Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Starter: Rosenhan questions 1. Who were Rosenhan’s participants for his study? 2. How many hospitals did they visit? 3. What did these pseudopatients have to do? 4. What did they do once they gained admission? 5. What were the two aims of the study? 6. What were the main findings? Follow-up questions (a) In his original study, all but one of the patients were given the label of paranoid schizophrenia with the other patient being labelled as bipolar. How does this show that there are issues with the reliability of diagnosis? (b) Rosenhan did a follow-up study where he told the psychiatric institutions that he would send them more pseudopatients (fake patients) over the next three months and they had to detect them. After three months they were confident that approximately a third of the new patients they were sent were pseudopatients and were shocked when they found out that Rosenhan had not actually sent any! Explain how this further highlights the poor validity (c) What were the implications of this study for the psychiatric profession? 1. 2. 3. 4. 5. 7 students – 4 male, 3 female 12 in 5 different states State hearing same sex “empty hollow thud” voice Acted normal and said symptoms have gone Aim 1: investigate whether psychiatric labels would be used in situations where they weren’t appropriate Aim 2: investigate whether the experience of being hospitalised in a psychiatric ward 6. None were ever detected as being pseudo- patients and the longest stay was 2 months Additional questions • The diagnosis of the different psychiatrists were inconsistent when they were presented with the same symptoms of Sz • Shows psychiatrists were unsure what Sz actually was as they were labelling someone with the disorder (insane) when they were actually sane • It brought widespread distrust in the ability of psychiatrists to accurately diagnoses mental illnesses – it also brought about a revision of the classification systems to incorporate a more in depth overview of mental illness 1. Negative symptoms of schizophrenia represent the loss of a usual experience T/F 2. Match the term to the definition A: A loss of motivation and lowered activity levels 1. Hallucinations 2. Delusions 3. Avolition 4. Poverty of speech B: Reduced frequency and quality of speech C: Sensory experiences that have no basis in reality, e.g. hearing voices D: Beliefs that have no basis in reality, for example thinking they are someone else or that they are the victim of a conspiracy 3. Co-morbidity is how commonly two or more conditions occur on their own T/F 4. Which of the following is an example of delusions? 1. Hearing voices. 2. Thinking that the neighbours are plotting to kill you 3. Lacking a desire to wash and go to work 4. Reduced frequency of speech. 5. White psychiatrists may tend to over-interpret symptoms of schizophrenia in black patients T/F Answers 1. True 2. 1 C 2D 3A 4B 3. False 4. 2 5. True Explanations of Schizophrenia Specification details: Biological explanations for schizophrenia: 1. the dopamine hypothesis 2. genetics, 3. neural correlates. Biological approach offers useful suggestions as to how it is caused. LEARNING OBJECTIVES • Describe / Draw the role of Dopamine (DA) in Sz • Outline / articulate evidence to support this hypothesis • Evaluate, using CASTLES the Dopamine Hypothesis • Outline the role of genes in Sz • Evaluate the role of genes using research evidence DOPAMINE HYPOTHESIS Draw the following: - Endocrine system - Nervous system - Neuron Human nervous system Peripheral nervous system (PNS) Autonomic nervous system Somatic nervous system Sympathetic nervous system Parasympathetic nervous system Central nervous system (CNS) Brain Spinal cord Lets remind ourselves how neurotransmitters work 1 5 2 4 3 Lets remind ourselves how neurotransmitters work What is dopamine? • known to be active in the limbic system - an area of the brain governing emotion • Regulates attention if this process is disturbed may lead to problems with attention, perception and thought DOPAMINE HYPOTHESIS The Dopamine hypothesis states that the brain of schizophrenic patients produces more dopamine than normal brains. Evidence for this comes from studies with drugs post mortems pet scans Dopamine Hypothesis Although the original Dopamine Hypothesis states that the brain of schizophrenic patients produces more dopamine than the brain of a “normal” person. It is now thought that schizophrenics have an abnormally high number of D2 receptors. Normal Level of Dopamine In The Human Brain Elevated Level of Dopamine In The Brain of a Schizophrenic Patient (specifically the D2 receptor) Neurons that use the transmitter ‘dopamine’ fire too often and transmit too many messages. There may be an excess of DA receptors at the synapse in schizophrenics Lowering DA activity helps remove the symptoms of schizophrenia ROLE OF DRUGS Amphetamines (agonists – prevent the breakdown of dopamine) lead to increase in DA levels Large quantities lead to delusions and hallucinations If these drugs are given to schizophrenic patients their symptoms get worse Randrup et al Rats given amphetamines developed schizophrenia type symptoms Parkinson’s disease • Parkinson’s sufferers have low levels of dopamine • L-dopa raises DA activity • People with Parkinson's develop schizophrenic symptoms if they take too much L-dopa Chlorphromazine (given to schizophrenics) reduces the symptoms by blocking D2 receptors Post-mortems Iversen (1979) and Seidman (1990) Post-mortem (after death) examinations have found that people with schizophrenia have a larger than usual number of dopamine receptors. Increase of DA in brain structures and receptor density (left amygdala and caudate nucleus putamen) Concluded that DA production is abnormal for schizophrenia What is a strength and weakness of a postmortem study? PET SCANS 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 • Suggests they were producing more DA than the control group PET Scans Gjedde and Wong (1987) There are more than twice as many dopamine receptors in schizophrenics compared to controls. Farde et al. (1990) There is no difference in the number of dopamine receptors between schizophrenics and controls. What is the main strength of a PET scan? What conclusions can be drawn from the research findings? Chickens hatch from eggs, but a mother chicken must keep an egg warm in order for it to hatch Which Came First? The Chicken or the Egg? Schizophrenia or Faulty Chemicals? Faulty chemicals cause schizophrenia but schizophrenia may cause faulty chemicals Drugs may influence other systems that impact on schizophrenia so we cannot be 100% sure about their effects There are lots of problems with the dopamine hypothesis! • The research is inconclusive… ensure you have both sides in your notes • There is a lack of correspondence between taking phenothiazines and signs of clinical effectiveness. It takes 4 weeks to see any sign that the drugs are working when they begin to block dopamine immediately. We cannot seem to explain this time difference. • It could be that the development of receptors in one part of the brain may inhibit their development in another Other EVALUATION POINTS • 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 good at explaining 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. TASK: read, absorb and understand some of the evaluation points using your text books. Make notes and ensure you can describe and evaluate the explanation: complete pgs in your packs GENETIC EXPLANTION • What is the logic behind conducting twin studies when investigating schizophrenia? • What is the logic behind conducting adoption studies when investigating schizophrenia? • What do we mean by concordance rate? Do you remember what concordance rate means? The probability of one twin having the disorder if the other already has it - expressed as a percentage MZ and DZ twins MZ = Monozygotic • Come from one egg • Identical twins – share 100% of their genes DZ = Dizygotic • Come from two eggs • Non-identical twins – share 50% of their genes Genetic vulnerability • Genetic explanation suggest that component to schizophrenia which predisposes some individuals to the illness • whether a person develops schizophrenia is at least partly due to their genes – may explain why patients often have other family members with schizophrenia • Look at: – Family studies – Twin studies – Adoption studies 1. Family Studies A01 • find individuals who have schizophrenia and determine whether their biological relatives are similarly affected more often than non-biological relatives Large-scale family study - Gottesman (1991) – additional material on the Blog • concluded if both parents suffer from schizophrenia, 46% chance of also developing the disorder (compared to a 1% chance for the general population) • Findings have shown greater degree of genetic relatedness, greater risk of developing schizophrenia 1. Family studies A03 • genes do play an important factor - however if genes were the only cause of schizophrenia then the percentages should be 100% Deterministic; just because we are ‘predisposed’ by our genes cannot mean we necessarily get the disorder schizophrenia • researchers accept that schizophrenia concordance rates in families to do with common rearing patterns or other environmental factors that have nothing to do with heredity 2. Twin Studies A01 • Twin studies help researchers work out whether nature or nurture has the greatest influence • Gottesman and Shields (1972) found that the concordance rate for schizophrenia in MZ twins was 48% compared to 17% for DZ twins. • He therefore suggests that schizophrenia is inherited through genes. • Also Joseph (2004) – showed concordance rate of 40.4% MZ and 7.4% for DZ. 2. Twin Studies A03 • Twin studies seem to indicate that there is a strong genetic component to the disorder • Twin studies demonstrate may be a predisposition to develop schizophrenia, however, both twins do not always develop schizophrenia suggesting environmental factors • Concordance rate for twins are not 100% therefore schizophrenia cannot be accounted for by genetics alone • Sample sizes of such twin studies always going to be very small…. difficult to generalise to the general population 2. Twin studies A03 L - higher concordance between MZ twins could be explained by greater environmental similarity rather than genetic similarity – MZ twins elicit more similar treatment than DZ twins (so can be explained by other theories) E - No single gene has been identified for schizophrenia, questioning genetics as a valid explanation for schizophrenia. S - Evidence for concordance rates for schizophrenia are based on older twin studies which are less reliable due to changes in the diagnostic criteria diagnosis is much rigorous than it was 40 years ago so some of those diagnosed as schizophrenic 40 years ago might not meet the criteria now 3. Adoption Studies A01 • genetically related individuals who have been reared apart due to being adopted • allow researchers to overcome the problem of disentangling genetic and environmental influences – Heston (1966) compared 47 adopted children whose biological mother had schizophrenia with a control group of adopted children with no history of schizophrenia in their biological family. – None of the control group was diagnosed with the illness; 16% of the offspring of schizophrenic mothers were diagnosed 3. Adoption studies A03 • results of adoption studies only reveal small percentages – still support the idea that genes must play a role within schizophrenia. • Tienara (1991) – 155 adoptees whose biological mothers had been diagnosed with schizophrenia , 10% also received a diagnosis of schizophrenia, – compared to just 1% of the 185 control adoptees (page 213) – this provides supporting evidence also • However, Tienara conducted his study within Finland, therefore we are not able to generalise this study to the rest of the world Genetic explanation overview Through research, Candidate genes have been implicated in the development of schizophrenia. Schizophrenia is thought to be polygenic – this means that its development is not determined by a single gene but a few (maybe as many as 108 genes) – this means that there is little predictive power from this explanation. Genes associated with the increased risk included those coding for the functioning of a number of neurotransmitters including dopamine Link to previous theory … Additional material to help you form an argument for or against the biological explanation of Sz Schizophrenia: stolen minds stolen lives: https://www.youtube.com/watch?v=Rv0b1unxUp M A specific gene that increases the risk of Sz >>> https://www.youtube.com/watch?v=fME16W4kc_ Q Neural Correlates: Brain dysfunction • Brain scanning techniques have made it possible to investigate living Sz brains • Both positive and negative symptoms have correlates Neural correlates of negative Neural correlates of positive •Activity in the ventral striatum •Reduced activity in the superior linked to the development of temporal gyrus and anterior avolition (loss of motivation) cingulate gyrus linked to the •ventral striatum believed to be development of auditory hallucinations involved in anticipation of a •Patients with auditory hallucinations reward – if there is abnormality in areas such as the ventral striatum, then this would result in a lack of motivation (avolition) showed lower activation levels in these areas than controls – reduced activity in these areas of the brain is a neural correlate of auditory hallucinations Suggested that the ventricles are 15% larger in Sz Ventricles: cavities that supply nutrients and remove waste Enlarged ventricles associated with negative rather than positive symptoms: Activity - Put the key phrases below in the appropriate part of the table: • Located deep inside the brain and affects movement and thinking skills. • Process information received from the eyes and the ears. • Schizophrenics have the same activity in these areas when they hallucinate as sane people do when they have genuine visual and auditory experiences. • Many schizophrenics have lower activity in this area, which could be linked to delusions and disorganised thoughts. • High levels in brain areas are linked to positive symptoms. • Smaller in schizophrenics so can link to loss of emotion (affective flattening). • Research has shown that this structure is larger in schizophrenics, which could cause motor dysfunction. • Responsible for basic feelings such as fear, lust and hunger. • Helps people think logically and organise their thoughts. • Low levels in certain brain areas are linked to negative symptoms as these are linked to a loss of pleasure. • Responsible for feelings of pleasure and also affects thinking and movement. Using your picture in the pack Match the text in the table to the areas of the brain. A Low levels of dopamine (hypodopaminergia) in the prefrontal cortex (responsible for thinking and decision making) in the negative symptoms of schizophrenia. B An excess of dopamine receptors in Broca’s area (which is responsible for speech production) may be associated with poverty of speech and/or the experience of auditory hallucinations. C Lower activation levels in the superior temporal gyrus and anterior cingulate gyrus are correlated with hallucinations. D Abnormality of areas like the ventral striatum may be involved in the development of avolition. Neural correlates of schizophrenia - evaluation A03 • Findings are inconsistent and therefore inconclusive • MRIs have made it possible to investigate living brain images which is an advance on merely having to rely on post mortems • However issues of causality. – Cause and effect can not be established with brain abnormalities - it is still uncertain whether structural abnormalities/reduced functioning predispose to schizophrenia, or whether the onset of the clinical symptoms causes these changes. Evaluation Summary • Biological explanations do account for schizophrenia, however the fact that there is no conclusive explanation that accounts for all schizophrenics - research is difficult to interpret and there have been contradictory findings. • It is difficult to establish cause and effect – as many participants have suffered from schizophrenia for a while and have been undergoing treatment. • Enlarged ventricles may be the result of taking antipsychotic medication for example • Biological explanations are reductionist in attempting to explain a complex multi- faceted disorder at the level of cells, genes and chemicals Evaluation Summary • Biological explanations are deterministic in the assumption that the disorder can be inherited and unavoidable • Biological explanations do account for schizophrenia, however the fact that there is no conclusive explanation that accounts for all schizophrenics means that psychological explanations need to be considered. • A ‘diathesis-stress’ relationship may be at work – an individual may have a genetic predisposition for schizophrenia but it may be due to environmental factors that lead to the onset of the condition What have I learnt? On a post it note: 5 key words each • What is the genetic explanation? • What is the dopamine H1 explanation? • What is the neural correlates explanation? to leave ACTIVITY • Describe and evaluate the biological explanation of schizophrenia • You must comment on how the evidence you use supports or challenges the explanation • You should comment on evidence both for and against the explanation • You could use your own skills and knowledge to make additional critical and evaluative points.