Schizophrenia

THE DIAGNOSIS AND CLASSIFICATION OF SCHIZOPHRENIA Classification of schizophrenia The classification of a mental disorder is the process of organising symptoms into categories based on symptoms 2 major systems of classification: The World Health Organisation's International Classification of Disease edition 10 (ICD) and the American Psychiatric Associations Diagnostic and Statistical Manual Edition 5 (DSM) Positive Symptoms: (added to behaviour) Hallucinations: sensory experiences of stimuli that have either no basis in reality or are distorted perceptions of things that are there. eg - voices talking to the sufferer Delusions: Involve beliefs that have no basis in reality - irrational. eg - believing to be an important historical, political or religious figure such as the queen Negative Symptoms: (taken away from behaviour) Avolition: involves the loss of motivation to carry out tasks, lowered activity levels. Anderson identified 3 signs of avolition: poor hygeine and grooming, lack of persistence in work/education and lack of education Speech Poverty: reduction in quality and frequency of verbal output, speech disorganisation involves disorganised and inconherent speech (this is classified as a positive symptom) Evaluation: Reliability - in the case of diagnosis, inter-rater reliability is to what extent two or more mental health professionals arrive at the same diagnosis Validity - to what extent to which we are measuring what we are intending to measure, one standard way of assessing validity of diagnosis is criterion validity Co-morbidity - the occurance of two illnesses or conditions together , eg if a person has both schizophrenia and personality disorder. When 2 conditions are frequently diagnosed together it calls to question the validity of classifying the two disorders separatly symptom overlap- occurs when two or more conditions share symptoms - calls into question the validity of classifying the two disorders separately Gender Bias - Longenecker - since the 1980's men have had more diagnosis of Sz than women - suggests a gender bias with women being underdiagnosed due to good interpersonal functioning Culture Bias - cultural bias due to cultural norms varying between cultures, distrust of black patients, westernised classifications of abnormality

THE BIOLOGICAL EXPLANATIONS: The Genetic Explanation: · Schizophrenia runs in families- this on its own is weak evidence of a genetic link · Identical twins share 100% of genetic materials · Non-identical twins and siblings share only 50% of genetic material · Gottesmann’s study – the concordance rate for identical twins to both have Sz is 48% versus 17% for non-identical twins and 9% for siblings · Shows a relationship between the degree of genetic similarity and shared risk of Sz · However it also shows that environmental factors MUST have a role- identical twins normally share environment and are treated the same due to looking the same, non-identical twins are more likely to share environment than siblings explaining higher % · The brain is the source of all mental states, Sz is a disorder of the mental state, if genes determine brain structure/ neurochemistry then these determine our thought processing and behaviours then we can inherit psychological traits and therefore Schizophrenia · Polygenic – schizophrenia requires a number of factors to work in combination – a number of genes increase risk · Aetiologically heterogeneous – different combinations of these genes can lead to the condition (Ripke et al: genetic makeup of 37,000 patient’s vs 113,000 controls – 108 separate genetic variations associated with risk of Sz) The Dopamine Hypothesis: · Neurotransmitters: the chemical messengers work differently in the brain of a patient with schizophrenia – in particular DOPAMINE. It is important in the functioning of several brain systems that may be implicated in the symptoms of schizophrenia · Hyperdopaminergia in the SUBCORTEX – the original focus of the dopamine hypothesis was high levels of dopamine in the sub cortex (central areas of the brain) – eg. Broca’s area which may be associated with speech poverty · Hyperdopamingergia in the CORTEX – most recent version of the hypothesis focus instead on abnormal dopamine systems in the cortex. Goldman-Rakic identified role of low levels of dopamine in the prefrontal cortex in negative symptoms Neural Correlates: · Measurements of the structure or function of the brain that correlate with experience – i.e schizophrenia. Both positive and negative symptoms have neural correlates. · Neural correlates of negative symptoms: THE VENTRAL STRIATUM involved in avolition/lack of motivation – abnormality in the ventral striatum. Juckel et al : negative correlation between activity levels in the ventral striatum and the severity of negative symptoms · Neural correlates with positive symtpoms: Lower activation levels in the SUPERIOR TEMPORAL GYRUS and ANTERIOR CINGULATE GYRUS were found with people with hallucinations – reduced activity in these areas neural correlate with auditory hallucination Evaluation: · Gottesmann study · Tienari et a : adoption study – children of Sz sufferers are still at heightened risk if adopted into low risk families · Ripke et al · Mixed evidence for dopamine hypothesis · Correlation or causation ?????

THE PSYCHOLOGICAL EXPLANATIONS Family Dysfunction: · The schizophrenic mother – Fromm-Reichmann’s psychodynamic explanation for schizophrenia, based on accounts of patients on their child hood. Particular type of parent = schizophrenogenic mother = cold, rejecting and controlling, which creates tension and secrecy. Leads to distrust which develops into paranoid delusions · Double-blind theory – Bateson et al- family climate is important, and emphasis on communication. Child receives mixed messages about what they’re doing wrong. When they get it wrong they are punished by the withdrawal of love, causes disorganised thinking and delusions · Expressed emotion (the accepted point) – the level of emotion (in particular negative emotion) expressed towards patient by carer. Contains the elements: verbal criticism, hostility and emotional over involvement. Serious source of stress which can trigger the onset of Sz in someone already vulnerable Cognitive Explanations: · Focuses on the role of mental processes · Ventral striatum associated with negative symptoms · Reduced info in the temporal and cingulate gyrus associated with hallucinations · Frith et al identified two kinds of dysfunctional thought processing that could underlie symptoms: 1. Metarepresentation: the cognitive ability to allow us to reflect on thoughts and behaviour – dysfunction would disrupt ability to recognise our own thoughts as being carried out by ourselves explaining hallucinations 2. Central control – the cognitive ability to supress automatic response, dysfunction could result in disorganised speech and thought disorder Evaluation: · Information gathered as a child may be distorted by the symptoms and therefore reducing validity of their recall · Almost no evidence to support schizophrenic mother or double blind · Leads to parent blaming · Stirling et al – 30 patients with 18 controls, range of tasks including stroop test – patients took over twice as long as controls – supporting dysfunction

DRUG THERAPIES Two Kinds: 1. Typical Antipsychotics 2. Atypical Antipsychotics Typical antipsychotics: -Have been around since the 1950’s -Example is chlorpromazine -taken as tablets, syrup or injection -Strong association to the dopamine hypothesis -Work as a dopamine ANTAGONIST as blocks the dopamine receptors in the synapse and reduce the activity of dopamine, in particular D2 receptor -Antagonists reduce the action of the neurotransmitters -Works only on positive symptoms -Also a sedative – related to its effect on histamine receptors Atypical antipsychotics: -Have been used since the 1970’s -Example is clozapine -not available as an injection due to its fatal side effect -Also a dopamine ANTAGONIST but also works on serotonin and glutamate receptors – helps to improve mood and reduce depression and anxiety as well as cognitive functioning -often prescribed to suicidal patients as mood enhancing effects- 30-50% of Sz patients want to commit suicide Evaluation: Effectiveness: -Thornley et al: compared chlorpromazine with a placebo control group – from 13 trials 1121 ppts showed that chlorpromazine was associated with better overall functioning, reduction in symptoms severity and relapse rate -Meltzer: Clozapine is more effective than typical antipsychotics, effective in 30-50% of resistant cases where typical antipsychotics failed Side effects: -Tardive dyskinesia: caused by dopamine super sensitivity and is involuntary facial movements – worse with typical antipsychotics -Neuroleptic malignant syndrome: most serious side effect for typical antipsychotics, caused when drug blocks dopamine action in the hypothalamus – results in high temperature, delirium and coma and can be fatal -Agranulocytosis: fatal, patients on clozapine need regular blood tests Dependence on the dopamine hypothesis: -original dopamine hypothesis not the complete explanation for Sz -dopamine levels in the brain apart from the sub cortex are actually too low rather than too high -If this is true, not clear how antipsychotics work as antagonists of dopamine – reducing dopamine -the dopamine hypothesis suggests then that antipsychotics shouldn’t work -undermined by the theory they rely on

PSYCHOLOGICAL THERAPIES CBT: -A method for treating disorders based on both cognitive and behavioural techniques -From cognitive viewpoint the therapy aims to deal with thinking, such as challenging negative thoughts -involves up to 20 sessions, only 1-2-1 therapy the NHS offers -Uses Ellis’s ABC model -The aim in general is to help patients identify irrational thoughts and trying to change them -How it helps: Helps to make sense of HOW their delusions and hallucinations impact their feelings and behaviour – just understanding where symptoms come from can be very helpful. -Offering psychological explanations for the existence of hallucinations (for example) can help reduce anxiety, psychologists also challenge irrational beliefs and provide alternative explanations for them, use Normalisation techniques, give homework Studies: - Jauhaur et al – meta analyses on the effectiveness of CBT and also investigated publication bias. Results = overall symptoms (CBT vs no CBT) -0.62 v -0.15 with no consistent evidence of publication bias across analyses. Conclusions = therapeutic effect on symptoms in the ‘small range’, reduced further when sources of bias are controlled -Jones et al – Cochrane review, all randomised controlled trials for CBT, 31 papers for 20 trials, no difference in overall effectiveness was found between CBT and other talking therapies, relapses and rehospitalisation was not reduced -Evaluative point = the ceiling effect – drugs already improved Sz as much as possible FAMILY THERAPY: -Takes place with the family to improve quality of communication and interaction, to reduce stress and expressed emotion and ensure compliance with drugs -The therapy works closely with the theory of expressed emotion -Pharoah et al identified a range of strategies which aim to improve functioning of a family, eg. Reduction of anger and guilt in family members and improving behaviour and beliefs towards Sz Studies: Pharoah et al – randomised and quasi randomised studies on families with Sz and compared it to standard care. Results = decrease in the frequency of relapse (RR = 0.55), reduce hospital admission (RR = 0.78) and compliance to medication (RR = 0.6). BUT methodological issues – problem of randomisation (majority of studies from china which stated they used randomisation when they didn’t) and the lack of blinding (observer bias) McCreadie et al – 52 families were offered family therapy, only 31 agreed and 14/30 didn’t attend – do people actually want family therapy? TOKEN ECONOMY: -a reward system to manage patients in psychiatric hospitals / modify bad habits or maladaptive behaviour -based on operant conditioning to reinforce positive and desirable behaviour -Tokens = secondary reinforcers (no value until reward is obtained), given immediately for desirable behaviour, this immediacy is important because it prevents delay discounting -Rewards = the positive reinforcement Studies: McMonagle and Sultana- meta analysis of randomised studies comparing token economy to standard care. Results = Only 3 trials could be included, there was no usable data on target or non-target behaviour, one small study found an improvement in negative symptoms. Conclusions – token economy may have an effect on negative symptoms, but it still remains worthy of careful evaluation Evaluation : -improve quality of live but do not cure

THE INTERACTIONIST APPROACH THE DIATHESIS MODEL: -means vulnerability, in this context stress means a negative psyshcological experience -The diathesis stress model states that both a vulnerability to Sz and a stress trigger are necessary in order to develop the condition -One or more underlying factors make a person particularly vulnerable to developing Sz but the onset of the condition is caused by stress -Meehl’s model – the original diathesis stress model, entirely genetic, the result of a single ‘schizogene’ – leading to the development of a biologically based schizotype personality. If a person does not have the schizogene then no amount of stress would lead to Sz, however in carriers of the gene, chronic stress through childhoods could result in the condition -The modern model – many genes appear to increase genetic vulnerability, no single ‘schizogene’ (Ripke et al). Modern model views a range of factors beyond the genetics- including psychological trauma (Ingram and Luxton) so trauma becomes the diathesis rather than the stressor. Read et al said that early trauma alters the brain – may affect the brain development, eg. The hypothalamic-pituitary-adrenal can become over active making a person more vulnerable to stress -Modern understanding of stress – in original model, stress was seen as psychological in nature, the modern definition includes anything that risks triggering Sz (Houston et al). The factor of cannabis – interferes with the dopamine system -Interactionist treatment – as the interactionist approach acknowledges both biological and psychological factors it is compatible with both biological and psychological treatment. The model is associated with combining drugs with psychological therapies, most commonly CBT. Study: Turkington et al – points out it is possible to believe in biological causes and use CBT to relieve psychological symptoms, but you have to adopt the interactionist approach- not possible to adopt a purely biological approach Evaluation: -Tienari et al – children adopted from Finish Sz mother, their adoptive parents assessed for child-rearing style and rates of Sz were compared to a control group of adoptees with no genetic risk. Results = child rearing styles of criticism, conflict and low levels of empathy implicated development of Sz in HIGH genetic risk children and not the control group. Suggests that genetic vulnerability and family stress are important in developing Sz -Houston et al – childhood sexual trauma emerged as a vulnerability factor whilst cannabis use was the trigger – shows the old idea that diathesis was biological and stress psychological was overly simple -Tarrier et al – 315 randomly allocated to a medication + CBT group, medication + counselling or a control group. Patients in the two combination groups showed lower symptoms levels than those who just had medication (controls)