Anxiety pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2]

Overview[edit | edit source]

The pathophysiology of anxiety is attributed to various theories that have been proposed which constitute: Biologic, psychoanalytic, learning, and genetic component. There is increased sympathetic tone, decreased levels of inhibitory neurotransmitter GABA, and alterations in neurotransmitters such as dopamine and serotonin. A gene coding for serotonin transport has also been implicated.

Pathophysiology[edit | edit source]

Various theories have been implicated in the pathogenesis of anxiety which are as follows:

Biologic component[edit | edit source]

• There is an increased sympathetic tone.
• There is a surge of catecholamines.
• Decreased levels of gamma - aminobutyric acid (GABA).
• Alterations in serotonergic and dopaminergic system.
• In anxiety states like panic attacks, the locus ceruleus is hyperactive.
• Hyperactivity of amygdala has been implicated in social anxiety. ^[1]

Psychoanalytic component[edit | edit source]

• Freud described that anxiety is developmentally related to childhood fears of disintegration that derived from the fear of actual or imagined loss of a love object or fear of bodily harm.
• He used the term "signal anxiety" to describe anxiety that triggers defense mechanisms used by the person to cope with the potential threat, but anxiety in fact, is not consciously experienced.

Learning theory[edit | edit source]

• Anxiety is produced due to continued stress.
• The anxiety eventually becomes a conditioned response to stressful situations of less severity.

Genetic studies[edit | edit source]

• About 5% individuals with anxiety have polymorphic variant of the gene associated with serotonin transporter metabolism.^[2]

References[edit | edit source]

Template:WH Template:WS