schizophrenia Flashcards

1
Q

Describe Type I and Type II schizophrenia

A

Type I : acute from characterised by positive symptoms and responsive to medication
Type II: chronic type characterised by negative symptoms and poorer prospects for recovery.

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2
Q

What are positive symptoms?

A
  • loss of touch with reality , such as hallucinations and delusions.
  • These generally occur in actute, short episodes
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3
Q

What are negative symptoms?

A
  • involve the displaying of behaviours concerning disruption of normal emotions actions.
  • these occur in chronic longer-lasting episodes , and are resistant to medication.
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4
Q

How is schizophrenia usually identified?

A
  • to be diagnosed with schizophrenia , 2 or more symptoms must be apparent for more than one of month, as well as reduced social functioning.
  • commonly occurs between 15 and 45 years of age, with an equal incidence rate between males and females, though males show onset an an earlier age.
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5
Q

Describe Schneider’s symptoms of schizophrenia

most are positive symptoms

A

1.** Passivity experiences and thought disorders:** thoughts and actions are percieved as under external control. Sufferers believe that thoguhts are being inserted, withdrwn or broadcast to others.
2. **Auditory hallucinations : **sufferers experience voices, often insulting and obscene which form running commentaries, or discuss the sufferers behaviour.
3. Primary delusions: sufferes usually experience delusions of grandeur belieiving they are someone important

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6
Q

Describe Slater and Roth’s negative symptoms of schizophrenia

A
  1. Thought process disorders: sufferers wander off the point, invent new words and phrases , stop mid sentence.
  2. Disturbances of effect : sufferers appear uncaring of others, display inappropriate emotional responses - e.g.
  3. Psychomotor disturbances: sufferers adopt frozen , statue like poses , exhibit tics and twitches and repetitive behaviours
  4. Avolition: sufferers display an inability to make decisions , have no enthusiasm or energy , lose interest in personal hygeine and lack sociability and affection.
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7
Q

How is schizophrenia diagnosed?

A
  • DSM-5 produced in the USA , and the ICD-10 by the WHO is used to diagnose schizophrenia
  • schizophrenia has a distinct set of symptoms that allows it to be diagnosed in a relibale and valid way.
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8
Q

H

Define reliability

A
  • Reliability concerns the consistency of symptoms measurement and affects diagnosis in two ways:
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9
Q

Describe the two different types of reliability

A
  1. Test-retest reliability: occurs when a clinician makes the same diagnosis on separate occasions from the same information
  2. Inter-rater reliability: occurs when different clinicians make identical , independent diagnoses of the same patient
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10
Q

Outline research on the relaibility of diagnosis for those with schizophrenia

A
  • Beck et al. (1962) Found a 54% concordance rate between experienced practitioners’ diagnoses when assessing patients. This suggests issues with reliability in the diagnosis process.
  • Söderberg et al. (2005) Reported an 81% concordance rate using the DSM classification system, indicating that reliability has improved over time with updated systems.
    Nilsson et al. (2000) Found a 60% concordance rate between practitioners using the ICD classification system. This implies that the DSM system may be more reliable than the ICD.
  • Read et al. (2004) Reported a test-retest reliability rate of 37% for schizophrenia diagnoses, showing poor consistency over time. Additionally, only 2% of British psychiatrists diagnosed schizophrenia from a case description, compared to 69% of American psychiatrists, demonstrating cultural differences and further questioning the reliability of schizophrenia diagnoses.
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11
Q

Evaluate research on the reliability of schizophrenia

A
  • The DSM classification system is regarded as more reliable than the ICD because the symptoms outlined for each catergory are more specific
  • even if reliability is not perfect , it allows practitioners to have a common viewpoint , permitting communication of research ideas and findings , which may ultimately lead to a better understanding of the disorder and the development of effective treatments
  • ## research shows that reliability of diagnoses has imporved as classification systems have been updated.
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12
Q

define validity

A
  • the accuracy of a diagnosis
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13
Q

Give and define the 4 ways validity can be assessed in the diagnosis of schizophrenia

A
  1. Reliability
  2. Predictive validity ( if diagnosis leads to successful treatment then it is valid)
  3. **Descriptive validity: paritents with schizophrenia should differ in symptoms from patients with other disorders.
    4.
    Aetelogical validity: **all should have the same cause for the disorder
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14
Q

Summarise Rosenhan’s research on the validity of diagnosis using the DSM-II classification system

A
  • 8 volunteers without mental illness pretended to hear voices and presented themselves at different mental hospitals. All were admitted, after which they acted normally.
  • The time it took to be released and how staff interpreted their behaviors were recorded.
  • In a 2nd part of the study, hospitals were informed that pseudo-patients would attempt entry within three months. Staff recorded suspected impostors, though no pseudo-patients were actually sent.
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15
Q

Evaluate and give the finding’s of Rosenhan’s research

A
  • The pseudo-patients were diagnosed with schizophrenia and remained hospitalized for 7 to 52 days.
  • In the second part, 193 patients were admitted, of whom 83 were suspected to be impostors by staff, though none were fake.
  • Highlighted flaws in diagnostic systems and raised awareness about the stigma of mental health diagnoses.
  • The study’s results might be influenced by clinicians’ expectations and the unusual nature of faking mental illness to gain hospital entry.
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16
Q

Give research on validity of diagnosis

A
  • Bailie et al surveyed 154 British psychiatrics to find that other than an agreement as to the influence of genetics, biochemical abnormalities and substance abuse , they had differing views on the cause of S. Suggests that aetiological validity of S is low.
  • Jager et al found that it was possible to use ICD-10 TO distinguish 951 cases of S from 51 PDD , 116 cases of acute and transient psychotic disorders. Suggests that diagnosis has high descriptive validity.
17
Q

Evaluate the validity of diagnosis in schizophrenia

A
  • the predictive validity of S diagnosis can be argeud to be low because different sufferers experience such a wide range of symptoms
  • Being labelled S has a long lasting negative effect on social relationships , work prospects , self esteem etc which is unfair if diagnoses is invalid
18
Q

Define comorbidity

A
  • the presence of one or more additional disorders or diseases simultaneously occuring with schizophrenia
  • schizophrenics often suffer from forms of depression , as well
  • also raises issues of descriptive validity as having simul. disorders suggests that S may not actually be a seperate disorders
19
Q

Give research on comorbidity

A
  • Sim et al reported that 32% of 142 hospitilised S had an additional mental disorder, illustrating the problem that CM can create in achieving reliable and valid diagnoses.
  • Bucekly reported that an estimated 50% S had comorbid depression , 15% panic disorder, 23% with OCD, 47% with substance abuse.
20
Q

How does culture bias affect the diagnosis of schizophrenia?

A
  • concerns the tendency to over-diagnose members of other cultures as suffering from S.
  • In Britain, Fearon found people with Afro-Caribbean hertiage in the UK and African Americans are up to 9 times more likely to be diagnosed with S compared to 1% of the general population.
21
Q

Give research which shows the culture bias when diagnosing Schizophrenia

A
  • Whaley believes that the reason for S for black Americans (2.1%) being greater than among white Americans (1.4%), is culture bias.
  • Fernado suggests that this occurs due to category failure where western defintions of mental illness are applied to no Western cultures
22
Q

Evaluate the effect of culture bias on diagnosis of S

A
  • Fernando argues that people from ethnic minorities experience greater levels of racism , povery etc. than the white population and higher levels of S , should be expected.
  • Cochrane argue that the racism and social deprivation immigrants suffer are bound to negatively affect mental health but that clinicians wrongly attribute their behaviour to their ethicity.
23
Q

Describe how gender bias affects the diagnosis of Schizophrenia

A
  • males tend to suffer more negative symptoms and have higher levels of substance abuse then females
  • females tend to have better recovery rates and lower relapse rates.
  • Men’s average age of diagnosis is 25 whereas women are 18-20. Cotton suggest that women’s underdiagnosis is due to women’s better social coping strategies leading to being less likely to seek treatment.
24
Q

Give research on gender bias in diagnosis

A
  • Haifner reported that males have more severe negative symptoms and higher levels of substance abuse.
  • Powell sent 290 psychiatrics 2 identical case studies where the gender and race of the patients where changed to either WF, WM, BF,BM , or NN. The researchers found overdiagnosis for black patients and underdiagnosis for females.
  • the most accurate diagnosiss was when the gender and race of the psychiatrist was the same
25
Q

Define symptom overlap and give some examples.

A
  • the perception that symptoms of S are also symptoms of other disorders.
  • Ophoff assessed genetic material from 50,000 particiapnts to find that of 7 gene locations on the genome assoicated with S , 3 of them were also associated with bipolar disorder, which suggests a genetic overlap.
26
Q

Evaluate the impacts of symptom overlap

A
  • the fact that there is genetic overlap between mental disorders suggests that gene therapies might be developed which simulataneously treat different disorders.
  • Ketter report that misdiagnosis due to SO can lead to years of delay in recieving relevent treatemnt , during time suffering and further degeneration can occur , aswell as high suicide levels.
27
Q

Give the genetic explanation of schizophrenia

A
  • sees S as transmitted through hereditary means.
  • Believes it to be a polygenic disorder, which increases an indidivuals overal vulnerability to developing schizophrenia
28
Q

Give research on the genetic explanations for schizophrenia

A
  • Gottesman & Shields (1976) reviewed 5 twin studies and reported a concordance rate of between 75% and 91% for MZ twins with severe forms of S , suggresting that genetics plays a role.
  • Torrey et al (1994) reviewing evidence from twin studies, found that if one MZ twin develops S , there is a 28% chance that the other twin will do to.
  • Kety & Ingraham: found that prevalence rates of S were 10 times higher among genetic than adoptive relatives of S suggesting that genetics > environmental factors.
  • The SWGPGC analysed the DNA of 36,989 S and 113,000 non-schizophrenics to identify 128 independent genetic variations at 108 locations on the human chromosomes that contribute to developing S. Of these 83 , had not been identified before.
29
Q

Evaluate the genetic explanations for schizophrenia

A
  • Twin studies suggest a genetic factor but do not consider socio-psychologcal factors between twins. Twin and family studies also fail to consider shared environmental influences.
  • if genes caused S on their own, concordance rates between MZ twins would be 100%, which they are not. Twin studies also produce confusing evidence , with heritability estimates ranging from 58% for MZ down to as low as 11%.
  • Leo (2006) argues that Kety’s adoption study evidence is not convincing as sample sizes were small makiing generalisations difficult , and many of the biological relatives with S were distant relatives , such as half siblings , with low biological similarity.
  • diathesis stress response: individuals inherit different levels of genetic predisposition to developing S , but it is environmental triggers that determine whether individuals go on to develop S.
30
Q

Describe the dopamine hypothesis

A
  • The DH believes that the onset of S is related to abnormal levels of the hormone and neurotransmitter dopamine.
  • dopamine increases the rate of firing of neurons during synapse which enhances communication between neurons. Snyder argued that if too much dopamine is released during synapse, it can lead to S.
  • DH was developed when phenothiazines and antipsychotic drugs lessened the symptoms of S, which decreased dopamine activity.
  • excessive amounts of dopamine in speech centres like Broca’s area may lead to auditory hallucinations and lower levels in areas like the frontal cortex are thought to contribute to negative symptoms like avolition
31
Q

Give research on the dopamine hypothesis

A
  • Randruo & Munkvad created S-like behaviour in rats by giving them amphetamines , which activate dopamine production , and then reversed the effects by giving them neuroleptic drugs, which inhibit the release of dopmine, supporting the DH.
  • Iversen (1979) reported that post mortems on people who had S found excess dopamine in the limbic system.
  • Javitt (2000) reported that the drugs phencylcidine and ketamine induce schizophrenic symptoms in non-sufferers by blocking neurotransmissions for glutamate receptors which leads to abnormal dopamine system functioning suggesting that there is a connection between D and S.
  • Leuhet et al conducted a meta analysis of 212 studie which tested the effectiveness of anti-psychotic drug treatments on dopamine balance vs a placebo. drugs were seen as more effective then placebo
32
Q

Evaluate the dopamine hypothesis as an explanation for schizophrenia

A
  • evidence is inconclusive as there is no consistent difference in dopamine levels between drug-free S and non-sufferers.
  • several neurotransmitters may be involved in the development of S , some drugs implicate serotonin’s involvement.
  • Healy (2000) beleives that pharmaceutical companies were keen to see the dopamine theory promoted to make huge profits.
  • LLoyd et al beleive that even if dopamine is a causative actor , it may be an indirect factor mediated through environemtal factors as abnormal family can lead to high levels of D which n turn trigger S symptoms
33
Q

Describe neural correlates as a biological explanation for schizophrenia

A
  • believes the development of S is related to structural and functional brain abnormalities
  • also believed that enlarged ventricles ( which is associated with damage to central brain areas ) is assoiared w negative symptoms of S.
34
Q

Outline research on neural correlates

A
  • Johnstone using CT scans first identified people with S had larger than average ventircles suggesting this structural difference may be linked to the cause of S.
  • Weyandt reported that enlarged ventricles are associaed with negative symptoms only , which implies EV cannot explain all symptoms of S.
35
Q

Evaluate neural correlates as a biological explanation for schizophrenia

A
  • ventricle studies are based on correlational research it is difficult to determine if there is a causal relationship, or a 3rd factor linked to both the EV and S such as a potenial side effect of medication.
  • must be a consideration to environmental factors such as substance abuse and stress levels, which mau have a damaging effect on brain tissue.
  • ## Ho et al performed MRI scans on recent schizophrenics and re-scanned them 3 years later. They found evidence of brain damage in the recent which worsened over time even with medication, especially in the frontal lobes. - supports NC
36
Q

Evaluate the biological explanation for schizophrenia

A
  • supported by biological treatments
  • assumes that S is biologically determined making sufferers feel disempoweered when diagnosed. Cogntive approaches have a soft determinist perspective
  • bioloigcally reductionist as fails to consider evidence for the range of psychological aspects of S such as EE.
  • a holistic explanation would consider the diathesis-stress approach in which the root cause of the disorder is a biological/genetic weakness however an env factor triggers the disorder.
37
Q
A