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BS42017- Translational Psychiatry and Neurology > BS42017 L4+5 > Flashcards

BS42017 L4+5 Flashcards

1
Q

what are the two diagnostic systems for sz?

A

ICD10 and DSM V

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2
Q

what are the four first rank symptoms of sz?

A
  • delusion
  • hallucinations
  • thought disorder: passivity of thought
  • passivity experiences: delusion of control
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3
Q

what kind of hallucinations occur commonly in sz?

A

auditory (visual are rare and typically occur in elderly confusional states)

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4
Q

what are auditory hallucinations?

A

they are not auditory misperception- it sounds like real speech in external space

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5
Q

what are command hallucinations?

A

an auditory hallucination- persistently hearing a voice in external space telling the patient what to do

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6
Q

what are delusions?

A

These are fixed rigidly held beliefs that are not understandable on the basis of a patient’s cultural background.

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7
Q

what are examples of negative symptoms? (7)

A

These are;

  • persistent loss of usual activities and interests
  • apathy
  • blunted emotional responses
  • speech reduction, social withdrawal
  • impaired attention
  • anhedonia
  • lethargy
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8
Q

what is passivity phenomena?

A

This is the patients belief that they are no longer in control of their actions, feelings or thoughts. They are controlled by an external agent that tells them how to act, feel or think. (relatively rare)

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9
Q

what does the positive and negative syndrome scale detail?

A

positive symptoms
negative symptoms
general psychopathology

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10
Q

what can symptoms of sz possibly be explained by?

A

abnormalities in the experience of;

  • salience (hallucinations and delusions)
  • agency (passivity phenomena)
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11
Q

what does Whitford’s theory state?

A

SZ arises because of some incompletely understood genetic trigger (e.g. sex hormone linked) during late adolescence/early adulthood. E.g. the trigger causes abnormal expression of oligodendrocyte-linked genes during pre-pubertal myelination of the association cortices.

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12
Q

components of Whitford’s theory of sz include; (6)

A
  1. Genetic abnormalities in schizophrenia
  2. Abnormal brain white matter (e.g. measured by fractional anisotropy DTI)
  3. Corollary discharge hypothesis and abnormalities
  4. Abnormal sense of agency and passivity phenomena symptoms
  5. Hyperdopaminergia, D2 receptor blockers antipsychotics, abnormal salience
  6. Grey matter abnormalities in schizophrenia.
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13
Q

what is the likelihood of developing sz if both parents have sz?

A

45%

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14
Q

if a child with a mother with sz is adopted by non-sz parents, what is the likelihood the child develops sz?

A

13% (same as if it was raisied by sz parents)

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15
Q

what are the problems with genetic sz studies?

A
  • even with many 1000s of patients there are still problems with replication between studies.
  • Multiple genes in each have a very small effect and the molecular genetics may explain the very small amount of variance.
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16
Q

genetic abnormalities could give rise to what?

A

white matter abnormalities (study by Kelly in 2018)

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17
Q

what is corollary discharge?

A
  • a motor command (move arm onto table) goes to the motor cortex and a copy is also made of this called the efference copy
  • the efference copy goes to the forward model.
  • the forward model is there to use the information about the motor command to predict what the sensory consequence will be (corollary discharge)
  • there is an area of the brain that compares what the actual sensory feedback is to the corollary discharge and tries to minimise the difference between the two
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18
Q

why do we have corollary discharge?

A

to inform the CNS about external movements ie. how you know the difference between the external world movement vs. self-generated eye movement.
e.g. when you’re on the train you can distinguish between your eye movements and the movement of the train

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19
Q

how does corollary discharge relate to sz?

A
  • Broca’s area produces speech and the speech is picked up by auditory system and processed in Wernicke’s area
  • there is also an internal corollary discharge loop
  • if corollary discharge loop is faulty due to impaired white matter tract integrity, your internal voice may not be recognised by the brain as self-generated (hence auditory hallucinations but not all due to this)
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20
Q

what are the two separate cues to the sense of agency?

A
  1. Sensorimotor system (corollary discharge)

2. (meta) cognitive system (interprets cues)

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21
Q

what two ways are action and effect linked? (voss 2010)

A
  • Predictively (action predicted to generate a given effect)- corollary discharge
  • Retrospectively (interference action caused effect-cognitive mechanism).
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22
Q

what action awareness do healthy subjects have? (predictive and retrospective component)

A

strong predictive component (corollary discharge) of intentional binding and minimal retrospective component

23
Q

what did Moore (2012) find out about sz predictive component?

A

Rather than being a total absence of prediction, patients were generating imprecise predictions rather than no predictions.

The outcome predictions were equally strong in high and low probability conditions (implying aberrant dopamine signalling).

24
Q

how does hyperdopaminergia come about?

A

If the brains response to constantly experiencing internally generated events as unexpected external events is to increase dopamine firing then hyperdopaminergia results.

25
Q

how can hyperdopaminergia be treated?

A

dopamine blockers

26
Q

the mesolimbic DA system is a critical component of what?

A

the attribution of salience

27
Q

what is salience?

A

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

28
Q

what are delusions and auditory hallucinations in terms of salience?

A

Delusions- beliefs with extremely high abnormal salience

Auditory hallucinations- abnormally high salience of internal thoughts.

29
Q

what happens to dopamine signalling during psychosis?

A

there is dysregulated dopamine transmission leading to stimulus independent release of dopamine. Dysregulated DA firing becomes a creator of “abnormal saliences” psychotic symptoms

30
Q

why are antipsychotics efficacious?

A

they all dampen DA signalling

31
Q

what is punishment avoidance and reward-learning associated with?

A

D2 and D1 receptors respectively

32
Q

the clinical efficacy of antipsychotics depends on what?

A

it ability to block the D2 receptors (basal ganglia indirect pathway)

33
Q

what does the atypical antipsychotic aripiprazole do to DA receptors?

A

it occupies D2/3 receptors in BG in dose dependent manner

34
Q

what kind of symptoms do antipsychotics work on?

A

only positive symptoms (no evidence of effect on negative symptoms)

35
Q

give examples of typical and atypical antipsychotics? (2,4)

A

typical- chlorpromazine, haloperidol

atypical- clozapine, olanzapine, risperidone, quetiapine

36
Q

when may clozapine be tried?

A

when failure to respond to a trial of three antipsychotics of different classes using an adequate dose for an adequate duration

37
Q

what are grey matter abnormalities due to?

A

neuropil elimination (not neuronal death)

38
Q

what aspects of sz can be modelled in animals? (5)

A
  • Locomotor changes (cf. psychomotor agitation)
  • “sensory gating” abnormalities, and lack of pre-pulse inhibition of acoustic startle
  • Impaired social interactions
  • Alterations in neurotransmitter levels or actions
  • Changes in cellular morphology or function (hippocampus and cortex) (e.g. parvalbumin-positive interneurons)
39
Q

how are speech and actions disorganised in sz? (3,3)

A

Speech-
- Loose associations; rapidly shifting between unrelated topics
- Preservation; repeating the same things over and over again
- Use of rhyming words without reason
Action-
- Difficulty starting or finishing tasks
- Behaviours that appear bizarre or lack purpose
- Unpredictable or inappropriate emotional responses

40
Q

what impairment predicts language disturbances in sz?

A

Working memory and executive function

41
Q

what does the DISC1 gene do?

A

it is necessary for pyramidal cell migration

42
Q

what do DISC1 knockout mice show?

A

abnormal social behaviour and reduced parvalbumin staining and abnormal interneuron activity.

43
Q

what are endophenotypes?

A

“endophenotypes” are simple, quantifiable, and heritable biological or behavioural traits that segregate with an illness.

44
Q

what is the neurodevelopmental hypothesis of sz?

A

developmental oxidative stress;

  • oxidative stress in cortical interneurons (genetic/environmental factors)
  • altered parvalbumin interneurons (juvenile/ prodromal)
  • excitation-inhibition imbalance (adult/ disease)
  • altered EEG oscillations/ cognitive deficits
45
Q

give examples of neurophysiological measures of sensory processing (3)

A
  • P50 (paired click), MMN and P3 ERPs
46
Q

what is the evidence for the dopamine hypothesis? (3)

A
  • Antipsychotics block D2 receptors
  • Drugs such as amphetamine that elevate brain dopamine levels can cause psychosis (cf. positive symptoms of sz).
  • Elevated D2 receptor levels in people with sz (post-mortem)
47
Q

what is the evidence against the dopamine hypothesis? (2)

A
  • Dopamine-inhibiting drugs modify dopamine levels within minutes, but can take much longer to be effective as antipsychotics
  • Abnormalities in other systems e.g. GABA and glutamate
48
Q

what is thought to underlie positive and negative symptoms?

A

hyperactive mesolimbic dopamine pathway and prefrontal hypoactivity

49
Q

in animal models and humans treatment with what improved working memory and attention?

A

a7 agonists

50
Q

what is reduced in CSF of sz patients (post mortem) in hippocampus and PFC?

A

glutamate levels

51
Q

what causes sz-like symptoms in humans and animals?

A

Non-competitive NMDA receptor antagonists such as ketamine and PCP

52
Q

Reductions in NMDAR-mediated excitation of parvalbumin-positive interneurons of the hippocampus and prefrontal cortex may play a role in what?

A

altered gamma activity and synchrony.

53
Q

what is reduced gamma synchrony between left and right auditory cortex associated with?

A

auditory hallucinations

BS42017- Translational Psychiatry and Neurology (4 decks)

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