Flashcards in 5.1.3 schizophrenia Deck (42)
what is disorganised schizophrenia
Disorganised (hebephrenic) Type
Must have all; disorganised speech,
disorganised behaviour, flat or
inappropriate affect and does not
meet the criteria for Catatonic Type.
what is catatonic sz
Immobility or stupor excessive motor
activity that is apparently purposeless, extreme negativity, strange voluntary movement as evidenced by posturing, stereotyped movements, prominent mannerisms, or prominent grimacing.
what is paranoid sz
Preoccupation with one or more delusions or frequent auditory
hallucinations, No disorganised speech, disorganised or catatonic behaviour, or flat or inappropriate affect,
what is undifferentiated sz
Variation between symptoms, not.
fitting into a particular type
what is residual sz
Absence of prominent delusions,
hallucinations, disorganised speech,
and grossly disorganised or catatonic
behaviour, A presence of negative
features of schizophrenia
About a quarter of people who have had a schizophrenic episode recover and do not get another one. And a quarter of those who have schizophrenia have it continually without any breaks. That leaves 50% who have periods of recovery and periods of symptoms. The positive symptoms, such as hallucinations and delusions, can be overcome the negative symptoms tend to remain.
A feature of schizophrenia is that there is psychosis, which refers to a separation from reality, unlike neurosis, where there are mental health issues but no separation from reality.
Another feature is that schizophrenia is a serious mental health condition with about 1% of the population experiencing it. The average life expectancy for someone with schizophrenia is around 10 or more years less of the average and this might be because of the physical health problems associated with schizophrenia or the highest suicide rate. E.g. duerr 2013 suggests that adolescence with psychotic symptoms are nearly 70 times more likely to attempt suicide.
Schizophrenia tends to be diagnosed during adolescence and up to the age of about 30.
People who are experiencing social problems, such as poverty and unemployment as well as possibly homelessness, more likely to develop schizophrenia than any other sections of the population
explanation of symptoms of sz
schizophrenia is a mental illness that can affect the way someone thinks, speaks or feels to such a degree that they lose their grip on reality. There are a number of ways of characterising schizophrenia, including giving first and second rank symptoms or positive and negative symptoms.
First rank symptoms include hearing voices and ideas about being guided by others. Second rank symptoms include flattened emotions.
according to the DSM-IV-TR, A diagnosis of schizophrenia requires 1 - 6 months of positive and negative symptoms.
In schizophrenia, positive symptoms are where there are additions to behaviour and symptoms that can be seen and noted i.e. the presence of something.
Negative symptoms are the absence of something, usually the absence of normal functioning
positive symptoms of sz
positive symptoms are additions to behaviour and actual symptoms that can be noted, such as delusions and
hallucinations.: refers to seeing or hearing things that are not there, but may also involve smells or feelings of being touched by someone or something. Hearing voices in some cultures is not seen as a side of a mental disorder, but other personal spiritual capability. In these cases the voices are often kind and positive, rise and other diagnosed with schizophrenia, the voices are often harsh and critical.
delusions AKA false beliefs: refers to a person thinking their movements are being controlled by someone else. A common form of delusion is the paranoid delusion, where the sufferer believes that someone is trying to mislead, manipulate or even kill them. Someone suffering from delusions of grandeur will think they are in prominent position of power, such as a king, or that they possess special powers, such as to cure cancer.
Thought insertion is when a person believes their thoughts do not belong to them and have been implanted by an external source. They experience a blurring of the boundary between yourself and others and feel that this border has become permeable. This can lead to the belief that thoughts, feelings and experiences can pass from one person to another
disordered thinking is inferred from a persons speech which may be characterised by derailment having a series of unrelated ideas, or tangentiality going off on a completely different topic. The person may switch from one topic to another and jumble seemingly unrelated ideas, making it difficult to follow the train of thought. Word salad refers to apparently random and incoherent stringing together of words while the term neologism refers to blending words together to create new words. Mixing up one’s words can be quite common and therefore this is only classed as symptomatic if it leads to dysfunctional Communication
basic eval of positive symptoms
positive symptoms tend to have greater weight when diagnosing schizophrenia but as explained previously, they can be affected by cultural differences so perhaps should not be weighted as strongly as negative symptoms, which might be more objectively measured
negative symptoms of sz
Negative symptoms are where normal functioning is not present, such as a loss of emotion, speech or motivation.
Such symptoms often start before positive ones, sometimes years before schizophrenia is diagnosed. this is known as the prodromal Period.
Some examples of negative symptoms are :
lack of energy and apathy e.g. no motivation to do daily chores, social withdrawal e.g. avoiding family and friends and not going out, flatness of emotions, not looking after their appearance, lack of pleasure and every day things in every day life, speaking little even when required to interact.
People with negative symptoms need help because they tend to neglect every day tasks such as preparing food or personal hygiene tasks.
eval of negative symptoms
negative symptoms seem less affected by cultural factors and it has been suggested that they can be more objectively measured. Hearing voices, for example, it’s difficult if not impossible to measure. Lack of energy, flatness of emotions or social withdrawal might be more easily monitored. However, prodromal features have been found to be present in many adolescence and cannot be taken to indicate the onset of schizophrenia on their own
prevalence of sz
It affects around 1 in every 100 people over the course of their life.
It affects men and women equally and seems to be more common in city areas and in some ethnic minority groups. It is rare before the age of 15, but can start at any time after this, most often between the ages of 15 to 35.
A key feature of schizophrenia is the lifetime prevalence which is 0.3 to 0. 7%. this varies with ethnicity, nationality and geographic origin in immigrants. Onset is slightly earlier in males early to mid 20s their females late 20s.
Males tend to have a poorer prognosis than females and females are over represented in late onset cases 40+.
Prognosis is variable and hard to predict.
A minority recover completely, most experience chronic, episodic impairment and some show progressive deterioration, with increasingly brief periods of remission and severe cognitive deficits.
Positive symptoms reduce overtime but debilitating negative symptoms of the remain
one biological explanation of sz : neurotransmitters as an explanation :
explain the dopamine hypothesis
the dopamine hypothesis is that sz is caused by excessive dopamine activity
this causes abnormal functioning of dopamine activity - dependent brain systems. resulting in sz symptoms. dopamine activity can increase / decrease brain activity depending on the system you’re looking at
dopamine hypothesis : what evidence is there for the hypothesis
The dopamine hypothesis states that the brain of sz patients produces more dopamine than normal brains
evidence comes from
studies with drugs
Which two dopamine pathways are there and how are they relevant to schizophrenia symptoms
Mesolimbic pathway is responsible for positive symptoms and the meso cortical pathway is responsible for negative symptoms
dopamine hypothesis : Explain the dopamine differences
Development of dopamine in one area can prevent development in other areas.
For a sample lack of activity in the prefrontal cortex and limbic system may lead to the lack of inhibition of their production in striatum in other words it releases more dopamine in the straighten
people with schizophrenia have enlarged ventricles and smaller frontal lobes.
Higher incidence of head injury in childhood.
All these features link with the prefrontal cortex, which stops developing in adolescence which is usually the onset of schizophrenia in males
dopamine hypothesis: Which drug is given to schizophrenics that reduces the symptoms and how does it do it
chlorpromazine and blocks D2 receptors
dopamine hypothesis: describe briefly the role of drugs
amphetamines which are agonists lead to increase dopamine activity levels.
Large quantities lead to delusions and hallucinations and if drugs are given to schizophrenic patients their symptoms get worse
dopamine hypothesis: describe a pet scan / study that used drugs
lindstroem et al 1999
radioactively labelled a chemical L dopa, administered to 10 patients with schizophrenia and 10 with no diagnosis, L-dopa taken up quicker with schizophrenic patients which suggests they were producing more dopamine activity than they control group.
gjedde and wong 1987
Concluded that there are more than twice as many dopamine receptors in schizophrenics compared to controls
dopamine hypothesis: describe the animal study that supports this hypothesis ￼
randrup and munkvad 1966
The aim was to study to see whether an excess of dopamine neurotransmitters maybe import responsible for schizophrenic symptoms, their procedure: injected rats with amphetamines which increase dopamine activity. they found that the rats showed many of the behavioural indicators of schizophrenia including stereotypical movement and findings were replicated with pigeons chickens cats dogs and squirrels
dopamine hypothesis: Briefly evaluate the dopamine hypothesis
there is a lack of correspondence between taking the drugs and signs of clinical effectiveness. It takes four weeks to see any sign that the drugs are working when they begin to block dopamine immediately and we cannot seem to explain this time difference
it could be that the development of receptors in one part of the brain may inhibit the development in another
Type 1 cases respond well to conventional anti-psychotic drugs. Drugs such as CHLOPROMAZINE: Only effective at relieving the Positive Symptoms of the Illness.
Not effective for negative symptoms. Therefore suggested that Type
2 is related to a different kind of abnormality such as brain structure.
PET scans have suggested that drugs did not reduce symptoms of patients diagnosed with disorder for 10 yrs or more
There may be other neurotransmitters involved
Possible that social and environmental factors trigger the condition.
dopamine hypothesis version 2 : who is davis 1991
Version 2: Davis (1991)
Davis' work addressed problems presented by a wave of conflicting data
postmortem studies, brain imaging data
and animal studies.
It became obvious that not all people with schizophrenia have an excess of dopamine
dopamine hypothesis version 2 : anti- psychotics
as many as 40% of people with schizophrenia do not experience relief from dopamine antagonists such as chlorpromazine, many people with schizophrenia who do experience some relief still experience the negative symptoms
dopamine hypothesis version 2 : clozapine
New drugs were being found to be particularly helpful to those people who did not get any relief from typical antipsychotics and these people seem to respond well to drugs like clozapine which block both dopamine and serotonin receptors
it seems that clozapine was effective in reducing both positive and negative symptoms and it is therefore possible that negative symptoms are linked to an excess of serotonin not just dopamine as initially stated in the first version of the dopamine hypothesis. Also it had been found that serotonin regulates dopamine in areas such as the mesolimbic pathway and this demonstrates the importance of considering how neurotransmitters actually influence and affect each other
dopamine hypothesis version 2 : what is hypodopaminergia and hyperdopaminergia
Davis hypothesise that schizophrenia was caused by hypodopaminergia in the frontal lobes and hyperdopaminergia in the striatum
hyperdopaminergia = too much dopamine activity
hypo= too little
he also suggested that negative symptoms result from hypodopaminergia in the frontal lobes and mesocortical pathways and that positive symptoms result from hyperdopaminergia in the striatum and mesolimbic pathway
Pet scanning had revealed that many schizophrenics have low blood flow in the frontal lobes known as hyper frontality and they also had low levels of metabolites for dope mean in their cerebrospinal fluid suggesting low levels of dopamine in the frontal regions (hypodopaminergia)
dopamine hypothesis version 3 : howes and kapur 2009
They hypothesise that the common pathway to psychosis is dopamine dysregulation in striatum
They discussed a wide range of genetic, environmental factors that may lead to excess dopamine in this region.
Presynaptic dopamine levels responsible for schizophrenia symptoms as opposed to irregularities of d2 receptors has previous versions highlighted.
It is a soft view a.k.a. psychosis proneness and is not an exclamation of schizophrenia and that sociocultural factors are critical in determining the actual diagnosis￼
dopamine hypothesis version 3 : howes and kapur 2009 what is aberrant salience
Dopamine dysregulation may alter the way a person appraises external stimuli.
Abnormal firing of dopamine neurons and the abnormal release of dopamine leads the individual to proceed links between unlinked stimuli.
Psychotic symptoms emerge overtime as the individual attempts to explain himself the experience of aberrant salience.￼
Psychosis is therefore Abaran salience driven by dopamine and filters through the individuals existing cognitive and socio-cultural schemas, thus allowing the same chemical i.e. dopamine to have different clinical manifestations in different cultures and different individuals
dopamine hypothesis version 3 : howes and kapur 2009 noise in the system
negative Symptoms And noise in the system : Dopamine dysregulation may increase the noise in the system and therefore drowning out dopaminergic signals link to stimuli indicating reward.
Net result would be reduced motivational drive that would lead over time to negative symptoms￼ Like social withdrawal
evaluation of dopamine hypothesis AO3 : evaluation for version 1
Amphetamine: induced psychosis.
STRENGTH: a strength of the dopamine hypothesis is that it is supported by research on rats treated with amphetamines￼ (randrup and munkrad 1966) and catherine tenn et al 2003 Found that rats given nine amphetamine injections over three weeks showed various schizophrenic like symptoms. This experimental evidence suggests that increase dopamine levels may be a cause of schizophrenia in humans
WEAKNESS: lana depatie and samrthji lai 2001 Showed that apomorphine, I don’t mean agonist, which stimulates D2 receptors, does not include psychotic symptoms in nonpsychotic clients know does it exacerbate symptoms in those already diagnosed with schizophrenia. This therefore challenges the suggestion that hyperdopaminergia is responsible for positive symptoms
evaluation of dopamine hypothesis version 2 (davis 1991)
the role of D2 receptions
STRENGTH: another strength is support for the role of D2 receptors, e.g. research by Solomon snyder 1985. He found that chlorpromazine Acts as an antagonist at many dopamine receptors, especially D1 and D2, and has antipsychotic effects. Halopendol is a dopamine antagonist with an hour a range of biochemical effects there is more effective in reducing schizophrenic symptoms. This finding suggests that excess activity on specific but not all dopamine receptors is implicated in the development of symptoms
Application to drug treatment
STRENGTH: Research into the role of neurotransmitters has led to effective drug treatments for people with schizophrenia.
For example research has demonstrated that dopamine antagonists that bind to receptors such as Halopendol and spiroperiodol can successfully reduce positive symptoms while atypical drugs such as clozapine which also blocks serotonin receptors have been successful in treating positive and negative symptoms. this means that people with schizophrenia can live in a community without need of residential care because their symptoms are controlled
evaluation of dopamine hypothesis version 3 howes and kapur 2009
second generation immigrants
WEAKNESS: A weakness of the neurochemical explanation is that they cannot explain why certain groups in society like second generation immigrants, I’m more likely to be diagnosed with schizophrenia. In the Netherlands,￼ Wim Veiling et al 2008 showed that Moroccan immigrants were more likely to be diagnosed with schizophrenia than Turkish immigrants.
This suggests that environmental factors such as social stress, actual or perceived discrimination, but interact with internal neurochemistry making some people more prone to psychosis
alternative explanation of sz - genes AO1
This explanation states that schizophrenia is a genetic illness. This means that a gene or number of jeans for schizophrenia can be passed down from parents to children.
It also predicts that like many of a genetic illnesses such as breast cancer, it should run in families.
This means that if one person in the family has the illness, others are likely to as well.
The lifetime risk of schizophrenia in the general population is one percent.
Therefore anything above this must be due to factors other than chance￼
claridge and davis 2003 argued that the contribution of genetic influences is one of few factual certainty is about schizophrenia. Even in the absence of the discovery of specific genes, this is clear from kinship data
alternative explanation of sz - genes evidence
Some of the earliest evidence for the genetic basis of schizophrenia comes from a unique case study conducted by Rosenthal 1963. He studied quadruplets in which all for girls were identical to each other. All four of them develop schizophrenia although they differ in terms of age of onset and the precise symptoms. They were known as the￼ genain quadruplets. The probability of four sisters or developing schizophrenia by chance is 0.000001 percent. This case study seems to suggest that schizophrenia is more likely to be caused by genetics rather than chance
however the girls also had a terrible upbringing. Both the father and the mother showed clear signs of instability and the childhood was disrupted due to the inability of the parents to probably care for the children so therefore this contradicts the genetic explanation as it actually seems that environmental factors could potentially play a more key role than genetics.
However it also could be used as evidence in favour for genes as both the parents showed signs of instability which could be symptoms of schizophrenia
while the genain quadruplets or an interesting case study, it is limited in its usefulness.
Today the main way in which psychologists investigate the genetic basis of a trait or behaviour is by using heritability studies.
There are three main types of heritability studies, family studies, twin studies and adoption studies
alternative explanation of sz - genes twin studies
some of the most striking evidence for the genetic basis of schizophrenia comes from looking at concordance rates between monozygotic i.e. identical twins and dizygotic fraternal twins
A study by Gottesman 1991 found that the concordance rate between identical twins was 48%, but only 17% for fraternal twins.
In other words, this means that if one of a pair of identical twins has schizophrenia, there is a 48% chance that the other twin will also have it. As identical and fraternal twins both share an environment, the higher concordance rate in the identical twins may be due to the shared jeans.
A problem with a lot of twin studies is that the findings with regards to concordance rates tend to be highly variable, fluctuating depending upon where and when the study was done.￼
claridge and davis 2003 reviewed twin studies in schizophrenia and reported concordance rates for identical twins ranging from 0 to 90%.
Generally the concordance rate for identical twins seems to be around 50% and this means that as of the rule of thumb, if one identical twin has schizophrenia, there is a 50-50 chance the other twin will also developed the disorder￼
gottseman and shields 1982: Found that heritability of schizophrenia varied depending upon the severity of the symptoms and with more severe cases of schizophrenia having higher concordance rates
gottseman and bertelsen 1989 found that people whose parents had an identical twins with schizophrenia had a 17% chance of being schizophrenic themselves whether or not the parent themselves had the illness
alternative explanation of sz - genes adoption studies
One way to overcome the issues of shared genes and environment is to look at concordance rates between adopted children and their birth families.
If the children have a high concordance rate with their birth families as opposed to their adopted families, it was adjust a genetic basis, whereas if they have more in common with her adopted families, it would be due to environment
tienari et al 2000 Studied 164 adoptees whose biological mothers had been diagnosed with schizophrenia and found that 11, 6.7% also received a diagnosis of schizophrenia compared with just four, 2% of 197 control adoptees born to non-schizophrenic mothers therefore it seems that genes play more of a part then environmental.
However an additional finding is that the children who are at a higher genetic risk tend to do well if they’re adopted family provide supportive environment, better in fact and the ones who did not have a genetic risk they were brought up in poor environments
alternative explanation of sz - genes EVALUATION
Gottesman found a relationship between genetic similarity and the probability of two people both having schizophrenia, Gottesman and shields 1966 identified a concordance rate of 42% for identical twins and 9% for fraternal twins, the greater rate for identical twins shows that was schizophrenia is not entirely a genetic disorder, biology certainly plays a significant role . therefore we would need to further study the relationship between environment and genetics
concordance rates in twin studies are far from 100% even for identical twins, suggesting a significant role for the environment.
Pedersen a Mortensen 2006 show the risk of developing schizophrenia increases with great exposure to city life and higher population density, this suggests that rural dwelling may help protect a person from developing a disorder to which they are genetically predisposed to. however clange and davis 2005 did find and theorised that if an identical twin has schizophrenia there is a 50-50 chance the other twin will have it too so this shows that the rates are still significant in terms of genes
dahoun et al 2017 concluded that disc1 is associated with presynaptic dopamine dysregulation, a key factor in schizophrenia. Egan 2001 found a link between decreased dopamine (hypodopaminergia) in the prefrontal cortex and one form of the COMT gene- the Val allele (inheriting two copies of these increases risk of developing schizophrenia by 50%, this shows how genetic variations underpin neurochemical differences which can predisposed a person towards schizophrenia.
schizophrenia can appear without family history of the disorder and the DNA code in one or more genes may spontaneously change or mutate and this may be due to environmental factors or error during cell division therefore further investigation and study has to take place￼
alternative explanation of sz - genes diathesis model
genes create a vulnerability for schizophrenia, rather than causing it.
you may possess the genes, but need other biological or environmental triggers to trigger schizophrenia.
Recently cannabis use has been looked at as a trigger. And apparently increases the risk seven times as cannabis interferes with a dopamine system￼
the social causation hypothesis: what is it
This suggests that schizophrenia is caused by factors relating to our social and physical environment such as living in an urban environment, being from a lower socio-economic class and being part of an ethnic minority group.
It seems that being born and brought up in such circumstances can be a causal factor in the development of schizophrenia
Pedersen and Mortensen 2001 found that the longer a child had been exposed to urban living, the greater the probability of developing schizophrenia. They also took into account factors associated with urban living there can also be independent risk factors for schizophrenia such as exposure to flu and birth complications and found that living in an urban environment still increased the risk even in the absence of these factors￼
the social causation hypothesis: living in an urban environment
living in an urban environment could be linked to schizophrenia because this means that the individual is experiencing a more stressful life due to positivity, unemployment etc
The link between urban city and schizophrenia has been researched by Pedersen and Mortensen 2001 who found that a change in location, increase the risk of schizophrenia.
They collected data from a Danish city registration and they found that in capital cities there was a more increased risk of schizophrenia and a high degree of more crowded areas increase the risk of schizophrenia
the social causation hypothesis: low socio-economic class
being from a lower socio-economic class could be linked to schizophrenia because families are affected by unemployment, poverty may be exposed to more stress than others and may not be able to access treatment which puts them at a more vulnerable risk to schizophrenia. The link between classes schizophrenia has been researched by Patel 1999 whose studies over the last 20 years indicated a close interaction between poverty and ill mental health
and farris + dunhan 1939 Analyse the prevalence of schizophrenia in Chicago and found that there was an increase in cases in the outskirts of the city moving inwards which reflects the rates of unemployment.￼
High levels of stress make people in low socio-economic groups are more vulnerable to schizophrenia
hJern et al 2004 showed that social adversity in childhood is associated with an increased risk of developing schizophrenia
the social causation hypothesis: ethnic minority group
being part of an ethnic minority group may be a causal factor in developing schizophrenia as in the Netherlands, immigrants from Morocco have an increased risk of schizophrenia.
Researchers suspect that adverse social experiences of immigrant groups or an explanation e.g. long-term separation from parents during childhood, not putative Risk factors such as pregnancy complications.
AKA racial and ethnic discrimination may contribute to the increased incidence, but only few studies have evaluated these hypothesis.
incident study of psychotic disorders in The Hague showed that risk of schizophrenia was increased for first and second generation immigrants from Morocco.
The risk was particularly high for second generation immigrants, Moroccan males and relatively low for Turkish immigrants.
There was also ethnic differences: Moroccan patients also had more severe symptoms than native Dutch patients and presented more persecutory decisions.
veling 2008 risk of psychotic disorders increased by belonging to a group with experiences of high level of discrimination and by having a weak or negative identification with their own ethnic group. Velling 2008 risk of schizophrenia was associated with perceived racial discrimination, week ethnic identity, lo ethnic density. This helps to explain research findings regarding the high incidence of schizophrenia and people facing socio-economic adversity who were also from ethnic minority groups. : Proactive suggestions for improving later mental health of children from ethnic minority communities e.g. celebrating cultural diversity and building positive ethnic identities
Living in neighbourhoods with many members of their own ethnic group is a protective factor and reduces the risk of schizophrenia.
Fernando 1988 found that Afro Caribbean people in the UK are 2 to 7 times more likely than the general population to develop schizophrenia