Anxiety Disorders
Aims:
· Describe the genetic, biological and psychological characteristics of:
o Phobias;
o Obsessive-compulsive behaviour.
· Assess the value of various explanations of these disorders.
Phobia’s
Definition: A pathological condition which stops the individual functioning normally.
Female to Male ratio for seeking help : 2:1.
I.e. they’re twice as likely to seek help.
Four clinical sub types of phobias have been found (Can these be separated???):
Animal
Situational
Natural environment
Injury
Psychological explanations:
Behavioral model;
Classical conditioning
Operant conditioning
Social learning theory.
Cognitive behavioral;
Diathesis stress model:
1. Behavioral model:
· Classical conditioning.
Certain stimuli elicit reflexive, involuntary responses. E.G. Pavlov’s Dogs…
E.G. Watson & Rayner (1920) infants fear of furry objects
Hans Eysenck (1970) attempted to link anxiety disorders such as phobias to personality dimensions, notably neuroticism and introversion (Inward looking, passive and withdrawn from social contact.)
· Operant Conditioning:
‘All behaviour is learned by its consequences’
B.F. Skinner (1981) claimed that all behaviour including inappropriate, phobic responses was learned through experiences that had consequences.
· Social Learning theory:
Albert Bandura’s Social Learning Theory (1963) claims that direct experience of the anxiety producing stimulus such as flying in an aircraft isn’t necessary for the acquisition of phobic response. – We learn much by observing and imitating people.
· Psychodynamic explanations for phobic anxiety disorders:
Freudian. Suggests that (Hypothetical) unconscious ‘urges’ drive us to think and behave in certain ways.
Displacement and suppression (Source of anxiety becomes attached to something else and buried deep in the unconscious mind) reduce and remove the mind from potential harm. Thus the original anxiety is displaced onto something which should not have originally resulted in a fear response.
e.g. The Case of Little Hans = fear of horses – jealous of fathers relationship with mother
and castration anxiety resulting in fear of horses. :S.
John Bowlby emphasized the importance of early emotional attachments in shaping later behaviour and saw that children who are insecurely attached may show agoraphobic symptoms, reflecting their fear of being left alone.
2. Cognitive behavioral explanations for phobic anxiety disorders
Ellis (1962) and Beck (1963) point out that the behavioral model ignores the role of cognition. They see phobias as being the result of an illogical association that we have made in our minds following an unpleasant experience.
Suggest that the catastrophic thoughts and irrational beliefs contribute to the development of a phobia.
Beck states that phobic’s tend to have belief systems whereby they know at a rational level that danger is minimal yet also truly believe that their feared object or situation will cause them physical or psychological harm.
Beck et al (1985) found that danger beliefs are activated when a person is in close proximity to a stimuli yet decrease with distance to zero. People with phobias are more preoccupied with their ‘fear of fear.’
Bieling and Alden (1997) found that people with social phobia scored significantly higher on controls on perfectionism and had lowered perceptions of their social ability.
3. Diathesis stress model explanation of phobias
Refers to the (probably) genetically inherited predisposition that we each have to develop certain illnesses, diseases, or other conditions. In this case the condition is stress or anxiety.
Suggests an interaction between vulnerability factors and triggering events
Holmes & Rahe (1967) explain the cumulative effects of major life events and the work of Kobassa (1979) highlight the effects of everyday minor hassles.
Kleiner & Marshall (1987) found that in a group of agoraphobics 84% had experienced family problems prior to the onset of their first panic attack this was confirmed by a number of other studies.
However, many people who do not experience the most adverse life events do not develop an anxiety disorder.
It is suggested that each individual have their own tolerance thresholds which form their predisposition to stress this being known as our diathesis / vulnerability factor.
This may be genetic or inherited through early experience.
Explanations being psychodynamic, cognitive and behavioral.
We all have fears and anxieties this only develops into a mental disorder when they become so severe that they prevent the individual getting on with life and their life becomes dysfunctional.
Obsessive-Compulsive Disorder
· Range of intensity from fairly minor to pathological affliction.
· One of the most severe of all anxiety disorders
· One of the most difficult to deal with.
· Obsessions dominate ones thinking and are persistent and recurrent thoughts images or beliefs entering the mind uninvited and which cannot be removed.
· Compulsions are the behavioral responses intended to neutralize these obsessions.
DSM-IV defines the diagnostic features of OCD as:
Recurrent obsessions or compulsions that are severe enough to be time consuming (I.e. take more than 1 hr a day) or cause marked distress or significant impairment.
At some point during the course of the disorder the person has recognized that the obsessions or compulsions are excessive or unreasonable. The disturbance is not due to the direct physiological effects of a substance (E.G. alcohol or drug abuse, or medication) or a general medical condition.’
Clinical characteristics:
· Sufferers are generally aware of how behaviors and thoughts are irrational but are powerless to overcome them. Often they attempt to hide them from others.
· Suffer severe anxiety however:
Initial obsessions and compulsions do not relieve initial anxiety
Rather they add to form additional anxieties as a consequence.
· Often suffer from severe depression – an understandable reaction.
· Onset from late teens to early twenties.
· Affects 2% of USA population (American Psychiatric Association.)
· Occurs equally in males and females though females are more likely to have compulsions involving cleaning.
Explanations of OCD:
· Research is in its infancy – evidence for each claim tentative.
· Some evidence that there is a genetic link and that biochemical imbalances may also be involved.
· Some drugs have proved successful treatment.
· Behavioral therapies effective therefore can’t be entirely biological.
Biological explanations of OCD:
Genetics, Biochemistry and Neuroanatomy.
· Genetics:
o Carey & Gottesman (1981) – 10% prevalence in 1st degree relatives.
o Hoeker & Schnurr (1980) – concordance rate of 50-60% in twin studies.
§ N.B. people share same environment and therefore evidence can be disputed.
o Repoport (1989) most people have individual fixed action patterns in their brain that have evolutionary significance for survival. Under stress they are triggered and cease when actions have been completed.
For people with OCD the patterns are triggered by an overly active sense of danger.
· Biochemistry:
o OCD resulting from insufficient or malfunctioning serotonin metabolism.
o Support comes from certain drugs which inhibit the re-uptake of neurotransmitter serotonin – Zohar et al. (1996) found beneficial in up to 60% of patients.
o Lydiard et al (1996) shows partial alleviation of symptoms only, therefore medication only alleviates and is not a cure.
· Neuro-anatomical explanations:
o Rapoport & Wise (1988) have suggested that OCD arises from structural dysfunction in the central nervous system. – probably the basal ganglia.
o Rapoport et al. (1994) have reported that surgery which disconnects the basal -ganglia from the frontal cortex brings relief in severe cases of OCD.
Evaluation: Biological explanations.
Genetics Vs environment debate continues.
Inconsistent findings regarding serotonin:
§ Studies on role of serotonin in OC have yielded inconsistent findings.
Much of the evidence is flawed and studies have not included controls to rule out the possibility that anti-depressant drugs bring relief because they alleviate the symptoms of depression that frequently accompany OCD.
Psychological therapy can be very successful treatment and this is difficult to account for in the serotonin hypothesis.
Possible dysfunction in the basal ganglia.
Aylward et al (1996) found no difference between this and matched control patients.
Psychological explanations of OCD.
1. Psychodynamic;
2. Behavioral;
3. Cognitive-Behavioral.
1. Psychodynamic:
· Freud states that OCD occurs from a fixation at the anal stage of development
Evaluation: Psychodynamic explanation.
· Hard to test the idea of unconscious motivation experimentally.
· Importance of obsessive personality style:
· There is evidence of an obsessive personality style.
· Peterson (1992) States such people do not seem any more likely to be diagnosed with OCD than anyone else.
2. Behavioral:
· An extreme form of learned avoidance behaviour.
· Initial event is linked to anxiety / fear initially fear is alleviated and then becomes a conditioned response.
Evaluation: Behavioral Explanation:
· Flawed argument:
o Behavioral explanation falls down in that the symptoms of OCD e.g. avoidance behaviour, creates anxiety. It’s hard to argue that people learn these responses to reduce fear.
· Effectiveness of behavioral therapies:
Baxter et al. (1992) behavioral therapies not only reduce symptoms of OCD but also bring about changes in biochemical activity.
Marks (1981) Behavioral therapy helps in reducing obsession behaviour but not the obsession thoughts.
3. Cognitive-Behavioral explanations
· Disorder is a consequence of faulty or irrational ways of thinking taken to a extreme.
· Specific or environmental stimuli are paired at some time with anxiety provoking thoughts and compulsive rituals are then used to try and neutralize them.
· Rachman & Hodges (1987) some people are more susceptible to developing obsession thoughts. Vulnerability factors include genetically determined hyper-arousability depressed mood and poor socialization.
Evaluation: Cognitive-Behavioral Explanation.
· Lack of evidence that OCD reduces through increased socialization.
· Emmelkamp et al. (1988) Effectiveness of CBT has shown a reasonably effective result in OCD.
· No long term solution – remains a difficult disorder to understand and treat effectively.
References:
Watson & Rayner (1920) - Infants fear of furry objects
(Classical conditioning.)
Hans Eysenck (1970) - Attempted to link anxiety disorders such as
phobias to personality dimensions, notably neuroticism and introversion
(Inward looking, passive and withdrawn from social contact.)
B.F. Skinner (1981) - Claimed that all behaviour including
inappropriate, phobic responses was learned through experiences that had consequences.
Albert Bandura’s
Social Learning Theory (1963) - Claims that direct experience of the anxiety
producing stimulus such as flying in an aircraft isn’t necessary for the acquisition of phobic response. – We learn much by observing and imitating people.
Ellis (1962) and Beck (1963) - point out that the behavioral model ignores
the role of cognition. They see phobias as being the result of an illogical association that we have made in our minds following an unpleasant experience.
Beck et al (1985) - Found that danger beliefs are activated when
a person is in close proximity to a stimuli yet decrease with distance to zero. People with phobias are more preoccupied with their ‘fear of fear.’
Bieling and Alden (1997) - Found that people with social phobia scored
significantly higher on controls on perfectionism and had lowered perceptions of their social ability.
Holmes & Rahe (1967) - Explain the cumulative effects of major life
events
Kobassa (1979) - Highlights the effects of everyday minor
hassles.
Kleiner & Marshall (1987) - Found that in a group of agoraphobics 84%
had experienced family problems prior to the onset of their first panic attack this was confirmed by a number of other studies.
Carey & Gottesman (1981) – 10% prevalence in 1st degree relatives
as genetic link for OCD
Hoeker & Schnurr (1980) – concordance rate of 50-60% in twin
studies with OCD. N.B. people share same environment and therefore evidence can be disputed.
Repoport (1989) - Most people have individual fixed
action patterns in their brain that have evolutionary significance for survival. Under stress they are triggered and cease when actions have been completed.
For people with OCD the patterns are triggered by an overly active sense of danger.
Zohar et al. (1996) - Support comes from certain drugs which
inhibit the re-uptake of neurotransmitter serotonin have been found beneficial in up to 60% of patients.
Lydiard et al (1996) - Shows partial alleviation of symptoms only,
therefore medication only alleviates and is not a cure.
Rapoport & Wise (1988) - Have suggested that OCD arises from
structural dysfunction in the central nervous system. – probably the basal ganglia.
Rapoport et al. (1994) - Have reported that surgery which
disconnects the basal ganglia from the frontal cortex brings relief in severe cases of OCD.
Aylward et al (1996) - Found no difference between this
and matched control patients.
Rachman & Hodges (1987) - Some people are more susceptible to
developing obsession thoughts. Vulnerability factors include genetically determined hyper-arousability depressed mood and poor socialization.
Peterson (1992) - States such people do not seem any more
likely to be diagnosed with OCD than anyone else.
Baxter et al. (1992) - Behavioral therapies not only reduce
symptoms of OCD but also bring about changes in biochemical activity.
Marks (1981) - Behavioral therapy helps in reducing
obsession behaviour but not the obsession thoughts.
Emmelkamp et al. (1988) - Effectiveness of CBT has shown a
reasonably effective result in OCD.
Concepts to note:
Define these terms:
· Autonomic nervous system
· Diathesis
· Displacement
· obsessive-compulsive disorders (OCD)
· Oedipus complex
· operant conditioning
· panic disorders
· phobic disorders
· repression
· somatic nervous system
What did they do or say?
· Asso and Beech
· Bandura
· Beck
· Brenner
· Ellis
· Eysenck
· Freud
· Holmes and Rahe
· Horowitz
· Kobasa
· Lader and Mathews
· Pavlov
Sunday 21 October 2007
Depression (Unipolar Disorder)
Depression (Unipolar Disorder)
Aims:
· Describe the clinical characteristics of unipolar depression;
· Outline genetic and biochemical explanations of depression;
· Discuss psychological explanations of depression.
The shit from having a bad day to clinical depression can be very gradual and go unnoticed to the sufferer until quite late.
The term clinical depression refers to a state of depression where the persons ability to cope with everyday life is seriously impaired.
Everyone (Especially if they have had any family history of suffering from depression) is vulnerable to developing it.
Up to 5% of the population can be diagnosed as having some form of depression and there is a 20% chance of having an episode of clinical depression at some point in one’s life
List of symptoms, loosely divided into those that have psychological and those who have physical consequences – overlaps occur considerably.
Psychological:
· Loss of concentration
· Indecisiveness
· Inability to experience pleasure
· Loss of appetite or food loosing its taste;
· Increase in harsh, negative, self-critical thoughts;
· Feeling that others are being over-critical;
· Guilt feelings;
· Feeling helpless and / or without hope that things can improve;
· Seeking to be alone more often;
· Changes in habitual behavior;
· Thoughts of suicide;
· Loss of interest in sexual matters or increased sexual promiscuity;
Physical:
· Feeling exhausted after 12 hours sleep;
· Sleep disturbance;
· Headaches, chest pains;
· Appetite or weight change;
· Increased alcohol / drug use.
If someone experiences most of these for >2 weeks there is a good chance that they are suffering from depression.
The above is for unipolar depression.
For bipolar depression they’re:
· Reactive depression – resulting from a reaction to external events;
· Endogenous depression – resulting from conditions within oneself
(Aetiology refers to the causes of an illness.)
Who is most at risk?
· Typically appears at 18-22
· Possibly linked to stressors during these years
What causes depression?
Single personal trauma / stressful life event è stress è symptoms of depression.
More often it is evoked by combinations of bad experiences. Physical causes include:
· Side effects of surgical operation or medication;
· Alcohol / drug abuse;
· Withdrawal from drugs;
· Thyroid disease.
Biological explanations of depression:
1. Genetic;
2. Biochemical;
Genetic Explanation of depression:
· Research concentrates on the individual sufferer, the families of sufferers, and the twin studies in which one twin suffers from unipolar depression.
· If an individual persistently has episodes of depression a genetic factor may be suspected. Several family and twin studies are reported that show concordance rates (when 1 member other than the twin suffering from the condition) between 30 – 40% which is higher than would occur by chance.
Evidence from family studies:
· Gershon (1990) reviewed ten family studies and found that rates of unipolar depression in 1st degree relatives ranged between 7 and 30%. However, this may arguably be genetically or environmentally produced.
· DSM-IV states that there is a high incidence of unipolar depression with those offspring of those with bipolar (manic) depression. However, that could be a reaction to exactly that situation.
Evidence from twin studies:
· Twin studies comparing MZ to DZ but cannot separate out the environmental and genetic effects.
· McGuffin et al. (1996) found 46% concordance in MZ twins compared with 20% DZ in total of 109 twin pairs with no evidence of the effect of shared environment.
· Bierut et al. (1999) carried out a study of 2662 pairs of twins in Australia and although they reported a hereditability factor of between 36 and 44 % they claimed that environmental factors played a larger role.
Evidence from adoption studies:
· Most show an increased risk in the biological relatives of people with depression rather than adopted relatives.
· Wender et al. (1986) found that biological relatives were 8 times more likely to have depression than adoptive relatives.
· It seems unlikely that a single unipolar gene will ever be identified.
Evaluation: Genetic explanations.
· Some genetic evidence, but, shared genes normally share the same environment; therefore it could equally be learned behavior.
· Risk seems to be increased for MZ twins however, the risks are never thought to be 100%. Genetics seems to be a risk factor but not a whole explanation.
· Predisposing factor: There may be a genetic component operating as a predisposing factor, with additional precipitating causes.
· Genetic uncertainty: Even if genetic factors do play a part in the origins of unipolar depression, it is not clear what the precise mechanism is that is transmitted. Without knowing the specific genes involved, it is impossible to understand how they code biological structures and functions that produce the symptoms of depression.
Biochemical explanations of depression:
The biochemical explanation claims that depression is the cognitive state resulting from imbalances in brain chemistry that can he controlled in many cases by antidepressant drugs known as tricyclic drugs. However, it does not claim that these imbalances are genetic in origin — and, indeed, they may be the consequence rather than the cause of some aspects of the depression. Three brain chemicals are principally involved. These are noradrenaline, serotonin, and dopamine.
Post-mortems of depressed people do not show abnormally low levels of noradrenaline. Serotonin levels are also associated with depressive symptoms, but we do not know whether a low serotonin level is the cause or the consequence of the depression. According to Iversen, low dopamine levels are associated with unipolar depression.
Cases of depression in old age were thought to be associated with the fact that dopamine production naturally diminishes after the age of 45. However, giving elderly sufferers a dopamine replacement doesn’t seem to help.
Although these three neurotransmitters may be involved in depression we do not know how. Researchers investigating the endocrine (hormonal) system have found that the adrenal cortex produces cortisol and cortisone — two hormones involved in metabolism of fats, carbohydrates and proteins. Cortisol production is increased as the individual experiences stress, and this may then trigger other physiological responses leading to the experience of depression. Hormonal (oestrogen and progesterone) imbalances are known to be involved in some menstruation-related depression, although the precise involvement isn’t known.
Some people appear to become more depressed and lethargic and have trouble sleeping during the winter months. This pattern can indicate a mood disorder called seasonal affective disorder (SAD). One suggestion is that this is caused by a lack of daylight.
Some evidence exists for links with the brain chemicals, particularly, serotonin and noradrenalin.
It’s been found that treatment with anti-depressive drugs, which contain serotonin are effective, whereas those drugs containing noradrenaline have no effect (Lam et al. 1996) Speculation concludes that SAD may be linked to serotonergic related mechanisms. Cannot be causal because treatment does not cure the problem, which returns when the drug treatment has ceased. Perhaps a genetic component?
Madden et al. (1996) reports a significant genetic influence in winter patterns SAD. Data was collected from 4,639 adult twins in Australia via a mailed questionnaire – however people lie.
Evaluation: Biochemical explanations.
1. Role of neurotransmitters:
· Significant body of evidence for this argument.
· Theories based on deficit of these chemicals are too simplistic – they do not have an immediate effect on neurotransmitter availability and take several weeks to affect mood.
2. Delayed effects:
· Much evidence implying noradrenaline comes from observations of resperine etc. these do not simply affect levels of noradrenaline – other properties of these drugs may relate to their reaction with noradrenaline.
3. Isolating cause and effect
4. Impairment of stress response system:
· Abnormal levels of regulation of cortisol suggest depression may be related to impairment of the stress response system.
· Such irregularities are not found in all people with depression and are sometimes found in people with other kinds of mental disorder.
5. Role of female hormones:
· Females more likely to suffer from depression, however, only few suffer from post natal depression – so not the inevitable response to hormonal changes.
6. Biological factors as predisposing factor:
· There is no definite evidence of biological features as the cause of depression, although there is a lot of support for the idea that they are a contributory factor. It is likely they predispose people to depression, but that environmental triggers are required before the disorder emerges.
Psychological explanations of depression:
1. Psychodynamic explanations for depression.
· Psychoanalysis:
Freud’s view is that where early relationships with parents are unsatisfactory because parents are neglectful, unloving, or abusive the child represses its feelings of anger towards the parents and these manifest themselves later as self-criticism, and lack of self esteem and self confidence. Depression develops from these negative feelings.
· Monotropy:
Bowlby’s (1973) attachment theory supports the idea that inadequate attachments also contribute to depression. Bowlby was supported by Robert Hinde (1977) at London zoo involving the removal of half a dozen or so infant monkeys from their parents and other monkeys and rearing them at various periods. Hinde investigated the nature of early social relationships and one way of testing this was to see what happened when they were disrupted. This research, which Hinde admits that he would not want to carry out now, caused great disruption in the animals behavior from which most never recovered. However, to generalize these findings with baby monkeys to humans is potentially simplistic and misleading.
Evaluation: Psychodynamic explanations
· Difficult to test:
Impossible to tell if Freud’s theory is true as impossible to demonstrate unconscious motivations.
· Presence of anger:
Some evidence people with depression show increased anger but findings are inconsistent. Studies unable to show this anger is directed inwards.
· Effect of loss of parent:
Some evidence that loss of parent in childhood is associated with later depression. However, such loss effects the environment in which the child lives as well as the child’s psychological functioning. It might be that the social and financial hardships that such a loss might entail create a vulnerability to depression.
2. Behavioral explanations of depression:
Lewinsohn (1974) suggests that when someone is deprived of social reinforcement such as feeling appreciated and encouraged and enjoying social interaction, they may become depressed. The individual displays the symptoms of depression, which are then reinforced by others paying them attention, and giving the sympathy that was lacking in the first place.
Martin Seligman’s theory of learned helplessness is influential.
Basically Seligman found that dogs that couldn’t escape from an electric shock learned that escape and avoidance were impossible, and didn’t even attempt to escape subsequently when it was possible. They had learned a ‘helpless’ reaction. Something similar may explain human depression. If you simply cannot achieve something, no matter how hard you try, you may give up and become depressed, knowing that you will never be able to achieve your goals. However, there are many other variables here. Some people are even more motivated to try harder when they fail. There may be a gender difference here, too. One study found that females tend to become depressed, whilst males tend to get angry, when frustrated by failure.
Seligman incorporated an element of cognition in order to refine his ‘learned helplessness’ model, It was developed from Aaron Beck’s faulty self-perception theory (1963). This proposed that people who suffer the symptoms of depression are likely to have negative views about themselves, the situation they are in, and their future prospects. Such feelings become an obsession and interfere with the individual’s ability to deal with the world. This leads to the symptoms of depression.
Beck claims that we inherit strategies for dealing positively with the world. However, environmental factors such as divorce and unemployment can undermine them.
3. Cognitive—behavioral explanations and Beck’s cognitive theory of depression
Most of the evidence for the cognitive—behavioural model comes from Aaron Beck’s work. He believed that depression is largely the result of negative thinking (which he called ‘cognitive errors’).
Beck’s view (1991) states there are three components to depression:
· regarding oneself as worthless
· believing that the world is filled with obstacles
· believing that nothing much is ever likely to change.
This seriously gloomy view distorts the ability to think logically about the world and relationships with it.
Evaluation: cognitive – behavioral explanations
· Research subjects:
Most of Seligman’s studies were conducted on college students, rather than on clinically depressed patients.
· Perception of control:
One of the key elements of hopelessness theory is that the depressed people have little control over their lives. Ford & Neale (1985) however, found that depression students did not underestimate their degree of control.
· Hopelessness as cause or effect?
It is not clear whether hopelessness is a cause of depression or a side effect of becoming depressed. If it is the cause, then it would have to precede the onset of depression.
A 5 year longitudinal study of children by Nolen-Hoeksema et al. (1992) found no connection between attributional style and depression in young children. However, they did find a connection as the children grew older, suggesting that attributional styles may develop over a number of years.
· Hopelessness expectancy:
Abramson et al. (1989) further reinforced the theory of hopelessness to inc. the role of expectancy. Outlining the sequence of events that they thought would lead to hopelessness. This begins with the negative event which interacts with the persons already held negative schemas and a stable and global attribution is made of why the event occurred. These beliefs lead to hopelessness expectation in the future that then may result in depression. They even suggest that hopelessness expectation is a sub type of depression.
DeVellis and Blalock (1992) is a longitudinal study of 57 adults tested the claim that hopelessness expectancy is a sufficient cause for depression. They found support for the link between expectancy and depression, but as moderating, rather than mediating factor, i.e. it does not by itself cause the depression merely by the degree.
4. Diathesis stress model:
No single explanation can account for depression.
Stressful life events
There is no doubt that the traumatic effects of stressful life events can build up overwhelming the ability to cope.
Some people are more vulnerable, genetically, endocrinologically and socially.
Brown & Harris’s longitudinal studies (1993) identify severe life events and long term difficulties as the two factors that trigger depression, especially when the person is feeling vulnerable because of lack of support or an inability to do anything about the situation.
Lock & Key hypothesis:
Parker et al. (1998) proposed a ‘lock and key’ hypothesis of depression which posits that the early adverse experiences establish locks that can be activated by keys mirroring the earlier adverse experience. Theses in turn induce depression. Interviewing 270 severely clinically depressed patients this worked in 1/3rd of their sample (Approx.)
The remaining 2/3rds were diagnosed as reactive depression – therefore not chronic depression.
Topic summary
Unipolar depression is a medical condition, typically first appearing in adolescents and young adults, which is recognised by an enduring group of symptoms including feelings of isolation, guilt, helplessness and even thoughts of suicide. It can be precipitated by environmental and/or biological triggers. Up to 5 per cent of the population may be diagnosed with a depressive illness at any one time.
Some types of depression may run in families and there is growing evidence that vulnerability to depression may be genetically transmitted. However, many behavioural scientists believe that some types of depression may have roots in learning arising from childhood experiences. Where the consequences of one’s actions lead, even unintentionally, to a desired consequence, the behavior may become learned. Showing symptoms of sadness may attract attention and support, which may thus reinforce the sad behaviour, leading ultimately to the experience of depression.
Beck’s cognitive—behavioural model suggests that people’s thinking becomes negative when one’s endeavors’ fail. One becomes self-critical and convinced that one cannot succeed, slowly leading to increasingly severe symptoms of depression.
On balance, it is probable that depression is caused by a combination of several factors — notably genetic predisposition, biochemical imbalances, early psychological deprivation, inadequate parenting, and an excessive exposure to adolescent and adult stressors.
References:
Gershon (1990) - Reviewed ten family studies and found that
rates of unipolar depression in 1st degree relatives ranged between 7 and 30%. However, this may arguably be genetically or environmentally produced.
McGuffin et al. (1996) - Found 46% concordance in MZ twins
compared with 20% DZ in total of 109 twin pairs with no evidence of the effect of shared environment.
Bierut et al. (1999) - Carried out a study of 2662 pairs of twins in
Australia and although they reported a hereditability factor of between 36 and 44 % they claimed that environmental factors played a larger role.
Wender et al. (1986) - Found that biological relatives were 8 times
more likely to have depression than adoptive relatives.
Robert Hinde (1977) - Supported Bowlby at London zoo involving
the removal of half a dozen or so infant monkeys from their parents and other monkeys and rearing them at various periods.
Lewinsohn (1974) - Suggests that when someone is deprived of
social reinforcement such as feeling appreciated and encouraged and enjoying social interaction, they may become depressed. The individual displays the symptoms of depression, which are then reinforced by others paying them attention, and giving the sympathy that was lacking in the first place.
Nolen-Hoeksema et al. (1992) - A 5 year longitudinal study of children
found no connection between attributional style and depression in young children. However, they did find a connection as the children grew older, suggesting that attributional styles may develop over a number of years.
Abramson et al. (1989) - Further reinforced the theory of
hopelessness to inc. the role of expectancy. Outlining the sequence of events that they thought would lead to hopelessness. This begins with the negative event which interacts with the persons already held negative schemas and a stable and global attribution is made of why the event occurred. These beliefs lead to hopelessness expectation in the future that then may result in depression. They even suggest that hopelessness expectation is a sub type of depression.
DeVellis and Blalock (1992) - Is a longitudinal study of 57 adults tested the
claim that hopelessness expectancy is a sufficient cause for depression. They found support for the link between expectancy and depression, but as moderating, rather than mediating factor, i.e. it does not by itself cause the depression merely by the degree.
Brown & Harris’s longitudinal
Studies (1993) - Identify severe life events and long term
difficulties as the two factors that trigger depression, especially when the person is feeling vulnerable because of lack of support or an inability to do anything about the situation.
Parker et al. (1998) - Proposed a ‘lock and key’ hypothesis of
depression which posits that the early adverse experiences establish locks that can be activated by keys mirroring the earlier adverse experience. These in turn induce depression. Interviewing 270 severely clinically depressed patients this worked in 1/3rd of their sample (Approx.) the remaining 2/3rds were diagnosed as reactive depression – therefore not chronic depression.
Concepts to note:
Define these terms:
· Bipolar (manic) depression
· Depression
· Dopamine
· Endogenous depression
· Monotropy
· Noradrenaline
· Reactive depression
· Seasonal affective disorder (SAD)
· Serotonin
· Tricyclic drugs
· Unipolar depression
What did they do or say?
· Beck
· Bierut
· Bifulco
· Bowiby
· Brown and Harris
· Ford and Neale
· Hinde
· Iversen.
· Kendler and Prescott
· Lewinsohn
· McGuffin
· Seligman
· Silberg
Aims:
· Describe the clinical characteristics of unipolar depression;
· Outline genetic and biochemical explanations of depression;
· Discuss psychological explanations of depression.
The shit from having a bad day to clinical depression can be very gradual and go unnoticed to the sufferer until quite late.
The term clinical depression refers to a state of depression where the persons ability to cope with everyday life is seriously impaired.
Everyone (Especially if they have had any family history of suffering from depression) is vulnerable to developing it.
Up to 5% of the population can be diagnosed as having some form of depression and there is a 20% chance of having an episode of clinical depression at some point in one’s life
List of symptoms, loosely divided into those that have psychological and those who have physical consequences – overlaps occur considerably.
Psychological:
· Loss of concentration
· Indecisiveness
· Inability to experience pleasure
· Loss of appetite or food loosing its taste;
· Increase in harsh, negative, self-critical thoughts;
· Feeling that others are being over-critical;
· Guilt feelings;
· Feeling helpless and / or without hope that things can improve;
· Seeking to be alone more often;
· Changes in habitual behavior;
· Thoughts of suicide;
· Loss of interest in sexual matters or increased sexual promiscuity;
Physical:
· Feeling exhausted after 12 hours sleep;
· Sleep disturbance;
· Headaches, chest pains;
· Appetite or weight change;
· Increased alcohol / drug use.
If someone experiences most of these for >2 weeks there is a good chance that they are suffering from depression.
The above is for unipolar depression.
For bipolar depression they’re:
· Reactive depression – resulting from a reaction to external events;
· Endogenous depression – resulting from conditions within oneself
(Aetiology refers to the causes of an illness.)
Who is most at risk?
· Typically appears at 18-22
· Possibly linked to stressors during these years
What causes depression?
Single personal trauma / stressful life event è stress è symptoms of depression.
More often it is evoked by combinations of bad experiences. Physical causes include:
· Side effects of surgical operation or medication;
· Alcohol / drug abuse;
· Withdrawal from drugs;
· Thyroid disease.
Biological explanations of depression:
1. Genetic;
2. Biochemical;
Genetic Explanation of depression:
· Research concentrates on the individual sufferer, the families of sufferers, and the twin studies in which one twin suffers from unipolar depression.
· If an individual persistently has episodes of depression a genetic factor may be suspected. Several family and twin studies are reported that show concordance rates (when 1 member other than the twin suffering from the condition) between 30 – 40% which is higher than would occur by chance.
Evidence from family studies:
· Gershon (1990) reviewed ten family studies and found that rates of unipolar depression in 1st degree relatives ranged between 7 and 30%. However, this may arguably be genetically or environmentally produced.
· DSM-IV states that there is a high incidence of unipolar depression with those offspring of those with bipolar (manic) depression. However, that could be a reaction to exactly that situation.
Evidence from twin studies:
· Twin studies comparing MZ to DZ but cannot separate out the environmental and genetic effects.
· McGuffin et al. (1996) found 46% concordance in MZ twins compared with 20% DZ in total of 109 twin pairs with no evidence of the effect of shared environment.
· Bierut et al. (1999) carried out a study of 2662 pairs of twins in Australia and although they reported a hereditability factor of between 36 and 44 % they claimed that environmental factors played a larger role.
Evidence from adoption studies:
· Most show an increased risk in the biological relatives of people with depression rather than adopted relatives.
· Wender et al. (1986) found that biological relatives were 8 times more likely to have depression than adoptive relatives.
· It seems unlikely that a single unipolar gene will ever be identified.
Evaluation: Genetic explanations.
· Some genetic evidence, but, shared genes normally share the same environment; therefore it could equally be learned behavior.
· Risk seems to be increased for MZ twins however, the risks are never thought to be 100%. Genetics seems to be a risk factor but not a whole explanation.
· Predisposing factor: There may be a genetic component operating as a predisposing factor, with additional precipitating causes.
· Genetic uncertainty: Even if genetic factors do play a part in the origins of unipolar depression, it is not clear what the precise mechanism is that is transmitted. Without knowing the specific genes involved, it is impossible to understand how they code biological structures and functions that produce the symptoms of depression.
Biochemical explanations of depression:
The biochemical explanation claims that depression is the cognitive state resulting from imbalances in brain chemistry that can he controlled in many cases by antidepressant drugs known as tricyclic drugs. However, it does not claim that these imbalances are genetic in origin — and, indeed, they may be the consequence rather than the cause of some aspects of the depression. Three brain chemicals are principally involved. These are noradrenaline, serotonin, and dopamine.
Post-mortems of depressed people do not show abnormally low levels of noradrenaline. Serotonin levels are also associated with depressive symptoms, but we do not know whether a low serotonin level is the cause or the consequence of the depression. According to Iversen, low dopamine levels are associated with unipolar depression.
Cases of depression in old age were thought to be associated with the fact that dopamine production naturally diminishes after the age of 45. However, giving elderly sufferers a dopamine replacement doesn’t seem to help.
Although these three neurotransmitters may be involved in depression we do not know how. Researchers investigating the endocrine (hormonal) system have found that the adrenal cortex produces cortisol and cortisone — two hormones involved in metabolism of fats, carbohydrates and proteins. Cortisol production is increased as the individual experiences stress, and this may then trigger other physiological responses leading to the experience of depression. Hormonal (oestrogen and progesterone) imbalances are known to be involved in some menstruation-related depression, although the precise involvement isn’t known.
Some people appear to become more depressed and lethargic and have trouble sleeping during the winter months. This pattern can indicate a mood disorder called seasonal affective disorder (SAD). One suggestion is that this is caused by a lack of daylight.
Some evidence exists for links with the brain chemicals, particularly, serotonin and noradrenalin.
It’s been found that treatment with anti-depressive drugs, which contain serotonin are effective, whereas those drugs containing noradrenaline have no effect (Lam et al. 1996) Speculation concludes that SAD may be linked to serotonergic related mechanisms. Cannot be causal because treatment does not cure the problem, which returns when the drug treatment has ceased. Perhaps a genetic component?
Madden et al. (1996) reports a significant genetic influence in winter patterns SAD. Data was collected from 4,639 adult twins in Australia via a mailed questionnaire – however people lie.
Evaluation: Biochemical explanations.
1. Role of neurotransmitters:
· Significant body of evidence for this argument.
· Theories based on deficit of these chemicals are too simplistic – they do not have an immediate effect on neurotransmitter availability and take several weeks to affect mood.
2. Delayed effects:
· Much evidence implying noradrenaline comes from observations of resperine etc. these do not simply affect levels of noradrenaline – other properties of these drugs may relate to their reaction with noradrenaline.
3. Isolating cause and effect
4. Impairment of stress response system:
· Abnormal levels of regulation of cortisol suggest depression may be related to impairment of the stress response system.
· Such irregularities are not found in all people with depression and are sometimes found in people with other kinds of mental disorder.
5. Role of female hormones:
· Females more likely to suffer from depression, however, only few suffer from post natal depression – so not the inevitable response to hormonal changes.
6. Biological factors as predisposing factor:
· There is no definite evidence of biological features as the cause of depression, although there is a lot of support for the idea that they are a contributory factor. It is likely they predispose people to depression, but that environmental triggers are required before the disorder emerges.
Psychological explanations of depression:
1. Psychodynamic explanations for depression.
· Psychoanalysis:
Freud’s view is that where early relationships with parents are unsatisfactory because parents are neglectful, unloving, or abusive the child represses its feelings of anger towards the parents and these manifest themselves later as self-criticism, and lack of self esteem and self confidence. Depression develops from these negative feelings.
· Monotropy:
Bowlby’s (1973) attachment theory supports the idea that inadequate attachments also contribute to depression. Bowlby was supported by Robert Hinde (1977) at London zoo involving the removal of half a dozen or so infant monkeys from their parents and other monkeys and rearing them at various periods. Hinde investigated the nature of early social relationships and one way of testing this was to see what happened when they were disrupted. This research, which Hinde admits that he would not want to carry out now, caused great disruption in the animals behavior from which most never recovered. However, to generalize these findings with baby monkeys to humans is potentially simplistic and misleading.
Evaluation: Psychodynamic explanations
· Difficult to test:
Impossible to tell if Freud’s theory is true as impossible to demonstrate unconscious motivations.
· Presence of anger:
Some evidence people with depression show increased anger but findings are inconsistent. Studies unable to show this anger is directed inwards.
· Effect of loss of parent:
Some evidence that loss of parent in childhood is associated with later depression. However, such loss effects the environment in which the child lives as well as the child’s psychological functioning. It might be that the social and financial hardships that such a loss might entail create a vulnerability to depression.
2. Behavioral explanations of depression:
Lewinsohn (1974) suggests that when someone is deprived of social reinforcement such as feeling appreciated and encouraged and enjoying social interaction, they may become depressed. The individual displays the symptoms of depression, which are then reinforced by others paying them attention, and giving the sympathy that was lacking in the first place.
Martin Seligman’s theory of learned helplessness is influential.
Basically Seligman found that dogs that couldn’t escape from an electric shock learned that escape and avoidance were impossible, and didn’t even attempt to escape subsequently when it was possible. They had learned a ‘helpless’ reaction. Something similar may explain human depression. If you simply cannot achieve something, no matter how hard you try, you may give up and become depressed, knowing that you will never be able to achieve your goals. However, there are many other variables here. Some people are even more motivated to try harder when they fail. There may be a gender difference here, too. One study found that females tend to become depressed, whilst males tend to get angry, when frustrated by failure.
Seligman incorporated an element of cognition in order to refine his ‘learned helplessness’ model, It was developed from Aaron Beck’s faulty self-perception theory (1963). This proposed that people who suffer the symptoms of depression are likely to have negative views about themselves, the situation they are in, and their future prospects. Such feelings become an obsession and interfere with the individual’s ability to deal with the world. This leads to the symptoms of depression.
Beck claims that we inherit strategies for dealing positively with the world. However, environmental factors such as divorce and unemployment can undermine them.
3. Cognitive—behavioral explanations and Beck’s cognitive theory of depression
Most of the evidence for the cognitive—behavioural model comes from Aaron Beck’s work. He believed that depression is largely the result of negative thinking (which he called ‘cognitive errors’).
Beck’s view (1991) states there are three components to depression:
· regarding oneself as worthless
· believing that the world is filled with obstacles
· believing that nothing much is ever likely to change.
This seriously gloomy view distorts the ability to think logically about the world and relationships with it.
Evaluation: cognitive – behavioral explanations
· Research subjects:
Most of Seligman’s studies were conducted on college students, rather than on clinically depressed patients.
· Perception of control:
One of the key elements of hopelessness theory is that the depressed people have little control over their lives. Ford & Neale (1985) however, found that depression students did not underestimate their degree of control.
· Hopelessness as cause or effect?
It is not clear whether hopelessness is a cause of depression or a side effect of becoming depressed. If it is the cause, then it would have to precede the onset of depression.
A 5 year longitudinal study of children by Nolen-Hoeksema et al. (1992) found no connection between attributional style and depression in young children. However, they did find a connection as the children grew older, suggesting that attributional styles may develop over a number of years.
· Hopelessness expectancy:
Abramson et al. (1989) further reinforced the theory of hopelessness to inc. the role of expectancy. Outlining the sequence of events that they thought would lead to hopelessness. This begins with the negative event which interacts with the persons already held negative schemas and a stable and global attribution is made of why the event occurred. These beliefs lead to hopelessness expectation in the future that then may result in depression. They even suggest that hopelessness expectation is a sub type of depression.
DeVellis and Blalock (1992) is a longitudinal study of 57 adults tested the claim that hopelessness expectancy is a sufficient cause for depression. They found support for the link between expectancy and depression, but as moderating, rather than mediating factor, i.e. it does not by itself cause the depression merely by the degree.
4. Diathesis stress model:
No single explanation can account for depression.
Stressful life events
There is no doubt that the traumatic effects of stressful life events can build up overwhelming the ability to cope.
Some people are more vulnerable, genetically, endocrinologically and socially.
Brown & Harris’s longitudinal studies (1993) identify severe life events and long term difficulties as the two factors that trigger depression, especially when the person is feeling vulnerable because of lack of support or an inability to do anything about the situation.
Lock & Key hypothesis:
Parker et al. (1998) proposed a ‘lock and key’ hypothesis of depression which posits that the early adverse experiences establish locks that can be activated by keys mirroring the earlier adverse experience. Theses in turn induce depression. Interviewing 270 severely clinically depressed patients this worked in 1/3rd of their sample (Approx.)
The remaining 2/3rds were diagnosed as reactive depression – therefore not chronic depression.
Topic summary
Unipolar depression is a medical condition, typically first appearing in adolescents and young adults, which is recognised by an enduring group of symptoms including feelings of isolation, guilt, helplessness and even thoughts of suicide. It can be precipitated by environmental and/or biological triggers. Up to 5 per cent of the population may be diagnosed with a depressive illness at any one time.
Some types of depression may run in families and there is growing evidence that vulnerability to depression may be genetically transmitted. However, many behavioural scientists believe that some types of depression may have roots in learning arising from childhood experiences. Where the consequences of one’s actions lead, even unintentionally, to a desired consequence, the behavior may become learned. Showing symptoms of sadness may attract attention and support, which may thus reinforce the sad behaviour, leading ultimately to the experience of depression.
Beck’s cognitive—behavioural model suggests that people’s thinking becomes negative when one’s endeavors’ fail. One becomes self-critical and convinced that one cannot succeed, slowly leading to increasingly severe symptoms of depression.
On balance, it is probable that depression is caused by a combination of several factors — notably genetic predisposition, biochemical imbalances, early psychological deprivation, inadequate parenting, and an excessive exposure to adolescent and adult stressors.
References:
Gershon (1990) - Reviewed ten family studies and found that
rates of unipolar depression in 1st degree relatives ranged between 7 and 30%. However, this may arguably be genetically or environmentally produced.
McGuffin et al. (1996) - Found 46% concordance in MZ twins
compared with 20% DZ in total of 109 twin pairs with no evidence of the effect of shared environment.
Bierut et al. (1999) - Carried out a study of 2662 pairs of twins in
Australia and although they reported a hereditability factor of between 36 and 44 % they claimed that environmental factors played a larger role.
Wender et al. (1986) - Found that biological relatives were 8 times
more likely to have depression than adoptive relatives.
Robert Hinde (1977) - Supported Bowlby at London zoo involving
the removal of half a dozen or so infant monkeys from their parents and other monkeys and rearing them at various periods.
Lewinsohn (1974) - Suggests that when someone is deprived of
social reinforcement such as feeling appreciated and encouraged and enjoying social interaction, they may become depressed. The individual displays the symptoms of depression, which are then reinforced by others paying them attention, and giving the sympathy that was lacking in the first place.
Nolen-Hoeksema et al. (1992) - A 5 year longitudinal study of children
found no connection between attributional style and depression in young children. However, they did find a connection as the children grew older, suggesting that attributional styles may develop over a number of years.
Abramson et al. (1989) - Further reinforced the theory of
hopelessness to inc. the role of expectancy. Outlining the sequence of events that they thought would lead to hopelessness. This begins with the negative event which interacts with the persons already held negative schemas and a stable and global attribution is made of why the event occurred. These beliefs lead to hopelessness expectation in the future that then may result in depression. They even suggest that hopelessness expectation is a sub type of depression.
DeVellis and Blalock (1992) - Is a longitudinal study of 57 adults tested the
claim that hopelessness expectancy is a sufficient cause for depression. They found support for the link between expectancy and depression, but as moderating, rather than mediating factor, i.e. it does not by itself cause the depression merely by the degree.
Brown & Harris’s longitudinal
Studies (1993) - Identify severe life events and long term
difficulties as the two factors that trigger depression, especially when the person is feeling vulnerable because of lack of support or an inability to do anything about the situation.
Parker et al. (1998) - Proposed a ‘lock and key’ hypothesis of
depression which posits that the early adverse experiences establish locks that can be activated by keys mirroring the earlier adverse experience. These in turn induce depression. Interviewing 270 severely clinically depressed patients this worked in 1/3rd of their sample (Approx.) the remaining 2/3rds were diagnosed as reactive depression – therefore not chronic depression.
Concepts to note:
Define these terms:
· Bipolar (manic) depression
· Depression
· Dopamine
· Endogenous depression
· Monotropy
· Noradrenaline
· Reactive depression
· Seasonal affective disorder (SAD)
· Serotonin
· Tricyclic drugs
· Unipolar depression
What did they do or say?
· Beck
· Bierut
· Bifulco
· Bowiby
· Brown and Harris
· Ford and Neale
· Hinde
· Iversen.
· Kendler and Prescott
· Lewinsohn
· McGuffin
· Seligman
· Silberg
Schizophrenia
Schizophrenia
‘Schizophrenia’ = Skhizein (To split) and Phren (Mind) in Greek.
Schizophrenia is completely different to DID.
Schizophrenia is a loss of contact with reality – sufferers are not aware of the effects of their behaviour on others around them.
Speculations on the origins and development of schizophrenia range from entirely ‘genetic and biological’ through to ‘genetic predisposition and environment trigger’ to the ‘entirely environmental/social.’
Clinical Characteristics:
Catatonic Schizophrenia is one type of schizophrenia, there are several and all hold several features in common:
· Sufferers cognitive, social and emotional state suffers a general deterioration leading to difficulties and breakdowns in normal relationships including those at work and home;
· Onset occurs between 15-45 years.
· Equally common in males as females;
· Occurs 4-5 yrs earlier in males than females.
· Symptoms always appear before the age of 50 – usually in teens and early twenties for males and females respectively.;
· In most countries across the world the lifetime risk of acquiring schizophrenia is 1%.
· Symptoms last at least 6 months before they can be taken as symptoms of schizophrenia;
· Auditory hallucinations and visual delusions occur. Other symptoms include severe disturbances in thought and a loss of self understanding.
· Sufferers are unaware of the impact that they have on others around them and seem to live in their own distorted worlds.
A distinction exists between acute and chronic onset:
1. Chronic = Insidious change in an apparently normal young person who gradually starts to lose drive and motivation and drift away from friends. After months or even years of this deterioration, more obvious signs of disturbance, such as delusional ideas or hallucinations appear.
2. Acute = more obvious signs of stressful event are represented in very disturbed behaviour within a few days..
Sub types of schizophrenia include:
1. Paranoid schizophrenia:
Delusions and or hallucinations are the predominant characteristics. Negative symptoms such as flattening of affect and poverty of speech are less apparent than in other types.
2. Hebephrenic (AKA Disorganised) Schizophrenia
Disorganised behaviour and rambling incoherent speech;
Marked flattening, inappropriateness of affect.
3. Catatonic Schizophrenia
Psychomotor abnormality is the central characteristic;
Adoption of strange postures and flailing limbs;
Often show negativism where they resist all instruction or attempts to move them
4. Undifferentiated schizophrenia
Labelled where they have insufficient symptoms to fit into a sub type or excessive symptoms to fit into one single type.
5. Post Schizophrenic depression (Not in DSM-IV)
Criteria met in last 12 months for classification but not currently present;
Depressive symptoms are long and severe.
6. Residual Schizophrenia
Criteria met in past though not at the present time;
Have been many signs of negative symptoms throughout the previous 12 months.
7. Simple schizophrenia (Not in DSM-IV)
Minimum of 12 months progression development of social withdrawal, apathy, poverty of speech and marked decline scholastic / occupational performance.
General criteria must be met as well as specific criteria for each sub type.
Positive symptoms:
Symptom
Explanation
Example
Delusions
False beliefs that the sufferer thought to be true.
Persecution – having special knowledge or a belief that powers, thought or actions are being controlled by an external force.
Hallucinations
Imagined sensory perceptions.
Auditory – hearing imagined voices (And holding prolonged conversations with these voices)
Thought Disorder
Confused thinking that is evident in what they say and how they say it.
Incoherent speech – jumping from one subject to another with little or no logical connection. The grammar may be strange and only makes sense to the speaker. They may claim that thoughts are being broadcast or stolen from them or are being controlled or influenced by an alien, demon, or foreign power.
Bizarre Behaviour
Strange and inappropriate behaviour (Contravening social norms)
Undressing in public or making odd faces, body gestures and postures for no apparent purpose.
Negative Symptoms:
Symptom
Explanation
Example
Blunted Emotional Responses
No emotional involvement in or response to things in their immediate environment
Unchanging facial expression, gestures, or tone of voice regardless of whether the environment would require a happy or sad response, or an inappropriate response e.g. laughing at a funeral.
Loss of drive
Little interest or motivation to work or enjoy leisure activities
Inability to wash and feed to take decisions and being entirely passive.
Social Withdrawal
Difficulty making and keeping friends acquaintances or more intimate relationships
Negativity and passivity and a reluctance to engage in social interaction
Poverty of Thought
Considerable reduction in cognitive activity: Thinking limited to immediate concerns.
Limited amount of speech and may answer questions with ‘yes’ ‘no’ or ‘I don’t know’
Genetic Explanations for Schizophrenia:
Sample sizes and modestly positive results do not add up to certainty, however, a summary of evidence to this end includes:
Twin studies showing higher than expected probability that if one twin presents symptoms the other is likely to do so;
The closer the relative to the sufferer, the higher the probability that they might develop schizophrenia;
Adopted children who’s natural family contained a member who had developed schizophrenia were more at risk;
A child adopted by a family where a member later develops schizophrenia is no more likely to develop the illness itself.
Where biological changes do occur they could be the result of the schizophrenia rather than the cause, or linked in ways we have yet to discover.
The longitudinal Copenhagen High Risk Study (1962 - early 90’s) examined children who’s mothers were diagnosed as having schizophrenic symptoms and found them much more likely to develop the illness compared to those who did not. There was less than 1 in 10,000 chance (p<0.0001) that these findings could have occurred by chance.
However, this study cannot differentiate between the effects of genes and the effects of the environment.
Adoption studies provide some of the strongest evidence in support of the argument that genetics play a key role in the development of schizophrenia.
Below shows the evidence indicating strong genetic links between genetics and schizophrenia. However, it must be remembered that sample sizes are small and that circumstances of each study were not directly comparable. Also, there are issues to do with the fact that not all social groups are equally likely to be diagnosed with schizophrenia.
Evaluation:
· Research evidence is pretty persuasive for genetic linked risk factors;
· Degree of risk for relatives is never 100% - even with Mz Twins its less than 50%, therefore genetics cant be a complete explanation.
· Search for the relevant gene:
o Without knowing the exact gene it’s impossible to isolate the underlying mechanisms that lead from genetic risk to symptoms of the disorder. The search for the gene continues.
Biochemical explanations of schizophrenia
Dopamine is a brain chemical that increases the sensitivity of the brain cells that promote the individual’s awareness of events around her or him when in danger or aroused and when under stress. If, however, the individual’s level of brain activity is already highly aroused, then the effects of additional dopamine activity may trigger the onset of a psychotic state, such as schizophrenia. (Anti- psychotic drugs block the dopamine-2 (D2) receptors and reduce the severity of some psychotic symptoms.) Studies of other brain chemical (serotonin and noradrenalin) activity are also being extensively researched.
Neurons are individual nerve fibres that carry electrical/chemical ‘messages’. Many millions are densely packed into brain structures. There are tiny gaps between their endings and messages are carried across them by a neurotransmitter substance.
Neurons that have dopamine as their transmitter substance (Dopaminergic neurons) are overactive in individuals who exhibit schizophrenic symptoms. The dopamine hypothesis suggests that ‘excessive activity’ in the dopamine neurons leading to increased dopamine production and limited absorption of existing dopamine is associated with schizophrenia.
An interesting parallel exists with Parkinson’s Disease, where a dopamine increasing drug (L Dopa) seems to have the opposite effect.
Further support for the dopamine hypothesis comes from the post-mortems of patients with schizophrenia. These have revealed specific increase of dopamine in the left amygdale (Falkai et al. 1988) and increased dopamine receptor density in the caudate nucleus putamen (Owen et al. 1978)
Wong et al. (1986) shows in live patients using pet scans that the dopamine receptor density in the caudate nuclei is indeed greater in those with schizophrenia than in controls. This however is not supported in subsequent studies.
Evaluation of Dopamine Hypothesis:
1. Current available evidence supports some form of the dopamine hypothesis.
Drugs alleviate positive symptoms but are not so effective with negative symptoms.
2. Effects of different drugs on different sub types (Type I and II):
Amphetamines worsen positive symptoms (associated with acute schizophrenia) and lessen negative symptoms (Associated with chronic) while phenothiazines (Anti-psychotics) alleviate positive symptoms but aren’t as effective in lessening negative symptoms.
3. Cause or effect cant be established
4. Role of dopamine in other disorders:
Dopamine also implicated in mania and other disorders which have quite different symptoms. Main evidence in dopamine schizophrenia is the effectiveness of phenothiazines in alleviating symptoms.
Neuroanatomical explanations
Advances in brain scanning (neuro-imaging) technology are allowing cognitive and medical researchers to seek structural, organic abnormalities in the brains of people who exhibit behavioural disorders. Two such scanning technologies are Positron Emission Tomography (PET) and Magnetic Resonance Imaging (MRI).
PET scans are used in the diagnosis of problems in bodily organs, particularly the brain. The patient is injected with glucose that contains a tiny amount of radioactive substance — which emits positrons that can be detected by the scanner. As various brain centres use up the glucose their size, location, and connectivity to other brain centres can be recorded.
MRI is a complex diagnostic technique whereby a patient is surrounded by a cylinder that contains a strong magnet. Radio waves from the cylinder cause the atoms of the body to resonate. Each type of body tissue resonates at a different, known, frequency. Since these are known, a computer can build these resonances into a two-dimensional picture. It can ‘see through’ bone and can produce detailed images of just about all parts of the brain and body.
These technologies have shown abnormal brain structures in many patients exhibiting schizophrenic symptoms, for example, the differences in the density of receptor cells for dopamine in schizophrenia patients who were being treated with anti-psychotic drugs and those who were not.
Evidence for neuro-anatomical explanations:
Brown et al (1986) found decreased brain weight and enlarged ventricles, which are the cavities in the brain that hold cerebrospinal fluid.
Flaum et al. (1995) also found enlarged ventricles along with smaller thalamic hippocampal and superior temporal volumes.
Buchsbaum (1990) found abnormalities in the frontal hippocampus and the amygdale. As more MRI studies are being undertaken, more abnormalities are being identified.
The critical time period for the onset of schizophrenia is not usually before adolescence. Therefore if the brain abnormalities precede the onset of clinical symptoms this would confirm the view that schizophrenia is a developmental disorder. Weinberger (!988) claims that despite much research evidence remains inconclusive as to whether there are progressive structural brain changes prior to the initial onset of schizophrenia or whether they follow the onset of clinical symptoms.
Castner (1998) subjected monkeys to brain damaging x rays during fetal development and found that they showed no ill effects in childhood compared to the control group, but at puberty they developed symptoms of schizophrenia such as hallucinations. There are of course ethical issues associated with animal research of this kind.
Evaluation: The neuroanatomical explanation
· Conflicting findings about structural abnormalities.
While MRI studies appear to provide conclusive evidence of structural abnormalities they don’t always agree on the area of the brain that is affected.
Flaum (1995) found no abnormalities in the temporal lobe region,
while Woodruff et al. (1997) found quite significant reductions in the temporal lobe compared with control.
· Structural abnormalities as cause or effect?
Because most studies using MRI techniques have been carried out on people already
diagnosed with schizophrenia it is not clear whether structural abnormalities
predispose to schizophrenia or whether the onset of clinical symptoms cause
structural changes.
· Types of Study:
Prospective studies, which could have shed light on the direction of causality have been carried out only on animals and it is difficult to generalise findings to humans.
Pregnancy and birth factors as explanations for schizophrenia.
Viral illness may damage brain structure and functioning.
This increases if the pregnant woman contracts the illness.
E.g. Influenza, measles and chicken pox.
There is a significant correlation between being born in the winter and early spring and developing schizophrenia. This increases after epidemics of viral infections. (Torrey et al 1988; 1996)
In the southern hemisphere a high proportion of those diagnosed with schizophrenia were born July to September (I.e. Winter months.)
These facts support schizophrenia having a biological origin.
However, not all schizophrenia is associated with brain damage and not all can be linked to viral infection.
Mednick et all (1988) suggestion is that if the mother is infected during the pregnancy there is pre birth exposure to the influenza A virus. It is thought that the 25-30 week foetus is most vulnerable because of accelerated growth of the cerebral cortex at this time.
Its hypothesised that the viral infection enters the brain and gestates until it is activated by hormonal changes in puberty. Alternatively there may be a gradual degeneration of the brain which eventually becomes so severe that symptoms of schizophrenia emerge.
Torrey et all (1988) furthered support for the viral hypothesis comes from the observation that throughout its history peaks in schizophrenia diagnosis have corresponded with major flue epidemics
There are conflicting views as to whether abnormalities result from genetic defect or from birth complications leading to brain damage.
A longitudinal study by Dalman et al. (1999) found significant links between birth complications and later development of schizophrenia, with pre-eclampsia being the most significant risk factor.
Evaluation: Pregnancy and birth factor explanations.
· Methodological problems:
Evidence suggests some link between infection and schizophrenia; however, Torrey inferred causation while doing a correlation study.
Data was based on DSM-II rather than the tighter DSM-III diagnostic range.
· Genetic predisposition:
Torrey et al. (1988) claims the link between viral infection and schizophrenia only exists between those that have a genetic predisposition. Also MZ & DZ twins sharing the same uterus are exposed to same virus and therefore correlation should be 100% - is this the case?
· Birth complications as sole cause?
It’s unlikely that birth complications like pre-eclampsia could be the sole cause of schizophrenia, because this is a common problem and not all such infants go on to develop schizophrenia.
Diathesis-Stress explanations for Schizophrenia
While 51% of all schizophrenics in high EE families suffered a relapse, 49% didn’t.
Other triggers that herald the onset of an episode include momentous life events (Serious illness, Unexpected Bereavement etc.) or a combination of factors which could in isolation be dealt with. E.g. Unemployment, lowered sense of self worth, heavy drinking, marital problems, minor criminal activity, apprehension by the police and a magistrate courts appearance could all trigger an episode.
Schizophrenia did not always develop in those genetically vulnerable.
The Finnish adoption study undertaken by Tienari (1987) investigated environmental factors by assessing the quality of parenting through a battery of tests and interviews. All of the reported cases of schizophrenia occurred in families rated as ‘disturbed.’the high risk sample in healthy environments had occurrences well below the general populations rates. However, unfortunately, low risk children from disturbed envornments did not develop schizophrenia.
The Israeli High Risk Study (Marcus 1987) investigated environmental factorsby assessing the parents on hostility, inconsistency and over involvement.
All the reported cases of schizophrenia had poor parenting ratings. However, all the cases also showed signs of neurological abnormalities at the time of initial assessment (13 years previous) which raises the question of whether these abnormalities had influenced the parent child interaction.
These studies are ongoing and many of the children have not yet passed through the critical period for the onset of schizophrenia. However, the evidence so far strongly supports the diathesis-stress model.
Psychological explanations of Schizophrenia
1. Dysfunctional families:
This discredited theory claimed that families who were secretive, critical and punitive, created such anxieties and tensions that the child was predisposed to developing schizophrenia later. Such explanations are not supported by studies of schizophrenia sufferers and their families, and would not account for biological influences.
Several retrospective clinical studies identified the dysfunctional family, and breakdowns in communication between its various members, as the key cause of schizophrenia.
However, they simply assumed that the patterns of behaviour between family members that they observed would also have been found in the past. Nor were there any control groups of families who had similar patterns of behaviour, but no evidence of schizophrenia amongst their members.
It is hardly surprising that communication becomes strained and routines are disrupted when a family is trying to live and cope with the behaviour of a schizophrenic member. It seems highly likely that the dysfunctional behaviour observed in some families with a schizophrenic member is caused by having to live with someone who has lost contact with reality. Furthermore, more recent studies of dysfunctional families show that few people reared in such homes actually develop schizophrenia and most schizophrenia sufferers come from ‘normal’, well adjusted families.
2. Expressed Emotion (EE):
It was obvious that families may be involved in the progress of the condition, but they are unlikely to have been the cause of it. However, the environment the schizophrenia sufferer returns to after treatment influences the likelihood of successful recovery. Homes where face-to-face interaction is characterised by intense emotional concern or criticism are less conducive to recovery than homes with more emotionally stable interactions. Relapse rates are highest where contact is most fraught.
Brown (1972) showed that patients who returned from hospital to homes where there was a high level of emotionality (High levels of Emotion were Expressed — HEE) were more likely to have a relapse, and would have it sooner than those with LEE (Low levels of Emotion Expressed) families. The kinds of emotions that were expressed were high levels of concern for the sufferers, leading to doing everything for them, being highly critical of their attempts to help themselves, and being very ‘strung out’ generally. These families were characterised by people (mothers usually) rushing around and driving themselves to exhaustion, looking after each other, fussing constantly and being overly possessive. Vaughn and Leff (1976) found 51 per cent of schizophrenic relapses in HEE families, compared to 13 per cent in LEE homes. The more contact the sufferer had with HEE relatives, the higher the relapse rate.
The evidence for the effect of other family members and their emotional responses on recovery from schizophrenia is now well established (and the care package for schizophrenia recovery usually includes some education and support for other family members).
Evidence for the importance of expressed emotion has been found in studies across different cultures so there can be little doubt of its importance in explaining relapse. Unfortunately for the EE explanation, there are also high relapse rates amongst those recovering from schizophrenia who are not in contact with any former family members, so the expressed emotion hypothesis may not be entirely true.
Cognitive explanations for schizophrenia
Whilst not disputing schizophrenia’s genetic and biological origins, cognitive psychologists regard schizophrenia as a thought disorder. They are interested in studying whether there are abnormalities in the cognitive processes of those with schizophrenia, and of their close relatives.
For example, cognitive psychologists are trying to find out if there are similarities in memory function in individuals diagnosed as suffering from schizophrenia and their nearest relatives. Some similarities have been found, but the data available so far fail to explain why only some people with cognitive malfunctioning actually develop schizophrenia while others in the family do not.
Research into similarities and differences in cognitive functioning between schizophrenia and non-schizophrenia sufferers is in its infancy and no acceptable conclusions about the origins or causes of schizophrenia have been established yet.
Cognitive psychologists suggest that disturbed thinking processes are the cause rather than the consequence of schizophrenia.
It is suggested that people with schizophrenia cannot filter information in this way and they simply let in too much irrelevant information.
Explanations that relate underlying biological impairments to psychotic symptoms are often referred to as neuropsychological theories’.
One such hypothesis has been proposed by Hemsley (1993) who suggested that the central deficit in schizophrenia is a breakdown in the relationship between information that has already been stored in memory and new, incoming sensory information.
Hemsley suggests that this processing break down in schizophrenia and those schemas are not activated. As a result, people with schizophrenia are subjected to sensory overload and do not know which aspects of a situation to attend to and which to ignore.
Hemsley further suggests that internal thoughts are sometimes not recognized as arising from memory and so are attributed to an external source are - experienced as auditory hallucinations.
Frith’s model (1992) was an attempt to explain the onset and maintenance of sonic of the positive symptoms of schizophrenia. His idea is that people schizophrenia are cognitively impaired in that they are unable to distinguish between actions that are brougi about b external forces and those that are generated internally. He believes that most of the symptoms of schizophrenia can be explained in terms of deficits in three cognitive processes:
· Inability to generate willed action;
· Inability to monitor willed action;
· Inability to monitor the beliefs and intentions of others.
According to Frith, faulty operation of this mechanism is due to a functional disconnection between frontal areas of the brain concerned with action arid more posterior areas of the brain that control perception. He has produced some evidence for his ideas by detecting changes in cerebral blood flow in the brains of people with schizophrenia when engaged in specific cognitive tasks.
Cognitive psychologists are attempting to find evidence for genetic links by examining whether malfunctioning cognitive processing is a family trait.
Park et al. (1995) identified working memory deficits in people with schizophrenia arid in their first-degree non-schizophrenic relatives, a study that has been supported by Faraone et al. (1999), who also found impairments in auditory attention. Faraone and colleagues claim that these memory and attention impairments are a manifestation of the genetic predisposition to schizophrenia and are even bold enough to claim that these are the cause.
They admit they cannot explain why their relatives do not develop the illness, even though they have the predisposing genes.
They suggest that further work is needed to establish whether some people have a low ‘dose’ of the genes, or, alternatively, whether they have not been exposed to any environmental agents that may trigger the disorder. Cannon et al. (1994b), who also identified verbal memory and attention, but not visual memory deficits, in people with schizophrenia and their non- schizophrenic siblings, suggested that the mediating factors that determine the expression of these genes are birth complications.
References:
Falkai et al. (1988) & Owen et al. (1978) - Further support for the
dopamine hypothesis comes from the post-mortems of patients with schizophrenia. These have revealed specific increase of dopamine in the left amygdale and increased dopamine receptor density in the caudate nucleus putamen
Wong et al. (1986) - Shows in live patients using pet scans that
the dopamine receptor density in the caudate nuclei is indeed greater in those with schizophrenia than in controls. This however is not supported in subsequent studies.
Brown et al (1986) - Found decreased brain weight and enlarged
ventricles, which are the cavities in the brain that hold cerebrospinal fluid.
Flaum et al. (1995) - Also found enlarged ventricles along with
smaller thalamic hippocampal and superior temporal volumes.
Buchsbaum (1990) - Found abnormalities in the frontal
hippocampus and the amygdale. As more MRI studies are being undertaken, more abnormalities are being identified.
Castner (1998) - Subjected monkeys to brain damaging x rays
during fetal development and found that they showed no ill effects in childhood compared to the control group, but at puberty they developed symptoms of schizophrenia such as hallucinations. There are of course ethical issues associated with animal research of this kind.
Mednick et all (1988) - Suggestion is that if the mother is infected
during the pregnancy there is pre birth exposure to the influenza A virus. It is thought that the 25-30 week foetus is most vulnerable because of accelerated growth of the cerebral cortex at this time.
Torrey et all (1988) - Furthered support for the viral hypothesis
comes from the observation that throughout its history peaks in schizophrenia diagnosis have corresponded with major flue epidemics
Dalman et al. (1999) - Longitudinal study which found significant
links between birth complications and later development of schizophrenia, with pre-eclapsia being the most significant risk factor.
Tienari (1987) - The Finnish adoption study investigated
environmental factors by assessing the quality of parenting through a battery of tests and interviews.
Marcus (1987) - The Israeli High Risk Study investigated
environmental factors by assessing the parents on hostility, inconsistency and over involvement.
Brown (1972) - Showed that patients who returned from
hospital to homes where there was a high level of emotionality (High levels of Emotion were Expressed — HEE) were more likely to have a relapse, and would have it sooner than those with LEE (Low levels of Emotion Expressed) families.
Vaughn and Leff (1976) - Found 51 per cent of schizophrenic relapses
in HEE families, compared to 13 per cent in LEE homes. The more contact the sufferer had with HEE relatives, the higher the relapse
Hemsley (1993) - Suggested that the central deficit in
schizophrenia is a breakdown in the relationship between information that has already been stored in memory and new, incoming sensory information.
Park et al. (1995) - Identified working memory deficits in
people with schizophrenia arid in their first-degree non-schizophrenic relatives, a study that has been supported by Faraone et al. (1999)
Faraone et al. (1999) - Found impairments in auditory attention.
Faraone and colleagues claim that these memory and attention impairments are a manifestation of the genetic predisposition to schizophrenia and are even bold enough to claim that these are the cause.
Cannon et al. (1994b) - Identified verbal memory and attention, but
not visual memory deficits, in people with schizophrenia and their non- schizophrenic siblings, suggested that the mediating factors that determine the expression of these genes are birth complications.
Concepts to note:
Define these terms:
· bizarre behaviour
· blunted emotional responses
· delusions
· diathesis-stress explanations
· dissociative identity disorder
· dopamine
· dopamine hypothesis
· expressed emotion (EE)
· functional schizophrenia
· hallucinations
· loss of drive
· neurochemical theory
· neurons
· organic schizophrenia
· poverty of thought
· schizophrenia
· social withdrawal
· thought disorder
What did they do or say?
· Brown
· Faraone
· Kendler
· Park
· Vaughn and Leff
‘Schizophrenia’ = Skhizein (To split) and Phren (Mind) in Greek.
Schizophrenia is completely different to DID.
Schizophrenia is a loss of contact with reality – sufferers are not aware of the effects of their behaviour on others around them.
Speculations on the origins and development of schizophrenia range from entirely ‘genetic and biological’ through to ‘genetic predisposition and environment trigger’ to the ‘entirely environmental/social.’
Clinical Characteristics:
Catatonic Schizophrenia is one type of schizophrenia, there are several and all hold several features in common:
· Sufferers cognitive, social and emotional state suffers a general deterioration leading to difficulties and breakdowns in normal relationships including those at work and home;
· Onset occurs between 15-45 years.
· Equally common in males as females;
· Occurs 4-5 yrs earlier in males than females.
· Symptoms always appear before the age of 50 – usually in teens and early twenties for males and females respectively.;
· In most countries across the world the lifetime risk of acquiring schizophrenia is 1%.
· Symptoms last at least 6 months before they can be taken as symptoms of schizophrenia;
· Auditory hallucinations and visual delusions occur. Other symptoms include severe disturbances in thought and a loss of self understanding.
· Sufferers are unaware of the impact that they have on others around them and seem to live in their own distorted worlds.
A distinction exists between acute and chronic onset:
1. Chronic = Insidious change in an apparently normal young person who gradually starts to lose drive and motivation and drift away from friends. After months or even years of this deterioration, more obvious signs of disturbance, such as delusional ideas or hallucinations appear.
2. Acute = more obvious signs of stressful event are represented in very disturbed behaviour within a few days..
Sub types of schizophrenia include:
1. Paranoid schizophrenia:
Delusions and or hallucinations are the predominant characteristics. Negative symptoms such as flattening of affect and poverty of speech are less apparent than in other types.
2. Hebephrenic (AKA Disorganised) Schizophrenia
Disorganised behaviour and rambling incoherent speech;
Marked flattening, inappropriateness of affect.
3. Catatonic Schizophrenia
Psychomotor abnormality is the central characteristic;
Adoption of strange postures and flailing limbs;
Often show negativism where they resist all instruction or attempts to move them
4. Undifferentiated schizophrenia
Labelled where they have insufficient symptoms to fit into a sub type or excessive symptoms to fit into one single type.
5. Post Schizophrenic depression (Not in DSM-IV)
Criteria met in last 12 months for classification but not currently present;
Depressive symptoms are long and severe.
6. Residual Schizophrenia
Criteria met in past though not at the present time;
Have been many signs of negative symptoms throughout the previous 12 months.
7. Simple schizophrenia (Not in DSM-IV)
Minimum of 12 months progression development of social withdrawal, apathy, poverty of speech and marked decline scholastic / occupational performance.
General criteria must be met as well as specific criteria for each sub type.
Positive symptoms:
Symptom
Explanation
Example
Delusions
False beliefs that the sufferer thought to be true.
Persecution – having special knowledge or a belief that powers, thought or actions are being controlled by an external force.
Hallucinations
Imagined sensory perceptions.
Auditory – hearing imagined voices (And holding prolonged conversations with these voices)
Thought Disorder
Confused thinking that is evident in what they say and how they say it.
Incoherent speech – jumping from one subject to another with little or no logical connection. The grammar may be strange and only makes sense to the speaker. They may claim that thoughts are being broadcast or stolen from them or are being controlled or influenced by an alien, demon, or foreign power.
Bizarre Behaviour
Strange and inappropriate behaviour (Contravening social norms)
Undressing in public or making odd faces, body gestures and postures for no apparent purpose.
Negative Symptoms:
Symptom
Explanation
Example
Blunted Emotional Responses
No emotional involvement in or response to things in their immediate environment
Unchanging facial expression, gestures, or tone of voice regardless of whether the environment would require a happy or sad response, or an inappropriate response e.g. laughing at a funeral.
Loss of drive
Little interest or motivation to work or enjoy leisure activities
Inability to wash and feed to take decisions and being entirely passive.
Social Withdrawal
Difficulty making and keeping friends acquaintances or more intimate relationships
Negativity and passivity and a reluctance to engage in social interaction
Poverty of Thought
Considerable reduction in cognitive activity: Thinking limited to immediate concerns.
Limited amount of speech and may answer questions with ‘yes’ ‘no’ or ‘I don’t know’
Genetic Explanations for Schizophrenia:
Sample sizes and modestly positive results do not add up to certainty, however, a summary of evidence to this end includes:
Twin studies showing higher than expected probability that if one twin presents symptoms the other is likely to do so;
The closer the relative to the sufferer, the higher the probability that they might develop schizophrenia;
Adopted children who’s natural family contained a member who had developed schizophrenia were more at risk;
A child adopted by a family where a member later develops schizophrenia is no more likely to develop the illness itself.
Where biological changes do occur they could be the result of the schizophrenia rather than the cause, or linked in ways we have yet to discover.
The longitudinal Copenhagen High Risk Study (1962 - early 90’s) examined children who’s mothers were diagnosed as having schizophrenic symptoms and found them much more likely to develop the illness compared to those who did not. There was less than 1 in 10,000 chance (p<0.0001) that these findings could have occurred by chance.
However, this study cannot differentiate between the effects of genes and the effects of the environment.
Adoption studies provide some of the strongest evidence in support of the argument that genetics play a key role in the development of schizophrenia.
Below shows the evidence indicating strong genetic links between genetics and schizophrenia. However, it must be remembered that sample sizes are small and that circumstances of each study were not directly comparable. Also, there are issues to do with the fact that not all social groups are equally likely to be diagnosed with schizophrenia.
Evaluation:
· Research evidence is pretty persuasive for genetic linked risk factors;
· Degree of risk for relatives is never 100% - even with Mz Twins its less than 50%, therefore genetics cant be a complete explanation.
· Search for the relevant gene:
o Without knowing the exact gene it’s impossible to isolate the underlying mechanisms that lead from genetic risk to symptoms of the disorder. The search for the gene continues.
Biochemical explanations of schizophrenia
Dopamine is a brain chemical that increases the sensitivity of the brain cells that promote the individual’s awareness of events around her or him when in danger or aroused and when under stress. If, however, the individual’s level of brain activity is already highly aroused, then the effects of additional dopamine activity may trigger the onset of a psychotic state, such as schizophrenia. (Anti- psychotic drugs block the dopamine-2 (D2) receptors and reduce the severity of some psychotic symptoms.) Studies of other brain chemical (serotonin and noradrenalin) activity are also being extensively researched.
Neurons are individual nerve fibres that carry electrical/chemical ‘messages’. Many millions are densely packed into brain structures. There are tiny gaps between their endings and messages are carried across them by a neurotransmitter substance.
Neurons that have dopamine as their transmitter substance (Dopaminergic neurons) are overactive in individuals who exhibit schizophrenic symptoms. The dopamine hypothesis suggests that ‘excessive activity’ in the dopamine neurons leading to increased dopamine production and limited absorption of existing dopamine is associated with schizophrenia.
An interesting parallel exists with Parkinson’s Disease, where a dopamine increasing drug (L Dopa) seems to have the opposite effect.
Further support for the dopamine hypothesis comes from the post-mortems of patients with schizophrenia. These have revealed specific increase of dopamine in the left amygdale (Falkai et al. 1988) and increased dopamine receptor density in the caudate nucleus putamen (Owen et al. 1978)
Wong et al. (1986) shows in live patients using pet scans that the dopamine receptor density in the caudate nuclei is indeed greater in those with schizophrenia than in controls. This however is not supported in subsequent studies.
Evaluation of Dopamine Hypothesis:
1. Current available evidence supports some form of the dopamine hypothesis.
Drugs alleviate positive symptoms but are not so effective with negative symptoms.
2. Effects of different drugs on different sub types (Type I and II):
Amphetamines worsen positive symptoms (associated with acute schizophrenia) and lessen negative symptoms (Associated with chronic) while phenothiazines (Anti-psychotics) alleviate positive symptoms but aren’t as effective in lessening negative symptoms.
3. Cause or effect cant be established
4. Role of dopamine in other disorders:
Dopamine also implicated in mania and other disorders which have quite different symptoms. Main evidence in dopamine schizophrenia is the effectiveness of phenothiazines in alleviating symptoms.
Neuroanatomical explanations
Advances in brain scanning (neuro-imaging) technology are allowing cognitive and medical researchers to seek structural, organic abnormalities in the brains of people who exhibit behavioural disorders. Two such scanning technologies are Positron Emission Tomography (PET) and Magnetic Resonance Imaging (MRI).
PET scans are used in the diagnosis of problems in bodily organs, particularly the brain. The patient is injected with glucose that contains a tiny amount of radioactive substance — which emits positrons that can be detected by the scanner. As various brain centres use up the glucose their size, location, and connectivity to other brain centres can be recorded.
MRI is a complex diagnostic technique whereby a patient is surrounded by a cylinder that contains a strong magnet. Radio waves from the cylinder cause the atoms of the body to resonate. Each type of body tissue resonates at a different, known, frequency. Since these are known, a computer can build these resonances into a two-dimensional picture. It can ‘see through’ bone and can produce detailed images of just about all parts of the brain and body.
These technologies have shown abnormal brain structures in many patients exhibiting schizophrenic symptoms, for example, the differences in the density of receptor cells for dopamine in schizophrenia patients who were being treated with anti-psychotic drugs and those who were not.
Evidence for neuro-anatomical explanations:
Brown et al (1986) found decreased brain weight and enlarged ventricles, which are the cavities in the brain that hold cerebrospinal fluid.
Flaum et al. (1995) also found enlarged ventricles along with smaller thalamic hippocampal and superior temporal volumes.
Buchsbaum (1990) found abnormalities in the frontal hippocampus and the amygdale. As more MRI studies are being undertaken, more abnormalities are being identified.
The critical time period for the onset of schizophrenia is not usually before adolescence. Therefore if the brain abnormalities precede the onset of clinical symptoms this would confirm the view that schizophrenia is a developmental disorder. Weinberger (!988) claims that despite much research evidence remains inconclusive as to whether there are progressive structural brain changes prior to the initial onset of schizophrenia or whether they follow the onset of clinical symptoms.
Castner (1998) subjected monkeys to brain damaging x rays during fetal development and found that they showed no ill effects in childhood compared to the control group, but at puberty they developed symptoms of schizophrenia such as hallucinations. There are of course ethical issues associated with animal research of this kind.
Evaluation: The neuroanatomical explanation
· Conflicting findings about structural abnormalities.
While MRI studies appear to provide conclusive evidence of structural abnormalities they don’t always agree on the area of the brain that is affected.
Flaum (1995) found no abnormalities in the temporal lobe region,
while Woodruff et al. (1997) found quite significant reductions in the temporal lobe compared with control.
· Structural abnormalities as cause or effect?
Because most studies using MRI techniques have been carried out on people already
diagnosed with schizophrenia it is not clear whether structural abnormalities
predispose to schizophrenia or whether the onset of clinical symptoms cause
structural changes.
· Types of Study:
Prospective studies, which could have shed light on the direction of causality have been carried out only on animals and it is difficult to generalise findings to humans.
Pregnancy and birth factors as explanations for schizophrenia.
Viral illness may damage brain structure and functioning.
This increases if the pregnant woman contracts the illness.
E.g. Influenza, measles and chicken pox.
There is a significant correlation between being born in the winter and early spring and developing schizophrenia. This increases after epidemics of viral infections. (Torrey et al 1988; 1996)
In the southern hemisphere a high proportion of those diagnosed with schizophrenia were born July to September (I.e. Winter months.)
These facts support schizophrenia having a biological origin.
However, not all schizophrenia is associated with brain damage and not all can be linked to viral infection.
Mednick et all (1988) suggestion is that if the mother is infected during the pregnancy there is pre birth exposure to the influenza A virus. It is thought that the 25-30 week foetus is most vulnerable because of accelerated growth of the cerebral cortex at this time.
Its hypothesised that the viral infection enters the brain and gestates until it is activated by hormonal changes in puberty. Alternatively there may be a gradual degeneration of the brain which eventually becomes so severe that symptoms of schizophrenia emerge.
Torrey et all (1988) furthered support for the viral hypothesis comes from the observation that throughout its history peaks in schizophrenia diagnosis have corresponded with major flue epidemics
There are conflicting views as to whether abnormalities result from genetic defect or from birth complications leading to brain damage.
A longitudinal study by Dalman et al. (1999) found significant links between birth complications and later development of schizophrenia, with pre-eclampsia being the most significant risk factor.
Evaluation: Pregnancy and birth factor explanations.
· Methodological problems:
Evidence suggests some link between infection and schizophrenia; however, Torrey inferred causation while doing a correlation study.
Data was based on DSM-II rather than the tighter DSM-III diagnostic range.
· Genetic predisposition:
Torrey et al. (1988) claims the link between viral infection and schizophrenia only exists between those that have a genetic predisposition. Also MZ & DZ twins sharing the same uterus are exposed to same virus and therefore correlation should be 100% - is this the case?
· Birth complications as sole cause?
It’s unlikely that birth complications like pre-eclampsia could be the sole cause of schizophrenia, because this is a common problem and not all such infants go on to develop schizophrenia.
Diathesis-Stress explanations for Schizophrenia
While 51% of all schizophrenics in high EE families suffered a relapse, 49% didn’t.
Other triggers that herald the onset of an episode include momentous life events (Serious illness, Unexpected Bereavement etc.) or a combination of factors which could in isolation be dealt with. E.g. Unemployment, lowered sense of self worth, heavy drinking, marital problems, minor criminal activity, apprehension by the police and a magistrate courts appearance could all trigger an episode.
Schizophrenia did not always develop in those genetically vulnerable.
The Finnish adoption study undertaken by Tienari (1987) investigated environmental factors by assessing the quality of parenting through a battery of tests and interviews. All of the reported cases of schizophrenia occurred in families rated as ‘disturbed.’the high risk sample in healthy environments had occurrences well below the general populations rates. However, unfortunately, low risk children from disturbed envornments did not develop schizophrenia.
The Israeli High Risk Study (Marcus 1987) investigated environmental factorsby assessing the parents on hostility, inconsistency and over involvement.
All the reported cases of schizophrenia had poor parenting ratings. However, all the cases also showed signs of neurological abnormalities at the time of initial assessment (13 years previous) which raises the question of whether these abnormalities had influenced the parent child interaction.
These studies are ongoing and many of the children have not yet passed through the critical period for the onset of schizophrenia. However, the evidence so far strongly supports the diathesis-stress model.
Psychological explanations of Schizophrenia
1. Dysfunctional families:
This discredited theory claimed that families who were secretive, critical and punitive, created such anxieties and tensions that the child was predisposed to developing schizophrenia later. Such explanations are not supported by studies of schizophrenia sufferers and their families, and would not account for biological influences.
Several retrospective clinical studies identified the dysfunctional family, and breakdowns in communication between its various members, as the key cause of schizophrenia.
However, they simply assumed that the patterns of behaviour between family members that they observed would also have been found in the past. Nor were there any control groups of families who had similar patterns of behaviour, but no evidence of schizophrenia amongst their members.
It is hardly surprising that communication becomes strained and routines are disrupted when a family is trying to live and cope with the behaviour of a schizophrenic member. It seems highly likely that the dysfunctional behaviour observed in some families with a schizophrenic member is caused by having to live with someone who has lost contact with reality. Furthermore, more recent studies of dysfunctional families show that few people reared in such homes actually develop schizophrenia and most schizophrenia sufferers come from ‘normal’, well adjusted families.
2. Expressed Emotion (EE):
It was obvious that families may be involved in the progress of the condition, but they are unlikely to have been the cause of it. However, the environment the schizophrenia sufferer returns to after treatment influences the likelihood of successful recovery. Homes where face-to-face interaction is characterised by intense emotional concern or criticism are less conducive to recovery than homes with more emotionally stable interactions. Relapse rates are highest where contact is most fraught.
Brown (1972) showed that patients who returned from hospital to homes where there was a high level of emotionality (High levels of Emotion were Expressed — HEE) were more likely to have a relapse, and would have it sooner than those with LEE (Low levels of Emotion Expressed) families. The kinds of emotions that were expressed were high levels of concern for the sufferers, leading to doing everything for them, being highly critical of their attempts to help themselves, and being very ‘strung out’ generally. These families were characterised by people (mothers usually) rushing around and driving themselves to exhaustion, looking after each other, fussing constantly and being overly possessive. Vaughn and Leff (1976) found 51 per cent of schizophrenic relapses in HEE families, compared to 13 per cent in LEE homes. The more contact the sufferer had with HEE relatives, the higher the relapse rate.
The evidence for the effect of other family members and their emotional responses on recovery from schizophrenia is now well established (and the care package for schizophrenia recovery usually includes some education and support for other family members).
Evidence for the importance of expressed emotion has been found in studies across different cultures so there can be little doubt of its importance in explaining relapse. Unfortunately for the EE explanation, there are also high relapse rates amongst those recovering from schizophrenia who are not in contact with any former family members, so the expressed emotion hypothesis may not be entirely true.
Cognitive explanations for schizophrenia
Whilst not disputing schizophrenia’s genetic and biological origins, cognitive psychologists regard schizophrenia as a thought disorder. They are interested in studying whether there are abnormalities in the cognitive processes of those with schizophrenia, and of their close relatives.
For example, cognitive psychologists are trying to find out if there are similarities in memory function in individuals diagnosed as suffering from schizophrenia and their nearest relatives. Some similarities have been found, but the data available so far fail to explain why only some people with cognitive malfunctioning actually develop schizophrenia while others in the family do not.
Research into similarities and differences in cognitive functioning between schizophrenia and non-schizophrenia sufferers is in its infancy and no acceptable conclusions about the origins or causes of schizophrenia have been established yet.
Cognitive psychologists suggest that disturbed thinking processes are the cause rather than the consequence of schizophrenia.
It is suggested that people with schizophrenia cannot filter information in this way and they simply let in too much irrelevant information.
Explanations that relate underlying biological impairments to psychotic symptoms are often referred to as neuropsychological theories’.
One such hypothesis has been proposed by Hemsley (1993) who suggested that the central deficit in schizophrenia is a breakdown in the relationship between information that has already been stored in memory and new, incoming sensory information.
Hemsley suggests that this processing break down in schizophrenia and those schemas are not activated. As a result, people with schizophrenia are subjected to sensory overload and do not know which aspects of a situation to attend to and which to ignore.
Hemsley further suggests that internal thoughts are sometimes not recognized as arising from memory and so are attributed to an external source are - experienced as auditory hallucinations.
Frith’s model (1992) was an attempt to explain the onset and maintenance of sonic of the positive symptoms of schizophrenia. His idea is that people schizophrenia are cognitively impaired in that they are unable to distinguish between actions that are brougi about b external forces and those that are generated internally. He believes that most of the symptoms of schizophrenia can be explained in terms of deficits in three cognitive processes:
· Inability to generate willed action;
· Inability to monitor willed action;
· Inability to monitor the beliefs and intentions of others.
According to Frith, faulty operation of this mechanism is due to a functional disconnection between frontal areas of the brain concerned with action arid more posterior areas of the brain that control perception. He has produced some evidence for his ideas by detecting changes in cerebral blood flow in the brains of people with schizophrenia when engaged in specific cognitive tasks.
Cognitive psychologists are attempting to find evidence for genetic links by examining whether malfunctioning cognitive processing is a family trait.
Park et al. (1995) identified working memory deficits in people with schizophrenia arid in their first-degree non-schizophrenic relatives, a study that has been supported by Faraone et al. (1999), who also found impairments in auditory attention. Faraone and colleagues claim that these memory and attention impairments are a manifestation of the genetic predisposition to schizophrenia and are even bold enough to claim that these are the cause.
They admit they cannot explain why their relatives do not develop the illness, even though they have the predisposing genes.
They suggest that further work is needed to establish whether some people have a low ‘dose’ of the genes, or, alternatively, whether they have not been exposed to any environmental agents that may trigger the disorder. Cannon et al. (1994b), who also identified verbal memory and attention, but not visual memory deficits, in people with schizophrenia and their non- schizophrenic siblings, suggested that the mediating factors that determine the expression of these genes are birth complications.
References:
Falkai et al. (1988) & Owen et al. (1978) - Further support for the
dopamine hypothesis comes from the post-mortems of patients with schizophrenia. These have revealed specific increase of dopamine in the left amygdale and increased dopamine receptor density in the caudate nucleus putamen
Wong et al. (1986) - Shows in live patients using pet scans that
the dopamine receptor density in the caudate nuclei is indeed greater in those with schizophrenia than in controls. This however is not supported in subsequent studies.
Brown et al (1986) - Found decreased brain weight and enlarged
ventricles, which are the cavities in the brain that hold cerebrospinal fluid.
Flaum et al. (1995) - Also found enlarged ventricles along with
smaller thalamic hippocampal and superior temporal volumes.
Buchsbaum (1990) - Found abnormalities in the frontal
hippocampus and the amygdale. As more MRI studies are being undertaken, more abnormalities are being identified.
Castner (1998) - Subjected monkeys to brain damaging x rays
during fetal development and found that they showed no ill effects in childhood compared to the control group, but at puberty they developed symptoms of schizophrenia such as hallucinations. There are of course ethical issues associated with animal research of this kind.
Mednick et all (1988) - Suggestion is that if the mother is infected
during the pregnancy there is pre birth exposure to the influenza A virus. It is thought that the 25-30 week foetus is most vulnerable because of accelerated growth of the cerebral cortex at this time.
Torrey et all (1988) - Furthered support for the viral hypothesis
comes from the observation that throughout its history peaks in schizophrenia diagnosis have corresponded with major flue epidemics
Dalman et al. (1999) - Longitudinal study which found significant
links between birth complications and later development of schizophrenia, with pre-eclapsia being the most significant risk factor.
Tienari (1987) - The Finnish adoption study investigated
environmental factors by assessing the quality of parenting through a battery of tests and interviews.
Marcus (1987) - The Israeli High Risk Study investigated
environmental factors by assessing the parents on hostility, inconsistency and over involvement.
Brown (1972) - Showed that patients who returned from
hospital to homes where there was a high level of emotionality (High levels of Emotion were Expressed — HEE) were more likely to have a relapse, and would have it sooner than those with LEE (Low levels of Emotion Expressed) families.
Vaughn and Leff (1976) - Found 51 per cent of schizophrenic relapses
in HEE families, compared to 13 per cent in LEE homes. The more contact the sufferer had with HEE relatives, the higher the relapse
Hemsley (1993) - Suggested that the central deficit in
schizophrenia is a breakdown in the relationship between information that has already been stored in memory and new, incoming sensory information.
Park et al. (1995) - Identified working memory deficits in
people with schizophrenia arid in their first-degree non-schizophrenic relatives, a study that has been supported by Faraone et al. (1999)
Faraone et al. (1999) - Found impairments in auditory attention.
Faraone and colleagues claim that these memory and attention impairments are a manifestation of the genetic predisposition to schizophrenia and are even bold enough to claim that these are the cause.
Cannon et al. (1994b) - Identified verbal memory and attention, but
not visual memory deficits, in people with schizophrenia and their non- schizophrenic siblings, suggested that the mediating factors that determine the expression of these genes are birth complications.
Concepts to note:
Define these terms:
· bizarre behaviour
· blunted emotional responses
· delusions
· diathesis-stress explanations
· dissociative identity disorder
· dopamine
· dopamine hypothesis
· expressed emotion (EE)
· functional schizophrenia
· hallucinations
· loss of drive
· neurochemical theory
· neurons
· organic schizophrenia
· poverty of thought
· schizophrenia
· social withdrawal
· thought disorder
What did they do or say?
· Brown
· Faraone
· Kendler
· Park
· Vaughn and Leff
Culture Bound Syndromes
Culture Bound Syndromes
Sam (1996) states that western psychological explanations don’t account for all the experiences and behaviour of people from other cultures, psychology being western culture bound and blind to influences from elsewhere
Defining Culture:
The word Culture refers to the beliefs, norms, and values (Standards of acceptable behaviour and thoughts) that govern the way people within a defined group (Such as society or a nation) interact with one another.
Each new member of the group has to learn these beliefs and understandings
Although ICD and DSM aim to be universal and scientific, culture bound syndromes do not fit comfortably into them. The DSM now lists 25 culture bound syndromes, but does not provide criteria for them. CBS raise a serious challenge to both of these classifications systems in this topic we will look at what are CBS. Finally whether CBS are really unique ways of being mad or localised manifestations of illness.
Definition of culture bound syndromes:
We musty always consider the ideas of ‘Value freedom’ and ‘value biases’
Behaviour that can be thought of as a disorder in one society may be thought of as an appropriate response or acceptable behaviour in another. In which case ICD-10 and DSM-IV aren’t going to be acceptable.
This would be described as a culture bound syndrome (CBS) as it is supposed to be specific to that culture. This is also known as a Culture bound Disorder (CBD) or Culture Specific Syndrome (CSS).
Not everyone accepts that CBS exist. ICD-10 defines them as localised forms of depression, anxiety and somatoform disorders – something being wrong with their bodies without there being physical evidence.
Culture bound syndromes of mental disorders are associated with ‘folk illnesses’ that are treated with ‘folk medicines’
ICD-10 defines CBS as behaviour that doesn’t easily fit into the usual categories and appears only amongst particular groups of people.
DSM agrees and adds the idea that other members of the specific culture consider them as illnesses.
Looking for patterns:
What we are interested to know is :
Do particular syndromes of pathological behaviour exist amongst specific groups of people at all?
Or, are they similar to syndromes that can be found everywhere, except that they are triggered by a feature of the culture in which they are found?
Every example of abnormal behaviour must be understood in terms of the norms and values of the group to which the person exhibiting it belongs. It wouldn’t make sense to apply DSM and ICD which reflect Western Cultural experiences, to the behaviour of some Malaysian Males.
Hall (1998) categorises CBS in the following way:
1. A psychiatric Illness (Not originally caused) which is locally recognised as an illness and which does not match a recognised western category;
2. A psychiatric illness (Not originally caused) which is locally recognised as an illness and resembles a Western category, but may lack some symptoms that are regarded as important in many cultures;
3. A psychiatric illness not yet recognised in the west;
4. A psychiatric illness (Which may or may not by organically caused) that is found in many cultures, but is only regarded as an illness in one or a few ;
5. Culturally accepted forms of illness which would not be regarded as acceptable in mainstream Western medicine;
6. A syndrome supposedly occurring in a given culture, but which does not in fact exist which is used to justify the expulsion or execution of an outcast in the same way as witchcraft was.
Arguments for and against the existence of culture-bound syndromes.
Here we ask the following three questions:
Do culture bound syndromes exist?
Can CBS be classified in any meaningful way?
Do the symptoms described as CBS actually exist everywhere (And as described by DSM and ICD) but influenced by culture or are the syndromes really specific to the culture in which they are found and do not exist anywhere else?
The development of the ‘global village’ will result in differences between people declining and therefore CBS declining
Yap (1974) believes that the conditions described in CBS actually exist everywhere but are triggered by factors in specific cultures making their forms vary.
Pfeiffer (1982), however, believes that the only way to understand these syndromes is as a response to the specific cultural circumstances that surround the individual but when clustered into a syndrome they are qualitatively different from other syndromes triggered by events in other cultures.
Universal or culturally relative?
Berry et al. (1992) argues that three positions can be taken in relation to abnormalities, mental disorders etc, these are:
1. Absolute:
Unchanging in terms of origin, symptoms etc. all cultures studies;
2. Universal:
Found in all cultures, but affected by cultural influences in terms of what brings them out, what forms they take etc.
3. Culturally relative:
Unique to some cultures and understandable only in terms of values and concepts held within those cultures.
Yap (1974) argues :
1. Human mental disorders are broad, spanning all cultures i.e. they are supra cultural. Thus it could be argued that symptoms emerge from within the individual and these symptoms cluster together to form discrete categories of mental illness. This was the precise starting point of contemporary psychiatry in the early work of Kraeplin in the late 19th Century;
2. Comparative psychiatry aims to establish common links across cultures in a similar manner to the way in which comparative psychology explores links seen as culturally specific expressions of common human problems and disorders that are addressed by the ICD and DSM. Yap (1974) believes that Latah is a local cultural expression of ‘primary fear reaction’
Commentary - CBS’s and the universal view of these disorders
Supracultural or specific to cultures? — Pfeiffer (1982) argues against the supracultural position on CBS’s. He agrees with Yap (1974) that the manifestations of illnesses, i.e. the human behaviours, may indeed be ‘a universally human character’, but argues that this is only one part of the issue. His view is that the diagnostic and classificatory systems of the Western world are so qualitatively different in nature to the folk illnesses and medicines specific to particular cultures that they cannot be integrated except by distortion. He writes:
‘The attempt to bring the culture-bound syndromes into a psychiatric diagnostic system is doomed to failure because the symptoms in the two spheres are selected and ordered from qualitatively disparate points of view.’
Why CBSs might not be ‘at home’ in the DSM?— Pfeiffer argues that CBSs must be viewed at the level of the individual culture, rather than from the vantage point of Washington DC, the home of the American Psychological Association, because they are specific in the following four aspects:
1. Cultures differ in those things that place people under unbearable stress; in one culture it may be work and status; in another, family relations.
2. Different cultures allow and ban certain expressions and behaviours. What might be permitted as a culturally acceptable release mechanism in certain cultures may not be allowed in others.
3. We may have culture-specific interpretations — a behaviour is one thing, but what we take it to mean and what sense we make of it, is entirely another. Think how certain women were ‘discovered’ to be witches because of culturally specific interpretations of their behaviour (Ussher 1992).
4. We have not explored the variety of cultural-specific ways of treating disorders, but folk medicine is a good example of the ways in which indigenous people treat their illnesses.
So, if CBS’s are a form of folk illness to be treated by folk medicine, then they are qualitatively inconsistent with the aims and purposes of the ICD and DSM
References:
Sam (1996) - States that western psychological explanations don’t
account for all the experiences and behaviour of people from other cultures, psychology being western culture bound and blind to influences from elsewhere
Hall (1998) - categorises CBS as a series of 6 points which
assess CBS existence.
Yap (1974) - believes that the conditions described in CBS actually exist
everywhere but are triggered by factors in specific cultures making their forms vary.
Berry et al. (1992) - argues that three positions can be taken in relation to
abnormalities, mental disorders etc
Pfeiffer (1982) - argues against the supracultural position on CBS’s. He
agrees with Yap (1974) that the manifestations of illnesses, i.e. the human behaviours, may indeed be ‘a universally human character’, but argues that this is only one part of the issue. His view is that the diagnostic and classificatory systems of the Western world are so qualitatively different in nature to the folk illnesses and medicines specific to particular cultures that they cannot be integrated except by distortion.
Concepts to note:
Define these terms:
Culture
Culture Bound Syndromes
What did they do or say?
Hall
Pfeiffer
Yap
Sam (1996) states that western psychological explanations don’t account for all the experiences and behaviour of people from other cultures, psychology being western culture bound and blind to influences from elsewhere
Defining Culture:
The word Culture refers to the beliefs, norms, and values (Standards of acceptable behaviour and thoughts) that govern the way people within a defined group (Such as society or a nation) interact with one another.
Each new member of the group has to learn these beliefs and understandings
Although ICD and DSM aim to be universal and scientific, culture bound syndromes do not fit comfortably into them. The DSM now lists 25 culture bound syndromes, but does not provide criteria for them. CBS raise a serious challenge to both of these classifications systems in this topic we will look at what are CBS. Finally whether CBS are really unique ways of being mad or localised manifestations of illness.
Definition of culture bound syndromes:
We musty always consider the ideas of ‘Value freedom’ and ‘value biases’
Behaviour that can be thought of as a disorder in one society may be thought of as an appropriate response or acceptable behaviour in another. In which case ICD-10 and DSM-IV aren’t going to be acceptable.
This would be described as a culture bound syndrome (CBS) as it is supposed to be specific to that culture. This is also known as a Culture bound Disorder (CBD) or Culture Specific Syndrome (CSS).
Not everyone accepts that CBS exist. ICD-10 defines them as localised forms of depression, anxiety and somatoform disorders – something being wrong with their bodies without there being physical evidence.
Culture bound syndromes of mental disorders are associated with ‘folk illnesses’ that are treated with ‘folk medicines’
ICD-10 defines CBS as behaviour that doesn’t easily fit into the usual categories and appears only amongst particular groups of people.
DSM agrees and adds the idea that other members of the specific culture consider them as illnesses.
Looking for patterns:
What we are interested to know is :
Do particular syndromes of pathological behaviour exist amongst specific groups of people at all?
Or, are they similar to syndromes that can be found everywhere, except that they are triggered by a feature of the culture in which they are found?
Every example of abnormal behaviour must be understood in terms of the norms and values of the group to which the person exhibiting it belongs. It wouldn’t make sense to apply DSM and ICD which reflect Western Cultural experiences, to the behaviour of some Malaysian Males.
Hall (1998) categorises CBS in the following way:
1. A psychiatric Illness (Not originally caused) which is locally recognised as an illness and which does not match a recognised western category;
2. A psychiatric illness (Not originally caused) which is locally recognised as an illness and resembles a Western category, but may lack some symptoms that are regarded as important in many cultures;
3. A psychiatric illness not yet recognised in the west;
4. A psychiatric illness (Which may or may not by organically caused) that is found in many cultures, but is only regarded as an illness in one or a few ;
5. Culturally accepted forms of illness which would not be regarded as acceptable in mainstream Western medicine;
6. A syndrome supposedly occurring in a given culture, but which does not in fact exist which is used to justify the expulsion or execution of an outcast in the same way as witchcraft was.
Arguments for and against the existence of culture-bound syndromes.
Here we ask the following three questions:
Do culture bound syndromes exist?
Can CBS be classified in any meaningful way?
Do the symptoms described as CBS actually exist everywhere (And as described by DSM and ICD) but influenced by culture or are the syndromes really specific to the culture in which they are found and do not exist anywhere else?
The development of the ‘global village’ will result in differences between people declining and therefore CBS declining
Yap (1974) believes that the conditions described in CBS actually exist everywhere but are triggered by factors in specific cultures making their forms vary.
Pfeiffer (1982), however, believes that the only way to understand these syndromes is as a response to the specific cultural circumstances that surround the individual but when clustered into a syndrome they are qualitatively different from other syndromes triggered by events in other cultures.
Universal or culturally relative?
Berry et al. (1992) argues that three positions can be taken in relation to abnormalities, mental disorders etc, these are:
1. Absolute:
Unchanging in terms of origin, symptoms etc. all cultures studies;
2. Universal:
Found in all cultures, but affected by cultural influences in terms of what brings them out, what forms they take etc.
3. Culturally relative:
Unique to some cultures and understandable only in terms of values and concepts held within those cultures.
Yap (1974) argues :
1. Human mental disorders are broad, spanning all cultures i.e. they are supra cultural. Thus it could be argued that symptoms emerge from within the individual and these symptoms cluster together to form discrete categories of mental illness. This was the precise starting point of contemporary psychiatry in the early work of Kraeplin in the late 19th Century;
2. Comparative psychiatry aims to establish common links across cultures in a similar manner to the way in which comparative psychology explores links seen as culturally specific expressions of common human problems and disorders that are addressed by the ICD and DSM. Yap (1974) believes that Latah is a local cultural expression of ‘primary fear reaction’
Commentary - CBS’s and the universal view of these disorders
Supracultural or specific to cultures? — Pfeiffer (1982) argues against the supracultural position on CBS’s. He agrees with Yap (1974) that the manifestations of illnesses, i.e. the human behaviours, may indeed be ‘a universally human character’, but argues that this is only one part of the issue. His view is that the diagnostic and classificatory systems of the Western world are so qualitatively different in nature to the folk illnesses and medicines specific to particular cultures that they cannot be integrated except by distortion. He writes:
‘The attempt to bring the culture-bound syndromes into a psychiatric diagnostic system is doomed to failure because the symptoms in the two spheres are selected and ordered from qualitatively disparate points of view.’
Why CBSs might not be ‘at home’ in the DSM?— Pfeiffer argues that CBSs must be viewed at the level of the individual culture, rather than from the vantage point of Washington DC, the home of the American Psychological Association, because they are specific in the following four aspects:
1. Cultures differ in those things that place people under unbearable stress; in one culture it may be work and status; in another, family relations.
2. Different cultures allow and ban certain expressions and behaviours. What might be permitted as a culturally acceptable release mechanism in certain cultures may not be allowed in others.
3. We may have culture-specific interpretations — a behaviour is one thing, but what we take it to mean and what sense we make of it, is entirely another. Think how certain women were ‘discovered’ to be witches because of culturally specific interpretations of their behaviour (Ussher 1992).
4. We have not explored the variety of cultural-specific ways of treating disorders, but folk medicine is a good example of the ways in which indigenous people treat their illnesses.
So, if CBS’s are a form of folk illness to be treated by folk medicine, then they are qualitatively inconsistent with the aims and purposes of the ICD and DSM
References:
Sam (1996) - States that western psychological explanations don’t
account for all the experiences and behaviour of people from other cultures, psychology being western culture bound and blind to influences from elsewhere
Hall (1998) - categorises CBS as a series of 6 points which
assess CBS existence.
Yap (1974) - believes that the conditions described in CBS actually exist
everywhere but are triggered by factors in specific cultures making their forms vary.
Berry et al. (1992) - argues that three positions can be taken in relation to
abnormalities, mental disorders etc
Pfeiffer (1982) - argues against the supracultural position on CBS’s. He
agrees with Yap (1974) that the manifestations of illnesses, i.e. the human behaviours, may indeed be ‘a universally human character’, but argues that this is only one part of the issue. His view is that the diagnostic and classificatory systems of the Western world are so qualitatively different in nature to the folk illnesses and medicines specific to particular cultures that they cannot be integrated except by distortion.
Concepts to note:
Define these terms:
Culture
Culture Bound Syndromes
What did they do or say?
Hall
Pfeiffer
Yap
Dissassociative Identity Disorder
Multiple Personality Disorder /
Dissociative Identity Disorder
DSM-IV locates the symptoms of multiple personality disorder (Failure to remember significant items and events) with other such dissociative conditions; hence multiple personality disorder is now called ‘dissociative identity disorder’ (DID)
(The ‘split’ in schizophrenia refers to the loss of contact with reality.)
In Dissociative Identity Disorder (DID) this integrity of the overall personality is said to break down and one or more independent sub personalities may appear.
Defining DID:
· Disassociation is a disorder in which a disruption ion memory leads to a separation of one part of a person’s identity from another. Disassociative Identity Disorder (DID) occurs when two or more distinct personalities (Referred to as ‘Alters’ or sub personalities’ exist within one person.
· Alters have their own distinct identity, personal history and self image. They often have their own name and age. Two or more of these control the persons behaviour from time to time.
Thigpen & Cleckley (1954; 1957) reported the case of ‘The three cases of Eve’
· Conducted 14 month long case study on the patient including over 100 hours of interviews, hypnosis, and several kinds of psychological tests.
· Chris Sizemoore was Eves real name;
· Wife and mother;
· Quiet and shy;
· Troubled housewife who sought psychotherapy;
· Complained of hearing an imaginary voice and suffered blackouts – did not disturb her;
· Had three distinct personalities – Eve white, eve black & Jane;
· Eve Black was confident and appealing;
· Much later eve claimed that she had 22 different personalities and they assisted in coping with difficulties;
· Multiple personality disorder usually involves average of 15 personalities.
o Each with different appetites, handwriting, skills, IQ and facial expressions and dress codes.
o Persons with DID display two or more personalities, often called ‘;sub personalities’ each with a unique set of behaviours, emotions and thoughts.
§ At any given time, one of the sub personalities dominates the persons consciousness and interactions with other people.
Not everyone believes that DID is a legitimate mental disorder. Some claim that it emerges as a patients response to therapy. Spanos (1994) states this is due to demand characteristics.
Just about all the cases of DID have been in N. USA. Relatively few exist elsewhere.
What is DID?
A cluster of problems that involve changes in a persons memory, sense of identity or consciousness.
Taking on a new identity and wandering from home for a time;
Four major sub-types of disassociate disorders are defined by DSM-IV-TR:
1. Dissociative Amnesia:
· Individuals unable to recall important personal information.
2. Dissociative Fuge:
· Dreamlike altered state of consciousness.
3. DID:
4. Depersonalisation disorder:
· Self perception is altered in a disconcerting way.
Alters (Ego states)
· In order to be diagnosed as suffering DID under current DSM guidelines an individual must have at least two separate modes of internal state and response.
· They should exist separately from one another and in extreme cases not even be aware of the others existence.
· Typically between two and four alters exist. Possibly more, this being not uncommon.
(Davison et al 2004)
Theoretical Explanations of Dissociative Identity Disorder
Psychodynamic Explanations:
· Supporters of the existence of DID claim the ‘alter’ protects the child’s personality from the memory of the trauma.
· Traumatic events could disrupt normal personality functioning and we can develop a means of coping with this potential disruption.
o Therefore our unconscious mind may deploy a defence mechanism.
§ Defends our rational ego from our irrational Id which are often in conflict
§ Painful thoughts and memories about early experiences may disrupt early personality development and therefore defence mechanisms are deployed here too.
§ A child suffering from abuse and neglect may develop another personality (Alter) to escape from the pain suffered by the child with the dominant or host personality.
§ N.B. Many children suffer abuse and neglect but few of them seem to develop DID.
§ Many children suffer abuse and neglect but few of them seem to develop DID.
Process map:
Healthy
↓
Defence Mechanism
↓
Alter(s) Development
↓
Conflict Resolution / Defences fail
↓
DID.
Case Study: Sybil.
1980’s è DID sufferer, eager for help
Screened on horizon in 1999 titled ‘Mistaken identity’
Professor Hubert Spiegel – doubts DID is a disorder.
Sybil “Do you want me to be Helen?”
Replies that’s unnecessary but you may if you would like to..
She preferred not to.
Relived experiences as if in another person when recalling them.
Did not display alters.
Overnight DID – a formerly fairly unknown / unheard of illness became more common.
Could this be behavioural reinforcement?
Kluft (1984) supports the role of abuse in DID – finds 97% of cases studied to involve physical or sexual abuse.
However, DID is relatively rare in comparison to known incidence of child abuse.
Behavioural Explanations.
Majority of behaviour is learned through the process of reinforcement where the consequences of something were unpleasant – the process of negative reinforcement, that this becomes reinforced.
Seligman (1971) claims that people may be biologically pre-programmed to react in several way, including exhibiting DID. This challenged behaviourists who only recognise factors in the environment as being able to provide reinforcement.
Psychodynamic model
Behavioural Model
Agree
Early traumas lead to DID
DID relieves otherwise damaging situations
Disagree
DID results from unconscious conflicts
DID reflects the. personality
DID is a learned response
DID reflects behaviour
Socio-cognitive explanations
State dependant learning
Knowledge acquired when in one emotional state is best remembered when in that state again. Memories when feeling sad may cluster into a sub personality, which could be recreated when made to feel sad again.
Self-hypnosis
Argues that children, who are highly suggestible to external influences, escape into a dream world through a form of self hypnosis. There are too many unknowns about what hypnosis is to be convinced by this explanation.
Comer (2004) argues that people with DID are particularly susceptible to hypnosis.
Others suggest that while using hypnosis to treat psychological problems therapists have unwittingly created ‘alters’ that DID sufferers report (Cohen 1995)
Trance like state Vs normal social, attention and cognitive processes in which it is a social role where people carry out their perceived obligations in line with their expectations of that role (Demand characteristics).
Despite these facts Coons (1989) found that most DID patients had not been hypnotized.
DID as a spontaneous ‘iatrogenic’ phenomenon.
Here it is claimed that people seek psychological help for a variety of reasons .
During therapy they start to talk about themselves as if they were someone else – creating another personality. The therapist asks them to elaborate on their behaviour as someone else. – They ere creating another personality. Iatrogenic means ‘created by the treatment – or mistreatment by - itself.’ In short induced unintentionally by therapeutic practice.
Spanos (1994) suggests that DID is created by role play influenced by their therapists goals and expectations
Gleaves (1996) notes that although the disorder occurs in other cultures, it is extremely rare in Europe and Japan leading to some e.g. Mersky (1992) suggesting its merely a ‘North American fad.’
Two explanations are put forward for DID:
The Post Traumatic Model
Sees DID resulting from traumatic early experiences as already described.
The Socio-Cognitive model (SCM)
Claims that DID is largely the result of iatrogenic factors.
Evaluation: DID as a spontaneous or Iatrogenic Disorder
Can iatrogenic factors alone explain DID?:
Gleaves (1996) argues that no disorder can be solely due to Iatrogenic factors.
This may be a common cause of DID but DID can occur spontaneously in their absence.
e.g. occurring in societies where exposure to mental health professionals is minimal.
Scroppo et al. (1998) suggests that people suffering from DID show increased imaginative activity, a reduced ability to integrate mental components, a complex and driven cognitive style and a highly unconventional view of reality.
Lilienfield et al (1999) argues that supporters of SCM do not deny that ‘much of the psychopathological raw material from which DID is sculpted exists prior to professional intervention.’ In short it contributes to DID no more than other social influences.
Shaped during therapy or spontaneous?:
It is recognised that in some instances DID may be feigned in order to avoid responsibility for criminal actions or to attract attention. This throws doubt on the existence of DID.
SCM model enthusiasts do not claim that DID is not a real phenomenon, they do however wonder if the condition’s best described as a response to trauma (PTSD) or as a ‘socially influenced product that unfolds largely in response to the shaping influences of therapeutic practices culturally based scripts and social expectations (Lilenfield et all (1999)
Are the patterns of abnormality consistent between sufferers of DID?
Sceptics maintain that iatrogenesis is one of the main reasons for the reported increase in numbers and believe that DID patients do not really share any underlying causes or psychological processes that one would expect to see in a real mental disorder (Cohen 1995)
In a study of 21 DID and 21 non DID patients Scroppo et al (1998) reported that the DID patients demonstrated fairly consistent patterns of behaviour in a number of different areas and also showed a distinctive and theoretically consistent set of perceptual and cognitive characteristics that clearly differentiated them from the non-DID participants.
Commentary: The increase in reported cases of DID
DID diagnosis have been on the increase for 30 years. This raises the question of whether it is really becoming far more common or whether clinicians are simply diagnosing it more frequently.
Tightening up the DSM.
Turkington & Harris (2001) state early editions of the DSM led to diagnosis of a wide range of abnormal behaviours being classified as DID. Fewer people with problems of identity which previously overlapped with schizophrenia are now classified as having DID. (Comer 1994)
Differences in acceptance of DID between the USA and the UK:
Although rates of reported cases of DID have soared in recent years, the vast majority have been due to diagnosis in the USA
Cohen (1995) in new Scientist describes a population of 1200 American doctors of whom 70% stated they have seen at least 1 case of DID. Only 12% did not believe in the diagnosis. Cohen found the condition contrived. If this is the case the increase may be due to largely due to a different interpretation of the DSM compared to UK clinicians.
The motivation for developing DID.
Mowrer’s View of the ‘Neurotic paradox’ (1948) is relevant here, people without a home, friends, possessions, and hope may feel prison is a refuge or sanctuary with food. Most view it as a punishment. This is the paradox.
References:
Davison et al. (2004) - Typically between two and four alters exist.
Possibly more, this being not uncommon.
Kluft (1984) - Supports the role of abuse in DID – find 97% of
cases studied to involve physical or sexual abuse.
Seligman (1971) - claims that people may be biologically pre-
programmed to react in several way, including exhibiting DID. This challenged behaviourists who only recognise factors in the environment as being able to provide reinforcement.
Comer (2004) - argues that people with DID are particularly
susceptible to hypnosis.
Coons (1989) - found that most DID patients had not been
hypnotized.
Spanos (1994) - suggests that DID is created by role play influenced
by their therapists goals and expectations
Gleaves (1996) - notes that although the disorder occurs in other
cultures, it is extremely rare in Europe and Japan
Mersky (1992) - suggested that DID is merely a ‘North American
fad.’
Gleaves (1996) - argues that no disorder can be solely due to
Iatrogenic factors. This may be a common cause of DID but DID can occur spontaneously in their absence. e.g. occurring in societies where exposure to mental health professionals is minimal.
Scroppo et al. (1998) - Suggests that people suffering from DID show
increased imaginative activity, a reduced ability to integrate mental components, a complex and driven cognitive style and a highly unconventional view of reality.
Lilienfield et al (1999) - argues that supporters of SCM do not deny that
‘much of the psychopathological raw material from which DID is sculpted exists prior to professional intervention.’ In short it contributes to DID no more than other social influences.
Lilenfield et all (1999) - SCM model enthusiasts do not claim that
DID is not a real phenomenon, they do however wonder if the condition’s best described as a response to trauma (PTSD) or as a ‘socially influenced product that unfolds largely in response to the shaping influences of therapeutic practices culturally based scripts and social expectations
Cohen (1995) - Sceptics maintain that iatrogenesis is one of the
main reasons for the reported increase in numbers and believe that DID patients do not really share any underlying causes or psychological processes that one would expect to see in a real mental disorder
Scroppo et al (1998) - In a study of 21 DID and 21 non DID patients
reported that the DID patients demonstrated fairly consistent patterns of behaviour in a number of different areas and also showed a distinctive and theoretically consistent set of perceptual and cognitive characteristics that clearly differentiated them from the non-DID participants.
Turkington & Harris (2001) - state early editions of the DSM led to diagnosis of a
wide range of abnormal behaviours being classified
as DID.
Comer (1994) - Fewer people with problems of identity which
previously overlapped with schizophrenia are now classified as having DID.
Cohen (1995) - In new Scientist describes a population of 1200
American doctors of whom 70% stated they have seen at least 1 case of DID. Only 12% did not believe in the diagnosis. Cohen found the condition contrived. If this is the case the increase may be due to largely due to a different interpretation of the DSM compared to UK clinicians.
Concepts to note:
Define these terms:
· Alters
· Defence mechanism
· Dissociative identity disorder (DID)
· Dissociation
· Iatrogenic
· Multiple personality disorder (MPD)
· Negative reinforcement
· Post-traumatic model (PTM)
· Socio-cognitive model (SCM)
· State-dependent learning
What did they do or say?
· Freud
· Gleaves
· Mersky
· Mowrer
· Seligman
· Skinner
· Spanos
· Thigpen and Cleckley
Dissociative Identity Disorder
DSM-IV locates the symptoms of multiple personality disorder (Failure to remember significant items and events) with other such dissociative conditions; hence multiple personality disorder is now called ‘dissociative identity disorder’ (DID)
(The ‘split’ in schizophrenia refers to the loss of contact with reality.)
In Dissociative Identity Disorder (DID) this integrity of the overall personality is said to break down and one or more independent sub personalities may appear.
Defining DID:
· Disassociation is a disorder in which a disruption ion memory leads to a separation of one part of a person’s identity from another. Disassociative Identity Disorder (DID) occurs when two or more distinct personalities (Referred to as ‘Alters’ or sub personalities’ exist within one person.
· Alters have their own distinct identity, personal history and self image. They often have their own name and age. Two or more of these control the persons behaviour from time to time.
Thigpen & Cleckley (1954; 1957) reported the case of ‘The three cases of Eve’
· Conducted 14 month long case study on the patient including over 100 hours of interviews, hypnosis, and several kinds of psychological tests.
· Chris Sizemoore was Eves real name;
· Wife and mother;
· Quiet and shy;
· Troubled housewife who sought psychotherapy;
· Complained of hearing an imaginary voice and suffered blackouts – did not disturb her;
· Had three distinct personalities – Eve white, eve black & Jane;
· Eve Black was confident and appealing;
· Much later eve claimed that she had 22 different personalities and they assisted in coping with difficulties;
· Multiple personality disorder usually involves average of 15 personalities.
o Each with different appetites, handwriting, skills, IQ and facial expressions and dress codes.
o Persons with DID display two or more personalities, often called ‘;sub personalities’ each with a unique set of behaviours, emotions and thoughts.
§ At any given time, one of the sub personalities dominates the persons consciousness and interactions with other people.
Not everyone believes that DID is a legitimate mental disorder. Some claim that it emerges as a patients response to therapy. Spanos (1994) states this is due to demand characteristics.
Just about all the cases of DID have been in N. USA. Relatively few exist elsewhere.
What is DID?
A cluster of problems that involve changes in a persons memory, sense of identity or consciousness.
Taking on a new identity and wandering from home for a time;
Four major sub-types of disassociate disorders are defined by DSM-IV-TR:
1. Dissociative Amnesia:
· Individuals unable to recall important personal information.
2. Dissociative Fuge:
· Dreamlike altered state of consciousness.
3. DID:
4. Depersonalisation disorder:
· Self perception is altered in a disconcerting way.
Alters (Ego states)
· In order to be diagnosed as suffering DID under current DSM guidelines an individual must have at least two separate modes of internal state and response.
· They should exist separately from one another and in extreme cases not even be aware of the others existence.
· Typically between two and four alters exist. Possibly more, this being not uncommon.
(Davison et al 2004)
Theoretical Explanations of Dissociative Identity Disorder
Psychodynamic Explanations:
· Supporters of the existence of DID claim the ‘alter’ protects the child’s personality from the memory of the trauma.
· Traumatic events could disrupt normal personality functioning and we can develop a means of coping with this potential disruption.
o Therefore our unconscious mind may deploy a defence mechanism.
§ Defends our rational ego from our irrational Id which are often in conflict
§ Painful thoughts and memories about early experiences may disrupt early personality development and therefore defence mechanisms are deployed here too.
§ A child suffering from abuse and neglect may develop another personality (Alter) to escape from the pain suffered by the child with the dominant or host personality.
§ N.B. Many children suffer abuse and neglect but few of them seem to develop DID.
§ Many children suffer abuse and neglect but few of them seem to develop DID.
Process map:
Healthy
↓
Defence Mechanism
↓
Alter(s) Development
↓
Conflict Resolution / Defences fail
↓
DID.
Case Study: Sybil.
1980’s è DID sufferer, eager for help
Screened on horizon in 1999 titled ‘Mistaken identity’
Professor Hubert Spiegel – doubts DID is a disorder.
Sybil “Do you want me to be Helen?”
Replies that’s unnecessary but you may if you would like to..
She preferred not to.
Relived experiences as if in another person when recalling them.
Did not display alters.
Overnight DID – a formerly fairly unknown / unheard of illness became more common.
Could this be behavioural reinforcement?
Kluft (1984) supports the role of abuse in DID – finds 97% of cases studied to involve physical or sexual abuse.
However, DID is relatively rare in comparison to known incidence of child abuse.
Behavioural Explanations.
Majority of behaviour is learned through the process of reinforcement where the consequences of something were unpleasant – the process of negative reinforcement, that this becomes reinforced.
Seligman (1971) claims that people may be biologically pre-programmed to react in several way, including exhibiting DID. This challenged behaviourists who only recognise factors in the environment as being able to provide reinforcement.
Psychodynamic model
Behavioural Model
Agree
Early traumas lead to DID
DID relieves otherwise damaging situations
Disagree
DID results from unconscious conflicts
DID reflects the. personality
DID is a learned response
DID reflects behaviour
Socio-cognitive explanations
State dependant learning
Knowledge acquired when in one emotional state is best remembered when in that state again. Memories when feeling sad may cluster into a sub personality, which could be recreated when made to feel sad again.
Self-hypnosis
Argues that children, who are highly suggestible to external influences, escape into a dream world through a form of self hypnosis. There are too many unknowns about what hypnosis is to be convinced by this explanation.
Comer (2004) argues that people with DID are particularly susceptible to hypnosis.
Others suggest that while using hypnosis to treat psychological problems therapists have unwittingly created ‘alters’ that DID sufferers report (Cohen 1995)
Trance like state Vs normal social, attention and cognitive processes in which it is a social role where people carry out their perceived obligations in line with their expectations of that role (Demand characteristics).
Despite these facts Coons (1989) found that most DID patients had not been hypnotized.
DID as a spontaneous ‘iatrogenic’ phenomenon.
Here it is claimed that people seek psychological help for a variety of reasons .
During therapy they start to talk about themselves as if they were someone else – creating another personality. The therapist asks them to elaborate on their behaviour as someone else. – They ere creating another personality. Iatrogenic means ‘created by the treatment – or mistreatment by - itself.’ In short induced unintentionally by therapeutic practice.
Spanos (1994) suggests that DID is created by role play influenced by their therapists goals and expectations
Gleaves (1996) notes that although the disorder occurs in other cultures, it is extremely rare in Europe and Japan leading to some e.g. Mersky (1992) suggesting its merely a ‘North American fad.’
Two explanations are put forward for DID:
The Post Traumatic Model
Sees DID resulting from traumatic early experiences as already described.
The Socio-Cognitive model (SCM)
Claims that DID is largely the result of iatrogenic factors.
Evaluation: DID as a spontaneous or Iatrogenic Disorder
Can iatrogenic factors alone explain DID?:
Gleaves (1996) argues that no disorder can be solely due to Iatrogenic factors.
This may be a common cause of DID but DID can occur spontaneously in their absence.
e.g. occurring in societies where exposure to mental health professionals is minimal.
Scroppo et al. (1998) suggests that people suffering from DID show increased imaginative activity, a reduced ability to integrate mental components, a complex and driven cognitive style and a highly unconventional view of reality.
Lilienfield et al (1999) argues that supporters of SCM do not deny that ‘much of the psychopathological raw material from which DID is sculpted exists prior to professional intervention.’ In short it contributes to DID no more than other social influences.
Shaped during therapy or spontaneous?:
It is recognised that in some instances DID may be feigned in order to avoid responsibility for criminal actions or to attract attention. This throws doubt on the existence of DID.
SCM model enthusiasts do not claim that DID is not a real phenomenon, they do however wonder if the condition’s best described as a response to trauma (PTSD) or as a ‘socially influenced product that unfolds largely in response to the shaping influences of therapeutic practices culturally based scripts and social expectations (Lilenfield et all (1999)
Are the patterns of abnormality consistent between sufferers of DID?
Sceptics maintain that iatrogenesis is one of the main reasons for the reported increase in numbers and believe that DID patients do not really share any underlying causes or psychological processes that one would expect to see in a real mental disorder (Cohen 1995)
In a study of 21 DID and 21 non DID patients Scroppo et al (1998) reported that the DID patients demonstrated fairly consistent patterns of behaviour in a number of different areas and also showed a distinctive and theoretically consistent set of perceptual and cognitive characteristics that clearly differentiated them from the non-DID participants.
Commentary: The increase in reported cases of DID
DID diagnosis have been on the increase for 30 years. This raises the question of whether it is really becoming far more common or whether clinicians are simply diagnosing it more frequently.
Tightening up the DSM.
Turkington & Harris (2001) state early editions of the DSM led to diagnosis of a wide range of abnormal behaviours being classified as DID. Fewer people with problems of identity which previously overlapped with schizophrenia are now classified as having DID. (Comer 1994)
Differences in acceptance of DID between the USA and the UK:
Although rates of reported cases of DID have soared in recent years, the vast majority have been due to diagnosis in the USA
Cohen (1995) in new Scientist describes a population of 1200 American doctors of whom 70% stated they have seen at least 1 case of DID. Only 12% did not believe in the diagnosis. Cohen found the condition contrived. If this is the case the increase may be due to largely due to a different interpretation of the DSM compared to UK clinicians.
The motivation for developing DID.
Mowrer’s View of the ‘Neurotic paradox’ (1948) is relevant here, people without a home, friends, possessions, and hope may feel prison is a refuge or sanctuary with food. Most view it as a punishment. This is the paradox.
References:
Davison et al. (2004) - Typically between two and four alters exist.
Possibly more, this being not uncommon.
Kluft (1984) - Supports the role of abuse in DID – find 97% of
cases studied to involve physical or sexual abuse.
Seligman (1971) - claims that people may be biologically pre-
programmed to react in several way, including exhibiting DID. This challenged behaviourists who only recognise factors in the environment as being able to provide reinforcement.
Comer (2004) - argues that people with DID are particularly
susceptible to hypnosis.
Coons (1989) - found that most DID patients had not been
hypnotized.
Spanos (1994) - suggests that DID is created by role play influenced
by their therapists goals and expectations
Gleaves (1996) - notes that although the disorder occurs in other
cultures, it is extremely rare in Europe and Japan
Mersky (1992) - suggested that DID is merely a ‘North American
fad.’
Gleaves (1996) - argues that no disorder can be solely due to
Iatrogenic factors. This may be a common cause of DID but DID can occur spontaneously in their absence. e.g. occurring in societies where exposure to mental health professionals is minimal.
Scroppo et al. (1998) - Suggests that people suffering from DID show
increased imaginative activity, a reduced ability to integrate mental components, a complex and driven cognitive style and a highly unconventional view of reality.
Lilienfield et al (1999) - argues that supporters of SCM do not deny that
‘much of the psychopathological raw material from which DID is sculpted exists prior to professional intervention.’ In short it contributes to DID no more than other social influences.
Lilenfield et all (1999) - SCM model enthusiasts do not claim that
DID is not a real phenomenon, they do however wonder if the condition’s best described as a response to trauma (PTSD) or as a ‘socially influenced product that unfolds largely in response to the shaping influences of therapeutic practices culturally based scripts and social expectations
Cohen (1995) - Sceptics maintain that iatrogenesis is one of the
main reasons for the reported increase in numbers and believe that DID patients do not really share any underlying causes or psychological processes that one would expect to see in a real mental disorder
Scroppo et al (1998) - In a study of 21 DID and 21 non DID patients
reported that the DID patients demonstrated fairly consistent patterns of behaviour in a number of different areas and also showed a distinctive and theoretically consistent set of perceptual and cognitive characteristics that clearly differentiated them from the non-DID participants.
Turkington & Harris (2001) - state early editions of the DSM led to diagnosis of a
wide range of abnormal behaviours being classified
as DID.
Comer (1994) - Fewer people with problems of identity which
previously overlapped with schizophrenia are now classified as having DID.
Cohen (1995) - In new Scientist describes a population of 1200
American doctors of whom 70% stated they have seen at least 1 case of DID. Only 12% did not believe in the diagnosis. Cohen found the condition contrived. If this is the case the increase may be due to largely due to a different interpretation of the DSM compared to UK clinicians.
Concepts to note:
Define these terms:
· Alters
· Defence mechanism
· Dissociative identity disorder (DID)
· Dissociation
· Iatrogenic
· Multiple personality disorder (MPD)
· Negative reinforcement
· Post-traumatic model (PTM)
· Socio-cognitive model (SCM)
· State-dependent learning
What did they do or say?
· Freud
· Gleaves
· Mersky
· Mowrer
· Seligman
· Skinner
· Spanos
· Thigpen and Cleckley
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