Depression Flashcards
Name 2 reasons why the monoamine hypothesis of depression cannot sufficiently explain depression.
- medications (targeting serotonin or norepinephrine) take 6 weeks or more to have and effect although the neurotransmittter at synapses are already altered .
- Studies of neurotransmitter in CSF, plasma have failed to find any deficits in depression patients compared to healthy individuals.
What stage of the brain is PET and fMRI used for depressed patients?
PET - idle brain
fMRT - when patients are doing a task (active)
What activities did fMRI and PET discover in a depressed brain?
- Activities in pulvina in thalamus (overactivity)
- Greater responses to negative stimuli in amygdala, insula and anterior cingulate.
- Lower responses to dorsal PFC and dorsal striatum (due to failture of dopamine pathways)
HOWEVER, ECT (result in lower FC activities) and TMC (the opp) is successful for depression -> why? –> maybe PFC and associations disrupted.
Describe the possible hypothesis of HPA and depression.
Increased cortisol by Corticotrophin releasing hormone (CRH) in hypothalamus (regulate more or less crh agent depending on the amt of cortisol in blood)-> affects pituitary gland-> affects ACTH –> affects adrenal gland and release cortisol -> hippocampal damage (degeneration) -> decreased inhibitory feedback on HPA axis (or hypothalamus) -> increased cortisol release.
How does effective treatments (ECT, lithium, antidepressant) restore HPA function?
- increased glucocorticoid receptor production -> hypothalamus more receptive to negative feedback from cortisol. (HOW???)
- May also restore hippocampal function.
5 Treatments for depression that increase BDNF (brain derived neurotrophic factor) .
- Lithium
- Antidepressants
- Estrogen
- Exercise
- Stimulation (ECT, TMS, VNS)
How does BDNF affects depression?
- Increased BDNF increase neurogenesis
- BDNF may be related to increased methyl groups that attached to histones that package DNA. Using anti depression increases acethyl groups to the histones and open up the dna and allow BDNF mRNA to be transcribed (no of methyl groups remain the same).
What does BDNF do in the brain?
- provide ongoing maintainece of neurons in the brain.
2. disruption will result in reduction in the size of the brain and cell loss.
Lithium increases gray matter volume in bipolar patients.
NIL
What is ketamine?
it is a NMDA (N-Methyl-D-Aspartate) blocker and a rapid treatment of depression by attacking the glutamate neurons. (glutamate antagonist)
Ketamine and depression?
- increased the production of BDNF in hippocampus
- able to sythesize proteins without gene expression. -> does not turn on DNA but turns off the supression of BDNF synthesis from existing mRNA.
What are the core symptoms in ICD 10?
Anhedonia, decresed drive & energy, decreased mood.
Criteria for diagnosing depression for iCD 10?
Mild: 2 core + 2 additional
moderate: 2 core + 3 - 4 additional
severe: 3 core + 4 or more additional
Symptoms last for at lest 2 weeks
Core symptoms in DSM 5?
Decreased Mood, anhedonia (or decreased in pleasure or interest in almost all activities)
Criteria for diagnosing depression for DSM 5?
At least 1 core symptom. Total of at least 5 symptoms that last for 2 weeks almost everyday and change in functioning (compared to the past)
