Social Anxiety Disorder by Borwin Bandelow & Dan J. Stein

Author:Borwin Bandelow & Dan J. Stein
Language: rus
Format: mobi
ISBN: 9780824754549
Publisher: Taylor & Francis
Published: 2004-04-27T21:00:00+00:00

12

The Promise of Neurobiology in Social Anxiety

Disorder

Michael Van Ameringen

and Catherine Mancini

McMaster University,

Hamilton, Ontario, Canada

I. INTRODUCTION

In spite of the high prevalence rate of social anxiety disorder (SAD) in the general population (1), little is known about its pathophysiology or neurobiology.

Neurobiological investigation of SAD has used a variety of approaches, reviewed in this chapter, including chemical and neuroendocrine challenges, evaluations of neurotransmitter functioning, and structural and functional neuroimaging studies.

A. Challenge Studies

Challenge studies use exogenous chemical agents to induce the individual’s naturally occurring anxiety symptoms. They tend to confirm an underlying biological mechanism of the disorder. Researchers have challenged patients with SAD with a variety of agents including lactate (2), caffeine (3), CO2 (4–6), cholecystokinin (CCK) (7), pentagastrin [a synthetic analogue of the cholecystokinin tetrapeptide (CCK4)] (8), and the benzodiazepine antagonist flumazenil (9). These substances have been successfully used to induce panic attacks in individuals with panic disorder. However, with the exception of pentagastrin or high concentrations of CO , these challenges have not shown consistent 2

panicogenic effects in SAD patients compared to controls. Flumazenil induced panic attacks in panic disorder patients (10) but failed to do so in a group of SAD patients (9).

Gorman administered 35% CO to patients with panic disorder and SAD as well as 2

normal controls. In this study, all subjects experienced increased anxiety and ventilation rates. The individuals with SAD showed an intermediate response between that of the controls and panic disorder patients (4). In a further similar study, Caldirola and colleagues gave 35% CO to patients with panic disorder, SAD and comorbid panic 2

disorder, SAD alone, and as well as healthy controls. Both the panic disorder and SAD

patients showed similar increased anxiogenic reactions to 35% CO compared to normal 2

controls. Those with comorbid panic disorder and SAD experienced similar reactions to those seen in patients with either disorder alone (6). These studies indicate that both

Social anxiety disorder 160

social SAD and panic disorder patients have a similar hypersensitivity to high-dose CO2

(35%) and therefore may share a common underlying biological vulnerability.

Van Vliet et al. demonstrated that SAD patients were more sensitive to pentagastrin infusions than normal controls, although the result did not reach significance (8). In a larger study, McCann and colleagues evaluated the response of patients with SAD and panic disorder as well as normal controls to pentagastrin infusion (11). A social interaction test was also included as part of the pentagastrin challenge. Both patient groups had similar rates of pentagastrin-induced panic attacks, implying that SAD and panic disorder patients may share a common pathophysiologic mechanism. However, the anxiety experienced by patients with SAD was not the same as that experienced in anxiety-provoking social situations, a finding that is reported in other studies. Overall, the results of the challenge studies do not support any specific underlying neurobiological abnormality although patients with SAD and panic disorder may share some common, unidentified vulnerability.

B. Neuroendocrine Assessments

Neuroendocrine assessments have been used in psychiatry in order to compare baseline and/or dynamic neuroendocrine measures in psychiatric patients and controls. Elevations in plasma cortisol have long been associated with stress in both animals and humans.

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