistic regression. RESULTS: SAD was a strong (78.6%) risk factor for the development of mental disorders during young adulthood. The major vulnerabilities were for panic disorder and depression. CONCLUSIONS: Because SAD creates a major vulnerability for mental disorders during young adulthood, clinicians should be sensitive to the presence of SAD, and children and adolescents with SAD should be treated. Future research should evaluate whether successful treatment of SAD and/or the provision of a preventive intervention during childhood/adolescence reduce the risk for future psychopathology.

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PMID: 18356763 [PubMed – indexed for MEDLINE]

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High risk studies and developmental antecedents of anxiety disorders.

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High risk studies and developmental antecedents of anxiety disorders.

Hirshfeld-Becker DR, Micco JA, Simoes NA, Henin A.

MGH Clinical and Research Program in Pediatric Psychopharmacology, 185 Alewife Brook Parkway, Suite 2000, Cambridge, MA 02138, USA. dhirshfeld@partners.org

The past two decades have witnessed significant growth in our understanding of the developmental antecedents of anxiety disorders. In this article, we review studies of offspring at risk for anxiety disorders, longitudinal studies of the course of anxiety disorders in clinical, epidemiologic, and at-risk samples, studies of hypothesized temperamental risk factors for anxiety, and give a brief overview of the literature on environmental risk factors. Clear developmental antecedents to anxiety disorders identified include (1) childhood anxiety disorders [in particular, separation anxiety and overanxious disorder/general anxiety disorder (GAD)], (2) behavioral inhibition which predicts later social phobia, (3) anxiety sensitivity which predicts later panic disorder, and (4) negative affectivity, which predicts a spectrum of psychopathology including anxiety disorders. Further prospective studies are needed to examine the roles of environmental factors such as parenting practices, peer influences, stressful life events, and perinatal stressors. Future studies could benefit from (1) beginning earlier in development and following individuals into adulthood, (2) assessing the overlap between multiple temperamental constructs, (3) greater use of observational measures of temperament and of parent-child and peer interactions, (4) greater attention to parental psychopathology which may confound associations noted, (5) exploration of other features of anxiety disorders (neurofunctional correlates, cognitive features, other aspects of emotional regulation) as potential precursors, and (6) intervention studies exploring whether modifying developmental antecedents can alter the course of anxiety disorders. Copyright 2008 Wiley-Liss, Inc.

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PMID: 18409200 [PubMed – indexed for MEDLINE]

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Characteristics of fatigue in panic disorder patients.

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Characteristics of fatigue in panic disorder patients.

Kaiya H, Sugaya N, Iwasa R, Tochigi M.

Outpatient Clinic for Anxiety Disorders, Akasaka Mental Clinic, Tokyo, Japan.

It was suggested that fatigue is one of characteristics of panic disorder. Fatigue was assessed in 360 patients with panic disorder using the Japanese version of the Multidimensional Fatigue Inventory (MFI-J). The scores for general fatigue and reduced activity were significantly higher in the patients than in the controls. These tendencies were also observed in men when the subject group was differentiated according to sex, but not in women. In contrast, the trend for higher score for physical fatigue was observed only in the female patients. Thus, the present study suggests that the characteristics of fatigue vary with sex in panic disorder.

PMID: 18412848 [PubMed – indexed for MEDLINE]

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Measurement of panic-like responses following intravenous infusion of sodium lactate in panic-prone rats.

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Measurement of panic-like responses following intravenous infusion of sodium lactate in panic-prone rats.

Sajdyk TJ, Keim SR, Thielen SR, Fitz SD, Shekhar A.

Indiana University Medical Center, Indianapolis, Indiana, USA.

This unit describes a putative animal model for panic disorder. The basic premise is that pharmacological disruption of critical brain regions implicated in the circuitry of anxiety will lead to a condition similar to that of the human disorder. A clinically relevant test, the sodium lactate challenge, is utilized to assess parallels between the human condition and this rat model.

PMID: 18428590 [PubMed – indexed for MEDLINE]

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A panic attack-like unusual stress reaction.

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A panic attack-like unusual stress reaction.

Schenberg LC, Dos Reis AM, Ferreira Póvoa RM, Tufik S, Silva SR.

Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, ES, Brazil.

Ever since the seminal studies of Hans Selye, activation of hypothalamus-pituitary-adrenal (HPA) axis is emblematic of stress. Consequently, the lack of HPA axis responses following the undisputable psychological stress of a panic attack stands out as one of the most intriguing findings of contemporary psychiatry. On the other hand, the defensive behaviors and aversive emotions produced by stimulation of the dorsal periaqueductal gray matter (DPAG) have been proposed as a model of panic attacks. Therefore, we examined whether the plasma levels of ‘stress hormones’ corticotropin and prolactin show any change following the DPAG-evoked freezing and flight behaviors of the rat. Rats bearing an electrode into the DPAG and an intra-atrial catheter were stimulated at 9:00 a.m., 18-24 h after the catheter implantation. Blood samples were withdrawn just before 1-min stimulation of DPAG, immediately after (5 or 15 min) and throughout 3 to 27 h following stimulation. In another experiment, samples were withdrawn either before or following a prolonged stimulation (5 min) of the DPAG with flight threshold intensity. Hormones were measured by either chemiluminescent or double-antibody immunoassays. Hormone plasma levels following freezing and flight behaviors were compared to those of resting or restraint-stressed rats. Data show that stress hormones remain unaltered following the DPAG-evoked defensive behaviors. Not even the 5-min stimulation of DPAG with the flight threshold intensity changed corticotropin plasma levels significantly. As far as we known, this is the first demonstration of the lack of stress hormone responses following the intense emotional arousal and physical exertion of a fear-like behavior in rats. Data add new evidence of DPAG involvement in spontaneous panic attacks.

PMID: 18423636 [PubMed – as supplied by publisher]

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