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Cognitive Psychology > Schizophrenia > Flashcards

Schizophrenia Flashcards

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1
Q

What is it?

A

Disorder of the dopaminergic system

Cognitive processes are split off from volition (power to use ones own will) behaviour and emotion

Characterized by three clusters of symptoms:
Positive
Negative
Cognitive

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2
Q

What are positive symptoms?

A

Anything that ‘adds’ to normal behaviour, e.g. delusions, hallucinations, disorganised speech, catatonic behaviour

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3
Q

What are negative symptoms?

A

Anything that takes away from normal behaviour e.g. blunted responses, lack of motivation, feeling flat, no emotion, slow reactions, loss of apathy, no pleasure or happiness, not clean

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4
Q

What are cognitive symptoms/abnormalities?

A

Jumbled thoughts, attention span affected, speed of processing affected, working memory, social cognition, reasoning and problem solving

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5
Q

How much of the population does it affect and how much does it shorten lifespan?

A

1% , 9 years or more

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6
Q

When does it usually begin and what precedes it?

A

Begins late adolescence/ early childhood

Usually preceded by prodromal signs such as social isolation, odd behaviours and ideas, blunted affects

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7
Q
  1. Do positive and negative symptoms appear the same in everyone?
  2. Do symptoms respond the same to treatments?
A
  1. no - they vary greatly from one person to another

2. no - they each respond differently

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8
Q

Diagnosis: What are the criteria for diagnosing schizophrenia?

A

Two or more of the following for a significant amount of time during a 1 month period. Must include one of 1-3

  1. DELUSIONS
  2. HALLUCINATIONS
  3. DISORGANISED SPEECH
  4. Disorganised or catatonic behaviour
  5. Negative symptoms
  • Symptoms must also lead to social dysfunction
  • Last 6+ months
  • Other disorders/impairements such as autism must first be excluded
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9
Q

Biological basis for schizophrenia. What are the three lines of evidence?

A
  1. Genes
  2. Brain structure
  3. Neurotransmitters
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10
Q

Genetic predisposition. What are the % chances of getting schizophrenira if a close relative has got it?

A 
Monozygotic twin (identical) 50%
Dzygotic twin (non-identical) 15%
Child 13%
Sibling 10%
Nephew 4%
General population 1%
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11
Q

Under the microscope: What do we see?

A

More ‘black’ areas in patients with schizophrenia = more fluid

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12
Q

What is happening with the grey matter?

A

Less grey (neurons) matter - reduced dendritic complexity and synaptic density > leads to a disturbance of neural communication

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13
Q

What is happening with the white matter?

A

white matter is the axons connecting different areas of brain so reduction of myelin in schizophrenia, this leads to a discoordination of brain regions (myelin helps with action potential)

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14
Q

Which areas of the brain does it affect?

A

Prefrontal cortex area
Hyperthalmus area
all link to Brain stem

Nigrostriatal tract (thalmus - green)
Mesolimbic tract (thalmus, blue)
Mesocortical tract (pre-frontal cortex, blue)
Tuberoinfundibular tract (hypothalamus, pink)
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15
Q

What are the four tracts affecteed in schizophrenia and dopaminergic system?

A 
Nigrostriatal tract (thalmus - green)
Mesolimbic tract (thalmus, blue)
Mesocortical tract (pre-frontal cortex, blue)
Tuberoinfundibular tract (hypothalamus, pink)
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16
Q

What effect does dopamine have?

A

Too much dopamine in the system causes schizophrenic tendencies.

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17
Q

What are dopamine antagonists?

A

Dopamine antagonist: Drugs block action of neurotransmitter doamine at its postsynaptic receptor

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18
Q

What are dopamine agonists?

A

Produce psychotic episodes

19
Q

Abnoramlities in dopamine transmission: How is it affected at the ‘pre-synaptic neuron’?

A
  1. Too much dopamine released because…
    - of increased excitatory input to dopamine neuron
    - of decreased inhibitory input (so a higher likelihood of firing)
    - of decreased number of dopamine autoreceptors (receptors in pre-synaptic nerve) so lack of regulation of cell, causing too much dopamine in cell
    - slow reuptake in synaptic cleft as a result of decreased dopamine transporters
20
Q

How is dopamine transmission affected in the post-synaptic?

A

Receiving neuron becomes more sensitive to dopamine as a result of;

  1. increased number of dopamine receptors on post-synaptic membrance
  2. Biochemical changes make the post-synaptic neurone more responsive
21
Q

What are the subtypes of dopamine receptors?

A

D2, D3 and D4 receptors, which are found in different locations around the brain

22
Q

How do atpical antipsychotic drugs work?

A

Drugs work to block these D2/D3/D4 receptors, helping alleviate symptoms and the amount of dopamine in the action potential

23
Q

What do the D3 and D4 receptors do?

A

These are the site of action for atypical antipsychotic drugs. Atypical antipsychotic drugs relieve symptoms.

e.g. clozapine relieve symptoms as it is an antagonist, it inhibits activity. A post mortem found an increase of these receptors in the brain

24
Q

What is a dopamine transporter?

A

located on pre-synaptic membrane and responsible for removing DA from the synaptic cleft

25
Q

What is a dopamine autoreceptor?

A

A receptor located in the presynaptic terminal of the same neuron that produces the neurotransmitter. Decrease the likelihood of neurotransmitter release.

26
Q

What is a receptor?

A

‘valve’ on membrane on post-synpatic neurone

27
Q

What is a D2 receptor?

A

Located on the post-synaptic membrane.

28
Q

How do D2 antagonists work?

A

Block all receptors so no dopamine flowing, no receptor activity.

This is a problem as it blocks receptors all over the brain, including those at the basa ganglia, which simulates parkinsons (caused by a lack of dopamine)

Dopamine also usually inhibits release of protactin from pituitary gland

29
Q

What areas of the dopaminegic system is affected in schizophrenia?

A

Pre-Frontal cortex and limbic system

30
Q

what side effects do we get from D2 antagonists?

A

Because they block all receptors in the brain, not just those affected.

  • block receptors at basa ganglia, which simulates parkinsons. This causes something called Extra pyramidal symptoms
  • DA usually inhibits the release of prolactin from the pituitary gland. Drugs results in a full blockage of dopamine, meaning an increase of prolactin so get problems with infertility and no sex drive. This is called Hyperprolactinemia.

No improvement on negative symptoms

31
Q

What positive effects are there from D2 antagonists?

A

Improves positive symptoms

32
Q

D2 Partial agonist drugs: What do these do?

A

Stabilise the amount of dopamine in the brain. This is because it modulates the functionality of receptors and helps regulate the side effects of the drug.

  • Improves the positive symptoms
  • Does not increase production of prolactin (resulting in hyperprolactinemia)
  • Controls the negative symptoms better
33
Q

What are the problems with the dopamine hypothesis?

A

20% of patients do not improve

Time for drugs to have an effect

PCP (drug) does not act directly on dopamine system but can induce psychotic episodes. Why is this is psychotic episodes are a result of a dopamine imbalance?

34
Q

What is NMDA?

A

These are glutamate neurotransmitter receptors located in the post-synaptic membrane of a neuron.

PCP (drug) does not act directly of DA system but can produce positive and negative psychosis symptoms…Why is this is psychotic episodes are a result of a dopamine imbalance?

Because…PCP are antagonists at the NMDA receptors (which uses glutamtes)

The glutamate system in the brain interacts with the dopamine system. The blockage of NMDA receptors produce Hypofrontality - which is decreased activity in the pre-frontal cortex and THIS is associated with cognitive and negative symptoms.

35
Q

What is GABA?

A

Main inhibitory neurotransmitter in the brain

GABA interacts with the dopamine system causing a reduced reuptake in GABA in particular parts of the brain (pre-frontal cortex) related to functionality of dopaminergic system in that area.

36
Q

What area of the brain is linked with positive symptoms

A

Hyperactivity in mesolimbic system (central parts of limbic system)

37
Q

What area of the brain is linked with negative symptoms?

A

Hypoactivity (decreased activity) in the pre-frontal cortex

38
Q

What is a negative loop system?

A

The human brain is a negative feedback loop systems.

This means that whenever there is a difference between what a person experiences in reality that is different from the ideal set point established by this person’s brain, an urge to behave to correct the situation is created by the brain.

For example, each person has a comfortable room temperature as his ideal set point. When the room temperature dips below the ideal, the person will take action to correct the situation and re-establish the environment to match the comfortable room temperature set point established by this person. The creativity and adaptability of being human means you can choose from a wide variety of solutions to increase your warmth. You can put on warmer clothes. You can exercise, increasing your own internal temperature. You can build a fire, or turn up the heat, or sit in a sunny spot in the room.

But any action you take is generated by the signal your brain gives you that what you want does not match what you are getting. It is the mismatch between what you want and what you are getting that creates the signal for you to take action

39
Q

What is the overall symptom of positive symptoms?

A

Idea that the patient feels he is the subject of something that’s happened outside of him. Being the passive object of other people’s actions.

40
Q

What is a hypothesis for the cognitive cause of positive symptoms?

A

Dysfunction of the system used by the brain to alert itself to self-generated motor commands e.g. speaking, talking, moving arm. It is something expected & intentional by the person. So feels like it is someone else saying or doing these things

Self-generated action is predicatabe, and elicits less brain activity and is less relevant

41
Q

What is relevent stimuli?

A

externally generated action e.g. listening

relevent because it requires more brain activitiy as it is less predictable

42
Q

What is irrelevent stimuli?

A

self-generated action e.g. talking

43
Q

When applied to ones own thoughts and actions, what happens if we lose the ability to distinguish between relevant and irrelevant stimuli?

A

misattribution of self-generated action to others

Disturbed connectivity in the brain may be at the root of this affect…
Brain may be unable to dampen the cortical responses to self-generated and expected sounds/actions (like a regular person would) and reacts to them as if they are externally generated

Cognitive Psychology (8 decks)

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