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Neurobiology of Mental Illness > Lecture 3 - Schizophrenia > Flashcards

Lecture 3 - Schizophrenia Flashcards

1
Q

Describe schizophrenia in one sentence.

A

A psychotic disorder with positive and negative symptoms

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2
Q

What are positive symptoms?

A

Symptoms that were not present before illness onset

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3
Q

What are negative symptoms?

A

Symptoms involving a deviation from or loss of normal functioning.

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4
Q

Name 4 positive symptoms in schizophrenia.

A
  • delusions
  • hallucinations
  • thought disorder
  • lack of insight
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5
Q

Name 5 negative symptoms in schizophrenia

A
  • social withdrawal
  • self neglect
  • loss of motivation
  • emotional blunting
  • paucity of speech
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6
Q

Why is schizophrenia often difficult to diagnose?

A

Negative symptoms match to symptoms of depression.

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7
Q

What are the stages of schizophrenia?

A

Prodromal
Active
Residual

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8
Q

What is the first stage of schizophrenia and what does it involve?

A

Prodromal (pre-stage):

  • minimal, but detectable symptoms
  • sleep disturbances, depressed mood, anxiety, irritability, paranoia
  • ultra high risk (UHR) for full-blown schizophrenia
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9
Q

If you are classed as UHR for schizophrenia, what is the percentage likelihood that you will go on to develop a psychotic episode?

A

20-50% within 1-2 years.

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10
Q

What is one of the greatest predictors of a psychotic episode?

A

If you have had a previous psychotic episode.

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11
Q

Define a psychotic episode

A

A full-blown breakdown of your senses. No specific timeframe.

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12
Q

When does schizophrenia typically begin?

A

Early adulthood, 18-21.

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13
Q

Describe sex differences in schizophrenia.

A

Men seem more likely to develop it, have more negative symptoms than positive, and have less chance of recovery than women.

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14
Q

What are some predictors of schizophrenia?

A
  • Living in a big city during formative years (0-15 y/o).
  • Being an immigrant
  • Cannabis use in teenage years (suggests a developmental element - no relationship in adult life)

Picchoni and Murray (2007)

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15
Q

Why is being an immigrant a risk factor for schizophrenia?

A

Increased isolation and stress.

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16
Q

What are the neurodevelopmental risk factors for schizophrenia?

A
  • Mother gets the flu during first 3 months
  • Adverse life events (mum living in a war zone)
  • Maternal malnutrition
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17
Q

Why is schizophrenia viewed as a neurodevelopmental disorder?

A

There are crucial stages where, if something happens, your risk of schiz goes up dramatically.

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18
Q

What is occurring in the brain during the stage when the risk factors for schizophrenia have the most influence?

A

Synaptic pruning

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19
Q

What are the most consistent neurological findings in schizophrenia, and according to who?

A

Schizophrenics have a reduction of gray matter volume in their:

  • prefrontal cortex
  • medial temporal cortex
  • superior temporal lobe
  • also have larger ventricles

compared to matched controls

(Chung & Cannon, 2015)

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20
Q

What do large ventricles represent?

A

Reduction in gray matter volume - ventricles increase in size to fill out the empty space caused by tissue loss. Ensures brain doesn’t move around within the skull.

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21
Q

What was the loss of gray matter in schizophrenics explained away as?

A

Due to the anti-psychotic medication they received.

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22
Q

How was it shown that gray matter loss was indeed due to schizophrenia and not to their anti-psychotic medication?

A

Thompson et al., (2001) compared annual gray matter loss between medicated schizophrenics and medicated non-schizophrenics.

Authors found that schizophrenics remained to have a much greater loss in gray matter than matched non-schizophrenics receiving the same medication.

Their gray matter loss was also more temporal and prefrontal than the losses of the medicated non-schizophrenics.

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23
Q

What are the structural differences found using volumetric MRI in schizophrenia (Chung & Cannon, 2015)?

A

Consistent differences in white matter tracts between schizophrenics and controls.

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24
Q

What does DTI stand for and what is it?

A

Diffusion Tensor Imaging.

The mapping of the diffusion process of molecules.

It is a way to measure the quality of white matter tracts (fiber density, axonal diameter, myelination) by sending a magnetic field and trapping water molecules in voxels of the brain.

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25
Q

How does DTI work?

A

The measure that DTI uses is FA - fractional anisotropy, which is the number of directions diffusion occurs in. If water molecules can diffuse in all directions, you have an anisotropy/FA value of 0 (more diffusion directions & lower tract quality). If the molecules can only go in two directions, you have a very high FA value (less diffusion directions & higher tract quality).

White matter tracts, which are the axon bodies of neurons, tend to have quite high FA values, at least to begin with. The higher the value, the higher quality they are - greater myelination and healthier axons. This means there is more direct communication/coherent flow of molecules from one area to another.

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26
Q

What is the tract called between the frontal and parietal cortex?

A

Superior Longitudinal Fasciculus (SLF)

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27
Q

What did Karlsgodt et al., (2008) find about the white matter tracts between the frontal and parietal cortex?

A
  • Higher SLF values correlated with improved working memory performance.
  • Quality of white matter tracts had more of an impact in schizophrenia patients compared to controls.
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28
Q

What does FA stand for, and how can it be defined?

A

Fractional anisotropy:

Represents a scalar value from 0, reflecting isotropic movement of water molecules (uniformly in all directions), to 1, anisotropic movement of water molecules (different amounts of each direction).

–> used in reference to the quality of white matter tracts, as the more isotopic/uniform diffusion is, the less efficient it will be in moving from one location to another. This is why a high FA value represents high quality of white matter.

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29
Q

What could explain findings in Karlsgodt et al., (2008)?

A

Suggests patients are reliant on the SLF tract for working memory function, which may result due to a lack of a compensatory mechanism. Healthy individuals may not have premium quality tracts, but have other ways of improving their working memory.

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30
Q

Define a neurotransmitter.

A

A chemical released by nerve cells to send signals to other nerve cells.

31
Q

Where is the biggest source of dopamine?

A

In the substantia nigra and ventral tegmental area (striatum)

32
Q

Which evidence suggests a link between dopamine and schizophrenia?

A
  • If dopamine receptors in the substantia nigra are blocked by Da antagonists, schizophrenia symptoms are attenuated.
  • More dopamine release correlates with symptom severity.
  • Dopamine receptor binding is increased in patients with psychosis.
  • amphetamines induce positive schizophrenia symptoms (such drugs increase extracellular dopamine)

Deserno et al., (2013)

33
Q

What does the first Dopamine hypothesis of Schizophrenia posit?

A

Howes and Kapur (2009):

Schizophrenia is characterised by an excess in dopaminergic transmission/D2 occupation.

34
Q

Why is dopamine assumed to be a reward signal in the brain?

A
  • If dopamine is released during a particular action, that action occurs more often.
  • The more dopamine is released, the more significant (/salient) the event will be perceived.
35
Q

What do antagonists do in relation to dopamine?

A

Occupies dopamine receptors, decreasing the amount of dopamine transmission that is possible.

36
Q

Which dopamine receptor is involved in reward and saliency?

A

D2

37
Q

What is the D2 dopamine receptor involved in?

A

Reward and saliency

38
Q

What are the counters to the first dopamine hypothesis of schizophrenia?

A

The level of dopamine metabolites in cerebrospinal fluid does not significantly differ between schizophrenics and healthy controls.

There is also no clear link between dopamine transmission and symptoms.

39
Q

What shows that increased baseline occupancy of D2 receptors by dopamine characterises schizophrenia?

A

The greater the increase in D2 receptor availability, the greater the decrease in positive symptoms after 6 weeks of anti-psychotic treatment.

As the decrease in symptoms is associated with an increase in D2 receptor availability, and symptoms were theorised to result from dopamine transmission, this evidence suggests that the greater availability of receptors reflected lesser extents of dopamine transmission/lower levels of dopamine, and that this was why (positive) symptoms decreased.

40
Q

What does the second dopamine hypothesis of schizophrenia propose?

A

Too little dopamine in the PFC (prefrontal hypodopaminergia) leads to negative symptoms

  • Too much Da in the subcortical striatum (hyperdopaminergia) leads to positive symptoms
41
Q

What are the counters to the second dopamine hypothesis of schizophrenia?

A
  • There is no evidence to suggest there’s actually too little dopamine in the PFC of schizophrenics.
  • Doesn’t take into account the neurodevelopment of the disease, or genetics.
42
Q

What is the third dopamine hypothesis of schizophrenia?

A

Only attempts to explain the negative symptoms of schizophrenia.

Says that a mixture of genetic and sociocultural factors (e.g. stress, drugs) causes a faulty dopamine system.

Faulty system leads to random dopamine release, causing minor events and stimuli to be perceived as largely important (leads to delusions too).

43
Q

Why are antipsychotics an issue in the long term, according to the third dopamine hypothesis of schizophrenia?

A

Antipsychotics are dopamine antagonists, so they do not prevent increased dopamine release. Therefore, they plug the dam and disallow dopamine transmission, but as soon as antipsychpotics are withdrawn and the dopamine D2 receptors are no longer occupied, the build up of dopamine causes even more severe symptoms than before.

44
Q

What is the issue with the third dopamine hypothesis of schizophrenia?

A

It only addresses the positive symptoms.

45
Q

What is the third dopamine hypothesis of schizophrenia more accurately called?

A

The dopamine hypothesis of psychosis-in-schizophrenia.

46
Q

Why are so few findings directly replicated across studies?

A
  • Schizophrenia is a highly heterogeneous disorder.
  • A (significant) minority of schizophrenia patients do not experience hallucinations.
  • most resting state studies in schizophrenia assume resting networks are stable, trait-based markers for psychopathology.

Alderson-Day, McCarthy-Jones & Fernyhough (2015)

47
Q

What is one consistent findings from functional studies in schizophrenia?

A

Evidence of over-connectivity between the auditory and frontal cortex.

(Yoon et al., 2015)

48
Q

Define hallucinations

A

Perception without a stimulus

49
Q

Define delusions

A

Fixedly held beliefs that are not shared by others from the individual’s community.

50
Q

Define thought disorder

A

Distorted or illogical speech; a failure to use language in a logical and coherent way.

51
Q

Define lack of insight

A

Failure to appreciate that symptoms are not real or caused by illness.

52
Q

What did Cardno & Gottesman (2000) show about geneticelements to schizophrenia?

A

There does appear to be a genetic element. Meta analysis of twin studies, and found:

There is a greater rate of schizophrenia between MZ twins than there are between same gender DZ twins.

Suggests that there could be a gene or allele that increases the risk for schizophrenia, and that when shared, the incidence of schizophrenia between twin pairs is higher.

53
Q

What are typical antipsychotics?

A

Ones which target the dopaminergic system by blocking dopamine D2 receptors. Induces changes in the basal ganglia and cortical areas.

54
Q

What are atypical antipsychotics?

A

Ones which do not target dopamine directly, but occupy serotoninergic receptors (5-HT2A). Enlarges the thalamus.

55
Q

What is hypodopaminergia?

A

Too little dopamine activity

56
Q

What is hyperdopaminergia?

A

Too much dopamine activity

57
Q

What else did Yoon et al., (2015) find about functional connectivity and schizophrenia?

A

(aside from correlation between functional connectivity and positive symptoms)

Greater connectivity between frontal and auditory cortices in schizophrenia patients with hallucinations compared to those without hallucinations.

58
Q

What did Crossley et al., (2009) find about WM-task related connectivity and neuroimaging correlates?

A
  • negative coupling between the frontal gyrus and STG in controls (deactivation of the STG during the WM task)
  • positive coupling in those with first episode phase schizophrenia
  • neutral coupling in those with at risk mental states.

Suggests that an failure to deactivate the STG during tasks that engage the PFC seems a physiological feature of schizophrenia, and may reflect aberrant fronto-temporal connectivity.

Implies that this over-active link between the two regions can be apparent in such WM tasks. WM tasks cause activation of the PFC/frontal areas, which may activate temporal areas in schizophrenics, something which does not occur with controls on the same task - in fact temporal areas seem to be inhibited.

59
Q

What is the P50?

A

A response that occurs 50ms after an auditory sound.

If a second click is presented within 500ms, the auditory cortex’s response is much lower.

(aids habituation mechanisms)

60
Q

How is the P50 aberrant in schizophrenics?

A

Schizophrenics do not actually appear to show the P50 response - they do not have a decreased response to the same stimuli when presented successively (within 500ms).

Suggests that the auditory cortex is unable to gate information in schizophrenia.

61
Q

What did Kwon et al., (1999) find about auditory steady state responses in schizophrenia?

A

Gamma range neural synchronisation is thought to reflect information processing and integration of various features of an object, in neural networks.

Neural synchronisation was measured in response to auditory stimulation of different rates (20-40Hz).

At lower frequencies of stimulation, no differences in power (EEG magnitude squared) were found. However, at 40Hz, schizophrenia patients showed reduced EEG power, and also showed delayed onset of phase synchronisation and delayed desynchronization.

Suggests that failure to support the entrainment of intrinsic gamma-frequency oscillators could be the underlying mechanism of early-stage processing deficits in schizophrenia. The reduced power at 40Hz could reflect a dysfunction of the recurrent inhibitory drive on auditory neural networks.

62
Q

What is sensory gating?

A

Neurological processes which filter out redundant stimuli in the brain from all possible environmental stimuli.

63
Q

What is the P50 ratio?

A

The amplitude of the P50 to the second stimulus divided by the amplitude of the P50 to the first stimulus.

64
Q

What can temporarily reverse the lack of P50 response in schizophrenics?

A

Nicotine patches. Some evidence suggests there is a gene that regulates both nicotinic reception, sensory gating and is also implicated in schizophrenia.

65
Q

What does mismatch negativity represent?

A

A error prediction response/signal in EEG activity which occurs outside of conscious control (even fetuses show it).
Activity decreases 150-200ms after the violation in prediction.

66
Q

How is mismatch negativity different in schizophrenics?

A

It is diminished.

67
Q

What are the two components of MMN?

A
  • supratermporal component-pre-perceptual change detection

- frontal component-involuntary attention switch caused by auditory change

68
Q

What does the MMN depend on?

A

The presence of a short term memory trace in the auditory cortex (needs a few seconds of auditory pattern to decide whether the most recent stimulus is different to prediction).

(Naatanen et al., 20017)

69
Q

What did Horton et al., (2011) find about MMN in schizophrenics?

A

In controls, the amplitude of MMN in response to a violating stimulus increases from a change of -3v at 5% change in frequency (as the MMN) to a change of -4.5v in response to a frequency change of 20%.

In schizophrenics, the amplitude of responses did dip slightly, but remained fairly constant, at around -1.5v across all frequency changes.

70
Q

What is the P300?

A

A later, conscious response to a mistake. Positive EEG response occurring 300ms after the mistake, and only seen when the task involves detecting the presence of a deviancy. Not present if its not asked for.

71
Q

What is the relationship between the size of the P300 and confidence in devincy detection?

A

The larger the P300 response, the more confident you are that a deviancy in a pattern has been detected.

72
Q

How is the P300 different in schizophrenics?

A

The P300 is smaller in schizophrenics compared to controls.

P300 is also eve smaller in more severe schizophrenics, compared to less severe schizophrenics.

73
Q

What is the relationship between P300 timing and mental efficiency?

A

Negative correlation between timing and mental efficiency:

Shorter latencies are associated with superior cognitive performance on neuropsychological tests.

Neurobiology of Mental Illness (10 decks)

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