Depression revision
Specification 2014
Clinical characteristics of depression
What is depression?
• An affective (mood) disorder.
• Characterised by sadness and ...
Apply knowledge and understanding of models, diagnosis and classification of depression
•Endogenous depression (caused by ...
• Always comes up as 24/25 mark question
• 8/9 marks AO1
• 16 marks A02
What would you write for 16 marks?!
Biological explanations for depression for example genetics and biochemistry
Evidence to suggest that depression has a bio...
Biological explanations for depression for example genetics and biochemistry
Initially people to
Psychological explanations for depression:
Psychodynamic and diathesis stress model
• Depression occurs when the no...
Psychological explanations for depression: Psychodynamic & diathesis stress model
No single explanation can account for de...
Biological therapies are designed to redress the imbalance of biochemicals through drugs, ECT and in rare cases Psychosurg...
ECT: Only used if antidepressant drugs have no effect and if there is a risk that the person
will commit suicide (Mental H...
Psychological therapies for depression – psychodynamic therapy
• Freud introduced Psychoanalysis in the beginning of the 2...
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    1. 1. Depression revision Specification 2014
    2. 2. Clinical characteristics of depression What is depression? • An affective (mood) disorder. • Characterised by sadness and withdrawal. • Can range from mild, moderate to very severe, and can even result in suicide. • In 2011 6045 suicides in England • In Europe, around 5% of people suffer from depression at any one time. • Nearly everyone suffers from depression at some point in their lives, so it is very common. Two types of depression – unipolar and bipolar. • We are studying unipolar depression, of which there are two types: Major Depressive Disorder (MDD)– severe but usually short-lived depressive episode. Can include psychotic symptoms. Dysthymic Disorder (DD) – less severe, but usually chronic (very long-lasting). Low mood must last at least 3 years to be diagnosed. • There are two manuals used by doctors and psychiatrists to diagnose depression. • They are the DSM IV (Diagnostic and Statistical Manual: Version 4) and the ICD-10 (International Classification for Diagnosis: Version 10). • The DSM is usually used in England, and the ICD in America, but because the ICD is more widely- used, we will focus on it’s diagnostic criteria. General criteria which must be met 2/3 = mild 3/3 = severe 2/7 = mild 3/7 = moderate 4+/7 = severe Depressive episode lasts 2 weeks Mood that is abnormal and lasts most of the day almost every day Loss of confidence/ self esteem The episode cannot be attributed to substance abuse or organic illness Loss of interest or pleasure in activities that are normally pleasurable Unreasonable feelings of guilt Decreased energy or increased tiredness Thoughts of death and suicide Inability to concentrate and proneness to indecision Changes to psychomotor activity, e.g. agitation or lethargy Sleep disturbance Change in appetite with weight change
    3. 3. Apply knowledge and understanding of models, diagnosis and classification of depression •Endogenous depression (caused by internal biological mechanisms). Usually more severe and long lasting •Reactive depression (caused in response to external mechanism) Underlying cause •Melancholic symptoms (DSM) or Somatic (ICD) Biological in origin (e.g. appetite changes, weight loss, constipation, reduced sex drive and early morning waking) •Non-melancholic symptoms are psychological in nature (e.g. slowed cognitive functioning) Types of symptoms •Seasonal affective disorder (SAD) – symptoms occur mainly in the winter months •Brief recurrent depression – the episodes are fairly frequent but of short duration Course of the disorder •Some of the subtypes of depression found in the classification manuals still need validating. •Premenstrual dysphoric disorder (pre menstrual depression) shares some characteristics of depression but also involves anxiety symptoms and specific somatic (physical) symptoms. Validity of diagnostic criteria Differentwaysofclassifyingdepressivedisorder AO2: Neither of these terms are used in the DSM or ICD Ao2: Issue with this classification is that most patients with depression suffer from both. Where do you draw the line between each one? Melancholic depression is associated with more severe symptoms, poor response to placebo treatment and good response to ECT. This suggests that the melancholic category is a valid category although there are issues with the reliability of the diagnosis. Ao2: Different courses and types of depression will have different treatments. AO2: It is included in the appendix of the DSM The validity of the syndrome is controversial Lack of reliable signs – No clear objective measure – Use of body language • Who makes the diagnosis – Psychiatrists are medical doctors who specialise in psychopathology – In the UK people who are depressed go see the GP who can refer them to a psychiatrist if it is thought appropriate – It is estimated that 50% of people showing depressive symptoms who visit the GP are not diagnosed with depression. To make a valid diagnosis rule out other possibilities 1st Normal sadness Anxiety • Very similar, but different treatments Dementia • People with depression perform poorly on tasks which require cognitive functioning. A diagnosis of depression rather than dementia can sometimes only be confirmed when the individual’s mood improves and normal cognitive functioning is restored. Physical illness • E.g. hyperthyroidism which is when the thyroid doesn’t work properly can result in depression. • When treated the depression usually disappears. Irritability • Depression in childhood is Often masked as a conduct disorder Additional issues in the classification and diagnosis of depression • Treating depression as a disease • Dual diagnosis -Often occurs alongside other mental disorders such as schizophrenia, anxiety disorders, eating disorders and substance abuse. Normally primary condition is treated first • Gender -Why is depression diagnosis twice as high in females compared to males? • Socio-cultural background -Higher levels of mental health problems found in minorities. • Cultural differences -e.g. Eastern view on depression
    4. 4. • Always comes up as 24/25 mark question • 8/9 marks AO1 • 16 marks A02 What would you write for 16 marks?!
    5. 5. Biological explanations for depression for example genetics and biochemistry Evidence to suggest that depression has a biological origin - Physical symptoms - Drug treatments are successful - Depression runs in families - SAD- linked to serotonin levels - Similar symptoms across different cultures Family study Studies first degree relatives with depression (parents- siblings- offspring - we share 50% of our genes) Examines whether other members of the family also have depression People with a relative with bipolar are 3x more likely to be diagnosed with MDD compared to those undiagnosed with uni polar or bi polar. Gershon: Rate of 7-30% of depression between first degree relatives. Weissman: If someone has a relative diagnosed with depression before they turn 20, they are 8x more likely to be diagnosed with depression. Twin study Studies the concordance rates for depression in MZ and DZ twins . If depression is biological in cause it would be expected that there is a HIGHER CONCORDANCE for depression in MZ twins than in DZ twins McGuffin found a 46% concordance rate of depression in MZ twins verses 20% in DZ twins (109 pairs, no evidence of the effect of the shared environment) Bierut: Carried out research on 2662 twins in Australia and found a concordance of between 36-44% in MZ twins. Although they claimed environment played a larger role. (2662 twin pairs in Australia, environment played a larger role) Adoption study “Family studies like Gershon’s, and twin studies like McGuffin’s, can’t say genes are the only reason for depression, because they didn’t separate genes from environment“ Wender: Biological relatives were 8 x more likely to have depression than adoptive parents AO2: Unclear whether these findings are from genetic influence or shared environment Family studies often show inconclusive results AO2: Provides stronger quantitative data compared to family studies. Still very difficult to disentangle nature/ nurture. AO2: Best way to disentangle genetic factors from the environment since they study people brought up away from the influence of their genetic families. More AO2 • Genetics is only a risk factor- not 100% concordance rate • Genes or environment, nature - nurture • Genetic uncertainty – There does not appear to be a particular gene which results in depression. – An abnormality in the 5_HTT gene has been linked with depression – This gene is responsible for the transmission of the neurochemical serotonin • Diathesis stress model Environmental stressors Depressive reactionGenetics
    6. 6. Biological explanations for depression for example genetics and biochemistry Neurotransmitters Initially people to believed depression was caused by low levels of serotonin or noradrenaline More recent belief depression is the result of an overall imbalance between serotonin, noradrenaline, dopamine and acetylcholine. Neurotransmitters are chemical messages in the brain and nervous system that transmit nerve impulses from one cell to the next across the synapse. 1950s: was discovered that tricyclic drugs were effective in treating depression. They work by increasing the availability neurotransmitters in the brain called monoamines: • serotonin, • noradrenaline and • dopamine • NB in the functioning of the limbic system in the brain (appetite, emotion, etc). Noradrenalin • No abnormality in noradrenaline in post-mortems of depressed patients • Some abnormality in reserpine (function is to reduce the availability of noradrenaline) • Reserpine is used to treat high blood pressure and has unwanted side effect of producing depressive symptoms and suicidal tendencies Serotonin Mann et al found impaired transmission of serotonin in people with depression. • May act as the neuromodulator (controller) of a variety of brain systems. • If serotonin levels are low, activity in other systems is disrupted = depression. • Prozac is an effective antidepressant which increases the availability or serotonin the brain, but has no effect on noradrenaline. Dopamine • Thought to be involved in depression in old age • Dopamine content in brain diminishes considerably post 45 • Synthetic drug L-dopa has no antidepressant effect Hormones Endocrinology is the study of hormones. High levels of cortisol found in those who suffer from depression Techniques to supress cortisol secretion are successful as a depression treatment. Over activity of the HPAC stress circuit may lead to depression. Nemeroff found that those suffering from major depressive disorder suffered from enlarged adrenal glands which was not found in controls. Depression occurs the week prior to menstruation - 25% of women are affected – most do not receive a severe diagnosis. Result of an oestrogen (high)-progesterone imbalance (low) Biological rhythms Result of the changes in the number of daylight hours - or too much artificial light. Thought to be the result of Melatonin – the ‘dracula hormone’ released in dark conditions. Melatonin slows us down and makes us feel fatigued. People with SAD are very sensitive to melatonin. There is some evidence that serotonin and noradrenaline are also linked to SAD. Lam et al found drug treatments which include serotinin are effective (but do not cure the problem – depression returns when treatment ends), where as those including noradrenaline are not. Madden et al reports a significant genetic influence in winter-pattern SAD. Data collected from 4639 twins in Australia via mailed questionnaire. Special day light bulbs can now be purchased which can help those suffering from the type of depression Neurotransmitters Noradrenalin Serotonin Dopamine Hormones Endocrinology Biological rhythms Dracula hormone Treatment AO2 – evaluation 1. Role of neurotransmitters • Good amount of evidence that supports link between neurotransmitters and depression • Reductionist to say that excess or deficit of chemical in brain is cause of depression • Anti depressant drugs have an immediate effect on neurotransmitter availability but can take several weeks to have positive effect on mood. • Alternative theory is that depression may be linked to damaged neurons or BDNF (brain-derived neurotrophic factor) deficiency. 2. Role of hormones • Abnormal levels of cortisol suggest depression may the result of over use of the stress-response system. This is not a consistent finding. • Research for hormone imbalance theories are inconclusive (Clare 1985) • Social changes may occur at the same time as hormonal changes • Hormonal changes may trigger genetic predisposition to depression. 3. Biological factors as predisposing factor • No definite evidence that biological features are the cause of depression • Strong support for contributory factor • Predispose people to depression, but require environmental triggers (diathesis stress model) 4. Causal relationship • Depression causes biochemical changes rather than the other way around?
    7. 7. Psychological explanations for depression: Psychodynamic and diathesis stress model Freud: • Depression occurs when the normal grieving process following the death of a loved one does not diminish with time. • Begin to merge emotions to that of the loved one. • Introjection feelings for loved one are redirected to the self (.e.g sadness or anger) • Later Freud realised not everyone who was depressed had lost a loved one… • When loss is experienced this leads to anger but it is turned inwards as it is unacceptable (by super ego) to express it • Thus feelings of guilt, unworthiness and despair, which if intense may lead to suicide Symbolic loss • Can have the same effect as that of loosing a loved one. • E.g. Being fired, breaking up with a partner etc. • Symbolic losses can be interpreted the same way as death of a loved one. Melancholia: • Depression is like grief. • Freud – symbolic or actual loss may lead to re- experiencing parts of our childhood leading to dependency, clinging or regression to a childlike state. • Freud believed the greater the experience of loss in childhood the deeper the depression Relationship with parents An alternate psychodynamic view relates depression in adulthood to the individual’s early relationship with parents. • Hostile feelings towards the parent are introjected to the self in the form of self-accusation or self-hatred. • Could be the result of lack of love and care, support and safety or child abuse. • Repression of childhood trauma reappears in adulthood in the form of anxiety disorders or depression. The effects of separation and loss • Bowlby (1973) separation or loss of the mother in early childhood could result in severe depression in adulthood • Support for this view is by Hinde (1977) who examined the effects of separating infant rhesus monkeys from their mother. – Both mother and child displayed behaviours similar to the symptoms of depression in humans – Unwise to use primates to study human disorders. • Paykel (1981) reviewed 14 studies and found the evidence inconclusive. – 7 studies support the hypothesis, 7 studies did not support the hypothesis. • Depressed patients often report a parental style called “affectionless control” (Martin et al. 2004) AO2 • Issues: Falsifiability - difficult to test Freud’s ideas empirically because it is impossible to demonstrate unconscious motivations or abstract concepts such as symbolic loss. • No consistent evidence to suggest that depressed people show more anger. • If anger is directed inwards we would not expect depressed people to be hostile to others, but they are. • The effect of loss of parent does appear to be associated with later depression.. • It has been estimated that fewer then 10% of people who experience major losses in their early life go on to develop depression (Bonanno, 2004) • However it would be extremely difficult to isolate the separation from parent from other associated environmental variables such as financial loss, lack of adequate care, etc • Family discord and lack of adequate care predispose people to depression even in families where there is no actual separation (Harris, 2001)
    8. 8. Psychological explanations for depression: Psychodynamic & diathesis stress model No single explanation can account for depression, various contributory factors towards the disorder. Underlying genetic predispositions +childhood loss / negative thinking = depression if activated by the environment. Considerable evidence that social environment plays an important role in the development of unipolar depression. – Culture, gender, work environment, relationships, role of stressful life events. Brown and Harris 1978 • Result of a major study of depression among housewives in Camberwell, London. 2 factors contributing towards depression: 1. Severe life events 2. Long-term difficulties These had a particularly strong effect if vulnerability factors were experienced: a) Lack of paid employment b) 2 + children under 5 years c) Early loss of mother d) Lack of close confiding relationship. Mazure et al (2000) study on events, personality and depression • Previous research has shown that stressful life events precipitate episodes of MDD Q) Why do only some people who experience adverse events go on to develop depression? Becks’ highlighted the role of cognitive personality style. Method: • Matched pairs (86 participants in total) • Trained interviewers used standard scales to assess the number, severity and type of stressful events. • Cognitive personality characteristics were assessed by using Beck’s measures of sociotropy (Interpersonal dependency) and autonomy (need for independence and control) Findings: • Adverse life events, sociotropy and need for control were significantly related to depressive episode onset. The type of stressful event also had an impact on the effectiveness of treatment. Conclusion: • Adverse life events = potent risk factor in predicting depression • Cognitive- personality factors (e.g. need for control) increase susceptibility to depression • Interpersonal events (e.g. death of a loved one) has better treatment outcomes compared to adverse achievement events (e.g loss of job) Evaluation: • Studies important variables which may influence susceptibility to depression • However, it did not take into account factors such as social support networks, coping strategies and early trauma – play a large role in personality style • Study also found some evidence of gender differences in response to treatment 5 reasons why women are twice as likely to be diagnosed with depression 1. Biological factors – Evidence shows that hormonal factors in women may result in PMDD, Post- natal depression and menopause. – However men suffer from Andropause 2. Poorer quality of life & cultural pressures – Lower paid and lower status jobs, spill over between job and home, domestic chores, cultural pressure to be slim, attractive, good wife, mother, etc. These pressures lead to feeling of inadequacy. 3. Attributional style – Women are more likely to contribute failures to incompetence compared to men - linked to depression. (Beyer 1998) 4. Rumination – Women think about what is making them sad more than men. – These thoughts turn over and over in their minds. – Rumination is a predictor of depression (Nolen-Hoeksema and Corte 2004) 5. Adverse early life experiences – Sexual and physical abuse predisposed females to depression in adulthood (Veijola 1998) – There is no significant relationship between men who suffer from early life experience and adult depression in males. – In male adverse experiences were more likely to be expressed through antisocial behaviour and alcoholism • Support for life events theory and has been incorporated into the DSM diagnostic criteria under Axis IV. – Does not explain why many patients fail to report critical life events at the onset of their depression – Nor why some people have ongoing psychosocial stressors and yet do not become clinically depressed
    9. 9. Biological therapies are designed to redress the imbalance of biochemicals through drugs, ECT and in rare cases Psychosurgery Drug treatment Psychoactive drugs effect the nervous system in different ways, but they all increase or decease the availability of particular neurotransmitters Monoamine oxidase inhibitors (MAOIs) Tricyclics (TCAs) Selective serotonin re- uptake inhibitors (SSRIs) Blocks the production of monamine oxidase (an enzyme) used by the body to breakdown neurotransmitters such as serotonin and noradrenaline. Additionally improves availability of dopamine. Tofranil operates by blocking the re-uptake of noradrenaline and serotonin and making more of the neurotransmitters available. Example: prozac acts like tricyclics but targets reuptake of serotonin specifically Most frequent type of antidepressant prescribed MAOI AO2 • More effective in reducing symptoms of severe depression (Jarrett et al 1999) • Have to stick to a strict diet regime and avoid certain foods and medication (wrong combo can be fatal) • Recently been introduced as a skin patch which is less likely to produce dangerous food combos. • Not prescribed as often TCA AO2 • Milder than MAOIs • Less severe side effects. • Slower acting – have an immediate biological effect, but takes at least 10 days to reduce depressive symptoms. • Takes about 10 days for the cells to adapt to the TCA and begin releasing normal levels of neurotransmitters. • Need to continue medication after symptoms have improved due to 50% relapse rate (Montgomery, 1993). SSRI AO2 • More £ than tricyclics • Originally thought to have fewer side effects. • Josepth Wesbecker (1990) whilst staking Prozac shot 20 people at his former work place before killing himself • 2008 US military using Prozac to treat “stress” • Less side effects than tricyclics and MAOIs • Can be used with alcohol • Do not stop taking suddenly as can lead to unpleasant symptoms including dizziness, nausea, lethargy and headaches • SNRIs (Serotonin & noradrenaline) have more recently been developed. • SNRIs are more effective in treating depressive symptoms but may have more severe side effects Effective in reducing the symptoms of depression • Research shows that drugs can reduce symptoms of severe depression in around 65-75% of cases. • Compared with only 33% for placebos Treat the symptom and not the cause: • Drugs do not necessarily offer a long term cure. • Symptoms reoccur when drugs are not taken • Many psychologists believe that a biochemical imbalance is the result of rather than the cause of mental disorders. • Does not address the cause of the problem – i.e. why the person became depressed.  Combining drugs and psychological treatment • Some severely depressed people find it difficult to engage with psychological treatment • Short courses of antidepressant drugs are helpful Antidepressants can act as first line of defence to treat those who are suicidal. • In this way biological and psychological treatments can work together Alternative/ natural drug treatments • Hypericum – perforatum/ st john’s wart Sensational and shocking reports in the press about one or two individuals does not constitute evidence for a correlation Biological therapies for depression Drug treatment MAOIs TCAs SSRIs
    10. 10. ECT: Only used if antidepressant drugs have no effect and if there is a risk that the person will commit suicide (Mental Health Act 2007) ECT - The original procedures – less humane • used very high currents of electricity across both hemispheres of the brain • Severe side effects: memory loss, speech disorders& irreversible brain damage ECT - Modern procedure: - Much more humane: • Patient is given muscle relaxants & anaesthetic • Unilateral procedure is used • Administer 70 - 130 volts to the temple of one side of the head for 0.5 – 5.0 seconds • Induces convulsions for a brief period • Patient comes round from the anaesthetic with no recollection of the treatment • A course normally includes 6 sessions over a few weeks. Sackheim (2000) -double blind study 80 depressed patients allocated to: 1. UL ECT with 50% electrical dosages 2. UL ECT with 150 % electrical dosage 3. UL ECT 500 % above seizure threshold 4. BL ECT 150 % above threshold Depression severity, cognitive functioning and memory for personal and general knowledge were assessed by trained interviewers before, during, immediately after and 2 months after course of ECT • High dosage UL and BL were equally effective. • Week after treatment BL had greater memory& cognitive functioning impairment than all UL dosages. • 2 months after BL had the greatest memory impairment • 53% of the 62 patients who responded to ECT relapsed regardless of treatment group • UL ECT at high dosage is as effective as high dosage BL but produces less severe and persistent cognitive effects • Ethical issues? Unilateral or bi lateral? Traditional and modern ECT procedures AO2: Side effects When first introduced there were dangerous side effects including bone fractures, memory loss and confusion. There are “no detectable” changes in the brain structure with newer procedures. ECT can impair memory – particularly if bilateral ECT is used. AO2: Appropriateness Works more rapidly than antidepressant drugs or psychological therapies. Requires consent from patient or close relative. ECT has a history of terrible abuse being a means of punishing or controlling people in mental hospitals. Applying an electrical current to the brain is a frightening and forceful form on intervention. Even with newer techniques there are still side effects AO2: Effectiveness ECT is very effective in alleviating severe depression Studies indicate 60-70% of depressed people improve after treatment (Sackeim et al 2001). Precise understanding of how ECT reduces symptoms is not understood. - Like banging the sides of a TV? Likely that it works by increasing availability of noradrenaline or serotonin in the brain. It is so invasive it is difficult to isolate which element leads to the change. AO2: Transcracial Magnetic Stimulation – A safer alternative? Stimulates brain cells using magnetic fields without any direct contact with the brain. Painless, does not require the use of anaesthetics, electrodes or surgery. • Not sure how it works, but it is thought to increase the availability of noradrenalin and serotonin. Schulze-Rauschenbach (2005) found: • 46% of patients in the ECT group showed significant improvement • 44% in the TMS group showed significant improvement • ECT group showed signs of memory impairment - TMS did not.
    11. 11. Psychological therapies for depression – psychodynamic therapy • Freud introduced Psychoanalysis in the beginning of the 20th Century. Aim is not to “cure” or “remove symptoms” as this will not resolve the underlying issue. • Aim – for person 2 cope better with inner emotional conflicts that cause disturbance. • The purpose is to discover the unconscious conflicts and anxieties that have their origins in the past. • When the conflicts are brought in to consciousness the client is encouraged to work through them by examining and dealing with them is the a safe environment. • Confusing experiences from childhood are better understood through adult knowledge. AO2: Timescale • Conducted over a number of years which makes it expensive. • More current psychodynamic therapies are emerging which don’t deal with the past and are more affordable. Catharsis A psychological technique used to re lieve tension and anxiety by brin ging repressed feelings and fears to consciousness Free association Client asked to allow free flow of emotions, thoughts, connections, images and express these in words without censorship these should reflect the internal dynamic conflict. AO2: Appropriateness • Depressed people are 2 withdrawn & fatigued to deal with demanding therapy sessions. • People become easily disheartened & drop out of therapy before it has had any therapeutic effect. • For suicidal patients it is not an option as the process is long and slow. Word association The client has to respond to particular words with whatever comes instantly to mind. Dream analysis The client is asked to recount their dreams and the analyst helps them to interpret the hidden meanings. AO2: Effectiveness • Does it actually work? • Eysenck (1952) claimed it simply does not work! • However, there are studies with counter conclusions Transference This occurs when the client redirects feelings (of hostility)towards the therapist that are usually unconsciously directed towards a significant person in their life (usually a parent). Projective tests Many types of projective tests such as the Rorschach ink blot and the Thematic Apperception Test The client is asked to describe what they see in the ink blot or to tell a story around the picture AO2: Danger of emotional harm • Guide a client towards an insight that may prove emotionally more distressing than the original incident. • Therapists should never work beyond their competence in dealing with what may arise in therapy. Explanation Catharsis Free association Word association Dream analysis Transference Projective tests AO2: Time scale AO2: Appropriateness AO2: Effectiveness AO2: Danger of emotional harm Difficulties in evaluating the effectiveness of therapy – What is meant by a cure? – Corsini and Wedding (1995) claim that “cures” from using psychotherapy range from 30-60% – This range depends on what we mean by cure. – Bolger (1989) concept of “cure” is inappropriate and based on a model of physical symptoms only. – Should we assume psychological disorders follow a course similar to physical diseases? – The effectiveness is a subjective concept measured only by the extent to which clients feel that their condition has improved. Methodological issues – Firstly due to the fact that treatment can span several years and the point at which is assessed may skew data. – The variables being measured are rather abstract in nature. – Wedding (1995) explains that there are too many variables involved to enable a controlled and statically valid outcome study – lack of empirical principles. – At best we can make comparisons of symptoms experienced by the client at the beginning and end of treatment. Comparing research studies gains A02 points • Bysenck (1952) reviewed 2 outcome studies. – 66% of control group improved spontaneously – 44% of psychoanalysis patients improved – Therefore psychoanalysis does not work • Bergin (1971) – Patients in one of the control groups were in fact hospitalized and those in the other group were being treated by their GP. – Improvement in 83% of psychoanalysis group – Improvement in 33% in the control group.