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
Where does the ascending projections come from for the serotonin system
Locus coeruleus
26
Where does the LC extend
From rostral pons to the caudal midbrain
27
Key functions of LC
Arousal, support of alertness/selective/sustained attention
28
What us the LC activated by
Stressors-both positive and negative arousing stimuli
29
LC and the hippocampus and amygdala
Enhance memory consolidation, including for fear learning/extinction
30
What does the LC do to feeding
Suppresses feeding via hypothalamus (stress response)
31
Excess norepinephrine and LC
Linked to anxiety disorders including PTSD
32
What are the prevailing anti-anxiety Rx
Benzodiazepines (GABA agonists), and SSRIs Despite norepinephrine being linked to being a cause
33
How was the first anti-depressant discovered
By accident. Monoamine oxidase inhibitors used to treat movement disorders
34
What do monoamine metabolic enzyme inhibitors boost synaptic levels of
DA NA 5-HT
35
Second generation of anti-depressants
Tricyclic anti depressants: inhibitors of re-uptake transporters for monoamines --DA, NA, 5-HT
36
3rd generation of anti depressants
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
Disadvantages and risks of current anti depressants
- 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
Psychological therapies for MDD
Mainly cognitive behavioral therapy (CBT) with the goal to alter negative thinking patterns, promote reward system function, coping with life circumstances
39
CBT alone in individuals with MDD
Can produce ciliary changes in prefrontal and amygdala activity as wit RX alone
40
CBT and Rx treatment for MMD
Common to use them together
41
New drug targets for MDD
Under investigation, enkephalin receptor agonists (kappa receptor)
42
New accidental discoveries for MDD treatment
Off label uses for motion sickness (scopolamine)
43
Experimental in-patient crisis treatment and MDD
Ketamine | NMDA glutamate receptor antagonist
44
Electroconvulsive therapy (ECT)
Mild electrical current, scalp electrodes
45
Transcrnial magnetic stimulation and MDD
Non-invasive application of magnetic field over specific cortical region
46
Depression and deep brain stimulation
- implanted electrode in brain - current pattern can be adjusted to produce activation of target region. Works in movement disorders, experimental for MDD
47
Target regions for deep brain stimulation in MDD
Selected based on functional neuroimaging research studies showing altered regional activity relative to healthy control subjects
48
What is hyperactive in MDD patients and often the target of deep brain stimulation
Subgenual cortex | -inhibiting this produces rapid and significant reduction of symptoms
49
Nucleus accumbens and MDD
Antlers target for deep brain stimulation Aim to increase activity Might need to be combined with psychological therapy to be effective
50
What 3 areas are often messed up in MDD
Subgenual cortex Nucleus accumbens Periventricual zone along the 3rd ventricle
51
Brain maturation and psychiatric disorders
Brain regions differ in timing of complete maturity: probably involved in age-specific time-windows for vulnerability to psychiatric disorders
52
Altered mesolimbic dopamine system in schizophrenia may stem from what
Possibly stems from disruption of synaptogensis or mechanisms that stabilize and preserve effective synapses
53
When is the onset of schizophrenia
Early adult
54
Onset of depression
Can emerge in children, adolescents, adults of any age
55
When doesthe amygdala and hippocampus start to mature
About 2 years old
56
What is the last cerebral cortex to reach maturity
Prefrontal cortex
57
What is the risk of developing anxiety disorder, PTSD, and depression prior to prefrontal maturity due to
- lack of control of amygdala to prefrontal cortex (anxiety/PTSD) - lack of amygdala-prefrontal partnership in reward-related learning