Schizophrenia: Diagnosis, Causes, & Treatments - PDF

[(Validity & Reliability of...)] [Classification and Diagnosis ] Classification=the idea that symptoms that go together make a disorder Diagnosis= identifying symptoms in an individual and using a classification system to identify the disorder SCZ= severe mental disorder characterised by a disrup...

[(Validity & Reliability of...)] [Classification and Diagnosis ] Classification=the idea that symptoms that go together make a disorder Diagnosis= identifying symptoms in an individual and using a classification system to identify the disorder SCZ= severe mental disorder characterised by a disruption of language, thought, perception (including of reality), emotions, movement and sense of self It has a prevalence of roughly **1%**- and is more common in men, people in urban environments and lower socio-economic groups **DSM-5** requires **one positive** symptom for diagnosis (hallucinations, delusions) **ICD-10** requires **two negative** symptoms for diagnosis (speech poverty, avolition) **Reliability= consistency** **Test-retest** reliability= using same criteria for same person getting same outcome\* **Inter-rater** reliability= different clinicians using same criteria on same person getting same outcome\* **Validity= ability to measure what is claimed** **Criterion** validity= two different systems (DSM/ICD) used on the same person and getting the same outcome\* \*A **spearman's** statistical test for correlation can be used to correlate the 2 outcomes. If there is a significant positive correlation **above 0.8** (above chance) then it can be concluded that the diagnosis is reliable/valid. DIAGNOSIS RELIABLE- DSM-5 test-retest reliability +.92, DSM-5 inter-rater reliability +.97, very strong positive correlations (beyond chance), diagnosis is consistent DIAGNOSIS UNRELIABLE-8 sane confederates reported false symptoms at a psychiatric hospital, all but one diagnosed with SCZ, average stay 19 days, suggests possible overdiagnosis DIAGNOSIS/CLASSIFICATION LACKS VALIDITY- co-morbidity with depression 50%, OCD 23%, symptom overlap, bipolar and SCZ share delusions and avolition, diagnosis doesn't represent something clear and distinct, may lead to misdiagnosis (over or under), plus only 20% recover with treatment and 50% with limited improvement, a diagnosis should lead to successful treatment, which it doesn't DIAGNOSIS GENDER BIASED- men diagnosed more (1.4:1 ratio), could be men are genetically more vulnerable, or women have better social support, but in the US despite showing similar symptoms men still diagnosed more, androcentric assumption women are naturally more delusional? Decreased QoL for women- no access to treatment DIAGNOSIS CULTURALLY BIASED- hearing voices in some Afro-Caribbean cultures is a norm, but Afro-Caribbean British men 10x more likely to be diagnosed than white British men, discriminated against by biased diagnostic system, labels-stigma, lower QoL [Biological explanations of SCZ- GENETIC] Strong relationship between degree of genetic similarity and shared risk of SCZ The **closer the genetic relatedness**, the **greater the predisposed risk** (48% MZ vs 17% DZ vs 9% sibling vs 2% aunt/uncle) Polygenic- **108** genes involved (each slightly increases risk) Aetiologically heterogeneous- risk is affected by combinations Can be a mutation in parental DNA, positive correlation between paternal age (increased risk of **sperm mutation**) and risk of SCZ (the older a father is the more risk of sperm mutations) Twin studies- **MZ 48% vs DZ 17%** concordance rates SUPPORTING TWIN EVIDENCE- one study found 33% MZ and 7% DZ concordance rates, shows some degree of biological basis, but concordance is never 100 so cannot be solely genetic in origin, however, still supports role of genetics in SCZ TWIN STUDY FLAWS- MZ twins are often treated the same, therefore have the same experiences, and so are more likely to both develop SCZ than DZ twins treated differently, treatment of the twins is a CV, evidence from studies is unreliable OVERLY REDUCTIONIST- reducing to genetics alone and ignoring the role of environmental risk factors is determinist, there are bio risk factors such as smoking cannabis, and psych risk factors such as child/sex abuse- both external, genes are not a complete explanation GENETIC COUNSELLING VALUE- potential parents with SCZ in family advised on risks of having a child with SCZ, more prepared, can lead to better parenting (stress-free upbringing, less dysfunctional family, reduced EE). Could minimise risk of development or make living with condition more manageable [Biological explanations of SCZ- NEURAL] The **dopamine hypothesis**- increased dopamine activity (**hyperdopaminergia**) in the **subcortex** is associated with hallucinations and speech poverty (an excess of DA receptors in pathways linking subcortex to Broca's area) (Broca-auditory hallucinations) The **revised dopamine hypothesis**- reduced dopamine activity (**hypodopaminergia**) in the **prefrontal cortex** (thinking/decisions) linked to negative symptoms? PET scan evidence shows this (lower DA activity in PFC) Neural Correlates- VERY STUPID ANTS CAN GET STUCK TO GLUE **Low** activity in the **Venal Striatum** has a negative correlation with severity of negative symptoms eg avolition, so lower activity, worse symptoms **Low** activity in the **Anterior Cingulate Gyrus** and the **Superior Temporal Gyrus** is correlated with hallucinations Enlarged **Ventricles- 15% larger** in SCZ than control, associated with negative symptoms AMPHETAMINES EVIDENCE/ DRUGS WORK- amphetamines that increase DA have been found to mimic symptoms, and anti-psychotic drugs that reduced DA activity reduce symptoms, so though the role of DA is complex it clearly plays a role in SCZ symptoms GLUTAMATE ROLE- research from scanning and post-mortems show raised levels of glutamate in SCZs, and several candidate genes have been identified that influence glutamate activity, so the dopamine hypothesis alone doesn't explain SCZ fully. Also, the effectiveness of clozapine may be due to its dual impact on DA and glutamate AMPHETAMINE PSYCHOSIS NOT SCZ- evidence from rat research shows that amphetamines that increase DA can cause SCZ like symptoms and anti-psychotics that target DA reduce symptoms, but apomorphine increases DA with no symptoms of SCZ, and there are debates highlighting the differences between amphetamine psychosis and SCZ- so this argument alone isn't enough to support the role of dopamine PROXIMAL NOT DISTAL- shows correlations that explain symptoms, but cannot explain the cause, so is the explanation even useful? No understanding of cause means no treatments, incomplete explanation, cant establish cause/effect [Biological therapies for SCZ] **[Chlorpromazine]** (**typical** antipsychotic) -dopamine antagonists (block & reduce) -**blocks D2 receptors**, reducing DA activity (levels build up so production reduces) -reduces **positive** symptoms -has a **sedation** effect [Side effects] -possible **irreversible** tardive dyskinesia (facial tremors) -neuroleptic malignant syndrome, rare but **fatal** **[Clozapine]** (**atypical** antipsychotic) -normalises activity of **dopamine, serotonin** and **glutamate** -**temporary** effect -reduces **positive and negative** symptoms -reduces **depression, anxiety,** improves **mood** and **cognitive functioning** [Side effects] -less severe tardive dyskinesia -immune system side effects (some died from a blood condition) **[Risperidone]** -normalises **dopamine** and **serotonin** activity -**fewer** side effects -binds more **strongly** to DA and 5ht receptors so can be given in **lower doses** PLACEBO, EVIDENCE THEY'RE EFFECTIVE- 13 study meta review, Ch better than a placebo. Also, Cl more effective than Ch- effective in up to 50% treatment resistant cases. Meta analysis of 15 studies found both Ch and Cl had no significant difference when it came to symptom reduction, so antipsychotics, specifically Cl should be NHS 1^st^ line defence SIDE EFFECTS, NOT APPROPRIATE- both have fatal side effects (Ch neuroleptic malignant syndrome, Cl immune disorder) Ch has irreversible TD and Cl reversible TD- a patient in the US suffering TD received an out of court settlement due to this, so appropriateness/ ethics of prescribing is questionable NOT SURE WHY THEY WORK- most drugs tackle high levels of DA in the subcortex (Broca's area), but there's evidence this isn't the cause of SCZ as other areas of the brain eg the prefrontal cortex have low DA, so shouldn't they make symptoms worse? Unknown cause-effect, should they be prescribed if we can't identify why they work? CHEMICAL STRAIGHT JACKET- argued antipsychotics are used to calm patients, make them manageable/easier to work with, not for therapeutic benefit. BUT calming someone experiencing hallucinations may help with therapy compliance, so due to a lack of other options they may be useful as they do have some benefits [Psychological explanations- Family Dysfunction] **Family Dysfunction**= abnormal processes within a family such as poor communication, cold parenting and high levels of expressed emotion. These may be risk factors for the development and maintenance of SCZ. 1.**Schizophrenogenic mother**= **cold, rejecting**, controlling -creates a climate of tension explanations, this helps restructure the client's beliefs) R-therapist and client may develop **strategies to counter irrational** thoughts (e.g. **reality testing** and **positive self-talk** to drown out voices/ prove them wrong) ABCDE model: A. Identify **[A]ctivating event** (door bang) B. Explore **irrational [B]eliefs** (gun shot from mafia) C. Recognise **[C]onsequences** (hiding in cupboard) D. **[D]ispute** irrational beliefs (why would mafia be here) E. **Beliefs restructured** **[E]ffectively** (more rational thoughts & behaviour) **Doesn't cure** symptoms BUT can stop patterns of thinking, for **management/coping** CBT EVIDENCE & NICE- Jahar reviewed 34 studies of CBT for SCZ and found a significant (beyond chance, over 95% sure, \