A-Level Psychology
A-Level Psychology
Paper 3
Option 2
Schizophrenia
| | | | |
|The classification of schizophrenia. Positive symptoms, | | | |
|including hallucinations and delusions. Negative symptoms | | | |
|including speech poverty and avolition. | | | |
|Reliability and validity in diagnosis and classification of | | | |
|schizophrenia, with reference to co-morbidity, culture and | | | |
|gender bias and symptom overlap. | | | |
|Biological explanations for schizophrenia: genetics, the | | | |
|dopamine hypothesis and neural correlates. | | | |
|Psychological explanations for schizophrenia: family | | | |
|dysfunction and cognitive explanations, including | | | |
|dysfunctional thought processing. | | | |
|Drug therapy: typical and atypical antipsychotics. | | | |
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|Cognitive behavioural therapy and family therapy as used in | | | |
|the treatment of schizophrenia. Token economies, as used in | | | |
|the management of schizophrenia. | | | |
| | | | |
|The importance of an interactionist approach in explaining | | | |
|and treating schizophrenia; the diathesis - stress model. | | | |
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| | | | |
Background Reading
Schizophrenia is a mental illness that usually occurs in late adolescence or early adulthood, but it can occur at any time in life. In the Diagnostic and Statistical Manual (DSM) it is classified as a psychosis, as the sufferer has no concept of reality. Essentially the illness is due to a breakdown of the patient’s personality.
Schizophrenia is a worldwide disease i.e. culturally universal; however, both the symptoms and the incidence (how common it is) vary from culture to culture. Approximately 1% of the population develops schizophrenia during their lifetime, which is an enormous number. More than 2 million Americans suffer from the illness in a given year.
The peak of incidence for onset is 25-30 years and cases prior to adolescence are extremely rare. Overall there are no gender differences: a similar number of men and women are diagnosed with the disorder. However, the disorder often appears earlier in men than women (Warner 1994). Twice as many men as women between the ages of 15 and 24 years are diagnosed, but between 25 to 34 years the incidence of females rises, until after 35 years of age the two sexes are similar in rate of incidence.
Available treatments can relieve many symptoms, but most people with schizophrenia continue to suffer some symptoms throughout their lives; it has been estimated that no more than one in five individuals recovers completely.
Although recovery from schizophrenia is rare (1% of the population suffer from it), recent research has given hope to sufferers and their family members. Research has identified new, safer medications and has started to unravel the complex causes of the disease. New insights into the disorder have come from several areas of Psychology such as molecular genetics, the study of populations, brain imaging (e.g. MRI Scans) and brain function studies.
Schizophrenia is a severe long-term mental health condition. It causes a range of different psychological symptoms.
Doctors often describe schizophrenia as a type of psychosis. This means the person may not always be able to distinguish their own thoughts and ideas from reality.
Symptoms of schizophrenia
Symptoms of schizophrenia include:
• hallucinations – hearing or seeing things that don't exist
• delusions – unusual beliefs not based on reality
• muddled thoughts based on hallucinations or delusions
• changes in behaviour
Some people think schizophrenia causes a "split personality" or violent behaviour. This is not true.
The cause of any violent behaviour is usually drug or alcohol misuse.
Schizophrenia changes how a person thinks and behaves.
The condition may develop slowly. The first signs can be hard to identify as they often develop during the teenage years.
Symptoms such as becoming socially withdrawn and unresponsive or changes in sleeping patterns can be mistaken for an adolescent "phase".
People often have episodes of schizophrenia, during which their symptoms are particularly severe, followed by periods where they experience few or no symptoms. This is known as acute schizophrenia.
Positive and negative symptoms
The symptoms of schizophrenia are usually classified into:
• positive symptoms – any change in behaviour or thoughts, such as hallucinations or delusions
• negative symptoms – a withdrawal or lack of function that you would usually expect to see in a healthy person; for example, people with schizophrenia often appear emotionless and flat
Hallucinations
Hallucinations are where someone sees, hears, smells, tastes or feels things that don't exist outside their mind. The most common hallucination is hearing voices.
Hallucinations are very real to the person experiencing them, even though people around them can't hear the voices or experience the sensations.
Research using brain-scanning equipment shows changes in the speech area in the brains of people with schizophrenia when they hear voices. These studies show the experience of hearing voices as a real one, as if the brain mistakes thoughts for real voices.
Some people describe the voices they hear as friendly and pleasant, but more often they're rude, critical, abusive or annoying.
The voices might describe activities taking place, discuss the hearer's thoughts and behaviour, give instructions, or talk directly to the person. Voices may come from different places or one place in particular, such as the television.
Delusions
A delusion is a belief held with complete conviction, even though it's based on a mistaken, strange or unrealistic view. It may affect the way the person behaves. Delusions can begin suddenly, or may develop over weeks or months.
Some people develop a delusional idea to explain a hallucination they're having. For example, if they have heard voices describing their actions, they may have a delusion that someone is monitoring their actions.
Someone experiencing a paranoid delusion may believe they're being
harassed or persecuted. They may believe they're being chased, followed, watched, plotted against or poisoned, often by a family member or friend.
Some people who experience delusions find different meanings in everyday events or occurrences.
They may believe people on TV or in newspaper articles are communicating messages to them alone, or that there are hidden messages in the colours of cars passing on the street.
Confused thoughts (thought disorder)
People experiencing psychosis often have trouble keeping track of their thoughts and conversations.
Some people find it hard to concentrate and will drift from one idea to another. They may have trouble reading newspaper articles or watching a TV programme.
People sometimes describe their thoughts as "misty" or "hazy" when this is happening to them. Thoughts and speech may become jumbled or confused, making conversation difficult and hard for other people to understand.
Changes in behaviour and thoughts
A person's behaviour may become more disorganised and unpredictable, and their appearance or dress may seem unusual to others.
People with schizophrenia may behave inappropriately or become extremely agitated and shout or swear for no reason.
Some people describe their thoughts as being controlled by someone else, that their thoughts aren't their own, or that thoughts have been planted in their mind by someone else.
Another recognised feeling is that thoughts are disappearing, as though someone is removing them from their mind.
Some people feel their body is being taken over and someone else is directing their movements and actions.
Negative symptoms of schizophrenia
The negative symptoms of schizophrenia can often appear several years before somebody experiences their first acute schizophrenic episode.
These initial negative symptoms are often referred to as the prodromal period of schizophrenia.
Symptoms during the prodromal period usually appear gradually and slowly get worse.
They include the person becoming more socially withdrawn and increasingly not caring about his or her appearance and personal hygiene.
It can be difficult to tell whether the symptoms are part of the development of schizophrenia or caused by something else.
Negative symptoms experienced by people living with schizophrenia include:
• losing interest and motivation in life and activities, including relationships and sex
• lack of concentration, not wanting to leave the house, and changes in sleeping patterns
• being less likely to initiate conversations and feeling uncomfortable with people, or feeling there's nothing to say
The negative symptoms of schizophrenia can often lead to relationship problems with friends and family as they can sometimes be mistaken for deliberate laziness or rudeness.
The exact causes of schizophrenia are unknown. Research suggests a combination of physical, genetic, psychological and environmental factors can make a person more likely to develop the condition.
Some people may be prone to schizophrenia, and a stressful or emotional life event might trigger a psychotic episode. However, it's not known why some people develop symptoms while others don't.
Increased risk
Things that increase the chances of schizophrenia developing include:
Genetics
Schizophrenia tends to run in families, but no single gene is thought to be responsible.
It's more likely that different combinations of genes make people more vulnerable to the condition. However, having these genes doesn't necessarily mean you'll develop schizophrenia.
Evidence that the disorder is partly inherited comes from studies of twins. Identical twins share the same genes.
In identical twins, if one twin develops schizophrenia, the other twin has a one in two chance of developing it, too. This is true even if they're raised separately.
In non-identical twins, who have different genetic make-ups, when one twin develops schizophrenia, the other only has a one in seven chance of developing the condition.
While this is higher than in the general population, where the chance is about 1 in 100, it suggests genes aren't the only factor influencing the development of schizophrenia.
Brain development
Studies of people with schizophrenia have shown there are subtle differences in the structure of their brains.
These changes aren't seen in everyone with schizophrenia and can occur in people who don't have a mental illness. But they suggest schizophrenia may partly be a disorder of the brain.
Neurotransmitters
Neurotransmitters are chemicals that carry messages between brain cells.
There's a connection between neurotransmitters and schizophrenia because drugs that alter the levels of neurotransmitters in the brain are known to relieve some of the symptoms of schizophrenia.
Research suggests schizophrenia may be caused by a change in the level of two neurotransmitters: dopamine and serotonin.
Some studies indicate an imbalance between the two may be the basis of the problem. Others have found a change in the body's sensitivity to the neurotransmitters is part of the cause of schizophrenia.
Pregnancy and birth complications
Research has shown people who develop schizophrenia are more likely to have experienced complications before and during their birth, such as:
• a low birth weight
• premature labour
• a lack of oxygen (asphyxia) during birth
It may be that these things have a subtle effect on brain development.
Triggers
Triggers are things that can cause schizophrenia to develop in people who are at risk.
These include:
Stress
The main psychological triggers of schizophrenia are stressful life events, such as:
• bereavement
• losing your job or home
• divorce
• the end of a relationship
• physical, sexual or emotional abuse
These kinds of experiences, although stressful, don't cause schizophrenia. However, they can trigger its development in someone already vulnerable to it.
Drug abuse
Drugs don't directly cause schizophrenia, but studies have shown drug misuse increases the risk of developing schizophrenia or a similar illness.
Certain drugs, particularly cannabis, cocaine, LSD or amphetamines, may trigger symptoms of schizophrenia in people who are susceptible.
Using amphetamines or cocaine can lead to psychosis, and can cause a relapse in people recovering from an earlier episode.
Three major studies have shown teenagers under 15 who use cannabis regularly, especially "skunk" and other more potent forms of the drug, are up to four times more likely to develop schizophrenia by the age of 26.
The classification of schizophrenia. Positive symptoms, including hallucinations and delusions. Negative symptoms including speech poverty and avolition.
Mental illness is diagnosed using diagnostic criteria. The diagnostic tools mainly used are the DSM-5 and the ICD-10. These provide the clinician with information of what the specific disorders look like and they can be used a check list to diagnose mental illness.
It is important that classification systems such as the DSM and the ICD are valid and reliable and we will look at this later.
Schizophrenia symptoms can be split into positive and negative symptoms.
Positive symptoms are .............. symptoms experienced in .......................to normal experiences.
Positive symptoms involve the displaying of behaviours concerning loss of touch with reality, such as ................. and delusions. These generally occur in acute, short episodes, with more normal periods in between, and respond well to medication.
Negative symptoms are .............. experiences that represent the of a usual experience such as clear thinking or ‘normal’ levels of ....................
Negative symptoms involve the displaying of behaviours concerning disruption of normal emotions and actions. These occur in chronic, longer-lasting episodes, and are ...............to medication. Negative symptoms contribute most to sufferers not being able to function effectively in society, such as in relationships or at work.
Enduring negative symptoms are often referred to as the........................... characterised by the presence of at least 2 negative symptoms for 12 months or longer. Individuals with the deficit syndrome have been found to have more pronounced cognitive deficits and poorer outcomes than patients who don’t have this syndrome, with several studies (Milev et al, 2005) reporting worse functional outcomes in individuals with more prominent negative symptoms. Negative symptoms respond poorly to antipsychotic treatment, although the newer ....................... are claimed to be superior in this respect than the older ‘typical’ drugs.
The DSM - 5 classification of schizophrenia is as follows:
DSM-V (2013)
To meet the criteria for diagnosis of schizophrenia, the patient must have experienced at least 2 of the following:
Delusions
Hallucinations
Disorganized speech (e.g. frequent derailment or incoherence)
Disorganized or catatonic behaviour
Negative symptoms .e. affective flattening, alogia or avolition.
At least 2 of the symptoms must be the present for one month and one of these symptoms must be delusions, hallucinations, or disorganized speech.
Continuous signs of the disturbance must persist for at least 6 months,
-during which the patient must experience at least 1 month of active symptoms (or less if successfully treated),
-with social or occupational deterioration problems occurring over a significant amount of time. These problems must not be attributable to another condition.The American Psychiatric Association (APA) removed schizophrenia subtypes from the DSM-5.
What is the main difference between the ICD-10 and DSM-V?
|Positive Symptoms |Negative Symptoms |
|Hallucinations [pic] |Speech poverty |
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|Delusions |Avolition |
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|Disordered Thinking such as: | |
|Thought insertions |Flat Affect |
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|Thought withdrawal |Anhedonia |
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|Thought Broadcasts | |
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The Reliability and Validity in Diagnosing Schizophrenia
For a classification system to be useful it must be both reliable and valid. It can be complicated diagnosing schizophrenia as many people who develop the disorder may also have another condition such as depression, PTSD and OCD. When two condition exist it is known as co-morbidity.
There are also cultural biases in the diagnosis of schizophrenia - you can refer to the research we have previously looked at in this area.
There also seems to be a gender bias in the diagnosis of schizophrenia.
ome critics of the DSM diagnostic criteria argue that some diagnostic categories are biased towards pathologising one gender rather than the other. For example, Broverman et al. (1970) found that clinicians in the US equated mentally healthy ‘adult’ behaviour with mentally healthy ‘male’ behaviour, illustrating a form of androcentrism. As a result there was a tendency for women to be perceived as less mentally healthy when they do not show ‘male’ behaviour. Also interestingly, some research has indicated that a psychiatrist’s gender might affect their ability to diagnose.
Loring and Powell (1988) randomly selected 290 male and female psychiatrists to read two case articles of patients’ behaviour and then asked them to offer their judgment on these individuals using standard diagnostic criteria. When the patients were described as ‘male’ or no information was given about their gender, 56% were given a diagnosis of schizophrenia. However, when the patients were described as ‘female’, only 20% were given a diagnosis of schizophrenia. This gender bias did not appear to be evident amongst the female psychiatrists. This suggests that diagnosis is influenced not only by the gender of the patient but also the gender of the clinician.
Gender bias also occurs due to clinicians failing to consider that males tend to suffer more negative symptoms than women and have higher levels of substance abuse, or that females have better recovery rates and lower relapse rates. These misconceptions could be affecting the validity of a diagnosis as clinicians are not considering all symptoms.
Clinicians also ignore that there are different predisposing/risk factors between males and females, which give them different vulnerability levels at different points in life. This can possibly explain the gender difference in the onset of schizophrenia.
The following Study is good to use as an example of validity and inter-rater reliability (or not). This study shows how there are many issues with the reliability and validity of diagnosing schizophrenia. However, be careful because this study was carried out before the current classification systems were developed.
Rosenhan, D.L. (1973)
On being sane in insane places
Background
There is a long history of attempting to classify what is abnormal behaviour. The most commonly accepted approach to understanding and classifying abnormal behaviour is known as the medical model. This branch of medicine, which is concerned with treating mental illness, is known as psychiatry. Psychiatrists are medical doctors and are trained to regard mental illness as comparable to other kinds of (physical) illnesses. Beginning in the 1950s this medical approach has used the Diagnostic and Statistical Manual of Mental Disorders (DSM) to classify abnormal behaviour.
However, in the 1960s a number of psychiatrists and psychotherapists, known as the anti-psychiatry movement, started to fiercely criticise the medical approach to abnormality. David Rosenhan, a psychiatrist, was also a critic of the medical model and this study can be seen as an attempt to demonstrate that psychiatric classification is unreliable.
[pic]
Aim
The aim of this study was to test the hypothesis that psychiatrists cannot reliably tell the difference between people who are sane and those who are insane.
[pic]
The study actually consisted of two parts.
Procedure (main study)
The main study is an example of a field experiment. The manipulation (independent variable) was the made up symptoms of the pseudo patients, and the dependent variable was the psychiatrists' admission and diagnostic label of the pseudo patient. The study also involved participant observation, since, once admitted, the pseudo-patients kept written records of how the ward as a whole operated, as well as how they personally were treated.
The first part of the study involved eight sane people (a psychology graduate student in his 20s, three psychologists, a paediatrician, a psychiatrist, a painter, and a 'housewife') attempting to gain admission to 12 different hospitals, in five different states in the USA. There were three women and five men.
These pseudo-patients telephoned the hospital for an appointment, and arrived at the admissions office complaining that they had been hearing voices. They said the voice, which was unfamiliar and the same sex as themselves, was often unclear but it said 'empty', 'hollow', 'thud'. These symptoms were partly chosen because they were similar to existential symptoms (Who am I? What is it all for?) which arise from concerns about how meaningless your life is. They were also chosen because there is no mention of existential psychosis in the literature.
The pseudo patients gave a false name and job (to protect their future health and employment records), but all other details they gave were true including general ups and downs of life, relationships, events of life history and so on.
After they had been admitted to the psychiatric ward, the pseudo patients stopped simulating any symptoms of abnormality. However, Rosenhan did note that the pseudo patients were nervous, possibly because of fear of being exposure as a fraud, and the novelty of the situation.
The pseudo patients took part in ward activities, speaking to patients and staff as they might ordinarily. When asked how they were feeling by staff they were fine and no longer experienced symptoms. Each pseudo patient had been told they would have to get out by their own devices by convincing staff they were sane.
The pseudo patients spent time writing notes about their observations. Initially this was done secretly although as it became clear that no one was bothered the note taking was done more openly.
In four of the hospitals the pseudo patients carried out an observation of behaviour of staff towards patients that illustrate the experience of being hospitalised on a psychiatric ward. The pseudo patients approached a staff member with a request, which took the following form: 'Pardon me, Mr/Mrs/Dr X, could you tell me when I will be presented at the staff meeting?'. (or ‘…when am I likely to be discharged?’). See table 1.
In order to compare the results Rosenhan carried out a similar study at Stanford University with students asking university staff a simple question.
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Results
All of the pseudo patients disliked the experience and wished to be discharged immediately.
None of the pseudo patients was detected and all but one were admitted with a diagnosis of schizophrenia and were eventually discharged with a diagnosis of 'schizophrenia in remission' This diagnosis was made without one clear symptom of this disorder. They remained in hospital for 7 to 52 days (average 19 days), Visitors to the pseudo patients observed ‘no serious behavioural consequences'. Although they were not detected by the staff, many of the other patients suspected their sanity (35 out of the 118 patients voiced their suspicions). Some patients voiced their suspicions very vigorously for example ‘You’re not crazy. You’re a journalist, or a professor. You’re checking up on the hospital’.
The pseudo patients’ normal behaviours were often seen as aspects of their supposed illness. For example, nursing records for three of the pseudo patients showed that their writing was seen as an aspect of their pathological behaviour. 'Patient engages in writing behaviour'. Rosenhan notes that there is an enormous overlap in the behaviours of the sane and the insane. We all feel depressed sometimes, have moods, become angry and so forth, but in the context of a psychiatric hospital, these everyday human experiences and behaviours were interpreted as pathological.
Another example of where behaviour was misinterpreted by staff as stemming from within the patient, rather than the environment, was when a psychiatrist pointed to a group of patients waiting outside the cafeteria half an hour before lunchtime. To a group of registrars (trainee psychiatrists) he suggested that such behaviour was characteristic of an oral-acquisitive syndrome. However, a more likely explanation would be that the patients had little to do, and one of the few things to anticipate in a psychiatric hospital is a meal.
In four of the hospitals the pseudo patients carried out an observation of behaviour of staff towards patients that illustrate the experience of being hospitalised on a psychiatric ward. The results were compared with a university study. In the university study, nearly all the requests were acknowledged and responded to unlike the psychiatric hospital where the pseudo patients were treated as if they were invisible. See table 1.
Table 1: Responses of staff towards pseudo patients requests
|Response |Percentage making contact with patient |
| |Psychiatrists |Nurses |
|Moves on with head averted |71 |88 |
|Makes eye contact |23 |10 |
|Pauses and chats |2 |4 |
|Stops and talks |4 |0.5 |
Rosenhan noted that experience of hospitalisation for the pseudo patients was one of depersonalisation and powerlessness.
Powerlessness and depersonalisation were evident in the ways in which the patients were deprived of many human rights such as freedom of movement and privacy. Medical records were open to al staff members regardless of status or therapeutic relationship with the patient and personal hygiene was monitored and many of the toilets did not have doors. Some of the ward orderlies would be brutal to patients in full view of other patients but would stop as soon as another staff member approached. This indicated that staff were credible witnesses but patients were not.
It was estimated that the pseudo patients were given a total of 2,100 medication tablets, though only two were swallowed. The rest were either pocketed or flushed down the toilet. Often, when the pseudo patients visited the toilets to dispose of their tablets they found the medication of other patients that had already been placed there. As long as the patients were co-operative, then their behaviour went unnoticed.
The records the pseudo patients had made about the amount of time the nurses stayed in the ward offices was about 90 per cent of the time and the number of times medical staff came onto the ward, and the amount of time spent with psychiatrists, psychologists, registrars and so forth was, on average, under seven minutes per day.
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The Secondary Study
Procedure/Method
In the secondary study, the staff of a teaching and research hospital, which was aware of the first study, was falsely informed that during the next three months one or more pseudo patients would attempt to be admitted into their hospital. Staff members were asked to rate on a 10-point scale each new patient as to the likelihood of them being a pseudo patient.
This false information was the manipulated independent variable, and the dependent variable was the number of patients which staff subsequently suspected of being pseudo patients.
[pic]
Results/Findings of the Secondary Study
The table shows that many patients of the hospitals regular intake were judged to be pseudo patients. For example, around ten per cent of their regular intake were judged by one psychiatrist and another staff member to be pseudo patients.
Table 2: Judgement of all admissions patients as to the likelihood that they are pseudo patients
|Number of patients judged |193 |
|Number of patients confidently judged as pseudo patients by at least one staff member |41 |
|Number of patients suspected by one psychiatrist |23 |
|Number of patients suspected by one psychiatrist AND one other staff member |19 |
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Explanation
Rosenhan claims that the study demonstrates that psychiatrists cannot reliably tell the difference between people who are sane and those who are insane.
The main experiment illustrated a failure to detect sanity, and the secondary study demonstrated a failure to detect insanity.
Rosenhan explains that psychiatric labels tend to stick in a way that medical labels do not and that everything a patient does is interpreted in accordance with the diagnostic label once it has been applied.
He suggested that instead of labelling a person as insane we should focus on the individual’s specific problems and behaviours.
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Evaluation of the Procedure
Strengths
The participant observation meant that the pseudo patients could experience the ward from the patients’ perspective while also maintaining some degree of objectivity.
The study was a type of field experiment and was thus fairly ecologically valid whilst still managing to control many variables such as the pseudo patients’ behaviour.
Rosenhan used a range of hospitals. They were in different States, on both coasts, both old/shabby and new, research-orientated and not, well staffed and poorly staffed, one private, federal or university funded. This allows the results to be generalised.
Weaknesses
The hospital staff was deceived - this is, of course, unethical. Although Rosenhan did not conceal the names of hospitals or staff and attempted to eliminate any clues which might lead to their identification
Rosenhan did note that the experiences of the pseudo-patients could have differed from that of real patients who did not have the comfort of knowing that the diagnosis was false.
Perhaps Rosenhan was being too hard on psychiatric hospitals, especially when it is important for them to play safe in their diagnosis of abnormality because there is always an outcry when a patient is let out of psychiatric care and gets into trouble. If you were to go to the doctors complaining of stomach aches how would you expect to be treated?
Doctors and psychiatrists are more likely to make a type two error (that is, more likely to call a healthy person sick) than a type one error (that is, diagnosing a sick person as healthy)
When Rosenhan did his study the psychiatric classification in use was DSM-II. However, since then a new classification has been introduced which was to address itself largely to the whole problem of unreliability - especially unclear criteria. It is argued that with the newer classification DSM-III, introduced in the 1980s, psychiatrists would be less likely to make the errors they did. The DSM is currently in its fourth edition (DSM-IV)
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Evaluation of Explanation
The study demonstrates both the limitations of classification and importantly the appalling conditions in many psychiatric hospitals. This has stimulated much further research and has lead to many institutions improving their philosophy of care.
Rosenhan, like other anti-psychiatrists, is arguing that mental illness is a social phenomenon. It is simply a consequence of labelling. This is a very persuasive argument, although many people who suffer from a mental illness might disagree and say that mental illness is a very real problem
Reference
Rosenhan, D.L. (1973) On being sane in insane places. Science, 179. 250-58
Biological explanations for schizophrenia: genetics, the dopamine hypothesis and neural correlates.
From our lesson you should summarise the Dopamine hypothesis and the revised dopamine hypothesis.
Early research attention (Johnstone et al., 1976) was focused on schizophrenics having enlarged ventricles (fluid-filled gaps between brain areas). Enlarged ventricles are especially associated with damage to central brain areas and the pre-frontal cortex, which more recent scanning studies have also linked to the disorder. Such damage has often been associated with negative symptoms but cannot explain all symptoms and incidences of schizophrenia.
Allen et al. (2007) found that positive symptoms also have neural correlates. They scanned the brains of patients experiencing auditory hallucinations and compared them to a control group whilst they identified pre-recorded speech as theirs or others. Lower activation levels in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucination group, who also made more errors than the control group. We can thus say that reduced activity in these two areas of the brain is a neural correlate of auditory hallucination.
Is There a Specific Gene for Schizophrenia
Researchers have identified a gene that increases the risk of schizophrenia, and they say they have a plausible theory as to how this gene may cause the devastating mental illness.
After conducting studies in both humans and mice, the researchers said this new schizophrenia risk gene, called C4, appears to be involved in eliminating the connections between neurons — a process called "synaptic pruning," which, in humans, happens naturally in the teen years.
It's possible that excessive or inappropriate "pruning" of neural connections could lead to the development of schizophrenia, the researchers speculated. This would explain why schizophrenia symptoms often first appear during the teen years, the researchers said.
urther research is needed to validate the findings, but if the theory holds true, the study would mark one of the first times that researchers have found a biological explanation for the link between certain genes and schizophrenia. It's possible that one day, a new treatment for schizophrenia could be developed based on these findings that would target an underlying cause of the disease, instead of just the symptoms, as current treatments do, the researchers said.
"We're far from having a treatment based on this, but it's exciting to think that one day, we might be able to turn down the pruning process in some individuals and decrease their risk" of developing the condition, Beth Stevens, a neuroscientist who worked on the new study, and an assistant professor of neurology at Boston Children's Hospital, said in a statement.
The study, which also involved researchers at the Broad Institute's Stanley Center for Psychiatric Research at Harvard Medical School, is published today (Jan. 27) in the journal Nature. [Top 10 Mysteries of the Mind]
Schizophrenia risk
From previous studies, the researchers knew that one of the strongest genetic predictors of people's risk of schizophrenia was found within a region of DNA located on chromosome 6. In the new study, the researchers focused on one of the genes in this region, called complement component 4, or C4, which is known to be involved in the immune system.
Using postmortem human brain samples, the researchers found that variations in the number of copies of the C4 gene that people had, and the length of their gene, could predict how active the gene was in the brain.
The researchers then turned to a genome database, and pulled information about the C4 gene in 28,800 people with schizophrenia, and 36,000 people without the disease, from 22 countries. From the genome data, they estimated people's C4 gene activity.
They found that the higher the levels of C4 activity were, the greater a person's risk of developing schizophrenia was.
The researchers also did experiments in mice, and found that the more C4 activity there was, the more synapses were pruned during brain development.
Molecular cause?
Previous studies found that people with schizophrenia have fewer synapses in certain brain areas than people without the condition. But the new findings "are the first clear evidence for a molecular and cellular mechanism of synaptic loss in schizophrenia," said Jonathan Sebat, chief of the Beyster Center for Molecular Genomics of Neuropsychiatric Diseases at the University of California, San Diego, who was not involved in the study.
Still, Sebat said that the studies in mice are preliminary. These experiments looked for signs of synaptic pruning in the mice but weren't able to directly observe the process occurring. More detailed studies of brain maturation are now needed to validate the findings, Sebat said.
In addition, it remains to be seen whether synaptic pruning could be a target for antipsychotic drugs, but "it's promising," Sebat said. There are drugs in development to activate the part of the immune system in which C4 is involved, Sebat noted.
Follow Rachael Rettner @RachaelRettner. Follow Live Science @livescience, Facebook & Google+. Original article on Live Science.
General Genetic Link
One possible explanation of schizophrenia may be heredity i.e. genetics. The genetic explanation sees schizophrenia as transmitted through genes passed on to individuals from their families. We have to be careful when using this evidence as showing a genetic link because family members tend to share aspects of their environment as well as many of their genes. However, investigations that look at the genetic similarity between family members and how it is associated with the likelihood of developing schizophrenia are good evidence for understanding the influence that genes play. No one gene is thought to be responsible for this disorder – it’s more likely that different combinations of genes make individuals more vulnerable to schizophrenia. Having these genes does not necessarily mean an individual will develop schizophrenia
Family Studies
Family studies (Gottesman and Shields, 1991) find individuals who have schizophrenia and determine whether their biological relatives are similarly affected more often than non-biological relatives. Family studies have established that schizophrenia is more common among biological relatives of a person with schizophrenia, and that the closer the degree of genetic relatedness, the greater the risk.
Gottesman (1991) conducted a large-scale family study and found a strong relationship between the degree of genetic similarity and shared risk of schizophrenia. Children with two schizophrenic parents had a concordance rate of 46%, children with one schizophrenic parent a rate of 13% and siblings (where a brother or sister had schizophrenia) a concordance rate of 9%.
|Genes shared |
|12.5% | |3rd degree relatives|
|25% | |2nd degree relatives|
|50% | |1st degree relatives|
|100% | | |
Task - Briefly outline what can be seen from the table and graph above.
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Twin Studies
If monozygotic (MZ – genetically identical) twins are more concordant than dizygotic (DZ – who share only 50% of their genes), then this suggests that the greater similarity is due to genetic factors. Joseph (2004) calculated that the pooled data for all schizophrenia twin studies carried out prior to 2001 showed a concordance rate for MZ twins of 40.4% and 7.4% for DZ twins. More recent, methodologically sound studies (e.g. those using ‘blind’ diagnoses where the researchers assessing don’t know whether the twins are MZ or DZ) have tended to report a lower concordance rate for MZ twins than earlier studies. Despite this, however, such studies still support the genetic position because they show a concordance rate for MZ twins that is many times higher than for DZ twins.
Gottesman and Shields (1966) used patient records from psychiatric hospital from 1948 - 1964. They found that, in patients where both twins were hospitalised with schizophrenia or one with schizophrenia and the other with a related disorder the concordance rates for MZ were 54% and 18% for DZ. But when they included twins where one was diagnosed with schizophrenia and the other an unrelated psychiatric disorder the figure rose to 79% in MZ and 45% in DZ. This study suggests that there may be a genetic link to psychiatric abnormality but this is not always expressed as schizophrenia.
Task - How can such studies be evaluated?
Nature vs nurture
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Determinism
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Methodological flaws
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Are MZ twins treated more similarly?
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Adoption Studies
Because of the difficulties of disentangling genetic and environmental influences for individuals who share genes and environment, studies of genetically related individuals who have been reared apart are used.
Kety and Ingraham (1992) found that prevalence rates of schizophrenia were 10 x higher among genetic than adoptive relatives of schizophrenics, suggesting that genetics play a greater role than environmental factors. This is because the role of environment has been eliminated by looking at individuals who grew up away from their biological parents. So if the individual still develops schizophrenia this must be due to genes and not due to living with parents whose behaviour may have had an impact on development of the disorder.
You must learn all three biological explanations
From the evaluation task we complete in class you must have at least one highly effective evaluation point. After our class activity write these in your booklet.
Genes
Dopamine hypothesis
Neural correlates
Psychological explanations for schizophrenia: family dysfunction and cognitive explanations, including dysfunctional thought processing.
This can be a very difficult area to learn and we are going to stick to family dysfunction (double bind, expressed emotion and schizophrenogenic mother) and cognitive explanations (thought disturbances and deficits)
Double Bind theory
This theory was proposed by Bateson et al. (1972), who believes that family climate is important in the development of schizophrenia and emphasises the role of communication style within a family. The developing child regularly finds themselves trapped in situations where they fear doing the wrong thing, but receive mixed messages about what this is, and feel unable to comment on the unfairness of this situation or seek clarification.
When they ‘get it wrong’ (which is often) the child is punished by withdrawal of love. This leaves them with an understanding of the world as confusing and dangerous, and this is reflected in symptoms like disorganised thinking and paranoid delusions. Bateson was clear that this was just a risk factor in schizophrenia and not the only factor.
Expressed Emotion (EE)
Another feature of the theory is that of expressed emotion (EE), where families who persistently exhibit criticism and hostility exert a negative influence on the patient. This is primarily an explanation for relapse in recovering schizophrenics. However, it has also been suggested that it may be a source of stress that can trigger the onset of schizophrenia in a person who is already vulnerable due to their genetic make-up (diathesis-stress model).
EE is a family communication style in which members of a family of a psychiatric patient talk about the patient in a critical or hostile manner or in a way that indicates emotional over-involvement or over-concern with the patient or their behaviour. For example, research by Kuipers et al (1983) found that high EE relatives talk more and listen less. High levels of EE are most likely to influence relapse rates. A patient returning to a family with high EE is about 4 times more likely to relapse that a patient whose family is low in EE (Linszen et al 1997).
EE contains several elements:
• Verbal criticism of the patient, occasionally accompanied by violence
• Hostility towards the patient, including anger and rejection
• Emotional over-involvement in the life of the patient.
This suggests that people with schizophrenia have a lower tolerance for intense environmental stimuli, particularly intense emotional comments and interactions with family members. It appears that the negative emotional climate in these families arouses the patient and leads to stress beyond his or her already impaired coping mechanisms, thus triggering a schizophrenic episode. In contrast, a family environment that is relatively supportive and emotionally undemanding may help the person with schizophrenia to reduce their dependence on antipsychotic drugs and help reduce the likelihood of relapse (Noll, 2009).
The expressed emotion (EE) is considered to be an adverse family environment, which includes the quality of interaction patterns and nature of family relationships among the family caregivers and patients of schizophrenia and other psychiatric disorders. Influence of EE has been found to be one of the robust predictors of relapse in schizophrenia. This review article aims to provide a brief description of the origins and evolution of the EE as a construct from the available literature. The EE is modulated by multiple factors–some of which include certain personality profile, attribution factors by caregivers toward patient symptoms, and patient's vulnerability to stress. The psychosocial assessment and interventions specifically focused on family psychoeducation can potentially reduce high EE and relapse of symptoms as well. However, the theory surrounded with EE undermines the caregiver's positive attitudes toward the patients. Hence, it is important that the future studies should focus on both protective and vulnerable factors within the construct of EE in schizophrenia to facilitate comprehensive care.
INTRODUCTION
Expressed emotion (EE) refers to care giver's attitude towards a person with a mental disorder as reflected by comments about the patient made to an interviewer. It is a significant characteristic of the family milieu that has been found to predict symptom relapse in a wide range of mental disorders. The empirical data show that EE is one of the major psychosocial stressor and it has direct association with recurrence of illness. The importance of EE depends on research that has consistently established that persons with mental illness, such as schizophrenia, who live with close relatives who have negative attitudes, are significantly more likely to relapse. Research on EE was initiated in the 1950s, with researchers observing that close emotional ties between families could lead to sub-optimal stimulation and social withdrawal by the patient. The emotional expressions that form the basis of EE were selected purely based on their considerable relationship to relapse, rather than a particular theory of knowledge
The construct of EE comprises of the following factors/behavioral patterns: Criticism, hostility, and emotional overinvolvement (EOI). Like many other environmental stressors, EE behaviors are not pathological or unique to families of mental disorders, but they can cause relapse of psychiatric symptoms among people with a vulnerability to stress. It has been sufficiently established that high EE attitudes are reflected in actual interactions within the families of mental illness. Findings states that communication patterns in families with high EE relatives are usually characterized by more intense and negative verbal exchanges, oppositional or conflictual in nature and another significant finding is that interaction patterns in high EE dyads (of patient and caregiver) are more likely to be rigid
Hence, EE refers to the quality of family interactions, explicitly the existence of hostility, criticism, and EOI. Researchers have positioned EE within the diathesis-stress model of psychopathology, characterizing it as an environmental stressor that can potentially precipitate/cause relapse of psychosis among people with a genetic vulnerability.
Schizophrenogenic mother hypothesis
Introduced by Fromm-Reichman in 1948, putting the blame very much on the mother. The trigger is a domineering mother, micromanaging her child and refuse to acknowledge their independence.
The research in this area was correlation and often the mother's personality was assessed because she had a schizophrenic child. So this is a problem. why?
Can bad mothers and dysfunctional families cause young people to become schizophrenic? We know that, as recently as a generation ago, a large sector of Anglo-American psychiatry and clinical psychology believed that they could. Elite private hospitals offered patients with schizophrenia intensive forms of psychoanalytic therapy designed to uncover the trauma responsible for their suffering. Mothers of children with schizophrenia were given personality tests designed to discern what specific traits might be responsible for their children's distress; and family patterns of interaction were studied with an eye to unmasking the specific “crazy-making” dynamics.
Today, memories of that whole era make many people wince. Schizophrenia is now understood to be a brain disorder, best treated with medication. The psychiatric profession is appalled by the burden and pain that was once inflicted by telling families, and especially mothers, that they had literally driven their children crazy. That all said, there is a lot that remains imperfectly understood about how we got to the point we are at today. We are often told that, just when the psychogenic theories of schizophrenia had reached a peak of offensiveness and empirical vacuity, some new biological research came riding in, like the cavalry, and finally got things back on track. In fact, the historical record does not seem to bear this out.
Questions
1. Describe what is meant by expressed emotion.
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2. What three factors are involved in EE?
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3. What is the main problem with the notion of EE causing schizophrenia?
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Cognitive explanations - Background reading
A cognitive explanation for any phenomenon is one, which focuses on the role of mental processes. Compared to normal controls, research has found evidence of dysfunctional thought processing in people with schizophrenia i.e. they process information differently to those without the disorder. This is particularly evident in those who display the characteristic positive symptoms of schizophrenia such as delusions and hallucinations.
Cognitive explanations of delusions
During the formation of delusions, the patient’s interpretations of their experiences are controlled by inadequate information processing. A critical characteristic of delusional thinking is the degree to which the individual perceives him or herself as the central component in events (egocentric bias) and so jumps to conclusions about external events. This is manifested in the patient’s tendency to relate irrelevant events to themselves and consequently arrive at false conclusions. Muffled voices are interpreted as people criticising them, and flashes of light are a signal from God. Delusions in schizophrenia are relatively impervious to reality testing, in that patients are unwilling or unable to consider that they are wrong (Beck and Rector, 2005). They are considered to have impaired insight, an inability to recognise cognitive distortions and substitute more realistic explanations for events.
Cognitive explanation of hallucinations
Schizophrenia is associated with several types of abnormal information processing e.g. reduced processing of information in the temporal and cingulate gyri are associated with hallucinations. This lower level of information processing suggests that cognition is likely to be impaired.
Frith et al. (1992) identified two kinds of dysfunctional thought processing that could underlie some symptoms:
• Metarepresentation- dysfunction in this cognitive ability would disrupt our ability to recognise our own actions and thoughts as being carried out by ourselves rather than someone else. This would explain hallucinations of voices and delusions like thought insertion (the experience of having thoughts projected into the mind by others), both considered positive symptoms.
• Central control is the cognitive ability to suppress automatic responses while we perform deliberate actions instead. Disorganised speech and thought disorder could result from the inability to suppress automatic thoughts and speech triggered by other thoughts. For example, sufferers with schizophrenia tend to experience derailment of thoughts and spoken sentences (negative symptom) because each word triggers associations and the patient cannot suppress automatic responses to these.
Evaluation
There is strong support for the idea that information is processed differently in the mind of the schizophrenia sufferer.
Stirling et al. (2006) compared 30 patients with schizophrenia with 18 non-patients on a range of cognitive tasks including the Stroop Test, in which participants had to name the ink colours of colour words, suppressing the impulse to read the words in order to do this task. Patients took over twice as long as the control group to name the ink colours supporting Frith’s theory of central control dysfunction.
Sarin and Wallin (2014) reviewed recent research evidence relating to the cognitive model of schizophrenia. They found supporting evidence for the claim that the positive symptoms have their origins in faulty cognition. For example, delusional patients were found to show various biases in their information processing, such as jumping to conclusions and lack of reality testing. Likewise, schizophrenic individuals with hallucinations were found to have impaired self-monitoring and also tended to experience their own thoughts as voices. In addition, they found that patients with negative symptoms also displayed dysfunctional thought processes such as having low expectations regarding pleasure and success.
The claim that the symptoms of schizophrenia have their origin in faulty cognition is reinforced by the success of cognitive-based therapies. In cognitive-behavioural therapy for psychosis (CBTp), patients are encouraged to evaluate the content of their delusions or of any voices, and to consider ways they might test the validity of their faulty beliefs. The effectiveness of this approach was demonstrated in the NICE review of treatments for schizophrenia (NICE, 2014). This review found consistent evidence that, when compared with antipsychotic drugs, CBT was more effective in reducing symptom severity and improving levels of social functioning.
Despite a large body of evidence supporting the link between symptoms and faulty cognition (proximal causes), the cognitive theories do not tell us anything about the origins of those faulty cognitions (distal causes) and thus cannot be seen as explaining the causes of schizophrenia.
A strength of the cognitive explanation is that it can account for both positive and negative symptoms. In addition, it can be combined with other explanations e.g. biological ones to give a fuller understanding of the causes and maintenance of the disorder.
A problem with any psychological model of schizophrenia is that it deals adequately with one aspect of the disorder (e.g. cognitive impairment) but fails to explain, or ignores, another aspect (e.g. neurochemical changes). Howes and Murray (2014) addressed this problem with an integrated model of schizophrenia. They argue that early vulnerability factors (e.g. genes/birth complications etc) together with exposure to significant social stressors, sensitises the dopamine system, causing it to increase the release of dopamine. Increased dopamine activity results in paranoia and hallucinations, and eventually the development of psychosis. This contributes to the stress experienced by the individual, leading to more dopamine release, more symptoms and so on.
Therapies based on the Biological Approach
The following reading has been developed for patients and can help you understand how the drugs work. You do not have to remember the different trade names for the drugs but being able to identify one typical and one atypical by their generic name is desirable.
Drug therapy: typical and atypical antipsychotics.
Antipsychotics
About this leaflet
This leaflet may be helpful if:
• you have been prescribed antipsychotic medication
• a friend or relative has been prescribed antipsychotic medication
• you just want to find out about antipsychotic medication
It includes:
• What are antipsychotic medications?
• How are they supposed to help?
• How do they work?
• What kinds of antipsychotic medication are there?
• What are the possible side-effects?
• How long should it be taken for?
• How do I stop taking it?
• What alternatives are there?
What are antipsychotic medications?
They are a range of medications that are used for some types of mental distress or disorder - mainly schizophrenia and manic depression (bipolar disorder). They can also be used to help severe anxiety or depression.
What can they help with?
• The experience of hearing voices (hallucinations).
• Ideas that distress you and don't seem to be based in reality (delusions).
• Difficulty in thinking clearly (thought disorder).
• The extreme mood swings of manic depression/bipolar disorder.
• Some can help with severe depression.
How do they work?
They all affect the action of a number of chemicals in the brain called neurotransmitters – chemicals which brain cells need to communicate with each other. Dopamine is the main neurotransmitter affected by these medications. It is involved in how we feel:
• that something is significant, important or interesting;
• satisfied;
• motivated.
It is also involved in the control of muscle movements.
If parts of the dopamine system become overactive, they seem to play a part in producing hallucinations, delusions and thought disorder.
Although these medications were known as ‘major tranquillisers’ in the past, they are not designed to make you calmer or sleepy – so they are not the same as medications like Valium or sleeping tablets.
The basic aim is to help you feel better, without making you feel slowed down or drowsy. However, high doses may well make you feel too sleepy or 'drugged up'. They can be used in higher doses if you become very overactive, agitated or distressed - but this should usually only be for a short time.
What kinds of antipsychotic medication are there?
For the past 10 years or so doctors have talked about two different groups of antipsychotics:
• ‘Typical’ - the older drugs
• ‘Atypical’ - the newer drugs
Recent large independent research studies - not paid for by the drug companies – suggest that the new drugs are not really different – but are, in some situations, easier to use.
Choosing an antipsychotic
Most antipsychotics seem to be equally as good at controlling psychotic symptoms – Clozapine is the exception and is described later. Even so, individuals react differently to them, particularly with the side-effects. We cannot predict how well a particular person will respond to a particular drug – even whether a newer, or older drug, will be more helpful. It can often take some time, negotiation and ‘trial and error’ to find the best antipsychotic for a particular person.
Older antipsychotics: these first appeared in the mid-1950s. These older drugs are often called ‘typical’ or 'first-generation' antipsychotics. They all block the action of dopamine (see above), some more strongly than others.
Side-effects include:
• stiffness and shakiness, like Parkinson’s disease
• feeling sluggish and slow in your thinking
• uncomfortable restlessness (akathisia)
• some can affect your blood pressure and make you feel dizzy
• problems with your sex life
• problems with breast swelling or tenderness.
If you have any of these symptoms, you are probably on too high a dose. It should usually be reduced until the side-effects disappear. If you do need a higher dose to stay well, these side-effects can be controlled with anticholinergic drugs - used to treat Parkinson's disease. Orphenadrine and Procyclidine are the two most commonly used anticholinergics in the UK.
A longer-term problem is tardive dyskinesia (TD for short) – continual movements of the mouth, tongue and jaw. This affects about 1 in 20 people every year who are taking these medications.
Some older, ‘typical’ antipsychotics.
|Tablets |Trade Name |Usual daily dose (mg) |Max. daily dose (mg) |
|Chlorpromazine |Largactil |75-300 |1000 |
|Haloperidol |Haldol |3-15 |30 |
|Pimozide |Orap |4-20 |20 |
|Trifluoperazine |Stelazine |5-20 | |
|Sulpiride |Dolmatil |200-800 |2400 |
Newer antipsychotics : over the last 10 years, newer medications have appeared. They still block dopamine, but much less so than the older drugs. They also work on different chemical messengers in the brain (such as serotonin) and are often called ‘atypical’ or ‘second-generation’ antipsychotics. This is misleading - they have many of the same effects as the older drugs.
The newer antipsychotics are also being used to help treat some people's depression. There is growing evidence that this can be effective when combined with an antidepressant. Your psychiatrist will talk to you if this is an option to consider.
Side-effects
• Sleepiness and slowness
• Weight gain
• Interference with your sex life
• Increased chance of developing diabetes.
• Some can affect your blood pressure and make you feel dizzy.
• In high doses, some have the same Parkinsonian side-effects as the older medications (stiffness of the limbs).
• Long-term use can produce movements of the face (tardive dyskinesia) and, rarely, of the arms or legs.
Compared to the older drugs they seem:
• less likely to cause Parkinsonian side-effects (see above)
• less likely to produce tardive dyskinesia.
• more likely to produce weight gain
• more likely to produce diabetes
• more likely to give you sexual problems.
They may also help 'negative symptoms' (poor motivation, lack of interest, poor self-care), on which the older drugs have very little effect. Some people find the side effects less troublesome than those of the older medications.
Some of the newer ‘atypical’ antipsychotics.
|Tablets |Trade Name |Usual daily dose (mg) |Max. daily dose (mg) |
|Amisulpride |Solian |50-800 |1200 |
|Aripiprazole |Abilify |10-30 |30 |
|Clozapine |Clozaril |200-450 |900 |
|Olanzapine |Zyprexa |10-20 |20 |
|Quetiapine |Seroquel |300-450 |750 |
|Risperidone |Risperdal |4-6 |16 |
Clozapine: seems to be the only antipsychotic medication which works better than any of the others. It also seems to reduce suicidal feelings in people with schizophrenia.
It has many of the same side-effects as other newer antipsychotics, but can also make you produce more saliva.
It is different in that it seems to have very little, if any, effect on the dopamine systems which control movement, and so causes hardly any of the stiffness, shakiness or slowness that you can get with other antipsychotics. Although it does tend to make you drowsy, some people are prepared to put up with this because it makes them feel less sluggish than on the older antipsychotics. It also does not seem to produce the longer-term problem of tardive dyskinesia and can be used to help relieve this.
Side-effects
The main drawback is that it can affect your bone marrow, leading to a shortage of white cells. This makes you vulnerable to infection. If this happens, the medication is stopped at once so that the bone marrow can recover. So, if you take Clozapine you will need weekly blood tests for the first 6 months and 2 weekly blood tests after that. It can also cause weight gain, constipation, over-production of saliva and make epileptic fits more likely.
These problems mean that Clozapine is usually only suggested after at least two other antipsychotics have been tried. It is a difficult drug to monitor and can be difficult to take, but some people find that overall it gives them a much better quality of life.
‘Depot’ antipsychotics
The word ‘depot’ means that the medication is given not as tablets, but as an injection every 2 to 4 weeks. It releases the medication slowly over this time. The effects are generally the same as medications taken by mouth.
What's good about having a depot injection?
Unlike tablets, you only have to think about it once in a while. As there is someone else to remind you, it can be easier to remember to take than tablets.
What's bad about having depot injections?
• Nobody likes having injections – even though the pain is slight and doesn't last long.
• It takes a long time to know the effect of changing the dose. If the dose is changed, you may not know what the effect of this change is for several weeks or months – it can take 4 injections or so for the change to work its way through.
• If a particular dose is giving you side-effects, lowering it may make little difference for several weeks.
How well does medication work?
• About 4 in 5 people get help from them. They control the symptoms, but do not get rid of them. You have to go on taking the medication to stop the symptoms from coming back.
• Even if the medication helps, the symptoms may come back. This is much less likely to happen if you carry on taking medication, even when you feel well.
How long should I take an antipsychotic for?
This depends on a number of factors.
Schizophrenia
If you have had just one episode of schizophrenia, you have roughly 1 in 4 chance that your symptoms will not return after you get better. So you may well not need to carry on taking an antipsychotic.
For most people with schizophrenia, the symptoms will continue or come and go over the years. Some things to consider are:
• You may find that antipsychotic medication takes your symptoms away completely. It's more likely that they will just make the symptoms less intense and easier to cope with.
• As with any medication, you have to balance the help you get from it, against any side-effects it gives you.
• For many people the symptoms seem to come and go for no obvious reason – so there may be times when it is more helpful to take such medication, and times when you don't need it so much.
• If you have had more than one period of psychotic symptoms and stop the medication, the symptoms will usually return within 6 months.
• There is evidence that if major long-term problems are going to develop they do so in the first 5 years or thereabouts. So your doctor may feel that it is important to use medication to try and keep you well through these early years.
After reading this you will be asked to prepare materials on either Typical or Atypical antipsychotics. This should include:
Generic names
Mode of action
Effectiveness of treating positive/negative symptoms
Side effects
Research to support the use of the drugs
In our next lesson you will be asked to present your findings to other members of the class. There will then be exam questions on drug therapy.
You should use the table on the next page to take notes on both typical and atypical antipsychotics.
| |Typical |Atypical |
|Generic names | | |
|Mode of Action | | |
| | | |
| | | |
|Effectiveness in treating | | |
|negative/positive symptoms | | |
|Side effects |
| |
| |
| |
|Research |
|support |
| |
| |
|Challenging |
|points |
| |
| |
Cognitive behavioural therapy
CBT is now commonly used to treat patients with schizophrenia. It usually takes place for between 5-20 sessions, either in groups or an individual basis.
The aim of CBT involves helping patients to identify their irrational thoughts and trying to change them. This may involve argument or discussion of how likely the patient’s beliefs are to be true, and a consideration of less threatening possibilities. This will not get rid of the symptoms of schizophrenia but it can make patients better able to understand their thoughts and cope with them (Trowler et al., 2004)
HOW? Patients are helped to make sense of how their delusions and hallucinations impact on their feelings and behaviour. Just understanding where symptoms come from can be hugely helpful for some patients as it reduces the anxiety they experience, for example if they believe that the voices they are hearing are demons. Delusions are also challenged so that a patient can come to learn their beliefs are not based on reality.
Evaluation of CBT
Tarrier (2005) reviewed 20 controlled trials of CBT using 739 patients, finding persistent evidence of reduced symptoms, especially positive ones, lower relapse rates and speedier recovery rate of acutely ill patients. There were short-term benefits, however, with follow-ups needed to assess CBT’s long-term benefits.
More recent and methodologically sound meta-analyses of the effectiveness of CBTp as a sole treatment for schizophrenia suggests that its effectiveness may actually be lower than originally thought. One recent large-scale meta-analysis. Jahuar et al. (2014) performed a meta-analysis of 34 studies of CBT for schizophrenia. They concluded that CBT has a significant but fairly small effect on both positive and negative symptoms. However, even these small effects disappeared when symptoms were assessed ‘blind’ i.e. when assessors were unaware of whether the patient was in the therapy or control condition. Many studies of the effectiveness of CBT appear to have similar design problems and, in their meta-analysis, this uncertainty over whether non-drug therapies such as CBT really do offer superior outcomes to antipsychotic medication has led to conflicting recommendations even within the UK (Taylor and Perera, 2015). In England and Wales, NICE (2014) emphasise non-drug therapies such as CBT, whereas in Scotland, SIGN (2013) places more emphasis on antipsychotic medications This begs the question whether it should be used as a treatment if it only has a very small therapeutic effect.
Tarrier et al, (2000) suggests that CBT plus antipsychotics is effective in treating schizophrenia and more effective than drugs or CBT alone, supporting the case for combined treatments.
CBT is not suitable for all patients, especially those too disorientated, agitated or paranoid to form trusting alliances with practitioners.
CBT appears to be more effective when it is made available at specific stages of the disorder and when the delivery of the treatment is adjusted to the stage that the individual is currently at. For example, Addington and Addington (2005) claim that, in the initial acute phase of schizophrenia, self-reflection is not particularly appropriate. Following stabilisation of the psychotic symptoms with antipsychotic medication, however, individuals can benefit more from group based CBT. This can help normalise their experience by meeting other individuals with similar issues. Research has consistently shown that it is individuals with more experience of their schizophrenia and a greater realisation of their problems that benefit more from individual CBT.
CBT has fewer side effects than antipsychotic drugs but is more expensive treatment, as training of CBT practitioners is essential for it to be effective. This is a very important factor to consider at a time when reduced health-care budgets are common.
Family therapy
Families can play an important role in helping a person with schizophrenia recover and stay well. Family therapy is a form of psychotherapy based on the idea that as family dysfunction can play a role in development and maintenance of schizophrenia, altering relationships and communication patterns within dysfunctional families, and especially lowering levels of expressed emotion, should help schizophrenics to recover. Therefore the treatment involves the whole family not just the member with schizophrenia.
HOW? The main aims of the therapy are:
• Psychoeducation – helping the person and their carers to understand and be better able to deal with the illness.
• Forming an alliance with relatives who care for the person with schizophrenia.
• Improve positive and decrease negative forms of communication
• Increase tolerance levels and decrease criticism levels between family members
• Decrease feelings of guilt and responsibility for causing the illness among family members.
• Encouraging relatives to set appropriate limits whilst maintaining some degree of separation when needed.
Family therapy forms part of an overall treatment package and is commonly used in conjunction with routine drug treatment and outpatient clinical care. Therapists meet regularly with the patient and family members, for usually between 9 months and a year. The focus is on reducing symptoms and allowing family members to develop skills that can be continued after the therapy has ended. It also helps to reduce stress levels and increase the chances of the patient complying with medication. This combination of benefits tends to result in a reduced likelihood of relapse and re-admission to hospital.
Evaluation of family therapy
McFarlane et al. (2003) reviewed available evidence to find that family therapy results in reduced relapse rates, symptom reduction in patients and improved relationships among family members, which leads to increased well-being for patients. This suggests that family therapy is an effective treatment, with an indication that better family relationships are the key element.
Pharoah et al. (2010) reviewed the evidence of 53 studies published between 2002 and 2010 to investigate the effectiveness of family intervention. Studies chosen were conducted in Europe, Asia and N.America. The studies compared outcomes from family therapy to ‘standard care’ alone. The researchers concentrated on studies that were randomised controlled trials (RCTs) for the effectiveness of family therapy and concluded that there is moderate evidence to show that family therapy significantly reduces hospital readmission over the course of a year and improves quality of life for patients and their families.
The main results (comparing the 2 groups) were:
• Mental state – overall impression was mixed. Some studies reported an improvement in overall mental state because of family therapy, others didn’t.
• Compliance with medication – the use of family intervention increased patient’s compliance with medication.
• Social functioning – although appearing to show some improvement on general functioning, family intervention didn’t appear to have much of an effect on more concrete aspects such as living independently or employment.
• Reduction in relapse and readmission – There was a reduction in the risk of relapse and a reduction in hospital admission during treatment and in the 24 months after.
Pharoah et al (2010) meta-analysis established that family therapy can be effective in improving clinical outcomes such as mental state and social functioning. Pharoah noted that results of different studies were inconsistent and that there were problems with the quality of some evidence. Overall the evidence base for family therapy is fairly weak.
This treatment option may be particularly useful for younger patients who still live at home with their families and for patients who lack insight into their illness or cannot speak coherently about it, as family members may be able to assist here. Family members have lots of useful information and insight into a patient’s behaviour and moods and are often able to speak for them.
The Schizophrenia Commission (2012) estimates that family therapy is cheaper than standard care by around £1000 per patient over 3 years, suggesting it is a relatively cost-effective treatment.
A study by Garety et al (2008) failed to show any better outcomes for patients given sessions of family therapy compared to those who simply had carers but no family therapy. Individuals in both groups were found to have unexpectedly low rates of relapse, contrasting markedly with the rates found in the ‘no carer’ group. The researchers found that most of the carers in this study displayed relatively low rates of expressed emotion, which may reflect widespread cultural changes in carers’ knowledge and attitudes of schizophrenia. Garety et al suggest that, for many people, family intervention may not improve outcomes further than a good standard of treatment as usual.
Token economies
Token economies are a behaviourist approach to the management of schizophrenia, where tokens are rewarded for demonstrations of desired behavioural change. The technique is mainly used with long-term hospitalised patients to enable them to leave hospital and live relatively independently within the community. Token economies are particularly aimed at changing negative symptoms, such as low motivation, poor attention and social withdrawal.
The technique uses operant conditioning principles, where patients receive reinforcements in the form of tokens immediately after producing a desired behaviour e.g. getting dressed in the morning, making the bed (secondary reinforcer). The tokens can then later be exchanged for goods or privileges e.g. sweets, cigarettes, or a walk outside the hospital (primary reinforcer)
Evaluation of token economies
McMonagle & Sultana (2000) conducted a meta-analysis of token economy programmes involving 110 schizophrenics, finding slight evidence for improved mental state, especially with negative symptoms. This gives a degree of support to the treatment. However, there is limited support for the effectiveness of this method when random allocation to conditions was used in the research.
Token economies work best in unison with antipsychotic drugs and other personalised psychotherapeutic treatments. This should therefore not be seen as a “treatment” for schizophrenia in itself because they do not address symptoms, but perhaps as a technique to increase adaptive behaviours. (Dickerson et al. 2005)
A strength of token economies is that they can be tailored to meet the individual requirements of different patients, as the technique uses the same principles but to target different behaviours, this means that the technique has flexibility, allowing it to be used in a variety of settings.
A problem with token economies is desirable behaviour becomes dependent on being reinforced; upon release in the community, reinforcements cease, leading to high re-admittance rates.
Token economies are also not favoured by all clinicians, due to perceptions that participation in them is humiliating and that their benefits do not generalise to real-life settings. This raises ethical concerns with the use of token economies for patients as they are almost seen as ‘lab rats’ within a psychiatric institution
The importance of an interactionist approach in explaining and treating schizophrenia; the diathesis - stress model.
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The interactionist approach acknowledges that there are biological, psychological and societal factors in the development of schizophrenia. Biological factors include genetic vulnerability and neurochemical and neurological abnormality. Psychological factors include stress, for example, resulting from life events and daily hassles, including poor quality interactions in the family.
The diathesis-stress model
Diathesis means vulnerability.
In this context stress simply means a negative psychological experience.
The diathesis-stress model says that both a vulnerability to schizophrenia and a stress-trigger are necessary in order to develop the condition. One or more underlying factors make a person particularly vulnerable to developing the disorder but the onset of the condition is triggered by stress.
• In early diathesis-stress models, diathesis was seen as entirely genetic the result of a single ‘schziogene’. However, it is now clear that many genes appear to increase genetic vulnerability slightly (Ripke et al. 2014). Modern views of diathesis also include a range of factors beyond the genetic, including psychological trauma- so trauma is the diathesis not the stressor.
• In the original diathesis-stress model of schizophrenia, stress was seen as psychological in nature, in particular related to parenting. However, modern definitions of stress include anything that is a risk for triggering schizophrenia.
This can include such things as family dysfunction, substance abuse, critical life events etc. Much recent research had focused on cannabis use as a risk factor for triggering schizophrenia. However, most people do not develop schizophrenia after smoking cannabis so it seems there must be more than one vulnerability factors.
Treatment according to the interactionist model
Effectiveness of treatments is dependent upon factors such as cost, relapse rates, degree of side effects etc. as well as symptom reduction. Researchers normally compare different treatment options to assess the efficiency of each treatment.
However, research indicates combination treatments, where more than one treatment is administered simultaneously to patients, are generally most effective. This is reflective of the interactionist model of using both biological and psychological treatments.
• Which particular combination of treatments is best is affected by each patient’s individual circumstances and needs- for example, family therapy will only suit schizophrenic’s who have problems with dysfunctional family relationships and who have a great deal of contact and interaction with their families.
• Generally, treatment with antipsychotics is given first to reduce symptoms, so that psychological treatments will then have greater effect, though antipsychotics will generally still be given while these treatments are administered. It is unusual to treat schizophrenia using psychological therapies alone.
Evaluation of the interactionist approach
There is evidence to support the dual role of vulnerability and stress in the development of schizophrenia.
Tienari et al. (2004) followed 19,000 children adopted from Finnish mothers with schizophrenia. Their adoptive parents were assessed for child-rearing style, and the rates of schizophrenia were compared to those in a control group of adoptees without any genetic risk.
← They found that a child-rearing style characterised by high levels of criticism and conflict and low levels of empathy were implicated in the development of schizophrenia but only for the children with high genetic risk but not in the control group.
← This suggests that both genetic vulnerability and family-related stress are important in the development of schizophrenia-genetically vulnerable children are more sensitive to parenting behaviour. This is strong direct support for the importance of adopting an interactionist approach to schizophrenia, including hanging on to the idea that poor parenting is a possible source of stress.
There is also support for the usefulness of adopting an interactionist approach from studies comparing the effectiveness of combinations of treatments and biological treatments alone. As Turkington et al (2006) points out it is not really possible to use combination treatments without adopting an interactionist approach. outcomes and therefore highlight the importance of an interactionist approach.
Tarrier et al. (2004) randomly allocated 315 patients to a medication+ CBT group, medication+ supportive counselling group or a control group (medication only). Patients in the 2 combination groups showed lower symptom levels than those in the control group, although there was no difference in rates of hospital readmission. Studies like this show that there is a clear practical advantage to adopting an interactionist approach in the form of superior treatment outcomes.
Although combining therapies increases the cost of treatment, the greater effectiveness of treatment can make combination therapies more cost effective in the long term.
Questions
1. Explain what is meant by the terms diathesis and stress as they apply to schizophrenia (2)
2. Outline and evaluate the diathesis - stress model of schizophrenia (16)
3. Explain what is meant by the term token economy (2)
4. Discuss two therapies used to treat schizophrenia (16)
5. Outline the use of antipsychotic drugs to treat schizophrenia (6)
6. Describe and evaluate biological explanations of schizophrenia (16)
7. Briefly outline one or more cognitive explanations of schizophrenia and give one limitation of these explanations (6)
8. Explain what is meant by reliability and validity associated with the classification and/or diagnosis of schizophrenia (16)
9. Explain what is meant by positive symptoms in schizophrenia (2)
10. Outline the nature of hallucinations and delusions (6)
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From our activity on evaluation in the classroom make sure you have three evaluation points - this can include supportive research and general evaluation points.
Family interaction evaluation
addition, hallucinations, loss, deficit syndrome’,
Atypical, Atypical, motivation, resistant, atypical drugs
The Dopamine Hypothesis
The Revised Dopamine Hypothesis
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