Clinical Psychology Flashcards

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1
Q

ICD-11 diagnostic criteria for schizophrenia

A

Positive Symptoms (CORE symptoms) - an addition to/distortion of normal experience:
- Persistent delusions - convinced beliefs that a patient holds, which are not based in reality. e.g. falsely believing that someone is out to harm you.
- Persistent hallucinations - sensory experiences e.g. auditory hallucinations (hearing voices) or visual hallucinations (seeing a dead relative, etc).
- Thought disorder - an inability to think and speak in an organized manner.
- Experience of influence, passivity or control - the belief that your thoughts or actions are influenced or controlled by someone or someone else.

Negative Symptoms (further diagnosis) - level of functioning is being taken away:
- Avolition - lack of motivation
- Flattened affect (blunted emotional expression)
- Impaired cognitive function (reduced memory or attention)
- Catatonia (lack of movement or speech)

Age of onset
Early onset:
- Males - early to mid-20s
- Females - late 20s

Late onset:
- Females, more commonly - 40s

Prevalence between genders is closely similar - about 0.3-0.7% = not a significant gender difference

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2
Q

Types of Delusions

A
  • Persecutory: a strongly held beliefs that you are in danger or are being conspired against, and being pursued by others intending to harm you.
  • Grandeur: a strongly held belief that you are someone with special abilities or special powers, e.g. that you are a superhero
  • Delusions of reference: a strong held belief that events in the environment are related to you and have significant meaning. Things are a sign of prophecy or what to expect of the future, e.g. the belief that a TV programme is talking about you.
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3
Q

Aneja et. al (2018) - the study

A

Aneja et al (2018): carried out 3 case studies on early-onset schizophrenia before the age of 18 years.

Background:
- A boy from a troubled home with an aggressive father, began to show a decline in his academic studies and general behavior at 10 years old after parents’ divorce. Thus, he and his mother moved in with his grandparents and changed schools
- At 12 years old, he heard voices and over time, he believed his mother and other people were communicating with the voices.
- His behavior grew more erratic: muttering to himself and shouting at people who were not there.
- His schoolwork suffered and by 12 yrs, he stopped attending school at all. He was irritable, sad and often got into trouble for fighting.
- He barely slept and his level of self-care declined dramatically
- He was admitted to hospital several times and given a range of medications to attempt to control his worsening symptoms.
- The boy was diagnosed with early-onset schizophrenia and was released from hospital, on medication that kept his aggressive behaviors under control.
- He still suffered from negative symptoms e.g. apathy, social withdrawal and a resistance to going to school.

Symptoms:
- Spoke very little
- Poor sleep and self-care
- Preferred to be alone, away from other people
- Lack of insight into his condition
- Hearing voices that teased him
- Suspicious of his mother
- Muttered, laughed, and shouted at unseen others

Treatment:
- Sodium valproate (drug often treating BPD)
- His mood and behavior improved for a while but later became worse again
- Diagnosed with very-early-onset schizophrenia (VEOS).
- His aggressive and violent outbursts increased, and often admitted to hospital for his safety.

Methodological strengths and weaknesses
- STRENGTH: It has a detailed case history. The amount of detail highlighted that the boy had exhibited prodromal symptoms. This increases the validity of the schizophrenia diagnosis.

  • WEAKNESS: the case study is limited to 1 child and does not represent other cultures. India has stigma around people with mental disorders (Thomas, 2018). This means there were little community support and could have worsened symptoms due to family stress. This does not represent other VEOS in other cultures.
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4
Q

Aneja et. al (2018) - I&D

A

Application to real life
- it is difficult to use the ICD-11 diagnosis due to symptom overlap, e.g. catatonia and hallucinations can be experienced by ppl w/ depression or be caused by drug withdrawal, stress and sleep deprivation.
- So, different clinicians give different diagnoses, which decreases the reliability of the schizophrenia diagnosis.
- however, ICD-11 only requires to display symptoms for 1 month while DSM-5 requires 6 months, which means people could access treatment early.
- early treatment correlate with positive outcomes (Patel, 2014).
- ICD-11 removes a set of subtypes to classify schizophrenia e.g. catatonic, hebephrenic. The subtypes were primary symptoms a person displayed but symptoms often change.
- so, ICD-11 replaces the subtypes with dimensional descriptors and doctors rate each category of symptoms based on severity.
- this help access more treatment.

Use of children in psychological research
- the boy is 14 yrs old and so, he cannot give his informed consent.
- This meant that his mother had to give his consent on his behalf to participate in Aneja’s study and for him to write up a published case study.
- however, children would have been asked for their consent typically, and the study wouldn’t have proceeded without his cooperation.
- researcher must’ve found ways to make the study more accessible for the boy to know his rights to withdraw and how he would his data to be used.

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5
Q

Freeman’s Aim

A
  • To investigate whether participants without a history of mental illness have thoughts of a persecutory nature in VR
  • To investigate whether there are cognitive or emotional factors that predicted the likelihood of persecutory ideation being shown in VR
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6
Q

Freeman’s sample

A
  • 12 males and 12 females, all students/admin staff from UCL
  • mean age: 26 years
  • no history of mental illness
  • recruited via volunteer sampling: responded to ad within UCL
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7
Q

Freeman’s hypothesis

A

a small number of people will have thoughts of a persecutory nature in VR,
and these people will have higher levels of emotional distress and paranoia

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8
Q

Freeman’s research method

A

lab experiment: participants were trained on how to use the VR equipment, and entered a virtual environment (a library space) for 5 minutes

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9
Q

Freeman’s procedure

A
  1. Participants trained in how to use VR equipment, including:
    * Lightweight headgear to track head position
    * Handheld joystick to allow participant to move around the virtual space
  2. Half the participants completed the:
    * BSI (53-item questionnaire) to assess mood, anxiety and psychotic symptoms in the last 7 days
    * Two 20-item self reports (Spielberger State Anxiety Questionnaire & Paranoia Scale), to measure ideas of persecution and reference
  3. All participants completed the VR task: exploring a virtual library, where 5 avatars sat in 2 small groups (a three and a pair), occasionally smiling, looking over and talking to one another
  4. Participants were asked to “Explore the room and try to form some impression of what you think about the people in the room, and what they think about you”
  5. 5 mins after, all participants ‘exited the room’ and completed the questionnaires outlined above (half of them for the 2nd time)
  6. Participants were interviewed about their experiences, including any feelings of distress
  7. A clinical psychologist watched the videotaped interviews, rated them out of 6 for indications of persecutory ideation

Examples of items in Paranoia questionnaire:
* They were hostile towards me.
* They were laughing at me.
* They were watching me.

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10
Q

Freeman’s findings

A
  • Mean paranoia score: 31.8 (minimum: 20, maximum: 100)
  • no significant difference in paranoia scales between males and females
  • positive correlation between persecutory thoughts in questionnaires & the interviews
  • Most people had positive beliefs about the avatars, but some had more negative beliefs
  • VR persecutory ideation was positively
    correlated with paranoia, interpersonal sensitivity and
    anxiety,
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11
Q

Freeman conclusion

A
  • Emotional processes linked to anxiety and interpersonal sensitivity directly contribute directly to development of perseuctory ideation,
  • Showing that VR holds ‘great promise’ not only as a tool for enhancing theoretical understanding, but also to help individuals evaluate and reduce persecutory ideation
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12
Q

Psychological explanation of schizophrenia

A

a. Frith noted that schizophrenic people might have a deficient ‘metarepresentation system’ (system that makes people able to reflect on thoughts, emotions and behaviors).
* Could also be linked to theory of mind, as it controls self-awareness and how we interpret actions of others
* Those showing more negative symptoms might have a dysfunctional supervisory attention system (responsible for generating self-initiated actions)
* In a study, when ppts were asked to do things, such as name as many different fruits as possible, those with schizophrenia (with negative symptoms predominant) had great difficulty managing this

b. Frith noticed that in some people with schizophrenia, inner speech may not be recognised as being self-generated
* Therefore, when they hear ‘voices’, it’s their inner voice, but they’re unaware it’s themselves producing inner speech and believe it’s someone else
* Johnson et al. tested cognitive abilities of 99 people with schizophrenia, and 77 healthy controls
* Seen that people with schizophrenia performed worse across all cognitive tests, including those for working memory (involves tasks like dealing with inner speech)
* This might be the core determinant of overall cognitive impairment in schizophrenic people

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13
Q

Psychological treatments of schizophrenia

A

Cognitive behavioral therapy (CBT): aims to change or modify people’s thougths and beliefs, and also change the way they process information

Intention of CBT for schizophrenia: to help patients make sense of the psychotic experiences, and reduce the negative effects of the conditions, and any distress they may be feeling

  • Patients may be given help to understand that their thoughts and views aren’t facts, then given help with assessing them
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14
Q

Sensky et al. (CBT)

A

Aims: to compare the efficacy of one-to-one CBT and a befriending intervention for people with schizophrenia
Procedures:
a. Patients were recruited if they fitted the following criteria:
* Aged 16-60 years
* Had a diagnosis of schizophrenia according to DSM and ICD
* Symptoms persisting for at least 6 months
* Showed no improvement with medications
* Didn’t abuse alcohol or drugs

b. There were 90 qualifying participants, randomly assigned to one of two groups:
* A manualised CBT specifically designed for schizophrenia
* A ‘befriending’ intervention

c. All had been prescribed a daily dose of at least 300mg of chlorpromazine for at least 6 months, but still experienced positive symptoms

d. Treatment was delivered by 2 nurses who received regular supervision
e. They were assessed by ‘blind raters’ before the treatment started (to establish a baseline), post-treatment (up to 9 months later), and 9 months after treatment ended (follow-up)
f. CBT sessions: therapists worked collaboratively with the patients to understand the development of their positive and negative symptoms, and to reduce distress
g. Befriending: received same duration of interaction with a therapist. Therapists were empathic and non-directive. Talked about hobbies, sport and current affairs

Findings:
* Both interventions resulted in significant reduction in both negative and positive symptoms of schizophrenia, and depression scores on Comprehensive Psychiatric Rating Scale
* However, at the follow-up, those who had CBT continued to improve, whereas befriending group didn’t

Conclusions:
CBT is effective at reducing symptoms of schizophrenia in those previously resistent to antipsychotic medication

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15
Q

Biochemical explanations for schizophrenia: the dopamine hypothesis

A

Dopamine hypothesis

Dopamine excess as cause

  • 1960s - Researchers proposed that schizophrenia was caused by an excess of the neurotransmitter dopamine - in the brain’s limbic system and mesolimbic pathways (Carlsson and Lindqvist, 1963).
  • This excess can be caused by many factors, e.g. excess L-Dopa, the substance that dopamine is made from.
  • Synapses using dopamine may also be overactive due to differences in the number of receptors on the postsynaptic cell.
  • New evidence caused scientists to update this explanation. For example, many people who were taking dopamine antagonists e.g. chlorpromazine still suffered with -ve symptoms and some experienced no improvement.

Dopamine deficiency as cause

  • 1990s - Researchers suggested that a lack of dopamine in the prefrontal cortex and mesocortical pathways may explain the negative and cognitive symptoms (Davis et al., 1991).
  • Symptoms e.g. disorganised thinking and speech could certainly result from problems with dopamine regulation as this neurotransmitter is important for shifting and directing attention.
  • However, new evidence revealed that the updated hypothesis was still over-simplified.
  • Overactivity in the mesolimbic pathways was thought to result from excess D2 dopamine receptors and/or low levels of the enzyme beta-hydroxylase, which breaks down dopamine.
  • However, in 2006, Arvid and Maria Carlsson proposed the dopamine deficiency hypothesis, suggesting that the brain compensates for low levels of dopamine by increasing the number of receptors on the postsynaptic cell.
  • This process is known as upregulation.
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16
Q

Biochemical explanations for schizophrenia: genetic explanations

A

Genetic explanations

Classic family and twin studies

  • there is a strong argument for the heritability of schizophrenia.
  • the concordance rate (consistency) for monozygotic (MZ) twins is 42% but only 9% for dizygotic (DZ) twins (Gottesman and Shields, 1966).
  • Since the siblings in MZ and DZ groups were raised in the same household, the higher concordance rate in MZ twins was thought to be due to the greater amount of shared DNA.
  • Hilker et al 2017 carried out a twin study with over 30k twin pairs, using several Danish registers.
  • They looked at related disorders and diagnosis of schizophrenia
  • Hilker et al concluded that heritability of schizophrenia was 79%

Adoption studies

  • Adoption studies separate influence of genetics and environment
  • This is achieved by comparing a child raised by an adoptive family with their bio parent who they are not raised by
  • Tienari et al 2000 found schizophrenia in 6.7% of adoptees w a bio mother w schizophrenia, compared to just 4% of a control group (adoptees born to mothers w/o schizophrenia)
  • This suggests that there is a genetic influence in the dev of schizophrenia.
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17
Q

Describe the Biochemical Treatment of Schizophrenia

A

Typical Anti Psychotics
Dopamine blockers that prevent dopamine from bonding to the receptor that thus reduces dopamine activity (called dopamine antagonists)
– This therefore reduces the positive symptoms of schizophrenia (hallucinations and delusions)
– The downside of typical antipsychotics is that there are many side effects.

Atypical antipsychotics:
– These block both dopamine and serotonin receptors
– The have a lower risk of side effects
– Shown to be more effective for ‘treatment-resistant’ patients

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18
Q

Evaluate the Biochemical Treatment of Schizophrenia

A

Efficacy:
– Antipsychotics have been studied through randomised control trials (RCT) that are typically double blind placebo controlled and have consistenly shown:
50% of those taking antipsychotic showed significant improvement
30-40% showed partial improvement
– However, a significant minority showed little to no improvement in their functioning.

Side effects:
– Side effects can be unpleasant, debilitating or even fatal
– Dizziness, drowsiness, restlessness
– Nausea, constipation, excessive weight gain
– Uncontrollable spasms and abnormal movements of the face and body (tardive dyskenesia)

19
Q

Describe the biological treatment of schizophrenia - ECT

A

ECT (Electron Convulsive Therapy)
– Involves purposefully inducing a seizure by delivering electrical pulses to one or both sides of the brain
– Pulses are 70-150 volts and last up to one second
– Treatments usually undergo 6-12 sessions
Two to three times a week during treatment period
– Or at longer intervals as ‘maintenance sessions’ to prevent symptom relapse
– Patients are typically given muscle relaxants so that the seizure does not harm the patient
– The theory as to why ECT has an effect is that it affects post synaptic responses to central nervous system transmittors
– ECT can be effective when fast, short-term improvement of severe symptoms is needed.

20
Q

The diathesis-stress model

A

The diathesis-stress model suggests that some people are predisposed to psychotic disorders (due to genetics of adverse childhood experiences) but only developed symptoms when faced with situational stressors e.g. divorce or death of loved one. So, it is not 100% concordance rates.

21
Q

ICD-11 symptoms for Major Depression Disorder (unipolar)

A

Symptoms:
Changes in Mood (unipolar)
- Long period of feeling empty, sad, hopeless and despair
- Loss of interest in enjoyable activities nearly everyday
- Impairs ability to function normally
- Difficulty concentrating, excessive feelings of worthlessness or guilt
- Recurrent thoughts of death
- Changes in eating and sleeping patterns

22
Q

ICD-11 diagnostic criteria for Major Depression Disorder (unipolar)

A

Diagnostic criteria
- Must never had a manic, mixed or hypomanic episode
- A depressive episode of at least 2 weeks of daily depressed mood and decrease in interest in activities

Duration:
1 episode depressive disorder
The presence of 1 depressive episode w/o history of previous episodes

Recurrent depressive disorder
At least 2 depressive episodes separated by several months or more

23
Q

ICD-11 symptoms for Bipolar Disorder

A

Changes in mood:
- Long period of feeling empty, sad, hopeless and despair
- Loss of interest in enjoyable activities nearly everyday

Manic symptoms:
- Long periods of feeling euphoric or ‘high’
- Rage, irritability, and feeling of increased energy
Easily distracted, racing thoughts
- Sudden interest to take on new activities
- Overconfidence in one’s own abilities
- Rapid speech
- Sleeping less
- Engaging in risky behavior (promiscuity, drugs, gambling)

24
Q

ICD-11 diagnostic criteria for Bipolar Disorder

A

Duration:
- the person may alternate between depressive and manic episodes that last a week or more
- they may experience mixed episodes where aspects of both mania and depression may be apparent within the same day or week.
- BPD is characterised by lability of mood -> the changeability and intensity with which moods may be experienced and expressed.

25
Q

ICD-11 BPD type 1

A
  • At least 1 manic or mixed episode
  • Manic episodes last at least 1 week
  • Mixed episodes consist of 2 weeks -> mixture of manic and depressive episodes
  • Depressive episode consist of at least 2 weeks of daily depressed mood and decreas in interest in activities
26
Q

ICD-11 BPD type 2

A
  • 1 or more hypomanic episode and at least 1 depressive episode.
  • Hypomanic episodes: less extreme version of a manic episode. This also involves several days of persistent elevated moods and increased irritability.
  • Hypomanic episodes do not necessarily impair ones ability to function.
  • No history of manic or mixed episodes.
27
Q

Beck Depression Inventory (BDI) (Aaron Beck)

A

Beck Depression Inventory (BDI)
- can only be used w/ ppl over the age of 13
- ppl should think abt the **last 2 weeks, inc the day the test is taken when answering.
- 21 items (e.g. self-dislike, pessimism and indecisiveness) and takes around 5–10 mins to complete.
- scored on a 4-point scale from 0 (symptom is absent) to 3 (symptom severe).
- ppt answer best fits how they are feeling recently e.g. last week or last few weeks.
- helps to determine the severity of a person’s symptoms.
Gebrie (2018) found that:
* a score of 14–19 is common in ppl w/ mild depression
* score of 20–28: moderate depression and 29–63 severe depression.
- designed to be used by health professionals.

28
Q

Biochemical explanations - genetic explanations. Twin studies.

A

Twin studies
- Kendler et al. (2006) found a concordance rate of 44% for female monozygotic (MZ) twins vs only 16% for female dizygotic (DZ) twins;
- males - there were concordance rates of 31% for male MZ twins and 11% for male DZ twins.
- the study suggests that depression has a genetic component but that the condition is more heritable in females.
- BPD appears to be more heritable than unipolar depression, returning rates of 62% concordance in MZ twins compared with just 8 per cent for DZ twins (Bertelsen et al., 1977)

29
Q

Biochemical explanations - genetic explanations. Candidate gene.

A

Candidate gene:
- genetic research focused on genes coding for postsynaptic serotonin receptors (e.g. 5-HT2c) and presynaptic transporter molecules (e.g. 5-HTT).
- 5-HTT gene has a polymorphism that results in 2 different alleles.
- Individuals who inherit 2 short alleles have an increased risk of depression than those who inherit either 2 long alleles or mixed alleles.
- Caspi et al. (2003) found that ppl carrying 2 copies of the short allele were more likely to become depressed following a stressful life event
- more negative life events = stronger effect

HOWEVER
- large studies (GWAS) have failed to identify consistent patterns of genes associated w/ depression (Hek et al., 2013).

30
Q

Biochemical explanations - genetic explanations. Monoamine Hypothesis.

A
  • noradrenaline, a neurotransmitter central to the brain’s emotion centres e.g. hippocampus (Schildkraut, 1965).
  • Researchers observed that reserpine (a drug used to treat high blood pressure) causes depression as a side effect.
  • it reduces noradrenaline levels -> proposed that noradrenaline deficiency as potential cause of depression.
  • Researchers also observed another neurotransmitter, serotonin (e.g. Prange et al., 1974).
  • it controlled noradrenaline levels.
  • an imbalance of serotonin = noradrenaline levels drop -> a depressive episode.
  • if serotonin allowed noradrenaline levels to become too high it could lead to manic episodes.
31
Q

Biochemical explanations - genetic explanations. Serotonin and Dopamine imbalances.

A

Serotonin and Dopamine imbalances:
Serotonin levels can **rise and fall bc of:

  • Changes in diet affect mood as serotonin is created from an amino acid called tryptophan
  • Production can also be inhibited by cortisol, a hormone associated with chronic stress (Dinan, 1994).
  • Problems with the receptor sites on the postsynaptic cell could also interfere with the communication between neighbouring neurons.
  • receptors may become oversensitive, when serotonin levels are low.
  • postsynaptic cell may also attempt to compensate this by creating more receptors (upregulation) = more problems
  • serotonin is absorbed back into the presynaptic cell via transporter molecules in the presynaptic cell membrane.
  • Problems with these molecules = serotonin is either not cleared out of the synapse effectively or;
  • if taken back quickly, it can reduce the availability of serotonin molecules for binding on the postsynaptic cell.
  • Serotonin levels may fall if there’s too much monoamine oxidase - an enzyme that breaks down serotonin.
32
Q

Oruc et al.
Research method

A
  • Correlational study - analyses the association between diagnosis of bipolar and specific alleles of 2 candidate genes
    * Researchers examined the frequency of these 2 alleles using blood samples from people with and without diagnosis of bipolar disorder (type 1),
    * Assessed via diagnostic interview and hospital case notes
33
Q

Oruc et al.
Aim

A

to determine whether specific polymorphisms of 2 genes associated with serotonin transmission (5-HT2c and 5-HTT gene) were more common in people with bipolar disorder

34
Q

Oruc et al.
Sample

A

Sample to be studied:
1. All Croatian participants: 25 males, 17 males
2. Aged 31-70
3. Had bipolar disorder (type 1), from psychiatric hospitals in Zagreb, Croatia
4. Average age of onset was 32
5. 16 of the participants had at least 1 first-degree relative (i.e. parent/sibling) with a mood disorder
6. Recruited via opportunity sampling

Control sample:
1. Age-and-sex matched control group: 25 females, 15 males
2. Recruited via opportunity sampling of hospital staff, friends and family
3. None had first-degree relatives with a psychiatric diagnosis

35
Q

Oruc et al.
Procedure

A
  1. Blood samples were analysed to see which alleles participants were carrying for two specific genes:
    * the serotonin receptor 2c gene (5-HTR2c), which codes for a specific type of serotonin receptor
    * The serotonin transporter gene (5-HTT), which codes for the serotonin transporters.
  2. Each gene had two possible alleles; the alleles of the 5-HTR2c gene are called Cys (C) and Ser (S), whilethe 5-HTT alleles are referred to as 1 and 2.
36
Q

Oruc et al.
Findings

A
  1. No significant difference in the specific polymorphisms of interest on either of the genes
  2. There WERE SOME sex differences in allele frequency:
    * A difference in the distribution of the S allele of the 5-HTR2c gene (somewhat more common in heterozygotic females with bipolar disorder than female controls)
  3. Females with bipolar slightly more likely to carry allele 1 of the 5-HTT gene than female controls
37
Q

Oruc et al.
Conclusion

A
  • The 2 specific polymorphisms of genes associated with serotonergenic function didn’t appear to play a major role in increasing risk of bipolar disorder
  • Study suggests that females may be more vulnerable to genetic alterations to serotonergenic transmission
38
Q

Biochemical treatments

A

a) Tricylics

  • improve depressive symptoms by blocking serotonin transporter molecules (SERT) and noradrenaline transporter molecules (NET) in the presynaptic cell membrane
  • This means molecules of these neurotransmitters can’t be reabsorbed and remain in the synapse, ready to bind to postsynaptic receptors
  • Some tricyclic drugs are more effective at binding SERT, and some are better at binding to NET
    * This may be why certain tricyclics work better than others for some people.
  • Tricyclics also bind to a range of different types of receptors, which is why they have certain side effects.

b) MAOIs

  • Stops monoamine oxidase from breaking down monoamines (serotonin, noradrenaline and dopamine), which increases serotonin and noradrenaline levels
    • Increases amount of serotonin available for release into the synapse
    • There are two subtypes of MAO (enzyme), subtype A and subtype B. MAO-A is better at breaking down serotonin and noradrenaline, whereas MAO-B is better at breaking down dopamine. Drugs that inhibit MAO-A seem to have more of an antidepressant effect than those that block MAO-B.
      * Although MAOIs are effective in improving depressive symptoms, they’re only used if other drugs haven’t worked
      * Because they can have harmful interactions with other drugs and certain foods
      * MAOs in the gut break down monoamines from food. When inhibited, tyramine can build up, increasing risk of a stroke
      * Very important for people taking MAOIs to avoid foods with lots of tyramine

c) SSRIs
* Increases the amount of serotonin available to bind with 5HT receptors on the postsynaptic cell
* SSRIs bind to SERT in the presynaptic cell membrane
* Means that serotonin that has been released into the synapse can’t be reabsorbed for recycling, and remains in the synapse
* The reuptake process has therefore been inhibited
* Notable example of SSRI: fluoxetine (Prozac)

39
Q

Beck’s cognitive theory of Depression
(Psych Explanation)

A
  • Depressive thoughts are caused by negative thoughts that develop into dysfunctional core beliefs that form a reality for this person that may be far-fetched/unrealistic for others.
  • This is a form of Cognitive Distortion that causes them to have a negaitve bias and see things in a negative way
  • There is a negative cognitive triad of these kinds of negative thoughts:
  • – Negative views about oneself - “I am worthless”
  • – Negative views about the world - “Everybody hates me because I am worthless”
  • – Negative views about the future - “I’ll never be good at anything because everyone hates me and I am worthless”
  • —- These thoughts feed into one another and can exacerbate (make worse) each other as a vicious cycle of negativity
  • These thoughts are thought to have developed as a result of negative experiences during childhood, leading to negative schema
  • When facing future events/experiences, these schema are activated and they expect things to turn out badly
  • – These schema/beliefs also affect how people interpret information from their future experiences for further processing
  • – Evidence that does not match their beliefs is filtered out and evidence that confirms their negative information is exaggerated (magnified) and the importance of contradictory information is minimised. Eg. “I only got a good grade because my teacher felt sorry for me”
  • Beck beliefed that the invidual’s low mood and physiological symptoms are due to an underlying process of incorrect information processing.
40
Q

Seligman’s Learned Helplessness/Attributional Styles (1960s) (Psych exp)

A
  • Learned helplessness is a state that occurs as a result of a person having to endure an unpleasant situation when they perceive the unpleasantness to be inescapable
  • The theory states that the individual is unable to control the situation and prevent suffering, so they eventually stop trying to resist it.
  • Seligman believed that depression was a direct result of real or perceived lack of control over the outcome of your situation.

After research about learned helplessness was done including one conducted on dogs where they would not try to escape the electric shocks through easily jumped barrier after being conditioned to think they were unavoidable, Seligamn developed the theory of attributional styles

  • He believed that the way we attribute (give reason) for our circumstances can be the cause of depressive symptoms
  • People who are vulnerable to depression make attributions that are internal (that it is their fault (alone)), global (that thus more things are likely to go wrong) and stable (that things will stay bad forever
  • Conversely, people who are unlikely to be dperessed make attributions that are external, specific and unstable

Eg.
More depression vulnerable:
* Inernal: “I wasn’t good enough for them”
* Global: “My friends think it’s my fault, I’m rubbish at my job , I’m going to fail my exams
* Stable: I’m going to be singel forver

Less depression vulnerable:
External: “we weren’t spending enough time together
Specific: “At least I’ve got my friends, my job and I’m doing okay” (The negativity is not spreading
Unstable: I’ll meet someone new when I’m ready (eventually things will change)

41
Q

Supporting Study: Seligman et al. (1988) Aim and Sample

A

Aim: To replicate past study results that showed a correlation between depressive attributional style and severity of depressive symptoms. (How well attributional style could predict depressive symptoms)

Sample: 51 patients with a mood disorder (39 unipolar, 12 bipolar) all coming from the same outpatient clinic with a mix of genders and mean age 36

Control group: Ten participants with no diagnoses

42
Q

Supporting Study: Seligman et al. (1988) Procedure and Results

A

Procedure
* Completed the Beck Depression Inventory (BDI) and Attributional Style Questionnaire (ASQ) which particpants made attributions about 12 hypothetical positive and negative events and rate each one on a seven-point scale for internality, stability and globality
* They then completed 6 months of weekly cognitive therapy (average 22.5 sessions)
* Data collection began with an interview using teh Schedule for Affective Disorders and Schizophrenia (SADS)
* 32 were reassesd within a month of their last therapy session
* 26 were followed up 12 months later

Results
* Positive correlation between depressive attributions for negative events and severity of depressive symptoms before and after therapy
* Scores were lower for pessimism in the non-depressed control group compared to the experimental group
* The greater decrease in pessimism in therapy, the greater improvement in depressive symptoms
* —- These improvements were impressive and table over time
* Link between pessimism scores at the end of therapy and risk of relapse at 12 months
* Attributional style was fairly stable over time in the control group suggesting pessismism is a trait, not an effect of low mood or circumstances.

Conclusions
People with unipolar and bipolar disorder have a cognitive attributional style which favours internal, global and stable attributions of negative events which predicts depressive symptoms in the individual

43
Q

Psychological Treatment: Beck’s Cognitive Restructuring

A

Congitive restructuring is the process of identifying and challenging negative thought processes in order to reduce patient’s reliance on dysfunctional beliefs and practice healthier thought processes.

Some of the techniques used in cognitive restructuring include:
* Psychoeducation – The therapist teaches their client about the link between their thoughts, feeling and behaviour and the problems that can result from their cognitive distortions and unhealthy thinking patterns.
* Homework – Clients are set and must complete homework exercieses between sessions. This could include keeping a thought and feelings diary throughout their week to disucss in the next session; this can help increase awareness of situations that trigger negative thinking
* Socrative Questioning – The therapist will ask questions to help the patient analyse and reflect on their thoughts; they will then seek to highlight alternative explanations for their negative attributions

The main goal of cognitive restructuring is to produce more objective, balanced views of the self, the world and the future.

Cogntive restructuring is typically done between five and twenty weekly sessions that train the person to embed these new thinking strategies into their everyday life.

Gradually they should begin to be able to restructure their own thoughts without support from the therapist

44
Q

Psychological Treatment: Rational Emotive Behaviour Therapy (REBT)

A

ABC Model
* A - Activating Events
* B - Beliefs
* C - Consequences
This was based upon the idea that therapy should be focused on our interpretation of events/situations compared to focusing on the events themselves.