We have all experienced anxiety symptoms, perhaps suffer from a particular ‘phobia’, or are a little bit obsessive about certain things, but to be clinically significant, these problems must be severe enough to cause marked distress and/or substantially interfere with our day-to-day lives. Because of the recognizable quality of some of the symptoms of neurotic disorders, it may be helpful to divide them into three categories:

The common neuroses

·  Anxiety/phobic disorders: e.g. panic disorder, agoraphobia, generalized anxiety disorder (GAD), specific (understandable) phobias (e.g. snakes, spiders), hypochondriasis, social phobia.

·  Stress-related disorders: e.g. acute stress reactions, adjustment disorder, post-traumatic stress disorder (PTSD).

·  Obsessive–compulsive disorder (OCD).

·  Anxiety/phobic disorders: e.g. ‘non-understandable’ phobias (e.g. dirt, feathers), dysmorphophobia.

·  ‘Hysterical’ conversion disorders.

·  Dissociative/depersonalization–derealization disorder.

·  Somatoform disorders.

·  Chronic fatigue syndrome (CFS)/eating disorders (see b p. 398).

·  Other ‘culture-bound’ disorders.

This chapter deals with the anxiety, phobic, and stress-related disorders. Anxiety symptoms are common in the general population.

·  Comorbidity is frequent (other neuroses, depression, substance misuse, personality disorder).

·  Anxiety disorders may often present with physical symptoms.

Historical perspective

The term ‘neurosis’ was coined by William Cullen in 1777, replacing ‘illness of the nerves’ (coined by Robert Whytt in 1764 to replace the old ‘vapours’), and meaning any disease of the nervous system without a known organic basis (which at the time also included epilepsy). Clinical descriptions of neurotic symptoms can be found in the works of Hippocrates. However, the ‘illness’ later vanished under the cloak of both pagan and Christian beliefs, with typical symptoms attributed to the work of spirits, possession, or divine punishment. It did not resurface properly until the Renaissance (the 1500s) thanks (in part) to the witchcraft trials, when doctors were called in to present diagnoses of known illnesses that could be mistaken for demonic possession (the first recorded ‘medical defence’!). Although there was much debate, the brain became the final resting place as the organ most likely to be involved in the aetiology of the condition.

The history of the neuroses is tightly bound to the (re)discovery of hypnosis (formerly the remit of faith healing). The work of Franz-Anton Mesmer (1734–1815)—mesmerism—and James Braid (1795–1860)— braidism—was brought to France by Azam in 1859, coming to the attention of Charcot, whose experiments with hysterics would have a profound influence on one particular assistant—Sigmund Freud. Freud’s first paper, published in 1886, shortly after his return to Vienna, was of a case of

‘traumatic hysteria’ in a male patient. It was his Studies on hysteria, written with Josef Breuer and published in 1895, that provided the starting point of his subsequent major concepts of psychoanalytical theory—including repression, psychic reality, and the subconscious.

The idea of repression of trauma (out of consciousness) and the appearance of ‘defences’ was highly influential, with the neuroses regarded as illnesses of the mind, needing psychotherapeutic treatment. Old arguments of emotional vs. physical factors resurfaced in the aftermath of the First World War, as some authorities found it difficult to attribute the illnesses seen in fit, healthy, young men (who had indisputably experienced traumatic events) to conversion hysteria or phobic neurosis. The encephalitis lethargicans epidemic in 1919, and the presence of numerous ‘hysterical’ symptoms (e.g. convulsions, mutism, feelings of passion, obsessions/compulsions, spasms) argued in favour of at least some of the neuroses having an organic basis.

In the 1920s, Walter Cannon proposed the concept of the ‘emergency reaction’, believing this ‘fight-or-flight’ response was mediated by the autonomic nervous system. He also noted that the physiological responses were too slow to account for feelings, and that some other ‘neural mechanism’ must be at work.

The dominance of the behaviourists in psychology relegated emotion to just another ‘way of acting’ in a particular situation (albeit internally perceived). Although an over-simplification, this led to the development of the ‘conditioning theory’ of anxiety. John Watson, the father of behaviourism, claimed to have produced an animal phobia in an 11-mth-old boy, ‘little Albert’, by making a loud clanging noise whilst the boy was playing with a rat. Watson proposed that neuroses arose out of traumatic learning situations and then persist to influence behaviour throughout life.

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This was adapted by the 1930s to include the concept of ‘instrumental conditioning’ (association of an emotionally arousing stimulus and a neutral response), and, in the 1940s, Mowrer attempted to translate Freud’s theory of anxiety neurosis into the language of learning theory: responses that reduce anxiety are learned—sometimes these reinforced behaviours may be aberrant, unhelpful, or simply bizarre, and present as neuroses. ‘Avoidance’ was postulated as the behaviour that was reinforced due to successfully removing a ‘negative reinforcer’ (e.g. fear). These ideas led to the rational treatment of phobias with desensitization techniques.

In the search for Cannon’s neural mechanism, neurophysiologists used lesioning experiments to identify the thalamus as a critical gateway for stimuli, and the hypothalamus as mediating the physiological response (via the HPA axis)—the Cannon–Bard theory. Other theories emerged over the years (e.g. the Papez Circuit, 1937), and understanding the emotional life of the brain remains at the forefront of research (see The emotional brain by Joseph LeDoux, 1998).

Inviting as psychological explanations appeared, the late 1950s also heralded the arrival of the BDZs. ‘Tranquillizers’ (e.g. Miltown®, Librium®, Valium®) became the ‘housewives’ choice’, effectively treating a multitude of neurotic symptoms. Unfortunately, the indiscriminate use of these drugs led to them being demonized as causing dependence problems (despite evidence for their effectiveness when properly used). The advent of the antidepressants artificially separated neurotic depression from the other neuroses, but nonetheless some utility was also seen in treating the anxiety disorders. A key study was the use of clomipramine in the treatment of OCD (see The boy who couldn’t stop washing by Judith Rapoport, 1989). The fact that clomipramine was the most serotonergic of the TCAs paved the way for the second-generation antidepressants (the SSRIs) used in neuroses (previously thought only to be amenable to psychological approaches).

Brain imaging demonstrated underlying functional changes in OCD patients (in the frontal cortex [left orbital gyrus] and bilateral caudate nuclei), which ‘normalized’ after successful treatment with medication (and interestingly with CBT techniques, although this took longer). For many patients with panic attacks, structural and functional changes were found in the temporal lobes. These findings resonated with the long-held observation that neurotic symptoms (e.g. anxiety, panic, somatic symptoms, depersonalization/derealization) were often reported in other ‘organic’ conditions (e.g. temporal lobe epilepsy).

Modern views are eclectic in their approach—e.g. the biopsychosocial model (see b p. 245). For the neuroses, early environmental influences (including social factors like maternal deprivation) can alter the sensitivity of physiological stress responses in adulthood. Hence, the experience of stressors (psychological or physical) may lead (e.g. through the effects of stress hormones such as cortisol, and other neurophysiological mechanisms) to alterations in the structure and/or function of the brain, which in turn manifest as clinical symptoms (i.e. behavioural and/or emotional change).

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Panic attack: 

period of intense fear characterized by a constellation of symptoms (see Box 9.1) that develop rapidly, reach a peak of intensity in about 10min, and generally do not last longer than 20–30min (rarely over 1hr). Attacks may be either spontaneous (‘out of the blue’) or situational (usually where attacks have occurred previously). Sometimes attacks may occur during sleep (nocturnal panic attacks), and rarely, physiological symptoms of anxiety may occur without the psychological component (non-fearful panic attacks).

Recurrent panic attacks, which are not s to substance misuse, medical conditions, or another psychiatric disorder. Frequency of occurrence may vary from many attacks a day to only a few a year. Usually a persistent worry about having another attack or consequences of the attack (which may lead to phobic avoidance of places or situations—see b p. 364), and significant behavioural changes related to attack.

Physical symptoms/signs related to autonomic arousal (e.g. tremor, tachycardia, tachypnoea, hypertension, sweating, GI upset), often compounded by HVS (in 50–60% of cases, see b p. 356).

Concerns of death from cardiac or respiratory problems may be a major focus, leading to patients presenting (often repeatedly) to emergency medical services.

Panic disorder may be undiagnosed in patients with ‘unexplained’ medical symptoms (chest pain, back pain, GI symptoms including IBS, fatigue, headache, dizziness, or multiple symptoms).

Thoughts of suicide (or homicide) should be elicited; acute anxiety (particularly when recurrent) can lead to impulsive acts (usually directed towards self). Note: risk of attempted suicide substantially raised where comorbid depression, or alcohol or substance misuse.

Symptoms associated with panic attacks

In order of frequency of occurrence:

·         Palpitations, pounding heart, or accelerated heart rate.

·         Sweating.

·         Trembling or shaking.

·         Sense of shortness of breath or smothering.

·         Feeling of choking or difficulties swallowing (globus hystericus).

·         Chest pain or discomfort.

·         Nausea or abdominal distress.

·         Feeling dizzy, unsteady, light-headed, or faint.

·         Derealization or depersonalization (feeling detached from oneself or one’s surroundings).

·         Fear of losing control or going crazy.

·         Fear of dying (angor animus).

·         Numbness or tingling sensations (paraesthesia).

·         Chills or hot flashes.

Emergency treatment of an acute panic attack

·         Maintain a reassuring and calm attitude (most panic attacks resolve spontaneously within 30min).

·         If symptoms are severe and distressing consider prompt use of BDZs (immediate relief of anxiety may help reassure the patient, provide confidence that treatment is possible, and reduce subsequent ‘emergency’ presentations).

·         If first presentation, exclude medical causes (may require admission to hospital for specific tests).

·         If panic attacks are recurrent, consider differential diagnosis for panic disorder and address underlying disorder (may require psychiatric referral).

Obsessive–compulsive disorder (OCD)

A common, chronic condition, often associated with marked anxiety and depression, characterized by ‘obsessions’ (see b p. 101) and ‘compulsions’ (see b p. 89). Obsessions/compulsions must cause distress or interfere with the person’s social or individual functioning (usually by wasting time), and should not be the result of another psychiatric disorder. At some point in the disorder, the person recognizes the symptoms to be excessive or unreasonable.

Content of obsessions/compulsions Checking (63%), washing (50%), contamination (45%), doubting (42%), bodily fears (36%), counting (36%), insistence on symmetry (31%), aggressive thoughts (28%).

Epidemiology Mean age: 20yrs, 70% onset before age 25yrs, 15% after age 35yrs, 5=4, prevalence: 0.5–3% of general population.

Acute stress reaction (ICD-10)

A transient disorder (lasting hours or days) that may occur in an individual as an immediate (within 1hr) response to exceptional stress (e.g. natural catastrophe, major accident, serious assault, warfare, rape, multiple bereavement, fire). The stressor usually involves severe threat to the security or physical integrity of the individual or of a loved person(s).

Symptoms tend to be mixed/changeable with an initial state of daze, followed by depression, anxiety (as for GAD, see b p. 372), anger, or despair. Presence of social withdrawal, narrowed attention, disorientation, aggression, hopelessness, over-activity, or excessive grief defines mild (none of these symptoms present), moderate (2 present), or severe (4 present, or dissociative stupor) forms.

Acute stress disorder (DSM-IV)

Clear overlap with ‘acute stress reaction’ (symptoms of dissociation, anxiety, hyperarousal), but greater emphasis on dissociative symptoms, onset within 4wks, lasting 2 days to 4wks (after which diagnosis changes to PTSD).

As for PTSD—re-experiencing of events, avoidance, and hyperarousal (but lasting no more than 4wks).

Management

Psychological: the mainstay of management is essentially supportive psychotherapy to enhance the capacity to cope with a stressor that cannot be reduced or removed, and to establish sufficient support (esp. practical help, e.g. provision of carers/childcare, financial support and benefits, occupational therapy [OT] assessment, contact with specific support groups) to maximize adaption. Ventilation/ verbalization of feelings may be useful in preventing maladaptive behaviours (e.g. social isolation, destructive behaviours, suicidal acts) and understanding the ‘meaning’ of the stressor to the individual may help correct cognitive distortions.

Normal and abnormal grief reactions

Controversy surrounds how we should regard normal/abnormal grief, and whether they are distinct from depression or other stress-related disorders.1 It is very common for those suffering bereavement to have depressive symptoms. However, it is less common for people to experience a clear depressive episode that requires treatment.2 Normal grief is variable in its intensity and duration. Some commentators regard bereavement as just another stressor and argue that, depending on the phenomenology, grief may be regarded as an acute stress reaction/disorder, an adjustment disorder, or even a form of PTSD (‘traumatic grief’). Just as the former reactive/endogenous debate surrounding depression has led to recommendations that ‘clinical’ symptoms should be treated, a bereaved person should not be denied effective treatment on the basis of ‘understandability’, nor should arbitrary

Prolonged Grief Disorder (PGD) (aka Complicated Grief Disorder, Traumatic Grief)

Prigerson et al.1, a group of international researchers, have attempted to refine this syndrome for inclusion in DSM-V and ICD-11 with criteria to identify bereaved persons at heightened risk for enduring distress and dysfunction. Criteria require reactions to a significant loss that involve the experience of yearning (e.g., physical or emotional suffering as a result of the desired, but unfulfilled, reunion with the deceased) and at least 5 of the following 9 symptoms experienced at least daily or to a disabling degree:

·         feeling emotionally numb, stunned, or that life is meaningless;

·         experiencing mistrust;

·         bitterness over the loss;

·         difficulty accepting the loss;

·         identity confusion;

·         avoidance of the reality of the loss;

·         difficulty moving on with life.

Symptoms must be present at sufficiently high levels at least 6mths from the death and be associated with functional impairment.

Post-traumatic stress disorder

Severe psychological disturbance following a traumatic event (see b p. 380) characterized by involuntary re-experiencing of elements of the event, with symptoms of hyperarousal, avoidance, emotional numbing.

Symptoms arise within 6mths (ICD-10) of the traumatic event (delayed onset in 710% of cases) or are present for at least 1mth, with clinically significant distress or impairment in social, occupational, or other important areas of functioning (DSM-IV). Both ICD-10 and DSM-IV include:

• 2 or more ‘persistent symptoms of increased psychological sensitivity and arousal’ (not present before exposure to the stressor): difficulty falling or staying asleep; irritability or outbursts of anger; difficulty in concentrating; hypervigilance; exaggerated startle response.
• Persistent remembering or ‘reliving’ of the stressor in intrusive flashbacks, vivid memories, or recurring dreams; and in experiencing distress when exposed to circumstances resembling or associated with the stressor.
• Actual or preferred avoidance of circumstances resembling or associated with the stressor which was not present before exposure to the stressor.
• Inability to recall, either partially or completely, some important aspects or the period of exposure to the stresso
• Risk of developing PTSD after a traumatic event 8–13% for men, 20–30% for women. Lifetime prevalence estimated as 7.8% (4:5 = 1:2).1 Cultural differences exist. Some types of stressor are associated with higher rates of PTSD (e.g. rape, torture, being a prisoner of war).