Patients with Generalized Anxiety Disorder and a History of Trauma: Somatic Symptom Endorsement

Brawman‐Mintzer, Olga; Monnier, Jeannine; Wolitzky, Kate B.; Falsetti, Sherry A.

doi:10.1097/00131746-200505000-00010

Cited by 13 publications

(6 citation statements)

References 17 publications

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“…Although the relationship between exposure to a terrorist attack and GAD symptoms has not been previously examined, our results are consistent with past studies indicating that exposure to trauma, particularly assaultive trauma, is associated with GAD (Brawman-Mintzer, Monnier, Wolitzsky, & Falsetti, 2005; Roemer, Molina, Litz, & Borkovec, 1997), and that an emotional connection to victims is associated with stress symptoms (Dixon, Rehling, & Shiwach, 1993; Terr et al, 1999). Indeed, past studies have shown that disasters may have a negative effect on mental health when a loved one or acquaintance is harmed or when an individual personalizes the event (Dixon et al, 1993).…”

Section: Discussionsupporting

confidence: 92%

Screening for generalized anxiety disorder symptoms in the wake of terrorist attacks: A study in primary care

Ghafoori

Neria

Gameroff

et al. 2009

Journal of Traumatic Stress

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Little is known about the mental health impact of terrorism beyond posttraumatic stress disorder (PTSD) and depression. The associations between exposure to the September 11, 2001 (9/11) attacks in New York City and generalized anxiety disorder (GAD) symptoms were examined in a sample of 929 primary care patients. After controlling for PTSD, depression, panic and substance use disorders, and pre-9/11 trauma, patients who screened positive (vs. negative) for GAD symptoms were roughly twice as likely to report having a loved one at the 9/11 disaster site, twice as likely to know someone who was killed by the attacks, and twice as likely to know someone who was involved with the rescue/recovery efforts after the disaster. Implications for treatment and future research are discussed.

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Section: Discussionsupporting

confidence: 92%

Screening for generalized anxiety disorder symptoms in the wake of terrorist attacks: A study in primary care

Ghafoori

Neria

Gameroff

et al. 2009

Journal of Traumatic Stress

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“…Dysregulation of the HPA axis has also been associated with panic disorder (Abelson et al, 2007), chronic fatigue syndrome (Van Houdenhove et al, 2009), obsessive-compulsive disorder (Gustafsson et al, 2008), fibromyalgia (Tanriverdi et al, 2007), generalized anxiety disorder (Lenze et al, 2011), and bipolar disorder (Daban et al, 2005). Importantly, stressful life events have been implicated in the onset of each of these disorders (Kendler et al, 1995; Hatcher and House, 2003; Gupta and Silman, 2004; Brawman-Mintzer et al, 2005; Garno et al, 2005; Goodwin et al, 2005; Sarkhel et al, 2011), and dysregulation of the HPA axis may be an etiological link between stress and the subsequent development of pathology.…”

Section: Introductionmentioning

confidence: 99%

Synaptic regulation of the hypothalamic–pituitary–adrenal axis and its modulation by glucocorticoids and stress

Levy¹,

Tasker²

2012

Front. Cell. Neurosci.

120

104

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Dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis has been implicated in a range of affective and stress-related disorders. The regulatory systems that control HPA activity are subject to modulation by environmental influences, and stressful life events or circumstances can promote subsequent HPA dysregulation. The brain is a major regulator of the HPA axis, and stress-induced plasticity of the neural circuitry involved in HPA regulation might constitute an etiological link between stress and the development of HPA dysregulation. This review focuses on the synaptic regulation of neuroendocrine corticotropin-releasing hormone (CRH) neurons of the hypothalamic paraventricular nucleus, which are the cells through which the brain predominantly exerts its influence on the HPA axis. CRH neuronal activity is largely orchestrated by three neurotransmitters: GABA, glutamate, and norepinephrine. We discuss our current understanding of the neural circuitry through which these neurotransmitters regulate CRH cell activity, as well as the plastic changes in this circuitry induced by acute and chronic stress and the resultant changes in HPA function.

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“…It has been reported that up to 94.8% of GAD patients were exposed to any trauma (40). GAD may resemble PTSD in this respect and the mechanism of hypocortisolemia may be similar.…”

Section: Discussionmentioning

confidence: 96%

Evaluation of hypothalamo-pituitary-adrenal axis activity by using dexamethasone suppression test in patients with panic disorder and generalized anxiety disorder

Hacımusalar¹,

Eşel²

2017

Dusunen Adam

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Evaluation of hypothalamo-pituitary-adrenal axis activity by using dexamethasone suppression test in patients with panic disorder and generalized anxiety disorderObjective: The aim of this study was to investigate the role of hypothalamo-pituitary-adrenal (HPA) axis activity on the pathophysiology of anxiety disorders by examining the HPA axis activity in patients with panic disorder (PD) and generalized anxiety disorder (GAD).Method: Baseline and post dexamethasone suppression test (DST) serum concentrations of cortisol and dehydroepiandrosterone-sulfate (DHEA-S) were measured in patients with PD (n=24), GAD (n=21) and in healthy controls (n=20). Results:The baseline cortisol levels in GAD group were found lower than those of the patients with PD and healthy controls. Cortisol suppression by dexamethasone in GAD group was found to be lower than PD patients and healthy controls. Baseline and post-DST DHEA-S levels in the patients with PD and GAD were similar to those of the healthy controls. Yöntem: PB (n=24) ve YAB (n=21) olan hastalarda ve sağlıklı kontrollerde (n=20) bazal ve deksametazon baskılama testi (DST) uygulaması sonrasında kortizol ve dehidroepiandrosteron-sülfat (DHEA-S) değerleri ölçüldü.Bulgular: YAB grubunun bazal kortizol düzeyleri kontrol ve PB grubuna göre düşük bulundu. Ayrıca YAB grubunda deksametazonun kortizolu baskılaması kontrol ve PB grubuna göre düşük bulundu. PB ve YAB hastalarında bazal ve DST sonu DHEA-S düzeyleri kontrol grubuna benzer bulundu.Sonuç: YAB hastalarında bazal kortizol düzeyinin düşük olması ve DST'de kortizol baskılanmasının yetersiz oluşu bu hastalarda hem kortikotropin salgılatıcı hormon reseptörlerinde, hem de glukokortikoid reseptörlerinde bir aşağı ayarlama (down-regulation) olduğunu akla getirmektedir.Anahtar kelimeler: Dehidroepiandrosteron, deksametazon, yaygın anksiyete bozukluğu, panik bozukluğu

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Patients with Generalized Anxiety Disorder and a History of Trauma: Somatic Symptom Endorsement

Cited by 13 publications

References 17 publications

Screening for generalized anxiety disorder symptoms in the wake of terrorist attacks: A study in primary care

Screening for generalized anxiety disorder symptoms in the wake of terrorist attacks: A study in primary care

Synaptic regulation of the hypothalamic–pituitary–adrenal axis and its modulation by glucocorticoids and stress

Evaluation of hypothalamo-pituitary-adrenal axis activity by using dexamethasone suppression test in patients with panic disorder and generalized anxiety disorder

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