Understanding anxiety

Only 34.9 per cent of those with any disorder are known to seek help, most of them women, one-in-three of whom had visited their general practitioner, compared to one-in-six men.

Anxious individuals fear the loss of control, the unknown, negative evaluation by others and illness/death. Along with feeling helpless and needy they also have the fantasy that they should be omnipotent and omniscient, able to control their environment and lives in order to feel the “safety” of being all-knowing and self-sufficient.

Neuroscience and Biological Models

The amygdala, a part of the limbic system, has been studied the most in relation to the fear response. Through its link with the hippocampus, the amygdala is where emotions and memory are combined. It is part of the mammalian subcortical brain that quickly registers strong emotional stimuli such as fear and aggression as well as pleasurable feelings such as sexual drive and sociability.

This is so that we can make a fast decision whether the person coming towards us is friend or foe. The amygdala sends out efferent fibres that mediate autonomic, endocrine and behavioural responses to these emotions. Hyperactivation of the amygdala is seen in many types of anxiety. In PTSD there is both hyper- and hypo- activation.

The ventral hyperactive region is related to acquired fear responses (eg flashbacks, exaggerated startle response) and the dorsal hypoactive region is involved in the autonomic blunting, emotional numbing and dissociation of PTSD.

One of the amygdala’s myriad connections is with the medial prefrontal cortex (MFPC) that regulates the fear provoking stimuli coming from below.

Specific and social phobias are due to an exaggerated fear response, whilst PTSD and panic disorder have the fear component as well as inadequate emotional regulation by the hypoactive MFPC. The fear response is sensitized by early or more recent trauma.

Like other mammals, humans have a panic system which is associated with separation distress. Infants signal their need for parental care by distress vocalizations. Panic attacks stem from sudden arousal of the separation-distress system, whether it is an actual or symbolic separation. They can be modulated particularly by opioids but also by oxytocin and prolactin. There is a deficit of opioids in panic disorder. This could partly explain the anxiety disorders’ comorbidity with substance misuse.

Hormonal and autonomic responses to threat are mediated via the hypothalamic-pituitary-adrenal (HPA) axis. The hypothalamus receives afferent fibres from the amygdala, which then activates the sympathetic autonomic nervous system (causing increased heart rate, sweating, pupillary dilation) and the parasympathetic system (causing urinary and gastrointestinal disturbances).

The fight-or-flight or acute stress response leads to increased secretion of cortisol which increases glucose metabolism in the short term but in the long term leads to a decreased immune response, higher risk of CVAs and myocardial infarcts, poor memory retrieval and impaired learning and depression.

The stress response also leads to an increased production of noradrenaline from the amygdala and related limbic system structures. It is thought that there is chronic central hypersecretion of noradrenaline in anxiety, with consequent hyporesponsiveness of central post-synaptic receptors. Serotonin has both anxiogenic and anxiolytic effects. The GABA (the major inhibitory neurotransmitter) – benzodiazepine receptor molecule is disrupted in anxiety disorders.

Psychological Models of Panic Disorder

The cognitive-behavioural model views panic as a learned fearfulness of bodily sensations. The initial panic attack develops from misfiring of the fear system often triggered by stressful life events in psychologically vulnerable individuals. This panic attack becomes the traumatic event and causes further heightened arousal, misinterpretation of physical sensations and fear. A fear of fear develops.

Although the initial panic attack is thought to be precipitated by a past experience, intrapsychic conflict and unconscious causes of fear are not considered central to cognitive-behavioural therapy (CBT).

One psychodynamic model posits that the panic prone individual has an inherent fear of the unfamiliar, making them more dependent on their parents for a sense of safety. Children with insecure attachments will experience any separation with significant distress and will have an ongoing fear of a recurrence of separation. This fearful dependency can also arise from developmental traumas such as over-controlling parents or parents who threaten abandonment. The child then sees the parents as unreliable and rejecting and this can elicit angry feelings in the child. This in turn leads to feelings of inadequacy and further feelings of anger at being dependent upon unreliable parents. Thus anger, often unconscious, disrupts attachments and can be associated with fear.

A Proposed Integrated Model of Panic Disorder

Panic prone individuals may be genetically predisposed to the development of an oversensitized fear network and separation-distress system from early life. Traumatic early developmental memories can also cause the exaggerated fear response. Trauma memories are encoded in the amygdala which is also involved in the expression of anger. Psychological distress due to intrapsychic conflicts (e.g. feeling controlled by others yet feeling unable to be assertive because of a concomitant wish to be dependent), fear of separation and negative affects such as anger, activate the sensitized fear system which is inadequately modulated by higher cortical centres such as the MPFC.

Anger may be triggered with fear. This can lead to more fear as the expression of anger may cause the loss of the attachment figure or more intrusion by them. Thus the separation-distress system can be activated by anger as well as fear. An anxious individual will feel that relationships are more easily threatened, that they themselves are more needy and incompetent and that others are more critical and abandoning. This puts attachments at risk and heightens the onset of panic.

Management

Simplistically, medications act from the bottom up, that is, on the amygdala and basal ganglia and psychotherapy works from the top down by augmenting prefrontal cortex processing and emotional regulation. However, psychodynamic psychotherapy also acts at the subcortical unconscious level through the emotional and psychic attachment between therapist and patient.

Overactivity in the core fear system can be reduced by anxiolytics such as benzodiazepines. Antidepressants such as the SSRIs (e.g. fluoxetine), SNRIs (such as duloxetine), NaSSA (e.g. mirtazapine) and tricyclics (e.g. nortriptyline) increase levels of serotonin and noradrenaline in the synaptic space.

CBT works in the here and now through re-educating patients to correct misconceptions, to modify negative mental representations of events and to change their self-regulation of thoughts, feelings, and behaviours, e.g. sleep hygiene, moderate exercise, healthy diet, a decrease in caffeine and other substances, and challenge negative thinking. Possible causes of fear and interpersonal difficulties as manifested in the therapeutic relationship are not examined.

Although short-term CBT has been used with effect on some anxiety disorders, it requires the patient to continually practise the techniques they are taught. In the treatment of patients who have early implicit memories of trauma, where fear has neither words nor logic, cognitive processes cannot be activated immediately.

Long term psychodynamic therapy allows emotional connectedness between patient and therapist, helps to modify implicit memories by creating a secure environment for open communication, intimacy and trust. The patient learns to sit with their anxiety rather than avoid it and feels held and contained by the therapist.

Repressed unconscious feelings such as anger and fear that the patient has towards significant others from the past and present can be named, owned and worked through. The dyad co-create a meaningful narrative initially through mainly unconscious thought (where 95 per cent of our thinking occurs), affect, intuition, perceptions, play, dreams and myths. The compulsive need for absolutes and certainty diminishes – one becomes more open to seeing and experiencing what is rather than what should be.

Psychological flexibility makes ambiguity more tolerable and calm is achievable in the face of uncertainty as one’s sense of agency increases. Imagination and creativity are given space so that one can grow and better realize one’s potential. Changes at the subcortical level are slow but profound, emotional rather than intellectual.

Long term therapy has been shown to have more enduring effects than short term work, even after termination of treatment. The patient comes to know themselves better, learns to process and regulate their emotions and undo habitual ways of thinking via the prefrontal cortex, thus making conscious what was previously unconscious.

I know that there is so much more to know, and in the journey to more knowing, we are growing.

Rosalind Foy is a psychiatrist in private practice in Brunswick Heads. Her particular interest is in long-term psychotherapy of anxiety, depression and personality vulnerabilities in adolescence through to older age.

Bibliography

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