Psychiatry (depression and psychosis) Flashcards
What does the extended limbic system do?
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
What parts of the brain are involved in the Limbic System?
Insula, hippocampus, amygdala, OFC/mPFC, hypothalamus, fornix, cingulate, mammillary bodies
What psychiatric disorders can occur from a dysregulated limbic system?
Affective disorders, personality disorders, psychosis, autism, psychopathy, addiction
What differences in the brain did Drevets (1997) find in those with depression? What imaging technique did they use?
Decrease in volume of subgenual cingulate
and decrease of metabolism of subgenual cingulate
PET - glucose metabolism
What differences in the cortex did Schmaal et al (2016) find in those with depression?
Decrease in thickness of the subgenual cingulate
Decrease in ventromedial PFC, cingulate and medial temporal lobe
HOWEVER effect size was small
What is the relationship between the subgenual cingulate thickness and the length of depression?
It gets worse the longer the depressive illness exists - not often seen in adolescence
What did Schmaal et al (2016) find with adolescents with MDD and cortical thickness?
No significant difference in subgenual cingulare
Decrease in ventromedial PFC
Effect sizes small
What 4 regions is the subgenual cingulate (Cg25) connected to?
the limbic system, frontal regions, brainstem and thalamus/hypothalamus
What did Mayberg suggest the subgenual cingulate did? What was the name of this theory?
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
What happens with activity in the Cg25 and frontal areas during transient sadness?
Increase in activity in Cg25 and decrease in frontal areas
What happens with brain activity if you treat depression?
This activity in the Cg25 decreases
What example of another type of experiment/study has shown to create a reduction in Cg25
Tryptophan depletion
What did surgeons discover about the Cg25? what alternative treatment did it lead to?
If you lesion it then it can improve depression
Deep brain stimulation
What results were found about the hippocampus in those with MDD in Schmaal et al’s (2016) study?
Smaller hippocampus but ONLY present in those with RECURRING MDD and this was more pronounced in those with early onset MDD
What other subcortical area was found to be smaller in those with early onset MDD
Amygdala
Which parts of the hippocampus are shown to be affected after the first presentation of depression?
CA4 and CA2/3
What parts of the hippocampus starts to get affected after recurring episodes of depression?
CA1 and subiculum
Why might the hippocampus get affected by depression?
Its sensitive to serotonin and cortisol
Neurogenesis is thought to be disrupted with depression
Greater neuronal death in the CA1 in depression
What results were found about the amygdala and depression in Victor et al’s (2010) study
Hyperactivity is found to be characteristic of depression
Thought to be basis for mood-congruent attentional bias
What 3 other key findings are there about amygdala and depression?
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
How can you treat the amygdala for those with treatment-resistant depression?
Vagal nerve stimulation - reduces hyperactivity
What did Woolley and McGuire (2005) find about cortical volume and schizophrenia
Lower total volume of both grey and white matter and lower overall brain volume
Greater ventricular volume
Smaller intracranial volume
What is the significance of the finding that those with schizophrenia have a smaller intracranial volume?
Provides evidence that is a developmental disorder
What did Olabi et al (2011) find out in their longitudinal study on brain matter volume for those with SCZ?
Greater DECLINE in grey, white matter and whole brain volume
Greater INCREASE in ventricular volume
When do the differences in brain volume start to appear in those with schizophrenia compared to controls?
18-40 years old
What relationship is found between brain thickness and schizophrenia?
Globally thinner cortex
Greatest effects in frontal & Temporal areas
What types of functions in the brain are particularly affected by cortical thinness in those with schizophrenia?
executive functions: decision-making, planning, self-monitoring, judgments, achieving goals, language, knowledge, social behaviour
Is there an effect of antipsychotic drugs on cortical thinness or is it an effect of disease?
Both:
Effects 2-3x larger for those on drugs
Global thinness is also dependant on the severity of symptoms
Is cortical thinning present after the first presentation of schizophrenic symptoms?
Yes, in the temporal and frontal regions
What is the limitation of Van erp et al (2018) on cortical thinning and schizophrenic patients?
- Those not on antipsychotic drugs is rare
- Hard to find schizophrenic people after first episode
What part of the brain is affected in those with schizophrenia with auditory hallucinations? What is the association and the role with this area?
Superior temporal lobe
Grey matter volume associated with the frequency and severity of auditory symptoms and that area is to do with speech
What part of the brain is associated with negative symptoms in schizophrenia?
Frontal lobe
What limbic structures have shown a reduction in volume for those with schiozphrenia?
Hippocampus, accumbens, amygadala and thalamus
What is the role of the accumbens?
Reward area
What parts show an increase in volume for those with schizophrenia?
lateral ventricle, pallidum and putamen
Why might the pallidum and putamen show an increase in volume? how is this proven?
drug related
Twin/first degree relative study showed no increases even when other areas show similar differences compared to control
What differences in the brain have been found in unaffected first degree relatives (twin/sibling) of those with schizophrenia?
Overall grey matter volume is smaller
Reduction in hippocampal volume compared to age/sex
What pattern has been shown about how white matter tracts are affected by schizophrenia?
It affects the connection between the frontal, temporal and subcortical regions
Except for the corpus callosum that connects the two hemispheres
What did Cropley et al’s (2017) study demonstrate about when white matter changes appear?
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
What relationship has been shown between rates of decline in fractional anisotropy and medication?
The decline is worse for untreated patients
What are the 4 dopamine pathways relating to schizophrenia
- Mesolimbic (reward system)
- Mesocortical (cortical control, motivation)
- Nigrostriatal (coordination of movement)
- Tuberinfundibular (reg of pituitary gland)
What is the relationship between the 4 dopamine systems and SCZ?
- Reward system - Increase in dopamine = positive symptoms
- Mesocortical - Too little dopamine = negative, cog and affective symptoms
- Nigrostriatal - antipsych drug effects
- Tuberinfundipular - Drug side effects
How has evidence supported the theory that too much dopamine is being taken up pre-synaptically?
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
How has evidence supported the theory that more dopamine is released in those with SCZ
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
How has evidence supported the theory of too little dopamine in the mesocortical pathway
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)
