Chapter 16 - Schizophrenia Flashcards

1
Q

What was an ancient treatment for psychosis? (Neolithic, > 7000 years ago)

A

Trephination

A hole is drilled into the skull to release spirits and treat headaches

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2
Q

Before the 1900’s, what did people think psychosis was the result of?

A

Stress and strain of personal/ social interactions

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3
Q

In 1911, what did Hideyo Noguchi do and what did he find?

A

Examined brains of psychotics

Found that the brains were damaged by syphillis

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4
Q

True or false? Schizophrenia will persist for life only.

A

False. Can cycle in and out of remission.

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5
Q

What are the early and later definitions of schizophrenia? (Know conventional symptoms)

A

Early: Paranoia, delusions, hallucinations, abnormal emotions, thought disturbances
Later: Dissociated thinking (lack of logic)

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6
Q

What are five “types” of Schizophrenia?

A
  1. Disorganized
  2. Catatonic
  3. Paranoid
  4. Undifferentiated
  5. Residual
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7
Q

Is Schizophrenia a genetic disorder?

A

Shows strong genetic predisposition but identical twins do not have 100% concordance. (twin adoption study) (may be due to developmental/environmental difference)

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8
Q

What signs does the schizophrenic twin usually exhibit?

A

Lower birth weight
More tearful, sensitive, vulnerable
Early neurological signs (eye movement)

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9
Q

What happens with the ventricles in patients with Schizophrenia? What does this suggest?

A

Enlarged.

Cortical atrophy and neural degeneration. (Consequence, not root cause!)

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10
Q

Early-onset schizophrenia in adolescence is characterized by a (loss/gain) in _____ matter.

A

Loss, gray

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11
Q

With respect to the limbic system, what is observed with patients with Schizophrenia?

A

Smaller hippocampus and amygdala

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12
Q

Schizophrenia patients have a (smaller/larger) cerebellar vermis?

A

Smaller

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13
Q

During frontal cortex development, what may also be observed in patients? What is this consistent with?

A

Abnormal neuronal migration

Consistent with impaired performance on frontal lobe dependent tasks.

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14
Q

In patients, frontal lobe neuronal complexity is (less/more)?

A

Less

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15
Q

How is the hippocampus organized in patients?

A

Cells are disorganized, results in abnormal inputs and outputs

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16
Q

In the hippocampus, what is correlated with severity of disease?

A

Degree of disorganization

17
Q

Using PET and fMRI, what has been observed in the frontal lobes of patients?

A

Lower metabolic activity, even at rest

18
Q

What is the effect of antipsychotics?

A

Increase frontal lobe activity

19
Q

What are the two main theories of Schizophrenia?

A
  1. Dopamine hypothesis

2. Glutamate hypothesis

20
Q

Why is it difficult to study Schizophrenia and why?

A

Hard to separate cause from effect because Schizophrenia = heterogenous disease (could have different causes for different symptoms)

21
Q

[Dopamine hypothesis] With amphetamine psychosis, what is the dose required by amphetamine addicts and why?

A

3000 mg/day (5 mg for normal person keeps them awake!)

Due to drug tolerance

22
Q

[Dopamine hypothesis] With amphetamine psychosis, what is the dose required by amphetamine addicts and why?

A

3000 mg/day (5 mg for normal person keeps them awake!)

Due to drug tolerance

23
Q

[Dopamine hypothesis] What are the effects of using too much amphetamine?

A

Paranoia, delusions of persecution, auditory hallucinations, strange motor behaviour

24
Q

Amphetamines make schizophrenic symptoms (better/worse)?

A

Worse

25
Q

Amphetamines make schizophrenic symptoms (better/worse)?

A

Worse

26
Q

What do typical antipsychotics do and with which hypothesis does this support?

A

Block D2 receptors

Dopamine hypothesis

27
Q

In Parkinson’s patients, what drug can produce schizophrenic symptoms?

A

L-DOPA

28
Q

What does the ‘Dopamine Hypothesis’ suggest?

A

Schizophrenia may result from excessive synaptic dopamine or excessive postsynaptic sensitivity to dopamine

29
Q

What are the four main problems with the DA hypothesis?

A
  1. DA antagonists don’t help all patients
  2. Atypical antipsychotic drugs (works better!)
  3. Dopamine metabolites in CSF, blood, urine (normal levels)
  4. Therapeutic lag (DA receptors blocked quickly but symptoms reduced later)
30
Q

Atypical antipsychotic drugs have low activity of what and is it (more / less / just as) effective for positive symptoms? Negative symptoms?

A

Low D2 activity
Just as effective for positive symptoms
More effective for negative symptoms
(Note: can increase dopamine release, and L-DOPA combined with atypical works better!)

31
Q

What is the ‘Glutamate Hypothesis’?

A

Schizophrenia may be caused by decreased activity at NMDA receptor

32
Q

What acts as an NMDA antagonist?

A

Phencyclidine (PCP)

33
Q

What acts as an NMDA antagonist?

A

Phencyclidine (PCP)

34
Q

What can PCP induce?

A

Positive and negative symptoms similar to schizophrenia (psychomimetic)

35
Q

Prolonged administration (2 weeks) resulted in what in monkeys?

A

Decreased performance on prefrontal cortex dependent tasks

36
Q

What is the ‘Integrative Model’ for treatment?

A

Identify those with biological predispositions (brain abnormalities) and provide them with lower stress environments