psych ao3
Rosenhan (1973) found that all pseudo-patients were diagnosed with schizophrenia,
however the pseudo-patients gave specific schizophrenia symptoms so indicates
criterion validity.
Andrews et al (1999) assessed 1500 people with the DSM-IV and ICD-10, finding
agreement in diagnosis for depression, substance dependence and anxiety,
highlighting good criterion validity.
Kim-Cohen et al (2005) reviewed DSM-IV diagnosis of conduct disorder using
several data collection methods and found the diagnosis was a valid
representation of the children’s experiences.
- Cooper et al. (1972) reported that New York psychiatrists are twice as likely than
London psychiatrists to diagnose schizophrenia when shown the same video-taped
clinical interviews, so criteria may not be objectively interpreted
- Lopez (1989) claims that taking cultural beliefs into account in diagnosis can lead to
misdiagnosis if symptoms are considered to be cultural norms rather than symptoms.
- Cultures view mental health differently, the Plains Indians may claim to hear dead
relatives speak to them as be considered normal but in North America this would be
a symptom of schizophrenia.
- Malgady et al (1987) found linguistic and cultural differences in diagnosis, with
clinicians of non-Hispanic origin rating symptoms of Hispanic people less severe than
Hispanic clinicians would do.
- Eating disorders such as bulimia nervosa are more prevalent in western culture (up
to 7.2% females) than in non-western cultures (up to 3.2% females), so culture
affects more than just the diagnosis (Makino et al, 2004).
- Lin and Cheung (1999) claimed that due to Asian traditions of viewing the body and
mind as unitary, patients tend to focus more on physical discomforts than emotional
symptoms, leading to an overrepresentation of somatic complaints.
- Luhrmann et al. (2015) found that in some cultures hearing voices was a negative
experience while in others it is a positive experience so culture may determine your
experience of mental health.
- Chadda (1995) found that patients reporting symptoms of the culturally specific
disorder ‘Dhat’ were found to meet the criteria for an unspecific emotional disorder in
the DSM IIIR as there was no criteria for ‘Dhat’ as a disorder in its own right.
- López and Núñez (1987) argued that the sets of diagnostic criteria and interview
schedules for schizophrenic, affective, and personality disorders at that point in time
paid little attention to cultural factors.
- Lee (2006) found that using the DSM in Korea for diagnosis of ADHD was as valid as
using it in the USA so cultural differences had no impact on diagnosis.
- Littlewood and Lipsedge (1997) suggested that Black and Irish people in Britain are
more likely to receive a diagnosis of serious mental disorder due to bias in diagnosis
Brown et al (2001) found two independent interviews using the DSM-IV criteria
resulted in the same diagnosis of anxiety and mood disorders in 362 outpatients.
- Goldstein (1988) used the DSM III to re-diagnose 199 patients with an original
diagnosis from the DSM II and found reliability between the two versions.
Iverson (1979) found that post-mortems of schizophrenic patients showed high
levels of dopamine in the brain.
- In patients with schizophrenia phenothiazine drugs (which block dopamine receptors)
show signs of improvement and a reduction in schizophrenia symptoms, which is
evidence that dopamine plays a role in schizophrenia.
- Dépatie and Lal (2001) found that apomorphine, which stimulates dopamine
receptors, did not result in schizophrenia symptoms, suggesting that dopamine may
not be the cause of schizophrenia.
- Aarsland et al (1999) found that treatments for Parkinson’s disease (Ldopa) that
increase dopamine production result in schizophrenia symptoms
(hallucinations/delusions) suggesting dopamine features significantly in
schizophrenia.
- Amphetamine drugs were found by Krystal et al (2005) to increase the concentration
of dopamine in the synaptic gap, but only produce the positive symptoms of
schizophrenia, suggesting there is more than dopamine involved in schizophrenia.
- Krystal et al (2005) found that glutamate NDMA receptors in the brain are stimulated
with ketamine drugs which can cause positive and negative schizophrenia
symptoms, so dopamine may not be the only neurotransmitter involved.
- Carlsson et al (1999) suggest that the glutamate hypothesis expands on the
dopamine hypothesis with both neurotransmitters being involved in schizophrenia.
- Carlsson et al. (2000) found that hyperdopaminergia and hypoglutamatergia may
play a role in schizophrenia.
- Explanations about the role of dopamine in schizophrenia are strengthened by
objective, scientific evidence such as Bird et al. (1979) who found that post-mortems
of schizophrenic patients showed high levels of dopamine in the brain.
- Phenothiazine drugs block dopamine receptors and result in a reduction in
schizophrenia symptoms, which could be evidence that dopamine plays a role in
schizophrenia.
- Wong et al. (1986) who carried out PET scans on schizophrenic patients finding an
increased density of dopamine receptors which could lead to increased reuptake of
dopamine.
- Moskovitz et al. (1978) found that treatments for Parkinson’s disease (L-dopa) that
increase dopamine can result in schizophrenia symptoms.
- Gottesman (1991) found that there was a 48% chance of having schizophrenia if a
person had a MZ twin with schizophrenia, so neurotransmitters alone may not be a
full explanation of the disorder.
- Concordance rates are not 100% in MZ twin studies, so research from a
diathesis-stress model that includes environmental triggers would be a more holistic
method to research the range of causes of the disorder.
Family members can look out for any early indications of symptoms as they can
be made aware that they have an increased risk of developing schizophrenia.
- Gottesman (1991) found that there was a 48% chance of having schizophrenia if a
person had a MZ twin with schizophrenia.
- Kendler et al (1985) found that first line family members were 18 times more likely to
develop schizophrenia than the general population.
- However, this shows that there must be other factors otherwise the concordance rate
would be 100% for MZ twins who are genetically identical.
- Gottesman and Shields (1982) found that there was a 58% concordance rate (7 out
of 12 twins) of schizophrenia in MZ twins reared apart.
- Gottesman (1991) found that there was a 46% chance of developing schizophrenia
if both parents had schizophrenia.
- MRI scans of MZ twins, one with and one without schizophrenia, suggest it is a brain
disease not a genetic disposition.
- Walsh et al (2008) found that in cases where no family history was evident the
patients had a rare CNV genetic mutation.
- Hence understanding genetic mutation can help to explain causes of
schizophrenia in people where there is no previous family history of the
disorder
- Gottesman and Shields (1966) did not find 100% concordance rate between twins
developing schizophrenia, so neither explanation can fully explain schizophrenia.
Drug therapy is based on reducing dopamine uptake in the brain however this
assumes dopamine is the cause when there is evidence from Gottesman that
suggests genetics play a role in schizophrenia
- Anti-psychotic drugs allow patients to stay in society rather than become
institutionalised.
- Phenothiazine drugs block dopamine receptors and patients show signs of
improvement and a reduction in schizophrenic symptoms.
- Phenothiazine drugs such as Chlorpromazine block dopamine receptors and
according to Ban (2007) patients show positive signs of improvement and a
reduction in schizophrenic symptoms.
- Bustillo et al (2001) found that Assertive Community Treatment’s (ACT) have clear
effects on the prevention of psychotic relapse and rehospitalization, so drug therapy
based on biological explanations is not sufficient on its own.
- Meltzer et al (2004) found patients using haloperidol had reduced symptoms of
schizophrenia and showed improvements in day to day functioning.
- Emsley (2008) found that risperidone injections reduced both positive and negative
symptoms of schizophrenia, with 64% of patients having no symptoms two years on.
However, drug therapy is only based on a biological neurotransmitter
explanation of schizophrenia and excludes other factors such as the
environment or genetics
- Adityanji and Kaizad (2005) found that in 0.05% of patients, antipsychotic drugs
lead to neuroleptic malignant syndrome which causes nausea, high blood pressure,
confusion, coma, and in 10% of cases, death.
- Anti-psychotics have serious side effects such as a decrease in motivation so
schizophrenics may prefer not to take them.
- Clozapine and Olanzapine carry a high risk of significant weight gain which can
impact on the patient's adherence to their medication programme, ultimately reducing
the effectiveness of drug therapy.
- Rosa et al. (2005) found only 50% of patients complied with taking their
anti-psychotics.
- Pickar et al. (1992) showed clozapine was most effective with the placebo least
effective when 21 schizophrenic patients were given either a placebo, clozapine or
fluphenazine.
- A meta-analysis (Hartling et al., 2012) reviewed 114 studies and found it difficult to
reach overall conclusions of antipsychotic effectiveness due to possible bias, brief
follow-up trials, and use of selective populations.
- Social adversity explanations would suggest schizophrenia is related to the
environment for example, Eaton (1980) found that schizophrenia is associated with
city life rather than biological factors.
- Drug therapy only works with some patients who have schizophrenia PET scans
have shown that blocking dopamine does not work in patients who have had
schizophrenia for over 10 years.
Family therapy may only help the client's family support the client when they are
experiencing the symptoms of schizophrenia rather than control the cause (1) as
family therapy does not regulate the dopamine imbalance in the brain that is
said to be a possible cause of schizophrenia.
- The family must be engaged and positive about the therapy in order for the
treatment to help the client feel supported otherwise relapse may occur as Vaughn
and Leff (1976) found a 48% chance of relapse in patients in families with high levels
of negative attitudes to therapy.
- Family therapy is a more holistic approach as it addresses the social and
emotional issues and burdens for the whole family in supporting patients in daily
functioning to reduce relapse.
- Pitschel-Walz et al. (2001) found in their meta-analysis an average decrease in
relapse rates of 20% for schizophrenic patients whose families attended family
therapy interventions.
- Pharoah et al (2010) found a positive impact on patient recovery, reduction in
relapse and improved social functioning as a result of family therapy.
- Magliano et al (2005) found improved social functioning of caregivers of family
members with schizophrenia, so treating a wider impact of schizophrenia.
- Psychoeducation (part of family therapy) can increase family knowledge of the
illness which helps them support the patient in medication routines.
- Vaughn and Leff (1976) found patients in families with high levels of negative
attitudes, there was a 48% chance of relapse compared to 6% in families without
negativity, supporting using family therapy to tackle emotions.
- Effective family therapy usually runs alongside a drug based therapy, therefore it is not a therapy that can be used alone.
Changing thought processes may not be effective where the cause of offending
behaviour is antisocial personality disorder.
● Offenders may want to change their behaviour to rehabilitate themselves and prevent
recidivism, so CBT would be an effective therapy.
● Lipsey (2009) analysed 548 studies and found CBT was more effective in reducing
further criminal behaviour than other interventions.
● Howells et al. (2005) found CBT did not significantly reduce aggression in offenders,
so it may not be effective for violent crimes like assault.
● Re-offending may be reduced using CBT as offenders are taught to understand
thinking processes that immediately precede their criminal behaviour so it may stop
them acting in a criminal way.
● Armelius and Andreassen (2007) reported that CBT was effective for the first year
of release but there was no evidence of more long term effects so it may not be
helpful in reducing recidivism in the long-term.
● Lipsey et al. (2007) suggests that recidivism can be reduced by 25% in the 12
months following effective CBT intervention, so this has long term benefits in
reducing re-offending.
● If offenders lack commitment or have been forced to undertake the CBT programme,
there may be attrition and they would drop out so it would not be helpful as they will
not have learned the skills to prevent them re-offending.
● Wilson et al. (2005) found in their meta-analysis that CBT reduced recidivism by up
to 30% when compared to non-treatment groups.
● Levy et al. (2014) found that it was important to deal with the underlying problems
such as joblessness and poverty, which CBT does not change.