Schizophrenia
Positive symptoms
Positive symptoms are a change in behaviour or thoughts. It is when
something is gained such as delusions
(bizarre beliefs that seem real to the person), hallucinations (unreal perceptions of
surroundings), or experiences
of control E.G thinking an alien is controlling them.
Negative symptoms
Negative symptoms represent a withdrawal or lack of
something E.G motivation. Negative symptoms include apathy (lack of interest or emotion), social withdrawal, alogia (poverty
of speech no fluency slowed thoughts), avolition (cant initiate goal directed behaviour)
, flat effect (having no emotion).
Clinical
Characteristics
·
Chronic onset – slow and
gradual deterioration. Most commonly seen in younger people aged 18-25. They can often experience more obvious
symptoms such as hallucinations.
·
Acute onset – Obvious
symptoms occur quickly can be after a stressful life event. Most usually known
in older people. This is the least common way.
DSM-IV-TR
® Text revision version of DSM-IV published in July 2000.
® Diagnostic and statistical manual of mental disorder
® Produced by the American psychiatric association
® Most widely used diagnostic tool worldwide.
ICD
® International classification of diseases.
®
Produced by world health
organization (WHO)
Classification systems for
diagnosing Sz are the ICD and DSM. To be diagnosed the patient has to have had
the symptoms for at least 6 months.
Sub types listed in DSM but removed from DSM5: paranoid Sz, Hebephrenic
Sz, Catatonic Sz, undifferentiated Sz, and Residual Sz. = these
had a negative impact upon validity. DSM 5 updated in 2013.
Cormorbidty = presence of one or more disorders. E.G Having
depression as well as bipolar.
Issues with
diagnosis and classification of Schizophrenia:
·
Psychological harm to patient if they receive wrong
diagnosis or no diagnosis.
·
It’s a waste of money and resources if a patient is treated
with therapy and drugs and then turns out not to have the disorder.
·
You want to diagnose it correctly as it helps psychologists
to becoming closer to understanding what causes Sz.
·
Is Sz actually a mental health issue?
·
Reliability of diagnostic manuals
·
Inter-rater reliability (extent to which psychiatrists agree on diagnosis)
·
Validity
·
Co-morbidity ( when Sz sufferer has 1 or more disorders E.G Depression and Sz)
·
Cultural differences
·
Advantages and disadvantages of labelling
-Advantages of labelling = help communicate better between clinicians, help research cause of Sz
-Disadvantages of labelling= can become a self fulfilling prophecy and Goffman 1968 said labelling had negative consequences and that people react badly to it.
Cultural
differences:
·
Could genuinely be more likely to have Sz.
·
Environmental factors EG Stress of living in poverty, or
diet or unemployment
·
Social factors such as cannabis smoking.
·
Genetic pre-disposition to get the disorder.
Criticism
of diagnosis of Sz:
ROSENHAN ET AL 1973 :
Rosenhan did a study showing that 8
healthy ‘pseudopatients’ could gain admissions to 12 psychiatric hospitals in
America by pretending to have auditory hallucinations such as the word ‘empty, thud, hollow’. When admitted they behaved normally. All wanted to be discharged so they
behaved very well and followed all instructions from staff. They remained in
the hospital from 7-52 days. Follow up study completed
where Rosenhan warned hospitals he was sending people out, 21% of them were
found out… yet Rosenham didn’t actually send anyone out!!
ESSAY Q = DISCUSS THE ISSUES SURROUNDING THE CLASSIFICATION AND
DIAGNOSIS OF SZ
AO1 8 MARKS A03 = 16
MARKS
·
Explanation of how reliability affects diagnosis
·
Inter rater reliability tests
·
Reliability improved since rosenhams landmark study
·
Copelands study
·
Does sz exist? If experts cant agree then maybe it has no
objective truth behind it Thomas Szasz said that mental illnesses are a myth.
CULTRAL
DIFFERENCES:
®
Copeland et al (1971) gave a description of a patient to
134 US psychiatrists and 194 British psychiatrists.
®
69% of US psychiatrists diagnosed schizophrenia, but only
2% of British psychiatrists gave same diagnosis.
®
Harrison et Al said that afro-Caribbean people are 8x
more likely to get Sz. Could be due to environmental factors such as stress of
unemployment, or cannabis smoking. Could be due to how they were bought up to
show their emotions.
Type 1
= positive symptoms
Type 2 = negative
symptoms
Inter rater reliability
= getting the same result regardless of who you ask. For example Copeland
demonstrated that the inter rate reliability between British and American
psychologists is very low.
Copenhagen High Risk Study 1994 family and Sz (genetic
causes)
Kety et al study in Denmark 207 offspring with mothers
who have Sz Condition 1 = high risk group condition 2 = low risk group. All
kids ages 10-18. Matched pairs design, matched on age, gender, socio economic
factors.
Follow up in 1974 . 16.2% high risk diagnosed with Sz.
1.9% low risk diagnosed. Schizotypal
personality disorder was diagnosed in 18.8% of group 1 and in 5% of group 2.
+ prospective not retrospective study
+natural experiment high ecological validly. Also
longitudinal study with 2 follow ups
-
Population bias done in Denmark can’t be generalised to
different cultures e.g. Africa
-
Natural experiment
extraneous variables could affect the IV
+ new
York high risk study is a supporting study showed same resilts.
-
Could also use nature VS nurture debate could be copying
behaviour
Biological explanations of Sz include: genes (DNA), biochemical (dopamine)
and anatomical (structure of brain).
Carlson 1991 = Claims that the DSM has become more reliable
as it has been updated, however a review in 2001 showed that it has an
inter-rater reliability of 0.11
Klosterkotter 1994 = Assessed nearly 500
admissions to a psychiatric unit in Germany and found that positive symptoms
are more useful in diagnosis.
Cromer 2003 = dopamine neurons play key role in attention,
perception and thought.
Test retest reliability = repeating the test and making
sure you get the same findings
BIOCHEMICAL EXPLANATION
OF SZ:
·
This is the most supported explanation of Sz.
·
Sz sufferers have high levels of dopamine binding
·
The drug LSD can imitate symptoms of Sz
·
Neurotransmitters DRD1, DRD2 have been linked to Sz.
·
Neurons send messages via electrical impulses over the
synapse.
·
Neurotransmitters released fit onto dopamine receptors. The
receptors are shaped specially to fit.
·
In Sz sufferers messages from neurons transmit dopamine
fire too easily
·
Symptoms of Sz have been observed in Parkinson’s patients
who took ‘levodopa’
EVALUATION OF
BIOCHEMICAL:
+ supports idea dopamine plays key role, anti psychotic drugs block the activity of
dopamine in the brain so they are dopamine antagonists. By reducing binding they
eliminate symptoms such as hallucinations.
+Post mortem studies support biochemical explanation. Autopsies
of patients with Sz revealed increase in dopamine in left dopamine receptor.
This was confirmed with PET scan.
-Mixed results of drug treatments, drugs that work on dopamine do not benefit all Sz suffers E.G
not very effective at treating negative symptoms (type 2)
-Clonazapine most effective
drug in Sz treatment it works with serotonin and not dopamine
- We don’t
know if dopamine is the cause or effect of Sz. However it wouldn’t explain
LSD
Giving Sz like symptoms.
GENETIC EXPLANATION OF SZ:
The closer the biological link with a Sz suffer, the greater the link
of child or relative developing Sz.
KENDLER 1995 showed that 1st
degree relatives are 18 x more at risk than general population.
Cousins = 2%, Siblings = 9%,
Children = 13% = average risks for developing Sz = 1%
Kety 94(Copenhagen high risk study), Erlenmeyer kimling 97( new York high
risk study) = LONGITUDINAL STUDIES BOTH
CARRIED OUT OVER 25 YEARS + = STRONG FAMILIAL LINK IN SZ
TWIN STUDIES:
Gottseman 1991 Meta analysis of
40 studies. Found 48% concordance rate for Mz twins and 17% for Dz twins, =
large genetic component with environmental link.
Jospeh 2004 meta analysis concordance rate
for identical twins = 40.4% and 7.4% for non identical twins.
EVALUATION OF META ANALYSIS:
+ gather large amount of data from meta analysis can infer cause and
effect
+gives more weight to conclusions
-
Suffer from publication and cultural bias
-
May have reduced reliability as dissimilarities in methods
used in studies.
ADOPTION STUDIES:
Finnish adoption study 2000 = 7% adopted
children of mothers with Sz developed the disorder. Compared to 1.5% of the
control group.
Danish adoption study = high rates of
chronic Sz in adopted children of biological parents with Sz.
EVALUATION OF GENETIC
EXPLANATION:
-
Family studies are often
inconclusive because they are retrospective. Prospective longitudinal studies
EG Copenhagen and NY provide better quality data
-
Difficult to isolate
genetic factors as environmental factors also play a key role.
-
The fact Sz runs in
families could be nurture and not nature
-
Scientists cannot find
the specific gene that causes it
-
Genetic explanation been
criticised for being reductionist
-
Adoption studies have
advantage of separating environmental +genetic factors more clearly
NEURO
ANATOMICAL EXPLANATIONS:
MRI studies E.G Brown 96, Flaum 95 show definite anatomical
abnormalities in Sz patients especially those with negative symptoms. In the
past structural differences had been noticed but all evidence is from post
mortem studies.
Structural changes
could be a consequence not a cause of Sz, MRI allows you to see brain of living Sz
patient.
Such anatomical abnormalities
have been found more often in patients with negative/chronic symptoms,
supporting the division between Type I and Type II.
Szesko et al found that the ‘asymmetry’
found in normal brains in the prefrontal cortex is absent in people with
schizophrenia.
However L researchers do not agree on which
areas of the brain are affected.
·
DECREASED BRAIN WEIGHT
·
ENLARGED VENTRICLES
·
ABNORMALITIES IN FRONTAL CORTEX (SZESKO FOUND THIS)
Measles, scarlet fever, polio and influenza A contracted either during pregnancy or in
early childhood have been suggested as explanations of Sz.
Jones and Cannon 98 =
children who suffered viral infections are 5 times more likely to develop Sz.
Torrey 88 and 96 = If the mother suffers Type A flu between weeks
25 and 30 of pregnancy (phase of major brain development) the viral
infection enters the brain of the foetus.
There it stays until activated at puberty (hpth 1) or cause a slow and
gradual degeneration of the brain that eventually results in S (hpth 2)
EVALUATION OF VIRAL:
L Correlational data therefore may not
establish cause and effect.
L Obsolete diagnostic criteria.
L Difficulty in isolating contributory factors
in pregnancy.
J Historically flu epidemics are linked with an increase in S
cases. L Not all researchers agree on
this conclusion from evidence.
PSYCHOLOGICAL
EXPLANATIONS FOR SZ:
Psychosocial factors:
- Socio economics = Sz is more common
among people with lower socio-economic status. Living in poorer
conditions with financial worries brings a number of stressors that can
trigger the onset of the condition.
- Migrant populations. Migrants who move into a new environment are
at higher risk. In the UK Sz is more frequent among African Caribbean
groups. However this might reflect racial bias in diagnosis
Family relationships
- Double blind theory. Contradictory messages from parents may result
in the development of schizophrenic symptoms such as flat effect and
withdrawal. Conflicting messages from a parent prevent the development of
a coherent model of reality. Families with high emotional tension have
been described as ‘schizophrenogenic.’
- Expressed emotion a negative emotional climate at home has been
linked to Sz. In particular high levels of expressed emotion (hostility,
criticism but also over involvement)
LIFE EVENTS
A specific
stressful life event, such as bereavement or divorce, can trigger a
schizophrenic episode.
Brown and
Birley reported that 50% of people experience a stressful life event in the 3
weeks before a schizophrenic episode (a control group of healthy people
reported low levels of traumatic experiences).
The people they studied had previously experienced S and the stressful
event caused a relapse.
However not
all evidence supports the role of life events.
Van Os (94) reported no link between life events and the onset of
S. Also supporting evidence tends to be
correlational.
COGNITIVE EXPLANATIONS
The disorganised and disordered thinking characteristic of S
is the cause rather than the consequence of the disorder.
Attention deficit theory (Frith 79)
The
mechanisms that operate in ‘normal’ brains to filter incoming information are
defective in people with S. They let in
too much irrelevant information, because they are unable to select what is
relevant. Frith tested the hpth and found that S sufferers have reduced cerebral blood flow in certain areas of the brain (indicating
reduced activity) during certain cognitive tasks.
Neuropsychological theories = Physiological
abnormalities lead to cognitive malfunctioning:
i.
Failure to activate schemas (Hemsley 93)
The main problem in S is the breakdown in the
relationship between stored
information and new sensory input.
Schemas are knowledge packages in our memory built from experience that
we use to make sense of reality and interpret new events. Hemsley suggests that schemas are not
activated in S. This has been used to
explain positive symptoms such as delusions and auditory hallucinations.
ii.
Faulty cognitive processes (Frith 92)
This is an explanation of how some of the
positive symptoms develop.
A disconnection between frontal areas of the
brain regulating action and posterior areas controlling perception causes a
fault in a mechanism which he calls ‘meta-representation’. This is what regulates cognitive processes
that allow us to have goals and to pursue them and to understand the intentions
of others.
Genetic
links
Cognitive psychologists are trying to find
out whether cognitive malfunctioning is hereditary. There is some evidence that first degree
relatives of S sufferers have various cognitive deficits such as working
memory malfunctioning (Park 95) or an impaired auditory attention
(Faraone 99). These would be an
indication of the presence of the gene that predisposes to S and even causes S.
EVALUATION.
It is
not clear why some members of the family with malfunctioning cognitive
processes don’t develop the disorder. It
could be that it depends on the degree to which one has the gene(s) or on the
presence of environmental triggers.
EVALUATION OF
COGNITIVE EXPLANATIONS
L Cognitive
explanations describe S symptoms in terms of cognitive processes rather than
finding the causes. They may help
however J to explain how such symptoms
develop.
L They need to be combined with biological
factors such as genes or physiological abnormalities to give a full
explanation.
L Hemsley’s theory has little supporting
evidence, although recently J the results
of animal research offer some support.
L
Frith’s
faulty processes theory has been criticised as reductionist, though it does
offer a useful framework J for explaining many of the symptoms
of S.
THE PSYCHODYNAMIC
EXPLANATION
Freud saw the distorted beliefs
characteristic of SZ as the regression of the ego into a pre-ego state. This may be caused by an excessively critical
and uncaring mother (or parent). The
unrealistic picture of the world typical of SZ (e.g. delusions) is similar to
that of early childhood. The ego
attempts to regain control are the cause of auditory hallucinations.
EVALUATION OF THE PSYCHODYNAMIC EXPLANATION
J Later
psychodynamic psychologists (such as Fromm-Reichmann) found that SZ sufferers
do tend to have what they call ‘schizophrenogenic’ mothers.
J Observational
studies of how parents behave in the presence of their SZ children support the
theory. However L is such observed
parental behaviour cause or effect? We
would need evidence that parents behaved coldly and uncaringly in the early
stage of the child’s life for the Freudian explanation to be supported.
L The theory
has no scientific research support.
L This
explanation leads to parental blame.
L Even Freud
regarded his psychoanalytic theory as unsatisfactory to explain psychoses.
THERAPIES
BIOLOGICAL
THERAPIES
DRUG THERAPY
Conventional antipsychotic drugs such as
phenothiazines are dopamine antagonists - they reduce the amount of
available dopamine or the number of dopamine receptor sites. By doing this they
can stop hallucinations and delusions experienced by the patient.
Among the serious side effects of
conventional antipsychotic drugs are symptoms similar to those of Parkinson’s
disease, as well as low blood pressure and blurred vision. Tardive
dyskinesia is a serious condition probably caused by phenothiazines destroying
parts of the brain. Around 30% of those taking phenothiazines develop tardive
dyskinesia.
Atypical antipsychotic drugs such as
clozapine work mainly by blocking serotonin receptors. Clozapine has
been shown by research to be more effective than conventional antipsychotic
drugs. The immune system can be damaged by prolonged use of clozapine.
One problem
with long term drug therapies is that outpatients may stop taking them because
of their side effects or simply because they forget. One way to overcoming this problem is to
provide depot medication. Depot
injections release the drug slowly, so they only need to be given at intervals
of a week or more.
Another promising strategy that has been introduced to help sufferers to
carry on taking their prescribed drug therapy is motivational
interviewing. This non-coercive
technique aims at making the patient feel that he/she is in control of the
decision of following the therapy voluntarily.
ECT
|
Electroconvulsive Therapy has received some bad press as a result of
what the treatment used to be. Yet "ECT has a higher success rate for
severe
depression than any other form of treatment." It has also been shown to be an effective form of treatment for certain types of schizophrenia (those accompanied by catatonia, extreme depression, mania and other affective components). In recent years there has been a resurgence of interest in ECT because it has evolved into a safe option.
ECT has a higher success rate on severe depression and certain cases
of catatonic SZ than any other form of treatment. Although its benefits in treating SZ are
not as impressive as for depression, it can bring about a rapid cure in cases of alogia and catatonic
unresponsiveness. It is particularly useful for
people who suffer from psychotic depressions or other severe psychoses and
cannot take medication due to problems of health or lack of response &
pregnant women.
·
When a patient
is intent on harming themselves or others, ECT is a good option because it
works rapidly. Suicide attempts are
very rare after ECT.
·
Today the
method is painless, & with modifications in technique it bears little
relationship to the unmodified treatments of the 1940s.
·
Side effects: short term memory loss.
·
In some cases,
after the initial success, the patient relapses into the condition.
|
PSYCHOLOGICAL
THERAPIES
CBT
People may have distorted beliefs
and these make their behaviour maladaptive.
This is often the case with S.
The therapy aims at replacing disordered and delusional thoughts with
thoughts that are more constructive and more in line with reality. Patients are encouraged to find a rational
explanation for the origin of their symptoms and evaluate the content of their
beliefs. They are also set behavioural
tasks aimed at making their behaviour more adaptive.
J A
consistent body of research evidence has shown that CBT is effective in
relieving both negative and positive symptoms of S.
J Research shows that CBT has positive effects
fairly soon into the treatment programme.
L CBT is generally conducted on patients
who also receive drug treatment. Its
effectiveness has therefore not been assessed independently.
FAMILY INTERVENTIONS
The type of communication
within a family can cause S or contribute to a relapse. This type of therapy programme involves other
family members and aims at reducing level of negative expressed emotion
within the family. Key family
members are trained to develop more effective and positive communication
styles. In the case of a patient being
discharged form hospital, the family is trained prior to the patient’s returned
at lowering expressed emotion levels and adjusting expectations.
EVALUATION.
Pharoah’s meta-analysis study
(2003) found that f.i. reduces the
rates of both admissions to hospital and of relapse. It also improves levels of compliance with
drug therapy. The outcomes of the
therapy are however quite varied. Also,
it can really only be used with people who live with their family.
PSYCHODYNAMIC THERAPY
As the conflicts that have
pushed the ego to regress to a pre-ego stage are largely unconscious, the AIM
of the therapy is to bring them to the conscious mind where they can be
dealt with. The therapist tries to
connect with the patients by offering help with the perceived problem.
Freud was pessimistic about
the appropriateness of psychoanalysis to treat psychoses in general.
However other forms of
psychotherapy have been tried with some success.
EVALUATION.
The findings of research into the
effectiveness of psychodynamic treatments are contradictory. Gottdiener carried out a meta-analysis
which shows that 66% of patients receiving psychotherapy improved compared with
35% of the group that didn’t receive psychotherapy. Within the psychotherapy group,
psychoanalysis was as successful as CBT.
However there are some methodological issues with this study, as it
spanned many years, so different diagnostic and methodological tools were used.
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