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Neuro Block 8 > Motivational Systems And Psychiatry > Flashcards

Motivational Systems And Psychiatry Flashcards

1
Q

What is schizophrenia a disorder of

A

Mesolimbic dopamine system and prefrontal cortex

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2
Q

When does schizophrenia emerge

A

Early adulthood

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3
Q

Positive symptoms of schizophrenia

A

-hallucinations, paranoid delusions, dissociated from reality. Common type of hallucinations: ‘hearing voices in my head”. Erratic eye movements, related to constantly shifting attention

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4
Q

Negative symptoms of schizophrenia

A

-impaired attention, executive function, behavioral control, flattening of emotional expression (flat affect)

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5
Q

Neurobiology of schizophrenia

A

Excessive activity of mesolimbic DA system (opposite of Parkinson’s)

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6
Q

Rx for schizophrenia

A

Dopamine receptor antagonists, referred as “typical anti-psychotics’ or ‘neuroleptic’ drugs

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7
Q

One potential serious complication of anti-psychotics or neuroleptics

A

Tardive dyskinesia

  • involuntary movements of facial/mastication/tongue muscles.
  • can also develop Parkinson’s like signs including cogwheel rigidity
  • extra-pyramidal side effects
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8
Q

Role of serotonin in schizophrenia

A
  • some atypical anti-psychotics can also affect serotonin NT
  • normal functions of serotonin systems include promoting memory retrieval
  • some hallucinogenic act by activating serotonin receptors
  • speculative explanation for efficacy of Rx that modulates serotonin: schizophrenia involved excess serotonin signaling which drives hallucinations and delusions
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9
Q

Role of glutamate dysregulation in schizophrenia

A
  • role of dysregulation of glutamate in prefrontal cortex and straitum: excess glutamate release by axon terminals
  • dysregulation of glutamate occurs in corticostriatal projections, i.e. Part of the basal nuclei “cognitive loop” or emotive loop
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10
Q

Two major groups of nuclei (multi raphe) of serotonin systems

A

Ascending/rostral

  • caudal midbrain
  • rostral pons

Caudal/descending raphe nuclei
-in pons/medulla

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11
Q

Which serotonin system is involved with schizophrenia and how

A

Rostral/ascending system

  • caudal midbrain
  • rostral pons

Spritzing serotonin all over cerebrum

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12
Q

Group of nuclei located at the midline in brainstem sections

A

Nuclei raphe

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13
Q

Early generation diet pills and rostral/ascending system

A

Act via increasing serotonin in hypothalamus, normally mediates stress-induced interruption of eating

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14
Q

Serotonin levels regulate what

A

Aggressive behavior, natural reward (eating)

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15
Q

Different raphe nuclei and effects on anxiety

A

They have opposing affects on anxiety, due to difference in projections targets and receptors types. Ascending serotonin systems have widespread, diffuse projections in cerebrum, but important targets include amygdala, prefrontal cortex, other subcortical sites

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16
Q

What is used for Rx for anxiety/panic/ PTSD, and as anti-depressants

A

SSRIs

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17
Q

Core symptoms of MMD

A
  • loss of interest, pursuit, and pleasure from usual rewarding activities
  • inability/disinterest in performing any daily plan, motivational ‘paralysis’
  • feelings of hopelessness/worthlessness
  • causes severe dysfunction in daily work/social life
  • lasts more than 1 month
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18
Q

Additional diagnostics criteria for MDD

A
  • increases anxiety/agitation
  • excessive sleeping or insomnia
  • excessive appetite or absence of appetite
  • lethargy or high ‘psychomotor’ activity
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19
Q

Crisis point requiring emergency intervention for MDD

A

Suicidal ideation/planning

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20
Q

Onset of MDD

A

-chronic/insidious, but often triggered by chronic stress, trauma, grief

Course: may be episodic or chronic state

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21
Q

What do anti depressants target

A

norepi, serotonin, and dopamine systems

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22
Q

Efectiveness of ant depressant Rx discovery

A

Through historical/medical accident, not by any pathophysiological understanding of the neurobiology basis of depression

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23
Q

What lead to the monoamine hypothesis of depression

A

The effectiveness of anti-depressants

24
Q

What is the monoamine hypothesis of depression

A

An imbalance of deficiency in monoamines is the cause of depression

25
Q

Where does the ascending projections come from for the serotonin system

A

Locus coeruleus

26
Q

Where does the LC extend

A

From rostral pons to the caudal midbrain

27
Q

Key functions of LC

A

Arousal, support of alertness/selective/sustained attention

28
Q

What us the LC activated by

A

Stressors-both positive and negative arousing stimuli

29
Q

LC and the hippocampus and amygdala

A

Enhance memory consolidation, including for fear learning/extinction

30
Q

What does the LC do to feeding

A

Suppresses feeding via hypothalamus (stress response)

31
Q

Excess norepinephrine and LC

A

Linked to anxiety disorders including PTSD

32
Q

What are the prevailing anti-anxiety Rx

A

Benzodiazepines (GABA agonists), and SSRIs

Despite norepinephrine being linked to being a cause

33
Q

How was the first anti-depressant discovered

A

By accident. Monoamine oxidase inhibitors used to treat movement disorders

34
Q

What do monoamine metabolic enzyme inhibitors boost synaptic levels of

A

DA
NA
5-HT

35
Q

Second generation of anti-depressants

A

Tricyclic anti depressants: inhibitors of re-uptake transporters for monoamines –DA, NA, 5-HT

36
Q

3rd generation of anti depressants

A

More selective inhibitors of re uptake transporters

  • selective serotonin re-uptake inhibitors (SSRIs)
  • selective norepi reuptake inhibitors
  • selective norepi and dopamine re uptake inhibitors
37
Q

Disadvantages and risks of current anti depressants

A
  • typically requires weeks to achieve noticeable effect
  • modest effect vs placebo for many patients
  • suicide risk for some adults, higher risk for children, possibly due to increases motivational drive but persistence anxiety and emotional pain
38
Q

Psychological therapies for MDD

A

Mainly cognitive behavioral therapy (CBT) with the goal to alter negative thinking patterns, promote reward system function, coping with life circumstances

39
Q

CBT alone in individuals with MDD

A

Can produce ciliary changes in prefrontal and amygdala activity as wit RX alone

40
Q

CBT and Rx treatment for MMD

A

Common to use them together

41
Q

New drug targets for MDD

A

Under investigation, enkephalin receptor agonists (kappa receptor)

42
Q

New accidental discoveries for MDD treatment

A

Off label uses for motion sickness (scopolamine)

43
Q

Experimental in-patient crisis treatment and MDD

A

Ketamine

NMDA glutamate receptor antagonist

44
Q

Electroconvulsive therapy (ECT)

A

Mild electrical current, scalp electrodes

45
Q

Transcrnial magnetic stimulation and MDD

A

Non-invasive application of magnetic field over specific cortical region

46
Q

Depression and deep brain stimulation

A
  • implanted electrode in brain
  • current pattern can be adjusted to produce activation of target region. Works in movement disorders, experimental for MDD
47
Q

Target regions for deep brain stimulation in MDD

A

Selected based on functional neuroimaging research studies showing altered regional activity relative to healthy control subjects

48
Q

What is hyperactive in MDD patients and often the target of deep brain stimulation

A

Subgenual cortex

-inhibiting this produces rapid and significant reduction of symptoms

49
Q

Nucleus accumbens and MDD

A

Antlers target for deep brain stimulation
Aim to increase activity
Might need to be combined with psychological therapy to be effective

50
Q

What 3 areas are often messed up in MDD

A

Subgenual cortex
Nucleus accumbens
Periventricual zone along the 3rd ventricle

51
Q

Brain maturation and psychiatric disorders

A

Brain regions differ in timing of complete maturity: probably involved in age-specific time-windows for vulnerability to psychiatric disorders

52
Q

Altered mesolimbic dopamine system in schizophrenia may stem from what

A

Possibly stems from disruption of synaptogensis or mechanisms that stabilize and preserve effective synapses

53
Q

When is the onset of schizophrenia

A

Early adult

54
Q

Onset of depression

A

Can emerge in children, adolescents, adults of any age

55
Q

When doesthe amygdala and hippocampus start to mature

A

About 2 years old

56
Q

What is the last cerebral cortex to reach maturity

A

Prefrontal cortex

57
Q

What is the risk of developing anxiety disorder, PTSD, and depression prior to prefrontal maturity due to

A
  • lack of control of amygdala to prefrontal cortex (anxiety/PTSD)
  • lack of amygdala-prefrontal partnership in reward-related learning

Neuro Block 8 (11 decks)

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