SZ MCQs

Question 1

Who first described SZ symptoms of patients as ‘Dementia Praecox’?

A) Eugen Bleuler (1911)
B) Emil Kraepelin (1898)
C) Kennedy West (1874)
D) Larry McCutcheon (1902)

Answer 1

B) Emil Kraepelin (1898)

Question 2

Which of the below was NOT identified as an original symptom by Emil Kraepelin (1898)?

A) Attention deficits
B) Memory deficits
C) Communication deficits
D) Goal-directed behaviour deficits

Answer 2

C) Communication deficits

Question 3

Who coined the term SZ?

A) Eugen Bleuler (1911)
B) Emil Kraepelin (1898)
C) Kennedy West (1874)
D) Larry McCutcheon (1902)

Answer 3

A) Eugen Bleuler (1911)

Question 4

What did Eugen Bleuler (1911) distinguish between?

A) Positive and Cognitive symptoms
B) Negative and cognitive symptoms
C) Positive and negative symptoms
D) None of the above, he did investigate symptoms

Answer 4

C) Positive and negative symptoms

Question 5

Which of the below are considered subdomains of negative symptoms?
(select all that apply)

A) Diminished emotional expression
B) Avolition
C) Anhedonia
D) Disorganised behaviour

Answer 5

A) Diminished emotional expression
B) Avolition

Question 6

What does this best describe?
“Affect= limited range of emotions, Alogia= Poverty of speech”

A) Diminished emotional expression
B) Avolition
C) Anhedonia
D) Disorganised behaviour

Answer 6

A) Diminished emotional expression

Question 7

Which of the below is NOT an aspect of Avolition?

A) Anhedonia
B) Apathy
C) Blunted affect
D) Social withdrawal

Answer 7

C) Blunted affect

Question 8

When are impairments in cognitive function often found?

A) Early adulthood
B) Late adulthood
C) Teenager
D) Early childhood

Answer 8

D) Early childhood

Question 9

How much more likely are siblings/children of affected individuals to develop SZ?

A) 10x
B) 20x
C) 30x
D) 40x

Answer 9

A) 10x

Question 10

Which of the below is NOT an environmental factor affecting risk of SZ??

A) Urban environment
B) Air pollution
C) Diet
D) Drugs

Answer 10

C) Diet

Question 11

Which of the below is NOT a neurotransmitter linked to SZ?

A) Dopamine
B) Serotonin
C) Glutamate
D) GABA

Answer 11

B) Serotonin

Question 12

Which of the below is the main excitatory neurotransmitter?

A) Dopamine
B) Serotonin
C) Glutamate
D) GABA

Answer 12

C) Glutamate

Question 13

What is the best description of the Dopamine hypothesis?

A) Important for the mesolimbic dopaminergic pathway projecting to the frontal cortex
B) Important for the mesolimbic dopaminergic pathway projecting to the hippocampus
C) Important for the mesocortical dopaminergic pathway projecting to the frontal cortex
D) Important for the mesocortical dopaminergic pathway projecting to the hippocampus

Answer 13

C) Important for the mesocortical dopaminergic pathway projecting to the frontal cortex

Question 14

Which of the below is NOT evidence for the Dopamine hypothesis?

A) Striatal DA correlates with negative symptoms
B) Dopamine agonists can induce psychotic symptoms
C) Post mortem/neuroimaging studies have shown altered levels of DA in midbrain
D) Increased striatal DA release in SZ correlates with more severe psychotic symptoms

Answer 14

A) Striatal DA correlates with negative symptoms

Question 15

What did Poels et al (2014) suggest?

A) Regulation of DA system is secondary to impaired glutamate function
B) Regulation of DA system is more important than impaired glutamate function
C) Dysregulation of DA system is secondary to impaired glutamate function
D) Dysregulation of DA system is more important than impaired glutamate function

Answer 15

C) Dysregulation of DA system is secondary to impaired glutamate function

Question 16

What did Moghaddam & Javitt (2012) suggest were the 2 phases of glutamate modulations?
(select 2)

A) NMDA mediated neuron dysfunction leads to loss of inhibitory control and decreased glutamate levels
B) NMDA mediated neuron dysfunction leads to loss of inhibitory control and increased glutamate levels
C) Glutamate-induced excitotoxicity leads to loss of glutamate connections and decreased glutamate levels
D) Glutamate-induced excitotoxicity leads to loss of glutamate connections and increased glutamate levels

Answer 16

B) NMDA mediated neuron dysfunction leads to loss of inhibitory control and increased glutamate levels

C) Glutamate-induced excitotoxicity leads to loss of glutamate connections and decreased glutamate levels

Question 17

Which of the below is NOT a neuroanatomical difference of SZ brains?

A) Increased neurons in prefrontal cortex
B) Enlarged ventricles
C) Weigh less
D) Abnormal cell structure

Answer 17

A) Increased neurons in prefrontal cortex

Question 18

Which of the below are considered problems when dealing with cognitive symptoms?
(select all that apply)

A) Difficult to understand underlying mechanisms
B) Difficulties due to short term problems
C) Difficult to assess as are constantly changing
D) Difficult to develop effective interventions

Answer 18

A) Difficult to understand underlying mechanisms
D) Difficult to develop effective interventions

Question 19

What was Barch and Ceaser (2012) hypothesis for cognitive symptoms?

A) Mechanisms within working and episodic memory creates impairments in proactive control
B) Mechanisms within working and episodic memory creates improvements in proactive control
C) Mechanisms within working and episodic memory creates improvements in goal directed behaviour
D) Mechanisms within working and episodic memory creates impairments in context processing

Answer 19

A) Mechanisms within working and episodic memory creates impairments in proactive control

Question 20

What is Proactive control associated with?

A) Representation of info in the Lateral preforntal cortex
B) Representation of info in the Bilateral prefrontal cortex
C) Representation of info in the Dorsolateral prefrontal cortex
D) Representation of info in the Trilateral prefrontal cortex

Answer 20

C) Representation of info in the Dorsolateral prefrontal cortex

Question 21

What theory did Braver et al (2009) create?

A) Bilateral mechanisms of behaviour
B) Intended actions hypothesis
C) Dual mechanism of control
D) Working memory inhibition

Answer 21

C) Dual mechanism of control

Question 22

What did Braver et al (2009) suggest Proactive control aimed to do?

A) Cope with the outcome of our previous actions
B) Prepare for an upcoming action
C) Create adjustments in behaviour
D) Reduce reliance on reactive control

Answer 22

B) Prepare for an upcoming action

Question 23

What did Minzenberg et al (2009) find in the meta-analysis to support the association between proactive control and SZ?

A) Showed reduced DLPFC activity in schizophrenia patients in tasks that require proactive control.
B) Showed increased DLPFC activity in schizophrenia patients in tasks that require proactive control.
C) Showed reduced DLPFC activity in schizophrenia patients in tasks that require reactive control.
D) Showed increased DLPFC activity in schizophrenia patients in tasks that require reactive control.

Answer 23

A) Showed reduced DLPFC activity in schizophrenia patients in tasks that require proactive control.

Question 24

Who studied processing speed in SZ patients?

A) Barch & Ceaser (2003)
B) Dickinson et al (2007)
C) Culbreth et al. (2018)
D) Moghaddam & Javitt (2012)

Answer 24

B) Dickinson et al (2007)

Question 25

What did Dickinson et al (2007) find when studying processing speed in SZ patients? A) Impairments in processing speed in patients B) Improvements in processing speed in patients C) Both A and B depending on patient, there were no conclusive findings D) None of the above

Answer 25

A) Impairments in processing speed in patients

Question 26

Which of the below is a potential explanation for reduced processing speed in SZ patients? A) Different tracts connecting brain areas B) Lack of integrity in patients white matter fibre tracts C) Working memory deficits D) Lack of association connections

Answer 26

B) Lack of integrity in patients white matter fibre tracts C) Working memory deficits

Question 27

What was found when styling episodic memory and SZ? A) Memory is more impaired than familiarity B) Recollection is more impaired than familiarity C) Familiarity is more impaired than memory D) familiarity is more impaired than recollection

Answer 27

B) Recollection is more impaired than familiarity

Question 28

Who studied decision making in SZ? A) Barch & Ceaser (2003) B) Dickinson et al (2007) C) Culbreth et al. (2018) D) Moghaddam & Javitt (2012)

Answer 28

C) Culbreth et al. (2018)

Question 29

What was found when styling physical/mentak effort in SZ patients? A) Those with SZ less likely to select an easy task compared to control group B) Those with SZ less likely to select a hard task compared to control group C) Those with SZ are more likely to select an easy task compared to control group D) Those with SZ are more likely to select a hard task compared to control group

Answer 29

B) Those with SZ less likely to select a hard task compared to control group

Question 30

What did Culbreth et al. (2018) find when studying decision making in SZ? A) Typical effort based decision making does not contribute to motivational impairments B) Typical effort based decision making does contribute to motivational impairments C) Atypical effort based decision making does contribute to motivational impairments D) Atypical effort based decision making does not contribute to motivational impairments

Answer 30

C) Atypical effort based decision making does contribute to motivational impairments

Question 31

What was hypothesised when testing reward responsivity in SZ? A) Increased reward responsivity, therefore less likely to exert effort B) Increased reward responsivity, therefore more likely to exert effort C) Reduced reward responsivity, therefore less likely to exert effort D) Reduced reward responsivity, therefore more likely to exert effort

Answer 31

C) Reduced reward responsivity, therefore less likely to exert effort

Question 31

Which of the below is NOT a stricture linked in effort-based decision making in healthy individuals? A) Medial frontal cortex B) Ventral striatum C) Dopamine systems D) Posterior cingulate

Answer 31

D) Posterior cingulate

Question 32

What was actually found when testing reward responsivity? A) Increased reward responsivity, therefore less likely to exert effort B) Increased reward responsivity, therefore more likely to exert effort C) Reduced reward responsivity, therefore more likely to exert effort D) No difference between SZ and controls

Answer 32

D) No difference between SZ and controls

Question 33

Which aspects of episodic memory are modulated in SZ? (select all that apply) A) Familiarity B) Recollection C) Relational memory and item memory D) Relational memory

Answer 33

B) Recollection D) Relational memory

Question 34

Which of the below is a good predictor of everyday functioning in SZ? A) Positive symptoms B) Number of genetic mutations C) Cognitive symptoms D) All of the above

Answer 34

C) Cognitive symptoms

Question 35

What did Moghaddam & Javitt (2012) assume? A) First, increased glutamate levels, followed by decreased glutamate levels B) First, decreased serotonin levels, followed by increased glutamate levels C) First, increased dopamine levels, followed by decreased dopamine levels D) First, increased dopamine levels, followed by decreased serotonin levels

Answer 35

A) First, increased glutamate levels, followed by decreased glutamate levels

Question 36

Emil Kraepelin assumed that the cause for schizophrenia is..? A) Dementia B) Psychological trauma C) Biological and genetic mechanisms D) All of the above

Answer 36

C) Biological and genetic mechanisms

Question 37

Which aspect of working memory seem to be impaired in individuals with schizophrenia? A) Central executive B) Episodic buffer C) Phonological loop D) Visuo-spatial sketchpad

Answer 37

A) Central executive

Question 38

What is observed in SZ individuals? A) Abnormal cellular structures in visual and auditory cortex B) Increased number of neurons in prefrontal cortex C) Abnormal cellular structures in hippocampus and prefrontal cortex D) Decreased number of neurons in parietal cortex

Answer 38

C) Abnormal cellular structures in hippocampus and prefrontal cortex