Psychiatry: Mental Disorders

Psychosis: Symptoms and Aetiology

Psychosis describes the misperception of thoughts and perceptions that arise from the patient’s own mind/imagination as reality, and includes delusions and hallucinations. It is a symptom, not a diagnosis. About 3% of the general population has clinically significant psychosis. Psychotic disorders include: schizophrenia, delusional disorder, schizoaffective disorder, psychotic depression and bipolar affective disorder.

Schizophrenia

History

• Emil Kraepelin (1893) divided psychotic disorders into manic depression, where normal function was regained between periods of relapse, and dementia praecox, characterised by irreversible deterioration of mental functions. The latter corresponds broadly to current concepts of schizophrenia.
• Bleuler coined the term, ‘schizophrenia’ in 1911.
• Kurt Schneider (1959) described first and second rank symptoms of schizophrenia (see Figure 6.1) – first rank symptoms are highly suggestive of schizophrenia but also occur in 8% of patients with bipolar affective disorder, while 20% of people with chronic schizophrenia never show them. Current ICD-10 and DSM-5 classifications are strongly based on these.

Epidemiology

• The annual incidence of schizophrenia is 15–20/100â•›000, with a lifetime risk of 0.7%. Lifetime risk is greater in men (1.4:1).
  Peak incidence is in late teens or early adulthood.

Symptoms

These can be divided into:

• Positive symptoms:
  • delusions, most commonly persecutory or delusions of reference
  • hallucinations
  • formal thought disorder (disorganised speech) e.g. loosening of associations, neologisms (new words, or words used in a special way).
• Negative symptoms:
  • poverty of speech, flat affect, poor motivation, social withdrawal and lack of concern for social conventions.
• Cognitive symptoms:
  • poor attention and memory.

Diagnosis

• Current diagnostic criteria are still broadly based on Schneider’s First Rank Symptoms. The diagnosis should not be made in the presence of drug intoxication or withdrawal, overt brain disease or prominent affective symptoms.
  • ICD-10 requires that certain symptoms (see Figure 6.1) are present for at least a month.
  • DSM-5 requires at least two of the following, including one positive symptom (1–3 below) are present for at least six
    months:

1. delusions
2. hallucinations
3. disorganized speech
4. disorganized or catatonic behaviour
5. negative symptoms.

Subtypes of schizophrenia

ICD-10 includes these subtypes. DSM-5 does not list subtypes because of their limited validity in predicting treatment response.

• Paranoid schizophrenia, the most common, in which delusions and auditory hallucinations are evident.
• Catatonic schizophrenia is uncommon (about 7% of cases).
  Psychomotor disturbances are prominent, often alternating between motor immobility (e.g. stupor) and excessive activity.
  Rigidity, posturing (e.g. waxy flexibility – maintaining strange postures), echolalia (copying speech) and echopraxia (copying behaviours) may occur.
• Hebephrenic schizophrenia: early onset and poor prognosis.
  Behaviour is irresponsible and unpredictable; mood inappropriate and affect incongruous, perhaps with giggling, mannerisms, and pranks; thought incoherence and fleeting delusions and hallucinations occur.
• Residual schizophrenia: there is a history of one of the types of schizophrenia described above, but in the current illness ‘negative’ and often cognitive symptoms predominate.
• Simple schizophrenia: uncommon; negative symptoms without preceding overt psychotic symptoms.

At risk of psychosis

• Acute psychotic illness may be preceded by a prodromal period during which patients exhibit symptoms such as anxiety, depression and ideas of reference (feelings of being watched).
• If a person is distressed, has a decline in social functioning and has transient psychotic symptoms, behaviour suggestive of possible psychosis or a first-degree relative with psychosis, they may be at risk of psychosis
• People at risk may be offered CBT and treatment of comorbid conditions, but not antipsychotic medication.

Aetiology

• Genetics: schizophrenia and affective psychoses are more prevalent in relatives of people with schizophrenia. The risk of developing schizophrenia is around 50% in someone who has a monozygotic twin with the disorder, 15% if a dizygotic twin is affected. Offspring of people with schizophrenia brought up in adopted families still have an increased (about 12%) chance of developing it. A number of genes affecting brain development probably contribute to this increased susceptibility. Advanced paternal age has been identified as a risk factor, probably owing to increased risk of chromosomal aberrations.
• Neurodevelopmental hypothesis: factors that interfere with early brain development lead to an increased risk of
  schizophrenia in adulthood. Evidence for this includes increased rates of schizophrenia associated with:
  • winter births (foetus more likely to be exposed to influenza);
  • obstetric complications, low birth weight and perinatal injuries;
  • developmental delay and poor academic performance ;
  • ‘soft’ neurological signs (e.g. abnormal movements, mixedhandedness);
  • temporal lobe epilepsy;
  • smoking cannabis in adolescence;
  • severe childhood bullying or physical abuse.

The neurodevelopmental hypothesis is also supported by findings of increased ventricular size and small amounts of grey matter loss from CT/MRI studies of people with schizophrenia.

• Social factors: Schizophrenia is also associated with socioeconomic deprivation, urbanity and an excess of life events in the 3 weeks before the onset of acute symptoms. In the UK, the incidence of all psychoses is higher in African Caribbeans and Black Africans than the White British population.
  People with schizophrenia living in families with high expressed emotion (relatives over-involved or making hostile or excessive critical comments) are more likely to relapse.
• Neurochemical changes: The way in which genetic, neurodevelopmental and social factors result in schizophrenia in vulnerable individuals is not clearly understood, but the final common pathway appears to involve dopamine excess or overactivity in mesolimbic dopaminergic pathways (stimulant drugs such as amphetamines release dopamine and lead to psychosis; antipsychotics, which block dopamine receptors, treat psychosis successfully).
  Raised serotonin and decreased glutamate activity have also been implicated.

Other psychoses

• Schizoaffective disorder – affective and schizophrenic symptoms occur together and with equal prominence
• Delusional disorder – a fixed delusion or delusional system (associated delusions) with other areas of thinking and functioning well preserved.
• Brief psychotic episodes – last less time than required for schizophrenia diagnosis (1 month in ICD, 6 months in DSM).

Schizophrenia: Management and Prognosis

This chapter mainly concerns the treatment of schizophrenia, the most common non-affective psychosis. The principles are relevant to all psychoses.

• People with schizophrenia and other psychotic disorders face considerable stigma, and public understanding of the disorder is limited. Care should be given with sensitivity, hope and optimism. Engagement is critical for the patient’s subsequent adherence and prognosis.
• Early detection and intervention is important.
• The longer the period between symptom onset and effective treatment (Duration of Untreated Psychosis), the worse the average outcome.
• The first few years after onset can be particularly distressing with a high risk of suicide.
• Therefore, in many developed countries, specialist Early Intervention in Psychosis teams support people in the first few years of their illness.
• People with psychosis are treated in the community rather than in hospital wherever possible, although admission may be necessary if the risks of serious neglect, suicide/deliberate self-harm or harm to others are high. If the patient refuses treatment, formal admission under the Mental Health Act may be required.
• After the first acute episode, the treatment focus shifts to promoting long-term recovery. People with schizophrenia face problems of social exclusion and barriers to returning to work or study.
• Including carers and family in care plans is important, unless this is against the patient’s wishes.

Medication

• Antipsychotics are effective in treating ‘positive symptoms’ in the acute episode (e.g. hallucinations, delusions, passivity phenomena) and in preventing relapses.
• Typical (conventional) and atypical (second-generation) antipsychotics are equally effective in the treatment of positive symptoms but have different side-effect profiles. ‘Atypical’ antipsychotics cause fewer motor side effects, but some are associated with weight gain and diabetes. The choice of antipsychotic should be made together with the patient, after explaining the relative side-effect profiles.
• After baseline investigations, treatment should be with the lowest dose that effectively controls symptoms to minimise side effects because these are associated with poor treatment adherence. The use of two antipsychotics concurrently should be avoided.
• Newly diagnosed patients should be offered oral medication.
  Liquid and oro-dispersible tablet formulations can be useful.
  Depot preparations may be used if this is the patient’s preference or avoiding covert non-adherence is a clinical priority. Patients who are agitated, overactive or violent may require sedation (with antipsychotics or benzodiazepines). This may need to be by intra-muscular injection.
• The medication should be taken at optimal dose for 4–6 weeks before deciding if it is effective. Patients should be regularly reviewed, noting the effectiveness of treatment, side effects, adherence and physical health. As weight gain, cardiac arrhythmias and diabetes may also be problematic during treatment with atypical antipsychotic drugs, patients require regular monitoring of weight, lipid and glucose profiles, and ECGs.
• Only clozapine has been shown to be effective in the treatment of psychosis that does not respond to treatment with other antipsychotic drugs. It is reserved for patients who do not respond to two other drugs. Blood monitoring is required because of potentially dangerous side effects.
• There is a high risk of relapse if antipsychotic medication is stopped within one to two years of an acute psychotic episode.
  Many clinicians advise continuing treatment for five years after an acute episode.
• People with schizophrenia can develop depression requiring treatment.

Psychological treatment

• NICE guidelines (2014) state that all people with schizophrenia should be offered individual cognitive behavioural therapy (CBT), and their families should be offered family interventions.
• CBT can help patients cope with persistent delusions and hallucinations.
  The aim is to alleviate distress and disability, and not necessarily to eliminate symptoms. Therapy might include encouraging a patient to:
  • learn to challenge or think differently about a voice (auditory hallucination) and to be less frightened of it;
  • develop strategies to cope with hearing voices – such as using distraction (e.g. listening to music) or telling the voices to go away;
  • challenge delusional beliefs and think of other possible explanations.
• Psychological support is important for all people with schizophrenia and their families. Family therapy helps families reduce their excessive expressed emotion, and there is good evidence that it is effective in preventing relapses.
• Art therapies can be particularly helpful for negative symptoms.
• Self-help groups and forums (e.g. Hearing Voices groups) enable people with psychosis to share experiences and ways to cope with symptoms.

Social support

• Helping people to return to work or study is crucial in maintaining their self-esteem and quality of life. Supported employment programmes should be offered. Where a return to work or study is not possible, day centres can provide daytime structure.
• Appropriate accommodation is important. People with residual symptoms (e.g. negative or cognitive symptoms) may not be able to live independently. Inpatient and community rehabilitation services aim to maximise independence (e.g. by teaching daily living skills). A range of supported living arrangements, from 24-hour staffed hostels to independent housing with support workers who visit once a week, are available depending on need.

Prognosis

• Seventy per cent of people experiencing a first psychotic episode will be well within a year, but 80% have a further episode within five years.
• Three-quarters of patients will discontinue their initial medication within the first 18 months, and those who do may be five times more likely to relapse over this period. In addition to taking medication, avoiding illicit drug use (in particular, cannabis) and excessive stress will reduce the risk of relapse.
• Only about 40% of people with schizophrenia will be in paid employment a year after their first episode; for those with multiple episodes, employment rates are even lower.
• Better prognosis is encountered in the developing world; this may be because of differences in social structure, greater family support or less stigma.
• Here are some factors associated with a good prognosis:

• The lifetime suicide risk is 10%. Suicide risk is higher:
  • in young men,
  • in the first few years of illness,
  • when there are persistent hallucinations or delusions,
  • when there is a history of illicit drug use,
  • when there have been previous suicide attempts.

Depression

Definitions and classification

• The most common symptom of depressive illness is a pervasive lowering of mood, although this is not essential for a diagnosis to be made. ICD-10 identifies three core symptoms, at least two of which should be present every day for at least two weeks:
  • low mood
  • anhedonia (loss of enjoyment in formerly pleasurable activities)
  • decreased energy (or increased fatiguability).
• Other symptoms include:
  • reduced concentration and attention
  • reduced self-esteem and self-confidence
  • ideas of guilt and worthlessness
  • feelings of hopelessness regarding the future
  • thoughts of self-harm
  • decreased sleep and/or appetite.
• The severity of the episode (mild, moderate, severe) depends on:
  • the number of symptoms present
  • the severity of symptoms
  • the degree of associated distress
  • interference with daily activities.
• Depression associated with psychotic features is always classified as severe.
• DSM-5 diagnostic criteria for major depressive disorder (its term for clinical depression) are similar, but one core symptom, either low mood or loss of enjoyment, is required.
• Mood disorders with recurrent episodes are described as unipolar if they include only depressive episodes, or bipolar if there is a history of at least one manic or hypomanic episode. Many unipolar depressed patients with a bipolar family history, very early onset and marked agitation subsequently meet criteria for bipolar disorder.

Clinical features

• Thought content often includes negative, pessimistic thoughts about:

• Biological symptoms (e.g. reduced sleep, appetite and libido) may be particularly prominent in older people, who less often complain of disturbed mood. There is often a sleep pattern of early waking (more than two hours before usual) and maximal lowering of mood in the morning (diurnal variation). Poor appetite is often associated with weight loss; in severe cases, food and fluids may be refused.
• Motor activity is often altered, with psychomotor agitation, retardation (of speech and/or movement), or both.
• Cognition may be impaired, with reduced attention, concentration and decisiveness.
• Depressive symptoms can be masked by severe anxiety, alcohol, hypochondriacal preoccupations or irritability.
• Anhedonia is usually accompanied by loss of motivation and emotional reactivity.
• Psychotic features may occur and are usually mood-congruent.
  Delusions are usually nihilistic (e.g. a belief that one is dead, has lost all one’s assets or one’s body is rotting), delusional or hypochondriacal, concerning illness or death. Where hallucinations occur they are usually auditory, in the second person and accusing, condemning or urging the individual to commit suicide.
• Atypical depression is characterised by initial anxiety-related insomnia, subsequent oversleeping, increased appetite and a relatively bright, reactive mood. It is more common in adolescence.
• Depression is often also comorbid with anxiety disorders, eating disorders, personality disorders and substance misuse.

Differential diagnosis

• Normal sadness, particularly in the context of bereavement or severe physical illness. The diagnosis depends on finding a pattern of characteristic features and on the degree and duration of associated disability. Predominant negative, guilty or suicidal thoughts support a diagnosis of depression, but such symptoms may be difficult to elicit if depression is severe.
• Psychotic depression should be differentiated from schizophrenia on the basis of thought content (mood-congruent psychotic features) and the temporal sequence in which the symptoms developed.
• Depressive retardation may be difficult to distinguish from the flat (unreactive) affect of chronic schizophrenia.
• Alcohol or drug withdrawal may mimic depression.

Epidemiology

• The lifetime risk of depression is about 10–20%, with rates almost doubled in women.
• First onset is typically in the third decade (earlier for bipolar disorder).
• Depression is strongly associated with socioeconomic deprivation.

Aetiology

• A genetic contribution is evident in both twin and adoption studies but less markedly for unipolar than bipolar depression. Current theories implicate gene-environment interactions – i.e. a genetic predisposition to depression if exposed to adverse life events.
• Monoamine neurotransmitter availability (particularly noradrenaline and serotonin) in the synaptic cleft is reduced in depressed patients, and antidepressants increase monoamine availability. It is now thought that this results in secondary neuroplastic changes that bring about the antidepressant effect. One suggested mechanism is that the greater monoamine availability leads to increased production of Brain Derived Neurotrophic Factor (BDNF) that promotes neurogenesis.

• Hypercortisolaemia has been reported in severe depression, while in atypical depression hypocortisolaemia has been reported.
• The limbic system and related areas such as the prefrontal cortex regulate emotion, reward and executive function, and dysfunctional changes have been implicated in depression.
  Deep brain stimulation of the subgenual cingulate cortex or the nucleus accumbens has an antidepressant effect.
• Psychosocial factors implicated are recent adverse life events (e.g. bereavement or deteriorating physical health) and adverse current social circumstances, especially unemployment and lack of a confiding relationship. Parental loss and major childhood stress or abuse appear to increase vulnerability to depression in adulthood. Stress leads to increased cortisol levels, which may cause depressed mood through decreasing expression of BDNF.
• Cytokines are also important modulators of mood. Interleukin 1 (IL-1) produces ‘sickness behaviour’ in rodents. A third of those treated with recombinant interferons develop depression.
• Several physical illnesses (most endocrine disorders, many cancers, some viral infections) and some medications (including steroids, isotretinoin (for acne)) are specifically associated with depression.
• Women are particularly vulnerable to episodes of depression in the weeks following childbirth.

Management

• Most depressive illnesses can be managed in primary care, although many are undetected. Psychiatric referral is indicated if suicide risk is high or if the depression is severe, unresponsive to initial treatment, bipolar or recurrent.
• Depressed patients often present with other conditions.
• Always assess risk of self-neglect and suicide.
• Treat comorbid physical illnesses or substance misuse problems.
• For mild depression, self-help groups, structured physical activity groups, guided self-help or computerised cognitive behavioural therapy (CBT) are often helpful.
• If these less intensive therapies do not help, individual CBT or interpersonal therapy (IPT) may be recommended. Behavioural activation or, where appropriate, behavioural couples therapy can also be of use.
• Psychological therapy should be given together with antidepressants for moderate or severe depression. These
  can have a 60–70% response rate but often fail because of inadequate dosage, duration or adherence.
• Continuing antidepressants for at least six months reduces relapse; in recurrent depression, prophylactic effects have been demonstrated for up to five years. When discontinuing antidepressants, taper slowly to avoid withdrawal symptoms. In bipolar depression, mood stabilisers (e.g. lithium) are preferable. CBT or mindfulness-based cognitive therapy can also help prevent relapse.
• Resistant depression may respond to combining an antidepressant (augmenting) with lithium, an atypical antipsychotic (aripiprazole, olanzapine, risperidone, quetiapine) or another antidepressant (e.g. mirtazipine).
• Electroconvulsive therapy (ECT) is very effective in severe cases, particularly where psychosis or stupor is present, and can be lifesaving if fluids and food are being refused.

Prognosis

• Single episodes of depression usually last three to eight months. About 20% of patients remain depressed for two years or more and 50% have recurrences; this rises to 80% in severe cases. Recurrent episodes tend to become increasingly severe with shortening of disease-free periods, emphasising the importance of prophylactic treatment.
• Lifetime suicide risk is 15% in severe depression but much lower in milder illness. There is an association between major depressive disorder/bipolar disorder and increased cardiovascular morbidity and mortality. Predictors of poor outcome include early onset, greater symptom severity and psychiatric or physical comorbidity.

Bipolar Affective Disorder

Definitions and classification

Bipolar affective disorder (previously called manic depression) is characterised by recurrent episodes of altered mood and activity, involving both upswings and downswings. Classificatory systems (ICD-10, DSM-5) define individual episodes and patterns of recurrence.
Individual episodes are classified as:

• depressive
• manic
• hypomanic (less severe and without psychotic symptoms)
• mixed (less usual) where features of both mania and major depression are present or alternate rapidly.
• In ICD-10, bipolar affective disorder is defined as at least two episodes, including at least one hypomanic or manic episode.
• In DSM-5, patterns of recurrence can be classified as:
  • bipolar I disorder – one or more manic or mixed episodes and usually one or more major depressive episodes;
  • bipolar II disorder – recurrent major depressive and hypomanic but not manic episodes;
  • cyclothymic disorder – chronic mood fluctuations over at least two years, with episodes of depression and hypomania (but not mania) of insufficient severity to meet diagnostic criteria.

Clinical features

The cardinal clinical feature of a manic or hypomanic episode is alteration in mood, which is usually elated and expansive but may also be characterised by intense irritability. DSM-5 emphasises changes in activity and energy as well as mood. Associated features include:

• increased psychomotor activity (distractibility, decreased need for sleep);
• exaggerated optimism;
• inflated self-esteem;
• decreased social inhibition, with apparent disregard for potentially harmful consequences of:
  • sexual overactivity
  • reckless spending
  • dangerous driving
  • inappropriate business, religious or political initiatives;
• heightened sensory awareness;
• rapid thinking and speech:
  • uninterruptible (pressured) speech
  • flight of ideas.
• (in mania only) mood-congruent delusions and hallucinations, usually auditory.
  Insight is often absent. Manic and hypomanic episodes are distinguished on the basis that hypomania is less severe, causing less disruption to work and social or interpersonal life, and psychotic symptoms are absent. Manic episodes have a median duration of four months. Depressive episodes tend to last longer (median six months). Recovery may or may not be complete between episodes.

Differential diagnosis

• Substance abuse (particularly amphetamines or cocaine).
• Mood abnormalities secondary to endocrine disturbance (idiopathic Cushing’s syndrome or steroid-induced psychoses) or epilepsy.
• Schizophrenia: persecutory or grandiose delusions, auditory hallucinations and increased psychomotor activity may occur in both conditions.
• Schizoaffective disorder should be diagnosed where affective and schizophreniform symptoms (e.g. First Rank Symptoms) are equally prominent.
• Personality disorders (emotionally unstable or histrionic) may mimic some features of the mood or behavioural disturbance of mania and hypomania.
• Attention-deficit hyperactivity disorder (ADHD) in younger people and transient psychoses induced by extreme stress, although in both elevation of mood is rare.
• Bipolar disorder can also be comorbid with conditions including substance use, personality disorders, obsessive–compulsive disorder and anxiety.

Epidemiology

• Lifetime prevalences are:
  bipolar I disorder 1%
  bipolar II disorder 0.4–2%
  cyclothymia 2.5%.
• The female : male ratio is approximately equal for bipolar I disorder; some but not all studies show a female excess in the bipolar II group.
• Peak age of onset is in the early twenties. The illness often starts in childhood and adolescence. There may be a second smaller peak of onset in later life (45 to 54 years)
• Several studies have shown greater prevalence rates in higher social classes, probably reflecting differences in access to diagnosis.
• Black African and African Caribbean people are more likely to present with mania and to present with more severe psychotic symptoms than are white European people –social exclusion and late diagnosis, and thus treatment, have been suggested as reasons for this.

Aetiology

• There is evidence for a strong genetic component, with evidence of heritability of mood disorder from other family members in 60% or more people. The lifetime risk of bipolar disorder is increased in first degree relatives of a person with bipolar disorder (40–70% for a monozygotic twin; 5–10% for other first degree relatives). Autism, ADHD, bipolar disorder, major depression and schizophrenia share some of the same genetic risk factors.
• A number of studies have reported abnormalities in the hypothalamic-pituitary-adrenal (HPA) axis in bipolar disorder which are consistent with reduced HPA axis feedback – e.g. chronically elevated cortisol levels in depression
• The hypothalamic-pituitary-thyroid (HPT) axis is also implicated; approximately 25% of those with rapid cycling bipolar disorder have evidence of hypothyroidism
• Magnetic resonance imaging (MRI) findings include smaller prefrontal lobes and enlarged amygdala and globus pallidus. There may be diminished prefrontal modulation of subcortical and medial temporal structures (eg, amygdala, anterior striatum and thalamus) that results in dysregulation of mood.
• Prolonged psychosocial stressors during childhood, such as neglect or abuse, are associated with HPA axis dysfunction in later life, which may result in hypersensitivity to stress. People with a history of childhood sexual or physical abuse appear to be more at risk and to have a worse prognosis.
• There is a markedly increased risk of manic episodes in the early postpartum weeks; this may relate to dopamine receptor supersensitivity associated with postpartum falls in oestrogen and progesterone levels.
• Sleep disturbance can induce mania. Disturbance of circadian rhythms (e.g. in jet lag and sleep loss) may precipitate an episode, as may a recent life event. There appears to be an increase in manic episodes in the spring and early summer.
• Psychodynamic models of mania suggest denial of loss or loss-associated conflict in order to avoid depression, or loss of superego (‘conscience’) control. These are not frequently invoked in mainstream psychiatry.

• ‘Secondary’ mania may be precipitated by severe physical illness, particularly stroke.

Management (NICE guideline 2014)

• A coordinated care programme, with rapid access to support at times of crisis, is essential. Hospitalisation is required for those at significant risk of harm.

Treating manic and hypomanic episodes

• Effective first line drugs for treatment of acute mania are haloperidol, olanzapine, quetiapine or risperidone.
• Lithium has a slower onset of action, but lithium or valproate can be considered if the first-line drugs above are ineffective.
  Benzodiazepines may be used in the short term for acute behavioural disturbance. Lorazepam and antipsychotics may be useful for rapid tranquillisation.

Treating depressive episodes

• Antidepressants may precipitate mania or ‘rapid cycling’ (with four or more episodes a year), so they should not be prescribed without an antimanic/mood-stabilising agent. If a patient is taking an antidepressant at the onset of an acute manic episode, the antidepressant should be stopped. For episodes of moderate or severe depression in bipolar disorder, 2014 NICE guidelines recommend quetiapine, olanzapine, lamotrigine or a combination of olanzapine and fluoxetine.

Treating bipolar affective disorder

• Structured psychological interventions (individual/family/group) should be offered.
• When planning long-term pharmacological treatment to prevent relapse, it is important to take into account drugs that have been effective during episodes of mania or bipolar depression.
• Discussions should include whether to continue this treatment or switch to lithium because lithium is the most effective long-term treatment for bipolar disorder. Lithium reduces the risk of suicide; it may also be useful in cyclothymia. Lithium therapy requires blood monitoring.
• Valproate, olanzapine and quetiapine are also effective treatments.
• Weight and cardiovascular and metabolic indicators of morbidity should be routinely monitored in people with bipolar disorder.
• The teratogenic toxicity associated with valproate severely limits its use in women of child-bearing potential. Lithium is also teratogenic.

Prognosis

• The lifetime prognosis following a single manic episode is poor, with 90% of patients having manic or depressive recurrences (averaging four episodes in 10 years). In bipolar I disorder, both the frequency and severity of episodes tend to increase for the first four or five episodes but then plateau.
• A minority who develop rapid cycling have a particularly poor prognosis and seldom respond to lithium. However, they respond better to antiepileptic mood stabilisers.
• Long-term functional prognosis (work, family, etc.) (particularly in untreated patients) is almost as poor as in schizophrenia.
• There is an overall increase in premature mortality, only partially explained by a suicide rate of 10%. Prognosis for
  bipolar II disorder is better, although there remains a high suicide risk.
• Cyclothymia runs a chronic course and approximately 30% of patients risk developing full-blown bipolar disorder.
• There is an association with violence that is almost completely explained by the greater risk of violence in those patients with comorbid substance misuse.

Stress Reactions (Including Bereavement)

Major psychological stress involves threat or loss. Reactions to a broad range of major stressors (physical or sexual assault, transport accidents, natural disasters, war) are often similar in nature and involve:

• emotional responses (fear from threat and sadness at loss);
• physical symptoms (autonomic arousal and/or fatigue);
• psychological responses, which may be conscious (e.g. avoidance behaviour) or unconscious (e.g. denial or dissociation).
  Abnormal stress reactions represent exaggerated or maladaptive responses. They may be acute and self-limiting (acute stress reactions) or prolonged (post-traumatic stress disorder [PTSD], adjustment disorder or abnormal grief).

Acute stress reactions

• ICD-10 criteria for acute stress reactions require rapid onset (within minutes or hours) of extreme responses to sudden and severe stressful events.
• There is a mixed and usually changing picture of symptoms that include:
  • an initial state of feeling dazed or perplexed;
  • depression, anger, despair;
  • purposeless overactivity and withdrawal;
  • intense subjective anxiety with autonomic arousal (sweating, dry mouth, tachycardia, vomiting);
  • dissociative symptoms, which predict increased risk of PTSD, include wandering aimlessly;
  • reduced sleep and nightmares.
• Initial management involves:
  • helping to reorient and ‘ground’ the individual;
  • practical support (e.g. temporary housing following a natural disaster);
  • brief cognitive behavioural therapy (CBT) to improve outcome and reduce the rate of chronic PTSD.
• There is no evidence that anxiolytics or hypnotics are effective, and they carry a risk of dependence.
• In most cases symptoms resolve rapidly (within a few hours at the most) where removal from the stressful environment is possible.
  If the stress continues or cannot by its nature be reversed, the symptoms usually begin to diminish after 24 to 48 hours and are minimal after about three days.
• Persistence of symptoms for more than one month indicates the development of PTSD.

Adjustment disorders

• Adjustment disorders include a range of abnormal psychological responses to life adversity (e.g. job loss, house move or divorce).
• The onset is usually within weeks of the stressful event and the duration less than six months, unless there are factors leading to persistence (e.g. ongoing litigation). Adjustment disorders usually improve following resolution of their precipitating cause.
• The presentation includes a broad mix of symptoms of anxiety (autonomic arousal, insomnia, irritability) and depression (sadness, tearfulness, worry). The diagnosis should be made only where there are insufficient symptoms to justify a diagnosis of a specific anxiety or depressive disorder.
• Initial management may involve encouragement to ventilate feelings and to develop appropriate problem-solving strategies.
  Sometimes formal CBT is required.
• Adjustment to chronic or terminal illness may manifest as anxiety, depression or exaggerated disability. There may be a sequence (similar to that in bereavement) of:

Management involves adequate symptomatic control (particularly of pain), honest explanation, supportive psychotherapy and family counselling.

PTSD

• The onset of PTSD follows a severe stressful experience that is of an exceptionally threatening or catastrophic nature; this can include assault, accident, disaster, act of terrorism or battle. It may occur in adults or children. ICD-10 states that onset is usually within six months of stressor (although it may rarely exceed this); DSM-5 that symptoms persist for at least one month.
• The characteristic features of PTSD involve:
  • persistent intrusive thinking or re-experiencing of the trauma, such as traumatic memories, recurrent dreams or nightmares and re-enactments (‘flashbacks’) of the traumatic event;
  • avoidance of reminders of the event (e.g. the scene of an accident), and thoughts, feelings and conversations associated with the trauma;
  • numbing, detachment and estrangement from others, loss of interest in significant activities and sense of a foreshortened future;
  • increased arousal with autonomic symptoms, hypervigilance, sleep disturbance, irritability, poor concentration and exaggerated startle response.
• Alcohol or substance misuse may be a symptom and/or long-term complication.
• Depression may be comorbid or secondary to PTSD.
• Risk for PTSD is proportional to the magnitude of the stressor but may be greater following man-made rather than natural disasters and if some stress continues. Lack of social support, the presence of other adversities at the time of the trauma and premorbid personality are vulnerability factors.
• Effective treatments include:
  • trauma-focused CBT;
  • eye movement desensitisation and reprocessing therapy (EMDR);
  • antidepressant drugs (e.g. paroxetine or miratzapine) – these have been shown to be effective but should not be used first line unless patients do not wish to engage in psychological treatment.
• Debriefing is no longer indicated because it does not, as previously thought, prevent PTSD (in debriefing, patients were encouraged to recall the stressful events in detail soon after the trauma and were then supported through the associated emotions.)
• Many PTSD victims recover over the first few months. If the syndrome persists over one to two years, it may become chronic, possibly for the rest of a victim’s life, as with many Holocaust survivors.

Bereavement and grief

• Bereavement is associated with increased mortality (from cardiovascular disease and cancer) and may precipitate depression and even suicide.
• ‘Normal’ grief may last up to two years. The classic stages of grieving are:

• The sequence of stages is often less clear-cut than this linear model suggests. Bereavement may be characterised by jumbled feelings as people pass in and out of these stages.
• Normal grieving requires no specific management apart from support and encouragement to ventilate feelings and accept them as normal. Symptoms often recur briefly on anniversaries.
• ‘Abnormal’ grief is characterised by delayed onset, greater intensity of symptoms or prolongation of the reaction. Suicidal ideas may be harboured during abnormal pining (a wish to be with the deceased) or despair.
• In ICD-10, abnormal grief reaction is coded as an adjustment disorder. DSM-5 lists persistent complex bereavement disorder as a disorder for further study, and a separate diagnostic category is also being considered for ICD-11. It is more likely where:
  • the relationship with the deceased was problematic (ambivalent or overinvolved);
  • the death was sudden;
  • normal grieving was impeded by social constraints (e.g. ‘putting on a brave face for the children’).
• Abnormal grief reactions last longer than normal grief – at least six months after the bereavement. Symptoms are intense and disabling, including:
  • confusion about one’s role in life or diminished sense of self, feeling life is empty since the loss or that it is difficult to move on;
  • feeling numb, stunned or shocked since the loss, or feeling angry or struggling to accepting it.
• Abnormal grief may respond to CBT, encouraging structured review of the relationship and giving vent to the emotions produced.
  Complex bereavement or adjustment disorder should not be diagnosed if criteria for depressive disorder are met.

Anxiety Disorders

Anxiety

• Anxiety is an unpleasant emotional state involving subjective fear, bodily discomfort and physical symptoms. There is often a feeling of impending threat or death, which may or may not be in response to a recognisable threat.
• The Yerkes–Dodson curve shows that anxiety can be beneficial up to a plateau of optimal function, beyond which, with increasing anxiety, performance deteriorates.

Anxiety disorders

• Pathological anxiety can involve:
  • generalised anxiety, as in generalised anxiety disorder (GAD);
  • discrete anxiety attacks caused by an external stimulus (in phobias) or without external stimulus (in panic disorder).
• Anxiety disorders may present alone but are also frequently comorbid with other disorders including depression, substance misuse or another anxiety disorder.
• Anxiety occurs in other disorders such as depression.

Epidemiology

• Around 6% of the general population have an anxiety disorder at one time. The anxiety disorders comprise:
  • generalised anxiety disorder (GAD) (2–4%)
  • panic disorder (1%)
  • phobias (agoraphobia, social phobia, specific phobias)
  • obsessive–compulsive disorder.
• Anxiety disorders are more common in women, younger adults and the middle-aged.
• Lower rates are reported in young men and older people. In older people this may be because of the difficulty in detecting anxiety in old age using standard measures.

Aetiology

Biological

• Low levels of GABA, a neurotransmitter that reduces activity in the central nervous system, contribute to anxiety.
• Mouse studies have found that the frontal cortex and amygdala undergo structural remodelling induced by the stress of maternal separation and isolation, which alters behavioural and physiological responses in adulthood.
• Heightened amygdala activation occurs in response to disorder-relevant stimuli in post-traumatic stress disorder, social phobia and specific phobia.
• The medial prefrontal cortex, insula and hippocampus have also been implicated.
• Alcohol and benzodiazepine abuse can worsen or cause anxiety and panic attacks.

Genetics

• First degree relatives of people with an anxiety disorder have a quadrupled risk of developing an anxiety disorder.
• Some of this risk is disorder-specific and some is not.
  • The genetic factors of panic attacks appear to overlap with depression by about 50%.
  • GAD and depression are genetically related.
• For social phobia and agoraphobia, genetic risk appears to be mainly due to inheritance of personality traits (low extraversion and high neuroticism).
• Inheritance of specific phobias appears to be independent of personality.

Childhood

• There is an association with childhood abuse, separations, demands for high achievement and excessive conformity.

Stress

• Anxiety disorder can arise in response to life stresses such as financial problems or chronic disease.
• Anxiety disorders are precipitated and perpetuated by physical health problems:
  • a degree of anxiety when facing physical illness, especially when the diagnosis is unclear, is normal;
  • concerns about incontinence or being ill when out may perpetuate agoraphobia;
  • Panic disorder is 10 times more common in people with chronic obstructive airways disease, probably because breathlessness precipitates the symptoms of panic (see Figure 11.2).

Panic disorder

• Recurrent episodic severe panic (anxiety) attacks, which occur unpredictably and are not restricted to any particular situation.
• Panic attacks are discrete periods of intense fear, impending doom or discomfort accompanied by characteristic symptoms:
  • palpitations, tachycardia
  • sweating, trembling, breathlessness
  • feeling of choking
  • chest pain/discomfort
  • nausea/abdominal discomfort
  • dizziness, paraesthesia
  • chills and hot flushes
  • derealisation/depersonalisation
  • fear of losing control, ‘going crazy’ or dying.
• Typically, they only last a few minutes.
• ‘Anticipatory fear’ of having a panic attack may develop, with consequent reluctance to be alone away from home. DSM-5 states that for panic disorder to be diagnosed, panic attacks must be followed by at least a month of persistent worry about having another attack or maladaptive behavioural changes related to the attack.
• According to the cognitive model, panic attacks occur when catastrophic misinterpretations of ambiguous physical sensations (such as shortness of breath or increased heart rate) increase arousal, creating a positive feedback loop that results in panic.

• Selective serotonin reuptake inhibitors (SSRIs) and cognitive behavioural therapy (CBT) or self-help
  materials based on CBT principles are recommended first-line treatments.
• Tricyclic antidepressants (imipramine and clomipramine) may be helpful where SSRIs are ineffective.
• Benzodiazepines are not recommended.

Generalised anxiety disorder (GAD)

• GAD is characterised by generalised, persistent, excessive anxiety or worry (apprehensive expectation) about a number of events (e.g. work, school performance) that the individual finds difficult to control, lasting for at least three weeks (according to ICD-10) or six months or longer (according to DSM-5). The anxiety is usually associated with:
  • subjective apprehension (fears, worries),
  • increased vigilance,
  • feeling restless and on edge,
  • sleeping difficulties (initial/middle insomnia, fatigue on waking),
  • motor tension (tremor, hyperactive deep reflexes),
  • autonomic hyperactivity (e.g. tachycardia).
• GAD may be comorbid with other anxiety disorders, depression, alcohol and drug abuse.
• Differential diagnoses include:
  • withdrawal from drugs or alcohol,
  • excessive caffeine consumption,
  • depression,
  • psychotic disorders,
  • organic causes such as thyrotoxicosis, parathyroid disease, hypoglycaemia, phaeochromocytoma and carcinoid syndrome.
• Treatment with individual guided self-help (CBT principles) and psychoeducational groups often helps.
• If not or if symptoms are more severe, the next step is face-to-face CBT or applied relaxation.
• SSRIs or serotonin noradrenaline reuptake inhibitors (SNRIs) are the recommended pharmacological treatments where these are required. Pregabalin is sometimes used as a second-line treatment.
• CBT (self-help material or face-to-face) for GAD seeks to:
  • identify morbid anticipatory thoughts and replace them with more realistic cognitions
  • learn and use distraction, breathing and relaxation exercises.

Benzodiazepines should only be used in crises and usually not beyond two to four weeks.

Phobic disorders

Agoraphobia

• Agoraphobia is often comorbid with panic disorder and is characterised by fear and avoidance of places or situations from which escape may be difficult or in which help may not be available in the event of having a panic attack.
• Diagnosis requires that anxiety is restricted to being in the following situations that are therefore avoided:
  • crowds
  • public places
  • travelling away from home
  • travelling alone.
• Some people with marked agoraphobia experience paradoxically little anxiety because they avoid all phobic situations. They may, for example, leave the house only occasionally to visit a very restricted number of places.
• CBT is considered the mainstay of treatment and usually involves graded exposure to avoided situations,
  but SSRIs are also effective. Treatment response depends on the patient’s engagement with treatment and motivation for change.

Social phobia

• Social phobia is prevalent and treatable.
• It is equally common in men and women. Onset is usually by mid-adolescence, but affected individuals often do not seek help for many years.
• It is characterised by a persistent fear of social situations in which the individual is exposed to unfamiliar people or to possible scrutiny by others and fears that he or she will be humiliated or embarrassed (e.g. by blushing, shaking, vomiting).
• Management includes CBT, self-help materials, graded self-exposure and social skills training. Drug treatments should not be first line but, if psychosocial treatment fails or the patient does not want it, may help. SSRIs are most commonly used.

Specific phobias

• Specific phobias are characterised by fear of specific people, objects or situations (e.g. flying, heights, animals, blood).
• Treatment is typically by graded exposure therapy and response prevention. Short-term use of benzodiazepines may be helpful if the phobia is only rarely encountered (e.g. flying twice a year).

Obsessions and Compulsions

Obsessions and compulsions

Obsessions are unwelcome, persistent, recurrent, intrusive, senseless and uncomfortable for the individual, who attempts to suppress or neutralise them and recognises them as absurd (egodystonic) and a product of his or her own mind. Obsessions may be:

• thoughts (e.g. blasphemy, sex, violence, contamination, numbers);
• images (vivid, morbid or violent scenes);
• impulses (e.g. a fear of jumping in front of a train);
• ruminations (continuous pondering);
• doubts.
  Obsessions should be distinguished from volitional fantasies (thoughts that are not displeasurable (egosyntonic)).
  Compulsions are repetitive, purposeful physical or mental behaviours performed with reluctance in response to an obsession.
  They are carried out according to certain rules in a stereotyped fashion and are designed to neutralise or prevent discomfort or a dreaded event. The activity is excessive and not connected to the triggering thought (obsession) in a realistic way. The individual realises the behaviour is unreasonable. Compulsions include:
• hand-washing, cleaning;
• counting, checking;
• touching and rearrangement of objects to achieve symmetry;
• mental compulsions (e.g. checking and repeating thoughts);
• hoarding;
• arithmomania (counting);
• onomatomania (the desire to utter a forbidden word);
• folie du pourquoi
• (the irresistible habit of seeking explanations for commonplace facts by asking endless questions);
• inappropriate and excessive tidiness.
  Compulsions should be distinguished from rituals and ‘normal’ superstitious behaviour (actions that have a magical quality and are culturally sanctioned, such as touching wood for good luck).
  If resistance to the obsessions or compulsions is attempted, anxiety usually increases until the compulsive activity is performed.
  Mild obsessions and compulsions are common in the general population and in many other disorders (see Figure 12.1).
  Recent evidence suggests that there is comorbidity between the spectrum of obsessive–compulsive disorders and a range of other psychiatric disorders including bipolar affective disorder, Tourette’s syndrome, pathological gambling and hypochondriasis.

Obsessive–compulsive disorder (OCD)

Clinical characteristics

• OCD is characterised by time-consuming (>1 hour/day) obsessions and/or compulsions. An ICD-10 diagnosis of OCD requires that obsessions or compulsions are present most days for at least two weeks, are distressing and interfere with activities.
• Avoidance of stimuli or activities that trigger obsessive–compulsive symptoms is very common. Resistance is characteristic but may not persist.
• Onset is usually during adolescence.
• OCD can be divided into four subtypes, characterised by:
  • obsessions and compulsions (usually hand-washing) concerned with contamination (most common subtype);
  • checking compulsions in response to obsessional thoughts about potential harm (e.g. leaving the gas on);
  • obsessions without overt compulsive acts;
  • hoarding (the acquisition of, and difficulty in discarding, items that appear worthless to others).
• Complications include depression and abuse of anxiolytics or alcohol. Severe OCD can lead to as much distress and functional impairment as psychotic illness.

Epidemiology

The lifetime prevalence of OCD in the general population is 2–3%. Men and women are affected equally.

Aetiology

• People with OCD are more likely to have a family history of OCD (50% of cases), tics or Tourette’s syndrome.
• Some studies report an association with parental overprotection.
• Biochemical abnormalities (especially involving serotonin) are now thought to be important in the pathophysiology of OCD.
• OCD may be caused by an abnormality of the cortico-striatothalamic circuit, which mediates social behaviour. A fundamental problem appears to be an inability to inhibit or suppress inappropriate mental or physical acts. Neuroimaging has shown functional abnormalities in the frontal cortex and basal ganglia.
• Psychoanalytic theories view OCD as a defence against cruel and aggressive fantasies (filling the mind with obsessional thoughts prevents undesirable ideas entering consciousness) and defensive regression to the anal stage of development.
• Behavioural theories propose that compulsive behaviour is learned and maintained by operant conditioning processes, the anxiety reduction following the compulsive behaviour strengthening, and ultimately increasing, the need to perform the compulsion in response to an obsessional thought.
• OCD and related tic disorders may occur suddenly in children.
  These were known as paediatric autoimmune neuropsychiatric disorders associated with streptococci (PANDAS), but doubt has been cast more recently on the relationship between streptococcus and the behaviours. More recently the terms ‘childhood/paediatric acute neuropsychiatric syndrome’ (CANS/PANS) have evolved to describe these acute onset disorders without defining aetiology.

Body dysmorphic disorder (BDD)

• This disorder (also called dysmorphophobia) is characterised by a preoccupation with an imagined defect in appearance or markedly excessive concern with a slight physical anomaly.
• Time-consuming behaviours include mirror-gazing, comparing particular features with those of others, excessive camouflaging tactics to hide the defect, skin-picking and reassurance-seeking; the sufferer may even request surgery.
• Around 0.5% of the general population have BDD.
• It is related to OCD and hypochondriacal disorder.

Management of OCD and BDD

• Psychoeducation helps people understand their disorder.
• First-line treatment is with cognitive behavioural therapy (CBT), together with medication.
• CBT involves exposure followed by response prevention; the patient is encouraged not to perform the unwanted compulsive behaviour (e.g. hand-washing) while simultaneously being exposed to a situation associated with it (e.g. wiping a toilet seat).
  CBT can be self-help, group or individual therapy.

• Drug treatment is with selective serotonin reuptake inhibitors (SSRIs) or clomipramine. These drugs are effective even in the absence of coexistent depressive symptomatology. They may take up to 12 weeks to have an effect.
• Neuroimaging studies show that similar changes in the caudate nucleus occur in response to both CBT and to SSRIs. Overall response to CBT and/or drugs is about 75%; in contrast, placebo responses in clinical trials are low (5%).
• Psychosurgery (cingulotomy, capsulotomy) is very rarely used but may be effective in the most severe and treatment-resistant cases. Deep brain stimulation has been used successfully recently, but in a small, select number of patients.

Course and prognosis

• OCD may follow an episodic or chronic course. Patients with prominent compulsions, comorbid tic disorders, persistent life stresses or premorbid anankastic personality fare worst.
• Traditionally, OCD was thought to carry a low risk of suicide; recent research, however, contradicts this.

Anankastic personality disorder

• Also called ‘obsessive–compulsive personality disorder’.
• Characteristic features include:
  • rigidity of thinking,
  • perfectionism that may interfere with completing tasks,
  • moralistic preoccupation with rules,
  • excessive cleanliness and orderliness,
  • objectively high standards that are seldom achieved,
  • a tendency to hoard,
  • emotional coldness.
• These are egosyntonic life traits with no obvious onset.

Eating Disorders

People with anorexia nervosa restrict what they eat and may compulsively overexercise to maintain an excessively low body weight.
People with bulimia nervosa have intense cravings, secretively overeat, and then try to prevent weight gain (e.g. by vomiting).
There is an important overlap. Some people with mixed symptoms are diagnosed with eating disorder not otherwise specified.

Epidemiology

• Anorexia and bulimia nervosa are three times more common in women. In childhood anorexia the sex ratio is nearly equal.
• Eating disorders usually begin in adolescence or early adulthood.
  Bulimia has a later onset (typically 18–19 years).
• Prevalence rates in young women are:
  • 1–2% for anorexia nervosa
  • 1–3% for bulimia nervosa.

Aetiological factors

Genetics

• Twin studies indicate a genetic component. First degree relatives have increased rates of eating disorders, anxiety disorders including OCD, depression, obsessional personality and (in bulimia) alcohol and substance abuse.

Personality

• Anxious, obsessive–compulsive and depressive traits and low self-esteem are common.
• People with anorexia often have constricted affect and reduced emotional expressiveness. Those with bulimia tend to be impulsive.

Biological

• Altered brain serotonin (5-HT) function contributes to dysregulation of appetite, mood and impulse control.

Childhood environment

• Sexual, physical or emotional abuse.
• An overprotective or overcontrolling environment, or one where food, eating, weight or body shape are overvalued.
• Troubled interpersonal or family relationships.
• Being ridiculed because of size or weight.

Culture

Cultures that place a high value on being thin and consequent media messages/adverts encouraging dieting may contribute.

Anorexia nervosa

• There are ‘restrictive’ (minimal food intake and exercise) and ‘bulimic’ (episodic binge-eating with laxative use and induced vomiting) subtypes.
• Diagnosis (ICD-10/DSM-5) requires:
  • a morbid fear of fatness;
  • deliberate weight loss;
  • distorted body image;
  • Body Mass Index (BMI, weight [kg]/ht [m]2) <17.5;
  • amenorrhoea (primary prepubertally, or secondary; oral contraceptive pill may still cause vaginal bleeds);
  • loss of sexual interest and potency in men; in prepubertal boys development will be arrested.
• Associated clinical features include:
  • preoccupation with food (dieting, preparation of elaborate meals for others);
  • self-consciousness about eating in public, socially isolating behaviour;
  • vigorous exercise;
  • constipation;
  • cold intolerance;
  • depressive and obsessive–compulsive symptoms.
• Physical signs/complications include:
  • emaciation: often disguised by make-up/clothes;
  • dry and yellow skin;
  • fine lanugo hair on the face and trunk;
  • bradycardia and hypotension;
  • anaemia and leucopenia;
  • consequences of repeated vomiting, including hypokalaemia, alkalosis, pitted teeth, parotid swelling and scarring of the dorsum of the hand (Russell’s sign).
• Differential diagnosis
  • Organic causes of low weight (e.g. diabetes mellitus), which are not usually associated with abnormal attitudes to weight or eating. Diabetes may, however, coexist with anorexia.
  • Psychiatric causes of low weight include depression (which may also coexist with anorexia), psychotic disorders with delusions concerning food, and substance or alcohol abuse.
• Management
  • Patients value their emaciated state and are usually ambivalent about treatment. Good therapeutic rapport and motivational counselling are important.
  • Exclude other diagnoses and monitor physical health.
  • For adolescents, family interventions are first line.
  • For adults, effective psychological therapies include cognitive behavioural therapy (CBT), interpersonal psychotherapy (IPT), focal psychodynamic therapy and family therapy.
  • Specialist inpatient programmes typically provide a structured, symptom-focused treatment regime to achieve weight restoration. In very severe cases, nasogastric feeding may be instigated without the patient’s consent under the Mental Health Act.
  • Coexistent depression should improve with weight gain, even without antidepressants.
  • Treatment is usually as an outpatient but hospitalisation may be needed because of:
    – severe or rapid weight loss, or BMI <13.5, because of high risk of fatal arrhythmia or hypoglycaemia
    – significant suicide risk
    – physical sequelae of starvation or purging.
• Prognosis
  • Anorexia has the highest death rate of any psychiatric disorder (see Figure 13.1 for prognosis).
  • Osteoporosis is a long-term complication.

Bulimia nervosa

• Diagnosis (ICD-10/DSM-5) requires the presence of:
  • a morbid fear of fatness;
  • craving for food and binge-eating (of large amounts in a short time (e.g. >2000 kcal in a session));
  • recurrent behaviours to prevent weight gain (e.g. self-induced vomiting; misuse of laxatives, diuretics, enemas;
    omitting insulin; if diabetic; fasting or excessive exercise);
  • preoccupation with body weight and shape.
  • episodes are not exclusively during episodes of anorexia nervosa.
• Associated clinical features include:
  • normal or excessive weight (which often fluctuates);
  • loss of control or in a trance-like state during bingeing;
  • intense self-loathing and associated depression;
  • in ‘multi-impulsive bulimia’, alcohol and drug misuse, deliberate self-harm, stealing and/or sexual disinhibition coexist; poor impulse control is the common pathology.
  • Physical signs/complications include:
  • amenorrhoea, which occurs in 50% (despite normal weight);
  • hypokalaemia, which may cause dysrhythmias or renal damage;
  • signs of excessive vomiting; acute oesophageal tears can occur during forced vomiting.
• Differential diagnosis
  • Consider anorexia nervosa, affective disorder and obesity.
  • Rare causes of overeating include Kleine–Levin and Klüver–Bucy syndromes.
• Management involves:
  • medical stabilisation;
  • psychotherapy (usually CBT or IPT) to establish a regular eating programme, re-establish control of diet and address underlying abnormal cognitions;
  • antidepressants; these are effective, best established for fluoxetine (60 mg) but less effective than CBT.
• Prognosis
  • With CBT or IPT, 30–40% achieve remission, gains which are typically maintained.

Binge-eating disorder and obesity

• This involves binge-eating with associated subjective loss of control and distress, without purging, and typically leads to obesity (BMI >30).
• Aetiological factors of obesity include:
  • weight-controlling genes
  • family and cultural influences
  • high availability of cheap calorific foods
  • a sedentary lifestyle.
• Management involves CBT, exercise and educational programmes. Anti-obesity medications such as orlistat (reduces absorption of dietary fat) are of short-term benefit. Surgery (e.g. gastric banding or bypass surgery) is indicated in severe cases.

Personality Disorders

Definition

• Personality disorders (PDs) are deeply ingrained and enduring patterns of behaviour that are abnormal in a particular culture, lead to subjective distress and sometimes cause others distress.
• PDs normally start in childhood or adolescence.
• The original distinction between PDs (lifelong and not treatable) and mental illnesses (briefer and treatable) is now less clear. People can recover from PDs, and there are now effective treatments for borderline PD.

Epidemiology

• In the adult population, PD of at least mild severity occurs in:
  • 5% of the general population
  • 20% of GP attendees
  • 30% of psychiatric outpatients
  • 40% of psychiatric inpatients.
• People with borderline and (to a lesser extent) antisocial PDs are particularly likely to present to emergency and psychiatric services (because of self-harm and severe emotional reactions to crises).
• Just under half of prisoners have antisocial PD.

Aetiology

Genes and environment contribute about equally to personality.

• Genetic influences are shown by twin studies. XYY individuals display higher criminality irrespective of IQ or social class.
• Schizotypal PDs are more common in relatives of people with schizophrenia.
• An underactive autonomic nervous system has been implicated in antisocial PD.
• Adverse intrauterine, perinatal or postnatal factors leading to abnormal cerebral maturation may predispose to PDs.

• Childhood sexual abuse and borderline PD are strongly linked.
• Poor parenting and an adverse childhood environment (during personality development) are implicated in cognitive and psychodynamic theories.
  • Cognitive theory suggests that people with PDs developed ways of coping with early life adversity (e.g. turning anger against oneself rather than expressing it if this could result in parental violence) that manifest as maladaptive traits later in life (e.g. problems in interpersonal relationships).
  • Psychodynamic theories suggest that PDs result from insecure attachment in childhood and thus in adult relationships.

Classification and characteristics

• Patients (particularly those with severe PDs) often fulfil criteria for more than one PD diagnosis. DSM-5 groups PDs into three clusters that are more likely to overlap. The ICD-10 classification does not include narcissistic PD but is otherwise similar to that of the DSM.
• Figure 14.1 shows the diagnostic criteria.
• People should usually be assessed more than once, collateral history sought and comorbid psychiatric disorders treated before a diagnosis of a PD is made.

Management

• People with PD have in the past been excluded from health and social care, and active work to engage them is needed to reverse this. Progress is slow but tolerance of frustration is required for effective treatment.
• Structure, consistency and clear boundaries (i.e. agreement of behaviour that is acceptable and unacceptable) are critical. Multidisciplinary and multi-agency work is often required.
• Most people with PDs have a reduced ability to cope with everyday problems, so may need help with housing and other social matters.
• Comorbid psychiatric illness and substance misuse disorders are prevalent, and their detection and treatment are a priority.
• Drugs are sometimes used to treat specific PD traits, e.g. mood stabilisers for impulsivity (not generally recommended because of lack of evidence). Short-term sedative medication may be used cautiously in borderline PD for crisis management.
• Admission to hospital, day hospital care or crisis team input may be necessary during periods of crisis.
  The evidence base is strongest for the treatment of antisocial and borderline PD.

Borderline PD

• Adapted cognitive behavioural therapy (CBT), dialectical behaviour therapy (DBT) and mentalisation-based treatments can help.
• Threats and acts of deliberate self-harm and suicide can be difficult and time-consuming.
• Ending of or changes in treatments or services may evoke strong emotions and reactions.

Antisocial PD

• Treatment outcomes for antisocial PD are modest, and prevention by targeting children with conduct disorder, a third of whom are likely to develop it, is best (e.g. by providing parent-training/education programmes).
• Psychological therapies require patient cooperation, and motivation to engage in treatment predicts success. For those with a history of offending behaviour, group-based cognitive and behavioural interventions focused on reducing offending and other antisocial behaviour can be effective.
• In the UK there are treatment centres for people with dangerous and severe personality disorders in prisons and secure psychiatric units.

Prognosis

• Most individuals with PDs show decreased aggressive behaviour with age, although the ability to form successful relationships remains poor.
• Borderline PD carries a relatively favourable prognosis with recovery in over 50% at 10–25-year follow-up. It is associated with an increased risk of bipolar affective disorder.
• Schizoid and schizotypal patients tend to remain isolated.
• Dissocial PD carries a particularly poor prognosis.
• Comorbid alcohol and substance misuse is associated with violence and an increased risk of accidental death. There is an increased risk of suicide: 30–60% of completed suicides show evidence of a PD.
• Obsessional PDs are at high risk of progression to obsessive compulsive disorder or depression.
• Paranoid and schizotypal PD may progress to psychosis.
  Schizoid PD does not predispose to schizophrenia.
• Some PDs may confer susceptibility to physical illness (e.g. obsessional PD and duodenal ulcer).

Psychosexual Disorders

• The range of sexual behaviour is extremely wide, with concepts of normality being socially or legally, rather than physiologically, determined.
• Moral and legal objections to some forms of sexual behaviour and an increasing awareness of the seriousness of sexually transmitted infections – particularly the human immunodeficiency virus (HIV) – and of what might be expected from a sexual relationship have encouraged the increasing medicalisation of sexuality.
• Current psychiatric classifications (DSM-5, ICD-10) emphasise that sexual disorders have an element of psychological distress rather than being defined by behaviour alone. They can be divided into disorders of sexual function, preference and identity.

Disorders of sexual function

• Some degree of sexual dissatisfaction is present in as many as 20% of women and 30% of men.
• The commonest problems identified in population surveys and referrals to sexual disorder clinics are:
  • in men: failure of erection and/or ejaculation;
  • in women: low sexual interest, inability to allow penetration (vaginismus), pain on intercourse (dyspareunia), lack of sexual enjoyment and orgasmic dysfunction.
• Assessment involves detailed history-taking from, and examination of, both partners in order to identify the nature of the problem, its duration, the couple’s knowledge of and attitudes to sex and the reasons why help is currently being sought.
  Aetiological factors to be considered in the initial assessment include:
• psychological factors and recent life events;
• past sexual abuse;
• a poor general relationship with the sexual partner;
• physical conditions impeding sexual function, which include:
  • neurological conditions (e.g. multiple sclerosis)
  • diabetes
  • hypothyroidism
  • pelvic surgery;
• sexual dyfunction: this may be a manifestation of poor psychological adjustment to surgery (particularly mastectomy, colostomy or amputation);
• psychiatric conditions:
  • depression (loss of libido, generalised anhedonia)
  • alcohol dependence or misuse
  • anxiety disorders;
• some prescribed drugs including:
  • beta-blockers
  • diuretics
  • antipsychotics
  • benzodiazepines
  • antidepressants
  • recreational drug misuse, especially of opiates.
• Management usually involves:
• treatment of underlying medical or psychiatric conditions
• medical treatments:
  • Oral phosphodiesterase inhibitors such as sildenafil (Viagra) are the drugs of choice for erectile dysfunction.
  • Low-dose antidepressant drugs, which have a side effect of delaying time to ejaculation, are also commonly prescribed to men with premature ejaculation.
  • Other treatments for erectile dysfunction include mechanical devices (vacuum pumps, penile bands and intracavernosal use of drugs e.g. alprostadil).
• psychological treatments:
  • Cognitive–behavioural-based therapies, which aim to facilitate communication, decrease anxiety about performance failure, and identify and explore underlying developmental and personality problems.
  • Education, particularly dispelling myths about what is considered appropriate or normal sexual behaviour.
  • Traditional sex or couples therapy, which (irrespective of the presenting dysfunction) involves the setting of a hierarchy of sexual ‘assignments’, structured on behavioural principles.
• Prognosis with treatment is good in 50–70% of cases, with best results being for premature ejaculation in men and vaginismus in women. Other favourable prognostic factors include a good quality of general relationship, high motivation and early progress within treatment.

Disorders of sexual preference

• Disorders of sexual preference (paraphilias) are much more common in men than in women.
• They may be classified into:
• variations of the sexual object
• variations of the sexual act.
  Variations of the sexual object include:
• paedophilia: sexual activity or fantasy involving children; associated with child pornography and abuse;
• fetishism: the object of sexual arousal is an inanimate object (e.g. an item of clothing or a non-genital body part);
• transvestism: sexual arousal obtained by cross-dressing;
• bestiality: sexual activity with animals;
• necrophilia: intercourse with a corpse.
  The aetiology of these conditions is unclear.
  Management usually involves behaviour therapy (which may involve elements of aversion therapy and conditioning more appropriate responses).
  Antiandrogens are sometimes used in paedophilia to help (usually) men reduce or control their sexual desire.
  Variations of the sexual act involve the induction of both sexual arousal and (usually) orgasm by specific actions. Almost all people presenting to the courts or for psychiatric treatment with such variations are men. The variations include the following:
• Exhibitionism (indecent exposure), which is the most common.
  • Genital exposure is accompanied by emotional tension and excitement and sexual arousal.
  • Exhibitionists make up one-quarter of the sexual offences dealt with by the courts, with psychiatric referral usually arising from this route.
  • Exhibitionists fall into two main groups:
    – those with aggressive personality traits or antisocial personality disorders, in whom the act frequently involves
    masturbation;
    – those of inhibited temperament, where the exposed penis is often flaccid.
  • Treatment may include psychodynamic, behavioural and hormonal (antiandrogen) components.
• Voyeurism (observing sexual acts).
• Frotteurism (rubbing the genitalia against a stranger in a crowded place).
• Sadomasochism (inflicting pain on others (sadism) or having it inflicted on oneself (masochism)). There are no systematic trials of treatment, although behavioural techniques are often used.

Disorders of sexual identity (transsexuality)

• This involves a strong wish to be of the other sex and a conviction that one’s biological sex is wrong. Cross-dressing reflects this wish rather than bringing sexual excitement.
• It often begins in childhood, when it is characterised by:
  • cross-dressing,
  • taking cross-gender roles in games and fantasy,
  • an attraction for pastimes usually regarded as more appropriate for children of the opposite sex.
• Gender atypical behaviours in boys are common but they usually disappear because they are discouraged at school and by parents. Most boys who show gender atypical behaviour grow up to be heterosexual although adult homosexual men are more likely to report gender atypical behaviour in childhood than are heterosexual men.
• Boys with clinical disorders of sexual identity do not regard themselves as homosexual as they grow up but rather as a woman (in a man’s body) who is attracted to men.
• Most adult transsexuals are men. Transsexuals usually seek gender-reassignment surgery (with associated hormonal treatment).
  Outcome following such treatment is best where the patient:
  • is psychologically stable,
  • has adopted the cross-gender role consistently for at least two years prior to surgery,
  • accepts that surgical treatment is not a ‘cure’,
  • is willing to participate in presurgical psychotherapy.

Unusual Psychiatric Syndromes

• The features of the best described psychiatric syndromes are summarised below.
• Although these syndromes have now been subsumed into the ICD-10 and DSM-5 classification systems, their names are still in regular use.
• They can be divided into psychotic (characterised by delusions and hallucinations) and non-psychotic syndromes.

Psychotic syndromes

Delusional misidentification syndrome

• The two most common subtypes are:
  • Capgras’ syndrome, characterised by a delusional belief that a person known to the patient (e.g. spouse or parent) has been replaced by an imposter who is their exact double;
  • Fregoli’s syndrome, which involves the delusion that strangers or other people the patient meets (e.g. nurses, doctors) are the patient’s persecutors in disguise.
• It most commonly occurs in schizophrenia, affective disorders and dementia or other organic illness. Treatment is of the primary disorder.
• There is some evidence that it relates to the pathophysiology of face recognition, with hyporecognition in Capgras’ and hyperrecognition in Fregoli’s syndrome.
• Violence towards those who are the subject of the delusions is rare but the risk should be assessed carefully.

Delusional parasitosis

• This is also known as Ekbom’s syndrome (although this term is also used to describe the neurological disorder of ‘restless legs’).
• It is twice as common in women.
• Sufferers believe that insects are colonising their body, particularly the skin and eyes. They often claim to feel dermal sensations and to visualise the bugs, although no one else can see them.
• Initial presentation is often to public health workers (with persistent demands for deinfestation), dermatologists or infectious disease physicians, with insistent, repeated and bizarre requests for investigation and treatment.
• Delusions may be circumscribed or part of a schizophrenic or depressive illness.
• Antipsychotics are the mainstay of treatment.

Folie à deux (induced or shared delusional disorder)

• A delusional belief that is shared by two or more people (usually within a family), of whom only one has a psychotic illness.
• The psychotic individual (principal) tends to be more intelligent and better educated than the non-psychotic (more submissive) recipient(s) and has a dominating influence over them.
• The delusion is usually persecutory or hypochondriacal.
• The pair are often isolated from others by distance or by cultural or language barriers.
• The diagnosis of the principal is most commonly schizophrenia but may be an affective disorder or dementia.
• Folie à deux is classified as induced delusional disorder in ICD-10; DSM-5 does not list it separately from delusional disorder.
• Primary treatment of the principal is of the underlying condition.
  A period of separation of the involved individuals, followed by supportive individual and/or family therapy, may be
  helpful.

De Clerambault’s syndrome (erotomania)

• The patient (usually female) has the unfounded and delusional belief that someone (usually a man of higher social status) is in love with her. The patient makes inappropriate advances to this person and becomes angry (and sometimes violent) when rejected.
• The syndrome may exist in isolation, as part of an affective (usually manic) disorder or, more rarely, schizophrenia.
• Underlying conditions should be treated; where no other underlying condition is identified, antipsychotics may be useful.
• Management frequently involves hospitalisation (sometimes compulsory) to prevent harassment or injury. When men are affected they present a greater forensic risk.

Othello syndrome (morbid or pathological jealousy)

• The patient (usually male) is delusionally convinced that his partner is being unfaithful. He goes to great lengths to produce ‘evidence’ of the infidelity (e.g. stains on underclothes/sheets) and to extract a confession.
• It may occur in long-term alcohol abuse, dementia, schizophrenia, cocaine addiction and as a side effect of treatment with dopamine agonists in Parkinson’s disease.
• Paradoxically, the partner is sometimes driven to true and actual infidelity.
• There is a substantial risk of violence (even homicide); thus, distant separation may be warranted and compulsory hospitalisation and treatment are often necessary. It tends to reoccur with a new partner.

Cotard’s syndrome

• This is characterised by nihilistic delusions in which the patient believes that parts of his or her body are decaying or rotting or have ceased to exist. Patients may also believe themselves to be dead or (paradoxically) unable to die and therefore eternally alive.
• It is almost invariably found in the context of psychotic depression.
• Electroconvulsive therapy (ECT) is often required because of the severity of the associated depression.

Non-psychotic syndromes

Munchausen’s syndrome

• Munchausen’s syndrome is termed ‘factitious disorder’ in ICD-10 and DSM-5.
• It is characterised by deliberately feigned symptomatology, usually physical (e.g. abdominal pain) but sometimes psychiatric (e.g. with feigned hallucinations, multiple bereavements or sexual abuse).
• These result in multiple presentations to A&E departments, usually to several hospitals, with frequent admissions often culminating in surgical procedures.
• Patients often use multiple aliases, are often of no fixed abode and usually have no regular GP. When discovered, the patients usually discharge themselves against medical advice.
• The syndrome characteristically occurs in people with severe personality disorders.
• Management is difficult, although confrontation without rejection may prove helpful.
• Important differential diagnoses are dissociative and somatisation disorders (where symptoms are not consciously produced) and undiagnosed illness.
• Occasionally the disorder can be by proxy, as when a parent fakes illnesses in a child (Munchausen’s syndrome by
  proxy).

Couvade syndrome

• This is the experience of symptoms resembling those of pregnancy (abdominal swelling and/or spasms, nausea and vomiting, etc.) in expectant fathers. Anxiety and psychosomatic symptoms (e.g. toothache) are also common.
• The prevalence of mild forms is as high as 20%.
• The condition (which in some cultures is quite acceptable and may even be expected) is usually self-limiting and responds to counselling but often recurs in subsequent pregnancies.

Ganser’s syndrome

• This is a rare, dissociative disorder. Symptoms are seen as a defence against intolerable stress.
• Characteristic symptoms are:
  • approximate, absurd and often inconsistent answers to simple questions. The patient may say ‘2 + 2 = 5’, or, when asked the colour of snow, reply ‘green’;
  • clouding of consciousness;
  • true and/or pseudohallucinations (visual or auditory);
  • somatic symptoms.
• There may be an underlying depressive illness warranting treatment in its own right.
• It is overrepresented in prison populations.
• Spontaneous improvement often occurs and is characteristically accompanied by amnesia for the abnormal behaviour.
  Recovery may be hastened by admission to hospital and psychotherapeutic exploration of underlying conflicts.
• Factitious disorder is a differential diagnosis.