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Schizophrenia |
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, | |||||||||||||||||||||||||||||||||||||
