Schizophrenia Flashcards
(37 cards)
What is schizophrenia?
When is the typical onset?
How common is it?
-psychotic mental illness characterized by a loss of reality, often with a breakdown of personality
-usually appears in late adolescence or early adulthood, with a peak onset between 25-30 years
-often appears earlier in men than in women, with twice as many men diagnosed between ages 15-24
-affects approximately 1% of the population
Outline positive and negative symptoms and schizophrenia
-positive symptoms involve an excess or distortion of normal functions, including hallucinations and delusions
Hallucinations:
-false perceptions
-most common example is auditory hallucinations, where one or more voices instruct the person to do certain things or make negative comments
Delusions:
-false beliefs, including delusions of:
Control: Belief that their thoughts or actions are controlled by an external force, often attributed to spirits or radio transmitters
Grandeur: Belief in having extraordinary powers or importance (e.g., thinking they’re Jesus Christ)
Persecution: Belief that others want to harm, threaten, or manipulate them (e.g., thinking they’re being spied on)
-negative symptoms involve a loss of normal function
-e.g. speech poverty (reduced speech fluency) and avolition (lack of motivation)
-impacts daily life and social interaction
Outline reliability and validity in terms of schizophrenia
Reliability:
-consistency of a diagnosis
-consistency across different psychiatrists = inter-rater reliability
-a diagnosis is reliable if psychiatrists reach the same conclusion independently
Validity:
-accurately measuring what is intended
-for schizophrenia, it questions if diagnostic tools provide the correct diagnosis
Outline Rosenhan’s (1973) study
-aimed to see how situational factors affect schizophrenia diagnoses
-8 pseudopatients pretended to have auditory hallucinations, claiming to hear voices saying “empty,” “hollow,” and “thud”
-were admitted to 12 different psychiatric hospitals, where the staff never recognised their sanity
-average stay of 19 days before they were released once they had proven their sanity
-reveals a lack of reliability and validity in psychiatric diagnosis
-staff interpreted normal behaviours as symptoms of mental illness
-highlights influence of situational factors and questions the DSM’s effectiveness
Outline and evaluate comorbidity in the context of schizophrenia
-refers to the presence of more than one disorder alongside a primary diagnosis
-e.g. having both schizophrenia and a personality disorder
-overlapping symptoms might lead to misdiagnosis
-so raises questions about the validity of classifying both conditions
Strength - research support
-Buckley et al. (2009) found that approximately 50% of patients with schizophrenia also have depression
-47% have schizophrenia and substance abuse issues
-29% have schizophrenia and PTSD
-23% have schizophrenia and OCD
-shows that schizophrenia often coexists with other mental illnesses
Outline and evaluate culture in the context of schizophrenia
-Harrison et al. (1984) found that individuals of West Indian origin were over-diagnosed by white doctors in Bristol due to ethnic bias
-Copeland et al. (1971) found that when patients were described to psychiatrists, 69% of US psychiatrists diagnosed them with schizophrenia, whereas only 2% of British ones did
-suggests symptoms of ethnic minorities may be misinterpreted
-hence ethnicity can influence diagnostic outcomes
-raises concerns about the reliability of schizophrenia diagnoses
-furthermore, hallucinations may be culturally acceptable in some African cultures
-may lead to potential misinterpretation by psychiatrists from different backgrounds
-Escobar (2012) noted that White psychiatrists might over-interpret symptoms in Black patients due to cultural differences in language and mannerisms, as well as stereotypes about mental health in Black communities
-therefore, greater attention to cultural factors in psychiatric diagnosis is essential
Outline and evaluate gender bias in the context of schizophrenia
-it is argued that DSM diagnostic categories often diagnoses one gender more than the other
Strength - research support
-Broverman et al. (1970) found that US clinicians associated mentally healthy ‘adult’ behavior with ‘male’ behavior
-leads to women being perceived as less mentally healthy if they didn’t conform to these standards
-suggests androcentrism
-Loring and Powell (1988) showed that psychiatrists diagnosed 56% of patients who were described as male or not described by gender with schizophrenia
-compared to only 20% for female patients
-however, this bias was not evident among female psychiatrists
-indicates that both patient and clinician gender influence diagnosis
Limitation - clinicians may overlook that males often exhibit more negative symptoms and substance abuse
-in contrast, females have better recovery rates and lower relapse rates
-further affects diagnostic validity
-furthermore, differences in predisposing risk factors between genders can impact vulnerability levels
-explains disparities in the onset of schizophrenia
Outline and evaluate symptom overlap in the context of schizophrenia
-considerable overlap between symptoms of schizophrenia and other conditions, like bipolar disorder
-share positive symptoms (e.g. delusions) and negative symptoms (e.g. avolition)
Strength - research support for the influence of symptom overlap on reliability and validity of diagnosis
-Ellason and Ross (1995) noted that individuals with dissociative identity disorder (DID) exhibit more schizophrenic symptoms than those diagnosed with schizophrenia
-lowers validity of schizophrenia’s classification and diagnosis
-furthermore, a patient may be diagnosed with schizophrenia according to the ICD, while the DSM might classify them as bipolar
-suggests schizophrenia and bipolar disorder may not be distinct but potentially one condition
Limitation - research contradicts influence of symptom overlap on reliability and validity of diagnosis
-Serper et al. (1999) found that despite significant symptom overlap between schizophrenia and cocaine abuse, accurate diagnoses were still possible
-suggests that symptom overlap doesn’t always undermine diagnostic validity
Limitation - symptom overlap can delay appropriate treatment
-Ketter (2005) highlighted that this is due to the confusion caused by symptom overlap leading to misdiagnosis
-results in increased suffering and higher suicide rates
Strength - useful real world applications
-Ophoff et al. (2011) identified genetic overlap
-found that three of seven genes located on chromosomes associated with schizophrenia were also linked to bipolar disorder
-suggests the potential for developing gene therapies that could treat multiple disorders simultaneously
Outline and evaluate the genetic explanation of schizophrenia, including:
-specific genes
-schizophrenia appears to be polygenic
-requires several genes to work in combination
-aetiologically heterogeneous, as different studies have identified various candidate genes that may be involved in its development
-one study found that individuals affected by schizophrenia were more likely to have a defective version of a gene called PPP3CC
-this is associated with the production of calcineurin, a regulator of the immune system
-in contrast, another study identified a gene located on chromosome 5 linked to the disorder in a small number of extended families
-suggests that multiple genes may be implicated in the condition
-remains unclear whether it is one single gene or several working together that contribute to the illness
Limitation - genetic factors cannot be the sole explanation
-concordance rates for identical twins (MZ twins), range from 40% to 60%
-as these rates are not 100%, it indicates that genes cannot fully explain the disorder
-an individual may be predisposed to schizophrenia
-increases their risk without it being the only cause
-furthermore, it is biologically reductionist
-focuses solely on genetic factors and overlooks other biological or psychological influences, such as biochemistry or family dynamics
Limitation - difficult to separate the impact of nature and nurture
-both family and twin studies often involve individuals who share the same environment
-may inflate concordance rates, regardless of genetic factors
-possible that the high concordance rates among MZ twins arise due to more similar treatment than (DZ) twins or ordinary siblings
-not solely due to genetic influences
-furthermore, even MZ twins who are raised apart share the same prenatal environment
-could also serve as a confounding variable
-makes it challenging to differentiate between genetic and environmental influences
Limitation - family studies often rely on retrospective data when comparing individuals who have already been diagnosed with schizophrenia
-can be unreliable due to potential issues with memory and record accuracy
-however, prospective data is more reliable
-follows individuals over time
-can make comparisons before and after the onset of their condition
Limitation - not everyone with the disorder has a genetic predisposition
-two-thirds of people with schizophrenia do not have a relative with a similar diagnosis
-may be due to possibility of mutations in parental DNA, particularly in paternal sperm cells
-triggered by factors like radiation, poison, or viral infection
-furthermore, research support for the role of mutations
-found a positive correlation between paternal age and the risk of schizophrenia
-risk increases from around 0.7% for fathers under 25 to over 2% for fathers over 50
Limitation - research into the location of specific genes related to schizophrenia has not produced definitive results
-makes it impossible to understand the underlying mechanisms that connect genetic risk to the disorder
Outline and evaluate the genetic explanation of schizophrenia, including:
-inheritance
-evidence suggests that schizophrenia runs in families and is partly genetic
-family studies indicate that the closer the genetic relationship to someone with schizophrenia, the greater the chance of developing the disorder
Strength- research support for genetic link from family studies
-Gottesman (1978) reports that while the rate of schizophrenia in the general population is 1%, the chances of first-degree relatives (e.g. parent or sibling) developing the disorder is 12%
-40% likelihood for child to develop it if both parents have schizophrenia
-Tsuang et al. (1990) estimated that a first-degree relative of a schizophrenic is 5-20 times more likely to develop it
-shows that the closer the genetic relationship to someone with schizophrenia, the greater the chance of developing the disorder
Strength - research has found a much higher concordance rate in MZ twins in comparison to DZ twins
-Gottesman and Shields (1972) found a concordance rate of 42% for MZ twins and 9% for DZ twins
-furthermore, Cardno et al. (1999) conducted study in London using the Maudley Twin Register
-found 40% concordance rate in MZ twins, but 5.3% in DZ twins
-shows MZ twins have an increased risk of developing schizophrenia compared to DZ twins
-suggests a degree of heritability
Strength- research support from adoption studies
-Heston (1966) compared 47 children of schizophrenic mothers who had been fostered or adopted during the first month of their life with a control group of 50 children who had been raised in the same homes as these children
-none of the control group developed schizophrenia, but 17% of the children with schizophrenic biological mothers did
-these 47 children were far more likely to have been diagnosed with other psychological abnormalities and to be involved in criminal activities than the control group
-shows that sharing genetic material with a schizophrenic mother increased a child’s chances of having schizophrenia and other mental illnesses
-even when not being raised by her or sharing the same environment
Strength - adoption studies are more effective than family or twin studies
-adoption studies isolate the effects of environmental and genetic factors to look at levels of schizophrenia in adopted children
-can compare them with their biological and adoptive parents
Outline the dopamine hypothesis explanation of schizophrenia
-dopamine is an excitatory neurotransmitter in the brain
-original dopamine hypothesis stated that schizophrenia was caused by excessive activity of dopamine
-causes the neurons that respond to dopamine to fire too often and transmit too many messages
-may produce many symptoms of schizophrenia
-hypothesis suggests that schizophrenia is caused by a high density of dopamine receptors and by a high level of sensitivity in these receptors, leading to messages from neurons that transmit dopamine firing too easily or too often
-Snyder (1976) suggests that too much dopamine released into the synapse leads to the onset of schizophrenia
-original version of the hypothesis focuses on the possible role of high levels or activity of dopamine in the subcortex
-e.g. an excess of dopamine receptors in Broca’s area might be associated with poverty of speech and/or the experience of auditory hallucinations (Broca’s area is responsible for speech production)
-updated dopamine hypothesis emphasizes abnormal dopamine systems in the brain’s cortex, particularly the prefrontal cortex (responsible for thinking and decision-making)
-could explain the negative symptoms of schizophrenia
-more probable that both hyperdopaminergia and hypodopaminergia are correct explanations, as high and low levels of dopamine in different regions are implicated in schizophrenia.
-Davis et al. (1991) updated the theory as high levels of dopamine are not found in all schizophrenics
-the modern anti-schizophrenic drug clozapine, which has very little dopamine-blocking activity, works effectively against the illness
-suggests that high levels of dopamine in the mesolimbic dopamine system are associated with positive symptoms
-whereas high levels in the mesocortical dopamine system are associated with negative symptoms
Evaluate the dopamine hypothesis explanation of schizophrenia
Limitation - newer drugs such as clozapine are more effective than traditional ones
-they affect dopamine as well as other neurotransmitters, such as serotonin
-appears that several neurotransmitters may be involved in the development of schizophrenia
-therefore, the hypothesis is too simplistic
-furthermore, alongside dopamine and serotonin, some research has implicated glutamate
Strength - practical applications using research
-led to the development of effective treatment options, e.g. clozapine
-much more effective than neuroleptics at relieving schizophrenic behaviour
-suggests that psychiatrists understand the role of neurotransmitters when treating different types of schizophrenia
-improves the patient’s quality of life.
Strength - research shows that schizophrenics have more dopamine receptors
-more neurons firing may lead to an overproduction of messages
-autopsies show that schizophrenics generally have a larger number of dopamine receptors
-Owen et al.: have increased dopamine in the caudate nucleus and putamen in the left amygdala
-Falkai et al. (1988): increased amount of dopamine in the left amygdala
-supports presence of dopamine abnormalities in the brains of schizophrenics
-however, not all schizophrenics, especially those with negative symptoms, have dopamine abnormalities
-dopamine abnormalities seem to be associated more with positive symptoms
-suggests that it may only explain certain aspects or types of the illness
-Davis et al. (1991) argue that the diversity of types and symptoms in schizophrenia implies that other neurotransmitters involved
Limitation - difficulty establishing cause and effect
-uncertain whether high dopamine levels lead to schizophrenia, or whether schizophrenia increases dopamine levels the result of schizophrenia
-Lloyd et al. believe that if dopamine is a causative factor, it may be an indirect one mediated through environmental factors
-may be due to abnormal family circumstances can lead to high levels of dopamine, which triggers the schizophrenia symptoms
-suggests the differences in the biochemistry of schizophrenics could just as easily be an effect rather than a cause of the disorder, so conclusions about factors affecting schizophrenia must be drawn with caution
Outline the neural correlate explanation of schizophrenia
-suggests structural and functional abnormalities in specific brain areas are associated with development of schizophrenia
-evidence was originally limited to post-mortems on brains of schizophrenics
-but research now utilises non-invasive scanning techniques, such as fMRI
-provides a picture of the brain in action through magnetic fields and radio waves
-allows for a comparison of the functioning of the brains of individuals with schizophrenia with that of non-sufferers
-typically achieved by giving participants tasks like social cognition and thought processing
-as these are associated with functional abnormalities in schizophrenia
-proposes that schizophrenia is caused by enlarged ventricles (fluid-filled gaps between brain areas)
-enlarged ventricles are especially associated with damage to central brain areas and the prefrontal cortex
-often linked to negative symptoms
-Johnstone et al. (1976) found that schizophrenics had enlarged ventricles, while non-sufferers did not
-implies schizophrenia is related to a loss of brain tissue
Evaluate the neural correlate explanation of schizophrenia
Limitation - enlarged ventricles may only explain certain symptoms of schizophrenia
-Weyandt (2006) reported that enlarged ventricles are specifically associated with negative symptoms
-implies that this explanation cannot account for all symptoms and types of the illness
-furthermore, research into the role of enlarged ventricles remains inconclusive
-some non-schizophrenics have enlarged ventricles, and some schizophrenics that don’t
-challenges notion that schizophrenia is solely linked to loss of brain tissue
-as not every person with enlarged ventricles would suffer from the illness
Limitation - difficult to establish cause and effect relationship
-evidence suggests that schizophrenics who do not respond to medication are those with enlarged ventricles
-raises the possibility that enlarged ventricles may be an effect of long-term suffering from schizophrenia rather than a contributing factor to its development
Outline what antipsychotics are
Compare typical and atypical antipsychotics
-chemical treatment usually prescribed in the form of tablets, intravenous means, or both
-based on the dopamine hypothesis, which assumes that dopamine activity is linked to schizophrenia
-aims to treat psychotic illnesses, such as schizophrenia
-however, they do not cure the illness
-can only reduce the symptoms to imrpvoe wellbeing enable a degree of normal functioning to occur
Differences:
1. Atypicals have less of a risk of extrapyramidal (an area of the brain-particularly the motor function) side effects, such as tardive dyskinesia.
2. Research has indicated that atypicals have a beneficial effect on negative
symptoms.
3. Atypicals are suitable for a treatment-resistant schizophrenic patient, as they are more likely to work when typicals have failed.
Outline how typical antipsychotics treat schizophrenia
-primarily used to combat the positive symptoms of schizophrenia, such as delusions and hallucinations
-e.g. chlorpromazine
-reduces or blocks the effects and actions of dopamine
-hence reducing the symptoms of schizophrenia
-drugs like chlorpromazine are classified as dopamine antagonists
-because they bind to dopamine receptors, particularly the D2 receptors
-reduce their action without stimulating the dopamine system of the brain
-hence antipsychotic drugs can eliminate the hallucinations and delusions experienced by individuals with schizophrenia
-therefore, antipsychotic drugs like chlorpromazine work by blocking dopamine production through blocking the receptors in synapses that absorb dopamine
-ultimately normalise neurotransmission by ensuring that the postsynaptic cells receive less dopamine and cannot be affected by it
Summary:
- They are dopamine antagonists.
- They bind to the dopamine receptors, particularly the D2 receptors.
- In binding to the receptors, they block the stimulation of these receptors, preventing them from absorbing dopamine.
- This normalizes neurotransmission as the postsynaptic cells receive less dopamine
Outline how atypical antipsychotics treat schizophrenia
-atypical antipsychotics combat the positive symptoms of schizophrenia, and claimed to have beneficial effects on negative symptoms too
-e.g. clozapine
-these drugs work on the dopamine system, but they also block serotonin and glutamate receptors
-drugs like clozapine function by temporarily occupying the D2 receptors and then rapidly dissociating to allow normal dopamine distribution
-means the receptors still receive dopamine, but only in smaller amounts
-atypical antipsychotics are associated with lower levels of side effects, such as tardive dyskinesia, when compared to typical antipsychotics
-tardive dyskinesia is linked to various involuntary, repetitive movements caused by long-term or high-dose use of typical antipsychotics.
Summary:
- They work on dopamine receptors as well as serotonin and glutamate receptors.
- They occupy the D2 receptors.
- By doing so, they dissociate dopamine, allowing receptors to receive it in smaller amounts.
Evaluate the use of drugs to treat schizophrenia
Limitation - possible side effects with typical antipsychotics
-Kapur et al. (2000) estimate that between 60-70% of D2 receptors in the mesolimbic dopamine pathway must be blocked for typical antipsychotics to be effective
-unfortunately, this also means that a similar number of D2 receptors in other areas of the brain are blocked
-one of the side effects caused is tardive dyskinesia
-often results in patients discontinuing their medication
-furthermore, there are several dopamine pathways in the brain
-although blocking dopamine receptors in one of them can be beneficial, blocking receptors in other pathways may be harmful to the individual
Strength - atypical antipsychotics generally do not cause the movement issues often associated with typical antipsychotics
-e.g. atypical antipsychotics lower the chances of tardive dyskinesia
-Jeste et al. (1999) found that 30% of patients on typical antipsychotics for nine months experienced tardive dyskinesia, compared to only 5% of those on atypical antipsychotics
-furthermore, atypical antipsychotics may ultimately be more appropriate for treating schizophrenia due to fewer side effects
-can make patients more likely to continue with their medications
-allows them to experience greater benefits, and can treat wider range of symptoms
-however, atypicals are not completely free of side effects
-they are associated with risks like diabetes and cardiac arrest, which can be fatal
Limitation - research about which antipsychotics are more effective at treating schizophrenia is inconclusive
-meta-analysis by Leucht et al. (1999) found that two atypical drugs were only slightly more effective than typical drugs
-furthermore, the claim that atypical drugs effectively treat negative symptoms has received limited support
-suggests that atypicals may not necessarily be a superior treatment
Strength - drug therapy has proven effective in reducing the symptoms of schizophrenia, especially positive symptoms
-these drugs are relatively inexpensive to produce
-makes them cost-effective and easy to administer
-have had positive effects on many sufferers, enabling them to live relatively normal lives outside of institutional settings
-furthermore, estimated that fewer than 3% of people with schizophrenia in the UK live permanently in hospitals, largely due to medication
Antipsychotic drugs have also been shown to be more effective than placebos. Leucht et al. (2012) found that patients who continued their antipsychotic medication were only 27% likely to relapse, compared to a 64% relapse rate for those given a placebo. This demonstrates that drugs are successful in preventing relapse. However, these medications are only palliative, meaning they treat the symptoms of schizophrenia rather than providing a cure. If a patient stops taking their medication, their symptoms often return. From a psychodynamic perspective, critics argue that drugs address only the symptoms, not the underlying cause of the illness. This can lead to a “revolving door” phenomenon, where patients are discharged and re-admitted to the hospital repeatedly. Patients may take their medication, feel better, then mistakenly assume they are cured, stop their medication, and subsequently become ill again.
There are ethical concerns surrounding the use of antipsychotic drugs. When considering side effects, potential fatalities, and social consequences, a cost-benefit analysis may lean toward a negative outcome. In the USA, there was a significant out-of-court settlement awarded to a tardive dyskinesia sufferer under the Human Rights Act 1988. Additionally, some in the psychiatric community believe that the widespread use of antipsychotics is heavily influenced by the powerful interests of pharmaceutical companies, which profit substantially from their ongoing use.
Outline the schizophrenogenic mother as part of the family dysfunction explanation of schizophrenia
-proposed by Fromm-Reichmann (1948)
-suggests that schizophrenia arises from being reared by a cold and dominant mother
-both overprotective and rejecting
-although she may appear self-sacrificing, she uses the child to satisfy her own emotional needs
-hence individuals raised with this mothering style develop schizophrenia due to the confusion stemming from their mother’s contradictory behaviour
-modern day psychologists reject this theory
-Roff and Knight (1981) found a link between mothering style and schizophrenia
-but has also been found that it is also implicated in many other disorders
Outline the double-bind hypothesis as part of the family dysfunction explanation of schizophrenia
-proposed by Bateson (1956)
-suggests schizophrenia is a reaction to a parent presenting the child with a no-win situation, created by contradictory communication between tone of voice and content
-leads to social withdrawal in order to escape double-bind situations
-prolonged exposure to such interactions prevents the development of an internally coherent construction of reality
-this later manifests as typical schizophrenic symptoms, e.g. delusions and hallucinations, incoherent thoughts and speech, and paranoia
-e.g. a mother may say, “Come and give mummy a cuddle,” but then freezes when the child approaches and subsequently tells the child off for not being affectionate
Outline the expressed emotion as part of the family dysfunction explanation of schizophrenia
-families constantly criticise and be hostile towards recovering schizophrenics
-these individuals may react by relapsing and experiencing positive symptoms, such as delusions
-Kuipers et al. (1983) found that high EE relatives tend to 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 four times more likely to relapse than a patient whose family is low in EE
-suggests that schizophrenics have a lower tolerance for intense emotional situations, critical comments and family dynamics
-causes stress beyond the patient’s coping mechanisms and triggers an episode
Evaluate the family dysfunction explanation of schizophrenia
Double bind:
Limitation - little evidence of double-bind communication being associated with schizophrenia
-even when it occurs, it may be due to having a schizophrenic in the family rather than being the sole cause of the disorder
-lowers internal validity of theory
-however, Berger (1965) found that schizophrenics reported a higher recall of double-bind statements by their mothers than non-schizophrenics
-although it may not be reliable, as patients’ recall may be affected by their illness
Strength - research support
-Bateson (1956) reported case study in which a recovering schizophrenic was visited in the hospital by his mother
-he embraced her warmly, but she stiffened, and when he withdrew his arms, she said, “Don’t you love me anymore?”
-supports the idea of double-bind communication
-however, critics argue that this is weak evidence, as it is a case study
-lacks population validity and cannot be generalised
Limitation - contradictory research
-e.g. Liem (1974) found no difference in parental communication patterns in families with a schizophrenic child compared to families without a family member with schizophrenia
-furthermore, Hall and Levin (1980) found no difference between families with and without a schizophrenic member in the degree to which verbal and non-verbal communication were in agreement
Expressed emotion:
Strength - research support
-Hooley et al. (1998) conducted a meta-analysis of 26 studies
-found schizophrenics returning to a family environment with high EE experienced more than twice the average rate of relapse
-supports claim that EE could be responsible for a patient’s relapse
-furthermore, Kavanagh (1992) also conducted a meta-analysis
-found that the relapse rate for schizophrenics living with high EE families was 48%, compared to 21% for those who returned to low EE families
Limitation - overlooks role of individual differences
-not all patients in high EE homes relapse
-not all patients in low EE homes avoid relapse
-Altorfer et al. (1988) found that one-quarter of the patients they studied showed no physiological responses to stressful comments from their relatives
-hence vulnerability to the influence of high EE may be psychologically based
-furthermore, if not all patients are equally vulnerable to high levels of expressed emotion, then other factors must be involved
-suggests a more holistic approach would be better suited to explaining different factors affecting response to high EE
Family dysfunction:
Limitation - research in this area is correlational
-many studies show a link between family dysfunction and schizophrenia
-uncertain if family dysfunctions causes schizophrenia, or if having a family member with schizophrenia leads to these dysfunctions
-cause and effect cannot be established
-lowers internal validity
-furthermore, there is limited research support for family dysfunction as a direct cause of schizophrenia
-suggests it is more likely to be a maintenance factor
Limitation - these theories do not explain why some children in dysfunctional families do not develop schizophrenia
-implies it cannot be the only cause
-weakens validity of theories
-furthermore, it is more likely that individuals have a biological predisposition to schizophrenia
-diathesis-stress model suggests biological vulnerability combined with a harmful family environment may trigger the illness
-a single element of nurture alone is likely insufficient to cause the disorder
Outline cognitive deficits
-includes issues with attention, communication, and processing information
-affects perception of thoughts as inner speech
-schizophrenics often struggle to interpret others’ behaviour, which impacts social interactions
-difficulties in processing visual and auditory information may contribute to symptoms like reduced emotional expression, disorganized speech, and delusions
Outline cognitive biases
-involves selective attention
-Bentall (1990) found that individuals experiencing auditory hallucinations may misinterpret their inner voice as speech from an external source
-these individuals often see themselves as powerless in comparison to others in their social network
-leads to feelings of worthlessness and incompetence
-most people experience an inner voice when thinking, such as when making decisions or solving problems
-but those who feel powerless may hear voices that reinforce their negative self-view
-the perceived power imbalance between themselves and others mirrors their relationship with the voice they hear
-the greater the perceived gap, the more powerful and controlling the voice becomes