Generalized anxiety disorder: Some biochemical aspects

Munjack, Dennis J.; Baltazar, Patricia L.; DeQuattro, Vincent; Sobin, Paul; Palmer, Ruby; Zulueta, Anicia; Crocker, Benjamin; Usigli, Rudolfo; Buckwalter, Galen; Leonard, Michele

doi:10.1016/0165-1781(90)90133-p

Cited by 32 publications

(4 citation statements)

References 39 publications

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“…Anxiety is a common reaction to a significant life stress. It is characterized by fear and apprehension that may or may not be associated with a clearly identifiable stimulus (30–32). BZDs are considered as first line in the pharmacotherapy of anxiety (33).…”

Section: Discussionmentioning

confidence: 99%

Passionflower in the treatment of generalized anxiety: a pilot double-blind randomized controlled trial with oxazepam

et al. 2001

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Section: Discussionmentioning

confidence: 99%

Passionflower in the treatment of generalized anxiety: a pilot double-blind randomized controlled trial with oxazepam

et al. 2001

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“…This can take the form, for instance, of worrying about one's finances, misfortune to one's children when there is no danger present, or problems with one's health when there is no cause for concern. Plasma MHPG levels have been Behavioral and bioloeical effects of vohimbine Sevy et al, 1989;Mathew Mathew et al, 1980Sevy et al, 1989Munjack et al, 1990Mathew et al, 1981Sevy et al, 1989Curtis et al, 1989Munjack et al, 1990Cameron et al, 1990Charney et al, 1987bNesse et al, 1985bStein et al, 1992 Tancer and Siever et al, 1983Siever et al, 1983 Siever et al, Lee et al, 1990Curtis et al, 1989Hollander et al, 1991;Lee et al, 1990 shown to be increased in GAD patients in comparison to normal controls (Munjack et al, 1990;Sevy et al, 1989), while conflicting results have been obtained for resting plasma norepinephrine (Table IV). Other studies have shown an increase in plasma epinephrine in comparison to controls (Mathew et al, 1980(Mathew et al, , 1981.…”

Section: Noradrenergic Contributions To Generalized Anxiety Disorder mentioning

confidence: 89%

Noradrenergic mechanisms in stress and anxiety: II. Clinical studies

Bremner

Krystal

Southwick

et al. 1996

Synapse

272

111

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Studies in animals have shown a relationship between alterations in noradrenergic brain system function and behaviors of anxiety and fear. These findings have generated the hypothesis that the symptoms seen in patients with anxiety disorders may be related to alterations in noradrenergic function. A number of clinical studies have tested this hypothesis, utilizing measures of catecholaminergic function such as heart rate and blood pressure, measurement of norepinephrine and its metabolites in urine and plasma and adrenergic receptor binding in platelets, as well as pharmacological challenge to the noradrenergic system. Acute stressors, such as public speaking, have been associated with an increase in heart rate, blood pressure, and norepinephrine and its metabolites in urine and plasma. Findings in patients with panic disorder at baseline related to heart rate, blood pressure, baseline norepinephrine and its metabolites, and platelet adrenergic receptors have been mixed, while the most consistent findings have been blunted growth hormone response to clonidine and increased 3‐methoxy‐4‐hydroxy‐phenylethylene‐glucol (MHPG) and anxiety following stimulation of the noradrenergic system with yohimbine. Baseline measures of noradrenergic function in patients with posttraumatic stress disorder (PTSD) have also been mixed, while an increased heart, blood pressure and norepinephrine response to traumatic reminders, as well as increased behavioral (as well as different brain metabolic) response to yohimbine, have been found in PTSD. There are fewer studies of noradrenergic function in the other anxiety disorders, and the findings there have not been consistent. These studies provide evidence for increased noradrenergic responsiveness in panic disorder and PTSD, although there does not appear to be an alteration in baseline noradrenergic function in these patients. © 1996 Wiley‐Liss, Inc.

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“…One study found elevated plasma levels of norepinephrine and decreased A2-adrenergic function in GAD patients (Sevy, Papadimitriou, Surmount, Goldman, & Mendlewicz, 1989). Norepinephrine activity is elevated in GAD, causing receptor downregulation, while other studies have not been able to replicate these findings (Matthew, Ho, Francis, Taylor, & Weinman, 1982;Munjack et al, 1990). A response to clonidine (an A2 adrenergic agonist) has been seen in patients with GAD, suggesting a decrease in A2 adrenergic receptor sensitivity, as seen in MDD (Abelson et al, 1991).…”

Section: Neurobiologymentioning

confidence: 99%

Generalized Anxiety Disorder Across the Lifespan

Portman¹

2009

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Generalized anxiety disorder: Some biochemical aspects

Cited by 32 publications

References 39 publications

Passionflower in the treatment of generalized anxiety: a pilot double-blind randomized controlled trial with oxazepam

Passionflower in the treatment of generalized anxiety: a pilot double-blind randomized controlled trial with oxazepam

Noradrenergic mechanisms in stress and anxiety: II. Clinical studies

Generalized Anxiety Disorder Across the Lifespan

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