Depression Flashcards
Describe depression.
- Episodes can be mild, moderate or severe.
- 8-12% of UK population affected each year.
- 121m people worldwide
Describe the Monamine Theory and evidence for it.
- Decreased serotonin in depression.
- Common excitatory neurotransmitter: releases a lot of Dopamine
- Anti-depressants target serotonin
- Tryptophan diets = lower mood: effect Cinglulate 25 area of brain: ‘Sadness’ area. Tryptophan is a precursor to serotonin.
What is the most common treatment for depression and how does it work?
- SSRI’s.
- block reuptake of serotonin and noradrenaline
- Short-term: transport anti-depressants back to pre-synapse. Long-term: reduction in number of receptors available, more serotonin in synaptic cleft left.
What is the success rates of treatment?
- 33% finish treatment after 14 weeks of citalopram
- 47% shown greater than 50% reduction in baseline symptoms
What are the 4 secondary types of treatment?
- CBT
- Electroconvulsive therapy
- TMS
- DBS
What is the percentage genetic risk of depression?
40-50%
What brain changes increase the risk of depression?
- Stroke to the left side
- Lesion in PFC
- Lesion/disorder affecting the basal ganglia (e.g. Parkinsons)
What is not constant in neural correlates of depression?
Structural effects
What does Clark et al. (2009) state about neural correlates of depression?
- Frontal lobes and basal ganglia are important areas
- Dysregulation of medial/orbitofrontal circuit
- Amygdala dysregular in mood disorders
- Decreased volume in the ACC
- Functional hyperactivity in the subgenal cingulate
- 41% decrease in serotonin binding potential
- 27% decrease in medial temporal lobe (amygdala and hippocampus
- Serotonin used to modulate emotional behaviour and causes cognitive dysfunction possibly
Why is Brodmann area 25 important?
- Seems to be linked to serotonin and ‘sad’ area of the brain.
- Depressed patients have no activation in this area when hearing sad stories, but activation normalises after treatment (SSRIs for 6 weeks - Mayberg et al., 2006)
What did Liotti et al. (2002) find about cerebral blood flow?
No difference in activation between healthy and depressed when measuring cerebral blood flow with PET.
How effective has DBS been?
4/6 patients responded well, but no control
Where does DBS have no effect on depression?
Nucleus Accumbens
What did Wagner et al. (2006) find?
- Depression leads to cortical inefficiency
- On a Stroop task, depressed patients performed as well but needed more frontal activation to do so
What is the estimated effect of depression on memory?
2-3% reduction in paragraph recall with every depressive episode
What brain region is smaller in depression and why?
What controversy has this caused?
- Hippocampus
- Higher levels of cortisol seen in depression: cortisol is toxic to the hippocampus and causes it to shrink
- Unknown if this is a side-effect of depression or a cause
How can the effects of shrinkage be prevented in depression?
- Anti-depressants help protect hippocampus
- Duration of untreated depression is negatively correlated with volume of the hippocampus
What has been found about Affective Processing in depression?
- Biased to more negative aspects of the environment
- More likely to recall negative memories
- Depressed patients are impaired at recognising happy faces
- Go/nogo task: depressed faster responses to sad faces
- Greater frontal activation for negative words: more effort to suppress negative than controls
Define executive control.
Executive control is the ability to focus on the aspect of the environment and suppress the rest during a task: frontal cortex implicated in ability.
What has been found about Executive Control in depression?
- Depressed patients are worse at Stroop tasks: required to read word and suppress colour.
- indicates cortical inefficiency in executive tasks: takes more effort to perform at the same level
- Dysregulation of dorsal and lateral PFC during EF tasks
What has been found about Memory in depression?
- Hippocampal pathology suggests a memory deficit
- Depressed patients have issues with recall compared to controls
- Longer duration of illness = worse memory
What causes the missing reappraisal of emotions in depression?
Increased connectivity of amygdala and VLPFC (is missing)
What has been found about feedback sensitivity in depression?
- Ruminate over failures and criticism
- Exaggerated response to negative feedback in labs
- More likely to fail again if failed once
- Depression does not decrease amygdala activity after negative feedback like healthy
- Altered positive valence processing
What are the neural correlates associated with affective processing?
- Hyperactivity in the amygdala = negative responses
- Serotonin regulates affective processing: decreased in depression therefore irregular affective processing
- Cg25 has a role in affective bias and implicated in depression
- Greater frontal activation for negative words
