Definition

Anxiety is an unpleasant and often distressing sense of uneasiness, apprehension and/or nervousness. Anxiety is considered to be a standalone, non-pathological symptom (i.e. a normal response to an environmental stessor such as workplace or examination stress), as well as a central feature of ‘anxiety disorder’, a term that is inclusive of generalised anxiety disorder (GAD), phobias, panic disorder, obsessive–compulsive disorder (OCD) and post-traumatic stress disorder (PTSD).¹

Epidemiology

The lifetime prevalence rate of GAD ranges from 10.6 per cent to 16.6 per cent. This disorder is most prevalent in women, and appears to increase with advancing age. For the more specific anxiety disorders, the lifetime prevalence rates range from 0.5–1.3 per cent for OCD, 1.0–1.2 per cent for panic disorder, 1.2–2.1 per cent for PTSD, 3.6–5.3 per cent for phobias and 2.6–6.2 per cent for GAD.²

Aetiology and pathophysiology

Anxiety disorders are complex conditions that appear to originate from a number of causes. Genetic predisposition and/or familial history, for instance, have been associated with panic disorder, GAD, phobias and OCD.³ Physiological factors, including group A beta-hemolytic Streptococcus infection and trauma or postpartum events are, respectively, also implicated in OCD and panic disorder. But most attention has focused on the neurochemical aetiology of these disorders. Elevated central nervous system catecholamine levels (e.g. panic disorder), impaired gamma-amino butyric acid metabolism (e.g. panic disorder), carbon dioxide sensitivity (e.g. panic disorder), abnormal serotoninergic and noradrenergic activity (e.g. GAD and PTSD), reduced dopamine (D2) receptor and transporter binding (e.g. phobias), abnormal number and/or function of serotinergic receptors (e.g. OCD), neurological disease (e.g. OCD), increased limbic system activity (e.g. PTSD), impaired lactate metabolism (e.g. panic disorder), and basal ganglia dysfunction and prefrontal hyperactivity (e.g. OCD) are just some of the many neurochemical causes of these disorders.⁴

The pathogenesis of anxiety disorders is only partly explained by these physiological elements. The development of these conditions is also influenced by socioenvironmental factors such as stress, illicit drug use (e.g. marijuana and lysergic acid diethylamide, or LSD), diet (e.g. caffeine), poor social support (e.g. PTSD) and the demise of close relationships (e.g. panic disorder). Behavioural elements also may be implicated in the pathogenesis of anxiety disorder, including the development of abnormal or irrational conditioned responses to fearful situations (e.g. panic disorder), life events (e.g. GAD) or stressful situations (e.g. OCD).^4,5

Clinical manifestations

Anxiety is an elusive symptom that can manifest in any person, at any time, in any given situation and to any degree. Anxiety can manifest in any health condition and the physiological features of anxiety can mimic other disorders. As a result, distinguishing anxiety from other medical conditions may be a challenge for some clinicians. A critical first step to identifying anxiety disorder is to understand that anxiety is only one symptom of this condition. Other symptoms that commonly manifest in this group of disorders are irritability, poor concentration, insomnia, restlessness, muscle tension, avoidance behaviour, preoccupation with an event or situation, easy fatigability, tachycardia, palpitations, shortness of breath and an exaggerated startle response.^1,3,4

The duration of anxiety is also important. Panic disorder, for instance, is an acute condition that manifests rapidly and peaks within 10 minutes. PTSD can be acute (i.e. occurring soon after an event) and chronic (i.e. occurring more than 3 months after an event). Conditions such as GAD, OCD and phobias are chronic and can exist for many months, years or decades. While the intensity of symptoms is often most severe in acute panic disorder, the severity of symptoms in other anxiety disorders varies greatly.^1,3,4