Introduction to Clinical Neuroscience Flashcards

1
Q

Schizophrenia

A

Breakdown of effective integration of emotion, thought, and action

  • Delusions, hallucinations, odd behaviour, incoherent thought, inappropriate effect
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2
Q

Schizophrenia as a diagnosis

A
  • Diverse disorder, multiple types with varied profiles
  • Have to meet a set of criteria, not a set thing, fuzzy search
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3
Q

Positive symptoms

A

Experience MORE than what is actually there

e.g. Hallucination, delusion

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4
Q

Negative Symptoms

A

Absence of experiences

e.g. Blunted emotion, reduced emotional processing, facial affect

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5
Q

Causal Factors - Schizophrenia

A
  • Evidence for a genetic contribution (inherit increased risk)
  • Multiple cases
  • Infections, autoimmune disorders, toxins, traumatic injury stress
  • Interference with normal development of susceptible individuals
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6
Q

Chlorpromazine

A

Calms many agitated schizophrenics and activates many emotionally blunt schizophrenics

“levelling effect”

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7
Q

Reserpine

A

Also found to be effective for treating schizophrenia, no longer used

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8
Q

Antipsychotic drugs –> Use/Side effects

A
  • Both drugs are not effective for 2-3 weeks
  • Parkinson-like motor effects
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9
Q

Dopamine Theory of Schizophrenia

A
  • Link between dopamine and parkinson’s disease established
  • Antipsychotics side-effects suggest role for dopamine-drugs work by decreasing dopamine levels
  • Schizophrenia associated with dopamine overactivity
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10
Q

Reserpine - How does it work

A

Depletes brain of dopamine and other monoamines by making vesicles leak

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11
Q

Amphetamine and cocaine

A

Dopamine agonists and produce psychosis

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12
Q

Chlorpromazine

A

Antagonizes dopamine activity by binding and blocking dopamine receptors

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13
Q

Higher the affinity a drug has for dopamine receptors…

A

The more effective it is in treating schizophrenia

Haloperidol - The exception

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14
Q

How does Chlorpromazine work?

A
  1. Chlorpromazine binds to postsynaptic dopamine receptors; it does not activate them, blocks ability of dopamine to activate them
  2. Blockage of dopamine receptors by chlorpromazine sends a feedback signal to the presynaptic neuron, which increases the release of dopamine
  3. The feedback signal increases the release of dopamine, broken down into the synapse, resulting in elevated levels of dopamine metabolites
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15
Q

Limitations of Dopamine Theory

A
  • Clozapine, an atypical and effective neuroleptic, acts at D1, D4, and serotonin receptors, but has only some binding to D2 receptor
  • Neuroleptics acct quickly at synapse, but do not alleviate symptoms for weeks
  • Schizophrenia associated with brain damage: little damage to dopamine circuitry
  • Neuroleptics only effective for some
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16
Q

Depression

A

Normal reaction to loss

Abnormal when it persists/has no cause

17
Q

Mania

A

Overconfidence, impulsivity, distractibility, and high energy

18
Q

Affective disorders

A
  • Psychiatric disorders characterized by disturbances of mood or emotion
    • Also known as mood disorders
    • Includes depression and mania
19
Q

affective disorders - Prevalence

A

Very common

5% suffer from unipolar, 1% for bipolar

20
Q

Affective Disorders - Genetics

A

Concordance rate higher for bipolar than unipolar

21
Q

Antidepressant drugs

A

Monoamine Oxidase Inhibitors

Tricyclic Antidepressants

22
Q

Monoamine Oxidase Inhibitors

A

○ Eg. Iproniazid

	○ Prevents breakdown of monoamines
 
	○ (E.g. dopamine, serotonin)
23
Q

Tricyclic Antidepressants

A

○ Eg. Imipramine

	○ Block reuptake of serotonin and norepinephrine

	○ Safer than MAQIs
24
Q

Selective Monoamine reuptake Inhibitors

A
  • Include Prozac, Paxil, Zoloft, and others
    • No more effective than tricyclics, but side effects are few and they are effective at treating other disorders
    • Selective Norepinephrine-reuptake inhibitors (SNRIs) are also effective
    • Not necessarily getting more effective, but more specific –> less side effects
25
Q

Diathesis-Stress Model of Depression

A
  • Diathesis = genetic susceptibility
    • Diathesis + Stress = depression
    • Support is indirect: depressed people…
      ○ Tend to release more stress hormones
      ○ Fail dexamethasone suppression test - normal negative feedback on stress hormones not functioning in many depressed patients
26
Q

Treatment of Depression with Brain stimulation

A
  • Chronic stimulation near the anterior cingulate gyrus helped relieve depression on treatment-resistant patients
27
Q

Explain how Serotonin works in terms of Depression, How SNRI’s effect this

A

Serotonin is deactivated in the synapse by reuptake into the presynaptic neuron, causing symptoms of depression

SNRI’s: Block reuptake of serotonin, increasing activation of serotonin receptors