Anxiety disorders include fear and anxiety. Anxiety refers to apprehension over an anticipated problem. Fear is a reaction to immediate danger. Fear happens at the moment and anxiety involves a future threat. In all anxiety disorders, except for a panic disorder, the symptoms must persist for at least 6 months. The symptoms must persist for at least one month for a panic disorder.

Clinical profile-specific phobia (e.g: snakes, spiders, heights):

The object of phobia may also elicit intense disgust. Specific phobias are highly comorbid.

Clinical profile social anxiety disorder:

The social anxiety disorder can be about a specific social situation (e.g: speaking in public) and doesn’t necessarily include all social situations. Severe social anxiety is highly comorbid with depression and alcohol abuse. People with social anxiety can demonstrate aggressive and hostile behaviour in the face of potential social rejection.

Clinical profile panic disorder:

Panic attacks are unrelated to specific situations.

Clinical profile panic attack:

Depersonalization, derealization and fears of losing control or dying may also occur during the panic attack. A panic attack can be characterised as a misfire of the fear system.

Clinical profile agoraphobia:

Clinical profile generalized anxiety disorder (GAD):

Worry refers to the cognitive tendency to chew on a problem and to be unable to let go of it. Anxiety disorders are highly comorbid with other anxiety disorders. It is also highly comorbid with other psychological disorders. Anxiety disorders are highly comorbid with substance abuse, depression and personality disorders.

Women are more likely than men to develop anxiety disorders. The culture may influence the focus of fears, the way that symptoms are expressed an even the prevalence of different anxiety disorders.

Mowrer’s two-factor model of anxiety disorders suggests two steps in the development of an anxiety disorder:

1. Classical conditioning
2. Operant conditioning
   This is avoiding the conditioned stimulus and this acts as a reinforcer.

Classical conditioning can occur through direct experience, modelling (seeing something happen) or verbal instruction. People with panic disorder seem to sustain classically conditioned fears longer. Anxiety disorders are partially heritable.

The fear circuit (hippocampus, amygdala, medial prefrontal cortex) in the brain is engaged when people feel anxious or fearful. Elevated activity in the amygdala may explain different anxiety disorders. The medial prefrontal cortex helps to regulate amygdala activity. People with anxiety disorders have less activity in that area. GABA is a neurotransmitter and helps inhibit anxiety. Serotonin helps modulate emotions. Anxiety disorders are related to increased levels of norepinephrine. It is involved in activation of “fight or flight”.

Behavioural inhibition is a tendency to become agitated and cry when faced with novel toys, people or other stimuli. This may be a predictor of anxiety disorders. People with neuroticism are more likely to develop anxiety disorders.

Cognitive factors include sustained negative beliefs about the future, perceived lack of control and attention to threat. People with panic attacks engage in safety behaviours and they believe that this kept them alive. A perceived lack of control may be caused by traumas or strict parents. Safety behaviours are behaviours used to reduce anxiety.

There is prepared learning in humans. We are biologically prepared to fear certain things (e.g: snakes). People can fear other stimuli, but these fears are often quickly extinguished and more natural (prepared) fears are sustained longer.

Social anxiety disorders may be caused by classical and operant conditioning. People with social anxiety also often have too much focus on negative self-evaluations and beliefs about how the other will perceive him and this may perpetuate the social anxiety. People with social anxiety might also attend more to internal cues than to external (social) cues.

The locus coeruleus is the major source of the neurotransmitter norepinephrine in the brain. This part of the brain might be overly active in people with panic disorder and certain drugs can increase activity in the locus coeruleus increasing probability of a panic attack. Classical conditioning of panic attacks in response to bodily sensations is called interoceptive conditioning. A person experiences somatic signs of anxiety which are followed by a panic attacked and the panic attack then becomes the conditioned response to the somatic changes. People with panic attacks catastrophically fail to interpret their bodily responses. Bodily sensations are interpreted as signs of impending doom, which will increase the anxiety, which increases the physical sensation, which increases the beliefs about impending doom. It is a vicious cycle. There is a gene that increases the risk of panic disorder. The anxiety sensitivity index measures the extent to which people respond fearfully to their bodily sensations and is a predictor of panic attacks.

The fear-of-fear hypothesis states that agoraphobia is driven by negative thoughts about the consequences of experiencing anxiety in public. In other words, fear of fear.

GAD is explained in the following way. Worrying is used to reduce strong negative emotions. It is also possible that people who find it difficult to accept ambiguity are more likely to worry and develop GAD.

All effective psychological treatment for anxiety disorders makes use of exposure. Exposure should include as many features of the feared object as possible and include as many situations as possible. Extinction of the fear does not involve forgetting the fearful associations but learning new, non-fearful associations.

There are several treatments for anxiety disorders:

Anxiolytics are medications that reduce anxiety. D-cycloserine (DCS) enhances learning and can enhance the effect of exposure therapy.