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Psychology & Neuroscience of Affective Disorders > Neuroanatomical models of affective disorders > Flashcards

Neuroanatomical models of affective disorders Flashcards

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1
Q

What is the Brodmann Area (BA) 10 known as?

A
  • Frontal Polar Cortex
  • Anterior Rostral Medial PFC
  • one of the most recently evolved areas
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2
Q

How does Frith (2007) consider the Brodmann Area (BA) 10?

A

> “key region in mentalising”

> In healthy people, BA 10 activated during fMRI in 3 tasks:

  1. Mentalising
  2. Person perception
  3. Self-perception
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3
Q

What do mentalising tasks refer to?

A

Understanding the behaviour of characters in terms of mental states
- stories, cartoons

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4
Q

What do tasks on people perception refer to?

A

Questions about long-term dispositions

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5
Q

What do self-perception tasks refer to?

A

Questions about one’s own long-term dispositions

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6
Q

Which brain areas were discovered as related to inappropriate behaviour when damaged?

A

> Right anterior temporal
- affected in Frontotemporal Dementia

> Ventral meidal PFC
- with damage / loss of tissue

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7
Q

What is Frontotemporal Dementia?

A

Group of neurodegenerative disorders

  • leading to loss of tissue
  • resulting in inappropriate social behaviour
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8
Q

What is observed in patients with amygdala damage?

A
  • Less risk averse

- Abnormalities on gambling tasks: take riskier gamble

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9
Q

What is the role of the amygdala in social and emotional behaviour?

A

Detecting both positive AND negative emotionally salient stimuli

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10
Q

How did Walle Nauta extend the definition of the structures involved in the limbic system (1960?

A

Included the “Limbic Forebrain Structures”

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11
Q

What are the limbic forebrain structures (Walle Nauta, 1960)?

A
  1. Orbitofrontal cortex
  2. Hippocampus
  3. Amygdala
  4. Hypothalamus
  5. Septal region
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12
Q

What is the location and role of the orbitofrontal cortex?

A
  • Part of ventral medial PFC
  • Extends laterally
  • Sits just above eyeballs
  • Damage impacts social behaviour
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13
Q

What is the location and role of the hypothalamus?

A
  • Subcortical

- Projects to hormonal system

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14
Q

What is the location and role of the septal region?

A
  • In the septum
  • Contains very small nuclei
  • thought relevant to emotions
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15
Q

Which damaged brain areas do not lead to abnormal social behaviour?

A

Parietal and occipital cortex

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16
Q

How does posterior cortical atrophy (form of Alzheimer’s) show that damaged parietal and occipital regions do not lead to abnormal social behaviour?

A

> Memory is retained
-> doesn’t start in hippocampus

> Visual problems BUT behaviour remain intact

  • > starts in back of the brain
  • damaging parietal and occipital cortex
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17
Q

What are prefrontal-striato-thalamic loops?

A

> Dorsolateral frontal cortex connected with part of striatum
- to Caudate nucleus AND Putamen (by small bridges)

> Caudate nucleus and Putamen are connected to Thalamus

=> closed loop of reciprocal systems

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18
Q

What are the parallel frontal subcortical systems?

A

Prefronto-striato-thamalic loops that start from frontal cortex, connecting to subcortical structures

  • motor
  • oculomotor
  • dorsolateral prefrontal
  • lateral orbitofrontal
  • anterior cingulate

Cortex -> Striatum -> Globus pallidum, Substantia nigra -> Thamalus

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19
Q

What are the most relevant prefrontal-striato-thamalic loops to the limbic system?

A

> Lateral orbitofrontal loop

> Anterior cingulate loop

  • evolutionarily older
  • always considered part of limbic system
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20
Q

What is the aetiology of Parkinson’s disease?

A

Degeneration of dopaminergic neurons in substantial nigra (DA projections to motor cortex)

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21
Q

How are the frontal subcortical loops involved in Parkinson’s disease?

A

> Degeneration of DA neurons in substantial nigra

> Ventral tegmental connected to midbrain (striatum, nucleus accumbens) and PFC
-> mesocorticolimbic pathways

> Patients with Parkinson’s disease suffer from

  • anxiety
  • depression
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22
Q

Why are many models of affective disorder based on the idea of frontal subcortical loop systems?

A

Because the dopaminergic, monoaminergic, and glutamatergic NTs modulate the frontal subcortical loop systems

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23
Q

What does the top-down frontal cognitive control model of social and emotional functions suggest?

A

Frontal cortex controls information in other cortical and subcortical areas

  • “when an automatic response needs to be overcome”
  • for non-standard situations
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24
Q

What does the bottom-up subcortical control model of social and emotional functions suggest?

A

Ventral (medial) frontal cortex stores linkages of

  • subcortical “somatic markers” in hypothalamus
  • action knowledge in posterior areas

e. g. risky gambling game:
- hypothalamus may signal via increase in arousal, detected by ventral (medial) frontal cortex

-> helps making smart decision, avoid risky situations

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25
Q

Who constructed the bottom-up subcortical control model of social and emotional functions, and how?

A

Damasio group

  • patients with ventral medial frontal cortex damage had problems in rapid and complex decision making
  • they knew decisions were bad but couldn’t stop themselves
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26
Q

What does the reciprocal fronto-temporo-subcortical integration model of social and emotional functions suggest?

A

Frontal cortex stores specific information:
- context-dependent knowledge of sequences of social actions/events

  • > cortex necessary to enable context-appropriate social behaviour
  • explains inappropriate behaviour of people with damage to frontal cortex
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27
Q

How did Miller and Cohen (2001) conceptualise the top-down frontal cognitive control model of social and emotional functions?

A

“the role of the PFC is modulatory rather than transmissive”
- “PFC guides activity flow along task-relevant pathways in more posterior and/or subcortical areas”

  • task-relevant pathways of PFC activity = “map that specifies which pattern of “tracks” is needed to solve the task”
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28
Q

Where does the idea of frontal disinhibition stem (subcortical urges after frontal damage) come from?

A

> Hierarchy of spirits (vapours) in Galen’s physiological system (131-201 AD)

> Hierarchy of souls in Renaissance (1517)

-> Modern hierarchy: frontal cortex in the old brain (intellective soul) and subcortical areas in the old heart (sensitive soul)

> Review of behavioural changes following frontal lobe ablations in monkeys (Stanley and Jaynes, 1949)

> Review of frontal functions in animals (Brutkowski, 1965)

  • > Modern accounts assuming disinhibition is a given (not often critically appraised):
  • frontal cortex suppresses information in other parts of the brain
29
Q

What is MacLean’s Triune Brain model (1979)?

A

Evolution of brain:

  1. Reptilian
  2. Paleomammalian (Limbic system)
  3. Neomammalian

“the only part of the brain that can tell us what we perceive to be real the things is the limbic brain”

30
Q

What is the parallel between MacLean’s Triune Brain model (1979) and the Renaissance Hierarchy of Souls (1517)?

A
  1. Reptilian brain = Vegetative soul
  2. Paleomammalian brain = Sensitive soul
  3. Neomammalian brain = Intellective soul
31
Q

What does the alternative model of social and moral cognition and emotion propose?

A

> Historically we like hierarchies in brain models
- these aren’t bad or incorrect BUT need to be criticised

  • > Alternative model not based on hierarchy, BUT on integrated networks of systems
  • integration happens via temporal binding: synchronous/phased neural activity
32
Q

What is the alternative model of social and moral cognition and emotion?

A

> Frontal cortex: structured event knowledge

> Subcortical: central motive states
(emotional value to goal/context)

> Temporal cortex

  • posterior: sensory social features
  • anterior: conceptual knowledge
33
Q

In the alternative model of social and moral cognition and emotion, what is the function of the frontal cortex?

A

Structured event knowledge

  • complex, long duration, multi-stage
  • over learned, highly structured
  • for unfamiliar context
  • social/emotional
34
Q

In the alternative model of social and moral cognition and emotion, what is the function of the subcortical regions?

A

Central motive states

  • emotional value to goal/context
  • agression, anxiety, attachement, happiness, sadness, hunger, sexual arousal
35
Q

In the alternative model of social and moral cognition and emotion, what is the function of the temporal cortex?

A

> Posterior temporal cortex: sensory social features
- social perceptual features (gaze, face, voice, body posture)

> Anterior temporal cortex: conceptual knowledge
- social functional features (social behaviours)

36
Q

What do Price and Drevets show about the neurocircuitry of mood disorders?

A

> Affective disorders are network conditions

> They alter networks of frontal and subcortical regions

> However, disruption of frontal-subcortical circuitry is unclear

37
Q

What are the points of criticism on the models of affective disorders?

A
  1. Relationship between symptoms and psychological components is often unclear
  2. Relationship between neuroanatomical structures and psychological functions is often based on poorly tested hypotheses
    (e. g. frontal disinhibition)
  3. Same neuroanatomical structures and psychological functions appear across different disorders without specificity
  4. No adequate models of the differences between mood states and trait vulnerability
38
Q

What does the fMRI measure?

A

> Blood oxygenation level dependent (BOLD) effect

  • > relative to baseline condition
  • > BOLD contrast between baseline task and activation task
  • corresponds to local field potentials
  • recording through electrodes in the brain
  • summation of neurons firing

> Measure functional connectivity between regions
- compare BOLD signal under different psychological tasks

=> Relationship between specific cognitive function that is probed and anatomical representation
- relate to a specific symptom

39
Q

What are the limitations of fMRI studies?

A

> Different subjective experience of stimuli confounds activation differences

> Whole-brain illusion: signal drops out near air-filled cavities or bones

> Multiple comparisons across many voxels of brain decrease statistical power

> Participant needs lots of repetitions to get valid signal, as BOLD effect is approx. 2%

> BOLD effect is slow, peaking after several seconds

> Same region can be activated for seemingly different tasks/stimuli

40
Q

How can you reduce the confounding from the subjective experience of stimuli between participants in fMRI studies?

A
  • Control subjective experience by obtaining ratings as covariates
  • Choose tasks/stimuli and group comparisons which minimise differences in subjective experience
41
Q

What is a the whole brain illusion in fMRI studies?

A

Signal drops out near air-filled cavities or bones

42
Q

What can you do against the whole brain illusion in fMRI studies?

A
  • Loot at images to determine drop out
  • Use optimised sequences

However, this will decrease effect size

43
Q

What can you do against the loss of statistical power in fMRI studies, resulting from the multiple comparisons across many voxels of the brain?

A

Define regions of interest before analysing the data

-> have a hypothesis

44
Q

What can you do against the potential activated regions shown by the fMRI in regions which are not necessary for the task in question?

A
  • Use Transcranial Magnetic Stimulation (TMS) or neurofeedback to confirm causal role
  • Do a lesion or virtual lesion study (temporarily disrupt brain region of interest)
45
Q

What can you do to facilitate the numerous repetitions required to get valid signal in an fMRI study?

A

Do not squeeze too many experiments and conditions into fMRI session

46
Q

What can you do to counter the slowness of the BOLD effect in an fMRI?

A

Use MEG, EEG or simultaneous fMRI-EEG if time matters

47
Q

What can you do against the risk that the same region is activated for seemingly different tasks and stimuli in an fMRI study?

A

Do not make reverse inferences

i.e. this region was activated, therefore this process was engaged

48
Q

What did the fMRI meta-analysis of Sacher and colleagues (2012) show on the differences in brain region activity between people with MDD and healthy controls?

A

> MDD decreases grey matter volume in medial frontal areas

> Ventral striatum abnormalities in MDD

> Abnormalities with sub-general metabolism

49
Q

What did the fMRI meta-analysis of Hamilton and colleagues (2012) show on the difference in response to thinking of negative stimuli between people with MDD and healthy controls?

A

> Amygdala more active in those with depression

> Dorsolateral anterior cingulate cortex more active in those with depression

> Dorsolateral PFC more active in healthy controls

-> confirmation of brain regions involved in depression
However, direction of effects is unclear
-> details are not reproducible BUT network are

50
Q

What are the benefits of comparing people with bipolar disorder and people with schizophrenia?

A
  • Comparable stress levels

- Control for medication effects

51
Q

What did the meta-analysis of Arnone and colleagues (2009) show on grey matter volume between people with bipolar disorder and people with schizophrenia?

A

Amygdala volume affected by

  • mood stabilisers
  • antidepressants
  • antipsychotics

-> confounding factors effecting regions of interest

=> demonstrates importance of controls in meta-analysis

52
Q

What are the limits neuroimaging studies using cross-sectional designs for comparing healthy controls and symptomatic patients?

A

Problems related to:

  • medication effects
  • distress
  • different motivations to participate
  • mood state is often not properly controlled for in meta-analysis
53
Q

What are the limitations of neuroimaging studies using longitudinal designs?

A
  • Need to disentangle correlates of symptoms from correlates of vulnerability
  • You can compare direct effects of medication if imaging occurs both prior and after medication
  • Expensive and harder to do
54
Q

What are general design issues in neuroimaging studies?

A
  • Co-morbidity often poorly controlled
  • Sample sizes are often too small due to price of imaging
  • > impacts statistical significance
55
Q

What improves the use of neuroimaging?

A

Imaging biomarkers

56
Q

What are the FDA and European Medicine Agencies for biomarkers?

A
  1. Positive predictive values
    - at least 80%
  2. Diagnostic biomarkers (that aid in diagnosis)
  3. Predictive biomarkers (e.g. risk of recurrence)
  4. Surrogate endpoint
    - biomarker is used instead of clinical measures in trial
57
Q

What did the fMRI meta-analysis of Fu and colleagues (2013) show on the prediction of the treatment response of medication-free patients suffering of depression?

A

> Pregenual and anterior subgenual cingulate areas:
- increased activation predictive of positive response to treatment

> Posterior subgenual cingulate, right amygdala, striatum, and insult:
- increased activation increases likelihood of poor treatment response

However, these were underpowered studies
-> most didn’t report predictive accuracies

58
Q

What does “pregenual” mean?

A

In front of corpus callosum

59
Q

What is a “leave-one-out cross-validation”?

A
  • Run a model while leaving a subject out

- Re-run leaving another subject out, and so on

60
Q

What made the high accuracy (mean of 74%) of adequately powered neuroimaging meta-analyses in predicting the treatment response?

A
  • Machine learning models

- Leave-one-out cross-validation

61
Q

What does the cognitive model of vulnerability to depression by Abramson and colleagues (1978) suggest?

A

Vulnerability to depression is due to blaming oneself in an overgeneral fashion

  • “I hate myself”, “I’m useless”, “it’s all my fault”, “I can’t do anything”
62
Q

What are the functions associated to the subgenual cingulate/area?

A
  • Linked to how prone one is to experiencing guilt and self-blame
  • Active when donating to charity AND in people who are prone to guilt and empathy
  • Abnormal metabolism in people with current major depression
63
Q

What are the functions associated to the septa area?

A
  • Active when donating to charity

- Neurodegeneration in this area associated with loss of guilt and pity

64
Q

How is the rejection sensitivity clinically expressed in major depression?

A

> To self

  • common low self-worth
  • overgeneralisation occurs

> To others

  • common non violent irritability and anger
  • uncommon agression/violence
  • no overgeneralisation
65
Q

How does the right anterior temporal lobe contribute to blame differentiation?

A

Anterior temporal lobe represents conceptual meaning of social behaviour

  • more active for social concepts
  • less active for general concepts

-> it’s activation guards against overgeneralisations that would lead to low self-worth

66
Q

What is the hypothesis the role of the communication between the anterior temporal and subgenual lobes in the vulnerability to depression?

A

Vulnerability to depression associated with disruption in communication between

  • anterior temporal lobe: social concepts
  • subgenual lobe: self-blame/guilt
  • There should be disruption when experiencing self-blame or guilt
  • There should be no disruption when experiencing anger or when blaming others
67
Q

Was the hypothesis on the role of the communication between the anterior temporal and subgenual lobes in the vulnerability to depression confirmed (Green et al., 2010; Lythe et al., 2015)?

A

Hypothesis confirmed

> Green et al. (2010): participants fully remitted from depression (still vulnerable) showed selective disruption of connectivity

  • during self-blame
  • did not occur during anger or blaming others
  • Functional miscommunication observed in frontal lobe, hippocampus and hypothalamus

> Lythe et al. (2015):

  • higher connectivity for self-blame in Brodmann area 25 in subegenual (posterior)
  • lower connectivity for self-blame in Brodmann area in subgenual (anterior)
  • Connectivity between subgenual and anterior temporal lobes predicted (75% accuracy) who would go on to develop another episode
68
Q

What are the fMRI findings on the communication between the anterior temporal and subgenual lobes?

A

> Subgenual cingulate areas selectively involved in proneness to self-blaming/guilt emotions

> Individual differences in overgeneralised self-blame associated with differences in coupling between anterior temporal and anterior subgenual areas

> Vulnerability to recurrence in MDD: high coupling in anterior temporal-posterior subgenual networks

Psychology & Neuroscience of Affective Disorders (16 decks)

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