Mood disorders

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Mood disorders

  • Mood disorders are disturbances of emotion
  • Clinical depression has a severe and debilitating effect on the individual and those around them, and may lead to difficulty in obtaining employment.
  • Clinical depression is very difficult to treat
  • There are two types of depression; unipolar, and bipolar
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Unipolar depression

Comer (2008) defines unipolar depression/major depression as 'a severe pattern of depression that is disabling and is not caused by factors such as drugs or a general medical condition.'

*Classified under the DSM-IV-TR as a mood disorder (aka major depressive disorder)

  • Emotional (Affective) symptoms = depressed mood, sadness, feeling low.
  • Cognitive symptoms = feeling guilty, thinking they are worthless, suicidal thoughts
  • Behavioural symptoms = social withdrawal, restlessness.
  • Physical symptoms = changes in sleep patterns, energy levels or appetite.

Requires the presence of five of the following:

  • Sad, depressed mood.
  • Loss of interest and pleasure in usual activities.
  • Difficulties in sleeping.
  • Shifts in activity level, lethargic or agitated.
  • Poor appetite and weight loss, or increased appetite and weight loss.
  • Loss of energy and great fatigue.
  • Negative self concept, feelings of worthlessness and guilt.
  • Difficulty in concentrating.
  • Recurrent thoughts of death or suicide.
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Unipolar depression

  • This is the most common form of depression, where a person suffers from deep depressive moods and it is therefore an emotional disorder
  • In any one year, 5-7% of adults suffer from this type of depression (higher in women than men, perhaps more likely to talk about it). 
  • With severe unipolar depression, individuals may suffer from delusions and hallucinations which are to do with the person having done something wrong and being punished.
  • Diagnosis requires that there has been no history or presence of mania (an emotional state of intense, but infounded elation.)
  • Blazer (1994) states that many people diagnosed with unipolar depression have other psychological problems, such as eating disorders.
  • Unipolar depression may have a gradual onset or appear suddenly, it occurs in all social classes of all ages, but is more common in middle and old age.
  • Blazer found the highest incidence to be between 15-24 and 35-44.
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Bipolar depression

  • Emotional (Affective) - Feelings of euphoria and highly elevated mood states, irritability due to not getting own way, lack of feelings of guilt and inhibition.
  • Cognitive - Delusional ideas, grandiose plans, thinking that other people are persecuting them, reckless and irrational decision making.
  • Behavioural and psychological - High energy, increased work activity, increased social and sexual activity, reckless and dangerous behaviours.
  • For an episode to be classed as mania, the above symptoms must persist for at least one week, along with distress or impairment of mental function

Three/four of the following symptoms at least one is elevated/irritated mood:

  • unusual talkativeness/rapid spech
  • Distractability and attention easily diverted
  • Less than usual amount of speech needed
  • Inflated self-esteem, belief that one has special talents/powers
  • Increase in activity level, at work/socially or sexually
  • Flight of ideas/racing thoughts
  • excessive involvement in pleasureable activities
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Limitations of the DSM

Limitations of the DSM.

*gender and culture bias as made by western males.

*difference in normative values between western and non-western societies.

*ignores individual differences?

*may be another cause for behaviour.

*An individual's normative behaviour, personality and history are different.

*subjectivity - GPs.

*degree of symptoms - how far is this taken into account?

*depression is stigmatised in some cultures.

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Biological theories of depression

Genetics

Family history and twin studies suggest that mood disorders, partiularly bipolar depression, have a genetic basis, with a risk of developiong a mood disorder at least double where there is no family history (Wallace et al, 2002). In family studies, a proband is generally identified, and info concerning close relatives is gathered. In a large scare study (900 patients) by Winokur in 1995 found rate of unipolar was 10.4% in first degree relatives, compared to 4.9% in a control. Weissman et al (1987) found 50% of offspring display depressive symptoms. 

Twin studies have shown concordanance rates for identical twins for bipolar twins are much higher than DZ twins or other relatives (70% MZ concordanance, 23% DZ).

Some twin studies have also shown concordanance rates for mood disorders are higher in women than men (Kendler et al, 2002). However, other studies show no difference between men and women. So far, it has not been possible to pinpoint a single gene responsible for mood disorders. The present view is that mood disorders result from mult-gene, rather than a single gene action.

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Mc Guffin et al (1996)

AIM: To investiate the genetic component of depression

METH: The researchers got a sample of 214 twin pairs through probands, who'd been treated as patients with depression. (Proband, is a person with a disorder, whose relatives are then investigated to discover genetic transmission of the disorder.)

RESULT: The concordanace rate for unipolar depression was 46% for MZ twins and 20% for DZ twins, both substantially higher than the lifetime depression rate for the general population.

CONC: Genetic factors play a moderate role in family patterns of depression, and may be particularly important in recurrent depression

EVAL: DZ twins and normal siblings have the same genetic similarity, but its difficult for intended factors alone to explain the much higher concordanance rate for DZ twins over normal siblings.

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Genetic explanations evaluation

  • Family studies' results are hard to attribute to genetics alone, since psychological factors, such as being reared by ill relatives cannot rule out environmental factors. 
  • Twin studies cannot rule out environmental factors altogether, as twins are raised in very similar environments, with similar psychological experiences.
  • Adoption studies would be more convincing as nature and nurture are convienetly seperated, but there is a limited sample to obtain in this area of study.
  • The search for a particular gene responsible for major depression has proved difficult, owing to a number of factors - eg, unipolar depression is highly heterogenerous (has many subtypes.) 
  • Studies that have investigated the interaction of genetic inheritance and environments suggest that, rather than cause depression, genes likely influence how sucepible we will be to the effects of life events.
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Biochemical factors

The monoaime hypothesis (MAOH)

Monoamnie oxidase is an enzyme which breaks down the monoamine transmitters, which are dopamine, serotonin and noradrenalin. It is a depletion of these neurotransmitters which seems to cause depression.

Evidence comes from drugs used in the '50s to treat high blood pressure, known as reserpine. A common side effect was depression. This drug reduced the levels of 5-H1AA, a substance which is produced when serotonin is broken down (high levels of seotonin = bipolar, low levels of serotonin = unipolar.)

Levels of serotonin can be measured by looking for 5-H1AA in urine and cerebrospial fluid (CSF), suggesting that there is less serotonin at the synapse. A problem with this, is that you cannot tell whether this is directly linked to serotonin in the brain, or whether the rest of the body is involved. This type of research is therefore correlational, which can't determine cause and effect.

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Biochemical factors

MAOIs are drugs that inhibit the enzyme, and so increase the levels of monoamnie transmitters (don't break them down). These were very effective at treating depression, until their toxic effects became known.

In the synaptic cleft, neurotransmitters, such as serotonin are only active for a short amount of time, after which they are destroyed or inactivated. Tricyclics block the synaptic reuptake of all amines into the neurons, and so increasing their avalibility. Now SSRIs are used, which selectivley stop only the serotonin reuptake, allowing more to cross the synapse. This seems to relieve most patients of depression.

Cortisol helps people respond to stress during the fight and flight response. People with unipolar depression have unusually high levels of cortisol in their bodies. Even when the immediate stressful event has disappeared.

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Evaluation of biochemical factors

  • This theory is one of the longest standing, and is the most persistant explanation of depression (Claridge and Davis, 2003).
  • There is much research to support this hypothesis, by looking at 5-H1AA and the effects of drugs that affect the monoamine transmitters.
  • However, most of the research is based on correlations
  • Claridge and Davis, 2003, found that if you give people drugs to reduce the levels of serotonin, they don't get depression. This cannot be explained by this hypothesis.
  • Antidepressant medications were discovered that didnt have the same effects (Eg, increasing the avalibility of neurotransmitters)
  • Antidepressants immediatly increase levels of neurotransmittters, but there's a delayed effect on alleviating the symptoms, (ie, they can take 7 weeks.) Everything is therefore not known, as if the neurotransmitters were increased, depression should stop immediatly. Researchers now believe an interaction between various neurotransmitters occur.
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Brain structure explanations

There is some evidence that the limic system and the frontal lobes are implicated in depression:

  • Injury or stroke that affects the frontal part of the brain, can lead to depression. The frontal lobes are a major regulatory component of the limbic system, as this system controls the emotion and drives of a person.
  • Neuroimaging studies have found structural abnormalities in the frontal region of the brain of unipolar patients. Using MRI, Coffey et al (1993) demonstrated depressed patients have lower frontal lobe volume than did controls.
  • Using electronenceptiolographical recording (EEG) Henrique and Davidson (1990) discovered frontal hypoactivation in a sample of 15 unipolar depressed patients. This wasn't found in normal controls.
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Evaluation of brain structure

  • Findings that show defiects in brain structures of depressed patients, don't show cause and effect.
  • Henrique and Davidson (1990) proposed a diathesis-stress model (due to both inherited factors and environmental factors) to explain brain abnormalities and found: 'individuals who display frontal EEG asymmetry are more vunerable to depression, given sufficient environmental stress'.
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Cognitive theories of depression

Conginitive explanations state that people come depressed as they think in negative and self-defeating ways. Beck created this theory, calling it the dysfunctional thinking explanation. It has three components: the cognitive triad, faulty info processing and negative self-schemas.

Beck suggested that schemas develop, providing a cognitive framework for viewing events pessimistically. The cognitive triad has 'the self' at the top, and 'the future' and 'the world' on the two bottom points.

It refers to the negativie cognitions that individuals have of themselves, the world and the future (eg 'the self' - I am hopeless, or 'the future' - is bleak). According to this theory, defeated self critical and hopeless thoughts affect people in a variety of other areas, like mood, behaviour and physiology.

People with such a triad believe it's futile to attempt to do much, as the world and future are bleak. Such patterns predisopose people to experience depression. 

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Cognitive theories of depression

Our reactions and beliefs about the world (even dysfunctional ones) originate in schemas developed in childhood. Our schemas are shaped by our early experiences. An individual with negative schemas, will not, necessarily become depressed, but it is more likely if they then encounter a similar negative experience in later life. Schemas allow us to process info fast and selectivley ue to expectation. If these are negative, we can interpret that fits into a maladaptive or inappropriate way of thinking

Once the negative triad is activated, the individual will concentrate on processing the information relevant to it, and not on more personally positive info.This will lead to a reinforcement of the negative beliefs and will perpetuate the depression.

EG--> negative early experience -> leads to formation of dysfunctional beliefs/schemas-> a critical life experience (Eg redundancy from work) -> leads to assumptions being activated -> consequent bias info processing (over emphasis on negative achievements) -> leads to symptoms of an emotional disorder.

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Cognitive theories of depression

Beck also believes that negative and illogical thoughts deepen a person's depression, and lower their motivation to take constructive action, which could change their situations. This means their information processing is cognitivley biased.

Examples of illogical thinking are:

  • Magnification and minimisation: some people magnify their difficulties and failures, while minimising their achievements and sucesses
  • Selective abstraction: This is when an individual arrives at a conclusion, based on only one factor, rather than considering a number of possible reasons.
  • Arbitary inference: an individual arrives at a negative conclusion about themselves in the absence of any supporting evidence
  • Overgeneralisation: this is when an individual arives at a sweeping conclusion based on a single, and often trivial, event

Abramson et al (1989) proposed the hoplessness theory of depression, which is having a pessimistic, attributional style coupled with a negative life event, that can lead to a feeling of hopelessness. This would then, likely, result in depression.

However, distinguishing cause and effect is difficult in this study

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Cognitive theories of depression

Evidence suggests that depressed people may process info differently to non-depressed people. Yost and Weary (1996) compared attibutions of a group of 58 depressed students, and 57 non depressed students.

They found participants were more likely to blame external factors. This encouraged a helpless attitude, as they were more likely to see people as victims of their circumstances.

However, when making self attributions, the depressed people were more likely to judge negative behaviours and events as due to their own personal shortcomings (blaming internal factors).

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The learned helplessness theory

Seligman (1974) first proposed that learned helplessness may be a useful model for depression. Learned helplessness in operant condtioning, if a punishment is too harsh or escape from punishment is too difficult, punishment will not stop a particular response to a stimulus. Individuals continue doing the behaviour and accept their punishment.

Deficits are said to occur in three areas:

  • Motivation - there's no point trying if you have already learned you have no control
  • Cognitive - Learning you have no control results in passive acceptance
  • Emotional - this passivity is a kind of depression
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Learned helplessness

Abramson et al (1978) reformulated the helplessness theory and proposed the types of attributions people make of uncontrollable events are an important element in whether or not they become depressed. The kinds of attributions are:

  • internal/external - caused by something in the individual or in the environment
  • global/specific - will affect all situations, or just specific to one
  • stable/unstable - will always be that way, or can change

An internal, stable and global attribution would reflect a pessimistic style that would leave someone at risk for depression. The more recent hopelessness theory (abramson et al '89) proposed having a pessimistic style coupled with a negative life event can lead to a feeling of hopelessness, which would result in depression

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Evaluation of cognitive theories

  • This theory is one of the most influential models explaining negative thought processes.
  • Our emotional reaction seems to come from how we interpret/predict the world around us
  • This main problem is that the theory is correlational, and the argument is a circular one. Does depression caise the negative thinking, or does negative thinking cause depression?
  • When participants are tested in research, they have often been on drugs to manage the depression, which may affect the results of any studies.
  • Thoughts are subjective experiences that are hard to test and measure
  • Also, most people seeking help already have negative emotions, and so it is not possible to assess their cognitive processes prior to the onset of the disorder
  • It's difficult to see whther negative thinking plays a causal role in depression
  • Eysenck and Keene(2000) concluded there is mixed evidence for bias info processing in depressed people
  • Damasio (2000) found that neurouimaging techniques have shown emotional processing can occur before cognitive processing - suggesting emotions control cognitions. In this case, Beck's theory is incomplete.
  • The focus on internal cognitions doesn't view environmental/social factors in which people live.
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Psychodynamic explanations of depression

According to this theory, childhood experiences, particularly in the oral stage of development (0-2 years) a child's needs may be overly gratified or insufficiently gratified, either way resulting in a child which is orally fixated. This could result in the personality type where the person suffers from low self esteem or over dependance.

Freud believed that personality is contructed from three structes and all behaviour is a product of their interaction:

Id - pleasure principle, innate part of the personality. Demands immediate gratfication. It is the 'I must have' part of the personality, driven by sexual and aggresive insticts (mania?)

Ego - reality principle, develops to meet the needs to the id. When the superego develops, it acts as a balance between the id and the superego.

Superego - morality principle, develops from society's morals, codes and expected behaviours.

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Psychodynamic explanations of depression

In depression, the superego part of the personality may be winning out, as it is stunting the Id. The ego may not be balancing them effectively - hence the superego, as oppose to the id is winning out, and therefore there is little pleasure or gratification in the personality.

Freud suggested that to avoid the distress caused by any conflict, an individual could employ defence mechanisms, which would help to prevent anxiety - arousing thoughts and impulses from reaching consciousness. Defence mechanisms work on an unconscious level and protect an individual by distorting reality. Freud felt that regression (going back to an earlier, childlike state) may be linked to depression. 

In childhood, you no longer have to rely on yourself, and can rely, and blame others for your failures. You don't have to deal with your troubles, such as grief or loss.

Other psychodynamic theorists, such a Klien and Bowlby don't emphasise the notion of regression, but stress the importance of early mother-infant relationships, and the link between the nature of that relationship and the susceptablity to depression. Bowlby's attachment theory proposed if a child is depreived of a warm and loving attachment to a mother figure, later depression could occur.

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Psychodynamic explanations of depression

Freud proposed that as a result of the loss of a loved one, a person suffers a period of introjection, which is the process of identifying with a loved one. This results in a person incorprating (talking to themselves) any negative feelings towards the loved one, resenting the desertion of the loved one and feeling guilty. The period that follows introjection is mourning, where memories of the lost one are recalled, which enables a seperation to be made. 

However, for the overly dependant (fixated in oral stage) the emotional bonds can't be broken, and anger continues to be turned on words and directed on the self, resulting in depression. Freud also proposed that depression can occur due to imagined or symbolic losses.

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Evaluation of psychodynamic theory

  • The psychodynamic approach is idographic, and so focuses on the individual. This means that the individual's problems are taken into account, and they are not just diagnosed on the basis of others.
  • An important contribution to the psychodynamic approach has been in emphasising the importance of loss to the onset of depression.
  • Depressed people often express anger to others, which isnt what one would expect if the theory suggest anger is turned inwards.
  • There is little experimental evidence for Freud's theories, as most of his work was based upon case studies. This makes the approach highly subjective, unscientific and un-testable, as his findings are often biased to fit his theories.
  • His case stdies were mainly of the middle aged, upper class Austrian women. This means these cant be generalised to the wider population. This is also a problem, as he developed his ideas on childhood from adults talking reterospectivley of their pasts.
  • Golombok (2000) disputes the role of the family as a cause of mental illness. In a review the researcher concluded that once poverty is controlled for there is no significant relationship between family type and psychological development.
  • Theres been some evidence depressed people are high in dependance (Nietzel and Harris, 1990)
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Treatments - biological

Antidepressant medication

Antidepressants have become more widley used due to the development of new drugs and increasing awareness. The drugs were originally used on TB patients, and it was found they elevated the mood of TB patients. It was then found the medication that depleted certain neurotransmitters appeared to cause depression, and those that increased specific neurotransmitters reduced depression. 

Antidepressants used are:

  • Monoamine oxidase inhibitors (MAOIs)
  • Tricyclic antidepressants (TCAs)
  • Selective serotonin reuptake inhibitors (SSRIs)
  • Lithium carbonate (could be used as AO2)
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Monoamine oxidase inhibitors (MAOIs.)

  • Early drugs that inhibit monoamine oxidase, and enzyme present in the synaptic cleft that helps break down neurotransmitters noradrenalin, dopamine and seotonin.
  • MAOIs are only used in atypical depression, when the patient doesn't respond to other antidepressants
  • Because of side effects, some of which are dangerous
  • Because of dietary requirements and restrictions
  • They are toxic in large doses (not good for suicidal patients)
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Tricyclic antidepressants (TCAs)

  • Imipramine was found to elevate the mood of those with schizophrenia who were depressed
  • They affect several differen neurotransmitters
  • Used to treat severe depressive symptoms, usually for unipolar deression.
  • They are toxic (risk for the sucidal) in high doses
  • They have side effects such as dry mouth, blurred vision and erectile dysfunction
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Selective serotonin reuptake inhibitors (SSRIs)

  • More recent type of antidepressant and chemically unrelated to the others
  • Work by selectivley inhibiting the reuptake of serotonin only
  • Now the preferred type of antidepressant 
  • Have fewer side effects and not fatal in overdose
  • As with all medications, there are a few side effects, such as nausea, diarrhoea and sexual dysfunction

HOWEVER, NONE OF THESE ANTIDEPRESSANTS CAN BE USED ON BIPOLAR PATIENTS

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Lithium Carbonate (ao2?)

  • A drug used to treat bipolar disorder (manic depression)
  • It isn't clear how it works but it is effective both during the depressed and manic phases
  • It isn't effective in the treatment of unipolar depression, suggesting a diferent aetiology in these two forms of depression
  • Lithium is usually taken continually, as discontinuation can lead to mania (Suppes et al, 1991) 
  • The side effects are potentially life threatening and early use of this drug led to cases of kidney damage or failure due to the incorrect dosage. Even at lower doses, there are side effects, including arrhythimia, blurred vision and lack of coordination.
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Evaluation of antidepressants

  • The mechanisms of action of all antidepressants are not fully understood. It is accepted it is not as simple as increasing a particular neurotransmitter. If this was the case, results should be rapid, whilst noticeable effects can take three to five weeks.
  • Due to the side effects, coupled with the long period before they 'kick in' many patients discontinue use before the antidepressant effect is felt
  • There have been some reports that SSRIs (eg, Seroxat) have been associated with suicidal urges (Cole et al, 1990)
  • A review of numerous studies comparing antidepressants with placebos in blind trials show depression was lifted in 50-70% of cases, which is around 40% higher than in placebo groups (Thase and Kupfer, 1996).
  • Most depressions arise in response to significant life difficulties, and although they treat symptoms, do not cure the circumstances, or cause. Individuals may require psychotherapeutic intervention to deal with their problems and exogenous stressors.
  • The efficacy of antidepressants doesn't mean there is an underlying biological cause for depression. It could be that depression causes the neurotransmitter imbalance (cause and effect.)
  • A small number of depresed people don't respond to antidepressants alone, and may require additional treatment (eg, ECT or hospitalisation.)
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Electrocompulsive therapy (ECT) (bio)

ECT is only used on severely depressed patients who do not respond to antidepressants. ECT requires electrical stimulation of the brain so that seizure is induced. Patients are first given a fast-acting anaesthetic and a muscle relaxant to control potentially damaging physical side effects. Electrodes are attachment to the patient's temples and a 70- to 150 volt shock is given, lasting up to one second. The shock produces a convulsion that lasts up to one minute. After treatment, the patient is confused, feels nauseous and has a headache.  Typically, a course of treatment would be six to nine treatments given over a period of two to three weeks. Lerer et al recommended no more than two treatments a week to avoid unnecessary cognitive impairments. The exact mechanism underlying the effects of ECT is not well understood, but it is likely that resultant changes in neurotransmitters may be responsible for the anidepressants effects. Nobler et al (1994) have linked ECT to blood flow in the frontal-temporal reigons of the brain as they found that successful ECT treatment was generally associated with reduction in blood flow in this region.

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Evaluation of ECT

  • ECT is known to affect short term memory (retrograde amnesia) and it is common to have no recall of events immediatley prior to the ECT.
  • Animals studies and neuroimaging studies on humans have found no evidence of structural brain change caused by ECT (Devanand et al, 1994) 
  • Many critics of ECT view it as unethical, particularly as, in extreme cases, it can be administered against a person's will. However, it has proved effective in cases where other treatments dont work or in life threatening situations where rapid response is needed.
  • Weiner and Coffer (1988) reviewed controlled and placebo studies of ECT and found ECT significantly decreases severe depression.
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Cognitive treatment for depression

Cognitive behavioural therapy

Beck was a psychoanalytically trained psychiatrist who noticed his depressed patients were overwhelmed with negative and dysfunctional thinking patterns.

He developed a treatment, known as cognitive-behavioural therapy (CBT) which has become widley applied for depression and other mental disorders.

Beck's basic tenet is that when people think negativley, they will feel and act depressed, and therefore the therapy attempts to identify the negative beliefs and alter dysfunctional behaviours.

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CBT

CBT is a brief therapy (no more than 20 sessions over 16 weeks) which is directive and focuses on current dysfunctional thinking patterns. Homework assignments are set between visits. Typically the treatment includes the following features:

  • Behavioural activation - the client and therapist draw up a list of activities that the client previously found enjoyable, they then deal with any issues to rekindling them. Engagment in such activities should result in lifting mood.
  • Graded task assignments - clients are helped to engage in sucessively more demanding but rewarding activities
  • Thought catching of 'automatic negative thoughts' - this is fundamental to the treatment. Clients are taught to notice the association between thoughts and feelings and note this down.

(eg, asking someone to go on holiday (emotion arousing experience), automatic negative thought is 'she doesnt like me' and the challanges to this maladaptive thought may be 'kate has already booked her holiday, there is no evidence she doesnt like me, in fact, we always go to lunch together.

Clients are taught to challenge negative thoughts and replace them with more realistic ones. An important part of therapy is to reduce depression by giving clients copings strategies to deal with any emerging depressive symptoms.

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CBT - Elkin et al (1985)

AIM: to investigate the efficacy of different treatments for depression

METH: 250 patients with major depression were randomly assigned to one of four conditions for 16 weeks. The groups were CBT, interpersonal therapy, drug therapy (imipramine -TCA) and a placebo group. 18 months after treatment, a follow up analysis was carried out,

RESULTS: Patients responded equally well to active treatments, but severly depressed initatilly fared better on medication. Recovery, was 36% for CBT, higher than the placebo group but similar to other treatment conditions. After 18 months, the psychotherapy groups had maintained their improvement above medication and placebo groups.

CONC: there is evidence that CBT is at least as effective as medication, and there are no side effects. Psychotherapy appears to have a long term advantage over medication.

EVAL: This is useful as it contained a control group

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Interpersonal psychotherapy

Interpersonal psychotherapy was first proposed by Klerman et al (1984) and is based on the assumption that depressed people have difficulties with interpersonal relationships. It attempts to allievate symptoms and improve interpersonal functioning, particularly with significant others. It does this by 'clarifying, refocusing and renegotiating the interpersonal context associated with the onset of depression' (Weissman and Klerman, 1990). IPT is a brief therapy, lasting for 12 to 16 weeks, sessions are usually weekly and one to one. The therapy is foucused on the 'here and now' rather than the historical origins of problems. There are three phases:

  • The initial phase - lasts for a couple of sessions, is for assessment and the formulation of treatment goals. The client is taught the 'sick role' ie, learns about the illness and although the client is encouraged to be active, theres no expecation of normality.
  • The second phase - identifies interpersonal problems that are thought to contribute to depression. Info is gathered in relation to areas commonly associated with depression (inc. gried, role disputes and role transitions) and interpersonal deficits.
  • The termination phase - focuses on consolidating learning and on preparing for the use of skills in future difficulties.

The therapist uses nondirective exploration, through gathering information, insight and role playing to encourage emotional expression and teach more effective communication methods.

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Eval of cognitive treatment

  • Robinson et al (1990) reviewed 57 studies and found CBT as being more effective than either psychotherapies or drug therapy, post treatment patients' depression levels remained significantly reduced.
  • Research into the efficacy of CBT over other forms of therapy has mixed results, and studdies often have methological errors. However, the study by Elkin was a large scale study with excellent controls, and found similar improvements across psychotherapies.
  • Cognitive therapies have been criticised on ethical grounds - the therapist decides what thoughts and behaviours are acceptable, and then attempts to change what the client believes.
  • Cognitive therapy isn't suitable for bipolar and works best with motivated people
  • IPT is not as well researched as CBT and there is little evidence to evaluate how, or if, it is effective. But Frank et al (1990) found patients recieving IPT stayed well for twice as long as those recieving a placebo
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