Clinical Psychology

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The 4 D's of Diagnosis

Deviance - behaviour not in the norm. It can be the same for different disorders. Paedophilia is clearly indicated by deviance.

Danger - harm to the individual or others. Can be hard to interpret and comes in different levels. Mental Illness include a 25% danger of unnatural death.

Distress - negative feelings. Hard to measure as people are affected in different ways. Hypocondriasis includes high levels of distress.

Dsyfunction - unsucessful every day behaviour. Several events can cause dysfunnction. Major depressive disorder needs dysfunction to be diagnosed. 

Davis (2009) adds Duration- how long symptoms last. Issues of construct validity. Schizophrenia requires diagnosis that includes duration. 

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The DSM

Created by the Americal Psychological Association, the Diagnostic and Statistical Manual of Mental Disorders (DSM) provides criteria for diagnosis. The most recent version is DSM-5

Brown et al (2014) found overdiagnosis of Anorexia Nervosa using DSM when issues about weight loss and phobia were discussed. 

DSM-5 has changed since the DSM-IV-TR as it left the multi-axial system and now has three sections (contents, codes and emerging models and measures) which aims to harmonise it with the ICD. Changes occur due to updated reserach and changes in attidudes e.g. removing homosexuality as an illness. Each update works on validity and reliability. 

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Evaluating the DSM

  • Goldstein (1988): Reliability in the DSM III, but diagnostic differences from the DSM II to III showed updates to DSM cause disruption in the reliability of diagnosis. 
  • DSM-5 had field trials to test reliability, but they were not transparent, lowering credibility. 
  • Does not link to biological evidence and brought in social norms, but is seen to confirm the medical model and to be scientific and credible. 
  • Brown et al (2001): boundary and symptom length problems. Generally reliable. 
  • Sinchenfield (2003): validity and reliability in the diagnosis of pathological gambling. 
  • Kirk and Kutchins (1992): methodological problems in the studies of relibility of the DSM.
  • Steeka & Ghamei (2014): only 1/2 of clinicians use DSM-5; concerns about its reliability.
  • Cooper (2014): the reduced reliability (0.6) is acceptable as there is a focus on treatment. but
  • Spizer and Fleis (1974) found reliability is only 0.7, which they say is not good.
  • Lee (2006): Diagnosis of ADHD has validity in Korea. 
  • Pies (2013): DSM-5 = Bible for Diagnosis. 'Informative but fallible'. Needs more biological evidence and phsychodynamic explinations; Shopping list of symptoms: less valid.
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Cultural Issues in the DSM

Evard (2012) say hearing voices could be a mental illness in western culture but could be exceptional in another culture. 

The DSM is an American manual so could be hard to generalise. But if it is not generalisable accross cultures then it may not be valid. Though could be used across cultures. 

Cultural-bound syndromes could be seen as a difficulty in generalisation of diagnosis. E.g. in the DSM there is Genital Restract Syndrome found mainly in Africa and Asia.

Section three focuses on cultural issues to take into account. E.g. what features could be affected by culture. 

Challenges of the use of the word 'Bizzare' included cultural interpretation, yet it was still included.

Flaum et al (1991): more focus on negative symptoms allows for increased objectivity.

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The ICD

The International Classification of Diseases and Related Health Problems (most recent being ICD-10) is more widely used than the DSM as it is created by the World Health Organisation.

It looks at both physical and mental health conditions and is also used to measure mortality and morbidity.

It is split into categories up to XXII. Mental and Behavioural Disorders is category V.

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Comparing the ICD and DSM

The NHS uses ICD-10, but the DSM-5 has a big influence on UK as it helps guide reaseach, bring new ideas and influences clinical guidelines; widley known research is often in US.

The ICD-10 is currently being updated and DSM-5 may influence the mental health section. 

  • Andrews et al (1999): Only 68% agreement between  ICD-10 and DSM-IV 
  • Hoffman et al (2015): DSM-5 and ICD-10 agreed in diagnosing 'healthy' or severe alcoholism, but 1/3 with mild alcohol disorder according to DSM-5 received no diagnosis from ICD-10.Evana et al (2013) found that more used the ICD (51%) than DSM (44%). Reed et al (2011) found ICD (70%) more than DSM (23%)
  • Reed (2013) suggest to change to ICD as it is made by WHO, is free and open, is available so all, is multilingual and covers all health conditions.
  • Jakobsen et al (2005): significant agreement between ICD and DSM showing reliability. 
  • Andreasen (2000) suggest emphasis is on psychosis in Schizophrenia for both systems, improving relibility as symptoms are easier to access. So reliability is gained at the expense of validity. 
  • Tarrahi et al (2014) found agreement was good at 0.81.
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Models of Health

Medical Model: 

  • Illnesses diagnosed using symptom lists and a 'cure' or 'treament' is offered.
  • Illness is seen as a problem that needs to be fixed as human are like machines.
  • Help is often in the form of medication to rebalance biological factors

Recvery Model:

  • Focused on the recovery of mental health and less focus on diagnosis. 
  • Arnella (2015): the model is good as it moves away from mending broken brains and relief of symptoms and focuses on the holistic person and how personal relationships can help healing.The holistic model is gaining ground since drugs are expensive.
  • Laverenne et al (2013) used a case study of a group therapy to show how groups can act as an 'ego boundary' for those with mental disorders.

In both models, there is  a lack of focus on socio-economic issues and Beresford (2015) says the recovery model predisposes that there was mental health in the first place in both models. 

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Schizophrenia- Symptoms

First-rank symptoms are the most common (e.g. hallucinations), second-rank symptoms are those that may come as side effects/less common (e.g. flat emotions).

Positive symptoms are additions to behaviour and includes: 

  • Delusions - false beliefs that can be illogical and are held after being disproved. Includes paranoid delusions, delusions of grandeur (thinking they are someone of importance), alternate delusions (believing things unrrelated to them are related to them) and delusions of persecusion (feeling someone is trying to harm them).
  • Hallucinations - hearing, feeling or seeing things that are not there. Different interpretations across cultures. Can be positive or negative.
  • Thought disorders make someone's speech hard to follow- they may lose concentration or be disorganised. 'Thought blocking' is when someone feels like the thought is taken out of their head. 'Thought intertion' is when it is believed that thoughts are put there by someone else. 'Thought broadcasting' is when it is believed that others can read their thoughts.
  • Movement disorders could mean agitated movement such as repeating things over and over. Could also mean catatonia where they do not move or respond much. 
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Schizophrenia- Symptoms Cont.

Negative symptoms: lack of something

  • Apathy- lack of energy or motivation to do daily tasks or chored.
  • Social Withdrawal- avoiding family memebers and friends and not goign out.
  • Flatness of emotions- lack of emotion/expression
  • Lack of self care- not bothering about self care
  • Lack of pleasure in things that previously gave pleasure.
  • Speaking very little, even when required to interact.

Cognitive symptoms: to do with the way someone processes sensory information 

  • Memory difficulties
  • Concentration and attention difficulties 
  • Difficulty with executive function
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Schizophrenia- Features & Types

  • Psychosis- a separation from reality 
  • It affects about 1% of the population
  • Life expectancy is around 10 years shorter
  • Durerr (2013): adolescents with psychotic symptoms are 70 x more likley to commit suicide
  • It tends to be diagnosed in adolescence up to around 30 years old. 
  • People who experience social problems are more likley to be diagnosed. 

Paranoid: suspicious of others and having delusions of grandeur as well as some hallucinations. 

Disorganised: speech is disorganised, inappropriate moods for situations, no hallucinations.

Catatonic: withdrawal and isolation and little physical movement

Residual: low levels of positive symptoms and psychotic symptoms are present. 

Schizoaffective Disorder- symptoms of Schizophrenia along with a mood disorder 

Undifferentiated- when their diagnosis does not fit into any of these categories.

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Schizophrenia - Diagnosis

Other than diagnosis using the DSM and ICD, it has been suggested that Schizophrenia can be diagnosed using:

  • Blood Testing: 'Schizophrenia Bulletin' article shows that blood testing could be used. Perkins (2014) analysed blookd samples of a group and found biomarkers of inflammation, oxidative stress and metabolism and hormones linked to psychosis.
  •  Eye Tracking- there have been issues of eye movement for those with Schizophrenia. Sweeny et al (1944) found psychotic patients had slow eye movements and Benson (2012) found that they had some success in identifying patients from controlls. 
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Schizophrenia - Cultural Differences

Lurhmann et al (2015): hearing voices is seen as negative in the US, but is seen as more positive in India and Ghana. 

Myers et al (2012): using the recovery model tended to generate more stress for those with schizophrenia if their life was already stressful. 

Kulhara et al (2009) reviewed various studies and found that more people have a 'favourable outcome' in developing countries but it may not be culture. Factors should be looked at more.

Chandrasena (1986) found more incidence of catatonic schizoprenia in Shri Lanka compared to British people. In Sri Lanka, however, patients were less likley to have intervention.

Lin et al (1996): Schizophrenia is found in all cultures and there are more similaries than differences. Prevalence also seems to be similar, as well as symptoms. 

However, even if similarities are found across cultures doesn't mean it is the same illness. 

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Reliability & Validity of ICD/DSM for Schizophreni

Reliability:

  • Jokobsen et al (2015): diagnosis (ICD) showed 93% sensitivity and 87% predictive value. 
  • Hiller et al (1992): Compared ICD and DSM and found ICD gave higher reliability and agreement was high (around 50%) for both. 
  • Cheniaux et al (2009) found Schizophrenia was more frequent using ICD than DSM (type I or II error). They also found reliability dropped below 0.5 for schizoaffective disorder.

Validity: 

  • Pihlajamma et al (2008) used case notes and found validity but there were issues in diagnosis when there was co-morbidity. 
  • Jassib et al (2002):ICD and DSM show good agreement but differences in diagnosis and boundaries for diagnosis+ need revising. ICD-10 seems to be less valid than 9

Overall the ICD compares well for reliability with DSM and studies use inter-rater reliability. Studies also use careful controls- however, results of studies show some lack of reliability to some. In validity, it matches diagnosis from different systems, but studies of validity are hard to do.

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Neurotransmitter Explanation for Schizphrenia

The Dopamine Hypothesis; (evidence from Carlsson et al, 1999, review)

  • Hietala et al (1994) found dopamine receptors have been linked to psychosis. 
  • They found that development of certain receptors could inhibit the development of others.
  • Increase of dopamine in the mesolimbic pathway links to positive symptoms
  • Increase of dopamine in the mesocortical pathway links with negative symptoms. 
  • PET/fMRI scans show 'supersensitivity' to dopaminecould be genetic or from lesioning. 
  • Enlarged ventricles and smaller frontal lobes have been linked with schizophrenia. 
  • Drugls linke amphetamine produce similar symptoms and have the same link to dopamine. 
  • Phenothiazine can alleviate symptoms by blocking dopamine receptors. 
  • Drugs that increase dopamine production increase positive symptoms. 
  • Some genes linked with dopamine production are found in those with the illness. 
  • Stress from imaging may affect study results and PET shows blocking receptors does not always reduce symptoms. There are also delays for relief even after receptors are blocked.
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Neurotransmitter Explanation for Schizphrenia

The Glutamate Hypothesis (Carlsson et al, 1999)

  • It could be something more than dopamine, judging by the weaknesses. Therefore, Carlsson wanted to look into more detail. They looked at animal studies where animals treated by an NMDA antagonist It led to a lack of glutamate but not always an increase in dopamine. NMDA are psychostimulants and lead to psychosis and inhibit dopamine.
  • PCP (angel dust) leads to lowe glutamate and increased dopamine. Glutamate receptor antagonists can cancel the PCP behaviour despite the access dopamine.
  •  The glutamate hypothesis could be said to work with the dopamine hypothesis and add to it rather than go against it. The evidence is complex but the wide range of evidence relates blocking glutamate and increasing dopamine links to schizophrenia. 
  • Generalising animal studies to humans is difficult so could lack validity. 
  • Using PET scanning could put people under stress and cause the results.
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Genetic Explanation for Schizophrenia

Using MZ (identical) and DZ (non-identical) twins to study Schizophrenia is useful as it can be used to compare nature and nurture where twins are brought up in the same environment so the only difference is either genes or non-shared environment.However, MZ twins may share DNA but even in the womb there is a non-shared environment. MZ twins may be treated more alike than DZ twins so environment, again, may not be so controlled.

Gottesman and Shields (1996) did a twin study and found that there are genetic factors involved in Schizophrenia. They found a 58% concordance rate in MZ twins with schizophrenia and 26% in DZ twins suggesting a strong genetic link but a link that does not completley explain schizophrenia.

They concluded that the diathesis-stress model (which explained that genetic factors are triggered by the environment) is the best explination of these results.

Tiwari et al (2010) found that there is evidence for common genes and rare copy numbers that could add to increased predisposition to Schizophrenia. Some genes that make someone susceptible to bipolar disorder also overlap with those for Schizophrenia. They cite Sullivan et al (2003) with a 81% heritability for schizophrenia. 

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Genetic Explanation for Schizophrenia

Tiwari et al (2010) also foudn that less than 1/3 people with Schizophrenia have a family history, suggesting complexity. 

There have been chromasome problems like the missing 22q11 found in 52% of cases. 

Common varients include alleles that unrelated individuals would share. 

DNA pooling shows different allele frequencys, Mah et al (2001) found Plexin A2 as a marker.

Other factors include the environment: Maternal infection, taking cannabit and epigenetic modification (when genes act on the organism throughout it's development) during pregnancy affect development of Schizophrenia. 

Environmental factors can affect body mechanisms that are driven by genes such as stress. 

Shiffman et al (2006) found a female-specific association with RELN. 

However, the area is very complex and hard to study and we cannot be sure about the area yet.

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Non-Biological Explanation of Schizophrenia

The Social Causation Hypothesis: (Tiwari et al, 2010)

  • There are environmental factors like growing up in an urban environment, cannabis usage, male gender, stress and malnutrition that increase prevalence for Schizophrenia.
  • Being in a lower social class has been linked to Schizophrenia. However, this could be that they are more likley to be brought by the police or social services to get help. 
  • Cooper et al (2005) suggest those in social class 5 are diagnosed more than class 1.
  • Social adversity, particularly in childhood, links to development. 
  • Immigrant populations (such as Afro-Carrabean and black populations) are pointed to be 4 times as likley to suffer thant he indigenous population. It is not thought to be genetic, but down to the fact that they are strangers in that society. 
  • Brown (2010) found that when immigrants were in neighbourhoods where their own ethnic group did not predominate, there was a higher rate of psychosis. They cite Mortensen et al (1999), who found higher risk in capitals than rural areas; Veling et al (2008), who found more diagnosis in ethnic minorities in an area; Kirkbride et al (2007), who found less social support and connectedness linked to psychosis; and March et al (2008) who found some social pathways may explain why some people are diagnosed.
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Antipsychotic Treatments for Schizophrenia

Antipsychotic Drugs act on neurotransmitters to supress hallucinations and delusions. Typical antipsychotics -first generation- are well established (e.g Chlorpromazine) that have side effects like tiredness, muscle spasms, low sex drive and low blood preassure. Atypical -second generation- are newer (like Risperidone) and have less extrapyramidal effects like Parkinson's.

Atypical drugs seem to be better for negative symptoms and hallucinations and delusions and typical for positive symptoms more. Typical drugs tend to work on the dopamine system and atypical on the glutaminetgic system.

Meltzer et al (2004) found that one typical drug gave significant improvements in all aspects compared to a placebo. 2/2 atypical drugs showed improvements

Guo et al (2011) found thatthere were similar percentages of patients stopping treament (405) showing around 60% effectiveness. Clozapone has the lowest amound of discontinuing treatment. 

Hartling et al (2012) found core illness symptoms were similar for all drugs. Some were better than others at reducing certain symptoms and some higher risk of Tardive Dyskinesia for clorpromazine.

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CBT to Treat Schizophrenia

Cognitive Behavioural Therapy focuses on thinking and execuative function and works on changing maladaptive schemas and thoughts- including working on helping people focus on thinking, understanding reality and improving negative symptoms. Social supports links to social causation.

Beck (197) focused on maladaptive cognitions (thinking that is not helpful in a situation).

Dickerson (2000) found that those with Schizophreania have symptoms and social disability throughout their lives- fewer than 60% achieve full remission. 

Special CBT has been created for Schizophrenia as people may be stressed by symptoms and cope with it in a way that worsense symptoms. CBT aims to replace this. Symptoms are challenged rationally (belief modification) and reatribution of hallucinations as not-real, as well as normalising psychotic experiences, help to cope with symptoms. 

Four different processes of CBT include challenging key beliefs, group therapy, family sessions and structured activities. 

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CBT to Treat Schizophrenia

Hoffman et al (2012) found that CBT was strongest for anxiety and Schizophrenia was not regarded as best treated. 

Chadwick and Lowe (1994) considered reattribution and found that 3/6 patients did reattribute the voices to themselves and a different 3/6 reported fewer hallucinations. 

Kingdon and Turkington (1991) foudn 54% of patients had no symptoms five years after normalising and using CBT. 62/65 were living in the community. 

Drury et al (1996 a&b) found after 7 weeks, CBT for acute phases lowered psychotic symptoms. 

NICE Guidelines (2014) suggest that after the first eposode, medication is reccomended and then CBT. CBT should be a first intervention with or without family intervention. CBT and drug treatment are both recommended. 

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Other Treatments for Schizophrenia

Assertive Community Therapy (ACT) is a group therapy and involves clients with difficulties meeting personal goals, getting on with people, making friends and living independently. 

  • Laverenne et al (2013) showed community therapies can act as a boundary for individuals. 
  • There is a focus on those who need the most help, help with independence, rehabilitation and recovery and workinging with other people and professionals to support eachother. 
  • van Vugt et al (2011) found treatment team structure was most related to better outcomes.
  • Nishio et al (2011) looked at the transition into the commuinty and found a decrease in the number of days and in frequencey of hospitalisations. One year after, there was no change in life satisfaction, but the Global Assessment of Functioning scores increased.
  • Harvey et al (2012) found outcomes for staff was not good including emotional exhaustion.
  • Dixon (2002) says ACT has been the model for mental health practice since the 1980s
  • Bond et al (2001) suggests there is large evidence for it's effectiveness.
  • Gremory (2001) says the client has no choice- there is social control.11% feel forced into it. 
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Unipolar Depression - Symptoms

Unipolar - one state e.g. also known as Clinical Depression fo Major Depressive Disorder (MDD). 

Psychological Symptoms: 

  • Anxiety, Irritability, despair, hopelessness, irrational fears, suicidal ideation. 

Social Symptoms: 

  • Problems at school/work, avioding social activities, avoiding friends, family life difficulties. 

Cognitive Symptoms: 

  • Lack of pleasure in usual activities, loss of memory, difficulty concentrating, low sex drive.

Physical Symptoms: 

  • Headaches, digestive problems, changed appetite, lethargy/disturbed sleep, slow movement.
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Unipolar Depression - Types and Features

Types:

  • Mild depression- some impact on daily life
  • Moderate depression- significant imact on daily life
  • Severe depression- life is extremely hard to cope with 
  • Postnatal depression- after having a baby
  • Bipolar depression- a mix of mania and depression
  • SAD- seasonal affective disorder, where depression is in winter months

Features: 

  • Twice as common in women as it is in men and males are more lilkey to commit suicide. 
  • In USA, depression affects around 14.8 million and around 3.4% with MDD commit suicide. 
  • In UK, around 4.7 million or more have depression. Over a lifetime, 10-25% of women will have depression and around 5-12% of men.
  • Those with depression have a shorter life span and after one episode there is 50-60% chance of it happening again. 
  • It is most common in ages 25-44 and is one of the most common mental illnesses (Mind). 
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Co-Morbidity

Co-Morbidity is when an individual is diagnosed with more than 1 mental illness/disorder at once. 

Kessler et al (1966) sugges that MDD often appears with other disorders including personality disorders, Schizophrenia, anxiety disorders, drug misuse, eating disorders and Autism. 

This can have implications for diagnosis, treatment and every-day life. 

Goes et al (2007) found that there is a link beteween psychosis and MDD. 

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Brain Structure and Unipolar Depression

Limbic system: 

  • Hippocampus is thought to be involved in stress/emotion regulation and depression. Some studies show smaller hippocampal volume links to MDD. 
  • Amygdala is thought to link to emotional reactivity (strong emotions). Siegle et al found that those with depression had more activity here during emotional tasks.

Prefrontal Cortex:

  • Thought to link to executive control including memory and self control. Siegle et al found lower activity in the prefrontal cortex during executive tasks for those with unipolar depression.
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The Monoamine Hypothesis

A monoamine is a type of neurotransmitter that contains amino acids and includes dopamine, serotonin and noradrenaline in the Central Nervous System (CNS). Monoamine transporter action stops when there is reuptake and they are thought to be important for emotions and cognitions. 

Serotonin is thought to regulate neurotransmitters and without regulation there can be erratic brain frunctioning and thinking patterns. It can cause the production of neorepinephrine (increasing anxiety) and can help regulate behaviour: mood, sleep and appetite. Lack of serotonin links to anxiety and compulsions. Karg et al (2011) found that changes in the gene encoding of serotonin transporters links to depression triggered by stress. 

Dopamine is thought to also link to emotions. If there is not enough dopamine, it is thought it can lead to depression. This is the opposite to Schizophrenia, acting as a strength as it equalises and makes sense e.g. depression is underactive brain and Schizophrenia, overactive. 

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Alternate Explinations

Genetic/environmental factors:

The diathesis-stress model shows that a stress trigger could cause an underlying biological/genetic vulnerability to depression to come to light. Heritability is thought to be about 30-40% showing a genetic link. Therefore, there may be biological predisposition. It has also been shown that stress can increase the likelihood of depression. These could link.

Synaptic plasticity:

Lee and Kim (20120) suggest synaptic plasticity (how synapses can get stronger or weaker) as a deeper explanation. Antidepressants are delayed before they start taking effect. They claim it could be neurotrophic factors (factors that affect growth and survival of neurons) that leads to plasticity. The hippocampus can change in those who are depressed. If it continues to produce new neurons it can decrease in size because of weaker neurons from this. Neurogenesis (growth) is increased when using SSRIs, and studies show there is more brain-derived neurotrophic factors in depressed people. Ther

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Brown et al (1986)

They considered factors involved in depression in UK women. They looked at self esteem and support factors. They believed that the existence of crisis support could protect against the onset of depression.

They found that 50% of those recorded went on to have a depressive episode/crisis time. Of that 50%,, 11% had the onset of depression and of those. The majority of women with core crisis support found it useful and had a large impact on if they developed depression or not. 42% with support had onset and 42% without support had onset. 

They concluded that it was more likley that someone who had a negative life event developed depression and that those with negative evaluation of self were more likley to develop depression. Only one person had depression without a provoking agent or negative evaluation of self. Those who were married or had someone closer to them had a lower chance of depression. 

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Non-Biological Explanation: The Cognitive Model

  • Beck, in the 1960's created the model that considers that there are three aspects of thinking that lead to depression: cognitive errors (negative views), faulty patterns of thought or schema and distorted processing of information. 
  • Seligman put forward the idea that depression is a form of learned helplessness where people learn to give up trying as they have only exprienced faulture. He looked at the cognitive triad (negative view of the self, of the world and of the future), cognitive errors and schemata.
  • The main issue concerns the meaning assigned to an event.
  • Genetic and early expriences link to the formation of schema and through events we form beliefs and assumptions. The person will adhere to these beliefs.
  • This can lead to negative automatic thourhgs where negative thoughts automatically stem from core beliefs because of negative past experiences and schema.
  • According to the cognitive model, overcoming depression involves changing these problems. 
  • Types of negative schema are cognitive schemata (that lead to seeing actual or threatened loss), affective (leading to sadness), physiological (that makes a person feel tired and unable to do things), motivational (that lead to helplesness and a lack of direction) and behavioural schemata (that lead to social withdrawal and inactivity). 
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Evidence for the Cognitive Model

Evaluations of CBT (Cognitive Behavioural Therapy) can help to evaluate this model. E.g. Hollon et al (2002) found that CBT is useful using controlled trials. 

Bothwell and Scott (1977) found that faulty thinking and errors in cognitive processing linked with the symptoms of depression continuing.

Watkins and Baracaia (2002) found that knowing more about mental processes helps to reduce relapse and stop them constantly ruminating. 

Teichman et al (2002) looked at details within relationships. Self-concept was the most marked link with the severity of the depression. 

Strunk and Adler (2009) found that how optimistic or pessimistic someone was depended on their symptoms and depression (negative correlation). 

Disner et al (2011) concluded that there is different brain functioning in different brain structures for the range of processes. However, emotion processing regions combined with cognitive control mechanisms underlay the model. E.g. 70% more activity in the amygdala when processing negative stimuli.

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Types of Processing Information

Bottom up processing - moving from certain components to explain a more complex entity. (stimuli trigger biologial responses eg. amygdala activity)

Top down processing - moving from complexity to explain components e.g biological responses 

Bottom up processing is said to link to bias in top down processing

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Antidepressants - Treatments for Depression

  • Selective Seritonin Reuptake Inhibitors (SSRIs) include Fluoxetine, Sertraline and Paroxetine and block the reuptake of serotonin so there is more in the synapse. Symptoms include stomach upset, sexual dysfunction and serotonin syndrome. 
  • Tricyclic antidepressants are older medications including amitriptyline and clomipramine and they inhibit the reubtake of seotonin and norephinephrine.Symptoms include high blood preassure, low sex drive, dry mouth and bloating. 
  • Atypical antidepressants are newer drugs such as bupropion and trazadone. They target other neurotransmitters- those that target serotonin, dopamine and norepinephrine can be called Serotonin Norepinephrine Reuptake Inhibitors (SNRIs). Side effects inclulde bloating, swelling and loss of appetite. 
  • Monoamine Oxidase Inhibitors (MAOIs) are the oldest form of antidepressants and cannot be used with SSRIs or with certain food and drinks such as wine, cheese and preserved meats as it can lead to serotonin syndrome. One example is phenelzine. Symptoms include sweating, tremors, elevated temperature, high blood preassure and palpitations. 

Withdrawal symptoms (antidepressant discontinuation syndrome) is found when someone stops medication; it includes anxiety, diziness, insomnia, stomach upsets and flu-like symptoms..

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Evidence for Antidepressants as a Treatment

WHO 2005 reported that drugs are 'well documented treatments' and seems to back the use of medication to an extent with the goal of complete remmission (by which other interventions are needed). They give vonvlusions about specific drugs from a range of studies and claim that SSRIs are more effective than Trycyclic antidepressants. 

Geddes et al (2003) found that those who had drug treatment had a 18% relapse rate compared to 41% of a placebo group. Treatment also lasted up to three years.

Psychology Today posted an article that criticised the way drugs for depression are widely prescribed without sufficient attention to the individual's past history and without alternative therapies being used. The article also cites a study where relapse rate was higher in those who took medication along with another treatment. 

Caporiono and Karver (2012) found that psychotherapy was mre acceptable to adolescent girls when combined with drug treatment- drug treament on its own is not accepted as much.

Kuyken et al (2008) found that Mindfulness Based Cognitive Behavioural Therapy (MCBT) was more effective than medication,. Those on MBCT reported gaining better life skills over drugs.

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CBT to Treat Depression

Developed from Beck's cognitive model, as discussed earlier, the person is treated by focusing on their negative automatic thoughts and faulty thinking patterns and how they can change these using different tools.

Different faulty thinking includes 'all or nothing' thinking, 'catastrophising', 'magnification and minimisation' of events and problems, jumping to conclusions, a 'negative mental filter' and disqualifying the positive. 

In practice, CBT involved an introduction where a contract is made for around six, fifty minute sessions. There will be a review and introduction on the process. In the sessions, there will a be an agenda for what will happen in that session and then the client will talk about their own thinking to help the therapist. The therapist then summarises what the client has said and asks questions to help understand more and challenge ideas. At the end, the therapist will go over what the client has leaned and make sure that they have support. They will eventually be discharged.

One technique is the Downward Arrow Technique of Burns. The therapist would ask why a negative automatic statement matters untill it gets to the route of the statement- the initial schema. Once this is found, they may disprove it or argue against it.  

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Comments

miss.mannning

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Excellent overview of the whole of the topic! 

miss.mannning

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Excellent overview of the whole of the topic! 

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