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Neuroimaging > Psychiatry (depression and psychosis) > Flashcards

Psychiatry (depression and psychosis) Flashcards

1
Q

What does the extended limbic system do?

A

The basis for emotion = Emotion recognition, experience and regulation
Outside world and inside world (hunger,thirst,tiredness) converge to modulate
Biasing memory - with emotionally salient

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2
Q

What parts of the brain are involved in the Limbic System?

A

Insula, hippocampus, amygdala, OFC/mPFC, hypothalamus, fornix, cingulate, mammillary bodies

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3
Q

What psychiatric disorders can occur from a dysregulated limbic system?

A

Affective disorders, personality disorders, psychosis, autism, psychopathy, addiction

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4
Q

What differences in the brain did Drevets (1997) find in those with depression? What imaging technique did they use?

A

Decrease in volume of subgenual cingulate
and decrease of metabolism of subgenual cingulate
PET - glucose metabolism

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5
Q

What differences in the cortex did Schmaal et al (2016) find in those with depression?

A

Decrease in thickness of the subgenual cingulate
Decrease in ventromedial PFC, cingulate and medial temporal lobe
HOWEVER effect size was small

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6
Q

What is the relationship between the subgenual cingulate thickness and the length of depression?

A

It gets worse the longer the depressive illness exists - not often seen in adolescence

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7
Q

What did Schmaal et al (2016) find with adolescents with MDD and cortical thickness?

A

No significant difference in subgenual cingulare
Decrease in ventromedial PFC
Effect sizes small

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8
Q

What 4 regions is the subgenual cingulate (Cg25) connected to?

A

the limbic system, frontal regions, brainstem and thalamus/hypothalamus

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9
Q

What did Mayberg suggest the subgenual cingulate did? What was the name of this theory?

A

1) regulate shifts in mood state by shifting activity between:
frontal cognitive and attention areas (happiness/sadness etc)
insula, hypothalamus, hippocampus and Cg25 (resting, sleeping etc)
Activity is high in one and low in the other
2) Limbic-Cortical Dysregulation System

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10
Q

What happens with activity in the Cg25 and frontal areas during transient sadness?

A

Increase in activity in Cg25 and decrease in frontal areas

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11
Q

What happens with brain activity if you treat depression?

A

This activity in the Cg25 decreases

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12
Q

What example of another type of experiment/study has shown to create a reduction in Cg25

A

Tryptophan depletion

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13
Q

What did surgeons discover about the Cg25? what alternative treatment did it lead to?

A

If you lesion it then it can improve depression
Deep brain stimulation

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14
Q

What results were found about the hippocampus in those with MDD in Schmaal et al’s (2016) study?

A

Smaller hippocampus but ONLY present in those with RECURRING MDD and this was more pronounced in those with early onset MDD

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15
Q

What other subcortical area was found to be smaller in those with early onset MDD

A

Amygdala

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16
Q

Which parts of the hippocampus are shown to be affected after the first presentation of depression?

A

CA4 and CA2/3

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17
Q

What parts of the hippocampus starts to get affected after recurring episodes of depression?

A

CA1 and subiculum

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18
Q

Why might the hippocampus get affected by depression?

A

Its sensitive to serotonin and cortisol
Neurogenesis is thought to be disrupted with depression
Greater neuronal death in the CA1 in depression

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19
Q

What results were found about the amygdala and depression in Victor et al’s (2010) study

A

Hyperactivity is found to be characteristic of depression
Thought to be basis for mood-congruent attentional bias

20
Q

What 3 other key findings are there about amygdala and depression?

A

Increased amygdala blood flow in familial depression
Increased amygdala reactivity to negative emotions predicts a response to CBT
Lower amygdala volume in those with genetic risk factor for anxiety/depression

21
Q

How can you treat the amygdala for those with treatment-resistant depression?

A

Vagal nerve stimulation - reduces hyperactivity

22
Q

What did Woolley and McGuire (2005) find about cortical volume and schizophrenia

A

Lower total volume of both grey and white matter and lower overall brain volume
Greater ventricular volume
Smaller intracranial volume

23
Q

What is the significance of the finding that those with schizophrenia have a smaller intracranial volume?

A

Provides evidence that is a developmental disorder

24
Q

What did Olabi et al (2011) find out in their longitudinal study on brain matter volume for those with SCZ?

A

Greater DECLINE in grey, white matter and whole brain volume
Greater INCREASE in ventricular volume

25
Q

When do the differences in brain volume start to appear in those with schizophrenia compared to controls?

A

18-40 years old

26
Q

What relationship is found between brain thickness and schizophrenia?

A

Globally thinner cortex
Greatest effects in frontal & Temporal areas

27
Q

What types of functions in the brain are particularly affected by cortical thinness in those with schizophrenia?

A

executive functions: decision-making, planning, self-monitoring, judgments, achieving goals, language, knowledge, social behaviour

28
Q

Is there an effect of antipsychotic drugs on cortical thinness or is it an effect of disease?

A

Both:
Effects 2-3x larger for those on drugs
Global thinness is also dependant on the severity of symptoms

29
Q

Is cortical thinning present after the first presentation of schizophrenic symptoms?

A

Yes, in the temporal and frontal regions

30
Q

What is the limitation of Van erp et al (2018) on cortical thinning and schizophrenic patients?

A
  • Those not on antipsychotic drugs is rare
  • Hard to find schizophrenic people after first episode
31
Q

What part of the brain is affected in those with schizophrenia with auditory hallucinations? What is the association and the role with this area?

A

Superior temporal lobe
Grey matter volume associated with the frequency and severity of auditory symptoms and that area is to do with speech

32
Q

What part of the brain is associated with negative symptoms in schizophrenia?

A

Frontal lobe

33
Q

What limbic structures have shown a reduction in volume for those with schiozphrenia?

A

Hippocampus, accumbens, amygadala and thalamus

34
Q

What is the role of the accumbens?

A

Reward area

35
Q

What parts show an increase in volume for those with schizophrenia?

A

lateral ventricle, pallidum and putamen

36
Q

Why might the pallidum and putamen show an increase in volume? how is this proven?

A

drug related
Twin/first degree relative study showed no increases even when other areas show similar differences compared to control

37
Q

What differences in the brain have been found in unaffected first degree relatives (twin/sibling) of those with schizophrenia?

A

Overall grey matter volume is smaller
Reduction in hippocampal volume compared to age/sex

38
Q

What pattern has been shown about how white matter tracts are affected by schizophrenia?

A

It affects the connection between the frontal, temporal and subcortical regions
Except for the corpus callosum that connects the two hemispheres

39
Q

What did Cropley et al’s (2017) study demonstrate about when white matter changes appear?

A

Differences appear early but old compared to cortical thickness/volume (35+)
Show a greater decline in fractional anisotropy in multiple white matter tracts compared to controls

40
Q

What relationship has been shown between rates of decline in fractional anisotropy and medication?

A

The decline is worse for untreated patients

41
Q

What are the 4 dopamine pathways relating to schizophrenia

A
  1. Mesolimbic (reward system)
  2. Mesocortical (cortical control, motivation)
  3. Nigrostriatal (coordination of movement)
  4. Tuberinfundibular (reg of pituitary gland)
42
Q

What is the relationship between the 4 dopamine systems and SCZ?

A
  1. Reward system - Increase in dopamine = positive symptoms
  2. Mesocortical - Too little dopamine = negative, cog and affective symptoms
  3. Nigrostriatal - antipsych drug effects
  4. Tuberinfundipular - Drug side effects
43
Q

How has evidence supported the theory that too much dopamine is being taken up pre-synaptically?

A

McGowan et al (2004); PET scan data using F-Dopa which is a precursor to dopamine. Found an increase in uptake in the ventral striatum

44
Q

How has evidence supported the theory that more dopamine is released in those with SCZ

A

Abi-Dargham (1998): SPECT imaging using specific tracer that binds to D2 receptors. Gave ptps an amphetamine and worked out how much dopamine knock-off there was after stimulus
SCZ group = less of a knock suggesting more dopamine

45
Q

How has evidence supported the theory of too little dopamine in the mesocortical pathway

A

Abi-dargham (1998): PET scan with tracer for D1 receptors. Found in the Dorso-lateral PFC there’s a difference in binding in D1 receptors
Meaning there’s compensatory receptors due to too little receptors
Ptps didn’t do well in n-back tasks (WM)

Neuroimaging (11 decks)

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