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Disorders

Characteristics of Disorders Anxiety,

Psychotic and AffectiveExplanations and treatments of one

Disorder Schizophrenia

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Characteristics of Disorders

Anxiety Disorders

Anxiety disorders give a continuous feeling of fear and anxiety which is disabling and imposes on daily functioning. They can be triggered by something that may seem serious or trivial to others; they may even be triggered by non-existent threats that nevertheless seem very real to the person themselves. In the UK in 2000 the Office of

National Statistics reported that 1 adult in 6 in the UK had a neurotic disorder anxiety or depression. Anxiety disorders encompass many different disorders including panic disorders, OCD, Phobias, Post Traumatic Stress Disorder and other generalised anxiety disorders.

PHOBIAS

Phobias essentially are a definite, persistent fear of a particular object or situation. A stimulus such as a snake, dog, and a man’s beard will provoke an immediate response, which may be similar to a panic attack. The individual may experience physical symptoms such as shortness of breath or palpitations, and may feel intense terror and begin to lose control. Even though the individual knows that the fear is irrational they can still not control the immense terror the stimulus produces. This response alone is not enough to be actually diagnosed with a phobic disorder, if the fear disrupts the individuals day to day life, over a period of time then the disorder may be diagnosed.

DSM-IV Classification for specific phobia Marked and persistent fear that is

excessive or unreasonable Exposure to phobic stimulus provokes

immediate anxiety response (fight or flight mechanism)

The person recognises the fear as excessive and unreasonable

The phobic situation is avoided The phobia disrupts the person’s normal

life The phobia has lasted more than 6

months in people under 18 years of age. The phobia can start at any age as they

are often learned or occur after traumatic experiences.

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Affective Disorders -Bipolar We all have different moods; sometimes we are happy and sometimes we are sad, and

these are natural responses to events in our lives. However, you will see that the characteristics of mood or affective disorders are disabling moods. This means that the disorder is so disabling that it prevents the individual from leading a normal life, at work socially or within their family, which would cause them to be diagnosed with depression or bipolar disorder. Bipolar is when moods alter between manic episodes and depression. These changes can be months or years apart or can be on a daily basis.

DSM-IV Classification for bipolar

Mania is described in the DSM as a period of distinct elevated, expansive or irritable mood :

inflated self-esteem or grandiosity – think you can conquer the world!

decreased need for sleep (e.g., feeling rested after only 3 hours of sleep – or even days without sleep)

more talkative than usual or feeling pressure to keep talking

racing thoughts or thoughts that seem to jump from topic to topic

distractibility (e.g., attention is easily drawn to unimportant details)

increased goal-directed activity (either socially, at school or work, or sexually) or psychomotor agitation

excessive involvement in pleasurable activities that have a high potential for negative consequences (e.g., going on buying sprees, foolish business investments, promiscuous sex).

Extreme manic episodes can sometimes lead to such psychotic symptoms as delusions and hallucinations

DSM classification for depression: Insomnia most nights or continuous sleep

day and night Fidgeting or lethargy Tiredness & withdrawal from social

interaction Feelings of guilt or worthlessness and self

blame Inability to concentrate Recurrent thoughts of death, planning

suicide.

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Data appears to show that bi polar exists in between 1% (for the most serious of cases) and 5% of the average population with less serious symptoms of bipolar. It is equally prevalent in men and women and across all cultural groups. The onset of full symptoms generally occurs in late adolescence or young adulthood. Diagnosis is based on the person's self-reported experiences, as well as observed behavior. Episodes of abnormality are associated with distress and disruption and an elevated risk of suicide, especially during depressive episodes. In some cases, it can be a devastating long-lasting disorder. In others, it has also been associated with creativity, goal striving, and positive achievements.

Genetic factors contribute substantially to the likelihood of developing bipolar disorder, and environmental factors are also implicated. Bipolar disorder is often treated with mood stabilizing medications and, sometimes, other psychiatric drugs. Psychotherapy also has a role, often when there has been some recovery of the subject's stability. In serious cases, in which there is a risk of harm to oneself or others, involuntary commitment to a mental hospital may be used. These cases generally involve severe manic episodes with dangerous behavior or depressive episodes with suicidal possibilities. There are widespread problems with social stigma, stereotypes, and prejudice against individuals with a diagnosis of bipolar disorder. People with bipolar disorder exhibiting psychotic symptoms can sometimes be misdiagnosed as having schizophrenia, another serious mental illness.

Characteristics of Psychotic Disorders - Schizophrenia

Schizophrenia is a mental disorder characterized by a disintegration of the process of thinking and of emotional responsiveness. It most commonly manifests as auditory hallucinations, paranoid or bizarre delusions, or disorganized speech and thinking, and it is accompanied by significant social or occupational dysfunction. The onset of symptoms typically occurs in young adulthood, with a global lifetime prevalence of around 1.5% of the population. Diagnosis is based on the patient's self-reported experiences and observed behaviour.

Genetics, early environment, neurobiology, psychological and social processes appear to be important contributory factors; some recreational and prescription drugs appear to cause or worsen symptoms. Current psychiatric research is focused on the role of neurobiology, but this inquiry has not isolated a single organic cause. As a result of the many possible combinations of symptoms, there is debate about whether the diagnosis represents a single disorder or a number of disorders.

Unusually high dopamine activity in the neurotransmitters of the brain has been found in people with schizophrenia. The mainstay of treatment is antipsychotic medication; this type of drug primarily works by suppressing dopamine activity. Dosages of antipsychotics are generally lower than in the early decades of their use. Psychotherapy, and vocational and social rehabilitation, are also important. In more serious cases—where there is risk to self and others—involuntary hospitalization may be necessary, although hospital stays are shorter and less frequent than they were in previous times.

Psychosis is the general term for disorders that involve a loss of contact with reality. It covers many disorders, which may involve delusions (hallucinations that cause a person to lose their

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sense of what is really happening in their life). It can therefore lead to withdrawal from the outside world as the person becomes more confused and disorientated. Psychotic disorders tend to be characterised by delusions and disorganised speech or behaviour, they include all types of schizophrenia.

DSM-IV Classification for schizophrenia:

Delusions – believe things about their life that are unreal for example think they are Jesus

Auditory and Visual Hallucinations (20% have visual hallucinations but 60% auditory) Auditory are through to be the most destructive as they are the most convincing – they are also often menacing commanding the person to carry out violent acts –often toward themselves but occasionally towards others!

Disorganised speech – does not make logical sense

Disorganised behaviour – uncoordinated or not related to obvious normal responses (opening or un-opening buttons or playing with hair continuously etc)

Paranoia – think people or organisations are out to kill or harm them in some way

Social or occupational dysfunction At least six months duration No other explanation such as

developmental disorders or medication side effects like drug taking

Age of onset average for 17 – 21 for men and 21 – 30 for women.

There is a continuum of seriousness of symptoms – from 10% not responding to any treatment, often resulting in suicide to 25% managing to live relatively normal lives.

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Biological explanations of schizophrenia

Biological explanations blame our biology (nature) for the cause of schizophrenia, although there are many different assumptions for schizophrenia, the biological one has received the most research support to date. Two of these explanations are genetic factors and the dopamine hypothesis.

Firstly, family studies, Gottesman and Shields found individuals who have schizophrenia have biological relatives who are similarly affected more often than non-biological relatives, the greater the degree of genetic relatedness, the greater the risk. Genes appear to play an important role in schizophrenia because the concordance rate is higher in MZ twins than DZ twins. However environmental factors must also be important as the concordance rate is not 100% in monozygotic twins. Therefore, just because we are ‘predisposed’ by our genetics does not mean we necessarily will develop the disorder of schizophrenia. It appears that there is some interaction with the environment which triggers the gene to be turned on in some people and not in others. This interaction is explained by the ‘stress diathesis’ model which says stressful events may be the trigger to biological changes.

A second biological explanation is the dopamine hypothesis. Dopamine is a neurotransmitter that operates within the brain. The dopamine hypothesis states that messages from neurons that transmit dopamine fire too easily or too often, leading to the characteristic symptoms of schizophrenia. Evidence to support this comes from patients who do not suffer with psychosis or hallucinations and have been given excess dopamine for other conditions like Parkinson’s and have been found to develop the symptoms of schizophrenia. Secondly, antipsychotic drugs (dopamine antagonists) block the activity of dopamine in the brain, and so reduce the stimulation of the dopamine system, eliminating hallucinations and delusions in many patients.

Schizophrenics are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing. Comer (2003) states that dopamine neurons play a key role in guiding attention, therefore disturbances may well lead to the problems relating to attention, perception and thought, found in people with schizophrenia.

Biological Treatments for Schizophrenia:

Biological treatments work on the assumption that the disorder is caused by chemical imbalances in the brain such as too much dopamine being taken up by the neurotransmitters. Therefore drugs are aimed at reducing the function of these neurotransmitters so reducing hallucinations.

Antipsychotics

Antipsychotics are usually recommended as the first-line treatment for treating the symptoms of an acute schizophrenic episode. Antipsychotics work by blocking the effect that dopamine has on the brain.

Antipsychotics can usually reduce feelings of anxiety or aggression within a few hours of use, but they may take several days or weeks to reduce other symptoms, such as hallucinations or delusional thoughts.

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Antipsychotics can be taken orally (as a pill) or given as an injection. Several 'slow release' antipsychotics are available whereby you only need to have one injection every two to six weeks.

You may only need to take antipsychotics until your acute schizophrenic episode has passed. However, their long-term use is usually recommended to prevent further acute schizophrenic episodes occurring.

There are two main types of antipsychotics:

typical antipsychotics - the first generation of antipsychotics that were developed during the 1950s, the older antipsychotics (which also went by the name of neuroleptics), were medicines like haloperidol or chlorpromazine which cause serious side effects (see below).

atypical antipsychotics - a newer generation of antipsychotics that were developed during the 1990s. The first of these, clozapine, has been shown to be more effective than other antipsychotics, although the possibility of severe side effects of leukaemia is 8 times greater when taking the medication (loss of the white blood cells that fight infection). They require that patients be monitored with blood tests every one or two weeks.

The side effects of typical antipsychotics can include:

drowsiness,

shaking,

trembling,

muscle twitches, and

spasms.

Side effects of both typical and atypical antipsychotics can include:

weight gain,

blurred vision,

constipation,

lack of sex drive, and

dry mouth.

Evaluation of biological explanations:

The biological model is today the strongest model for explaining the aetiology of schizophrenia. However the science is still in its early stages of development and drugs developed from biological theories about causes do not ‘cure’ the disorder, they only treat the symptoms. A great advantage of the biological model, however, is that it places the blame for the disorder on genetic or

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chemical imbalances in the body which takes the blame for the disorder away from the individual and the parents of the individual, reducing the experiences of guilt and social scapegoating. In the past parents have often felt blamed for their parenting style causing schizophrenia.

A major problem for the dopamine hypothesis is that drugs are used to treat schizophrenic patients by blocking dopamine activity can actually increase it, as neurons struggle to compensate for the sudden deficiency. Haracz (1982), reviewed post mortem studies of schizophrenics, found that most of those studied who showed elevated dopamine levels had received antipsychotic drugs shortly before death. Post-mortems of schizophrenics who had no medication had normal levels of dopamine. In addition, the development of sophisticated neuroimaging techniques, such as, PET scans has allowed researchers to investigate dopamine activity more precisely, these neuro-imaging studies have, as yet, failed to provide convincing supporting evidence of altered dopamine activity in the brains of individuals with schizophrenia making this an unreliable hypothesis (Copolov and Crook,2000).

We also know from the studies on genetics that although we need the abnormal gene to have schizophrenia, having the gene does not necessarily mean we will get schizophrenia, meaning this is a poor predictor of the disease developing. It only helps us know that we have an increased probability of developing the disorder if we have the gene. This means that biological explanations are reductionist as they do not explain why monozygotic twins do not have a 100% concordance rate in developing the illness.

On the other hand the biological models explanation that genetic factors are involved is highly reliable and scientific. Biological explanations can help us identify people early who may be at risk so that they can try and reduce their possible risk factors of developing the disorder (for example avoiding very stressful situations). Also the biological explanation has provided very useful medications which help some patients live almost normal lives without suffering from debilitating hallucinations, even though, as yet, they cannot cure the disorder. The biological model is still hampered by our lack of knowledge about brain structure and function but is probably the model that does offer the best chance of a cure for this disorder in the future.

Another problem with the biological model is that we cannot be sure that schizophrenia is only one specific condition. It may be made up of a cluster of different conditions which have similar symptoms. Evidence for this comes from the fact that 25% of people who are diagnosed with schizophrenia do not respond to any drug therapy at all and a small percentages of people appear to spontaneously recover. Until we are able to develop a scientific test we cannot be sure that all patients diagnosed with schizophrenia do have the same disorder.

Drug therapy is also controversial because many of the drugs have such sever side effects. Patients often want to stop taking their medication due to problems with the side effects. For example drugs cause sedation, slurring of speech and a shuffling walk. For this reasons over 50% of patients stop taking their drugs in the first year. There is also an 8% increased change of developing Acute Myeloid Leukaemia on some modern schizophrenic drug therapies like Clozapine. This can raise ethical dilemmas when patients may be at risk of harming themselves or others due to their disorder and do not wish to take their drugs (to what extent should a patient be forced to take a drug?).

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There are also alternative explanations for schizophrenia which say the problem may lie during early childhood rather than in genetic predisposition. Psychodynamic theorists say there is evidence of a correlation between early childhood disruption, poor parenting and the onset of schizophrenia. However these family behaviours may also be explained genetically through children being raised by a schizophrenic mother or father. Data from correlation does not prove cause and effect. Cognitive and behavioural explanations also say that at least some of the problem behaviours and problem cognitions maybe due to faulty learning rather than being biologically determined.

Schizophrenia: Psychological / Behavioural explanations

Classical / Operant and Social Learning Theory

Any behavioural explanation of schizophrenia has to incorporate fundamentals of conditioning (classical and operant) and/or social learning theory. Behaviourists would look not only at how patients develop faulty behaviour patterns but also at how they learn faulty thinking!

The behavioural explanation suggests that schizophrenia is a consequence of faulty learning. Children who do not receive reinforcement early in their lives will put larger attention into irrelevant environmental cues. For example: paying attention to the sound of a word rather than its procedural meaning. This behaviour will eventually appear ‘weird’ or strange to others and so will generally be avoided. These strange behaviours may be rewarded by attention and sympathy and so they are reinforced. This can continue until the behaviour becomes so strange that they are then labelled as schizophrenic. Eventually the behaviour and psychological state deteriorates into a psychotic state.

The principles of operant conditioning are used to explain the schizophrenic’s bizarre behaviour. The behavioural explanation claims that abnormality is learned dysfunctional behaviour. Punishment may lead the child to withdraw and consequently they are labelled as odd. The bizarre behaviour is rewarded with attention and this positive reinforcement encourages them to conform to the label according to Scheff’s labelling theory (1966). Consequently, more exaggerated versions of the disorder are displayed and so schizophrenia develops. Although this has some face validity it lacks conviction as a causal explanation. It is probably more relevant to the maintenance rather than the cause of the disorder as it does not explain how the bizarre behaviour originates. Nor does it account for the severity of the disturbance. Genetic and cognitive explanations may better account for the severity of schizophrenia, and these are ignored as the behavioural explanation is reductionist and environmentally deterministic, only accounting for nurture.

Behaviourists argue that learning plays a key role in the development of schizophrenia. One suggestion is that early experience of punishment may lead the child to retreat into a rewarding inner world. Others then label them as ‘odd’ or ‘strange’.

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Scheff’s (1966) labelling theory suggests that individuals labelled in this way may continue to act in ways that conform to this label. Bizarre behaviour is rewarded with attention, and becomes more and more exaggerated in a continuous cycle before being labelled as ‘schizophrenic’:

Behaviourists explain the fact that schizophrenia runs in families as a function of social learning. Bizarre behaviour by parents is copied by children. Parents then reinforce this behaviour and the behaviour becomes progressively more unusual, until eventually the child acquires the label of being ‘schizophrenic’.

Ullman and Krasner (1969) observed mental health nurses in their interactions with patients and concluded that staff actually reinforce schizophrenic behaviour by giving more attention to these patients.

Cognitive explanations for schizophrenia:

Beck explains the development of the disorder as due to the interplay of genetic, environmental, psychosocial and cognitive factors. The cognitive model of schizophrenia can, therefore, be considered a holistic approach to the disorder.

Schizophrenia patients generally score poorly on all cognitive tasks, although there is individual variation in each person’s profile of cognitive difficulty. The following are common areas of neurocognitive impairment in schizophrenia:

Scheff’s Labelling theory (1966)

Punishment

Withdrawal

Labelled as odd

Conforming to label

Reinforced by attention

Supporting research

Liberman (1982) suggests that if a child receives little or no social reinforcement early on in life (e.g. because of parental neglect), the child will, instead of focussing on social stimuli in the normal way, attend to inappropriate and irrelevant environmental cues (e.g. the sound of a word rather than its meaning). As a result, the child’s verbal and other behavioural responses will eventually appear to be bizarre. Those who observe the child’s behaviour will either avoid it or respond erratically. This will reinforce the bizarre behaviour, eventually deteriorating into a psychotic state.

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Intellectual Ability

Verbal Memory

Non-verbal Memory

Recognition

Motor Skills

Language

Attention

Processing Speed

The cognitive model explains schizophrenia in terms of the stress diathesis model. This means that genetic abnormalities create a predisposition for the development of the disorder, but the disorder only develops in response to stress. The more stressors accumulate, the greater the risk a susceptible person is. A person with a predisposition to develop schizophrenia has limited cognitive resources due to the biological factors outlined above. However, as long as life is relatively stress-free they are able to compensate for this and their behaviour appears normal.

Psychological Treatments for Schizophrenia:

At the current time there is no cure for schizophrenia and there are only drug therapies to help reduce symptoms of hallucinations or paranoia. Because schizophrenia has been through to be the main cause of schizophrenia, biological treatments and cures have been the main concentration of research. However research into different forms of psychological therapy have also taken place. We know that schizophrenia causes a distortion in thoughts and speech and also a loss of reality. We also know that it causes other forms of dysfunctional behaviour. Therefore a combination of cognitive and behaviour therapy is used to try and effect changes on these aspects of the condition. Today most schizophrenic patients will have a combination of therapies, for example drug therapy supported by cognitive behaviour therapy, although cost implications for therapies do effect the extent to which patients are given holistic care.

Cognitive-Behavioural Treatment of Schizophrenia: A Case Study

Bradshaw 1998

Cognitive-behavioural treatment (CBT) has rarely been applied as the primary treatment for the multiple, severe and persistent problems that characterize schizophrenia. However Bradshaw used CBT in the long-term outpatient care of a young woman with schizophrenia. Measures of psychosocial functioning, severity of symptoms, compliance with treatment and reductions in hospital visits were used to assess change over the 3- year treatment period and at 1-year follow-up. Results indicate considerable improvement in all outcomes.

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The case study of Carol:

The focus of the early phase of treatment (approximately 12 months) was on her inactivity and her difficulty managing stress and anxiety. Carol would spend much of her time in bed, watching TV and smoking. When she would consider doing some activity or was requested by her parents to do something, she would become anxious and hallucinations and delusions would increase. She would think that the task was too much for her and would withdraw to her room. She coped with the stress of her symptoms by apathy and withdrawal.

Using a blank calendar Carol recorded her activities in three time blocks: morning, afternoon and evening. She and the therapist reviewed the activities to identify what things improved or exacerbated her condition and to help Carol understand her reactions to different events.

Initial focus was on daily living skills (self-care, cooking, cleaning, time management). Exploration of previous interests and the use of an interest inventory were helpful in stimulating her interests and expanding the range of her activities. She had previous experience in arts and crafts and began to do paint by number paintings. This was followed by learning macramé and adding other activities such as bowling that could be done with other people. Mastery and pleasure ratings were later assigned to activities to evaluate the benefits of the activities and to identify cognitive distortions that minimised her sense of accomplishment and pleasure.

Stress management skills were developed in three ways. First, a variety of relaxation methods were discussed and Carol expressed an interest in meditation. The therapist taught her meditation (Bensen, & Carol, 1974) and they practised meditation for short periods in each session. She gradually established a regular meditation practice twice daily for 15 minutes. Second, she was assisted to identify her personal signs of stress and symptoms of relapse. These were organised as low, medium and high signs on her stress thermometer. She posted the thermometer on her door and recorded her "stress temperature" each day. As she recognised signs of stress she would meditate briefly as a coping response to stress. Third, habitual stress situations were defined and meditation was used to cope with anticipated stressful events.

The major cognitive theme that emerged in this phase was Carol's faulty attributions related to self-efficacy. She significantly underestimated or overestimated her ability to control others, events in the world and her own behaviour. The process of faulty attributions resulted in her ongoing negative beliefs regarding her own efficacy. Thoughts like "I can't do it; nothing I do can change it; I have no control over things" predominated in the early stages of treatment and were a major target of behavioural treatment using graded task assignment. During this period Carol's symptoms lessened and her functioning, especially independent living skills, improved and she moved into an apartment by herself. She had also developed skills in identifying and coping with stress and had experienced some increased sense of self-efficacy.

Carol started with a GPI of 30 (general psychological impairment scale) at the conclusion of the study her GPI score of 1 indicated only slight impairment. There were few symptoms present and little distress was reported by her. Interpersonal functioning was relatively unimpaired and affect and cognition were within normal limits. This shows that whilst Carol did have to take drug therapy to manage her condition, she still considerably improved her level of everyday functioning with the additional psychological therapy.

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Evaluation of Psychological Explanations and treatments:

The validity of the behavioural model is supported by the success of behavioural therapies used with schizophrenic patients. For example, Allyon (1968) also showed that schizophrenics have learned to make their own beds, comb their own hair etc. when given rewards for doing so when previously they could not perform these skills. However, psychological explanations probably best explain how schizophrenia symptoms are worsened or improved, but it do not explain where they came from in the first place and therefore will not offer a cure.

However, the success of training programmes in teaching new skills and reintegrating schizophrenics back into the community suggests that these are skills that schizophrenics failed to learn in the first place, which support behaviourist explanations. Bradshaw also successfully showed how symptoms can be successfully reduced by giving schizophrenics the skills they need to deal with their symptoms, together with increased self efficacy. This makes this psychological explanations highly useful to the understanding of how to treat schizophrenia to improve quality of life.

Some patients however, have some insight into their condition and are able to take part and co-operate in behaviour therapy sessions. However others are simply too ill to be able to respond to any form of behaviour therapy as their thinking and social skills are too disorganised.

The cognitive explanation is holistic and complete (and therefore less reductionist) than either the biological or behaviourist model as it includes both biological and environmental factors in its explanation. This enables us to understand why some individuals develop the disorder and some do not even though they may have the genetic disposition due to the stressors that they encounter in their different environments.

Psychological explanations do also however, have the disadvantage of putting blame on the individual, their family or their circumstances, implying that with the insight, motivation and support they can change. Some people would argue this is not ethical. On the other hand there are less ethical issues over behavioural treatments compared to biological ones as there are few side effects of behaviour therapy. However behaviour therapies are costly and time consuming compared to drug therapies which may be one reason why drug therapy is still the treatment of choice for most doctors.

Biological explanations are still more reliable and scientific however than behavioural or cognitive ones. For this reason, biological explanations still dominate and are hopefully going to be more useful in the future for helping cure the condition before it starts meaning that psychological therapies may not be necessary. Biological therapies are also the first line treatment for all patients with schizophrenia.

An ideal situation however, is to take a holistic approach to explanations and treatment. If we consider that the disorder is partly biological and partly environmental then those who have a predisposition to schizophrenia could be identified early and given psychological therapy to improve their skills and self efficacy and reduce their levels of stress, hopefully reducing the likelihood of schizophrenia then developing. This approach is supported by the stress diathesis model that says it maybe stress and a reduced ability to deal with stress which is the trigger for the disorder.

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