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Think of ‘madness’ and we probably think of schizophrenia. It is the ultimate when it comes to psychological disorders and abnormality, strange then that as a condition it is so loosely defined, to the point were some psychologists even question its very existence! That is not to question that some people (about 1% of the population) do suffer what we would term ‘schizophrenic symptoms,’ but given that the symptoms are so varied can we really group them all under on umbrella term of ‘schizophrenia?’ Schizophrenia is a massive health care issue. It is estimated that there are over half a million schizophrenics and that 10% of all NHS beds contain a schizophrenic. As a nation we spend an estimated £1.7 billion (£1,700,000,000) on treating schizophrenia each year. That is more than we spend on treating cancer! What is schizophrenia? Not an easy question to answer, but one thing it certainly is not is ‘split personality!’ This confusion probably arises due to the meaning of the word itself ‘split mind,’ but in fact schizophrenia is not a disorder of personality at all. It is probably best described as a detachment from reality in which the sufferer experiences hallucinations, delusions and a possible host of other symptoms. History of the term Emil Kraepelin (1898) first described a disorder that he called ‘dementia praecox’ or senility of youth. Typically the onset of what we now call ‘schizophrenia’ is in the late teens or early twenties in men and a little later in women. Kraepelin believed that mental disorders should be categorised as either:
This categorisation led to the development of the DSM (Diagnostic and Statistical Manual) still used today as a method of classifying mental disorders (particularly in the USA). It is also used as a basis for the ICD (International Classification of Diseases) used by the World Health Organisation in classifying all disorders (mental and physical). Note: you may see during the course of your extensive background reading the terms DSM-IV and ICD-10. These refer to the latest editions of the two classification systems. Eugen Bleuler (1908) called the disorder ‘schizophrenia’ and described its symptoms as a loosening of the threads that hold the mind together or as a loss of connections between thoughts.
The symptoms of schizophrenia The symptoms are so varied that it is useful to categorise them in one of a number of ways: Schneider (1959) described what he termed ‘first rank symptoms.’ To be diagnosed with schizophrenia one or more of these needs to be present:
Similarly the DSM-IV (categorisation system used by the American Psychiatric Association) believe that a schizophrenic has to be suffering one or more of the following symptoms:
The DSM-IV states that schizophrenia can be diagnosed if one of these is present OR two of the following: Other persistent hallucinations, breaks in the train of thought, catatonic behaviour, negative symptoms, change in personal behaviour. The next section will look at some of these in more detail.
First rank symptoms:
You may be familiar with the song ‘They’re coming to take me away ah ah!’ This was sung by a bloke calling himself Napolean 14th who was quite bizarre. The B side was the track played backwards. (This was in the days of vinyl when the recording medium had two sides!).
Major symptoms of Schizophrenia (according to Slater and Roth 1969) Thought disorder in which there are breaks in the train of thought and the person appears to make illogical jumps from one topic to another (loose association). Words may become confused and sentences incoherent (so called ‘word salad). Psychomotor disturbances (or catatonic behaviour) were the patient may adopt strange postures or engage in repetitive movements such as pacing or rocking (which I witnessed in one Victorian-style asylum I visited… as a student!). Catatonic refers to the tendency of some patients to hold a particular position for an extended length of time (in extreme cases several years!!!). Lack of volition: in which a person becomes totally apathetic and sits around waiting for things to happen. They engage in no self motivated behaviour. Their get up and go has got up and gone! Disturbances of affect, were the patient may show little in the way of emotional response or in some situations may exhibit inappropriate emotional responses:
First rank symptoms appear to be describing the ‘core’ characteristics of schizophrenia and the ones that most people find most concerning. Slater & Roth on the other hand see these so called ‘first rank’ symptoms as being secondary manifestations of other underlying processes. It is essential to remember that there is no one characteristic that must be present for a person to be diagnosed with schizophrenia! There is one other, particularly useful, way in which the symptoms can be broken down:
Types of schizophrenia The validity of schizophrenia has a single disorder is questioned by many. This is a useful point to emphasise in any essay on the disorder. The symptoms are so diverse and the possible causes so varied that it seems likely that we are in fact dealing with many different psychological disorders. One way round this problem is to consider different types of schizophrenia. Below are the main five subdivisions which just a brief description of each: Paranoid schizophrenia Characterised by type I or positive symptoms. Typically the paranoid schizophrenic experiences delusions of persecution or grandeur that are very detailed and complex. On average about 100 paranoid schizophrenics are arrested outside the Whitehouse, and in Britain sufferers are drawn to Downing Street or Buck House. Sometimes they are seeking money but often want to give advice on how to run the country or on impending disaster. This category is odd in that patients do not have any of the negative symptoms and other than their strange beliefs show no outward signs of their condition Disorganised schizophrenia (formerly hebephrenic) Hebephrenic means ‘silly mind.’ The characteristics of this disorder are silly and incoherent behaviour such as giggling and inane laughter and a tendency to talk about meaningless topics for hours! Negative symptoms such as disorganised behaviour and incoherent language are common. (Tune into the Radio 1 breakfast show any morning for a fuller understanding). Catatonic schizophrenia Characterised by impairment of body movement. This may involve wild and uncontrolled movements that put themselves or others in danger or may be simply holding one particular posture for long periods of time. ‘Waxy flexibility’ may also result, when someone attempts to move them they simply freeze in the new position instead. The movements may coincide with hallucinations, often about death and catastrophe. Simple schizophrenia Characterised by a withdrawal from reality resulting in declining academic performance, loss of friends and extreme apathy or loss of volition. Note: simple schizophrenia is not recognised by all categorisations of the disorder.
Evaluation of these categories of schizophrenia With the exception of paranoid schizophrenia the others types are difficult to distinguish in practice (even for psychiatrists specialising in the condition). On top of this the symptoms may change over time so that a patient displaying one set of symptoms may display a different set a few years later. Catatonic schizophrenia (the rocking and strange movements seen in films about the Victorian-style asylums) are very rare today. This could be due to much improved drug therapy or it could be that this was a mis-diagnosis in the first place. The film ‘Awakenings’ starring Robin Williams and Robert de Niro looks at a case of sleeping sickness* that could have been misinterpreted as catatonic schizophrenia. The different types are of little use in helping treatment or suggesting prognosis (unlike the Positive and Negative symptoms distinction). * The precise cause of sleeping sickness (an epidemic of which occurred in the 1920s) is not known. It could be due to a viral infection or perhaps even an auto-immune response triggered by a bacterium. The symptoms include very high fever and in some cases coma (hence the name). They can also include disturbances of movement and slowing of mental responses, hence the confusion with schizophrenia.
The course of schizophrenia
Exam advice: A question could ask you to describe the clinical characteristics of a psychopathological disorder (be it schizophrenia, depression or phobias). Schizophrenia, being an umbrella term has a wide variety of possible symptoms and be classed as having a particular type of the disorder as a result. You could mention the extent to which these types really are different and the extent to which they really do exist. As we shall see there are many issues related to diagnosis including social class and cultural background making definitions even more blurred. There are also some similarities between aspects of mania and schizophrenia.
Summary of characteristics (adapted from Gross & Rolls)
Most likely questions are on the models or explanations of the causes of the psychotic disorder. Think back to work on eating disorders at AS. At A2 you will be expected to describe or outline the various theories and then either evaluate them or compare them to other approaches. Important point to ponder: At the outset of the course you looked at the psychodynamic and behaviourist approaches. You are also familiar with the behaviourist, cognitive, psychodynamic and medical explanations of eating disorders. Each of these approaches to psychology has its own distinct, some would say entrenched, view on explanations to everything regarding the human condition. As a brief summary: Psychodynamic: initially based on the work of Freud. Theories concentrate on experiences in childhood, particularly during the various psychosexual stages of development (oral, anal etc.). Conflict between id, ego and superego are also central. Other ideas frequently cited include repression, regression and other ego defence mechanisms.
Behaviourist: ignores genetic factors and concentrates on learned behaviour. Three main strands exist: a. classical conditioning, learning by association b. operant conditioning, learning by being reinforced or punished c. Social learning (SLT), learning by the observation of others.
Cognitive: concentrates on faulty processing of information or inappropriate perceptions of ourselves.
Medical: believes disorders have one of four causes: a. genetic, the disorder is inherited b. biochemical, disorder is caused by disruption of the brains neurotransmitters c. neuro-developmental, the disorder is caused by damage to brain structures d. infection by virus or bacterium
Humanistic: uses environmental and social factors to explain disorders, for example role of family or social class. Some of these approaches are better suited or provide better explanations of certain disorders than others. As we saw at AS, a combination of behaviourist and cognitive approaches seems to offer a good account of eating disorders. The medical model seems to be the favoured account of schizophrenia and depression but clearly does not paint the whole picture.
Diathesis-stress: increasingly popular approach. · Diathesis refers to a genetic predisposition to the disorder · Stress refers to a triggering factor. A simple example of this, though obviously not psycho-pathological would be lung cancer. As you are doubtless aware some people can smoke 30 a day and live to 98. Others die much younger. The obvious conclusion being that some people, because of their genetic make up, are more susceptible to the disorder, smoking then triggers the disease. Note: the specification requires that you know biological (e.g. genetics, brain biochemistry) and psychological (e.g. social and family relationships). So in theory you can get away with knowing just one of each. However, in order to evaluate theories it is advisable for you to learn a few examples of each. Genetics and biochemistry are essential for the medical model. Family model is the most useful of the psychological but try to learn one other as well (e.g. psychodynamic). Make sure you learn the evidence on which they are based as well!
Genetic The incidence of schizophrenia in the general population is 1%. If the incidence within families is higher than this then it suggests a genetic link. This section of the topic shows considerable overlap with earlier work on intelligence with the main body of evidence coming from twin studies, family studies and adoption studies. As with intelligence it is vital to bare in mind that it is very difficult to separate out the effects of inheritance and environment (nature and nurture), even when monozygotic twins are reared apart. Twin studies Gottesman & Shields (1972) examined the records of 57 schizophrenics between 1948 and 1964. About 40% of the twins were determined to be MZ and about 60% DZ. If the pair were discordant, that is one had schizophrenia and the other did not then the none schizophrenic was followed (not literally James) for at least 13 years to see if it developed later. Concordance rates, (i.e. probability of a twin having schizophrenia if its twin has the disorder) were as follows: · Monozygotic twins 42% · Dizygotic twins 9% Gottesman (1991) in a review of over 40 other studies found · Monozygotic twins 48% concordance · Dizygotic twins 17% Heston (1970) found that if one MZ twin has schizophrenia that there’s a 90% probability that the other will have ‘some sort’ of mental disorder! What this suggests: · there is a genetic link for schizophrenia · schizophrenia is not entirely genetic, otherwise the concordance for MZ twins would be 100% However, as with all studies of this sort it is vital to consider the role of environmental factors. MZ twins are more likely to be brought up in similar conditions, be treated similarly, same class at school, have similar friends and experiences, even be dressed and treated similarly. Therefore it is not surprising that the concordance is so high. The usual way around this problem is to consider MZ twins reared apart. However, as Gottesman (1991) discovered the concordance rates are similarly high. But, the same proviso still applies. Twins that are adopted into different families still tend to be reared similarly and are often adopted into members of the same family! (Kamin 1977). One other evaluation point that is always worth mentioning, particularly for early studies, is that until the advent of sophisticated genetic testing it was very difficult to distinguish MZ and DZ twins, especially at birth. Some of the statistics for MZ twins may actually be DZ twins and vice versa. Be sure to emphasise the possible role of environmental factors to gain AO2 marks. Module 5 is testing all round understanding of psychology. Nature-nurture debate is crucial to all aspects of explaining human behaviour. One other point you could make (providing you follow what I’m about to say) is that we tend to assume that MZ twins are treated more alike because they are MZ twins. Lytton (1977) turned this on its head and suggested that the greater similarity of MZ twins ensures that they elicit a more similar response from their parents. That is the greater similarity of identical twins is a cause of their more similar parenting rather than an effect of it!
Family Studies Look at patterns of the disorder within families. As already mentioned your chances of developing the disorder are about 1%. Family studies examine the possibility of getting the disorder if parents etc. have the disorder. Again if this is greater than 1% then this could be seen as possible support for the genetic cause, however, the same provisos remain. Living with schizophrenics could increase your chances of developing it yourself. Gottesman (1991) in a review of other studies published the following findings:
Perhaps the most powerful of all evidence for a genetic link is the following. Note, this is not easy to get your head round so read it a few times or draw a family tree to clarify. If all else fails you could always ask! Gottesman & Bertelsen (1989). If your parent is an identical twin who has schizophrenia then you have a 17% chance of getting it too, (compare with one parent in table). However, if your parent does not have the disorder, but their identical twin does, then your chance of getting the disorder is still 17%. This is good evidence because it seems to minimise environmental causes since you are not living with a schizophrenic. However, you are living with someone who is predisposed to schizophrenia, (i.e. carries the genes for it), since they have the same genetic code as their twin who has developed it.
Dad (Richard) Uncle Robert (Richard’s MZ twin)
Ryan If Richard has schizophrenia then Ryan has a 17% chance of getting it too. (No surprises there). But this could obviously be due to environment rather than genetics since Ryan is living with his father. However, supposing dad (Richard) has an identical twin (Robert) who is genetically identical. Imagine a situation where uncle Robert is diagnosed with the disorder, so obviously has the genetic predisposition, but his brother Richard, (Ryan's dad) doesn't. Richard must also have the genetic predisposition (he shares his genes with Robert) but shows no outward signs of this. In such cases, the son still has a 17% chance of developing schizophrenia. This is very powerful evidence for a genetic cause since it shows that Richard (the father) who must be genetically predisposed to schizophrenia but has never shown the symptoms, has passed on the genes for it to his son, who has developed the disorder but without having been exposed to the behaviour. Bob's your uncle!
Adoption Studies One possible way of minimising environmental effects is to look at schizophrenics that have been brought up away from biological parents. Kety et al (1978) looked at adopted children in Finland who had developed the disorder. Findings Their biological parents, whose genes they possess, were more likely to have schizophrenia than the parents who had adopted them and brought them up. Conclusion Genes appear to play a role in schizophrenia although other factors must also be involved. The chromosome or specific gene(s) responsible have not yet been identified. The tips of chromosomes 5 and 22 have both been suggested as possible sites for the faulty genes but now appear to have discounted. Schizophrenics are often very heavy smokers. An area on chromosome 15, known to be responsible for the brain area involved in filtering information (implicated in some types of schizophrenia), is known to be stimulated by nicotine. It is thought that faulty neurons in this area may be causing the schizophrenia and nicotine may be acting as a treatment. Heston (1947) followed 47 children born to schizophrenic mothers but who were separated from them within the first three days of life. They were adopted into families not related to the biological mothers. Later in life (30s) they were compared with a control group of children who had been separated in similar circumstances at birth, but crucially, not born to schizophrenic mothers. Five of the 47 in the experimental group had gone on to develop schizophrenia (over 10%), whereas none of those in the control group had developed the disorder!
A few past paper questions for you to consider: January 1997 Describe and evaluate the possible contributions of genetic/neurological factors to schizophrenia. (30) Summer 1999 “Schizophrenia appears to be due to an abnormality in brain development that arises from mainly genetic but also environmental factors.” Discuss research into the causes of schizophrenia. (30) Other possible question: Describe and evaluate the possible contributions of biological factors to schizophrenia. (a) Outline the clinical characteristics of schizophrenia. (10) (b) Outline one explanation of schizophrenia, and evaluate this explanation in terms of research studies and/or alternative explanations. (20) (c) ‘There are many different kinds of depression, e.g. unipolar and bipolar, endogenous and reactive.’
Biochemical: (Is there a chemical cause for schizophrenia?) Anecdotal evidence: 1. Some hallucinogenic drugs such as LSD produce symptoms that are indistinguishable from schizophrenia. 2. Cocaine and amphetamines can produce hallucinations and delusions of persecution, again not dissimilar to those reported by schizophrenics. Smyhies (1976) found traces of hallucinogenic chemicals in the CSF (cerebro-spinal fluid) of schizophrenics. One role of the CSF is to mop up excess chemicals in the brain. Smythies findings therefore suggest that schizophrenics are producing more of these chemicals than normal. Dopamine hypothesis Hallucinogenic drugs are chemically similar to the neurotransmitter dopamine. Researchers therefore believed dopamine could be the cause. They concluded that the brains of schizophrenics were more sensitive to dopamine than the brains of non- schizophrenics. See your beautifully drawn diagrams of the dopamine pathway for details.
But · Chlorpromazine only reduces the positive symptoms of schizophrenia such as hallucinations and delusions. · Neuroleptic drugs (such as chlorpromazine) have their effect on the brain almost immediately, but they take weeks to affect the behaviour of the patients. The dopamine hypothesis is unable to explain this delay. · Chlorpromazine makes little or no difference to 30% of schizophrenics.
The role of serotonin Recently, Kane (1988) the drug clozapine has been used in the treatment of the disorder. Clozapine is more effective in reducing the negative symptoms of schizophrenia (e.g. disturbances of speech and flattening of affect). Clozapine seems to work by blocking serotonin sites in the brain. Conclusion Barlow & Durand (1995): both dopamine and serotonin are probably involved, but the precise role played by each is unclear. All the evidence provided is correlational. It implies an association between schizophrenia and chemicals in the brain. It does not prove cause and effect. It could be that schizophrenia has caused the abnormal chemical levels rather than the other way around.
Neuro-developmental: (do the brains of schizophrenics have an abnormal structure?) Johnson (1989) reported that some schizophrenics have a reduced blink reflex, evidence for neurological damage. Others have reported that some schizophrenics have difficult births which could have starved their brains of oxygen. This would also explain why the incidence of schizophrenia is declining as monitoring techniques at birth improve. Chua & Mckenna (1995) reported the following abnormalities in the brains of some schizophrenics: · Smaller corpus collosum · Less grey matter in the temporal lobes · Enlarged ventricles resulting in loss of brain tissue. · Reduced activity in the prefrontal cortex
However, none of these findings are consistent amongst schizophrenics. The most common abnormality amongst patients is the enlarged ventricles which would result in less brain tissue, particularly in the medial temporal lobes of the brain. This has been confirmed using techniques such as MRI scans. It could be argued that this does not show cause and effect. Perhaps the schizophrenia led to the abnormal brain structure. However, Harrison (1995) believes that these differences occur before the onset of schizophrenia, implying that they are more likely to be a cause than an outcome of the disorder. Since the abnormalities in brain structure do not increase over time, as is the case with diseases like Alzheimer’s, then it appears that the problems are due to a failure of the brain to develop normally in the first place.
One criticism often aimed at the possible relationship between brain damage and schizophrenia is that no one pattern of damage seems to correlate with the disorder. Perhaps, however this should not be surprising, given the variety of symptoms associated with schizophrenia. It seems that certain damage is associated with certain symptoms however. Damage to the temporal lobe is associated with some of the positive symptoms whereas damage to the frontal lobe is associated more with the negative symptoms. Any such differences between the brain of a ‘schizophrenic’ and ‘non-schizophrenic’ brain are so small that it is not possible to detect them in the individual. They only become apparent if groups of schizophrenics and non-schizophrenics are compared. Viral theory Significantly more schizophrenics are born in late winter or early spring (figures suggest up to 8% more likely than at other times of the year. Because various diseases such as colds, influenza, chicken pox etc. also show such a seasonal variation it was suggested that there might be a link. Support Torrey (1988) proposed a link with a viral infection in the mother during the second trimester of pregnancy (months 4 to 6). Barr et al (1990) found those in the fifth month of foetal development during the influenza pandemic of 1957 grew up to have a significantly higher risk of developing schizophrenia. This has been questioned by others in particularly because the effects are not seen worldwide. This increased risk was only evident in England, Wales and Finland and was not apparent in Scotland or the USA. However, more recently a new variation on this old theory has arisen. The theory suggests that some of our genes developed from viruses and became incorporated into our genetic make up. Blomberg estimates that about 1% of the human genome is made up of these retroviruses. These remain ‘dormant’ but can be activated by certain other viral infections that we contract or perhaps by other factors during foetal development or infancy. Blood samples were taken from 53,000 pregnant women in the USA during the 1950s and subsequently frozen. Buka (1999) checked the offspring of these women and found 27 schizophrenics in the Boston area. Buka found that their mothers’ blood was significantly more likely to contain antibodies (suggesting a viral infection during pregnancy). The most common infection found was herpes. Some of these quiescent genes are responsible for making proteins and these can be detected in the CSF of the brain. Karlsson found genetic material from these viruses in 29% of recently diagnosed schizophrenics. There was no sign of such material in healthy patients Retroviruses are responsible for AIDS and research is now ongoing to see if some of the drugs developed to treat AIDS can help with schizophrenia.
Diathesis-stress No essay on the causes of schizophrenia would be complete without a mention of this. It is particularly good since it can be used in either a question asking for medical explanations or one seeking information on the social and psychological explanations. Diathesis is a person’s genetic predisposition to a particular disorder. Because of the genes they've inherited some people are more likely to develop schizophrenia than others. However, this alone does not guarantee that they will. (Think of MZ twins, one of whom has the disorder and the other who does not). Stress refers to the environmental factors that trigger it, for example high levels of expressed emotion, major life events or a dysfunctional family. Support Tienari (1987) found that in all cases of schizophrenia that he studied one or other members of the sufferer's family were disturbed.
Marcus (1987) Israeli study, all parents
of schizophrenics studied had poor parenting skills. Social and psychological explanations of schizophrenia Family Models of schizophrenia Double bind hypothesis Bateson (1956) described the situation were families send out contradictory information to their children. For example parents who say they care whilst appearing critical or who express love whilst appearing angry. A classic example would be telling the child you’d like a hug and then pulling away when they try! Bateson believed that this caused confusion and self-doubt in the child leading to their withdrawal as they lose confidence in their own ability to express themselves. Most studies into this theory are retrospective (get the person to think back to childhood), this makes them notoriously unreliable. Pseudo-mutuality Wynne & Singer (1963) believined that the communication in some families was 'fragmented and disjointed.' Sentences show little continuity with Liverpool having a particularly good win at Leeds yesterday! Conversations switch focus from one topic to that really good curry we had last year in Bognor! To test their theory they counted the 'deviance score' for conversations. They would record families carrying out tasks and count the number of such defects in communication. The deviance score for schizophrenic families were significantly higher. But: Mischler & Waxler (1968) found that mothers do talk to their schizophrenic daughters in an unresponsive way, but talk to their 'normal' daughters in a 'normal' way, suggesting again that it is having a schizophrenic in the family that causes the abnormal communication rather than vice versa. Schizophrenogenic mother Fromm-Reichman (1948) coined the term to describe a mother likely to produce the disorder in her offspring. Typically these are cold, domineering conflict inducing, rejecting and very moralistic, particularly about sex. Her behaviour is often contradictory (compare to double bind), so for example saying ‘yes’ when her body language suggests ‘no.’ Fromm-Reichman believed that such a mother in conjunction with a weak and ineffectual father could 'drive' a child to schizophrenia. Little research evidence has found support for the theory. Support for the theory is limited although it is clear that the families of schizophrenics are often in some way different, often showing high levels of conflict and poor communication. However, we again come up against the problem of cause and effect. To what extent is the schizophrenia a result of these issues and to what extent may it be a cause? Goldstein & Rodnick (1975) believed family problems were a cause rather than a consequence. They found that often the family problems pre-dated the onset of schizophrenia. Tienari (1991) reported that children born to schizophrenic mothers and later adopted were far more likely to develop schizophrenia if adopted into a disturbed family. This provides good evidence for the diathesis-stress model; genetic predisposition followed by an environmental (family) trigger. Expressed emotion (EE) High levels of expressed emotion are typified by extremes of emotional content in conversations and daily life, for example high levels of hostility and criticism and of over concern with others. The researchers concluded that this is more important in maintaining schizophrenia than in causing it in the first place, (Brown et al 1958). Schizophrenics returning to such a family were more likely to relapse into the disorder than those returning to a family low in EE. The rate of relapse was particularly high if returning to a high EE family was coupled with no medication. Evaluation This is now well established as a 'maintenance model' of schizophrenia. Treatment of schizophrenia often involves education and training for other family members in reducing their levels of EE. But Some schizophrenics have little or no contact with their families when released back into the community, but their relapse rate does not appear to be any lower as a result. General evaluation of the family models It is difficult to know with any certainty whether the dysfunctional families reported in these studies have lead to schizophrenia in some family members or whether simply having a schizophrenic member in the family has lead to some degree of dysfunction. Yes you guessed it folks that good old cause and effect question yet again! Perhaps the effect is two way. Rosenfarb* et al (1995) observed recently diagnosed schizophrenic patients that have been discharged back into family care. Before the arrival of the patient the families had been classed as high in expressed emotion (support for EE causing schizophrenia). On arrival EE comments by other family members increased the schizophrenic symptoms (again). However, having the schizophrenic back in the family also increased the level of expressed emotion! *Did Rosenman marry Goldfarb?
RD Laing I have included this (and the bit about Szasz) as an area of general interest or extension piece for evaluating the medical model. Laing’s theories are similar to the family systems models but take an anti-medical approach. Basically, Laing does not see schizophrenia has a disorder, rather as a way of explaining away those people whose behaviour does not conform to societal norms. Laing’s ‘family interaction model’ of 1961 is similar to the theory proposed by Bateson. In his book ‘Self and Others,’ Laing proposes that schizophrenia is not something that happens inside a person but between people. In a number of family case studies looked at, Laing & Esterson conclude that schizophrenia did make sense in terms of the family relationships involved. Later models take a more radical and controversial approach seeing schizophrenia as a means of labelling and controlling. In the ‘conspiratorial model’ he suggests psychiatrists label and imprison schizophrenics in order to maintain their own definitions of normality. He takes this a stage further in his ‘psychedelic model’ suggesting that the schizophrenic just happens to be a particularly ‘eloquent critic of society.’ Schizophrenia is seen as a way of coping with the ‘disorder’ that is normality within society. However, the schizophrenic is not usually allowed to complete this healing process since psychiatrists intervene and administer ‘treatment’ of their own! Szasz Is a powerful critic of the psychiatric model. Psychiatrists see ‘mental disorders’ as being of physical origin. To Szasz this is contradictory. If illness has an organic (or physical cause) then it should be classed as a disorder of the brain. Although there are various biological models of disorders, such as schizophrenia, as yet none are proven. As Szasz points out in the majority of cases of patients with ‘mental illness’ there is no obvious physical defect in brain structure or genetic make up. (Exceptions are Alzheimers, Korsakoffs etc.). To Szasz, ‘mental illness’ is ‘a problem of living’ brought on by the bizarre nature and structure of societies. As such they should be seen in an ethical and social context and not simply treated by the administration of drugs.
Rosenhan (1973)
On being sane in insane places An all-time classic study in psychology that breaks some of the unwritten rules in that the real participants are the psychiatric establishment! This could be used as very clear evidence for some aspects of Laing’s theory and of labelling theory in general: Eight supposedly ‘normal’ stooges present themselves at various psychiatric establishments in America. The texts always emphasise their normality; they were in fact three psychologists, a psychiatrist, a psychology student, a paediatrician, a decorator and a housewife… (leave you to decide!). Each complained of hearing same sex voices which simply said ‘hollow’, ‘empty’ or ‘thud.’ All eight were admitted predominantly with a diagnosis of schizophrenia and in one case with manic or bipolar depression. On being admitted they stopped reporting the voices. During their stay the patients kept written records in the form of a diary. At first they tried to keep this from the staff until they all realised that the staff really didn’t care or see it as odd. All patients wanted to be released as soon as possible and apparently tried their best to behave in as friendly, cooperative and ‘normal’ manner as possible. Their average stay in the institutions that admitted them was 19 days with the shortest being 7 days the longest 52 days before they were able to convince staff that they were well enough to be released. Each was released with a diagnosis of ‘schizophrenia in remission’ meaning that although they were no longer displaying symptoms they were still schizophrenic. Such a diagnosis would make future employment difficult. Each patient had given a false name at the outset! During their stay they were famously administered (between them) a total of 2100 tablets, only two of which were actually swallowed. The only people to suspect they were not genuinely unwell were other patients (perhaps a case where the lunatics should have been taking over the asylum!) In a less well reported follow up study one of the hospitals was told about the results of the first study and warned that there may be other ‘pseudo-patients’ seeking admission in the coming months. In that time 193 patients were admitted and many of these were alleged to be stooges when in fact all were genuine. Sticky labels! One thing becomes very clear when the medical records of the pseudo-patients during their stay are read. Symptoms were not guiding diagnosis, rather diagnosis was influencing perception of the symptoms. Once labelled as schizophrenic that label sticks and determines how people view your case and your behaviour. The patients reported that the most simple of their behaviours were seen as being symptoms of their disorder. For example in three cases nurses had found their writing symptomatic of their disorder, ‘patient engages in writing behaviour’ appearing on their report. Another example reported by Rosenhan himself: A clear example of such translation is found in the case of a pseudopatient who had had a close relationship with his mother but was rather remote from his father during his early childhood. During adolescence and beyond, however, his father became a close friend, while his relationship with his mother cooled. His present relationship with his wife was characteristically close and warm. Apart from occasional angry exchanges, friction was minimal. The children had rarely been spanked. Surely there is nothing especially pathological about such a history. . . . Observe how such a history was translated in the psychopathological context, this from the case summary prepared after the patient was discharged. “This white 39-year-old male . . . manifests a long history of considerable ambivalence in close relationships, which began in early childhood. A warm relationship with his mother cools during his adolescence. A distant relationship to his father is described as becoming very intense. Affective stability is absent. His attempts to control emotionality with his wife and children are punctuated by angry outbursts and, in the case of the children, spankings. And while he says that he has several good friends, one senses considerable ambivalence embedded in those relationships also.” As Rosenhan points out, with physical illness it may be safer for the medical profession to play safe and risk admitting someone who is really well rather than risk missing someone who is ill. The danger with adopting the same approach to mental illness is that a diagnosis then stays with you for life and can adversely affect your relationships, job prospects and legal standing. Family and social theories are generally recognised as the better non-medical explanations of schizophrenia. Other theories you may want to accustom yourself with are the behaviourist, cognitive and psychodynamic. These are predictable and generally not as good (nor are they essential!). Behaviourist Conditioning: Ullman & Krasner (1969): believed that strange behaviour is inadvertently reinforced by others. For example, the staff in psychiatric hospitals paying more attention to those showing the worst symptoms. 1. Labelling theory: Scheff (1966). Children who for whatever reason withdraw into an ‘inner world’ are labelled because of their bizarre behaviour. This leads to attention, such as sympathy, which acts to reinforce the behaviour and causes the person to seek further attention by behaving even more strangely. 2. Social learning: Watching others being rewarded for behaving strangely. Evaluation Some of the strange behaviour of schizophrenics can be modified using behaviourist methods such as being reinforced for more appropriate behaviour. SLT does not explain how people can develop schizophrenia when there has been no chance to observe schizophrenic behaviour. It is possible to see how observable behaviours such as motor disturbances can be acquired in this way. However it seems unlikely that hallucinations, delusions and disturbances of thought could be acquired through reinforcement.
Psychodynamic According to Freud psychotic behaviour was due to inter-psychic conflict. Either the ego cannot cope with the demands being made upon it by the id, or the guilt caused by an overly conscientious superego. Since the ego is too weak to resolve the conflicts that arise between opposing elements of personality it retreats (regresses in Freud-speak) to the oral stage of development, a stage at which it felt safe and secure. At this age the child was unable to distinguish between itself and the outside world (good evaluation marks to be had here if you mention Piaget), and this, according to Freud causes the schizophrenic symptoms. But The symptoms of schizophrenia bare little resemblance to child-like behaviour.
Other comments on schizophrenia Validity of the disorder Is schizophrenia one disorder or a number of related disorders? Evidence for the latter: 1. Many of the symptoms occur in other mental disorders, e.g. i. thought disorder in mania ii. hallucinations in some forms of depression 2. The onset of the disorder can be sudden or insidious (person being unaware of the early stages). 3. Its course can be continuous (no breaks), or episodic. 4. Prognosis (outcome of the disorder): 50% go on to develop moderate or severe symptoms, 25% make a full recovery. 5. No one clear cause.
Seligman (1973) referred to depression as the ‘common cold’ of psychiatry because of its frequency of diagnosis. According to BPS figures a staggering 9 million people in Britain reported feelings of depression to their GP in 1998! However to continue Seligman’s analogy, although this ‘cold’ may have reached epidemic proportions in the West it is certainly not pandemic since many cultures and areas of the World report little or no depression Characteristics of depression Depression is an affective disorder in that it is characterised by disturbances of affect (or mood). During the course of any period of time it is not unusual for a person’s mood to alter. However with affective disorders this variation is more marked and is accompanied by other symptoms. These symptoms of depression do vary; the DSM-IV recognise three main types of depression, only two of which will be mentioned here, and only one of which will be covered in detail. A possible 6 mark question on the paper could ask you to describe the symptoms or characteristics of depression. Clearly ‘feeling sad’ is not going to earn you very much credit!
Emotional symptoms The symptoms we most associate with depression, those feelings of sadness, loss of mood and loss of pleasure from what were previously enjoyable activities. Mood may also alter during the course of the day, typically being lowest in the morning and gradually showing improvement as the day progresses. This may be associated with circadian rhythms. Physical symptoms Disturbances of sleep: patients sometimes report insomnia, but sleeping longer than before is also common, perhaps as patients attempt to escape their problems. Appetite can also decrease or it may increase in the form of comfort eating. Part of this may be due to boredom since typically depressed people tend to have lower activity levels. Motivational symptoms Apathy and loss of drive are common. Typically the depressed person will sit around waiting for things to happen, making no attempt to initiate activity or social contact. This could be because they don’t want people to see them in a depressed state. Cognitive symptoms These can vary from negative self thoughts, loss of self esteem and self confidence, feelings of despair and hopelessness, inability to concentrate on tasks for any length of time to feelings of inadequacy and blaming themselves for their situation and on occasions and suicidal thoughts.
Categories of depression Unipolar (major or clinical depression) This is what we normally consider to be depression and can comprise a combination of any of the symptoms mentioned above. Minor depression occurs when the patient suffers the low mood but without any of the cognitive or other disturbances. Bipolar (manic depression) Involves bouts of clinically depressed symptoms that alternate with periods of near normal mood and/or elevated mood (mania). Differences between unipolar and bipolar disorder
Endogenous or reactive depression This is a second way of distinguishing between depressions that relates more to causes rather than symptoms. Endogenous depression (as the name suggests) comes from within and is thought to be caused by chemical imbalance and is explained and treated best by the medical model. Reactive depression on the other hand is caused by external factors such as loss of job, death of relative etc. and is usually explained using psychological approaches such as behaviourist or cognitive models. Depression is also a major factor in a number of other related disorders such as Seasonal Affective Disorder (SAD), Premenstrual syndrome (PMS) and Postpartum depression (PPD). The latter was formerly known as post natal depression.
This is the most likely area to be examined and could ask you for the extent to which physiological or psychological models are able to explain the onset of the disorder. We shall look at medical explanations first, particularly the permissive amine theory and genetic evidence, and then consider the psychological models. It would be useful at some point during such an essay to suggest the medical model is used to explain endogenous depression and the psychological models used to explain reactive depression. Regardless of which way the question is worded it is useful to mention psychological models and medical models since each can be used to fill in the gaps left by the other. If the question asks for description and evaluation of the medical model, describe the medical model but use psychological explanations to evaluate.
Medical model A combination of genetic evidence and discussion of the permissive amine theory is needed here. Remember too that the two approaches are not mutually exclusive. A decreased sensitivity to a particular neurotransmitter is likely to be caused by a genetic abnormality! Genetic explanation All the usual points need to be borne in mind and spelt out to the examiner. Clearly you will want to mention trends within families, twin studies (MZ and DZ), adoption studies and gene research. These then need to be evaluated in terms of environmental influences and the extent to which they can explain patterns such as sex differences. Family patterns and studies Depression does tend to ‘run in families.’ Gershon (1990) found that the incidence of depression is up to three times higher in families with a history of the disorder than it is within the general population as a whole. Others have put this figure even higher. Weissman (1987) looked at the prevalence of affective disorders in general and found that family members with first degree relatives (parent, sibling) with a mood disorder were up to ten times more likely to suffer from one too.
Twin studies We’ll distinguish here between unipolar and bipolar disorders: Unipolar or major depression Allen (1976) reported the following concordance rates: MZ twins 40% DZ twins 11% Suggesting a genetic component to explain the difference between the two. Bipolar (or manic) depression MZ twins 72% (This is the highest concordance rate for any psychological disorder). DZ twins 14%
It is worth mentioning that different studies have produced varying percentage figures but the overall trend is usually the same. You must point out however the shortcomings of twin research:
Adoption studies Wender et al (1986) found that the biological parents of adopted children who had developed depression, were eight times more likely to have the disorder than the adoptive parents. As usual, adoption studies like this provide some of the most powerful evidence for a genetic component. Identifying specific genes for depression The first attempt was by Egeland et al (1987) who researched 81 members of the Old Order Amish Community of Pennsylvania. Four families within the community showed a much higher than expected incidence of bipolar (manic) depression. Of the 81 studied 14 were diagnosed with bipolar disorder and all had abnormalities on the tip of chromosome 11. This caused particular interest at the time since this location is adjacent to genes known to be involved in the production of serotonin (see biochemical section below). However, other studies have failed to replicate the findings suggesting that either this gene is not responsible or more likely; more than one gene is involved. Nemeroff (1998) has implicated a gene on the X chromosome. A possible link between genetic and biochemical influences… Ogilvie et al (1996) found that people with depression were far more likely to have abnormalities on a gene known as SERT that is used to make serotonin-transporter protein. New drugs used to treat depression are believed to act on serotonin-transporter protein.
Biochemical explanations Noradrenalin and serotonin are the likely candidates. Both are classed as amines. Background evidence Schildkraut (1965) found that too high a level of noradrenalin led to mania and too little to depression. The first finding should not come as a surprise if you consider the chemical similarity between noradrenalin and adrenalin! Schildkraut believed that serotonin behaved in the same way. We now know that this is not the case. Lemonick (1997) found that drugs used to treat depression increased levels of both noradrenalin and serotonin. Lithium carbonate used to level out some of the mood swings of manic depressives (such as Valerie in the video) decrease levels of noradrenalin and serotonin. How do these two neurotransmitters work to create depression? The permissive amine theory: Kety (1975) believed that fluctuations in noradrenalin levels affect our mood: high levels of noradrenalin leading to heightened mood and eventually mania, low levels to a lowering of mood and eventually to depression. But what about the role of serotonin which is clearly playing an important role too? Kety concluded that it is serotonin that controls the levels of noradrenalin by restraining the fluctuations.
Permissive in this sense refers to allowing or letting. One amine (serotonin) permits the other (noradrenalin) to fluctuate.
Evidence for the permissive amine theory. *Teuting et al (1981) examined the urine of depressed patients and found chemicals that suggest lowered levels of both serotonin and noradrenalin. *Imagine Mr Teuting speaking to the careers adviser at school. ‘And what would you like to do when you grow up master Teuting?’ ‘I’d like to collect urine samples’ comes the reply. ‘You’re taking the **ss!!!’ exclaims the careers officer! Kety (1975) found higher than expected levels of noradrenalin in manic patients. Bunney et al (1972) reported fluctuating levels of noradrenalin in bipolar disorder patients.
Evidence against the permissive amine theory Deakin & Graeff (1991) report that even following recovery from depression the deficits in serotonin and noradrenalin levels still remain which questions the cause and effect relationship assumed by the model. Research evidence for the other models of depression can be used to question the theory. Evaluation of the permissive amine theory Firstly there are problems of cause and effect (as always). We cannot be certain that fluctuating levels of noradrenalin are causing altered mood states. It could be altered mood states causing the fluctuation or a third variable that is causing both. Secondly, anti-depressives such as MAOIs (monoamine oxidase inhibitors) increase the levels of noradrenalin and serotonin within minutes. However, they have no effect on mood for many weeks suggesting that they are not working simply by increasing the levels of chemical in the brain. Kennett (1999) believes drugs like Prozac are causing structural changes within the brain such as making neurons more sensitive to amines. This would explain the time delay. Thirdly, not all depressives show reduced levels of these chemicals and similarly not all patients benefit from anti-depressives that work by increasing chemical activity. Finally there is the issue of ‘treatment aetiology fallacy.’ Just because increasing the level of a chemical solves a problem it doesn’t necessarily follow that it was lack of that chemical that caused the problem in the first place. MacLeod (1998) cites the example of aspirin curing headache as a more obvious example. Although taking aspirin cures our headache we would not assume that it was lack of aspirin that caused it in the first place!
For a fuller account of this theory see the back two pages borrowed and adapted from the ‘find the light’ mental health support group website. Hormones and depression Hormones are another family of biochemicals that we need to consider. These seem to be implicated in disorders such as PMS, PMD and possibly SAD. They may also help us explain why women are far more prone to depression. More on gender differences later when we briefly consider other, more feminist, perspectives.
Pre-menstrual syndrome (PMS) Halbreich et al (1983) found that 43% of women report depressive symptoms at some point in their menstrual cycle. Abramowitz et al (1982) reported that 41% of women admitted to a psychiatric hospital were admitted either on the first day of their monthly cycle or the day before. Post-partem depression (PPD) 20% of women report feelings of depression after the birth of a child. Normally this occurs within a few days but typically only lasts for about a week or so. It is still unclear whether this is due to levels of oestrogen or progesterone or to lowered levels of cortisol which make it difficult to cope with stress. PPD appears to be more common in women from families with a history of clinical depression suggesting that there may be a family predisposition to mood disorders of this kind.
Seasonal affective disorder You are already familiar with this from the work we did on biological rhythms. When I say that it may be linked to melatonin production does that ring any bells? If you recall we also mentioned that there is a close link between melatonin and serotonin…you see it all starts to fall into place by the time it’s almost too late! The most common form of SAD is experienced in the winter and is associated with falling light levels. In the summer light levels suppress melatonin production and darkness stimulates its production which is a factor in the onset of sleep. It is thought that lack of natural light in the winter months desynchronises our daily fluctuations of melatonin which in turn will affect serotonin production. Summer SAD is not so easy to explain. Kay (1994) suggests that changes within the Earth’s magnetic field may cause the alternation between winter and summer SAD. At first glance this does sound unlikely but there is surprisingly increasing evidence to support it. I’m not sure where you could tie this in but I’ll include it for general interest and in the hope (rather than the expectation) that a question on external factors of depression may come up. Following geomagnetic storms admissions to psychiatric wards for summer SAD increase significantly. Westhead (1996) found that pregnant women and new mothers are 60% more likely to suffer from depression if they live near power cables that also disrupt local magnetic fields. Bush (aaaaaaaaaaaaaaarghhhhh) just the mention of that name… reported significantly higher suicide rates (six times higher than expected) in 15 to 24 year olds living in the Alaskan hinterland. He put this down to the aurora borealis (or northern lights) that create changes within the Earth’s magnetic field. I will leave you to hypothesise about other possible causes of depression in young people living in a freezing cold climate in the back end of nowhere!
Psychological explanations of depression No surprises here! The usual collection of explanations based on some all too familiar approaches to the subject. As always I think it’s a useful exercise to spend a few minutes attempting to predict how each approach will seek to explain a given topic… useful since not only will it boost your confidence but also be good practice for the approaches section of the synoptic paper. As always with the approaches there is a mixture of the good, the bad and the downright ugly! Work out which is which for yourselves but as always keep opinions on the paper as objective as possible and always be sure to back up arguments with research! Psychodynamic approach As always Freud was the first to offer possible explanations of depression and was also the first to notice the similarity in feelings reported by patients suffering from depression and those who had recently suffered bereavement. Freud’s theory has a number of interconnecting strands. What follows is only a brief overview of what he saw as a complex process: Loss could be ‘actual,’ as in the case of death of a close friend or relative, or it could be ‘symbolic’, as in the case of a lost job etc. Either way loss in adulthood causes us to relive childhood experiences of loss explaining the clingy behaviour of some types of bereavement. In extreme cases regression to childhood may occur, particularly if the child had suffered bereavement during their own childhood. Hostility and aggression are also involved. Death causes feelings of anger at our loss and this has to be displaced inwards towards ourselves since outward expression of anger at such a sensitive time would not be acceptable to the superego. Anger directed towards ourselves causes the feelings of guilt and despair associated with many forms of depression. Freud also assumed that in most cases we would have had fallings out with the deceased which would also cause guilt on their death.
Evidence and evaluation Research for Freud’s ideas that early loss can make us more susceptible to depression in later life is mixed. At AS we looked at Bowlby’s work on maternal deprivation and separation. Bowlby suggested that early separation or loss can cause problems in forming later attachments (his so called ‘internal working model’). This inability to form loving relationships later in life may result in depression. Others, such as Parker (1992) have failed to find any link between early loss and later depression. As always Freud’s ideas on the workings of the unconscious mind are impossible to confirm one way or t’other. Freud also offered an explanation of bipolar disorder. The depressed phase is due to the Superego gaining overall control of personality and creating an overwhelming feeling of guilt and unworthiness. Eventually the Ego strikes back and is able to regain control of personality, but in so doing swings the balance too far the other way producing the manic backlash. This then leads to a further counter attack by the Superego producing alternating mood swings.
Cognitive approach Look back at your notes on schizophrenia and eating disorders (year 12) and you will notice the tendency for the cognitive model to treat the symptoms of a disorder as being the causes, for example faulty or distorted thinking or perceptions. Cognitive explanations of depression can broadly be split into two:
We’ll look at the first category for starters: Cognitive-behavioural explanation It should come as no surprise that these are combined; i. We have seen them used in this way before and ii. They do complement each other nicely, one concentrating on events outside the person and the other considering only events within the mind. Learned helplessness Seligman & Maier (1967) carried out their classic study in which dogs were given electric shocks to the feet. In the control condition the dogs could jump a small barrier and escape the shocks, but in the experimental condition the barrier was higher and the foot shocks were therefore inescapable. In the follow up trial dogs that could not escape in the first part of the study made no attempt to escape the shocks even when they were given the opportunity. Past experience had taught them that they had no control over outcomes, in effect they had learned to be helpless! Seligman noticed the similarity between learned helplessness and some of the symptoms of human depression in which patients become passive and accepting of their situation and make little or no attempt to resolve their problems. This similarity was reinforced by findings that showed a reduction in serotonin and noradrenalin levels in rats that had become helpless in this way.
Would humans placed in a similar situation behave in a similar way?
Hiroto (1974) got participants to endure inescapable loud noise.
In a follow up trial when they were provided with a handle that would
turn the sound off they sat back and endured it.
Seligman’s theory however, did not provide a full picture. Not everyone becomes helpless in these situations and Seligman was unable to explain the culture of self-blame or blaming others for their predicament. For example, many depressed patients blame themselves for their failings which does not tie in with Seligman’s idea that they see themselves as helpless. The experience of feeling out of control in one particular situation is an experience common to most people at some time but very rarely does it lead to clinical depression.
Cognitive explanation Seligman is seen as a link between behaviourist and cognitive explanations. Abramson et al’s theory (1978) can be seen as a logical extension of learned helplessness theory. They combined the theory with attribution theory. Basically any kind of experience we have in life we try and account for using attributions. However, according to this theory the depressed patient faced with an experience of failure, attributes the failure in a particular way according to three variables. We shall consider each using the unfamiliar experience of examination failure as an example: Internal or external?
The person blames themselves. In the case of exams, I failed to put in the necessary work or I wasn’t up to the task.
The person blames others or look for external excuse. We had a crap teacher or there was too much noise in the exam hall. Stable or unstable?
The idea that things will always be this bad and won’t get better in future. I just can’t do exams!
Things will improve. Next time I’ll be prepared and will succeed Global or specific?
The failure will apply in all other situations. There’s no point in sitting other exams because I’m no good at them.
The failure applies only to this examination. Maths and psychology will be fine.
Learned helplessness would equate to an internal, stable and global outlook. It’s all my fault, it will always be like this and regardless of the situation! Metalsky et al (1987) questioned students who had just failed a psychology exam. Those found to have an internal, stable, global outlook were still suffering mild depression two days later. Evaluation As always we have the problem of chicken or egg (cause and effect). Does this particular attribution lead to depression (as the theory implies) or does negative attribution arise from a depressed state of mind? Peterson & Seligman (1978) believe that it is causal and suggested that this internal, stable, global outlook is present in people prone to depression and acts to trigger depression in those suffering negative life events. The cause of this depressed attributional style is thought to arise in childhood. Rose et al (1994) attributed it (that word again) to abuse, parents being overly protective, harsh discipline within the family and to very high expectations from parents. In fact very similar to some of the possible triggers for anorexia. Much of the research has been done on laboratory experiments of students (as most university based research is). This clearly raises questions about generalisation and about the ecological validity of the research.
Much of the
research is questionnaire based (Peterson & Seligman’s Attributional style
questionnaire), with all the problems that arise because of this… demand
characteristics, fibs etc… Beck’s cognitive triad A cognitive perspective would not be complete without schemas! Remember memory? (no joke intended), Piaget etc? The triad involves unrealistically negative views about self, the world and the future. According to Beck this negative outlook would have originated in childhood, perhaps due to bereavement, overly critical parents or teachers etc. Essentially Beck believes that a depressed person has developed a negative set of schemas (schemata) upon which their expectations about life are based. For example they may have developed a self-blame schema which makes them feel responsible for all the things in their life that go wrong or an ineptness schema that causes them to expect failure every time. These negative schemas are caused by cognitive biases (faulty perceptions if you like): Some examples of cognitive biases suggested by Neck: Over-generalisation: an overall negative conclusion about all situations based on one, perhaps trivial event. For example a bad test result in a maths lesson convinces the person that they are stupid and should not be going to University! Arbitrary interference: an assumption arising from no evidence at all. For example you arrange a barbecue and it rains. Person assumes they are useless! According to Beck these three types of cognition: views, schemas and biases interact and in doing so reinforce each other eventually leading to clinical depression.
Evaluation There is plenty of evidence to suggest that Beck’s views on negative thinking do apply to depressed people. However, we still have the issue of what causes what. Davison & Neale (1998) believe that the process is two way. Depression leads to negative thinking which in turn worsens the effects of the depressed mood. A number of successful techniques have built up based on the cognitive approach such as Ellis’ Rational Emotive Therapy (RET) which encourage patients to recognise their negative thoughts and replace them with more realistic outlooks. Cognitive Behaviour Therapies in general have proved to be effective in treating a variety of disorders including depression, eating disorders and anxiety disorders. This also provides indirect evidence for the validity of the theory on which the therapies are based.
Culture, society, gender and depression Perhaps not a likely topic for an entire essay, this could certainly be questioned as a six-marker warm up question! Culture and depression Depression is far more widely reported in Western society. Is this due to its higher prevalence, its wider diagnosis or differences in diagnosis in other cultures? In the West we associate depression mostly with lowered mood, although as we saw at the outset there are distinct physical symptoms too. In Asian culture depression is very rarely reported or diagnosed. However, the physical symptoms that we associate with depression do appear to be common, namely apathy, tiredness, lack of volition (no attempt to initiate actions or interactions), loss of appetite etc. This unwillingness to report psychological symptoms may be due to the stigma some societies associate with illnesses of the mind and the discrimination that families may face as a result.
Family could provide another explanation of the apparent rarity in Asian culture. Extended families provide social support that we know can alleviate problems that are stress related (recall your AS). Stress and depression are known to be closely correlated.
Gender and depression More likely to be examined since it does shed some light on the possible causes of depression. Williams & Hargreaves (1995) reported that women are up to three times more likely to suffer depression than men. One theory for this discrepancy is that in fact men do suffer just as much depression as women but they fail to report it. Some of it may be hidden behind other behaviours such as alcohol or drug abuse or behind aggression. Research, however, suggests that men who do suffer depression were just as likely to report it as women. Some possible explanations for sex differences: Biological factors:
Biological factors alone seem unlikely as an explanation of the huge sex difference that exists. Other, non-biological factors have been implicated: Social and cultural factors
Generally the links between culture and gender and depression are complex, but in both cases stress and social support appear important.
Brain Chemistry Basics Extension for those who want to know more! Neurotransmitters are chemical messengers within the brain that facilitate communication between nerve cells. Let's illustrate with serotonin. Figure 1 depicts the junction between two nerve cells. Packets of serotonin molecules are released from the end of the presynaptic cell (the axon) into the space between the two nerve cells (the synapse). These molecules may then be taken up by serotonin receptors of the postsynaptic nerve cell (the dendrite) and thus pass along their chemical message. Excess molecules are taken back up by the presynaptic cell and reprocessed. Several things might potentially go wrong with this process and lead to a serotonin deficit. Just to enumerate a few possibilities: 1. Not enough serotonin is produced, 2. There are not enough receptor sites to receive serotonin, 3. Serotonin is being taken back up too quickly before it can reach receptor sites, 4. Chemical precursors to serotonin (molecules that serotonin is manufactured from) may be in short supply, or 5. Molecules that facilitate the production of serotonin may be in too short supply. As you can see, if there is a breakdown anywhere along the path, neurotransmitter supplies may not be adequate for your brain's needs. Inadequate supplies lead to the symptoms that we know as depression. The Primary Players Noradrenaline In the 1960s Schildkraut cast his vote with noadrenaline as the causative factor for depression in the now classic "catecholamine" hypothesis of mood disorders. He proposed that depression stems from a deficiency of noradrenaline in certain brain circuits and that mania arises from too much of this substance. There is indeed a large body of evidence that supports this hypothesis, however, changes in noradrenaline levels do not affect mood in everyone. Serotonin Obviously there must be some other factor that interacts with noradrenaline to cause depression. Serotonin has been found to be this other factor. Serious investigations into serotonin's role in mood disorders, however, have been going on for almost 30 years, ever since Prange et al put forward the so-called "permissive amine hypothesis". This view held that synaptic depletion of serotonin was another cause of depression, one that worked by promoting, or "permitting," a fall in noradrenaline levels. So, although, noradrenaline still played a major role in depression, serotonin levels could altered to indirectly raise noradrenaline levels. Newer antidepressants like Effexor are actually targeted at both serotonin and noradrenaline. Tricyclics (TCAs) also affect both noradreanline and serotonin, however, they have the added effect of influencing histamine and acetylcholine, which produces the side-effects that TCAs are known for, such as dry mouth or eyes, peculiar taste in mouth, sensitivity to light of the eyes, blurry vision, constipation, urinary hesitancy, and others. SSRIs (selective serotonin reuptake inhibitors) do not affect histamine and acetylcholine and thus do not have the same side-effects as the older medications.
The syllabus asks for any one anxiety disorder. There are a number of these: post traumatic stress disorder (PTSD), panic disorder and obsessive compulsive disorder (OCD). The one we do is phobias! When the paper asks for ‘any one anxiety disorder’ that is your cue to talk about phobias! It seems odd that fear of spiders is seen as a psychological disorder. About 14% of the population suffer from one phobia or another and most of these do not interfere with a person’s normal style of life. However, some such as social phobia and most notably agoraphobia do prevent people from leading life to the full.
Types of phobia Specific phobia The one that many of us are familiar with. Specific phobias are an irrational fear of a specific object, situation or creature. Most common are specific phobias of certain animals such as spiders (arachnophobia), snakes (ophidiophobia), but they may also include situations such as heights, thunderstorms, enclosed spaces (claustrophobia) and aerophobia (flying, not the fear of chocolate with lots of holes!). Particularly common are those involving blood and injections. The DSM-IV (diagnostic and statistical manual) that is used to categorise and define mental illness describes the following characteristics:
Social phobia This involves an undue concern about your own behaviour and particularly the reaction of others to your behaviour: Generalised social phobia involves the person being shy in most social situations Specific social phobia involves shyness being triggered by certain social situations such as public speaking.
A person suffering social phobia is afraid that others will see them being frightened or embarrassed, for example blushing or shaking. There are well documented cases of people avoiding shops because they may have to pay by credit card and are frightened that others will see their hand shaking. Agoraphobia On the face of it this appears similar to social phobia in that both involve fear of social situations. However, it is different in that agoraphobia involves the fear of panic attack. The DSM-IV actually classes the disorder as ‘panic disorder with agoraphobia.’ Usually the fear is triggered by one or a series of panic attacks in a public place. Symptoms include sweating, very rapid increased heart rate leaving people fearful for their lives and intense fear. In future this leaves people afraid to go out in case the attack occurs again in front of others. Many agoraphobics are confined to their houses for years.
Explaining phobias There should be no surprises here! Just a re-working of the oh so familiar approaches!
Medical or biological model Genetic factors Phobias (like noses) tend to run in families, for example if a person has blood and injection phobia then there is a 64% chance that some other person in the family will suffer the same. This compares to an incidence of about 4% in the general population. Torgersen (1983) reported the following concordance rates for agoraphobia: MZ twins: 31% DZ twins: 0% Evaluation Clearly there are the usual cases of nature or nurture! To what extent has the phobia been inherited and to what extent learned? Clearly, sharing a house with a mother that screams whenever she sees a spider may is likely to instil a fear of spiders in her offspring.
Biological arousal Some people are more easily aroused than others (tell me about it!). Since arousal is controlled by activity in the sympathetic branch of the ANS it could be that there is a biological predisposition to phobias. Lader & Mathews (1968) did find that agoraphobics and social phobes have a higher level of arousal. Clearly this could be tied in with the genetic argument since a higher state of physical arousal like this is probably inherited.
Biological preparedness (Seligman 1971) A little bit different to the usual medical explanations, this one takes an evolutionary stance. Basically it suggests that it could be an evolutionary advantage to have certain phobias meaning that we are more likely to develop some phobias than others. Clearly being frightened of snakes and spiders could help prolong our lives by ensuring that we stay well clear of them! Ohman et al (1975) used classical conditioning to induce a fear of either snakes and spiders or houses and flowers. They did this in the time honoured way of pairing the stimulus with electric shocks (like my number 3). After a shock-free period the fear for houses and flowers extinguished (died out) very quickly, whereas the fear of snakes and spiders persisted. This suggests that we may be predisposed to acquire phobias to situations or objects that are life-threatening. Evaluation The apparent ease with which we acquire phobias of spiders and snakes could just as well be explained by social conditioning. From an early age we are made aware of the dangers of such creatures through stories, books and films and simply by being warned. Personality type At first this seems out of place in a biological explanation. However social phobia may be caused by the personality characteristic of excessive shyness or introversion. Perhaps we inherit the personality type that then makes it more likely that we will become a social phobic. The extent to which personalities are determined by genes and environment is hotly debated! Generally the medical model does not offer a very convincing explanation of phobias. Many of their arguments can just as easily be explained using the psychological theories.
Psychological explanations of phobias Psychodynamic Have a guess! The specific case of Little Hans is classic Freudian thinking and we’ll consider that in a few moments. First let’s consider the broader picture: Conflict between the id and the ego causes anxiety. The id is the source of your selfish urges. These can be a source of anguish, embarrassment and stress so they tend to be repressed into the unconscious mind by one of a variety of defence mechanisms… stop me if this is not making sense. One of the defence mechanisms (check your list in ‘approaches’), is displacement. Anxiety caused by an object may be displaced onto something else. A classic case would be a woman’s fear of the male genitalia being displaced onto snakes or perhaps neck ties. Freud’s theory was based on his case study of Little Hans which you should all know backwards (it would probably make more sense that way). Briefly: Hans’ father was a friend of Freud who was concerned about Hans’ fear of horses. Freud concluded that this had come about because of an unresolved Oedipus complex. During the Phallic stage of development little boys develop an unconscious desire of their mother and become fearful that the father will find out. This fear is caused by castration anxiety, the worry that the father will chop off their ‘wedding tackle.’ In the case of Little Hans his unacceptable fear of his father had been displaced onto horses who bore some striking resemblances to his father (not to be quoted). Hans’ father wore glasses (similar to a horse’s blinkers), he had a moustache (similar to a horse’s reigns) and he’d been ridden to victory in the previous year’s Cheltenham Gold Cup (no not really!). Oh yes and Hans used to ride on his dad’s back and his dad had once told him to ‘trot away.’ To be fair Hans did seem overly fascinated with his ‘widdler’ but what little boy isn’t?
Evaluation Be careful here. Some of Freud’s ideas are still well respected and many of his theories were ground breaking, but to be fair this probably isn’t one of his finer moments. There appears to be a far more logical explanation of Hans’ fear as postulated by the behaviourists. Fromm (1970) sheds a different light on this particular case. He believes that the fear was not of the father but instead provides evidence for the fear being of the mother. On catching Hans playing with his ‘widdler’ (or ‘wi-wi-maker), his mother had threatened to take him to the doctors to have it chopped off! It was also his mother who on a number of occasions had threatened to leave Hans. There are clearly other explanations for Hans’ fear of horses which we shall come to with the behaviourist model. But for purposes of evaluation it would also be worth mentioning that there appears to be some association of horses and other events (behaviourist approach). Shortly before Hans’ problems started, his friend Lizzi had gone away and not returned. Her luggage was taken to the train station by a white horse, so we have an unhappy association with horses. Similarly Hans’ condition appeared to worsen after his tonsillectomy. Slap (not slap-head!) 1961, says that the fear of a surgeon in a long white coat also became added to his fear of his moustached father (again association), the white coat may have reminded him of white horses.
Behaviourist Back to reality! Obviously the stimulus-response lot are going to argue that phobias are learned and provide plenty of evidence and treatments to back up their claim. Returning briefly to Hans. We know that Hans had witnessed a horse falling over in the street and being pinned down by the cart it was pulling. Clearly this would have been distressing and frightening so an obvious explanation (for the behaviourists) is an association between horses and fear Just as Freud has Little Hans, the behaviourists have their Little Albert! Watson and Raynor (1920) classically condition a fear of white rats in an 11 month old boy, Albert. Over a period of weeks each time he plays with a toy white rat an iron bar is struck. At first this causes hesitation when dealing with the rat and eventually after 10 days or so (the third trial) he becomes distressed when the rat is seen. Worth mentioning is that the fear was immediately generalised to a toy white rabbit (sufficiently similar in appearance to the rat to illicit the response) whereas fear of cotton wool and of a toy dog was not so pronounced (evidence of discrimination).
Clearly the ethics of the study can be questioned. Watson & Raynor were both doctors so would have been aware of the long term effects their procedure may have had. It is clear when reading their report that they did consider the consequences in advance but went ahead on the grounds that this was no more distressing than the experiences he was likely to encounter in the real world. It had been their intention to treat Albert’s condition with a number of experimental techniques, including reconditioning in which he would have been given ‘candy’ each time the rat was presented. His mother removed Albert from the experiment before this could be done.
Conditioned, unconditioned and neutral stimuli (a brief explanation) For the purposes of this explanation think of ‘conditioned’ as learned and ‘unconditioned’ as already present.
Unconditioned stimulus: the loud noise From the outset this produces the Unconditioned response: the fear reaction The unconditioned stimulus is paired with the Neutral stimulus: white rat
Eventually after training the neutral stimulus becomes associated with the conditioned response and now becomes the Conditioned stimulus: white rat (after training) And this alone can now elicit the Conditioned response: fear of white rat
Operant conditioning Avoiding a situation or object that causes anxiety or fear is seen by behaviourists as being rewarding in itself. If you suffer from arachnophobia then avoiding spiders will result in you suffering less anxiety. As a result you will behave in a way that keeps you clear of spiders. Unfortunately this means that your fear will not be extinguished since the only way to lose a behaviour, in behaviourist terms, is by unlearning the association between fear and the stimulus that causes it. Mowrer’s ‘two-factor’ approach. This should sound familiar since we covered in year 12 with eating disorders. Mowrer believed that both classical and operant conditioning are involved in acquisition and maintenance of phobias.
As we have seen with Little Albert and other studies, we initially learn fear by association. Classical conditioning therefore explains how we acquire the fear.
Avoiding the fear-provoking stimulus then prevents us from unlearning the fear so as a result the fear is not extinguished. Operant conditioning therefore explains why a phobia is maintained.
Example: At a young age you’re out on a picnic with mum. A spider crawls over her hand, she screams and this frightens you. You have learned to associate spiders with being frightened. To unlearn this fear what you really need to do is relearn and associate spiders with things pleasant. But this means having to encounter spiders. Instead what you do is avoid them since this is reinforcing because it prevents anxiety. As a result you remain frightened of spiders. Only when you confront the fear and take positive steps to overcome it will you lose the fear. Evaluation There is some evidence to support the theory, particularly the case of Little Albert who clearly did acquire a phobia via classical conditioning and who did generalise it, as predicted by behaviourists, to similar objects such as rabbits. Some successful treatments for phobias are based on behaviourist theories Barlow & Durand (1995) report that 50% of people with a phobia for driving could remember a specific incident that had triggered the fear… again supporting the theory that phobias are learned following some incident or incidents. Mineka et al (1984) provided evidence for the SLT or modelling approach when they taught monkeys to fear snakes by getting them to watch video footage of other monkeys being frightened of snakes! However, about 50% of people with phobias cannot recall a specific event that triggered the fear. DiNardo et al (1988) reported that only about half of all people that have had frightening experiences of dogs go on to develop a phobia of dogs. Behaviourists are unable to explain this sort of individual difference using stimulus response theory. Other points worth making: the behaviourist theory is unreliable since much of the research is retrospective, relying as it does, on people thinking back to early childhood experiences. As always the theory is reductionist (explains a complex behaviour in very simple terms) and ignores biological or genetic factors. It is unable to explain why it is easier to become afraid of some things (snakes, spiders) than others such as flowers and houses.
Cognitive Explain phobias in terms of cognitive biases that exaggerate the threat being posed. Tomarken et al (1989) took participants that were frightened of snakes and/or spiders and compared them to people not afraid of these creatures. They would show them slides of snakes, spiders and non-fear provoking creatures. After each slide there would either be a tone, silence or an electric shock. The participants with phobias drastically overestimated the number of times the snake, spider etc. would be followed by an electric shock. Other studies have shown that phobics over-estimate the threat being posed. For example they see spiders in a jar trying to jump towards them or over estimate the size of the creature. People frightened of spiders, cockroaches etc. often perceive that these creatures always run towards them when encountered. Panic disorder and agoraphobia is explained in terms of the patient over-estimating the threat from their bodily arousal. An increase in heart rate is seen as potentially life threatening leading to even greater increase and discomfort. Evaluation The theory is descriptive but lacks explanatory power. It is able to describe the symptoms of phobias but unable to explain how these have come about. Why do some people over-estimate the threat from one particular creature and not others? As often happens with the cognitive theory of abnormal behaviour it is almost impossible to separate out cause and effect since it treats symptoms and causes as being alike. Does the warped perception cause the disorder or does the disorder lead to an over-estimate of the threat? A combination of the behaviourist and cognitive could also be considered. We learn phobias but because of the different ways in which different perceives the world, some people are more likely to develop fears than others. Compare this to the behaviourist-cognitive theories of eating disorders and depression.
Phobias is a relatively short topic, so nothing to be afraid of!
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