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Class: Psych > Basic Science of Mood Disorder > Flashcards

Basic Science of Mood Disorder Flashcards

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1
Q

The Amygdala is associated with what mood disorders/signs? (3)

A

1) Anxiety
2) Fear
3) Dysphoric emotions
- Unpleasant Mood
- Mental Anguish

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2
Q

The Nucleus Accumbens (Ventral Basal Ganglia - Ventral Caudate + Putamen) is associated with what mood disorders/signs? (2)

A

1) Anhedonia - Inability to feel pleasure

2) Decreased motivation

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3
Q

The Hypothalamus is associated with what mood disorders/signs? (1)

A

1) Neurovegatative symptoms (Sleep, appetite, etc. . )

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4
Q

What are the anatomical observations seen in depression?
A) Increasd volume (3)
B) Reduced volume (5)

A

A) Increased volume:

1) Ventricular enlargement
2) Increased CSF
3) Periventricular hyperintensity

B) Reduced volume in:

1) Caudate
2) Basal Ganglia
3) Hippocampus (Very Common)
4) Frontal Cortex
5) Gyrus Rectus

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5
Q

Anatomical Observation in MDD: Cortex

*Thicker _____ and _____

A

1) Orbitofrontal cortex

2) Subgenual cortex

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6
Q

Anatomical Observation in MDD: Cortex

*Higher risk of _______ independent of hx of MDD/anxiety

A

Thinner RIGHT LATERAL Cortex

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7
Q

Anatomical Observations in MDD: Cortex

*Correlates with having MDD/Anxiety.

A

Thinner MEDIAL LEFT Cortex

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8
Q

Which neuronal activity is activated during depression?

A

Areas mediating EMOTIONAL and STRESS response

  • Thalamus
  • Amygdala
  • Orbital cortex
  • Medial prefrontal cortex
    • including subgenual cingulate cortex Cg25
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9
Q

Which neuronal activity is deactivated during depression?

A

Areas implicated in ATTENTION and SENSORY processing

- Anterior cingulate cortex

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10
Q

Anatomical Volume in PTSD:
A) Smaller _____ may increase RISK of PTSD
B) Smaller _____ may result FROM PTSD

A

1) Hippocampus

2) Pregenual Ant. Cingulate Cortex

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11
Q

Neuronal activity correlates for OCD: (3)

A

ACTIVATED:

1) Head of Caudate
2) Ant. Cingulate Gyrus
3) Orbitofrontal Cortex

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12
Q

Neuronal activity correlates for PANIC DISORDER:

A

Have FEWER GABA receptors –> Increased activity

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13
Q

Benzodiazepine’s effect on GABA receptor

A

INCREASE affinity of GABA to the GABA receptor

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14
Q

Biogenic Amine Hypothesis:

What levels of NTs correlates with Depression

A

DECREASED availability of either 5-HT or NE or BOTH

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15
Q 
Evidence for Monoamine Hypothesis: DEPRESSION
What NT(s) is/are involved and what is it's concentration compared to normal?
A

1) 5-HT, DA, NE

2) DECREASED

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16
Q 
Evidence for Monoamine Hypothesis: MANIA
What NT(s) is/are involved and what is it's concentration compared to normal?
A

1) DA

2) INCREASED

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17
Q 
Evidence for Monoamine Hypothesis: ANXIETY
What NT(s) is/are involved and what is it's concentration compared to normal?
A

1) GABA -> DECREASED
2) NE -> INCREASED
3) 5-HT
- INCREASED (USMLE)
- DECREASED (Blumenfeld)

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18
Q

The Hippocampus and Prefrontal cortex are associated with what mood disorders? (5)

A

1) Cognitive abnormalities
2) Memory impairments
3) Hopelessness
4) Worthlessness
5) Guilt

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19
Q

Caveats to Monoamine Hypothesis:(3)

A

1) TREATMENT RESISTANCE (30-46%)
2) INCREASED monoamine transmission can STRENGTHEN memory of AVERSIVE life event
3) Long delay of efficacy

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20
Q

Caveats to the Monoamine Hypothesis:

Why is there a long delay in Monoamine therapy? (2)

A

1) Desensitization of presynaptic 5-HT inhibitory autoreceptors
- Takes time for these receptors to desensitize and allow more 5-HT to be released

2) Neuronal adaptation

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21
Q

What are the types of Neuronal Adaptation?

A

Changes in:

1) Gene expression
2) Neurogenesis
3) Synaptogenesis
4) Enhancement of survival

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22
Q

What is the Hypothalamic Pituitary Adrenal (HPA) Axis Hypothesis?

A

Problems in the GLUCOCORTICOID release feedback mechanism cause MOOD Disorders

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23
Q

Pathway of Hypothalamic control of Glucocorticoid release.

A

Hypothalamus (Periventricular Nucleus (PVN)) -> release CRF -> Ant. Pituitary -> Release ACTH -> Adrenal Cortex -> Release Glucocorticoid

24
Q

What is the Feedback mech of the HPA axis?

A

Glucocorticoid will feedback to inhibit Hippocampus and PVN

25
Q

What is the RESULT of HPA Axis hypothesis?

A

There is Hypersecretion of GLUCOCORTICOID due to the loss of feedback mechanism

26
Q

What is the role of the Hippocampus in the HPA Axis hypothesis?

A

INHIBIT PVN of the Hypothalamus

Remeber - the Hippocampus is smaller in pt’s with Depression

27
Q

What is the role of the Amygdala in the HPA Axis Hypothesis?

A

Excite PVN of the Hypothalamus

28
Q

What is the Neurotrophin Hypothesis?

A

Levels of growth factors such as Brain-Derived Neurotrophic Factor (BDNF) mediate the neuroanatomical changes during stress and antidepressant treatment.

29
Q

What is the mechanism and role of BDNF?

A

1) Glucocorticoids inhibits neurons from releasing BDNF.

2) Low levels of BDNF causes dendrites to regress.

30
Q

What is the result of low BDNF levels in the neurons of the Hippocampus?

A

1) Fewer synaptic connections

2) Smaller Hippocampus

31
Q

How does Monoamine therapy (SSRIs) affect BDNF concentration and hippocampus structure?

A

INCREASE BDNF -> Growth of Synpase/Dendrites in hippocampus

32
Q

Evidence for HPA Axis and BDNF Hypotheses

A

1) Depressed pt’s have Increased CRH levels -> Increased levels of Cortisol -> Increase GC
2) Enlarged Ant. Pituitary and Adrenal Cortex
3) Decreased levels of BDNF -> Decrease in neurogenesis -> Decrease in size of Hippocampus
4) Most Important: pt’s fail DEXAMETHASONE feedback test

33
Q

What is the Dexamethasone Feedback test?

A

Dexamethasone: a synthetic glucocorticoid which should initiate a negative feedback in a normal pt.

  • A pt with mood disorder will NOT elicit this feedback.
  • Evidence that something may be wrong with the HPA axis
  • Hypothalamus and Ant. Pituitary t is NOT responding to the glucocorticoid levels. Possible GC receptor issue.
34
Q

What are the effects of Antidepressants on the HPA Axis?

A

A) Increase BDNF levels which leads to changes in Hippocampus

  1) Gene Expression
  2) Neurogenesis
  3) Synaptogenesis
  4) Neuronal Survival

B) Increase GC receptor expression on Hypothalamus and Ant. Pituitary
- Reinstate the feedback mechanism of the HPA Axis

35
Q

What is the Altered Neurotransmission Hypothesis?

A

Other NTs (Other than Serotonin and NE) are involved in Depression

  • Decreased GABA
  • Decreased Glutamate
36
Q

What is the evidence for GABA’s involvement in depression? (3)

A

1) There are FEWER GABAergic neurons
- GABA levels are REDUCED in CSF and plasma
2) GABA agonists have antidepressant effects
3) Antidepressants affect GABAergic function

37
Q

What is the evidence for Glutamate’s role in depression? (2)

A

1) Glutamate levels as well as synthetic enzymes and transporters are reduced in prefrontal cortex in depression
2) Ketamine which inhibits NMDA receptors but INCREASES AMPA (GluR1) receptor levels has STRONG antidepressant effects.

38
Q

What is the Immune/Cytokine Hypothesis?

A

Humoral mediators of immunity affect mood.

39
Q

What increases cytokine levels? (4)

A

1) Stress
2) Inflammation
3) Infection
4) Immunotherapy

40
Q

What is the mechanism behind cytokine’s effect on mood?

A

1) Activate HPA axis
- Increased CRF release
- Resistance of GC receptors
2) Altered monoamine concentration

41
Q

What is the evidence for Immune/Cytokine Hypothesis? (3)

A

1) Pts with autoimmune dz or treated with recombinant interferon often suffer from depression.
2) Blocking cytokine pathways in mice has antidepressant-like phenotype
3) Antidepressants have anti-inflammatory effects

42
Q

What are some mood disorders with strong genetic links? (3)

A

1) Depression (2-5 xs higher)
2) Bipolar disorder (25x higher)
3) Anxiety disorder (3-5x higher)

43
Q

New treatment approach for Monoamine hypothesis

A

Vilazodone (5-HT receptor agonist)

44
Q

What is the mechanism of Vilazodone?

A

Activate 5-HT receptor on the postsynaptic neuron

- bypassing the presynaptic inhibitory autoreceptor.

45
Q

New treatment approach for HPA axis hypothesis.

A

CRH receptor antagonist

- prevent hypersecretion of GC

46
Q

New treatment approach for Neurotrophin hypothesis

A

BDNF receptor agonist and antagonist

47
Q

New treatment approach for Neurotransmission hypothesis

A

Sub-anesthetic doses of Ketamine

48
Q

New treatment approach for Immune hypothesis

A

IL-1B antagonist

- prevent cytokine pathway

49
Q

New treatment approach for Epigenetic mechanism

A

HDAC inhibitors

- BLOCK deactylation -> Promote transcription antidepressant factors

50
Q

What is the traditional Non-pharmacologic treatment?

A

Electroconvulsive Therapy (ECT)

51
Q

What is the mechanism for ECT? (2)

A

1) Electrodes induce grand mal seizure -> Increases in SENSITIVITY and NUMBER of 5-HT receptors
2) Increases Neurogenesis

52
Q

Who are the major pt population for ECT?

A

1) Suicidal pt
- Rapid onset
2) Non-responders
3) Elderly pt

53
Q

What is a major side effect with ECT?

A

Retrograde amnesia

54
Q

What is the newest invasive non-pharmacologic treatment?

A

1) Deep brain stimulation (DBS)

55
Q

What is the mech of DBS?

A

Hyper stimulation of the subgenual cingulate cortex (Cg25) -> Decrease activity of Cg25

56
Q

What is a caveat to DBS?

A

1) Control of timing

2) Need to find the best targer

57
Q

What is a less invasive non-pharmacologic treatment of Depression?

A

1) Vagal nerve stimulation
2) Repetitive transcranial magnetic stimulation
- activate the areas that were low in activation
3) Magnetic Seizure therapy

Class: Psych (2 decks)

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