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Psych370 > 18.1 Schizophrenia > Flashcards

18.1 Schizophrenia Flashcards

1
Q

what does schizophrenia mean? why?

A

the splitting of psychic functions

- primary symptom (at the time) was the break down of integration of emotion, action, thouoght

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2
Q

prev. of schizophrenia

A

1% lifetime, all races and cultural groups

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3
Q

what is waxy flexibility

A

react like a mannequin when touched - dont resist movement, hold new position until moved

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4
Q

what is schizophrenia with catatonia

A

schizophrenia characterized by long periods of immobility and waxy flex

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5
Q

what is echolalia

A

vocalized repetition of what’s just been heard

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6
Q

what is the major difficulty in studying and treating schizophrenia

A

developing an accurate definition of the disorder

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7
Q

why is defining schizophrenia so difficult (2)

A
  1. symptoms are complex and divers, overlap greatly with other psych disorder symptoms, and change during progression
  2. various neurological disorders like complex partial epilepsy have symptoms that suggest a diagnosis of schizophrenia
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8
Q

what does the DSM-5 prefer to call schizophrenia and why

A

schizophrenia spectrum disorders since it overlaps with several different brain diseases

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9
Q

what are schizophrenias two broad symptom clusters, and why are they so named

A

positive (represent an excess of normal function)

negative (represent a reduction or loss of normal function)

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10
Q

what are 5 examples of positive symptoms

A
  1. delusions
  2. hallucinations
  3. inappropriate affect
  4. disorganized speech or thought
  5. Odd behaviour
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11
Q

what are 3 examples of negative symptoms

A
  1. affective flattening - diminished emotional expression
  2. Avolition - reduction ro absence of motivation
  3. Catatonia - motionlessness
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12
Q

describe inappropriate affect

A

failure to react with the appropriate emotion to emotional events

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13
Q

describe disorganized speech or thought

A

illogical thinking, peculiar associations among ideas, belief in supernatural forces

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14
Q

describe ‘odd behaviour,’

A

difficulty performing everyday tasks, lack of personal hygiene, talking in rhymes

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15
Q

How do we diagnose schizophrenia

A

the frequent recurrence of any TWO symptoms listed above, provided that one of them is delusions, hallucinations or disorganized speech

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16
Q

Describe the first discovery that began to establish the genetic basis of schizophrenia

A

while schizophrenia has 1% prevalence, ts probability of occurring in a close biological relative (parent, child or sibling) is about 10%,
- occurs even if reared apart by a healthy family

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17
Q

Describe the second discovery that began to establish the genetic basis of schizophrenia

A

concordance rates for schizophrenia are higher in monozygotic twins (45-50%) than in dizygotic twins (10-17%)

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18
Q

Describe the third discovery that began to establish the genetic basis of schizophrenia

A

adoption studies found that the risk is increased by the presence of the disorder in bio parents, but not adoptive parents

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19
Q

what does the fact that monozygotic concordance for schizophrenia is less than 100% entail?

A

the presence of experiential factors

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20
Q

what is the current view of the ethology of schizophrenia

A

ppl inherit a potential for schizophrenia which may or may not be activated by experience

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21
Q

what support the diathesis-stress model of schizophrenia (ie biological predisposition plus experiential activation)

A

comparison of the offspring of a large sample of monozygotic twins who were discordant for schizophrenia (ie, only one had it)
- incidence in offspring was identical!

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22
Q

explain our current knowledge of the genetic basis of schizophrenia (5)

A
  1. many genes have been associated
  2. no single gene causes schizophrenia by itself
  3. some genes are more strongly associated than others
  4. genes act in combination with one another, and with experience, to produce the disorder
  5. the exact mechanisms of this interaction are as yet undetermined
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23
Q

what are the experiential factors implicated in schizophrenia (7)

A
  1. birth complications
  2. maternal stress
  3. prenatal infections
  4. socioeconomic factors
  5. urban birth
  6. urban residence
  7. childhood adversity
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24
Q

how are experiential factors thought to cause schizophrenia

A

by altering the normal course of neurodevelopment leading to schizophrenia in those with genetic susceptibility through epigenetic mechanisms

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25
Q

What two facts support the neurodevelopment theory of schizophrenia

A
  1. schizophrenia and autism share many features (genetic risk factors, environmental triggers)
  2. study of two 20th century famines, where fetuses whose pregnant mothers stuffered in the famine were more likely to dev. schizophrenia
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26
Q

what was the first antipsychotic, and what was its history of development

A
  1. chlorpromazine
    - developed as an antihistamine, ten a surgeon noticed that chlorpromazine given prior to surgery to counteract swelling had a calming effect, suggested it could help calm patients with psychosis
    - led to the discovery that it alleviates some symptoms, - agitated patients are calmed, and emotionally blunted are activated
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27
Q

what was the second antipsychotic

A

reserpine, the active compound from snakeroot

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28
Q

is reserpine still used as an antipsychotic

A

no, bc it produces a dangerous decline in BP at the doses needed for successful treatment

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29
Q

are reserpine and chlorpromazine similar in molecular structure?

A

nope!

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30
Q

what are the two similar antipsychotic effects of reserpine and chlorpromazine

A
  1. antipsychotic effects manifest only after the patient has been mediated for 2-3 weeks
  2. onset of the antipsychotic effect is typically associated with motor effects similar to the symptoms of parkinsons
31
Q

what did the two similar antipsychotic effects of reserpine and chlorpromazine suggest to researchers (2)

A

the they act through the same mechanism, which must be related to Parkinsons

32
Q

what finding in parkinsons patients allowed for the postulation of the dopamine theory of schizophrenia

A

the finding that the striatum (caudate plus putamens) of persons dying of parkinsons were depleted of dopamine
- suggested that a disruption of dopaminergic transmission might produce parkinsons and the antipsychotic effects of chlorpromazine and reserpine

33
Q

what is the dopamine theory of schizophrenia

A

schizophrenia is caused by too much domapine and that antipsychotics exert their effects by decreasing these levels

34
Q

what were the two established facts that lent support to the dopamine theory

A
  1. reserpine was known to deplete the brain of dopamine and other monoamines by breaking down the synaptic vesicles in which they are stored
  2. drugs like amphetamines and cocaine, which can trigger schizophrenic like episodes in healthy users are known to increase the extracellular levels of dopamine and other monoamines
35
Q

What did Carlsson and Lindqvist find when they examined the effects of chlorpromazine on extracellular levels of dopamine and its metabolites?

A

expected to find that chlorpromazine depletes the brain of dopamine (like reserpine), but didn’t

  • extracellular levels were unchanged by the drug
  • extracellular levels of metabolites increased
36
Q

what did Carlsson and Lindqvist conclude based on the fact that chlorpromazine didn’t reduced extracellular levels of dopamine

A

that reserpine and chlorpromazine antagonize dopamine synapses in different ways
reserpine - depletes the brain of dopamine
chlorpromazine - competitively binds to dopaminergic receptors

37
Q

what is the exact mechanism of action of chlorpromazine that Carlsson and Lindqvist proposed

A

receptor blocker - binds to dopamine receptors without activating them and tf prevents dopamine from doing so
- now know that many psychoactive drugs are receptor blockers, but chlorpromazine was the first to be identified

38
Q

what did Carlsson and Lindqvist propose to explain the increase in dopamine metabolites in the extracellular space?

A

lack of activity at postsyn dopamine receptors sent a feedback signal to the presynaptic cells that increased their release, which was then broken down in the synapses

39
Q

what important revision of the dopamine theory of schizophrenia came out of Carlsson and Lindqvist’s finding gs?

A

rather than high dopamine levels, the main factor is high levels of activity at dopamine receptors

40
Q

Explain Snyder and colleagues 1970 study that assessed the degree to which various antipsychotic drugs bind to dopamine receptors (process, not findings)

A
  1. added radioactively labeled dopamine to samples of dopamine receptor rich neural membrane from calf striatum
  2. rinsed away unbound dopamine molecules and measured the amount of radioactivity left to obtain a measured of the number of dopamine receptors
  3. measured each drugs ability to block the binding of radioactive dopamine to the sample - assumption was that the drugs with a high affinity for receptors would leave fewer sites open
41
Q

Explain Snyder and colleagues findings concerning the egree to which various antipsychotic drugs bind to dopamine receptors

A

chlorpromazine and other effective anti psychs had a high affinity for dopamine receptors, while ineffective antipsychotics had low affinity

  • ExCEPTIONs
  • Haloperidol; one of the most potent antipsychotics, relatively low affinity for dopamine receptors
42
Q

what was the solution to the problem that arose due to haloperidols relatively low affinity for dopamine receptors

A

dopamine binds to more than one receptor subtype - there are in fact FIVE

43
Q

what are phenothiazines, what types of dopamine receptors do they bind to,

A 
the chemical class of antipsychotic drugs similar to chlorpromazine 
- bind to D1 and D2 receptors
44
Q

what are butyrophenones and where to they bind

A

the chemical class of antipsychotic drugs similar to haloperidol - bind to D2, but not D1 receptors

45
Q

what did the discovery that butyrophenones bind selectively to D2 receptors entail?

A

schizophrenia involves dopamine hyperactivity specifically at the D2 receptor, since haloperidol (butyrophenone) and chlorpromazine (phenothiazine) are similarly effective

46
Q

What are typical antipsychotics

A

the first general of antipsychotics

47
Q

what is highly correlated to the effectiveness of any particular typical antipsychotic drug?

A

the degree to which it binds to D2 receptors

48
Q

which typical antipsychotic is an example of the high correlation between D2 binding affinity and antipsychotic effects?

A

spiroperidol, greatest affinity for D2 receptors, and most potent antipsychotic effect

49
Q

what two general findings can the D2 receptor theory not account for

A
  1. typical antipsychotics block D2 receptors within hours but their effects dont arise for weeks
  2. most antipsychotics are only effective in the treatment of schizophrenias positive symptoms
50
Q

what is the current version of the dopamine theory, in light of the 2 problems with the D2 receptor version

A

excessive activity at d2 receptors is one factor in the disorder but there are in fact several other relevant indicators

51
Q

what are atypical antipsychotics

A

drugs effective against schizophrenia but do not bind to D2 receptors

52
Q

what is an example of atypical anti psychs

A

clozapine, the first to be approved, has affinity for D1 receptors, D4 receptors and several serotonin and histamine receptors,
- only a mild affinity for D2 receptors

53
Q

what were the 2 initial claims about atypical antipsychotics

A
  1. more effective in treatment of schizophrenia than typical
  2. exert their effects without producing parkinsonian side effects
54
Q

are the 2 initial claims about atypical antipsychotics supported by the literature?

A

Nope - effects dont differ as a group from typical antipsychs, even tho they have a bunch of different effects within the group

55
Q

what did the discovery of atypical antipsychotics initially discredit

A

the Dopamine theory of schizophrenia - none of them act primarily as a D2 receptor antagonist

56
Q

what disconfirmed the purported discrepancy between the effects of atypicals and their lack of effects on D2

A

the fact they they do marginally antagonize the receptors

57
Q

what are the three facts to keep in mind about the role of D2 receptors in schizophrenia

A
  1. some effective D2 receptor antagonist have no antipsychotic effects
  2. some drugs that enhance the effects of glycine, or block the effects of glutamate, are effective treatments for schizophrenia (preliminary trials)
  3. growing appreciation of the role of glutamatergic dysregulation n the development of schizophrenia
58
Q

what are psychedelic drugs

A

drugs whose primary action is to alter perception, emotion and cognition

59
Q

what are classical hallucinogens

A

LSD, psylocibin

60
Q

what are dissociative hallucinogens

A

ketamine, phencyclidine

61
Q

are cannabinoids hallucinogens?

A

yes

62
Q

what are the two lines of research on psychedelics

A
  1. research the effects of psychedelics that are similar to symptoms of psychiatric disorders - use the drugs to model the disorders
  2. research the feelings of boundlessness, unity, bliss reported by some users and attempted to use them to treat psychiatric disorders
63
Q

what two factors stimulated the renewal of interest (following their prohibition in the 70s) in the study of psychedelics used to model and treat schizophrenia?

A
  1. development of techniques for imaging the effects of drugs in the human brain
  2. increased understanding of the mechanisms of psychedelic drug effects
64
Q

what are the two conclusions we can draw from research on psychadelics

A
  1. effects of classical hallucinogens mimic the positive symptoms of schiz by acting as antagonists of particular serotonin receptors
  2. dissociative hallucinogens mimic the negative symptoms of schizophrenia by acting as antagonists of glutamate receptors
65
Q

why has the study of the genetics underlying schizophrenia, despite the fact that the genes each contribute only a little, not been useles

A

bc identifying the genes can provide new insights into the causes, neural mechanisms and treatment of schizophrenia

66
Q

what are the several processes pointed to by the study of schizophrenia related genes that may play important roles in the development of the disorder (4)

A

some have been shown to disrupt

  1. neural proliferation and migration
  2. synaptic pruning during neurodev
  3. myelination
  4. transmission at glutamatergic and GABAnergic synapses
67
Q

what allowed for the rapid accumulation fo studies of brain changes in patients with schizophrenia

A

development of neuroimaging techniques in the 60s

68
Q

what did the first generation of neuroimaging studies show about schizophrenic brain changes

A

enlarged ventricles and fissures, indicating reduced brain volume

69
Q

what did subsequent (after the first gen) neuroimaging studies of brain changes in schizophrenia find (), and what did they focus on

A
  • focussed on specific cortical areas and subcortical structures, the following of which were found to be significantly decreased
    1. hippocampus
    2. Amygdala
    3. thalamus
    4. nucleus accumbent
70
Q

what is the general finding relating to schizophrenia related volume reductions (2)

A
  1. they develop in both gray and white matter

2. most consistently observed in the temporal lobes

71
Q

what are the two potential causes of reductions of brain volume in patients with schizophrenia

A
  1. reduced neuron size
  2. reduced dendritic and axonal arborization
    - both have been reported in individuals with schizophrenia
72
Q

what are the four important findings that have emerged from various meta-analyses of studies that assessed the brain development in patients with or at risk for schizophrenia

A
  1. those at risk but who haven’t been diagnoses display volume reductions in some parts of the brain
  2. extensive brain changes already exist when patients first seek medical treatment and receive their first brain scans
  3. subsequent brain scans reveal that the brain changes continue to develop after initial diagnosis
  4. alterations to different areas of the brain develop at different rtes
73
Q

what is the general consensus regarding the unity of schizophrenia
- what stands as evidence for this

A

NOT UNITARY

  • schizophrenia is not one disorder caused by a singular neural pathology
  • current diagnosis lumps together a group of related disorders under one label
  • suggested by the variability of symptoms, related genes, neural pathology, and the fact that treatments only have major lasting benefits in a small proportion of patients.

Psych370 (37 decks)

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