Schizophrenia Flashcards Preview

Translational psychiatry and neurology > Schizophrenia > Flashcards

Flashcards in Schizophrenia Deck (35)
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1
Q

When does schizophrenia typically start?

A

Adolescence or as a young adult

2
Q

What are examples of first rank symptoms?

A
  • Delusion
  • Auditory hallucination
  • Thought disorder e.g. thought withdrawal
  • Passivity phenomena e.g. ‘made’ feelings
3
Q

What is a delusion?

A
  • Fixed rigidly held belief not understandable on the basis of a patient’s cultural background
  • Typically dominates thinking and is socially disabling
4
Q

What are negative symptoms?

A
  • Persistent loss of usual activities and interests, apathy, blunted emotional responses, speech reduction
  • Social withdrawal, impaired attention, anhedonia, lethargy
5
Q

What is passivity phenomena?

A
  • Patients belief that they no longer control their actions, feelings or thoughts
  • External agent controlling them to act, feel or think
6
Q

What is presented in Whitford’s theory, which explains the symptoms of schizophrenia?

A

The concept of brain abnormalities and abnormal salience (hallucinations and delusions) and agency (passivity phenomena)

7
Q

What does Whitford’s theory suggest as the cause of schizophrenia?

A
  • SZ arises because of some incompletely understood genetic trigger during late adolescence/early adulthood
  • Myelin is structurally abnormal and consequently abnormal in ability to insulate axon membranes affecting velocity of axon potentials
  • Functional disconnections result in disruption of corollary discharge mechanisms
8
Q

What is the risk of SZ in monozygotic twins or a child with both parents having SZ?

A

45% increased risk of having SZ

9
Q

What is the risk to children of SZ mothers adopted soon after birth by non-SZ families?

A

13% increased risk - no increased risk of developing SZ for children of non-SZ parents similarly adopted

10
Q

What is the problem with molecular genetic studies in SZ?

A
  • They have not identified clinically useful findings for drug discovery nor does this seem likely
  • There are multiple genes implicated in SZ each with very little effect
11
Q

Where are the biggest white matter abnormalities in the brains of SZ patients?

A

Corona radiata and corpus callosum

12
Q

What is corollary discharge?

A
  • Efference copy of motor command is used to create a predicted sensory feedback (corollary discharge) which estimates the sensory consequences of a motor command
  • Actual sensory feedback compared with predicted feedback informs the CNS about external actions
  • This is how you know the difference between external world movement and self-generated eye movement
13
Q

How does abnormal corollary discharge relate to auditory hallucinations in SZ patients?

A

Auditory hallucinations are due to a failure of corollary discharge connections due to impaired white matter tract integrity from Broca’s area to superior temporal gyrus/Wernicke’s area so auditory hallucinations are untagged sub-vocal speech therefore not recognised by the brain as self-generated

14
Q

What is the altered sense of agency in SZ thought to be due to?

A

Dysfunction of perception and action therefore faulty integration of prior knowledge and expectations with evidence

15
Q

What are the 2 separate cues to sense of agency?

A
  • Sensorimotor system and cognitive system
  • The widely held view currently - physiological prediction deficit in sensorimotor function leads to distorted agency cues
16
Q

What are the 2 ways in which linkage of action and effect are generated?

A
  • Predicatively (action predicted to generate a given effect) - corollary discharge
  • Retrospectively (inference action caused effect) - cognitive mechanism
17
Q

In terms of predictive and retrospective components of intentional binding, what do SZ patients lack?

A
  • Absent predictive component with strong retrospective component
  • Higher incidence of first rank symptoms, such as delusions and hallucinations, associated with more reduced predictive component
18
Q

What is the key mechanism underlying the sense of agency?

A

Association between ones action and external effect

19
Q

What did the Moore et al (2012) review show about the prediction component of intentional binding?

A

Patients were generating imprecise prediction rather than no predictions

20
Q

Why could hyperdopaminergia occur in SZ?

A

If the brain’s response to constantly experiencing internally generated events as unexpected external events is to increase dopamine firing then hyperdopaminergia results

21
Q

The mesolimbic DA system is a critical component of the attribution of salience. Describe the process of salience

A

This is the process by which events and thought grab attention and influence goal-directed behaviour because of association with reward or punishment, linked to concepts of value

22
Q

How is salience related to delusions and auditory hallucinations?

A
  • Delusions - belief with extremely high abnormal salience
  • Auditory hallucinations - abnormally high salience of internal thoughts
23
Q

How does DA affect salience?

A

In health, DA mediates the process of salience acquisition and expression but does not create the process (DA release is dependent on external stimuli)

24
Q

What happens to DA release and thus salience in psychosis?

A
  • There is dysregulated DA transmission leading to stimulus independent release of DA
  • This leads to creation of abnormal saliences (psychotic symptoms)
25
Q

What property do all anti-psychotics have in common?

A

They dampen salience acquisition

26
Q

How was dampening of salience by anti-psychotics demonstrated in behavioural studies in rats in the 1950s?

A
  • Rats had a punishment avoidance schedule - associated bell with an electric shock, so would try to avoid
  • Rats + anti-psychotics - function not impaired and still responding to shock but there is a forgetfulness of motive i.e. reduced salience
27
Q

What pathways are punishment avoidance and reward-learning associated with respectively?

A
  • Indirect basal ganglia pathway and D2 receptors
  • Reward learning is associated with direct basal ganglia pathway and D1 receptors
28
Q

What property do anti-psychotics need to have to be clinically effective?

A

They need to block D2 receptors (indirect basal ganglia pathway)

29
Q

Name some examples of typical anti-psychotics

A

Chlorpomazine, haloperidol

30
Q

Name some examples of atypical anti-psychotics

A

Clozapine, olanzapine, risperidone, quetiapine

31
Q

Why are regular blood counts needed for patients on clozapine?

A

Risk of agranulocytosis

32
Q

What are some clinical factors of SZ associated with a good prognosis?

A
  • Female, abrupt onset, married, good pre-morbid social adjustment, short duration of illness, lack of negative symptoms, lack of cognitive impairment, no ventricular enlargement
  • Bold = if present tend to indicate poor prognosis
33
Q

10% of SZ patients commit suicide. What factors makes this more likely?

A

Early in illness, males with chronic illness, unemployed, tardive dyskinesia, previous high educational attainment, sudden stoppage of medication, recent discharge from hospital

34
Q

Grey matter abnormalities occur early in SZ. Why are these abnormalities thought to occur?

A
  • Due to neuropil elimination not neuronal death
  • Most likely loss of dendritic arbors and associated synaptic infrastructure
35
Q

What areas of the brain have been shown to atrophy in SZ?

A

Smaller hippocampus, amygdala, thalamus, nucleus accumbens