Lecture 4 Neurocognitive Deficits in UHR Flashcards

1
Q

What are the two lines of argument for cognitive deficits and transition to psychosis

A

These two areas of brain functioning may be associated with a greater risk of transitioning to psychosis:

  • Deficits in memory (hippocampal functioning)
  • Deficits in executive functions (fronto-striatal connections and frontal lobe)
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2
Q

What are the 4 neuropsychological memory tests used in UHR research

A

Rey auditory verbal learning test (RAVLT)
Story Recall
Paired associates
Design learning

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3
Q

What are some of the limitations with the neuropsychological memory tests?

A

RAVLT: not just testing memory, but the individuals organisational capacity, their lexicon, and this varies depending on education and English being first language (not so much anything to do with psychopathology. Also you can get better as the task goes on in trials, so worth noting how the paper reported the outcome measure

Story Recall: again not pure memory - you can do well on this task by simply having a good understanding of prose

Paired associate : not pure memory, but how well you can associate words

Design learning: it is generally an easy task (perform at ceiling) but despite this, good predictor of transition to psychosis

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4
Q

What is the trail making task

A

A test of cognitive flexibility, where the individual has to join the numbers in numerical order ASAP. Version A has no distractors, and version B has distractors (letters) - this measures EF as you need to inhibit your response to the distractors, in order carry on with the task ASAP.

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5
Q

What is the continuous performance test

A

Need to maintain attention in the task (boring and repetitive), and press when you see the same symbol twice in a row.
When people make an error, it is because they were not able to maintain their attention and omitted to seeing something important.

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6
Q

What is the EF test

A

The Wisconsin Card Sorting test.
You need to sort the cards out by number, colour or form, and then the rules will be changed without the individual knowing, and they have to then order the cards by learning from their mistakes.

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7
Q

What did Ozgurdal et al (2009) find when observing verbal memory in UHR and FEP individuals

A

The two groups had similar cognitive performance in terms of their verbal memory - we can hence see this as a core cognitive deficit in people with psychosis and those that are at risk.
BUT for the UHR group, their poor performance was on their sustained attention not memory.

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8
Q

Problems with Ozgurdal et als findings?

A
  • The potential impairments on cognitive performance was possibly buffered by the high IQ of the individuals in the sample (both in UHR and FEP group) - biased sample
  • ALSO, as we know not everyone in the UHR group transitions (Fusar-Poli et al) so is it worth looking at neurocognitive deficits, given majority of UHR will not transition.
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9
Q

What did Brewer et al (2005) want to find

A
  • Studied UHR individuals with a known outcome (followed up early participants in the PACE study, for which we know if they transitioned or not)
  • Seperated into UHR transition and UHR non transition individuals (and used healthy control)
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10
Q

Findings from Brewer et al (2005)

A
  • There was lower premorbid and performance in IQ in the UHR vs HC group
  • Impairments in visual and verbal memory were SPECIFIC to the UHR transition group
  • The differences between the groups were driven in visual reproduction (design learning) and story recall tasks.

This suggests that the tasks for which people who transition to psychosis do most poorly on, draw on rapid processing and rapid organisation of information - WHICH IS WHY selection of subtests and outcome measures are important.

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11
Q

What did Siedman et al (2010) find

A

Similar findings to Brewer et al:

  • Impaired neuropsychological functioning in UHR and genetic high risk individuals, compared to HC.
  • Processing speed and verbal memory were what was discriminating UHR from HC.
  • There was greater neuropsychological impairment in UHR transition than nontransition.
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12
Q

What is the argued performance in cognitive tasks related to psychopathology

A

HC > UHR-NT > UHR-T > FEP.

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13
Q

What is a delusion

A

A false, unshakeable belief or idea that is not in line with the individuals educational, cultural or social background. It is held with extreme conviction and subjective certainty
- Sims 1995

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14
Q

What are of brain functioning are delusions said to represent?

A

A frontal-striatal impairment.

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15
Q

What is the formation model of delusions (Freeman et al, 2002)

A

Delusions result from an intact reasoning mechanism, that helps us make sense of anomalous experiences.
In individuals with psychosis or UHR, they perhaps have impairments in attention and miss out parts of the conversation and information. They then need to make sense of what it is they heard.

This search for meaning, leads them to an atypical conclusion and appraisal, which is influenced by adverse environments, isolation, dysfunctional schemas of the self and world and attributional biases.

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16
Q

What are delusional beliefs said to be founded on

A

Dopaminergic and frontal-striatal pathways.

17
Q

What is the role of dopamine in delusional beliefs

A

Dopamine is released within the cortical striatal network, to help us make sense of meaningful connections between things in the environment, that occur at the same time
Atypicalities in this system (so hippocampal damage) may lead to dysregulation of the striatal dopamine system, leading individuals to make connections in the environment when there are no connections to be made.

These people are more likely to attribute salience to unmeaningful connections that do not require attention - here the development of delusional beliefs.

18
Q

What evidence is there for the dysregulation of the striatal dopamine system.

A
  • There is evidence for dysregulated dopamine levels in psychosis
  • This correlates positively with positive symptoms like delusional beliefs and hallucinations
  • Some anti-psychotic medication specifically targets dopaminergic connections
  • Also evidence for increased dopamine in UHR cases.
19
Q

Describe the study by Broome et al (2007)

A

-35 UHR vs 23 HC
-Bead task with 3 levels of difficulty
-Easy, Intermediate and Hard - difficulty depended on how the beads were split between the jars
Question was: how many beads had to be drawn for the individual to make a decision about which jar the beads were coming from?

20
Q

Findings from Broome et al (2007)

A

-The UHR group need significantly less informant then the HC group to make a decision on the task. They were more likely to jump to conclusions to make sense of the situation
-IN BOTH group, jumping to conclusions (less beads drawn) were correlated with severity of abnormal beliefs (PDI)
-Also correlations with jumping to conclusions and intolerance for uncertainty: Negative correlation with WM for UHR, they do not like waiting with uncertainty even if they have good memory.
Yet a positive correlation with WM for HC, they can afford to wait longer to gather information

21
Q

What did Ross et al (2015) find in their meta-analysis

A

People with higher delusions scores are more prone to making decisions with less evidence (in both clinical samples and the general population)

This association disappears though when looking at the clinical group alone (most likely due to small N and power)

22
Q

What did Woodbury et al (2010) find when observing transition rates and neurocognitive deficits

A
  • 13/73 UHR transitioned to psychosis.
  • The UHR group performed poorly across all domains compared to HC
  • Verbal IQ, verbal memory and olfaction differed SIGNIFICANTLY between transitions and non transition UHR.
23
Q

How did Lin et al (2013) contradict Woodburys findings

A

-Study from the Melbourne clinic looking at identifying predictors of psychosis onset
-Longest follow up, 15 years, 25% transition rate
-Used several cognitive measures and tests, but found that cognition at identification as UHR, was not a strong predictor of risk for transition.
READ THE ARTICLE

24
Q

Why should we be considering birth cohorts when looking at cognitive deficits?

A

Perhaps the cognitive differences emerge much earlier than we are currently assuming and investigating at (i.e. at birth) and we are therefore missing these differences by the time the individual reaches a UHR clinic.

25
Q

What did Reichenberg et al (2010) want to investigate

A
  • Wanted to investigate cognitive deficits in individuals earlier than when they reach UHR clinics or an ARMS.
  • Data was from the DUNEDIN cohort study, looking at the assessment of cognitive development at 7,9,11 and 13 using the WISC-R.
26
Q

What did Reichenberg et al (2010) find as outcome at age 32 in the cohort

A
  • 35 had schizophrenia diagnosis
  • 145 had recurrent depression
  • 556 were healthy comparison subjects
27
Q

What were the three questions concerning cognitive development in the DUNEDIN study

A

1) What is the developmental course of cognitive function prior to illness
2) Do different cognitive functions follow the same or different developmental course
3) Are neurodevelopment deficits specific to psychosis or common to other psychiatric disorders

28
Q

What are the three types of developmental course

A

1) Developmental deterioration - typical adult and those with degenerative illnesses
2) Developmental deficit - start from diff baseline
3) Developmental lag - overtime, pull away from typical development line

29
Q

Positives about the DUNEDIN study and cognitive development

A
  • They recruited from the general population and not just those in EI services
  • The study has information on premorbid functioning rom children
  • The study keeps the measures and domains separate over time
  • They do not talk or use retrospective assessments - EVERYTHING was measured when they said it was.
  • They measured cognitive performance at several time points, therefore are able to plot development accurately
30
Q

What were some of the findings from the DUNEDIN cohort regarding cognitive development

A
  • Lower childhood IQ predicted increased risk of schizophrenia/depression in adulthood. Those with FEP and depression had poor performance across all domains, compared to controls.
  • NO evidence of cognitive deterioration in any of the domains - can be optimistic about recovery
  • A number of subtests showed a developmental deficit (problem in the brain or early development and then stays steady) - verbal and visual knowledge, vocabulary
  • Some also show a developmental lag, from childhood to adolescence - arithmetic, visuospatial problem solving
31
Q

Do cognitive impairments predict transition to Psychosis - Bora et al (2014)

A

UHR transition are more cognitively impaired than UHR non transition, in all domains except sustained attention.

If you had the added effect of genetic risk and UHR, you do most poorly in cognitive performance.

But, the effect sizes are modest, suggesting a sig overlap between UHR transition and non transition.
Cognitive impairment has LIMITED capacity at predicting the outcome of those UHR if they transition or not