Flashcards in Schizophrenia Deck (24):
- 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?
- 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