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Neurobiology of Mental Illness > Schizophrenia > Flashcards

Flashcards in Schizophrenia Deck (24):
1

Describe schizophrenia.

- Psychotic disorder which shows positive and negative symptoms.
- Symptoms include: hallucinations, delusion, withdrawal, loss of motivation
- 3 phases: prodromal, active and residual
- Mainly occurs in early adulthood/late adolescence

2

What are the risk factors for schizophrenia?

- Males
- Living in a big city
- Cannabis use

3

What did Selemon and Zecevic (2015) describe as critical for the development of schizophrenia?

- Environmental factors have a causation role
- Neurodevelopment of the PFC
- Social stress = excess synaptic pruning = symptoms
- Dopamine hyperstimulation = decreased spine density = cognitive dysfunction

4

What did Cardno and Gottesman (2000) find about the genetic component of schizophrenia?

Monozygotic twins have a higher correlation of schizophrenia than dizygotic twins

5

What grey matter abnormalities are apparent in schizophrenia?

Decreased in: Medial temporal and superior temporal volumes

6

What effect do Grey Matter abnormalities have on the brain?

Causes enlarged ventricles and greater CSF levels

7

What did Chung and Cannon (2015) find?

- Progressive structure changes from high-risk to psychotic
- Disrupted cellular connectivity = schizophrenia
- Lower GM volume
- Clinical high risk have a steeper rate of cortical grey matter loss if they become psychotic (vs not-psychotic)
- White matter abnormalities in PF regions

8

Who investigated shrinkage in schizophrenia and what did they find?

- Thompson et al., 2001
- Accelerated GM loss
- Parietal lobe has the biggest deficits
- Over 5y significant shrinkage is seen in temporal lobes and frontal eye fields
- Loss rate is 3x higher than matched controls
- Those on anti-psychotics have less shrinking

9

What is the difference between typical and atypical anti-psychotics?

Typical: block dopamine type 2 receptors and effect basal ganglia and cortical areas

Atypical: Lower affinity and occupancy for DA, higher occupancy for serotonin and enlargement of thalamus

10

What did Karlsgodt et al. (2008) find?
What confounds this study?

- DTI
- Lower FA correlated with lower working memory deficits
- Schizophrenia could be a brain connectivity disorder: lower white matter integrity

Confounded by similar scores across patients and controls: some even did better on task than controls. - did this test a deficit of schizophrenia effectively?

11

What are the dopamine hypotheses based on?

DA is a reward signal. DA receptor antagonists block DA in substantia nigra which leads to psychotic symptoms.

12

Describe the first dopamine hypothesis

Excess DA in neurotransmission leads to positive symptoms.
Evidence: Anti-psychotics block receptors and work, but no clear link yet.

13

Describe the second dopamine hypothesis.

Too much DA in subcortical/striatum leads to positive symptoms, too little in prefrontal regions leads to negative symptoms.
No direct evidence, but better than 1.

14

Describe the third dopamine hypothesis. (2010/Howes & Kapur, 2009)

Presynaptic DA dysregulation.
- Multiple hits interact to cause striatal dopamine dysregulation: fronto-temporal dysfunction, genes, stress, drugs.
- Alters appraisal of stimuli = psychosis
- Anti-psychotics block DA receptors = decreased unusual salience = decreased psychosis

15

What is one issue with the third DA hypothesis?

It does not address negative symptoms.

16

What did Alderson-Day et al. (2015) find about hallucinations?

Resting state of left temporal lobe and left superior temporal gyrus disrupts inauditory and verbal hallucinations.

17

What did Yoon et al. (2015) find?

- Increased connectivity to bilateral dorsolateral PFC and decreased connectivity in left planum temporale and right dorsolateral PFC in first episode and ultra-high risk patients
- fronto-temporal intrinsic functional connection altered at early stages of psychosis
- over connectivity of auditory and frontal cortex

18

What type of task was used in Crossley et al.'s (2009) study and what did it show?

- N-back working memory task
- Connectivity of STG and middle forntal gyrus different in schizophrenia
- Failure to deactivate superior temporal lobe during PFC tasks

19

What does the P50 response tell us about schizophrenia?

- P50 is not suppressed in schizophrenia
- Failure of sensory gating mechanisms to inhibit responses

20

Who investigated Mismatch Negativity and what did they find?

- Naatanen and Kahkonen, 2009
- Temporal and frontal cortices for MMN affected
- Lower MMN response = more symptoms
- Linked to positive symptoms

21

Describe Horton et al.'s (2011) findings.

- Large MMN predicts good response to medication.
- Endophenotype marker of vulnerability to schizophrenia

22

What did Ford (1999) find about the P300 response?

- Lower P300 ERP in schizophrenia
- Linked to enduring negative symptoms, waning of attention and grey matter voume deficits
- P300 reflects amount of resources allocated to processing stimulus

23

Which 3 studies looked at ERPs?

- Uhlhaas & Singer, 2010: abnormalities in synchronised oscillatory activity of neurons. abnormal beta and gamma activity, rhythm anomalies generating networks of GABA interneurons
- Kwon et al., 1999: Less gamma power (as seen in EEG) = dysfunction of recurrent inhibitory drive on audiotry neural networks, unable to support 40Hz oscillations = abnormal temporal and perceptual binding = reality distortions
- Ford et al., 2002: No coherence of speech reception areas in left hemisphere during talking especially for those who hallucinate and lower fronto-temporal functional connectivity = misattribution of inner thoughts to external voices

24

What are limitations of using ERPs?

You have to average responses and may be individual variability