THE CLINICAL APPROACH - DEPRESSION

Question 1

What are the symptoms of unipolar depression?

Answer 1

Affective (mood) symptoms - feel sad, empty, hopeless, tearful, irritable, ma experience anhedonia (lack of enjoyment to pleasure in previously enjoyed activities), find it difficult to make decisions, suicidal thoughts
Both the DSM 5 and ICD 10 specify depressed mood and loss if interest/pleasure as key symptoms
Bodily symptoms - reduced energy levels or fatigue, changes in appetite (weight loss or gain of more than 5% in body weight), insomnia or hypersomnia, loss of sex drive
Cognitive symptoms - negative thoughts, blame themselves for things out of their control, lack of self-confidence, feel incompetent, recurrent thoughts of death
Behavioural symptoms - fatigue and loss of pleasure can lead to social withdrawal, signs of psychomotor retardation or agitation

Question 2

What did The Adult Psychiatric Mobility Survey find about depression?

Answer 2

found that in 2013, the prevalence of diagnosable depression was 3.3 per 100 population, up from 2.7 in 2007
It’s more common in women

Question 3

Why is depression difficult to diagnose validly?

Answer 3

has a high comorbidity
22.99% of women undergoing treatment for cancer also experience depression

Question 4

What is reactive depression (exogenous)?

Answer 4

depression that occurs as a reaction to a major life event (eg death of a loved one)
Previously, the DSM 5 cautioned psychiatrists against diagnosing depression if they’d experienced loss within the last two months
Dr Ronald Pies argues that you can differentiate depression and grief, and that they can also be experienced at the same time

Question 5

What is endogenous depression?

Answer 5

no external precipitating event or factor that appears to cause the condition, so it is presumed to stem from an internal process

Question 6

What are features of unipolar depression?

Answer 6

International studies show that lifetime prevalence for one or more major depressive episodes is 15% (10% for males, 20% for females)
Women may be more likely to develop depression because of different life events (eg pregnancy, periods, menopause) with change in hormones
Most commonly develops in early adulthood, yet older people are also vulnerable
Approximately 25% of all suicides involve people aged 65+, which could be because they start to lose loves ones aroundd them
Single people are at a higher risk than married people
Could be due to being lonely and no one to confide in, low self esteem and financially more strain
Risk factors: temperament, negative events in childhood, having a close relative with depression, and suffering from another disorder

Question 7

What is the evaluation for diagnosing depression?

Answer 7

The DSM 5 is unreliable at diagnosing depression, shown by Reiger who did field trials of the DSM 5 and the kappa statistic (measure of agreement) was just 0.28 for major depressive disorder (only agreement for 4-15% of times)
However it’s possible to use the DSM 5 in a more reliable way, as real world clinical diagnoses are based on semi-structured interviews - Shankman found ‘substantial reliability when using the SCID-5 to diagnose severity of major depressive disorder under the DSM 5 criteria
Many cultures do not recognise depression as a disorder or it is experiences in different ways, Watters says that some people may have ‘stomach pain’ or ‘tightness in the chest’ depending on whether they’re Chinese, Iranian or Korean - in these cultures, depression manifests itself in different ways
However the DSM 5 does include a section on how to conduct cultural formulation interviews which gives information about a person’s cultural identity and how that can affect their expression of signs and symptoms

Question 8

What are the key points of the monoamine hypothesis?

Answer 8

Argues that depression is the result of a chemical imbalance (low levels) of monoamine neurotransmitters - specifically serotonin and noradrenalin
These neurotransmitters control the brain’s emotional centres and are especially important as they form many connections with other parts of the brain
The low levels of the monoamine neurotransmitters cause low activity in the connections of the brain, meaning the activity slows down
Low levels leads to insufficient levels of stimulation

Question 9

What is MAOA?

Answer 9

an enzyme that degrades serotonin at the synapse
Early antidepressants were MAOA inhibitors as they stopped the MAOA from binding to the synaptic cleft, therefore preventing the serotonin from being degraded (stopping there from being low levels)

Question 10

Why was the monoamine hypothesis challenged and how did this lead to it being developed?

Answer 10

However, the hypothesis was challenged as being too simplistic because the MAOA inhibitors didn’t increase the availability of monoamine neurotransmitters so there had to be more to depression than low levels of serotonin and noradrenalin
Research argued that the receptor sites should compensate and become more sensitive to serotonin but they didn’t
In depression, serotonin and noradrenalin postsynaptic receptors become even more sensitive to reduce stimulation from serotonin than normal, therefore it wasn’t just low levels of serotonin but the fact the receptor sites were even less sensitive to serotonin in the case of depression
After a message has been sent over a synapse, serotonin is usually reabsorbed by the nerve cell - by preventing re-uptake, more serotonin is available to pass further messaged between nearby nerve cells
This increases serotonin levels in the brain, allowing more messages to pass between nerves, improving mood

Question 11

What are SSRIs?

Answer 11

drugs called selective re-uptake inhibitors, they work by blocking the re-uptake of serotonin at serotonin receptor sites (at the junction of neurons)
This means there is more serotonin to be absorbed by serotonin receptors on the post-synaptic terminal button

Question 12

What are strengths of the monoamine hypothesis?

Answer 12

It has resulted in the development of drugs to treat depression, which has improved the quality of life and reduce distress in patients experiencing depression by treating both noradrenalin and serotonin levels
SSRI drugs, specifically Prozac and Seroxat, seem to work by blocking the re-uptake of serotonin supporting the monoamine hypothesis
Patients with clinical depression have lower levels of serotonin metabolites (by-products) in cerebrospinal fluid than controls, strongly suggesting that they have lowered levels of serotonin
MDMA (ecstasy) works by increasing levels of serotonin at the synapse, and is associated with powerful feelings of euphoria - showing that reduced levels are implicated in depression

Question 13

What are the weaknesses of the monoamine hypothesis?

Answer 13

Low levels of monoamine neurotransmitters may provide a biological correlation with depression, but it doesn’t necessarily establish a causal relationship (cause could be psychological not biological)
Research noted that postsynaptic receptors were more responsive when antidepressants that increased serotonin levels were used, which they thought implied depression has a biological cause however the drug could work by correcting a biological process that is disturbed by a psychological factor (treatment aetiology fallacy)
Depression is too complex to be explained by just serotonin levels, and individual differences in release patterns and sensitivity can be a factor
MRI scans have shown physical differences in the brains of depressed people (eg smaller hippocampus) suggesting it could be that drugs that increase serotonin, increase the hippocampal mass and this is what lifts the mood

Question 14

What is the cognitive explanation of depression?

Answer 14

Beck argues that irrational thinking and cognitive distortions (way we think about things has been altered, so can’t see it the same as everyone else) can contribute to a person’s cognitive vulnerability to depression
Features of cognitive vulnerability:
The cognitive triad
Faulty information processing
Negative self schema

Question 14

What did Haase and Brown find about the monoamine hypothesis?

Answer 14

SSRIs don’t help everyone shown by the fact that only ⅓ of users were in full remission, suggesting the monoamine hypothesis isn’t the only explanation of depression

Question 15

What is the cognitive triad?

Answer 15

Depressed people make three major types of cognitive error:
The self - believe they are worthless, a failure, unattractive, etc (low self esteem)
The future - view the future in unavoidable negative ways
The world - perceived the world around them as hopeless (eg friend cancels a party, they see it as a sign no one likes them)
Becker developed the cognitive trias into cognitive distortion theory which argues that people with depression regularly engage in maladaptive, distorted, dysfunctional thinking and cognitive styles
They grouped these thought styles into nine categories, one example being excessive responsibility (if anything goes wrong, they blame themselves)

Question 16

What is faulty information processing?

Answer 16

Depressed people tend to selectively attend to the negative aspects of situations and ignore the positive ones, therefore there is a tendency to overestimate the downside
We are all illogical in that we often attend to some stimuli and not others, and we often jump to the wrong conclusions based on insufficient evidence or an irrational interpretation of the information to hand
Depressed people are irrational/illogical in a specific way, they attend to negative information and stimuli and reach the most negative conclusions

Question 17

What is a negative self schema?

Answer 17

Schemas are mental scripts/packets of information that contain our knowledge, perceptions and beliefs about various aspects of the world
Self schemas are scripts that contain all the information that relates to ourselves
Depressed people acquire a negative set of self beliefs in childhood as a result of negative or critical parents
With a negative self schema, interpreting new information about themselves positively can be difficult (eg I got a promotion because there was no one else available and they were desperate)
Two types of schema that operate in depression:
Negative interpersonal schema - a generalised representation of self/other relationships developed during childhood through interaction with attachment figures, lead to an unrealistic view of relationships
Schema based on personal achievement and based on a perception to failure to achieve personal goals - a sense of personal underachievement and a series of unhappy life events and experiences, lead to depressogenic schema (a set of dysfunctional thoughts and beliefs that lead to depressive symptoms)

Question 18

What are strengths of the cognitive explanation of depression?

Answer 18

Depression people often display faulty information processing and negative thinking (although might be a symptom not a cause), yet can test people with different levels of cognitive vulnerability and see who develops depression
CBT has been shown to be very effective, as Hollon et al found between 50-60% of depressed clients treated with CBT showed improvement
if the therapy based on cognition works, that implies that the cause must be related to cognition
cognitive techniques are a part of a successful treatment for depression, which implies that faulty information processing may be at the root of the disorder
Perez et al, Evans et al, D’Alessandro

Question 19

What did Perez et al find?

Answer 19

compared sufferers of major depression with a non-depressed control group and found that the depressed group paid significantly more attention to the sad words in the stroop task, suggesting that depressed people have a more negative cognitive style
Paying more attention to unhappy stimuli is called negative attention bias, the control group had a sad mood induced by means of sad music and recalling unhappy memories

Question 20

What did Evans et al find?

Answer 20

measured self belief of 12,003 women who were 18 weeks pregnant and those with the most negative self schema were more likely to get depressed

Question 21

What did D’Alessandro find?

Answer 21

students’ negative views about their future were strongly associated with an increase in depressed mood
Those with dysfunctional beliefs about themselves who did not get into their first choice college then doubted their futures and developed symptoms of depression

Question 22

What are weaknesses of the cognitive explanation of depression?

Answer 22

Cognitive theory fails to explain the variety of experience in depression such as gender bias (twice as many women suffer from depression than men yet there is no evidence to suggest that women have more negative schemas than men)
Maladaptive thinking may be the result and not the cause of depression, shown by the fact there is little evidence that negative thinking is present before the onset of depression
Some people are just ‘defensive pessimists’ who tend to be overly pessimistic about stressful events which can be beneficial for such individuals as it allows them to be prepared for negative outcomes (not disappointed)
Depression might have a useful evolutionary purpose
The diathesis stress model would suggest there is no one single cause of depression suggesting that the cognitive explanation is too reductionist and doesn’t look at the complex make up of individuals which could make them more prone to depression form a biological point of view
Seligman, Dr Paul Keedwell

Question 23

What did Seligman find about depression?

Answer 23

found that pessimists were less prone to depression than optimists after experiencing negative life events, such as death, as they spent more time bracing themselves mentally for unpleasant possibilitieS

Question 24

What did Dr Paul Keedwell argue?

Answer 24

that mild and moderate depression can help people to reasses their lives, by considering what has caused their depression
Surviving a depressive episode can lead to greater resilience, increased empathy and even lead to enhanced creativity

Question 25

What is the biological treatment of depression?

Answer 25

Antidepressants don’t cure depression but could help the patient to overcome it without experiencing symptoms
Antidepressants are agonists, they work by increasing levels of serotonin and noradrenalin (monoamine neurotransmitters)
Antagonist drugs block/inhibit activity which isn’t what we want
As a result, more of the neurotransmitter is available in the synapse for longer, thereby increasing activity in the affected neural pathway
Typical antidepressants are agonists working mostly on serotonin levels (MAOI inhibitors, tricyclics, SSRIs)
Atypical antidepressants are drugs which also target other neurotransmitters, such as noradrenalin and dopamine, as well as serotonin and also have antagonist effects (NaSSAs)

Question 26

What are MAOI inhibitors?

Answer 26

Have been around since the 1950s and include phenelzine
After normal neurotransmission across the synapse and the re-uptake of serotonin, the excess serotonin is degraded by the MAOI enzyme and is reabsorbed back into the cell
MAOI inhibitors work by preventing the degradation of neurotransmitters so they remain in the synaptic cleft ready for the next message to be passed
They are not selective so raise dopamine and noradrenalin levels as well as serotonin
Can cause severe side effects, for example dry mouth, blurred vision, constipation, drowsiness, dizziness, weight gain and excessive sweating
The user must also be careful which foods they eat as the drug can interact with foods such as cheese, pickles or wines
They can also interact with many common drugs and cannot be used with SSRIs
Tend to be a last resort if other drugs fail to work

Question 27

What are tricyclics?

Answer 27

Been used since the 1950s and include amitriptyline
They work by preventing serotonin and noradrenalin from being reabsorbed after they have crossed the synapse
They have many side effects like dry mouth, blurred vision, constipation, drowsiness, dizziness, weight gain and excessive sweating
Now only used if SSRIs don’t work

Question 28

What are SSRIs as a biological treatment of depression?

Answer 28

Developed in the 1980s and include fluoxetine
Serotonin in the synapse is normally removed by re-uptake, in this process the serotonin molecules are actively pumped back into the presynaptic neuron via the serotonin reuptake transporter
These drugs work by blocking the action of the serotonin reuptake transporter so that more serotonin is left in the synaptic cleft meaning it is available for constant use
Have fewer side effects, are far safer if an overdose is taken and has less interaction with other drugs (side effects can include nausea, insomnia, agitation, loss of appetite and sexual dysfunction)
Usually the first choice for doctors to treat depression, but do not work for everyone
NRIs work in the same way as SSRIs but target noradrenaline rather than serotonin, and SNRIs target both serotonin and noradrenalin

Question 29

What are NaSSAs?

Answer 29

Noradrenergic and specific serotonergic antidepressants, that were developed in the 2010s
They are used where SSRIs and SNRIs are not effective
They have the same agonist action, inhibiting the reuptake of serotonin and noradrenalin, but to a lesser extent
They are also antagonists as they act to block one specific serotonin receptor and one noradrenalin receptor
They have fewer side effects but can include dry mouth, dizziness, light headends and can affect sleep, appetite and bowel movements

Question 30

What are strengths of the biological treatments of depression?

Answer 30

The side effects can be managed with other drugs, making it more tolerable
Issues with MAOI inhibitors such as interactions with foods can be controlled by ensuring they have a good diet
Drug therapy may be required before patients can access and effectively utilise other treatments such as CBT
The Royal College of Psychiatrists, Ciprani et al, Pinquart et al

Question 31

What did The Royal College of Psychiatrists find?

Answer 31

reported that only 50-60% of people treated with antidepressants showed improvement compared to only 25-30% of those treated with a placebo

Question 32

What did Ciprani et al find?

Answer 32

all the drugs to be more effective than the placebos, showing that they do work as an effective treatment for depression

Question 33

What did Pinquart et al find?

Answer 33

concluded psychological therapies were more effective but drugs are cheaper and they avoid the waiting lists

Question 34

What are the weaknesses of biological treatments of depression?

Answer 34

Many antidepressants have unpleasant side effects, which can effect the ability of the patient to continue taking the drug
They relieve the symptoms of depression, but do not address the cause, so treat the biological factors but not the root causes
Should be used in combination with psychological therapies
Cognitive behavioural therapy has been shown to be very effective with mild to moderate depression - addresses the cause of depression which could lead to less chance of relapse
Kirsch et al, Harriman

Question 35

What did Kirsch et al find?

Answer 35

that antidepressants were no better than placebos in reducing symptoms for mild to moderate depression

Question 36

What did Harriman find?

Answer 36

some SSRIs increased the risk of suicide ideation and behaviour as well as hostility, and for older people they increased the risk of fractures - lower compliance rates

Question 37

What is a non-biological treatment of depression

Answer 37

CBT is a treatment based on Beck’s cognitive explanations of depression and aims to address the negative thinking a person may have

Question 38

What are the key points of CBT as a treatment of depression?

Answer 38

Can be one-to-one therapy, group therapy, or computerised therapy and typically sessions last 50-60 minutes, weekly or fortnightly for an average of 10 sessions
It is present and future orientated, by identifying thoughts and feelings in the present, not analysis were they may have origination like psychoanalysis
The aim is to reduce the symptoms of emotional disorders by challenging and changing dysfunctional beliefs and attitudes
First session typically involves setting the scene about what is expected, and the therapist and client work together to assess various aspects of the client’s functioning
Sessions will aim to identify what triggers depressive symptoms, identifying the thoughts they’re having, the feeling these thoughts lead to and the behaviour/physical symptoms they experience as a result
The therapist challenges the validity of the thoughts the client is having, for example they could be asked to find evidence that goes against their thoughts
Clients would be encouraged to keep a mood diary and reflect on their thoughts and their ability to deal with the emotions generated by these emotions

Question 39

What did Beck et al describe as the stages in cognitive therapy for depression?

Answer 39

Therapist teaches the client to identify and monitor negative automatic thoughts
The client’s response is challenged
Tasks that demonstrate the irrationality of the client’s beliefs are also used
The dysfunctional beliefs are then used to identify the individual’s core beliefs which correspond to their negative self schema developed in early life
The client is encouraged to plan ways to test the new, healthy and more flexible beliefs in everyday life

Question 40

What are the strengths of CBT as a treatment for depression?

Answer 40

CBT is practical and problem solving in nature, but is also empowering for the individual as they can learn and control excessively negative thoughts and emotions which can detrimentally affect their lives
CBT is very accessible, often free and a course of treatment can be successful in 10-12 weeks
It is widely regarded as the most appropriate first treatment for depression as there is considerable evidence for its effectiveness and little evidence for adverse side effects
Butler and Beck, Kuyken et al

Question 41

What did Butler and Beck find?

Answer 41

that Beck’s cognitive theory was highly effective for anxiety and depression and the relapse rates for depression was only 29.5% following CBT compared to 60% with antidepressant drug treatment

Question 42

What did Kuyken et al find?

Answer 42

that CBT was more effective than antidepressants in preventing relapse and improving the quality of life

Question 43

What are the weaknesses of CBT as a treatment for depression?

Answer 43

Holmes noted that a study by the National Institute for Mental Health showed that CBT was less effective than antidepressant drugs and other psychological therapies
There is insufficient evidence for the long term effectiveness of CBT, as evidence mainly comes from trials of highly selected patients with only depressive symptoms
Like biological treatments, there are problems with cause and effect (eg maladaptive thought processes may be the result and not the cause of the psychological disorder) therefore may not provide a cure for depression, but manages the symptoms
For it to work, the client has to have insight into their cognitions and beliefs