psychopathology: schizophrenia, depression and anxiety disorders
Created | Updated Nov 9, 2005
Schizophrenia
Schizophrenia refers to a disintegration of personality. It is a serious mental disorder that is characterised by severe disruptions in psychological functioning and a loss of contact with reality. They may experience a variety of disturbing and frightening symptoms.
Clinical Characteristics
According to the DSM-1V schizophrenia is diagnosed when 2 or more of the following symptoms are present for more then 6 months, along with reduced social functioning and when the symptoms are not due to substance abuse or any other medical conditioning.
• Thought disturbances – (+ve) reasoning that appears obscure and incoherent to others. e.g. thought insertion (controlled by aliens) and delusions (grandeur)
• Perceptual disturbances – (+ve) a tendency to perceive the world differently (hallucinations and hearing voices) and inability to recognise the emotional states of others.
• Disturbances of affect/violation – (-ve) withdrawal, flattened and inappropriate affect, reduced motivation and difficulty planning + carrying out actions.
• Emotional disturbances – display no emotions or inappropriate emotional reactions.
• Psychomotor disturbances – catatonia, stereotype (e.g. rocking) and frenetic activity (grimacing, giggling)
• Language impairments – may repeat sounds or use invented words (neologisms)
• Disturbances in social functioning – inability to maintain social relationships, poor social skills - poor quality of life.
Schizophrenia covers a family of loosely related disorders.
A distinction has been made:
Type 1 (positive/acute) presence of something normally absent.
Type 2 (negative/chronic) absence of something that is normally present.
3 main subtypes are:
Paranoid type - +ve symptoms. Awareness + language relatively unimpaired
Disorganised type – severe. Disorganised speech and behaviour, vivid hallucinations, flat emotion.
Catatonic – apathy and psychomotor disturbances.
Prognosis
- have a few acute episodes followed by full recovery
- periodic acute episodes throughout life but lead a relatively normal life when in remission
- persistent deterioration, can be partly alleviated by drug therapy.
Biological Explanations
Genetic causes
Family studies – children with 2 schizophrenic parents are about 46% more likely to develop the disorder BUT/ environmental?
Twin studies – Gottesman summarised 40 studies - MZ twins have 48% concordance rates compared to 17% for DZ twins.
BUT/ MZ share more similar environments
Fischer – offspring of discordant MZ twins had a higher risk of the disorder – hereditable.
Zimbardo – the closer the genetic link the higher the likelihood of developing the disorder.
Kendler – 1st degree relatives 18x more likely to develop the disorder
Adoption studies – When environment is matched the rates of schizophrenia is higher with schizophrenic biological parents then with adopted children and non-schizophrenic parents.
Finnish adoption study (Tienari) – 155 had schizophrenic mothers + control group. In adulthood 10% had developed the disorder compared to 1% of the control group.
Genes – Sherrington – found evidence for a cluster of genes on the 5th chromosome that may make individuals susceptible – not confirmed
- Not 100% concordance – genetic predisposition? Triggered by environment?
Biochemical causes
Dopamine shown to be connected with schizophrenia
• Large doses of amphetamines (which  dopamine activity) can create a condition that closely resembles acute paranoid schizophrenia. Small doses can trigger more symptoms in a schizophrenic.
• Anti-schizophrenia drugs which reduce +ve symptoms work by blocking the transmission of the neurotransmitter dopamine
• Davidson – found that the drug L-dopa which increases levels of dopamine can produce many of the symptoms of schizophrenia.
• Post mortems on schizophrenics and PET scans have found higher amounts of dopamine and dopamine synaptic sites.
- Over simplified – new drugs (clozapine) work by affecting other neurotransmitters especially serotonin.
- Drugs bloke dopamine rapidly but symptoms reduce slowely
- Dopamine could be a cause or effect.
Brain
• Enlarged ventricles – larger in schizophrenics due to brain cell loss. Associated with negative symptoms
BUT/ correlational – symptom rather then a cause
Non-schizophrenics can also have enlarged ventricles
• Post mortems show schizophrenics brains are 6% lighter and have fewer neurons in the cortex.
• MRI and CT scans have shown reduced brain weight, enlarged ventricles and abnormalities in the frontal cortex and hippocampus
• Frontal lobe damage may account for some of the negative symptoms
• Schizophrenics brains do not show the usual prefrontal activation of the cortex when given problem solving tasks.
• Generally the degree of brain abnormality correlates with the severity of the symptoms
- all the above remove blame from parents + family
Psychological Explanations
Family Relationships
Disturbed patterns of communication within families may be a factor in the development of schizophrenia.
1) Bateson’s ‘Double-Bind’ theory
Proposed that certain families that use maladaptive methods of communication – there is contradiction between what is said and how it is said (tone, body language) - confusion, self doubt and eventual withdrawal = schizophrenic symptoms established as a learned response to avoid social contact.
Lain – sane response to a disordered environment.
- Supported by clinical observations and retrospective accounts
- BUT/ SELECTED information he needed - biased
- Failure to replicate
- Abnormal communication may be a RESULT of schizophrenia rather then a cause
- This theory - blame + guilt
2) Schizophrenogenic families/mothers – Fromm-Reichman
Mothers whose actions are contradictory e.g. overprotecting and rejecting - faulty connections that can lead to schizophrenia.
BUT/ little evidence to support this view
3) Expressed Emotion – looks at development rather then onset
Brown examined progress of people with schizophrenia that had returned home after hospitalisation.
Families were labelled as low or high EE (characterised by high levels of hostility, criticism, over involvement and over concern)
Schizophrenics’ - high EE families – 58% relapsed
- low EE families – 10% relapsed
Vaughn + Leff – found that relapse was higher among patients returned to high EE families and that likelihood of relapse correlated with amount of time spent with family members.
Rosenfarb – observed discharged schizophrenics when returned to high EE families. Critical comments - increase in symptoms - increase in critical comments = vicious cycle
- Replicated. Cross cultural support
- Application – family counselling provided
- Evidence: dysfunctional families - schizophrenia
- BUT/ schizophrenia - dysfunctional families
- If family is at fault then all children should develop it.
- Schizophrenics who have minimal contact with family do not have a lower chance of having a relapse.
- High EE is less common in the families of 1st episode patients then those with re-admissions – suggesting that high EE may develop as a response to schiz
Social Relationships
Schizophrenia = 8x more common in low social classes
Many studies have found evidence that schizophrenia is more common in low social classes then high social classes
1) Social drift hypothesis
Schizophrenics drift down social ladder. Lose jobs - low skill/paid employment
In the UK it was found that male schizophrenics have lower status and lower paid jobs then their fathers (Goldberg + Morrison)
2) Social causation hypothesis
Members of lower social classes have more stressful lives (low income/poor housing/+ crime) - more vulnerable to schizophrenia
In the US it was found that fathers of schizophrenics were more likely to be from a lower social class (Turner + Wagonfeld)
Diathesis stress model
Combines genetic and psychological explanations
Suggests that individuals are born with a predisposition towards certain behaviours such as a mental disorder. However, the disorder may not appear except under certain circumstances which act as a trigger or stressor. Family environment may act as such a stressor.
Finnish Adoption Project (Tienari)
Children were assessed in terms of their risk of developing schizophrenia (degree of relatedness) then family environment was looked at.
So far all the participants who have developed schizophrenia were from disruptive households and ‘healthy’ participants have a very low incidence rate
BUT/ not yet complete. Most participants = too young.
- Hard to differentiate between genetic family influences from environmental genetic influences – if a parent has schizophrenia you may inherit it or it may develop from living with that person.
- Adoption studies suggest that both are important as not all children with schizophrenic parents develop the disorder.
Depression
Depression is a type of mood disorder in which the sufferer experiences feelings of great sadness, worthlessness, guilt, and finds the challenges of life overwhelming. Term used when the mood disturbance is so severe that the persons day-to-day functioning is impaired.
Unipolar + Dipolar = 2 main types.
Clinical Characteristics
Unipolar depression
• Cognitive – low self esteem, inappropriate guilt, self dislike, worthlessness, loss of interest*, negative thoughts of self + future, suicidal thoughts, poor memory, attention deficits, hopelessness, pessimism, lack of motivation, depressed mood*
• Behavioural – loss of appetite, disordered sleep, poor self-care and care of others, suicide attempts.
• Emotional – sadness, irritability, apathy, melancholy, self-involvement, guilt, passivity, loss of interest
• Physical – loss/increase of appetite and weight, lack of energy, headaches, sleep disturbances (insomnia/oversleeping), menstrual disruption.
- Reactive (external cause) or endogenous (no obvious cause)
- Diagnosed when 5 symptoms occur nearly everyday for a min. of 2 weeks.
- 4 – 5% in general population.
Biological Explanations
Genetics – predisposing factor?
Family studies
Depression seems to run in families suggesting a genetic influence.
Oruc - found that 1st relatives of depressives were 2/3 X more likely to be diagnosed with depression then 1st relatives of non-depressives.
1st relatives of severely depressed patients were at a higher risk of developing severe depression compared to the statistics for the general population. Relatives were 10-15% more likely to develop it compared to 1-2%.
- Shared environment?
- Inconclusive findings
Twin studies
• McGuffin tested about 200 twin pairs - 46% MZ concordance / 20% DZ
• Kendler and Prescott - about 4000 twin pairs. Depression 39% heritability. 61% environmental. no gender bias BUT/ Bierut - female twins had a stronger genetic component.
- 100% concordance
- Must be some genetic component
Adoption studies
• Wendler found that biological relatives of adopted depressives were 8X more likely then adopted relatives to develop depression
• Harrington et al. – biological relatives of adopted depressives more likely (20%) to develop depression then adopted relatives (5-10% likely)
-Removes Blame
Biochemical - Neurotransmitter
Deficiency of noradrenalin may cause depression.
• Teuting – analysed urine of depressed and normal people and found lower levels of products associated with noradrenalin in depressed
• Success of anti-depressant drugs that increase noradrenalin production.
• Mann found impaired serotonin activity in depressed
- Cause or effect?
- Effects of drugs not the same for everyone
Hormonal
Post-Partum depression (PPD), PMS, seasonal affective disorder (SAD) all linked to hormonal changes.
• Abramowitz – 41% of women admitted to a psychiatric hospital entered on or within a day of the start of menstruation.
• About 20% of women report moderate depression in the first weeks after giving birth.
• Carroll – suppressing cortisol secretion (stress hormone) alleviated depression
• Cooper – compared postnatal and normal women and found NO significant difference in depression levels.
- Cause or effect?
- social changes affect results for hormone changes
- everyone has hormonal changes – not everyone develops depression.
- may explain why more women suffer from depression.
may be a predisposing factor.
Viral causes – Borna virus
• Amsterdam – 12 carrying virus all uni/bi depressed. Non-depressed – none were carrying the Borna virus.
• Bode – blood survey of 3 continents. Virus present in 2% normal people, 30% severely depressed and 15% with chronic brain diseases.
- Does not explain all cases of depression.
Psychological Explanations
Psychodynamic - Freud
Hostile feelings towards parents are redirected towards the self in the form of self-accusation or self-hatred.
• Bowlby – separation from a primary caregiver in early childhood may increase susceptibility to depression later on.
• Bifulco – studied 250 women who had experienced maternal loss when younger than 17. 2X more likely to develop depression or anxiety disorders.
• Hinde – separated mother and baby monkey - exhibited depression.
• Finlay-Jones + Brown – depressed patients were more likely to have experience more stressful situations particularly loss in the past year then the controls.
- dreams of anger and hostility would be expected – but dreams of loss and failure were found.
- wouldn’t expect depressives to be hostile to others because feelings are ‘turned inwards’ – but they were often hostile to others
- usual criticisms of Freud
- inconsistent evidence
- difficult to test unconscious motives
Behavioural
Learned Helplessness (Seligman)
Seligman – if a rat or a dog was placed in an inescapable position and given electric shocks before being placed in an escapable position it would then ‘give up’ and show learned helplessness.
- generalised to humans
Maier and Seligman – exposed humans to inescapable noise. When they were placed in similar, escapable situations people would often fail to attempt escape.
• gender differences – depressed, angry – may explain diagnosis diffs.
- findings difficult to replicate
- Wortman and Brehm – helplessness improved subsequent performance.
- reductionist – doesn’t take cognitions into account
- animal studies – cant generalise to humans
Reinforcement (Lewinson)
Depressed people become trapped in a cycle of social withdrawal which leads to a lack of +ve reinforcement - depression.
If someone close to us dies or we lose our job we lose out on opportunities for +ve reinforcement. Also others may give us sympathy - +ve reinforcement (maintenance of depression)
- depression not always linked to a particular event - endogenous
- depression usually lasts after sympathy has stopped.
- people not always sympathetic
Cognitive – Beck
Depression caused by a bias towards negative interpretations of events – due to childhood experiences (e.g. loss, bullying, poor parenting). These biases are activated when similar situations are encountered.
Faulty cognitions - maladaptive emotions - depression
Cognitive Triad :
1) –ve views of self
2) –ve view of world
3) –ve view of future
• Scores on Automatic Thoughts Questionnaire correlate with scores on Beck Depression Inventory. ATQ score decreased after therapy.
• Craighead – D more likely to recall –ve info. Remembered wrong answers more then right answers.
- -ve thinking = cause or effect of depression?
- longitudinal studies support the view that –ve cognitions = an effect.
Cognitive-Behavioural – Abramson
Seligman failed to include cognitions so Abramson reformulated his theory.
When people experience failure they try and explain it, often attributing the failure to themselves (internal).
Abramson – depressed have a certain attributional style. Attributions for failure = internal, stable and global – this style arrises from maladaptive learning experiences.
• Internal/external – person or environment
• Stable/unstable – always happen or one incident
• Global/specific – one part of life or all areas.
Seligman – Attributional Styles Questionnaire to students after exams.
2 days later: unstable, specific attributions had recovered.
Stable, global attributions still depressed.
- Students – can’t be generalised to clinical patients
Ford + Neale found that contrary to expectations depressed people were more realistic about the future and did not underestimate the control they had.
Cog-B therapies = successful
But/ better for preventing recurrence of depression
Anxiety disorders - Phobias
Phobia – an irrational and persistent fear of an object, activity or situation that the person has no control over and it interferes with people’s ability to function normally.
Women 2x as likely to develop phobias – gender bias in diagnosis.
Clinical Characteristics
High levels of anxiety, recognise the fear is excessive, situation/object avoided, may produce panic attacks, sympathetic nervous system activated (adrenaline released), feelings of dread and panic, fleeing or freezing, breathing difficult.
3 categories:
• Agoraphobia – fear of open/public spaces
Usually started by panic attack then fear of having another one in public.
• Social phobias – fear of social situations, concern about own behaviour and reactions of others.
• Specific phobias – arachnophobia, hydrophobia, fear of heights.
- 6% of general population – higher in women – gender bias in diagnosis.
Biological Explanations
Genetic
Twin studies
• Slater + Sheilds - 41% MZ concordance / 4% DZ
• Torgersen – 31% concordance for agoraphobia on MZ twins. 0 for DZ
But/ none of the twins shared the same phobias.
- 100% concordance
- small sample size
- Must be some genetic component
Family Studies
• Solyom et al. 45% of phobic patients studied had a family history of the disorder. Control = 19%
• Noyes et al. inflated rates of agoraphobia (12%) and panic disorder (17%) in 1st relatives of phobic patients he interviewed.
• Ost – 64% of blood phobics had at least one close relative with the same.
• Fyer et al. 31% of 1st relatives of phobics also had phobias.
But/ only 2 had the same type of phobia
- not all differences are statistically significant – may have occurred through sampling error.
- could be caused by similar environments
- alternative explanation - imitation
- Must be some genetic component – predisposition?
Neurobiological
Phobics generally have a high level of autonomic arousal – sensitive to developing phobias – easily conditioned to fear a particular stimulus.
- cause or effect
- not much evidence
Biological Preparedness
Seligman – more likely to have phobias of potentially harmful objects (snakes, spiders) then of fluffy kittens so may have evolved with a preparedness to develop phobias - survival advantage.
• DeSilva – 88 phobic patients in Sri Lanka tended to exhibit fears that were biologically based - believed this proved universal nature of phobias
• Garcia + Koelling – showed that rats could be conditioned to avoid certain tastes (potentially poisonous) but not certain smells (harmless) – some organisms cannot be taught to avoid certain things.
- evolutionarily plausible (dark, heights)
- alternative explanation – observational learning
- snake + spider phobics don’t fear being hurt but having a panic attack whilst in contact with it.
- cant explain fears of harmless situations or objects (cotton wool)
Psychological Explanations
Psychodynamic - Freud
The root of phobias is from a traumatic event in childhood which has been repressed. This then manifests itself as a phobia due to conflict between the Id and the Ego when the person fears there unconscious wishes will express themselves  anxiety  impulses displaced to another object.
‘Little Hans’ – scared of horses – represented unconscious fear of his father as he associated horses with his father.
- cannot prove the psychodynamic theory wrong as it refers to unconscious wishes
- alternative explanation – classical conditioning
- based on case studies
- usual Freudian criticisms.
Behavioural
Classical Conditioning
Watson + Rayner – ‘Little Albert’ - paired loud noise (neutral stimulus) with a white rat (unconditional stimulus). He later became scared of most white fluffy objects (conditioned response).
- unethical
- failure to replicate
- Keuthen – 50% of phobics couldn’t remember any unpleasant experiences relating to the phobia. But/ may have repressed the memory
- DiNardo – after a traumatic experience with dogs: 50% developed phobia, 50% no phobia
Operant Conditioning – two process theory
avoidance of phobic stimulus - reduces anxiety - negative reinforcement
Social learning theory
Fears learned through imitation.
Mineka – monkeys could develop a snake phobia just by watching another monkey experience fear in the presence of a snake. BUT/ animal study - cant be generalised to humans
Control – Rotter
People with external loci of control are more likely to become depressed
Where parents don’t let their children outside without supervision - anxiety in child - phobia about going outside
- plausible
- systematic desensitisation 75% successful at dealing with specific phobias.
Cognitive-Behavioural - Beck
Irrational thoughts about the future possibility of a fearful situation - phobia
Anxious individuals have cognitive biases - exaggeration of threats posed by internal and external stimuli
e.g. sensation of crowded lift - associate lifts + suffocation - fear of lifts - generalised to similar situations - claustrophobia
• Matthews – threatening stimuli recognised faster by people with phobias – explained by them having more negative cognitions
• Beck – phobics often realises their fear is irrational but close proximity to the stimulus increases the sense of danger.
• Phobics more preoccupied with fear of fear rather then actual object.
- support from studies
- Cog-B therapies often very successful
- irrational thoughts – cause or effect?
Social factors
Holmes + Rahe – major life events are a contributing factor in the development of anxiety disorders.
Kobasa – minor daily hassles have a cumulative effect so can build up resulting in an anxiety disorder.
Kielner + Marshall – 84% of sample of agoraphobics had experienced family problems before the onset.
Gerlsman – phobics had lower than normal parental affection and were often over-protected.
- retrospective recall – unreliable
- demand characteristics
- correlational – cause or effect?
Diathesis stress model
Suggests that everyone has a certain tolerance threshold for stress and this varies between individuals. This may be genetically inherited or learned through experience. If the degree of environmental stress exceeds a certain threshold then anxiety symptoms result. But due to everyone being different the same set of stressors will result in symptoms for some people but not in others.
- plausible
- doesn’t explain the exact nature of the variable threshold
Schizophrenia refers to a disintegration of personality. It is a serious mental disorder that is characterised by severe disruptions in psychological functioning and a loss of contact with reality. They may experience a variety of disturbing and frightening symptoms.
Clinical Characteristics
According to the DSM-1V schizophrenia is diagnosed when 2 or more of the following symptoms are present for more then 6 months, along with reduced social functioning and when the symptoms are not due to substance abuse or any other medical conditioning.
• Thought disturbances – (+ve) reasoning that appears obscure and incoherent to others. e.g. thought insertion (controlled by aliens) and delusions (grandeur)
• Perceptual disturbances – (+ve) a tendency to perceive the world differently (hallucinations and hearing voices) and inability to recognise the emotional states of others.
• Disturbances of affect/violation – (-ve) withdrawal, flattened and inappropriate affect, reduced motivation and difficulty planning + carrying out actions.
• Emotional disturbances – display no emotions or inappropriate emotional reactions.
• Psychomotor disturbances – catatonia, stereotype (e.g. rocking) and frenetic activity (grimacing, giggling)
• Language impairments – may repeat sounds or use invented words (neologisms)
• Disturbances in social functioning – inability to maintain social relationships, poor social skills - poor quality of life.
Schizophrenia covers a family of loosely related disorders.
A distinction has been made:
Type 1 (positive/acute) presence of something normally absent.
Type 2 (negative/chronic) absence of something that is normally present.
3 main subtypes are:
Paranoid type - +ve symptoms. Awareness + language relatively unimpaired
Disorganised type – severe. Disorganised speech and behaviour, vivid hallucinations, flat emotion.
Catatonic – apathy and psychomotor disturbances.
Prognosis
- have a few acute episodes followed by full recovery
- periodic acute episodes throughout life but lead a relatively normal life when in remission
- persistent deterioration, can be partly alleviated by drug therapy.
Biological Explanations
Genetic causes
Family studies – children with 2 schizophrenic parents are about 46% more likely to develop the disorder BUT/ environmental?
Twin studies – Gottesman summarised 40 studies - MZ twins have 48% concordance rates compared to 17% for DZ twins.
BUT/ MZ share more similar environments
Fischer – offspring of discordant MZ twins had a higher risk of the disorder – hereditable.
Zimbardo – the closer the genetic link the higher the likelihood of developing the disorder.
Kendler – 1st degree relatives 18x more likely to develop the disorder
Adoption studies – When environment is matched the rates of schizophrenia is higher with schizophrenic biological parents then with adopted children and non-schizophrenic parents.
Finnish adoption study (Tienari) – 155 had schizophrenic mothers + control group. In adulthood 10% had developed the disorder compared to 1% of the control group.
Genes – Sherrington – found evidence for a cluster of genes on the 5th chromosome that may make individuals susceptible – not confirmed
- Not 100% concordance – genetic predisposition? Triggered by environment?
Biochemical causes
Dopamine shown to be connected with schizophrenia
• Large doses of amphetamines (which  dopamine activity) can create a condition that closely resembles acute paranoid schizophrenia. Small doses can trigger more symptoms in a schizophrenic.
• Anti-schizophrenia drugs which reduce +ve symptoms work by blocking the transmission of the neurotransmitter dopamine
• Davidson – found that the drug L-dopa which increases levels of dopamine can produce many of the symptoms of schizophrenia.
• Post mortems on schizophrenics and PET scans have found higher amounts of dopamine and dopamine synaptic sites.
- Over simplified – new drugs (clozapine) work by affecting other neurotransmitters especially serotonin.
- Drugs bloke dopamine rapidly but symptoms reduce slowely
- Dopamine could be a cause or effect.
Brain
• Enlarged ventricles – larger in schizophrenics due to brain cell loss. Associated with negative symptoms
BUT/ correlational – symptom rather then a cause
Non-schizophrenics can also have enlarged ventricles
• Post mortems show schizophrenics brains are 6% lighter and have fewer neurons in the cortex.
• MRI and CT scans have shown reduced brain weight, enlarged ventricles and abnormalities in the frontal cortex and hippocampus
• Frontal lobe damage may account for some of the negative symptoms
• Schizophrenics brains do not show the usual prefrontal activation of the cortex when given problem solving tasks.
• Generally the degree of brain abnormality correlates with the severity of the symptoms
- all the above remove blame from parents + family
Psychological Explanations
Family Relationships
Disturbed patterns of communication within families may be a factor in the development of schizophrenia.
1) Bateson’s ‘Double-Bind’ theory
Proposed that certain families that use maladaptive methods of communication – there is contradiction between what is said and how it is said (tone, body language) - confusion, self doubt and eventual withdrawal = schizophrenic symptoms established as a learned response to avoid social contact.
Lain – sane response to a disordered environment.
- Supported by clinical observations and retrospective accounts
- BUT/ SELECTED information he needed - biased
- Failure to replicate
- Abnormal communication may be a RESULT of schizophrenia rather then a cause
- This theory - blame + guilt
2) Schizophrenogenic families/mothers – Fromm-Reichman
Mothers whose actions are contradictory e.g. overprotecting and rejecting - faulty connections that can lead to schizophrenia.
BUT/ little evidence to support this view
3) Expressed Emotion – looks at development rather then onset
Brown examined progress of people with schizophrenia that had returned home after hospitalisation.
Families were labelled as low or high EE (characterised by high levels of hostility, criticism, over involvement and over concern)
Schizophrenics’ - high EE families – 58% relapsed
- low EE families – 10% relapsed
Vaughn + Leff – found that relapse was higher among patients returned to high EE families and that likelihood of relapse correlated with amount of time spent with family members.
Rosenfarb – observed discharged schizophrenics when returned to high EE families. Critical comments - increase in symptoms - increase in critical comments = vicious cycle
- Replicated. Cross cultural support
- Application – family counselling provided
- Evidence: dysfunctional families - schizophrenia
- BUT/ schizophrenia - dysfunctional families
- If family is at fault then all children should develop it.
- Schizophrenics who have minimal contact with family do not have a lower chance of having a relapse.
- High EE is less common in the families of 1st episode patients then those with re-admissions – suggesting that high EE may develop as a response to schiz
Social Relationships
Schizophrenia = 8x more common in low social classes
Many studies have found evidence that schizophrenia is more common in low social classes then high social classes
1) Social drift hypothesis
Schizophrenics drift down social ladder. Lose jobs - low skill/paid employment
In the UK it was found that male schizophrenics have lower status and lower paid jobs then their fathers (Goldberg + Morrison)
2) Social causation hypothesis
Members of lower social classes have more stressful lives (low income/poor housing/+ crime) - more vulnerable to schizophrenia
In the US it was found that fathers of schizophrenics were more likely to be from a lower social class (Turner + Wagonfeld)
Diathesis stress model
Combines genetic and psychological explanations
Suggests that individuals are born with a predisposition towards certain behaviours such as a mental disorder. However, the disorder may not appear except under certain circumstances which act as a trigger or stressor. Family environment may act as such a stressor.
Finnish Adoption Project (Tienari)
Children were assessed in terms of their risk of developing schizophrenia (degree of relatedness) then family environment was looked at.
So far all the participants who have developed schizophrenia were from disruptive households and ‘healthy’ participants have a very low incidence rate
BUT/ not yet complete. Most participants = too young.
- Hard to differentiate between genetic family influences from environmental genetic influences – if a parent has schizophrenia you may inherit it or it may develop from living with that person.
- Adoption studies suggest that both are important as not all children with schizophrenic parents develop the disorder.
Depression
Depression is a type of mood disorder in which the sufferer experiences feelings of great sadness, worthlessness, guilt, and finds the challenges of life overwhelming. Term used when the mood disturbance is so severe that the persons day-to-day functioning is impaired.
Unipolar + Dipolar = 2 main types.
Clinical Characteristics
Unipolar depression
• Cognitive – low self esteem, inappropriate guilt, self dislike, worthlessness, loss of interest*, negative thoughts of self + future, suicidal thoughts, poor memory, attention deficits, hopelessness, pessimism, lack of motivation, depressed mood*
• Behavioural – loss of appetite, disordered sleep, poor self-care and care of others, suicide attempts.
• Emotional – sadness, irritability, apathy, melancholy, self-involvement, guilt, passivity, loss of interest
• Physical – loss/increase of appetite and weight, lack of energy, headaches, sleep disturbances (insomnia/oversleeping), menstrual disruption.
- Reactive (external cause) or endogenous (no obvious cause)
- Diagnosed when 5 symptoms occur nearly everyday for a min. of 2 weeks.
- 4 – 5% in general population.
Biological Explanations
Genetics – predisposing factor?
Family studies
Depression seems to run in families suggesting a genetic influence.
Oruc - found that 1st relatives of depressives were 2/3 X more likely to be diagnosed with depression then 1st relatives of non-depressives.
1st relatives of severely depressed patients were at a higher risk of developing severe depression compared to the statistics for the general population. Relatives were 10-15% more likely to develop it compared to 1-2%.
- Shared environment?
- Inconclusive findings
Twin studies
• McGuffin tested about 200 twin pairs - 46% MZ concordance / 20% DZ
• Kendler and Prescott - about 4000 twin pairs. Depression 39% heritability. 61% environmental. no gender bias BUT/ Bierut - female twins had a stronger genetic component.
- 100% concordance
- Must be some genetic component
Adoption studies
• Wendler found that biological relatives of adopted depressives were 8X more likely then adopted relatives to develop depression
• Harrington et al. – biological relatives of adopted depressives more likely (20%) to develop depression then adopted relatives (5-10% likely)
-Removes Blame
Biochemical - Neurotransmitter
Deficiency of noradrenalin may cause depression.
• Teuting – analysed urine of depressed and normal people and found lower levels of products associated with noradrenalin in depressed
• Success of anti-depressant drugs that increase noradrenalin production.
• Mann found impaired serotonin activity in depressed
- Cause or effect?
- Effects of drugs not the same for everyone
Hormonal
Post-Partum depression (PPD), PMS, seasonal affective disorder (SAD) all linked to hormonal changes.
• Abramowitz – 41% of women admitted to a psychiatric hospital entered on or within a day of the start of menstruation.
• About 20% of women report moderate depression in the first weeks after giving birth.
• Carroll – suppressing cortisol secretion (stress hormone) alleviated depression
• Cooper – compared postnatal and normal women and found NO significant difference in depression levels.
- Cause or effect?
- social changes affect results for hormone changes
- everyone has hormonal changes – not everyone develops depression.
- may explain why more women suffer from depression.
may be a predisposing factor.
Viral causes – Borna virus
• Amsterdam – 12 carrying virus all uni/bi depressed. Non-depressed – none were carrying the Borna virus.
• Bode – blood survey of 3 continents. Virus present in 2% normal people, 30% severely depressed and 15% with chronic brain diseases.
- Does not explain all cases of depression.
Psychological Explanations
Psychodynamic - Freud
Hostile feelings towards parents are redirected towards the self in the form of self-accusation or self-hatred.
• Bowlby – separation from a primary caregiver in early childhood may increase susceptibility to depression later on.
• Bifulco – studied 250 women who had experienced maternal loss when younger than 17. 2X more likely to develop depression or anxiety disorders.
• Hinde – separated mother and baby monkey - exhibited depression.
• Finlay-Jones + Brown – depressed patients were more likely to have experience more stressful situations particularly loss in the past year then the controls.
- dreams of anger and hostility would be expected – but dreams of loss and failure were found.
- wouldn’t expect depressives to be hostile to others because feelings are ‘turned inwards’ – but they were often hostile to others
- usual criticisms of Freud
- inconsistent evidence
- difficult to test unconscious motives
Behavioural
Learned Helplessness (Seligman)
Seligman – if a rat or a dog was placed in an inescapable position and given electric shocks before being placed in an escapable position it would then ‘give up’ and show learned helplessness.
- generalised to humans
Maier and Seligman – exposed humans to inescapable noise. When they were placed in similar, escapable situations people would often fail to attempt escape.
• gender differences – depressed, angry – may explain diagnosis diffs.
- findings difficult to replicate
- Wortman and Brehm – helplessness improved subsequent performance.
- reductionist – doesn’t take cognitions into account
- animal studies – cant generalise to humans
Reinforcement (Lewinson)
Depressed people become trapped in a cycle of social withdrawal which leads to a lack of +ve reinforcement - depression.
If someone close to us dies or we lose our job we lose out on opportunities for +ve reinforcement. Also others may give us sympathy - +ve reinforcement (maintenance of depression)
- depression not always linked to a particular event - endogenous
- depression usually lasts after sympathy has stopped.
- people not always sympathetic
Cognitive – Beck
Depression caused by a bias towards negative interpretations of events – due to childhood experiences (e.g. loss, bullying, poor parenting). These biases are activated when similar situations are encountered.
Faulty cognitions - maladaptive emotions - depression
Cognitive Triad :
1) –ve views of self
2) –ve view of world
3) –ve view of future
• Scores on Automatic Thoughts Questionnaire correlate with scores on Beck Depression Inventory. ATQ score decreased after therapy.
• Craighead – D more likely to recall –ve info. Remembered wrong answers more then right answers.
- -ve thinking = cause or effect of depression?
- longitudinal studies support the view that –ve cognitions = an effect.
Cognitive-Behavioural – Abramson
Seligman failed to include cognitions so Abramson reformulated his theory.
When people experience failure they try and explain it, often attributing the failure to themselves (internal).
Abramson – depressed have a certain attributional style. Attributions for failure = internal, stable and global – this style arrises from maladaptive learning experiences.
• Internal/external – person or environment
• Stable/unstable – always happen or one incident
• Global/specific – one part of life or all areas.
Seligman – Attributional Styles Questionnaire to students after exams.
2 days later: unstable, specific attributions had recovered.
Stable, global attributions still depressed.
- Students – can’t be generalised to clinical patients
Ford + Neale found that contrary to expectations depressed people were more realistic about the future and did not underestimate the control they had.
Cog-B therapies = successful
But/ better for preventing recurrence of depression
Anxiety disorders - Phobias
Phobia – an irrational and persistent fear of an object, activity or situation that the person has no control over and it interferes with people’s ability to function normally.
Women 2x as likely to develop phobias – gender bias in diagnosis.
Clinical Characteristics
High levels of anxiety, recognise the fear is excessive, situation/object avoided, may produce panic attacks, sympathetic nervous system activated (adrenaline released), feelings of dread and panic, fleeing or freezing, breathing difficult.
3 categories:
• Agoraphobia – fear of open/public spaces
Usually started by panic attack then fear of having another one in public.
• Social phobias – fear of social situations, concern about own behaviour and reactions of others.
• Specific phobias – arachnophobia, hydrophobia, fear of heights.
- 6% of general population – higher in women – gender bias in diagnosis.
Biological Explanations
Genetic
Twin studies
• Slater + Sheilds - 41% MZ concordance / 4% DZ
• Torgersen – 31% concordance for agoraphobia on MZ twins. 0 for DZ
But/ none of the twins shared the same phobias.
- 100% concordance
- small sample size
- Must be some genetic component
Family Studies
• Solyom et al. 45% of phobic patients studied had a family history of the disorder. Control = 19%
• Noyes et al. inflated rates of agoraphobia (12%) and panic disorder (17%) in 1st relatives of phobic patients he interviewed.
• Ost – 64% of blood phobics had at least one close relative with the same.
• Fyer et al. 31% of 1st relatives of phobics also had phobias.
But/ only 2 had the same type of phobia
- not all differences are statistically significant – may have occurred through sampling error.
- could be caused by similar environments
- alternative explanation - imitation
- Must be some genetic component – predisposition?
Neurobiological
Phobics generally have a high level of autonomic arousal – sensitive to developing phobias – easily conditioned to fear a particular stimulus.
- cause or effect
- not much evidence
Biological Preparedness
Seligman – more likely to have phobias of potentially harmful objects (snakes, spiders) then of fluffy kittens so may have evolved with a preparedness to develop phobias - survival advantage.
• DeSilva – 88 phobic patients in Sri Lanka tended to exhibit fears that were biologically based - believed this proved universal nature of phobias
• Garcia + Koelling – showed that rats could be conditioned to avoid certain tastes (potentially poisonous) but not certain smells (harmless) – some organisms cannot be taught to avoid certain things.
- evolutionarily plausible (dark, heights)
- alternative explanation – observational learning
- snake + spider phobics don’t fear being hurt but having a panic attack whilst in contact with it.
- cant explain fears of harmless situations or objects (cotton wool)
Psychological Explanations
Psychodynamic - Freud
The root of phobias is from a traumatic event in childhood which has been repressed. This then manifests itself as a phobia due to conflict between the Id and the Ego when the person fears there unconscious wishes will express themselves  anxiety  impulses displaced to another object.
‘Little Hans’ – scared of horses – represented unconscious fear of his father as he associated horses with his father.
- cannot prove the psychodynamic theory wrong as it refers to unconscious wishes
- alternative explanation – classical conditioning
- based on case studies
- usual Freudian criticisms.
Behavioural
Classical Conditioning
Watson + Rayner – ‘Little Albert’ - paired loud noise (neutral stimulus) with a white rat (unconditional stimulus). He later became scared of most white fluffy objects (conditioned response).
- unethical
- failure to replicate
- Keuthen – 50% of phobics couldn’t remember any unpleasant experiences relating to the phobia. But/ may have repressed the memory
- DiNardo – after a traumatic experience with dogs: 50% developed phobia, 50% no phobia
Operant Conditioning – two process theory
avoidance of phobic stimulus - reduces anxiety - negative reinforcement
Social learning theory
Fears learned through imitation.
Mineka – monkeys could develop a snake phobia just by watching another monkey experience fear in the presence of a snake. BUT/ animal study - cant be generalised to humans
Control – Rotter
People with external loci of control are more likely to become depressed
Where parents don’t let their children outside without supervision - anxiety in child - phobia about going outside
- plausible
- systematic desensitisation 75% successful at dealing with specific phobias.
Cognitive-Behavioural - Beck
Irrational thoughts about the future possibility of a fearful situation - phobia
Anxious individuals have cognitive biases - exaggeration of threats posed by internal and external stimuli
e.g. sensation of crowded lift - associate lifts + suffocation - fear of lifts - generalised to similar situations - claustrophobia
• Matthews – threatening stimuli recognised faster by people with phobias – explained by them having more negative cognitions
• Beck – phobics often realises their fear is irrational but close proximity to the stimulus increases the sense of danger.
• Phobics more preoccupied with fear of fear rather then actual object.
- support from studies
- Cog-B therapies often very successful
- irrational thoughts – cause or effect?
Social factors
Holmes + Rahe – major life events are a contributing factor in the development of anxiety disorders.
Kobasa – minor daily hassles have a cumulative effect so can build up resulting in an anxiety disorder.
Kielner + Marshall – 84% of sample of agoraphobics had experienced family problems before the onset.
Gerlsman – phobics had lower than normal parental affection and were often over-protected.
- retrospective recall – unreliable
- demand characteristics
- correlational – cause or effect?
Diathesis stress model
Suggests that everyone has a certain tolerance threshold for stress and this varies between individuals. This may be genetically inherited or learned through experience. If the degree of environmental stress exceeds a certain threshold then anxiety symptoms result. But due to everyone being different the same set of stressors will result in symptoms for some people but not in others.
- plausible
- doesn’t explain the exact nature of the variable threshold
