Definitions and epidemiology

Anxiety is a normal, protective, psychological response to an unpleasant or threatening situation. Mild to moderate anxiety can improve performance and ensure appropriate action is taken. However, excessive or prolonged symptoms can be disabling, lead to severe distress and cause much impairment to social functioning. Figure 28.1 shows that as anxiety levels increase performance/actions increase. However, as the anxiety level increases beyond acceptable or tolerated levels, the performance declines.

Fig. 28.1 The Yerks Dodson curve.

The term ‘anxiety disorder’ encompasses a variety of complaints which can either exist on their own or in conjunction with another psychiatric or physical illness. Symptoms of anxiety vary but generally present with a combination of psychological, physical and behavioural symptoms (Fig. 28.2). Some of these symptoms are common to many anxiety disorders while others are distinctive to a particular disorder. Anxiety disorders are broadly divided into generalised anxiety disorder (GAD), panic disorder, social phobia, specific phobias, post-traumatic stress disorder (PTSD) and obsessive-compulsive disorder (OCD), see Table 28.1. Patient testimonials are presented in Box 28.1. Approximately two-thirds of sufferers of an anxiety disorder will have another psychiatric illness. This is most commonly depression and often successful treatment of an underlying depression will significantly improve the symptoms of anxiety. Many patients will also present with more than one anxiety disorder at the same time which can further complicate treatment. Anxiety disorders are the most commonly reported mental illness and as a whole have a lifetime prevalence of 21% (Baldwin et al., 2005) with specific phobias the most commonly reported.

Fig. 28.2 The symptoms of anxiety.

Table 28.1 A brief description of the common anxiety disorders

For all anxiety disorders together the overall female to male ratio is 2:1. The age of onset of most anxiety disorders is in young adulthood (20s and 30s), although the maximum prevalence of generalised anxiety and agoraphobia in the general population is in the 50–64 year age group.

Pathophysiology

Anxiety occurs when there is a disturbance of the arousal systems in the brain. Arousal is maintained by at least three interconnected systems: a general arousal system, an ‘emotional’ arousal system and an endocrine/autonomic arousal system (Fig. 28.3). The general arousal system, mediated by the brainstem reticular formation, thalamic nuclei and basal forebrain bundle, serves to link the cerebral cortex with incoming sensory stimuli and provides a tonic influence on cortical reactivity or alertness. Excessive activity in this system, due to internal or external stresses, can lead to a state of hyperarousal as seen in anxiety. Emotional aspects of arousal, such as fear and anxiety, are contributed by the limbic system which also serves to focus attention on selected aspects of the environment. There is evidence that increased activity in certain limbic pathways is associated with anxiety and panic attacks.

Fig. 28.3 Diagram of arousal and sleep systems. Arousal systems receive environmental and internal stimuli, cause cortical activation and mediate motor, autonomic and endocrine responses to arousal. Reciprocally connected sleep systems generate slow-wave sleep (SWS) and rapid eye movement sleep (REMS). Either system can be excited or inhibited by cognitive activity generated in the cortex.

These arousal systems activate somatic responses to arousal, such as increased muscle tone, increased sympathetic activity and increased output of anterior and posterior pituitary hormones. Inappropriate increases in autonomic activity are often associated with anxiety states; the resulting symptoms (palpitations, sweating, tremor, etc.) may initiate a vicious circle that increases the anxiety.

Several neurotransmitters have been implicated in the arousal systems. Acetylcholine is the main transmitter maintaining general arousal but there is evidence that heightened emotional arousal is particularly associated with noradrenergic and serotonergic activity. Drugs which antagonise such activity have anxiolytic effects. In addition, the inhibitory neurotransmitter γ-aminobutyric acid (GABA) exerts an inhibitory control on other transmitter pathways and increased GABA activity may have a protective effect against excessive stress reactions. Many drugs which increase GABA activity, such as the benzodiazepines, are potent anxiolytics.

Aetiology and clinical manifestations

Anxiety is commonly precipitated by stress but vulnerability to stress appears to be linked to genetic factors such as trait anxiety. Many patients presenting for the first time with anxiety symptoms have a long history of high anxiety levels going back to childhood. Anxiety may also be induced by central stimulant drugs (caffeine, amphetamines), withdrawal from chronic use of central nervous system depressant drugs (alcohol, hypnotics, anxiolytics) and metabolic disturbances (hyperventilation, hypoglycaemia, thyrotoxicosis). It may form part of a depressive disorder and may occur in temporal lobe lesions and in rare hormone-secreting tumours such as phaeochromocytoma or carcinoid syndrome.

Apart from the psychological symptoms of apprehension and fear, somatic symptoms may be prominent in anxiety and include palpitations, chest pain, shortness of breath, dizziness, dysphagia, gastro-intestinal disturbances, loss of libido, headaches and tremor. Panic attacks are experienced as storms of increased autonomic activity combined with a fear of imminent death or loss of control. If panic becomes associated with a particular environment, commonly a crowded place with no easy escape route, the patient may actively avoid similar situations and eventually become agoraphobic. When anxiety is precipitated by a specific cause then behaviour can become altered to ensure the sufferer avoids the cause. This avoidance behaviour can maintain the often irrational fear and strengthen the desire to avoid the threat.

Investigations and differential diagnosis

In patients presenting with symptoms and clinical signs of anxiety, it is important to exclude organic causes such as thyrotoxicosis, excessive use of stimulant drugs such as caffeine and the possibility of alcoholism or withdrawal effects from benzodiazepines. However, unnecessary investigations should generally be avoided if possible. Extensive gastroenterological, cardiological and neurological tests may increase anxiety by reinforcing the patient’s fear of a serious underlying physical disease.

Treatment

Treatment for anxiety disorders often requires multiple approaches. The patient may need short-term treatment with an anxiolytic, such as a benzodiazepine, to help reduce the immediate symptoms combined with psychological therapies and an antidepressant for longer term treatment and prevention of symptoms returning.

Pharmacotherapy

Benzodiazepines

Benzodiazepines are commonly prescribed to provide immediate relief of the symptoms of severe anxiety. A number of different benzodiazepines are available (Table 28.2). These drugs differ considerably in potency (equivalent dosage) and in rate of elimination but only slightly in clinical effects. All benzodiazepines have sedative/hypnotic, anxiolytic, amnesic, muscular relaxant and anticonvulsant actions with minor differences in the relative potency of these effects.

Table 28.2 Profile of selected benzodiazepines (Bazire, 2009; Taylor et al., 2009)

Pharmacokinetics

Most benzodiazepines are well absorbed and rapidly penetrate the brain, producing an effect within half an hour after oral administration. Rates of elimination vary; however, with elimination half-lives from 8 to 35 h (see Table 28.2

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