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Neuroscience 2: higher cognitive function > Module 1: L7 + L12-L17 - MDD and BIP > Flashcards

Module 1: L7 + L12-L17 - MDD and BIP Flashcards

1
Q

What are the symptoms of depression according to ICD-10 (DK)?

A
  • Depressive episode >/= 2 weeks
  • > = 2 core symptoms (low mood, reduced pleasure/interest, reduced energy)
  • > = 2 additional symptoms (reduced self esteem, self blame, thoughts about death/suicide, concentration difficulities, agitation/inhibition, sleep disturbance, appetite/weight change)
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2
Q

What are the symptoms of BIP according to ICD10?

A
  • > = 2 episodes of which >=1 mania/hypomania/mixed episodes
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3
Q

Describe the activity of the fronto-limbic network during emotion regulation.

A

Top-down control: dPFC is downregulating negative emotions

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4
Q

Describe how the activity of the fronto-limbic network during emotion regulation is affected by unipolar depression disorder and BIP.

A
  • Hypoactivity in dPFC
  • Hyperactivity in limbic + vPFC
    –> less top-down control –> emotions “take over” –> despression and/or mania
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5
Q

How does BIP type I and type II differ?

A

Type I: mania
Type II: hypomania

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6
Q

How does hypomania differ from mania?

A

Hypomania is still a functional state, whereas mania is highly dysfunctional. They differ in terms of severity and duration of:
- elevated mood/irritability
- speech, thoughts
- reduced sleep
- grandiosity
- sex drive
- reduced inhibition

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7
Q

What kind of bias does depressive patients show in the cognitive processing of emotional info?

A

Negative (enhanced fear recognition)

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8
Q

What kind of bias does BIP patients show in the cognitive processing of emotional info?

A

Positive (broader facial expression recognition impairments compared to unipolar depression)

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9
Q

Describe a way of screening pregnant women for the risk of postmortem depression.

A

Ratings of baby cries –> more negative –> predicts higher risk for PM depression

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10
Q

Describe the neural abnormalities of depression.

A
  • disturbance of monoamine system
  • elevated stress hormone cortisol in 50 % patients
  • chronic low inflammation
  • low glucose metabolism
  • reduced level of neurotrophic factors incl. BDNF
    –> less survival and regeneration of neurons (neural plasticity)
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11
Q

Describe the neural abnormalities of BIP.

A
  • dysregulated dopamine system (D2/D3)
  • elevated stress hormone cortisol
  • chronic low inflammation
  • reduced level of GABA transmission
  • elevated monoaminergic and glutamatergic neurotransmission in mania (neurotoxic effects)
    –> less survival and regeneration of neurons (neural plasticity)
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12
Q

Describe the structural changes in depression.

A
  • 10 % smaller hipocampus (more reduction with longer untreated illness)
  • reduced dendrite complexity
  • less complex and fewer astrocytes
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13
Q

Describe the structural changes in BIP

A
  • reduced hipocampus volume (not in patients treated with lithium)
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14
Q

Describe the monoamine hypothesis for major depression.

A

The hypothesis states that depression is the result of monoamine deficiency in the brain, based on experminents where inhibition of NE and 5-HT reuptake alleviated symptoms, as well as inhibition of monoamine oxidase (MAO).

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15
Q

Give examples of psychiatric conditions that have a high heritability.

A

Schizophrenia, bipolar disease,

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16
Q

Describe the hormonal system involved in the stress response.

A

HPA axis:
Hypothalamus (CRH) –> pituitary (ACTH) –> adrenal gland ==> glucocorticoids (cortisol)

Effects:
- increased blood glucose
- decreased reproductive function
- decreased immune function

Both neuronal and hormonal:
- increased fat breakdown
- increased glucose release from muscle and liver

17
Q

Describe the neuronal system involved in the stress response.

A

Sympathetic-adreno-medullar (SAM) axis:
Central nucleus of amygdala –> CRH neurons in paraventricular nucleus of the hypothalamus –> spinal cord –> preganglionic sympathetic fibers –> adrenal gland ==> adrenaline (+NE)

Effects:
- increased HR and ventilation
- increased pupil dilation
- increased vasoconstriction in skin
- decreased digestion

Both neuronal and hormonal:
- increased fat breakdown
- increased glucose release from muscle and liver

18
Q

How does glucocorticoids bind?

A

Glucocorticoid receptors (GRs) are intracellular receptors, so the glucocorticoids first pass the PM (lipophilic), and bind to the GR –> translocate to the nucleus –> binds to specific glucocorticoid responsive elements (GREs) on the DNA –> regulate genetranscription (or regulate genetranscription indirectly by protein-protein interactions)

19
Q

Which structure supress the activation of the stress response?

A

The hippocampus, also contribute to negative feedback as the hippocampal structure posses GRs

20
Q

What mental illnesses can chronic stress lead to?

A

Depreesion, anxiety and PTSD

21
Q

How does stress impact neuronal plasticity?

A

Glucocorticoids alters plasticity in a brain region dependdent matter:
–> decreased hippocampal volume in patients with MDD and PTSD
- dendritic trees in many brain regions are altered due to stress
- in rodents: dendrites of hippocampal CA3 neurons shorten after chronic stress exposure, and neurogenesis is inhibited in the dentate gyrus

22
Q

Describe the cortisolism, hypothalamic CRF release and GR sensitivity in both PTSD and MDD.

A

Blood cortisol levels:
PTSD: hypocortisolism
MDD: hypercortisolism

Hypothalamus CRF release:
Both: increased

GR sensitivity:
PTSD: increased sensitivity to negative feedback on HPA axis
MDD: blunted negative feedback on HPA axis

23
Q

Provide examples of drugs used as first-line treatment of bipolar disorder

A

Benzodiazepines, e.g., Diazepam
Lithium
Antiepileptics

24
Q

Provide examples of drugs used as first-line treatment of major depression.

A

Most common principle: inhibition of serotonin or NE reuptake:
- Selective serotonine reuptake inhibitors (SSRIs), e.g., escitalopram (lexapro, fluoxetine (prozac), sertraline (zoloft)
- tricyclic antidepressants (TCA), desipramine (NE selective)
- SNRI
- NRI

25
Q

What are the major side effects of SSRIs?

A
  • headache and nausea
  • tiredness
  • diarrhea
  • agitation
  • sleep disturbances
  • sexual dysfunction
  • arrythmia
  • suicidal behavior and personality changes
  • 5HT syndrome when overdosed in combi with e.g., TCA –> tremor, hyperthemia, cardiovascular shock
26
Q

Describe the use of lithium for treatment of bipolar disorder.

A
  • only efficient against mania in an acute attack (no acute effect on depression)
  • prevents mood swings
  • monovalent cation mimicking Na+: permeates Na+ channels + not pumped by the Na/K pump –> accumulaiton inside cells –> depol
  • inhibtion of signaling pathways:
    inhibition of inositol monophophatase –> inhibition of PI pathway –> block effects mediated by GPCRs
    inhibition of glycogen synthase kinase
    inhibition of cAMP production
27
Q

Describe the basic principles for electroconvulsive therapy (ECT).

A

High dose ultra brief pulse unilaterally

28
Q

What neuropsychiatric conditions are ECT used for?

A
  • mainly for severe depression (psychotic depression)
  • acute delirous conditions
  • mania, schizophrenia, PD …
29
Q

Describe the mechanisms of action of electroconvulsive therapy (ECT).

A

Resetting?

Psychological:
- changes bias to face expression
- diencephalon - HPA axis: CRH normalized after ECT

Hyperconnectivity hypothesis:
- therapeutic activity through modification of aberrant functional connectivity

Molecular: shift in sensitization of different receptors
- sensitization of 5-HT1A+3, and decreased sensitization of 5-HT2
- decreased sensitization of NE-Rbeta

30
Q

How are the glutamatergic system believed to be affected in MDD?

A
  • Decreased GABA and glutamate
  • altered glu-R expression and properties in different brain regions, e.g., NR2A subunit (NMDAR) decreased in GABA interneurons in ACC
31
Q

How are the immunesystem involved in MDD?

A
  • Patients with MDD have charateristic alterations in the populations of microglia cells
  • depression has been linked to increased cytokine levels
  • MDD –> (typically) smaller hippocampus (high density of microglia) –> decreased microglia population
  • Problems with causality: what comes first?

Neuroscience 2: higher cognitive function (20 decks)

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