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Affective (mood) disorders

Sep 12, 2021

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PSYC055
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l Epidemiological factors in mood disorders. l Aetiological factors in mood disorders, including
monoamine hypothesis of depression. l Clinical features of depressive disorders and mania, and of
dysthymia and hypomania. l Differential diagnosis of depression, including organic
(secondary) causes.
Learning Objectives
l Be able to assess a patient with low mood. l Be able to talk to a patient about starting an antidepressant
or mood stabiliser. l Be able to talk to a patient about electroconvulsive therapy
(ECT) treatment.
Classification, 62 Depressive disorders, 64 Epidemiology, 64 Aetiology, 64 Clinical features, 67 Diagnosis, 68 Differential diagnosis, 69 Management, 70
Course and prognosis, 77 Puerperal disorders, 77 Mania and bipolar affective disorder,
78 Epidemiology, 78 Aetiology, 79 Clinical features of mania or manic
episode, 79
Diagnosis, 80 Differential diagnosis, 81 Management, 82 Course and prognosis, 84 Summary, 84 Recommended reading, 86 Self-assessment, 86
Affective (mood) disorders 5
Testimony of a bipolar sufferer after a course of ECT treatment for a severe depressive episode
I have been high several times over the years, but low only once. When I was high, I became very enthusiastic about some
project or another and would work on it with determination and success. During such highs I wrote the bulk of two books and stood for parliament as an independent. I went to bed very late, if at all, and woke up very early. I didn’t feel tired at all. There were times when I lost touch with reality and got carried away. At such times, I would jump from project to project without completing any, and did many things which I later regretted. Once I thought that I was Jesus and that I had a mission to save the world. It was an extremely alarming thought.
When I was low I was an entirely different person. I felt as though life was pointless and that there was nothing worth living for. Although I would not have tried to end my life, I would not have regretted death. I did not have the wish or the energy to do even the simplest of tasks. Instead I withered away my days sleeping or lying awake in bed, worrying about the financial problems that I had created for myself during my highs. I also had a feeling of unreality, that people were conspiring to make life seem normal when in actual fact it was unreal. Several times I asked the doctor and the nurses to show me their ID because I just couldn’t bring myself to believe that they were real.
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62 Chapter 5 Affective (mood) disorders
5 Classification
Primary versus secondary mood disorder
A primary mood disorder is one that does not result from another medical or psychiatric condition. A secondary mood disorder, on the other hand, is one that results from another medical or psychiatric condition, e.g. anaemia, hypothroidism, substance abuse. Once a diagnosis of mood disorder has been made, it is important to con- sider the possibility of it being a secondary mood disorder, as a secondary mood disorder is often most effectively treated by treating the primary condition, e.g. anaemia, etc.
Unipolar depression versus bipolar affective disorder
Broadly speaking, a primary mood disorder is either unipolar (depressive disorder, dysthymia) or bipolar (bipolar affective disorder, cyclothymia) (Fig. 5.1). To meet the criteria for a bipolar mood disorder, the patient must have had one or more episodes of mania or hypo- mania. The unipolar–bipolar distinction is an important one to make, as the course and treatment of bipolar affect- ive disorder differ significantly from those of unipolar depression.
Unipolar mood disorders
In ICD-10, depressive disorders are classified according to their severity into mild, moderate, severe, and psychotic depressive disorder (Fig. 5.1). If a patient has had more than one episode of depressive disorder, the term recurrent
depressive disorder is used, and the current episode is classified as for a single episode, e.g. ‘recurrent depressive disorder, current episode moderate’ (Fig. 5.2). In DSM-IV the term major depression is used instead of depressive disorder. Major depression is simply subclassified as ‘single episode’ or ‘recurrent’.
Not all people suffering from depressive symptoms have a depressive disorder. Dysthymia can be described as a mild chronic depression characterised by depressive symptoms that are not sufficiently severe to meet a diagnosis of depressive disorder (Fig. 5.3).
Bipolar mood disorders
According to ICD-10, bipolar affective disorder consists of repeated (two or more) episodes of depression and mania or hypomania. In the absence of episodes of mania
All mood disorders
Primary mood disorders
Secondary mood disorders (Organic mood disorders)
Mild Moderate Severe Psychotic Bipolar l Bipolar ll
Mania
Figure 5.2 Recurrent depressive disorder.
Mania
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or hypomania, the diagnosis is one of recurrent depress- ive disorder. In the absence of episodes of depression, the diagnosis is either one of bipolar affective disorder or hypomania – i.e. recurrent episodes of mania are diagnosed as bipolar affective disorder. This is not only because sooner or later a depressive episode is almost certain to supervene, but also because recurrent episodes of mania resemble BAD in their course and prognosis.
According to DSM-IV, ‘bipolar disorder’ can be dia- gnosed after even a single episode of mania, whereas in ICD-10 a single episode of mania is simply diagnosed as a
‘manic episode’. The separation of bipolar disorder into bipolar I and bipolar II in DSM-IV may have implications for treatment response. Bipolar I consists of episodes of mania and major depression (Fig. 5.4), bipolar II of episodes of hypomania and major depression.
Cyclothymia can be described as mild chronic bipolar affective disorder and is characterised by numerous epi- sodes of mild elation and mild depressive symptoms that are not sufficiently severe or prolonged to meet the criteria for bipolar affective disorder or recurrent depressive dis- order (Fig. 5.5).
Mania
ICD-10 classification of affective disorders
F30 Manic episode F30.0 Hypomania F30.1 Mania without psychotic symptoms F30.2 Mania with psychotic symptoms F30.8 Other manic episodes F30.8 Manic episode, unspecified
F31 Bipolar affective disorder (BAD) F31.0 BAD, current episode hypomanic F31.1 BAD, current episode manic without psychotic symptoms F31.2 BAD, current episode manic with psychotic symptoms F31.3 BAD, current episode mild or moderate depression F31.4 BAD, current episode severe depression without
psychotic symptoms F31.5 BAD, current episode severe depression with psychotic
symptoms F31.6 BAD, current episode mixed F31.7 BAD, current episode in remission F31.8 Other bipolar affective disorders F31.9 Bipolar affective disorder, unspecified
F32 Depressive episode F32.0 Mild depressive episode F32.1 Moderate depressive episode F32.2 Severe depressive episode without psychotic symptoms F32.3 Severe depressive episode with psychotic symptoms F32.8 Other depressive episodes F32.9 Depressive episode, unspecified
F33 Recurrent depressive disorder F33.0 Recurrent depressive disorder, current episode mild F33.1 Recurrent depressive disorder, current episode
moderate
F34 Persistent mood disorders F34.0 Cyclothymia F34.1 Dysthymia F34.8 Other persistent mood disorder F34.9 Persistent mood disorder, unspecified
F38 Other mood disorders F38.0 Other single mood disorders F38.1 Other recurrent mood disorders F38.8 Other specified mood disorders
F39 Unspecified mood disorders
Single episode Recurrent
Bipolar disorder I Bipolar disorder II Cyclothymic disorder
Mood disorder due to a general medical condition Substance-induced mood disorder
Figure 5.5 Cyclothymia.Figure 5.4 Bipolar depression (bipolar I).
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64 Chapter 5 Affective (mood) disorders
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factors can affect the presentation not only of depression but also of other psychiatric and non-psychiatric condi- tions (see Table 7.3 on culture-bound syndromes).
Aetiology
Genetics
The prevalence rate for major depression in first-degree relatives is about 15%, compared to about 5% in the general population. Although first-degree relatives are at increased risk of depressive disorders they are not at increased risk of bipolar affective disorder or schizoaffec- ive disorder. The concordance rate for major depression in monozygotic twins is 46%, compared to 20% in dizy- gotic twins. There is thus an important genetic component to the aetiology of depressive disorders. The inheritance pattern is no doubt polygenic, but more research is needed to identify the genes involved.
Neurochemical abnormalities
The monoamine hypothesis of depression suggests that depression results from the depletion of the monoamine
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Age (years)
Males Females
Pr ev
al en
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er 1
00 0
pa tie
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Figure 5.6 Prevalence of ‘treated depression’ according to age and sex. Note prevalences and peaks. (Adapted from Key Health Statistics from General Practice 1998.)
Depressive disorders
Epidemiology
Figures for the lifetime incidence or lifetime risk of depressive disorders depend on the criteria used to define ‘depressive disorders’. Using the criteria for major depress- ive disorder (DSM-IV), the lifetime risk of depressive disorders is about 15%. The prevalence of depressive dis- orders at any one time or point prevalence is about 5%. This figure masks an uneven gender distribution, how- ever, as females are more affected than males by a ratio of about 2 : 1. The reasons for this uneven gender distribu- tion are unclear but are thought to be partly biological (genetic predisposition, hormonal influences) and partly sociocultural (social pressures, readiness to admit to depress- ive symptoms, diagnostic bias in clinicians). Although depressive disorders can occur at any age, their peak pre- valence in males is in old age, and in females is in middle age (Fig. 5.6). They are relatively uncommon in children, or present differently (see Chapter 13).
There are important geographical variations in the prevalence rates of depressive disorders, and these can at least in part be accounted for by sociocultural factors. For example, somatic presentations of depression are par- ticularly common in Asian and African cultures and may therefore not so easily be recognised as depression. As a clinician it is important to remember that sociocultural
. . . I have of late – but wherefore I know not – lost all my mirth, forgone all custom of exercises; and indeed it goes so heavily with my disposition that this goodly frame, the earth, seems to me a sterile promontory, this most excellent canopy, the air, look you, this brave o’erhanging firmament, this majestical roof fretted with golden fire, why, it appears no other thing to me than a foul and pestilent congregation of vapours. What a piece of work is a man! how noble in reason! how infinite in faculty! in form and moving how express and admirable! in action how like an angel! in apprehension how like a god! the beauty of the world! the paragon of animals! And yet, to me, what is this quintessence of dust? man delights not me: no, nor woman neither, though by your smiling you seem to say so.
Shakespeare, Hamlet, Act II, scene 2
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neurotransmitters noradrenaline, serotonin, and dopa- mine. In its revised version the monoamine hypothesis of depression recognises that depression may not result from an actual depletion of the monoamine neurotransmitters, but from a change in their receptors’ function.
Support for the original monoamine hypothesis of depression comes from several findings, notably: l Antidepressants increase the levels of the monoamine
neurotransmitters: – Monoamine oxidase inhibitors (MAOIs) inhibit the
degradation of monoamines presynpatically. – Tricyclic antidepressants (TCAs) inhibit the reuptake
of noradrenaline from the synaptic cleft. – Selective serotonin reuptake inhibitors (SSRIs) inhibit
the reuptake of serotonin from the synaptic cleft. l Amphetamines and cocaine increase the levels of mono-
amines in the synaptic cleft and can elevate mood. l Reserpine decreases the levels of monoamines pre-
synaptically and can depress mood. l Cerebrospinal fluid levels of 5-hydroxyindoleacetic acid
(5-HIAA), a serotonin metabolite, are decreased in depression sufferers.
Other neurological abnormalities
Computed tomographic (CT) and magnetic resonance imaging (MRI) findings in major depression include enlarged lateral ventricles and loss of volume in the frontal and temporal lobes, hippocampus, and basal ganglia; but these findings are inconsistent.
Endocrine abnormalities
The fact that depression occurs in a variety of endocrine disorders (Cushing’s syndrome, Addison’s disease, hypo- thyroidism, hyperparathyroidism) suggests that endocrine abnormalities play a role in the aetiology of depressive disorders. It has been found that plasma cortisol levels are increased in about 50% of depression sufferers and that about 50% of depression sufferers fail to respond to the dexamethasone suppression test. These endo- crine abnormalities may have their origin in disturbances of the hypothalamic–pituitary–adrenal axis.
Immune function
It has been postulated that disturbances in the hypothalamic– pituitary–adrenal axis in depression (see above) may at least in some cases result from changes in immune regulation.
Affective (mood) disorders Chapter 5 65
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Table 5.1 Organic causes of depression (note that this list is not exhaustive).
Neurological Stroke, Alzheimer’s disease/dementia, Parkinson’s disease, Huntington’s disease, multiple sclerosis, epilepsy, intracranial tumours
Endocrine Cushing’s syndrome, Addison’s disease, hypothyroidism, hyperparathyroidism
Metabolic Iron deficiency, vitamin B12/folate deficiency, hypercalcaemia, hypomagnesaemia
Infective Influenza, infectious mononucleosis, hepatitis, HIV/AIDS
Neoplastic Non-metastatic effects of carcinoma
Drugs L-dopa, steroids, beta blockers, digoxin, cocaine, amphetamines, narcotics, alcohol
Organic causes
The organic causes of depression are listed in Table 5.1.
Personality traits
Certain personality traits such as neuroticism and obses- sionality and certain personality disorders predispose to depression.
Environmental factors
Early adverse life events such as loss of a parent, neglect, or sexual abuse may predispose to depression in later life, and ‘an excess of life events’ occurs in the months preceding the onset of a depressive episode. A depressive episode that appeared to result from life events and lacked somatic symptoms used to be called a reactive depression and contrasted to an endogenous depression, but both epithets and their cognates have been abandoned in favour of the realisation that all depressive episodes ultimately result from a combination of both genetic and environ- mental factors.
The Brown and Harris study
In 1978, Brown and Harris studied working class women in inner London boroughs and found that certain cir- cumstances acted as so-called ‘vulnerability factors’ for depression:
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Three of the most influential psychological theories of depression are considered in Tables 5.2 and 5.3.
Table 5.2 Psychological theories of depression.
According to Depression results from
Attachment Maternal deprivation theory (Bowlby)
Psychoanalytical Loss of the loved object and mixed theory (Freud) feelings of love and hatred, so-called
ambivalence Cognitive theory Beck’s triad (negative appraisal of the
(Beck) self, of the present, and of the future) and Beck’s cognitive distortions (Table 5.3)
Table 5.3 Beck’s cognitive distortions in depression.
Cognitive distortion Explanation
Arbitrary inference Drawing a conclusion in the absence of evidence, e.g. Everyone on this ward hates me
Overgeneralisation Drawing a conclusion on the basis of a single incident, e.g. The nurse gave me an evil look – everyone on this ward hates me
Selective abstraction Focusing on a single event to the detriment of others
Dichotomous thinking ‘All-or-nothing’ thinking, e.g. If he doesn’t come to see me today then he doesn’t love me
Magnification/ Over- or underestimating the minimisation importance of an event
Catastrophic thinking Expecting disaster to strike, e.g. If I take the car out to the shops I’m more than likely to crash it and kill someone
Personalisation Relating independent external events to oneself, e.g. The nurse left her job because she was fed up with me
’Learned helplessness’ and depression
In 1975 Seligman demonstrated that dogs that had learnt that they could not escape from an electric shock did not try to escape from it even once the situation permitted them to do so. In other terms, once the dogs had learnt that they could not exert control over their environment, they permanently gave up the will to do so. Extended to human behaviour, this so-called ‘learned helplessness’ has provided an influential cognitive-behavioural model of depression.
Man’s Search for Meaning
We who lived in concentration camps can remember the men who walked through the huts comforting others, giving away their last piece of bread. They may have been few in number, but they offer sufficient proof that everything can be taken from a man but one thing: the last of human freedoms – to choose one’s attitude in any given set of circumstances – to choose one’s own way.
Victor Frankl (1905–1997), neurologist, psychiatrist, holocaust survivor, author of Man’s Search for Meaning,
and founder of logotherapy and existential psychotherapy
Frankl observed that those who survived longest in the con- centration camps were not those who were physically strong, but those who succeeded in retaining a sense of individual purpose and control over their lives.
l Loss of mother by death or separation before the age of 11.
l Excess of life events or major difficulties prior to onset of depression.
l Lack of a supportive relationship. l Three or more children under the age of 14 at home. l Not working outside the home.
Seasonal affective disorder
Seasonal affective disorder (SAD) is a depressive disorder that recurs every year at the same time of year and may be marked by increased sleep and carbohydrate craving. The condition is thought to result from changes in the seasons, particularly in the length of daylight, and may respond to bright artifical lights (light is given at 2500 lux in the morning and late evening). There is usually complete summer remission and occasionally summer hypomania or mania which, along with Shakespeare, may be at the origin of the expression ‘This is very midsummer madness’.
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Although the most common symptom of depression is depressed mood, many patients never complain of this and instead present because of other cognitive, behavioural, or somatic symptoms. For example, they may present because they are feeling tired all the time, because they cannot con- centrate on their job, or because they can no longer fulfil their marital or social obligations.
Mild depression is the commonest form of depression and tends to present, if at all, to GPs. The patient often complains of feeling depressed and tired all the time, and sometimes also of feeling stressed or anxious (‘mixed anxiety-depression’). There are none of the somatic features of depression and, although suicidal thoughts can occur, self-harm is uncommon.
Moderate depression is the classic textbook descrip- tion of depression that is often treated in primary care but that can be severe enough to be referred to a psychiatrist. Many if not most of the clinical features of depression are present to such an intense degree that the patient finds it difficult to fulfil his or her social obligations. Somatic features are present and anhedonia is charac- teristic. Suicidal ideation is common and may be acted upon.
Severe depression is an exaggerated form of moderate depression. It is characterised by intense negative feel- ings and psychomotor agitation or retardation. Depressive stupor may supervene upon psychomotor retardation, and urgent ECT treatment may be required (see later). Psychotic symptoms may be present in 10–25% and are usually mood-congruent, e.g. nihilistic delusions, delusions of guilt, delusions of poverty. Suicidal risk is high and, in the retarded patient, may be even more so once treatment is initiated and the mood begins to lift.
Dysthymia
Dysthymia is characterised by mild chronic depressive symptoms that are not sufficiently severe to meet the criteria for mild depressive disorder. Although dysthymia has sometimes been regarded as a ‘depressive personality’, genetic studies suggest that it is in fact a chronic, mild form of depressive disorder. If it develops into a depress- ive disorder, it is then referred to as ‘double depression’ (Fig. 5.7). Its lifetime prevalence is about 3% and, as it is a very chronic condition, its point prevalence is not actually very different. It is more common in females and in the divorced. Dysthymia may respond to drug treatment and to psychological treatments, although to date there is no firm evidence base for the latter.
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Clinical features
The clinical features of…
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