schizophrenia ao1 Flashcards

1
Q

what are neural correlates

A

Neural correlates are brain structures and functions linked to specific psychological processes or behaviours.​
Researchers look for brain abnormalities that may explain the symptoms of the disorder.​

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2
Q

cingulate gyrus

A

-emotion processing, cognitive control, and the integration of sensory and emotional information.​
- hypoactivity or altered connectivity in the ACC is associated with negative symptoms such as flattened affect and social withdrawal. (Low activity in the ACC is associated with high level of negative symptoms (flattened affect and social withdrawal)​
Reduced activity or structural abnormalities in the ACC have been linked to impairments in cognitive control and executive dysfunction in schizophrenia, often contributing to difficulties in attention and problem-solving.​

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3
Q

Low levels of brain activity in ANTERIOR CINGULATE CORTEX leads to high levels of negative symptoms such as:​

A

-Flattened affect​
-Social withdrawal​
-Difficulties in attention ​
-Problem-solving

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4
Q

superior temporal gyrus

A

auditory processing, including language, but also has been implicated as a critical structure in social cognition.​
A negative correlation has also been found between activation levels in the superior temporal gyrus and the severity of auditory hallucinations. Therefore, reduced activity in this area increases auditory hallucinations. (Allen et al) ​

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5
Q

role of striatum

A

neural correlates of negative symptoms: A negative correlation has been found between the activity levels in the ventral striatum (part of the brain). It was found that there is less activity in the VS in SZ compared to control. ​
Therefore, negative correlation between activity levels in the Ventral Striatum increases the severity of overall negative symptoms. (Juckel et al)

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6
Q

ventral striatum

A

Therefore, negative correlation between activity levels in the Ventral Striatum increases the severity of overall negative symptoms. (Juckel et al)​
All negative symptoms.

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7
Q

prefrontal cortex

A

may explain the negative and cognitive symptoms (e.g., lack of motivation, attention deficits).​
Research: Studies have shown that people with schizophrenia have reduced activity in this region, especially during tasks requiring working memory.​
Therefore, low levels of activity in the pre-frontal cortex, increase negative symptoms such as attention deficit, lack of concentration, lack of goal oriented tasks. Davis et al. (1991)​

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8
Q

According to the dopamine hypothesis, schizophrenia is the result of an excess of dopamine activity at certain synapse site. This could be caused by:

A

The release of excess dopamine by neurons.​
Over sensitive dopamine receptors​
An excess of dopamine receptors.

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9
Q

Hyperdopaminergia

A

in the Subcortex: The original version of the dopamine hypothesis focused on the possible role of high levels or activity of dopamine in the subcortex (central areas) of the brain. ​
E.g., an excess of dopamine receptors in Broca’s area may be associated with disorganised speech and/or the experience of auditory hallucinations. Positive symptoms

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10
Q

hypodopaminergia

A

n the Cortex: More recent versions of the dopamine hypothesis have focused instead on abnormal dopamine systems in the brain’s cortex. ​
E.g. low levels of dopamine have been found in the prefrontal cortex which have been associated with the negative symptoms of schizophrenia.​

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11
Q

Negative symptoms

A

low levels of dopamine in the cortex
speech poverty

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12
Q

Positive symptoms:

A

hallucinations

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13
Q

Kety and Ingraham

A

carried out another adoption study that supports Tienari’s findings. ​
Adoption studies like this are useful because they control for environmental factors.​
If schizophrenia was passed on from parents to children through environmental factors only, you would expect that adoptees whose biological parents had SZ, would not develop SZ if they live in a free SZ environment. ​

However, Kety and Ingraham found that adoptees whose biological parents had schizophrenia were 10 times more likely to develop schizophrenia than a control group of adoptees whose biological parents did not have schizophrenia, supporting a genetic basis of the disorder.​

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14
Q

genetic factors

A

To conclude that schizophrenia is totally genetic the concordance rate should be 100%​
schizophrenia is a highly polygenic disorder (Lee et al., 2012; Purcell et al., 2009)​
Ripke found 108 combinations of genes that are associated with the risk of SZ. They include the ones that affect the neurotransmitter Dopamine.​
Benzel et al. (2007) three genes: COMT, DRD4, AKT1 – have all been associated with excess dopamine in specific D2 receptors, leading to acute episodes, positive symptoms which include delusions, hallucinations, strange attitudes.

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15
Q

family studies

A

schizophrenia is more common among biological relatives of a person with schizophrenia, and the closer the degree of genetic relatedness, the greater the risk. ​
E.g. Gottesman found ​
MZ have a 48% risk to share SZ​
DZ 17% risk to share sz​
Sibling 9% ​
Parents 6%

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16
Q

twinn studies

A

Support genetic explanations as they show higher concordance rate for MZ twins than DZ twins.​
E.g. Joseph (2004) found a concordance rate of 40.4% for MZ twins and 7.4% for DZ twins.

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17
Q

adoption studies

A

Studies of genetically related individuals who have been reared apart allow genetics and the environment to be separated.​
For example, Tienari (2000) found 6.7% of adoptees (twins) whose biological mothers had SZ also developed SZ compared to 2% of adoptees whose biological mothers did not have SZ.​

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18
Q

appropriateness of drugs meaning

A

Refers to whether the antipsychotic medication is suitable for a specific patient, given their medical condition, diagnosis, and individual characteristics

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19
Q

key factors of drug approprotiatness

A

diagnosis
patient characteristica
side efects
drug interactions

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20
Q

Diagnosis:

A

: Whether the medication is the right treatment for the patient’s psychiatric condition (e.g., schizophrenia, bipolar

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21
Q

Patient Characteristics:

A

Consideration of the patient’s age, medical history, comorbid conditions (such as heart disease, diabetes), and other medications they may be taking.

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22
Q

Side Effects

A

How well the patient tolerates the medication and the likelihood of adverse effects. The choice of antipsychotic might depend on minimizing side effects or addressing specific concerns (e.g., weight gain, sedation).

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23
Q

Drug Interactions

A

Ensuring that the chosen antipsychotic doesn’t negatively interact with other medications the patient is taking.​

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24
Q

effectiveness of drugs

A
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25
Q

typical antipsychotics

A

First or old generation (chlorpromazine and Haloperidol)

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26
Q

atypical antipsychotics

A

Second or new generation. (Ziprazidone, Clozapine)

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27
Q

how typical antispcyhotics work

A

They work by binding with​
The D2 receptors in the ​
Mesolimbic and Meso-cortical pathway.​

They block the entrance to the D2 into the ​
Post-synaptic neuron.

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28
Q

how effective antipsychotics re ro treat sz symptoms

A

DA antagonists seem to be effective at reducing positive symptoms in most SZ patients. However, they are not effective on negative symptoms.​

1/3 of SZ do not get any improvement (positive or negative symptoms) at all with DA antagonist drugs.

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29
Q

types of typical d2 antagonistic drugs

A

High potency: Allow for a quick release: injections (Haloperidol)​
Low potency: Chlorpromazine at a lower dosage.​

The higher the potency, the stronger the side effects

30
Q

antpyical drugs

A

5HT2A Antagonist blocks less dopamine and blocks more serotonin (Clozapine) ​
5HT1A Agonist increases dopamine in the prefrontal cortex and reduces glutamate release (Ziprasidone) (quetiapine)

31
Q

atypical side effects

A

Fewer side effects (Parkinsonism, tardive dyskinesia)​
Problems: ​
Produce a potentially lethal blood disorder (agranulocytosis). Decreases the number of white cells. This can lead to low immunity and death.​
Increase of insulin (diabetes) and weight gain.

32
Q

typical side effects

A


They tend to produce Extrapiramidal side effects:​
Parkinsonism – tremors, rigidity, slowness of movement, temporary paralysis​
Dystonia – involuntary muscle contractions​
Tardive dyskinesia – involuntary movements of the mouth, lips, and tongue​
Weight gain

33
Q

difference between typical and atypical

A

ypical: Reduce D2 levels in the synapses. They bind to dopamine receptors without stimulating them. They Block dopamine and stop it being picked up. Most effective when given at the onset of schizophrenia.​
A-typical antipsychotic drugs act on the dopamine pathway but they only occupy the dopamine receptors temporarily. Therefore, they have lower side effects than the conventional antipsychotic drugs. They also block more serotonin. ​

34
Q

dysfunctional thought process

A

Frith et al. (1992) identified two kinds of dysfunctional thought processing: ​
Meta-representation is our ability to reflect on thoughts and behaviour and it allows us to identify our goals and intentions, as well as allowing us to interpret the actions of others. ​
Dysfunction in this area would disturb our ability to recognise our own actions and thoughts as being ours and carried out by ourselves, rather than being carried out by someone else. This therefore can explain hallucinations as the inner voice is experienced as coming from an external source.​

Central control is our ability to suppress automatic responses while we perform deliberate actions instead. ​
Having disorganised speech could be due to an inability to suppress automatic thoughts and speech triggered by other thoughts. ​
Many schizophrenics experienced derailment of thoughts and spoken words/sentences because each word triggers an association and the schizophrenic individual cannot stop the automatic responses to these associations.

35
Q

what is cbt

A

Cognitive behavioural therapy (CBT) is based on the idea that most unwanted thinking patterns, emotional and behavioural reactions are learnt over a long period of time.

36
Q

steps of cbt

A

identify hallucination
experimental situation
strategies to deal
homework

37
Q

identify hallucinations

A

Event ​
Overhearing someone saying “I know what’s on your mind”​
Interpretation​
Everyone can read my thoughts​
Feeling​
Paranoid, scared and believing that others will attack me for my thoughts​
Behaviour​
Take evasive action – avoiding situations that will bring me into contact with others

38
Q

experimental situation

A

Experimental situations: the therapist ask the patient to think of a situation where the faulty cognition occurs and do an experiment to prove if this cognition is true or not.

39
Q

homework

A

This therapy relies on the patient taking an active part, and they are given ‘homework’ between sessions, like keeping a diary of the contents of their delusions.​
Later on, their homework might be to try out ways of coping which they have learned during therapy.

40
Q

what is classification

A

of mental disorders involves taking sets of symptoms and putting them into categories e.g. symptoms of depressed mood, feeling hopeless, having low self-esteem, eating too much or too little, sleeping too much or too little, and having difficulty concentrating often occur together. Therefore, someone showing these symptoms has a particular disorder. We can go on to classify that disorder as part of a wider class of disorders

41
Q

what is diagnosis

A

once a set of symptoms is established and classified into disorders, individuals can be diagnosed according to their symptoms.

42
Q

icd

A

nternational Classification of the Causes of Disease (World Health Organisation) – recognises a range of subtypes: hebephrenic, paranoid and catatonic

43
Q

dsm

A

Diagnostic and Statistical Manual of Mental Disorder (American Psychiatric Association) – used to also recognise the subtypes but the most recent DSM-5 has dropped these.

44
Q

def of positive symptoms

A

Positive symptoms are when you experience things in addition to reality. For example, you might see or hear things that others don’t. Or believe things that other people do not.

45
Q

def of neg symptoms

A

when you lose the ability to do something you used to do before. For example, losing motivation to do things that you used to enjoy. They often last longer than positive Negatsymptom

46
Q

hallucinations

A

They are unusual sensory experiences. Voices may be heard either talking to or commenting on the sufferer, often criticising them. Hallucinations can be experienced in relation to any sense. The sufferer may see distorted facial expressions or people or animals who are not there

47
Q

delusions

A

Also known as paranoia, delusions are irrational beliefs. Delusions of grandeur – being an important historical, religious or political figure. Delusions of being persecuted perhaps by the government or aliens. Delusions of the body – sufferers might believe that they or a part of them is under external control.

48
Q

what is abolition

A

sometimes called ‘apathy’, can be described as finding it difficult to begin or keep up with goal-directed activity. Sufferers of schizophrenia often have sharply reduced motivation to carry out a range of activities.

49
Q

what is speech poverty and disorganised speech

A

Schizophrenia is characterised by changes in patterns of speech.

50
Q

classification issues

A


Duration for 6 months DSM5: Continuous signs of the disturbance persist for at least 6 months. This 6-month period must include at least 1 month of symptoms (or less if successfully treated) ​
ICD10:The course of schizophrenic disorders can be either continuous, or episodic with progressive or stable deficit, or there can be one or more episodes with complete or incomplete remission.

51
Q

comorbidity

A

he occurrence of 2 illnesses or conditions together. For example, a person has both SZ and a personality disorder. Where 2 conditions are diagnosed together it calls into question the validity of classifying the two disorders separately. For example, a person who is taken steroids may have hallucinations. However, these hallucinations may also happen because the person has SZ. Therefore, they may not treat SZ because the doctors believes that the hallucinations are due to the steroids.

52
Q

symptoms overlap

A

Occurs when 2 or more conditions share symptoms. Where conditions share many symptoms this calls into question the validity of classifying the 2 disorders separately.

53
Q

hebephrenic schisophrenia

A

The person’s behaviour is generally disorganised and not goal directed. Symptoms include thought disturbances (including delusions and hallucinations), an absence of expressed emotion, incoherent speech, large mood swings and a loss of interest in life – social withdrawal.​
It is usually diagnosed in adolescence/young adulthood

54
Q

catatonic

A

his is diagnosed if the patient has severe motor abnormalities such as unusual gestures or use of body language. Sometimes patients gesture repeatedly, using complex sequences of finger, hand and arm movements, which appear to have some meaning for them. This type often involves doing opposite to what is being asked or repeating everything that is said. The main feature is almost total immobility for hours at a time, with the patient simply staring blankly.

55
Q

paranoid schizophrenia

A

This type involves delusions of various kinds (persecution and grandeur); however, the patient remains emotionally responsive. They are more alert than patients with other types of schizophrenia. Paranoid schizophrenics tend to be argumentative. In some ways this is the least serious - but the most well-known. This often has a later onset than other types

56
Q

features of schizophrenia

A

Often positive symptoms such as hallucinations can be overcome but the negative symptoms remain.​
With treatment around 60% of patients manage a relatively normal life.​
Prognosis better in non-industrialised societies because of increases stress levels and a lack of community.​
Different types of schizophrenia, Paranoid, Disorganized, Catatonic (removed from DSM5)​

57
Q

what is the interactionist approach

A

Acknowledges there are biological, psychological and societal factors in the development of sz.

58
Q

diathesis strwss model

A

Acknowledges there are biological, psychological and societal factors in the development of sz.

59
Q

diathesis

A
60
Q

stress

A
61
Q

meehls model

A

Believed diathesis was entirely genetic, the result of a single ‘schizogene’​

This led to the development of a biologically based schizotypic personality, one characteristic is sensitivity to stress​

According to Meehl, if a person doesn’t have the schizogene then no amount of stress would lead to sz. However, in carriers of the gene, chronic stress through childhood and adolescence, particularly a schizophrenic mother could result in sz

62
Q

modern views of diathesis

A

range of factors beyond the genetic, including psychological trauma – trauma becomes the diathesis rather than the stressor.​

Read (2001) proposed a neurodevelopmental model in which early development in which early trauma alters the developing brain. E.g. The hypothalamic-pituitary-adrenal system (HPA) becomes over-active and the person is more vulnerable to later stress ​

63
Q

modern understanding of stress

A

Originally stress was seen as psychological in nature, in particular related to parenting.​
Nowadays a broader definition of stress has been adopted and refers to anything that risks triggering schizophrenia; cannabis use for example (Houston et al. 2008), can be a stressor as it disrupts the body’s dopamine system which triggers SZ symptoms.

64
Q

schizophrenic mother

A

Family dysfunction explanations attempt to link schizophrenia to childhood and adult experiences of living in a dysfunctional family. ​
Fromm-Reichmann (1948) proposed an explanation or schizophrenia based on accounts that she heard from her patients about their childhoods. She noted that many of her patients spoke about a particular type of parent which she called the Schizophrenogenic mother (Schizophrenia-causing). Schizophrenia comes from being reared by a cold and dominant mother who is both overprotective but rejecting. This type of mother tends to create a family climate characterised by tension and secrecy. This leads to distrust that later develops into paranoid delusions, and ultimately, Schizophrenia. ​
Although such a mother appears self-sacrificing, she actually uses the child to satisfy her own emotional needs. ​
Therefore, individuals brought up with this mothering style develop schizophrenia​
as they are confused by their mothers overprotective but rejecting nature. This produces hallucinations and delusions.

65
Q

double bind

A

Bateson (1972) agreed that family climate is important in the development of Schizphrenia but emphasised the role of communication style within a family. He proposed the double-bind hypothesis which suggested that schizophrenia is a reaction to a pathological parent presenting the child with a no-win situation. This is created by contradictory communication between tone of voice and content

The developing child regularly finds themselves trapped in situations where they fear doing the wrong thing but receive mixed signals about what this is and feel unable to comment on the unfairness of the situation.​
When they ‘get it wrong’ the child is punished by the withdrawal of love which leads them to see the world as confusing and dangerous – this is reflected in symptoms such as disorganised thinking and paranoid delusions

Prolonged exposure to such interactions prevents the development of an internally coherent construction of reality; in the long run, this shows itself as typically schizophrenic symptoms such as ​
Negative symptoms - flattening affect, incoherent thinking and speaking, poor or absent social skills ​
Positive symptoms - delusions and hallucinations, paranoia ​
Bateson was clear that this was not a sole explanation of schizophrenia but more so a ris

66
Q

expressed emotions

A

The Expressed Emotion (EE) explanation is the level of emotion – negative emotion in particular which is expressed towards a person by their carer. Schizophrenic families persistently exhibit criticism, hostility and a general negative influence upon recovering schizophrenics, who when returning to their families react to the expressed emotion by relapsing and experiencing positive symptoms, such as delusions.​
EE contains several elements:​
Verbal criticism – occasionally accompanied by violence ​
Hostility – including anger and rejection ​
Emotional over-involvement – in the patient’s life, including endless self-sacrifice. ​
These high levels of expressed emotion in carers directed towards the patient are a serious source of stress for patients and is used primarily to explain for relapses in patients

Kuipers et al. (1983) found that high EE relatives talks more and listen less. It is thought that high levels of EE are most likely to influence relapse rates. A patient returning to a family with high EE is about four times more likely to relapse than a patient whose family is low in EE.​

However, it can also be suggested that the source of stress generated from high EE families may trigger the onset of schizophrenia in a person who is already vulnerable (Diathesis-stress model)

67
Q

dysfunctional throughout processing

A

Frith et al. (1992) has identified two kinds of dysfunctional thought processing: ​
Metarepresentation is our ability to reflect on thoughts and behaviour and it allows us to identify our goals and intentions, as well as allowing us to interpret the actions of others. Dysfunction in this area would disturb our ability to recognise our own actions and thoughts as being ours and carried out by ourselves, rather than being carried out by someone else. This therefore can explain hallucinations as the inner voice is experienced as coming from an external source.​

Central control is our ability to suppress automatic responses while we perform deliberate actions instead. Having disorganised speech could be due to an inability to suppress automatic thoughts and speech triggered by other thoughts. Many schizophrenics experienced derailment of thoughts and spoken words/sentences because each word triggers an associations and the schizophrenic cannot stop the automatic responses to these associations.

68
Q

family therapy

A

aims to improve the communication and interaction between family members. As we know, high EE can cause a patient to relapse.

69
Q

pharaoh et al

A

Form therapeutic alliance with the family members​
Reduce the stress of caring for schizo relative​
Improve family’s awareness of relapse triggers​
Reduce anger and guilt in family members​
Help family achieve a carer-own life balance​
Improve beliefs about schizophrenia

70
Q

how family therapy works

A
  1. The therapist meets regularly with the patient and close family members, who are encouraged to talk openly about the patient’s symptoms, behaviour and progress.​
  2. They are taught to support each other and be caregivers, with each person given a specific role in the rehabilitation process.​
  3. There is an emphasis on openness, with no details remaining confidential, although boundaries of what is and is not acceptable are drawn up in advance.​
  4. Like CBT it is given for a set amount of time, usually between 3 months to a year, and at least ten sessions.​
  5. This type of treatment is aimed at reducing the level of expressed emotion (EE)​
    within the family, as EE has been demonstrated to increase the likelihood of relapse
71
Q

what is token economy

A

It is a system to encourage positive behaviour and change patterns of maladaptive behaviour, which has developed through spending a long period of time in an institution.

Token economies are a behaviourist approach to the management of schizophrenia, where tokens are awarded for desired behavioural change.​
When it was introduced in the 1970s, it was mainly used with long-term hospitalised patients to enable them to leave the hospital and live relatively independently in the community. ​
It is particularly aimed at changing negative symptoms of schizophrenia, such as low motivation, poor attention and social withdrawa

72
Q

how token economy works

A

Clinicians set target behaviours that they believe will improve the patient’s ​
engagement in their daily activities. For example, ​
The patient brushing their hair​
Persevering with a task. ​
Making their beds.

Tokens then are awarded whenever the patient engages in one of the target behaviours.​
These tokens can be exchanged for various rewards at a later date

Patients will engage more often with desirable behaviours because the behaviours become associated with these rewards and privileges.