Schizophrenia Flashcards
Describe the characteristics of Schizophrenia
Kurt Schneider (1959) suggested categorising the symptoms of either schizophrenia or negative symptoms.
- Positive symptoms, in addition to normal behaviours .
- Hallucinations, are perceptions that are unreal. Many people with schizophrenia report auditory hallucinations. Hearing sounds/voices. But can also present themself in a sensory modality. Katheryn Lewandowski (2009), estimated that 20% of people w schizophrenia have tactile hallucinations, whereby they are perceiving sensations as if someone or something is touching their skin. Formication= insects crawling.
- Delusions, are beliefs that are unreal. They are usually experienced with no evidence to offer in support of the delusion. Most common= persecution and grandiosity. Delusions of persecution, are based on the idea that a person or a group want to harm the individual. eg, believing that the government organisation, like M15, are following you as they believe you are a threat.
Delusions of grandiosity suggest that the individual is special in some way; the individual believes they are powerful, have superior knowledge, or believe they are e particular person.
- Disordered thinking is often evident through examining the speech of those individuals with schizophrenia. Described as ‘ derailment’. The persons thoughts and discourse seem to jump from one topic to another, no logical flow of discussion, for no reason. Patients speech = muddled. Individuals with schizophrenia may also report that the voices in their head are not thier own.
- Negative symptoms.
- Alofi, poverty of speech, reduction in the amount of speech and lacking meaning.
- Avolition, people are unconcerned with something going on in their surroundings. They show no desire to participate in activiites, may even be one they love. Distinct lack of goal directed behaviour.
- Anhedonia, where an individual does not react appropriately to pleasurable experiences.
- Flatness of affect, individual has no emotion. Little/no facial emotions.
-Catatonic behaviour, issues can range from fast, repetitive, useless movements to little or no movements at all. May one for no purpose, eg, wondering in circles. Echopraxia may occur, this is when people with schizophrenia mimic the the movements of others around them.
A individual may also remain immobile, but others can move them.
What is the biological explanation of ‘ Dopamine hypothesis’ in Schizophernia?
The biological explanation of schizophrenia focuses on dopamine dysregulation and its effect on brain pathways. The initial dopamine hypothesis proposed that schizophrenia was caused by an excess of dopamine, leading to positive symptoms. Griffiths et al. (1968) found that increasing dopamine with amphetamines induced psychotic symptoms, like paranoid delusions, in non-schizophrenic participants. However, this explanation was later refined, as it was overly simplistic.
The discovery of dopamine receptor subtypes (D1-D5) highlighted that D2 receptors, found in the limbic system, are critical in understanding schizophrenia. The limbic system, involved in emotions and memory, contains key pathways where dopamine dysregulation impacts symptoms:
Mesolimbic Pathway: This carries dopamine signals from the ventral tegmental area (VTA) to the nucleus accumbens. Excess dopamine activity in this pathway causes positive symptoms, like hallucinations. Antipsychotic drugs reduce dopamine activity here, alleviating these symptoms.
Mesocortical Pathway: This pathway carries signals from the VTA to the frontal lobe, regulating cognition and emotional responses. Kenneth Davis et al. (1991) noted reduced dopamine activity in D1 receptors in the frontal lobe, leading to negative symptoms, such as cognitive impairments and lack of motivation.
In summary, dopamine dysregulation in these pathways explains both positive and negative symptoms, providing a biological basis for schizophrenia.
Evaluate Dopamine Hypotheses as a biological explanation for Schizophernia
- Dopamine imbalances may be caused by genes. If dopamine imbalances are responsible for schizophrenia, the question then has to be what causes the dopamine imbalance? Many researchers believe that it may be a genetic predisopsition, and indeed twin and family studies indicate that there is some genetic basis for schizophrenia. Eg, the classic study involving Irving Gottesman et al (1991) looked at incidence of schizophrenia in cousins, grandchildren, half-siblings, paerents, siblings and non-identical twins. As genetics similary increased so did the probability of both individuals having schizophrenia. However, in 2014, the schizophrenia working group of the psychiatric genomics consortium reported that there were 108 genetic loci associated. So there is a genetic basis, not just a few abnorml dopamine genes.
- The role of serotonin. Dopamine is not the obly neurotransmitter implicated in schizophrenia. Serotonis, has also been identified to have a potential influence. Conventional antipsychotics have traditionally worked by primarly blockading the D2 receptor sites, but not all of those with schizophrenia benefit from these drugs. This suggests we cannot fully explain schizophrenia on its own.
- Dopamine- Cause or effect?
- Aklthough this hypothesis proposes that dopamine causes schizophrenia, it could also be proposed that schizophrenia causes the dopamine imbalances. Are the dopamine discrepanicies seen in some people with schizophrenia just another symptom of the disease? There is some hope, that as investigative techniques become less invasive, we will be able to conduct research that will be able to establish which comes first, a dopamine imbalance or schizophrenia?
- Research using PET scans hasnt yet been able to even detect differences in the dopamine activity of the brains of individuals with schizophrenia and those without. So it may be some time before we know forcertain if dopamine imbalances cause schizophrenia caused dopamine imbalances.
Apply the biological explanation of ‘Dopamine Hypothesis’ to a method of modifying behaviour, using drug treatments
One of the biggest benefits of using neurotransmitters such as dopamine to explain schizophrenia has to be its application to drug treatments. Phenzothiazine was the earliest type of antipsychotic drug and it revolutionaised psychiatry. It sedates the person and reduces symptoms of schizophrenia such as delusions and halluciantions by binding to dopamine receptors and blocking the build-up of dopamine. Prior to the introduction of phenothiazines in the 1950s, schizophrenia was generally considered to be untreatable. Apart from incerction in mental institutions, previous treatments include insulin shcok. and ECT. Both of these are controversial.
- One of the first controlled pieces of research investigating the effectivenss of phenothiaziness, reported that 75% of those given the drug were ‘much improved’ compared with only 25% of those recieving a placeb0. In addition, 48% of htose in the placebo condition were consdered to have gotten worse compared to none in the phenothiazine condition.
What is the biological explanation of ‘ Structural Abnormalities in Schizophrenia?’
Structural abnormalities in the brain are a key biological explanation for schizophrenia. Three major abnormalities are enlarged ventricles, cortical atrophy, and reversed cerebral asymmetry.
Enlarged Ventricles: Enlarged ventricles refer to fluid-filled cavities in the brain that are larger in individuals with schizophrenia. This is linked to a loss of brain tissue and impaired cognitive or emotional functioning. Weinberger et al. (1979) used CAT scans to show that individuals with chronic schizophrenia had significantly larger ventricles than controls, particularly in those with long-term symptoms. Similarly, Andreasen (1988) found a 20–50% increase in ventricle size using MRI scans, supporting the idea that ventricular enlargement is a hallmark of schizophrenia.
Cortical Atrophy: Cortical atrophy involves the loss of neurons in the cerebral cortex, leading to reduced brain mass and widened grooves (sulci). Research indicates that 20–35% of individuals with schizophrenia experience this. Antonova Vita et al. (1988) used CAT scans to confirm cortical atrophy as a common feature, though its severity varies based on factors like sex and ventricular enlargement rather than family history.
Reversed Cerebral Asymmetry: Normally, the left hemisphere of the brain is slightly larger than the right. In schizophrenia, this asymmetry is often reversed, which may contribute to language deficits like alogia (poverty of speech). Luchins et al. (1979) found increased reversals in the frontal and occipital lobes of individuals with schizophrenia, especially in those without cortical atrophy.
In summary, these structural abnormalities highlight the neurological basis of schizophrenia and show how brain dysfunction contributes to the disorder’s symptoms
Evaluate Structural Abnormalities as a biological explanation for Schizophenia.
The biological explanation of schizophrenia focuses on structural abnormalities in the brain, such as enlarged ventricles, cortical atrophy, and reversed cerebral asymmetry. While this explanation has strong scientific support, there are notable limitations regarding causation, specificity, and the role of other influences.
Strengths:
Reliable Evidence: Research consistently links structural abnormalities to schizophrenia. For example, McCarley et al. (1999) found that enlarged ventricles are one of the most reliable findings in schizophrenia studies. Similarly, Flashman and Green (2004) confirmed this link using advanced brain imaging techniques, adding to the validity and reliability of the explanation.
Scientific Credibility: The biological explanation is underpinned by objective and measurable methods, such as MRI and CAT scans, which enhance its scientific rigor. These tools allow researchers to identify abnormalities like ventricular enlargement or cortical atrophy without relying on subjective interpretations, providing robust evidence.
Practical Applications: Understanding structural abnormalities has informed medical treatments for schizophrenia, such as antipsychotics, which target dopamine dysregulation (linked to brain changes). These insights support the biological approach as a foundation for developing interventions.
Weaknesses:
Causation Issues: A major limitation is the difficulty in establishing whether structural abnormalities cause schizophrenia or are a result of the disorder. For example, Kenneth Lyon et al. (1981) argued that long-term use of antipsychotic medication could lead to enlarged ventricles, suggesting that the abnormalities might be an effect of treatment rather than a cause of the illness.
Lack of Specificity: Structural abnormalities are not unique to schizophrenia. Paul Roy et al. (1998) found similar brain changes in individuals with other disorders, such as bipolar disorder and schizoaffective disorder. This challenges the biological explanation’s ability to distinguish schizophrenia from other conditions.
Influence of Other Factors: Subtle variables, such as age, sex, and symptom severity, influence structural abnormalities. For instance, ventricular enlargement and cortical atrophy may worsen with age or in more severe cases, suggesting that these changes may not directly result from schizophrenia but reflect other aspects of the disorder.
Debate on Neurodevelopment vs. Neurodegeneration: It remains unclear whether structural abnormalities arise due to early neurodevelopmental issues (e.g., prenatal complications) or later neurodegenerative processes. Mathalon et al. (2003) proposed that both factors might contribute, complicating the explanation and reducing its simplicity.
Reductionism: The biological explanation focuses on brain abnormalities while overlooking psychological and social factors, such as trauma or family dynamics, which may play a significant role in schizophrenia’s onset and progression. This narrow focus may limit its explanatory power.
Conclusion:
The biological explanation of schizophrenia provides significant insights into the disorder, particularly through reliable findings on structural abnormalities and their links to symptoms. However, its inability to establish clear causation, the overlap of abnormalities with other conditions, and the neglect of psychological and environmental influences weaken its explanatory power. A more comprehensive understanding of schizophrenia would require integrating biological, psychological, and social approaches, as proposed by the diathesis-stress model.
What is the individual differences explanation of ‘Psychodynamic Approach in Schizophrenia?’
The psychodynamic approach explains schizophrenia as stemming from early developmental issues, particularly fixation, regression, and the role of parenting.
Fixation: Freud suggested that schizophrenia originates from fixation during the oral stage of psychosexual development, where satisfaction is gained from oral stimulation (e.g., feeding). If a child experiences too much or too little stimulation in this stage, they may become fixated, leaving them vulnerable to psychological issues later in life.
Regression: Freud also proposed that excessive stress in adulthood might cause a person to regress to the oral stage. As this stage lacks a developed ego, the individual’s behavior becomes dominated by the id, leading to disordered thinking.
Losing Touch with Reality: Regression results in the id operating without control from the ego or superego, causing the person to lose touch with reality. This explains symptoms like hallucinations and delusions, as desires and fantasies dominate their perception of the world.
Schizophrenogenic Mother: Frieda Fromm-Reichmann (1948) introduced the idea of the schizophrenogenic mother, describing a parent who is overprotective yet cold and rejecting. This contradictory behavior creates confusion and stress, stifling the child’s emotional development and increasing their vulnerability to schizophrenia.
This explanation emphasizes the role of early experiences, unconscious conflict, and parenting in the development of schizophrenia.
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Evaluate Psychodynamic Approach as an Individual Differences explanation for behaviour in Autism
Individual difference explanations, such as the psychodynamic approach, highlight the role of early experiences, family dynamics, and unconscious conflicts in the development of schizophrenia. These explanations are valuable but face significant criticism for being outdated, reductionist, and lacking empirical support.
Strengths:
1.Historical Influence:
The psychodynamic explanation was an important early attempt to understand schizophrenia. Concepts like the schizophrenogenic mother, proposed by Frieda Fromm-Reichmann (1948), brought attention to the role of family relationships and early emotional experiences in mental health.
2.Focus on Nurture:
By emphasizing the role of early experiences, the psychodynamic approach offers an alternative to biological theories, addressing the environmental factors that might contribute to schizophrenia.
Weaknesses:
1.Freudian Concepts Are Outdated:
Psychodynamic explanations rely on Freudian theories of fixation and regression, which are considered speculative and unscientific. Freud himself admitted he lacked evidence, stating, “I myself do not know whether there is more delusion in my theory than I should like to admit.”
2.Failure to Produce Effective Treatments:
Freud believed schizophrenia could be treated with psychoanalysis. However, studies such as Strupp et al. (1977) found that psychoanalytic therapies were largely ineffective for schizophrenia, as individuals often lack the emotional awareness needed for such approaches. Biological therapies, like antipsychotics, have been far more successful.
3.Inconsistent Evidence for the Schizophrenogenic Mother:
Research into the schizophrenogenic mother has been criticized for lacking consistency. Jacob Kasanin (1934) found maternal overprotection in only 33% of cases, which does not strongly support the theory. Moreover, research may have been biased, as early studies were not conducted “blind” to the hypotheses.
4.Overlooks the Role of Genetics:
Psychodynamic theories focus on nurture but ignore biological evidence. Adoption studies, such as Heston (1966), show that 10.6% of individuals with a biological mother with schizophrenia developed the disorder, compared to 0% in control groups. This highlights the importance of genetics, which the psychodynamic approach fails to account for.
5.Reductionist:
By focusing only on early relationships and family dynamics, the psychodynamic explanation oversimplifies the causes of schizophrenia. Modern approaches recognize that schizophrenia results from a combination of biological, psychological, and social factors.
Conclusion:
While individual difference explanations provide an important perspective on the role of family dynamics and early experiences, they are weakened by outdated concepts, limited evidence, and failure to consider biological factors. As such, these explanations
What is the Individual explanation of ‘Cognitive Approach in Schizophrenia?’
- Hallucinations – Morrison (1998) suggested that hallucinations occur when triggers (e.g., sleep deprivation) cause individuals to misinterpret internal thoughts as external voices. Negative emotional responses (e.g., anxiety, shame) reinforce these voices, creating a vicious cycle.
- Negative Symptoms – Beck et al. (2008) linked negative symptoms (e.g., avolition) to the cognitive triad, where individuals have negative beliefs about themselves, their future, and their experiences. Deficits in information processing reinforce these symptoms.
- Lack of Preconscious Filters – Frith (1979) proposed that individuals with schizophrenia struggle to filter irrelevant sensory information, leading to confusion and difficulty processing multiple interpretations of events. This contributes to disorganised thinking.
- Compromised Theory of Mind – Frith (1992) argued that schizophrenia involves deficits in understanding one’s own and others’ thoughts, leading to:
1.Disorders of willed action (explaining negative and disorganised symptoms).
2.Disorders of self-monitoring (causing hallucinations, e.g., hearing voices).
3.Disorders of monitoring others’ thoughts (leading to paranoia and delusions of persecution).
Evaluate Cognitive approach as an individual explanation for Schizophrenia
-Supporting Research – Barch et al. (1999) compared individuals with schizophrenia to a control group using the Stroop test. Those with schizophrenia were slower and made more mistakes, suggesting they have impaired attentional filters. This supports the cognitive explanation that faulty thought processing contributes to schizophrenia.
-Reductionist Account – Frith’s theory explains schizophrenia through cognitive deficits caused by dysfunction in brain areas like the frontal cortex. However, this is reductionist as it oversimplifies the disorder, ignoring biological and environmental factors that may contribute to its development.
-Not a Comprehensive Theory – The cognitive approach explains some symptoms, like disorganised thinking and delusions, but does not account for negative symptoms (e.g., avolition) or movement issues. It may only describe the effects rather than the root causes of schizophrenia, making it an incomplete explanation.
-Integrated Model of Schizophrenia Howes & Murray (2014) propose a more holistic model, suggesting that genetic vulnerabilities and environmental stressors (e.g., poverty) increase dopamine, leading to cognitive deficits. This suggests cognitive dysfunction is part of a larger interaction of biological and environmental factors rather than a sole cause.
-Conclusion – While the cognitive approach provides valuable insights, it is reductionist and incomplete. A more holistic approach considering biological and environmental influences gives a better understanding of schizophrenia.
What is the Social Psychological explanation of ‘Dysfunctional families’ in Schizophrenia?’
One social psychological explanation of schizophrenia is the role of dysfunctional families, specifically through double bind theory and expressed emotion (EE).
Double bind theory, proposed by Bateson et al. (1956), suggests that schizophrenia can develop due to repeated exposure to conflicting messages within the family. In a double bind situation, a child receives contradictory verbal and non-verbal messages, making it difficult for them to respond appropriately. For example, a mother may tell her child she loves them while acting cold and distant. This creates confusion because the child cannot ‘metacommunicate’ (comment on the contradiction). Over time, this leads to feelings of paranoia, anxiety, and eventually symptoms of schizophrenia, such as delusions and disorganized thinking.
Another explanation is expressed emotion (EE), introduced by Brown (1959). EE refers to the level of criticism, hostility, and emotional over-involvement from family members towards an individual with schizophrenia. High EE environments are characterized by excessive negative comments, rejection, and controlling behavior, which increase stress and the likelihood of relapse. Key features of high EE include critical comments, hostility, emotional over-involvement, low warmth, and low positive regard. These factors can overwhelm the individual, making it harder for them to manage their symptoms.
Overall, these theories suggest that dysfunctional family dynamics can contribute to both the development and maintenance of schizophrenia through stress, confusion, and negative emotional environments.
Evaluate ‘dysfunctional families’ as a social psychological explanation for Schizophrenia.
- Support for Expressed Emotion (EE).Vaughn and Leff (1976) found that 53% of individuals in high EE families relapsed within 9 months, compared to only 12% in low EE families.Suggests that high EE environments contribute to relapse, supporting the role of family dysfunction.
- Causation Issue (Double Bind)
Liem (1974) found no significant differences in communication styles between parents of schizophrenic vs. non-schizophrenic sons.Instead, parents may change their behavior in response to having a schizophrenic child.Suggests dysfunctional communication may be an effect, not a cause. - Real-World Applications. Family therapy, which aims to reduce EE in households, has been shown to lower relapse rates (Pharaoh et al., 2010).Supports the idea that modifying family interactions can improve outcomes for schizophrenia patients.
- Biological Explanations Overlooked.Genetic research (Schizophrenia Working Group, 2014) found 108 genetic loci associated with schizophrenia.Suggests schizophrenia is largely influenced by biology, rather than family dynamics.However, the diathesis-stress model argues that dysfunctional families may act as a trigger for those with a genetic predisposition.
- Holistic Approach Possible.Combining social and biological factors (e.g., genetics + EE) offers a more complete explanation.Family dysfunction alone cannot fully explain schizophrenia, but it plays a role in triggering and maintaining symptoms.
- Conclusion:
Social psychological explanations provide useful insights into environmental influences, but lack strong causal evidence and ignore genetic factors. A diathesis-stress approach is more comprehensive, acknowledging both biological vulnerability and family stressors.
What is the Social Psychological Explanataion of ‘Sociocultrual Factors’ in Schizophrenia?
Sociocultural factors explain schizophrenia by examining the impact of environment and social influences on mental health. Three key sociocultural factors include urbanicity, social isolation, and ethnicity/discrimination.
- Firstly, urbanicity refers to the higher prevalence of schizophrenia in urban areas compared to rural areas. Studies, such as those by Faris and Dunham, have found increased rates of schizophrenia in densely populated cities. This may be due to environmental stressors like overcrowding, pollution, and social adversity, which contribute to increased vulnerability to mental illness.
- social isolation has been linked to schizophrenia. Individuals with schizophrenia often have fewer social connections, which can be both a cause and consequence of the disorder. Faris (1934) suggested that a lack of social interaction leads to withdrawal, reinforcing symptoms. A longitudinal study by Jones et al. (1994) found that individuals diagnosed with schizophrenia were more likely to have experienced social isolation from early childhood.
- ethnicity and discrimination play a role, particularly in the overdiagnosis of schizophrenia among Afro-Caribbean individuals in the UK. Studies (e.g., Ineichen, 1984) show that they are more likely to be compulsorily admitted to psychiatric hospitals. The increased diagnosis rate cannot be explained by genetic factors alone, as studies in the Caribbean do not show the same trends (Mahy et al., 1999). Instead, migration stress and systemic discrimination in psychiatry likely contribute to this overrepresentation (Harrison et al., 1988).
Evaluate sociocultrural factors as a social psychological explanation for Schizophrenia
-One strength of urbanicity as an explanation is that research consistently shows higher schizophrenia rates in urban areas. This suggests that factors like overcrowding, pollution, and stress contribute to the disorder. However, McKenzie (2002) argued that urban living may not necessarily increase stress but could provide better access to healthcare, meaning diagnoses are more frequent rather than schizophrenia itself being more common. This challenges the direct link between urbanicity and schizophrenia.
-A major issue with urbanicity is the cause-and-effect problem. The social drift hypothesis suggests that rather than cities causing schizophrenia, individuals with schizophrenia are more likely to move to urban areas due to unemployment and financial struggles. Supporting this, Pedersen and Mortensen (2001) found that strong social networks in urban environments reduced the likelihood of developing schizophrenia. This suggests that urban living alone does not directly cause the disorder, but other factors play a role.
-Social isolation is another key factor, as people with schizophrenia often have fewer social connections. Research by Jones et al. (1994) found that individuals diagnosed with schizophrenia were more likely to have been socially isolated from childhood. However, it is unclear whether isolation causes schizophrenia or whether early symptoms, such as withdrawal, lead to isolation. This makes it difficult to establish a clear causal relationship.
- Ethnicity and discrimination also play a role, particularly in the overdiagnosis of schizophrenia in Afro-Caribbean individuals in the UK. Some researchers argue that discrimination within psychiatry, rather than actual increased prevalence, explains higher diagnosis rates. For example, some psychiatrists may misinterpret cultural differences as symptoms of schizophrenia. However, Jane Boydell (2001) found that the risk of schizophrenia increases in areas where fewer people of the same ethnic background live. This suggests that social factors, such as lack of community support and discrimination, contribute to schizophrenia.
- Overall, while social psychological factors provide useful insights into schizophrenia, they struggle with cause-and-effect issues and cannot fully explain the disorder. Biological factors, such as genetics and dopamine dysfunction, may interact with social factors, meaning a more holistic approach is needed.
What is the method of modifying behaviour ‘Antipsychotic drugs’ for Schizophrenia?
There are numerous antipsychotic medications that fall broadly into 2 cocepts; Conventional Antipsychotics and Atypical Antipsychotics.
- Conventional antipsychotics; these are ‘typical’ antipsychotics, first developed inn the 1950s. Conventional such as chloropromazine work by affecting nuerotransmission, specifically blocking the action of the neurotransmitter dopamine. Chloropromazine blocks other dopamine receptor subtypes D1,D2,D3,D4 and D5.
- It works by; after the presynaptic neuron releases dopamine into tje synapse, the recpetor sites on the postsynaptic neuron are blockaded by chloropamzine. Reducing activity in the post synapti neuron. Initially it causes a rise in the amount od dopamine secreted, hpwever it then drops because it is depleted and the amount of dopamine is the synapse decreases. Lower levels of dopamine in the synapse leads to a decreas ein neural activity, this decrease of dopamine in the mesolimbic pathway is said to be responsible for a decline of posotive symptoms such as hallucinations.
- Atypical Antipsychotics; eg, Clozapine, ‘newer’, have been developed since the 1990s. They work by acting as a dopmine antagonist, but the precise mechanism with which atypical antispychotics work is not yet clear. Aripiprazole is a newer atypical antipsychotic that is a dopamine antagonist slowing down dopamine transmission in the limbic system, but is also a parcial aganoist in other parts of the brain.
- Differences; some report thst stypicsl antipsychotics are differnt from conventional as they receive fewer dopamine D2 receptor sites and at more D1 and D4 receptor sites. A well as this, the time they occupy the D2 recpetor sites is differnt. Phillip Seeman 2002, reports of the ‘fast off’ theory. Proposing that atypical antipsychotics bin more loosely to the D2 receptor sites than the coventional antipsychotics. Meaning that the blockade has a theraputic effect.
Evaluate the method of modifying behaviour ‘Antiopsychotic Drugs’ for Schizophrenia in terms of Effectiveness, Ethical and social implications
Antipsychotic drugs are widely used to manage schizophrenia by reducing symptoms such as hallucinations and delusions. These drugs can be evaluated in terms of their effectiveness, ethical concerns, and social implications.
-One strength of antipsychotic drugs is their effectiveness. Research by Cole et al. (1964) found that 75% of patients who took conventional antipsychotics showed improvement compared to only 25% in the placebo group. Atypical antipsychotics, such as clozapine, have been found to be even more effective, especially for treatment-resistant schizophrenia. However, the effectiveness of these drugs is limited by non-compliance. Rettenbacher et al. (2004) found that only 54.2% of patients fully complied with their medication, which reduces the overall success of the treatment.
-A key ethical issue with antipsychotic drugs is their severe side effects, such as tardive dyskinesia and Parkinsonism, which can significantly impact quality of life. This raises concerns about whether the benefits outweigh the risks. Additionally, Thomas Szasz (1960) argued that antipsychotics act as chemical straitjackets, keeping patients under control rather than truly helping them. This suggests that the use of these drugs could violate patient autonomy and raise ethical concerns about informed consent.
- In terms of social implications, antipsychotics have revolutionized schizophrenia treatment by reducing the need for asylums and allowing patients to live in the community (Lawrie, 2011). This has improved quality of life and reduced the financial burden on healthcare systems. However, a major social concern is the risk of violence associated with non-compliance. Tiihonen et al. (2009) found that stopping medication was linked to a 37-fold increase in suicide risk, and the UK’s NCSH (2015) reported that 29% of homicides committed by individuals with schizophrenia involved patients who had stopped taking their medication. This highlights the importance of ensuring adherence to treatment.
- Overall, while antipsychotic drugs are effective in reducing symptoms and improving social outcomes, they come with ethical concerns regarding side effects and autonomy. Additionally, non-compliance remains a major issue, affecting both effectiveness and social consequences.
What is the method of modifying behaviour ‘Cognitive behavioural Therapy’ for Schizophrenia?
In the 1950s, CBT was developed by Aaron Beck and Albert Ellis, used to treat psychological behaviours such as depression.
- Irrational Thinking. A major symptom of schizophrenia is disordered thinking. The purpose of CBT is to help an individual consider and orgaise their disordered thoughts in a rational way. CBT helps to make the client aware of the connections between their disordered thinking and illness. These techniques can be used to deal with posotive symptoms of schizophrenia and making the client more self-reliant with their illness.
- Key components of CBT for Schizophrenia. Laura Smith et al (2003( has identified the key treatment components when using CBT for schizophrenia.
- Engagement Strategies.
Preliminary sessions are used to provide the oppurtunity to talk at length about potential worries and symptoms that are of particular concern to the client. During this stage, the therapist will try to develop a rapport with the client, which is important as client may have negative experiences with other therapists. THe therapist and client discuss any ‘natural coping strategies’ the client is using to manage their symptoms.
- Psycho-education. This stage serves 3 main functions. First it decastastrophies and normalises the experience of psychotic symptoms, offering alternative explanations of the clients experienceof their symptoms. The client hten increases their own understanding of the context in which their symptoms occur. Then the therapist can further access the clients understanding of their symptoms and illness.
-Cognitive Strategies,the client may be asked to keep a thought diary where they ercord how they felt, what they did and what they thought about the particular event. And, to record differnt views on the event, whcich are then discussed with the therapist.
- Behavioural skills training. A range of effective behavioural strategies can be taught, such as relaxation, activity scheduling, distraction and problem solving. These are useful in not only coping with residual symptoms not managed by mediaction but also any possible secondary symptoms or anxiety or depression. Problem solving= 5 steps. 1- identify a problem 2. generate possible solutions. 3. evaluate alternatives. 4. decide on a solution. 5. evaluate the outcome
- Relapse prevention strategies, the therapist and the lcient identify early warning indicators of relapse. These include the client identifiying thoughts, behaviours and feelings they experienced before becoming unwell. They are also asked to assess how they get on with others and what others may have noticed about them. The therpaist and client then discover plans that could be employed when these indicators are obserevd, including what the client would say to their family and friends, what their options are for support and what things they can do to do help themselves.
Evaluate the method of modifying behaviour ‘Cognitive behavioural Therapy’ for Schizophrenia in terms of Effectiveness, Ethical and social implications.
Cognitive Behavioural Therapy (CBT) is a psychological treatment for schizophrenia that aims to help patients challenge and manage their delusions and hallucinations. It can be evaluated in terms of effectiveness, ethical concerns, and social implications.
- One strength of CBT is that research supports its effectiveness. Kuipers et al. (1997) found that 50% of patients receiving CBT improved, compared to only 31% in a standard care group. This suggests that CBT is effective in reducing symptoms when used alongside medication. However, some studies contradict this finding. Jauhar et al. (2014) found that CBT only had a small effect on symptoms, raising doubts about its long-term impact. Additionally, Tarrier et al. (2004) found that after 18 months, patients who received CBT showed no greater improvement than those who received only standard care. This suggests that CBT’s benefits may be short-term rather than long-lasting. Bentall et al (1994) suggests cognitive therapy may be most effective for patients experiencing their first episode. It may not be suitable for everyone, those who get the most use out of CBT are those who want to get better and change their behaviour. A issue with these studys is that there is a lack of blind trials, which could be a potential cofounding variable.
- Finally, effectivness may be enhanced by the fact that the sample used in CBT studies are already biased towards having less severe symptoms and an increased willingness to work to overcome their illness.
- A key ethical issue with CBT is that it could be a negative experience for clients. Being diagnosed with schizophrenia is already distressing, and having to challenge one’s own beliefs in therapy could add to this stress. Kuipers et al. (1997) found that some patients found therapy helpful, but others felt that it was not a useful approach. This suggests that while CBT can benefit some, it may not be suitable for everyone. Additionally, psychiatrists may limit access to CBT based on their own beliefs. Kingdon and Kirschen (2006) found that some psychiatrists did not refer patients to CBT because they believed they would not benefit. This raises concerns about fairness and patient autonomy.
- In terms of social implications, CBT is not equally available to all patients. A 2014 audit by the Royal College of Psychiatrists found that the percentage of schizophrenia patients offered CBT varied from 67% to just 14% across different NHS trusts. This suggests that access to CBT is inconsistent, contradicting NICE guidelines that state all schizophrenia patients should have access to it. However, CBT is cost-effective in the long run. Kuipers et al. (1998) found that while CBT has an initial cost, it reduces the need for future psychiatric services, saving money over time. Despite this, NHS budgets often prioritise short-term costs over long-term benefits, meaning access remains limited.
- Overall, while CBT is effective for some schizophrenia patients, its impact may be short-term, and ethical and social barriers limit its availability. A combination of CBT and medication may be the most effective approach for long-term treatment.
