Schizophrenia Flashcards
What is Schizophrenia?
A type of psychosis/severe mental disorder categorised by a profound amount of disruption of cognition and emotion. Contact with external reality and insight are impaired. Affects a person’s language through perception, emotions and sense of self.
How many people are affected by Schizophrenia at one point in their life?
1% of the population. No more than 1 in 5 completely recover.
Definition of Positive Symptoms
Aren’t called positive because they are good but because they add something which ‘normal’ people don;t have.
What are some examples of Positive symptoms?
- Hallucinations
- Delusions/paranoia/grandeur
- Disorganised speech
- Disorganised/catatonic behaviour
What are hallucinations?
Disturbances of reality in any of the sense. False perceptions that either have no base in reality or are distorted perceptions of things that are. Most common are auditory hallucinations.
What are delusions?
Firmly held irrational beliefs that have no basis in reality. Common types:
- Delusions of persecution
- Delusions of grandeur
- Delusions of control
- Delusions of reference
Definition of negative symptoms
Known as ‘deficits’ if they’re present for at least a yea, and are something someone has lost.
Examples of negative symptoms
- Avolition
- Speech Poverty (Alogia)
- Affective Flattening
- Anhedonia
What is Avolition?
Lack of purposeful, willed behaviour. Reduction, difficulty or instability to start or continue with goal-directed behaviour. People with SZ often have a sharply reduced motivation to carry out a range of activities and results in lowered activity.
What is Speech Poverty (Alogia)?
Limited speech output with limited, often repetitive, content. Involves reduced frequency and quality of speech.
What is Anhedonia?
Loss of interest/pleasure, or reduced emotions to things that are pleasurable. Social aspect confused with depression - only physical anhedonia is reliable for SZ.
Who conducted the ‘Sane in Insane Places’ study?
Rosenhan (1973)
What was the ‘Sane in Insane Places study?
- Covert ppt observation
- Students reported a ‘dull thud’ which was not an actual symptom according to the DSM II
- All were diagnosed with SZ and hospitalised
- They were given meds/treatments and not allowed to leave until the university intervened, sometimes up to 2 months
- Rosenhan later phoned and said he was sending more fake patients. Over the next few weeks, 21% were diagnosed as ‘pseudopatients’ and sent home.
- He never actually sent any over.
The role of Dopamine Receptor Genes in SZ
(D2, DR2)
- Affects a number of dopamine receptor sites and transports proteins for dopamine
- Associated with negative and positive symptoms (Davis & Khan 1991)
The role of Glutamate Receptor Genes in SZ
(NMDA, AMPA)
- Affects a number of glutamate receptor sites. Especially important in the ventral striatum
- Associated with negative symptoms (Sorg et al 2013)
The role of GRK in SZ
(G-Protein Coupled Receptor Kinase)
- Makes epigenetic and sensitivity changes to receptors for a number of excitatory neurotransmitters. Higher levels increase effects (Funk et al 2014)
Gottesman’s study on SZ in families
(1991) Studied concordance rates in children with SZ parents or siblings 2x SZ parents: 46% concordance 1x SZ parent: 13% concordance 1x SZ sibling: 9% concordance
Joseph’s study on SZ in twins
(2004)
Meta analysis of data on MZ vs DZ twin concordance with SZ
MZ concordance: 40.4%
DZ concordance: 7.4%
Modern studies use ‘blind’ researchers. They show a lower but still big difference
Tienari’s study on SZ in adoptive families
(2000)
Compared siblings raised together vs apart
164 had SZ mothers = 6.7% developed SZ
197 were in a ‘control group’ = 2% developed SZ
Conclusion = genetic liability for SZ is ‘decisively confirmed’
What is the Dopamine Hypothesis?
States that SZ is caused by an imbalance of dopamine, either:
- They have too many D2 receptors
- Their D2 receptors are too sensitive/fire too often
- They produce too much dopamine
What is Dopaminergia?
Dopamine’s actions in the brain. If there is too much, it’s known as hyperdopaminergia. If there is too little, it’s known as hypodopaminergia.
What does Hyperdopaminergia cause in the subcortex?
It’s associated with positive symptoms. Broca’s area produces speech and too much dopamine here leads to the speech and hearing-related symptoms
What does Hypodopaminergia cause in the subcortex?
Associated with negative symptoms. PFC is the central executive and too little here leads to avolition/catatonia.
What are drugs that increase dopamine activity?
- Amphetamines
- L-dopa
What are drugs that decrease dopamine activity?
- Chlorpromazine
- Clozapine
What did Davis & Khan theorise about Dopamine in SZ?
- Too much in mesolimbic pathway > positive symptoms
- Too little in PFC > negative symptoms
What is the Double Bind Theory?
Bateson et al (1956): contradictory messages are responsible for children having/developing SZ. The parenting type is known as the ‘Schizophrenogenic Mother’
What did Kuipers et al say about Expressed Emotion?
- Families with high expressed emotion can trigger psychotic episodes
- These families describe SZ relatives in hostile, critical terms
- EE levels in family/friends is strongly correlated with relapse rates
What did Noll et al say about Expressed Emotion?
- Negative emotions can trigger SZ episodes in vulnerable people. Supportive environments may be protective. This is a diathesis-stress model.
What are the three stages of Beck & Rector’s Cognitive Model?
Stage 1: Cognitive Processing Biases
Stage 2: Misattribution of consequences to causes
Stage 3: Failure to test reality with memory or logic
What is the cognitive process of Delusions?
Inadequate information processing > Egocentric Biases > Failure to contextualise events
