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Flashcards in Schizophrenia Deck (24):

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


What are the risk factors for schizophrenia?

- Males
- Living in a big city
- Cannabis use


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


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

Monozygotic twins have a higher correlation of schizophrenia than dizygotic twins


What grey matter abnormalities are apparent in schizophrenia?

Decreased in: Medial temporal and superior temporal volumes


What effect do Grey Matter abnormalities have on the brain?

Causes enlarged ventricles and greater CSF levels


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


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


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


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

- 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?


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.


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.


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.


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


What is one issue with the third DA hypothesis?

It does not address negative symptoms.


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.


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


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


What does the P50 response tell us about schizophrenia?

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


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


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

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


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


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


What are limitations of using ERPs?

You have to average responses and may be individual variability