Psychosis Flashcards
what is psychosis?
a state defined by impaired contact with reality, general functioning and well-being OR a loss of contact with reality
Schizophrenia spectrum disorders - what?
all psychotic disorders bear similarity with SZ so they all come under the spectrum. SZ is the most prevalent. Most explanations and treatment for SZ are applicable to these too
a) schizoaffective = characterized by symptoms of SZ, and symptoms of a mood disorder, such as bipolar and MDD.
b) Schizotypal personality disorder - less severe form of SZ
c) Schizophreniform - short term SZ
incidence vs prevalence
Incidence is the rate of new (or newly diagnosed) cases of the disease
Prevalence is the actual number of cases alive, with the disease either during a period of time (period prevalence) or at a particular date in time (point prevalence)
LowSES & SZ; theory
1) Social causation theory -> stress of poverty causes the disorder
BUT it appears in all SES
SO
2) Is it the downward drift theory? = the disorder makes them fall in rank
But: no evidence to support downward drift in long-term data
Positive vs negative delusions & psychomotor symptoms
Positive = hallucinations, delusions, disorganised thinking and speech (something added on)
Negative = Poverty of speech, restricted affect, loss of volition & social withdrawal
psychomotor symptoms - awkward movements, repeated grimaces, odd, ritualistic behaviour (OCD link: OCD is a risk factor for SZ)
2 types of SZ (what, effect and cause)
People think that there should be 2 types of SZ:
Type 1 = positive symptoms (more likely to improve from the disorder & has biochemical abnormalities)
(relate to DT’s???)
Type 2 = Negative symptoms (more persistent cognitive deficits. May be tied to structural abnormalities) (in MDD theres reduction in blood flow to pfc, seen here too - volition & to reward system = loss of volition)
Biological views of SZ
Genetics
- received the most support
- Genetic factors: high genetic inheritance.
Biochemical abnormalities
• Dopamine hypothesis: DOPAMINE NEURONES FIRE TOO OFTEN AND TRANSMIT TOO MANY MESSAGES thus producing the symptoms of SZ (D-2 receptors)
^ the main suggestion for the cause of SZ
Problems with the dopamine hypothesis
- Second generation antipsychotic drugs = more effective than the normal ones
- The new drugs DO NOT BIND TO D-2 RECEPTORS but also to many D-1, D-4 receptors responsible for serotonin
- Suggesting that its abnormal activity of DOPAMINE AND OTHER neurotransmitters
**More complex models now also implicate additional (rather than alternative) neurotransmitters (e.g., GABA, serotonin) in the aetiology, rather than just DA alone
Abnormal brain structure
what & why?
- mainly linked to negative symptoms
- enlarged ventricles: atrophy/ lack of development?
- reduced reward pathway = MDD. Loss of volition
- loss of volume in amygdala and pfc = flat affect. MDD have high amyg activity = negative affect
maternal stress, excess dopamine damaging systems environmental factors,– pregnancy and delivery complications
ALWAYS CONSIDER THE DIATHESIS- STRESS MODEL
WHAT
The most popular explanation for schizophrenia – the ‘diathesis-stress’ model –>
– inherit a biological predisposition to schizophrenia
– is triggered by later exposure to extreme stress
- Disordered neuronal development –> cognitive, motor and social impairments provide vulnerability
- Stress leads to over activity of DA system –> pos symptoms (the greater the stress, increased risk of dysregulation and onset)
- Prolonged/recurrent stress = degeneration of neurons = structural damage = neg symptoms
Psychosocial factors
- substance use = enhances risk
- Stress
Psychological Views of SZ
Cognitive model
- congruent with bio in that hallucinations and related perceptual difficulties, the sufferers brain is producing strange and unreal sensations –> sensations triggered by bio factors.
- When people attempt to understand these unusual experiences, more features of the disorder begin to emerge. Misinterpretation of sensory problems
- Begin to dev delusions
- “rational path to madness” — tendency to jump to conclusions
- Dysfunctional schemas (poor self concept + low self esteem)
Cognitive model of delusions
- Delusions are extreme end of a continuum of ‘ordinary thoughts’
- cognitive distortions/hostility bias in interpretation of events
- the core of the model is an account of the way that causal attributions influence self-representations, which in turn influence future attributions: the attribution–self-representation cycle.
- We argue that biases in this cycle cause negative events to be attributed to external agents and hence contribute to the building of a paranoid world view
ToM in delusions
WHAT & evidence
• Difficulties monitoring own and representing other’s mental states
– May lead to delusions of paranoia and reference
– Reduced understanding of ToM (deception) jokes
(Marjoram et al., 2005)
– Reduced understanding of irony in SZ (diss)
– Deficits in inference of intentions and detection of
cognitive emotions (Craig et al., 2014)
BUT: show shame and awareness of others perceptions suggesting some ToM (McCabe et al., 2004)